Craniocerebral trauma

Introduction: Craniocerebral trauma Description of Craniocerebral trauma Craniocerebral trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., BRAIN; CRANIAL NERVES; MENINGES; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. Source: Diseases Database

Craniocerebral trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., BRAIN; $CRANIAL NERVES$; MENINGES; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. Source: MeSH 2007 http://www.rightdiagnosis.com/medical/craniocerebral_trauma.htm CRANIOCEREBRAL TRAUMA Craniocerebral trauma. The mechanical trauma of a skull causes a prelum (passing or permanent) a cerebral tissue, a tension and shift of its layers, passing sharp rising of intracranial pressure. Shift of cerebral substance can be accompanied by break of a cerebral tissue and vessels, a bruise of a brain. Usually these mechanical disturbances are supplemented with complex biochemical changes in a brain. Depending on, whether it is kept at a trauma an integrity of integuments of a skull and its tightness or they are broken, craniocerebral traumas section on closed and opened. The closed craniocerebral traumas traditionally divide into concussion, a bruise and a prelum; conditionally to them carry also a fracture of base of the skull and cracks of a crest at safety of an integument. The brain concussion is characterized by a triad of attributes: a loss of consciousness, a nausea or a vomiting, an amnesia. The focal neurologic symptomatology is absent. The bruise of a brain is diagnosed when the general cerebral signs are supplemented with attributes of a focal lesion of a brain. The bruise of a brain can arise both in a place of a trauma, and on the opposite party on the mechanism of a coutrecoup. Duration of a loss of consciousness at concussion - in most cases from several minutes up to tens. The prelum of a brain means development of a traumatic hematoma, more often subdural. At more simple there is " a light period ": the patient who has come to consciousness after a while again starts "to be loaded", becoming apathetic, flaccid, and then soporous. The fracture of base of the skull is inevitably accompanied by a bruise of a brain of this or that degree, characterized by penetration of a blood from a cavity of a skull in a nasopharynx, in periorbital tissues and under a conjunctiva, in a tympanic cavity (at an otoscopy cyanochroic painting of a tympanic membrane or its break is found out). The bleeding from a nose and ears can be consequence of a local trauma, therefore it is not a specific attribute of a fracture of base of the skull. In a peer measure " the sign of glasses " also quite often happens consequence of especially local trauma of the face. http://www.illnessofhuman.com/craniocerebral-trauma/

Background

Traumatic brain injury (TBI) continues to be an enormous public health problem, even with modern medicine in the 21st century. Most patients with TBI (75-80%) have mild head injuries; the remaining injuries are divided equally between moderate and severe categories. The cost to society of TBI is staggering, from both an economic and an emotional standpoint. Almost 100% of persons with severe head injury and as many as two thirds of those with moderate head injury will be permanently disabled in some fashion and will not return to their premorbid level of function. In the United States, the direct cost of care for patients with TBI, excluding inpatient care, is estimated at more than $25 billion annually. The impact is even greater when one considers that most severe head injuries occur in adolescents and young adults. TBI is associated with a catecholamine surge that results in an increased risk of infectious morbidity and mortality. As shown in an article by Schroeppel et al, the addition of multiple doses of betablockers dramatically reduces the mortality risk and significantly improves the patients chance for survival.[1] For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center, Back, Neck, and Head Injury Center, and Eye and Vision Center. Also, see eMedicine's patient education articles Concussion,Bicycle and Motorcycle Helmets, and Black Eye. Epidemiology Frequency The annual incidence of TBI in the United States has been estimated to be 180-220 cases per 100,000 population. In the United States, with a population of almost 300 million, approximately 600,000 new TBIs occur per year. As many as 10% of these injuries are fatal, resulting in almost 550,000 persons hospitalized annually in the United States with head injuries. Etiology While various mechanisms may cause TBI, the most common causes include motor vehicle accidents (eg, collisions between vehicles, pedestrians struck by motor vehicles, bicycle accidents), falls, assaults, sports-related injuries, and penetrating trauma. Motor vehicle accidents account for almost half of the TBIs in the United States, and in suburban/rural settings, they account for most TBIs. In cities with populations greater than 100,000, assaults, falls, and penetrating trauma are more common etiologies of head injury. The male-to-female ratio for TBI is nearly 2:1, and TBI is much more common in persons younger than 35 years. Motorcycle-related head injury Motorcycle-related head injuries deserve special mention. Motorcycle rights organizations dedicated to promoting safety and to preserving individual freedom suggest that safety should be a choice rather than a requirement; safety is a good choice, but individual motorcyclists should have the right to make a bad choice that ends in disaster if they so choose. A hallmark of the antihelmet movement is the argument that motorcyclists who do not wear helmets can perceive (ie, see and hear) their environment more effectively and, thus, can avoid impending accidents by anticipating them earlier. This argument is fallacious. Most accidents involving adult, otherwise responsible, motorcyclists are caused by moving objects hitting motorcyclists or by motorcyclists hitting a stationary object after being forced into an unusual position in an attempt to avoid something in their path. A full-face helmet restricts a relatively small portion of inconsequential downward and lateral peripheral vision. Similarly, it is highly improbable that a motorcyclist will hear an impending accident. A marginal increase in the ability to hear road noise and to see downward and laterally is not an improvement in the ability to avoid most accidents. The medical literature regarding motorcyclists head injury is clear. Head trauma is a devastating injury for motorcyclists a nd their families, and rehabilitation for survivors is prolonged and expensive. Injury expenses for motorcyclists who do not wear helmets far exceed that of motorcyclists who wear helmets. More importantly, the burden of caring for a motorcyclist with a head injury is frequently borne by the taxpayers, regardless of the insurance status of the injured motorcyclist. Pathophysiology Appropriate management of TBI requires an understanding of the pathophysiology of head injury. In addition to the obvious functional differences, the brain has several features that distinguish it from other organ systems. The most important of these differences is that the brain is contained within the skull, a rigid and inelastic container. Because the brain is housed within this inelastic container, only small increases in volume within the intracranial compartment can be tolerated before pressure within the compartment rises dramatically. This concept is defined by the Monro-Kellie doctrine, which states that the total intracranial volume is fixed because of the inelastic nature of the skull. The intracranial volume (V i/c) is equal to the sum of its components, as follows: V i/c = V (brain) + V (cerebrospinal fluid) + V (blood)

In the typical adult, the intracranial volume is approximately 1500 mL, of which the brain accounts for 85-90%, intravascular cerebral blood volume accounts for 10%, and cerebrospinal fluid (CSF) accounts for the remainder (< 3%). When a significant head injury occurs, cerebral edema often develops, which increases the relative volume of the brain. Because the intracranial volume is fixed, the pressure within this compartment rises unless some compensatory action occurs, such as a decrease in the volume of one of the other intracranial components. This is intimately related to the concept of intracranial compliance, which is defined as the change in pressure due to changes in volume. Compliance = Change in volume / change in pressure Compliance is based on the pressure volume index (PVI) within the intracranial compartment. The PVI describes the change in intracranial pressure (ICP) that occurs when a small amount of fluid is added to or withdrawn from the intracranial compartment. Simply stated, the brain has very limited compliance and cannot tolerate significant increases in volume that can result from diffuse cerebral edema or from significant mass lesions, such as a hematoma. The rationale for each treatment of head injury is based on the concept of the Monro-Kellie doctrine and how a particular intervention affects the intracranial compliance. When the volume of any of the components of the total intracranial volume is decreased, the ICP may be decreased. A second crucial concept in TBI pathophysiology is the concept of cerebral perfusion pressure (CPP). CPP is defined as the difference between the mean arterial pressure (MAP) and the ICP. CPP = MAP - ICP In practical terms, CPP is the net pressure of blood delivery to the brain. In the noninjured brain in individuals without long-standing hypertension, cerebral blood flow (CBF) is constant in the range of MAPs of 50-150 mm Hg. This is due to autoregulation by the arterioles, which will constrict or dilate within a specific range of blood pressure to maintain a constant amount of blood flow to the brain. When the MAP is less than 50 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate and blood flow becomes entirely dependent on the blood pressure, a situation defined as pressure-passive flow. The CBF is no longer constant but is dependent on and proportional to the CPP. Thus, when the MAP falls below 50 mm Hg, the brain is at risk of ischemia due to insufficient blood flow, while a MAP greater than 160 mm Hg causes excess CBF that may result in increased ICP. While autoregulation works well in the noninjured brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and, perhaps, globally in the injured brain. TBI may be divided into 2 categories, primary brain injury and secondary brain injury. Primary brain injury is defined as the initial injury to the brain as a direct result of the trauma. This is the initial structural injury caused by the impact on the brain, and, like other forms of neural injury, patients recover poorly. Secondary brain injury is defined as any subsequent injury to the brain after the initial insult. Secondary brain injury can result from systemic hypotension, hypoxia, elevated ICP, or as the biochemical result of a series of physiologic changes initiated by the original trauma. The treatment of head injury is directed at either preventing or minimizing secondary brain injury. Elevated ICP may result from the initial brain trauma or from secondary injury to the brain. In adults, normal ICP is considered 0-15 mm Hg. In young children, the upper limit of normal ICP is lower, and this limit may be considered 10 mm Hg. Elevations in ICP are deleterious because they can result in decreased CPP and decreased CBF, which, if severe enough, may result in cerebral ischemia. Severe elevations of ICP are dangerous because, in addition to creating a significant risk for ischemia, uncontrolled ICP may cause herniation. Herniation involves the movement of the brain across fixed dural structures, resulting in irreversible and often fatal cerebral injury. Maloney-Wilensky et al found that in patients with TBI, brain hypoxia as measured by brain tissue oxygen levels is associated with worse outcome.[2]Their review showed that, in 150 patients with severe TBI, those with brain tissue oxygen levels below 10 mm Hg had worse outcomes (odds ratio [OR], 4.0) and higher mortality (OR, 4.6). However, use of direct brain tissue oxygen probes proved to be safe, with only 2 adverse events in 292 patients. [2] The researchers suggest that treatment to increase brain tissue oxygen levels deserves investigation as a possible means of improving outcome in severe TBI. Presentation TBI may be divided into 2 broad categories, closed head injury and penetrating head injury. This is not purely a mechanistic division because some aspects of the treatment of these 2 types of TBIs differ. The clinical presentation of the patient with TBI varies significantly, from an ambulatory patient complaining of a sports-related head injury to the moribund patient arriving via helicopter following a high-speed motor vehicle accident. The Glasgow Coma Scale (GCS) developed by Jennett and Teasdale is used to describe the general level of consciousness of patients with TBI and to define broad categories of head injury.[3] The GCS is divided into 3 categories, eye opening (E), motor response (M), and verbal response (V). The score is determined by the sum of the score in each of the 3 categories, with a maximum score of 15 and a minimum score of 3, as follows: GCS score = E + M + V

Table 1. Glasgow Coma Scale (Open Table in a new window) Eye Opening Score 1 Year or Older 4 3 2 1 Spontaneously To verbal command To pain No response 0-1 Year Spontaneously To shout To pain No response

Best Motor Response Score 1 Year or Older 6 5 4 3 2 1 Obeys command Localizes pain Flexion withdrawal Flexion abnormal (decorticate) Extension (decerebrate) No response Localizes pain Flexion withdrawal Flexion abnormal (decorticate) Extension (decerebrate) No response 0-1 Year

Best Verbal Response Score >5 Years 5 4 3 2 Oriented and converses 2-5 Years Appropriate words 0-2 Years Cries appropriately

Disoriented and converses Inappropriate words Cries Inappropriate words; cries Incomprehensible sounds Screams Grunts Inappropriate crying/screaming Grunts

No response

No response

No response

Patients who are intubated are unable to speak, and their verbal score cannot be assessed. They are evaluated only with eye opening and motor scores, and the suffix T is added to their score to indicate intubation. In intubated patients, the maximal GCS score is 10T and the minimum score is 2T. The GCS is often used to help define the severity of TBI. Mild head injuries are generally defined as those associated with a GCS score of 13-15, and moderate head injuries are those associated with a GCS score of 9-12. A GCS score of 8 or less defines a severe head injury. These definitions are not rigid and should be considered as a general guide to the level of injury. Indications Traumatic injury and brain failure As a type of organ system failure, brain failure invariably affects consciousness. Consciousness is structurally produced in the cerebral hemispheres, including the pons and the medulla. These structures are all interconnected by the reticular formation, which begins in the medulla and extends to the midbrain, where it forms the reticular activating system. This pathway modulates the perception of events and controls integrated responses. Clinical evaluation of consciousness states is heavily dependent on the findings from the physical examination. When the physical examination yields visual and palpable clues to the integrity of consciousness, impairment thereof may be classified into one of the following categories:

Cloudy consciousness: This state is defined as a mild deficit in the speed of information processing by the brain. This results from macrotearing and histological-level disruption of cell-to-cell connectivity occurring throughout the brain disrupting physical connectivity between brain regions, exacerbated by vascular compromise of a mechanical and/or biochemical nature causing islands of nonfunctional or impaired tissue in the brain parenchyma. Cloudy consciousness may be noted after mild-to-moderate head trauma and may persist for several months. Memory of recent events is often diminished, but long-term memory typically remains intact. Lethargy: This state is defined as a decrease in alertness, resulting in impaired ability to perform tasks that are normally accomplished without effort. Patients rouse briefly in response to stimuli and then settle back into inactivity when left alone. They retain awareness of their immediate environment. Obtundation: This state is defined as a decrease in awareness and alertness, in which patients rouse briefly in response to stimuli and follow simple commands but are unaware of their immediate surroundings. When stimulation ceases, they settle back into inactivity. Stupor: In this state, patients cannot communicate clearly but can be aroused by continued painful stimulation. Arousal may be manifested only as withdrawal from painful stimuli. As soon as stimuli are removed, the patient settles back into inactivity. Coma: In this state, patients do not respond to even the most vigorous stimuli. Brain death: This state is equivalent to functional decapitation and is characterized by irreversible cessation of whole-brain function and hemisphere and brainstem function. The efficacy of the physical examination in the evaluation of consciousness diminishes when visual clues disappear (eg, during heavy sedation, therapeutic musculoskeletal paralysis). In such situations, monitoring of cerebral function by compressed spectral array is helpful in assessing the effect of therapy on neuronal function. Processed electroencephalogram (compressed spectral array) in consciousness assessment The processed electroencephalogram (EEG) does not require as many head electrodes to generate a satisfactory signal that can be used for clinical data in the intensive care unit (ICU). Brain wave monitoring by portable, noninvasive computer processed monitors allow quick recognition of some brain functions under titrated suspended animation in real time. These parameters are not effectively evaluated by raw signal EEG monitors, but some progress has been made using computerized processed signal EEGs. Advantages of the processed EEG during neuromuscular blockade are that data are more easily interpreted by clinicians not specifically trained in electroencephalography. The continuum from wakefulness to sleep involves a progressive decrease in the alpha band followed by increased activity in the beta, theta, and delta bands. The alpha rhythm contains waves of 8-12 Hz and is very responsive to volitional mental activity, increasing with excitement and decreasing with tranquility. These rhythms occur mainly in the posterior head and are the predominant brain activity in the normal brain. A technique has been developed to simplify pattern recognition and interpretation of the brain electrical activity using the key word SAFE:

S - SYMMETRY - Compare the pattern of asymmetrical patterns. Can indicate diminished perfusion to one hemisphere, cerebral embolism, or thrombosis. A - AMPLITUDE - Compare the altitude of the vectors. Asymmetric hemispherical amplitude suggests agitation under paralysis. Low amplitude suggests sedation and quiescence. F - FREQUENCY - Compare the distribution of vectors throughout all frequency bands. Absent or attenuated activity in the conscious side suggests sedation or anesthesia. E - EDGE - Observe the activity edge. Significant dips in one hemisphere compared to the other suggest focal brain ischemia. Agitation is represented by linear activity depicting intensity of brain activity and position of this activity within the brain topography. Sedation can be effectively titrated until this activity is reduced to normalcy using continuous infusion of sedative agents, while ensuring patient comfort under paralysis as the search for underlying pathology follows. Different classifications and combinations of

sedatives, analgesics, or antipsychotics can be tried until the combination that brings about the most appropriately calm cerebral function tracing is discovered. Attention can then be turned to protecting other organs from damage. Relevant Anatomy Several aspects of neuroanatomy and neurophysiology require review in a discussion of TBI. Although a comprehensive review of neuroanatomy is beyond the scope of this discussion, a few key concepts are reviewed. The brain essentially floats within the CSF; as a result, the brain can undergo significant translation and deformation when the head is subjected to significant forces. In a deceleration injury, in which the head impacts a stationary object, such as the windshield of a car, the skull stops moving almost instantly. However, the brain continues to move within the skull toward the direction of the impact for a very brief period after the head has stopped moving. This results in significant forces acting on the brain as it undergoes both translation and deformation. In an acceleration injury, as in a direct blow to the head, the force applied to the skull causes the skull to move away from the applied force. The brain does not move with the skull, and the skull impacts the brain, causing translation and deformation of the brain. The forces that result from either deceleration or acceleration of the brain can cause injury by direct mechanical effects on the various cellular components of the brain or by shear-type forces on axons. In addition to the translational forces, the brain can experience significant rotational forces, which can also lead to shear injuries. The intracranial compartment is divided into 3 compartments by 2 major dural structures, the falx cerebri and the tentorium cerebelli. The tentorium cerebelli divides the posterior fossa or infratentorial compartment (the cerebellum and the brainstem) from the supratentorial compartment (cerebral hemispheres). The falx cerebri divides the supratentorial compartment into 2 halves and separates the left and right hemispheres of the brain. Both the falx and the tentorium have central openings and prominent edges at the borders of each of these openings. When a significant increase in ICP occurs, caused by either a large mass lesion or significant cerebral edema, the brain can slide through these openings within the falx or the tentorium, a phenomenon known as herniation. As the brain slides over the free dural edges of the tentorium or the falx, it is frequently injured by the dural edge. Several types of herniation exist, as follows: (1) transtentorial herniation, (2) subfalcine herniation, (3) central herniation, (4) upward herniation, and (5) tonsillar herniation. Transtentorial herniation occurs when the medial aspect of the temporal lobe (uncus) migrates across the free edge of the tentorium. This causes pressure on the third cranial nerve, interrupting parasympathetic input to the eye and resulting in a dilated pupil. This unilateral dilated pupil is the classic sign of transtentorial herniation and usually (80%) occurs ipsilateral to the side of the transtentorial herniation. In addition to pressure on the third cranial nerve, transtentorial herniation compresses the brainstem. Subfalcine herniation occurs when the cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx. This may compromise the blood flow through the anterior cerebral artery complexes, which are located on the medial side of each frontal lobe. Subfalcine herniation does not cause the same brainstem effects as those caused by transtentorial herniation. Central herniation occurs when a diffuse increase in ICP occurs and each of the cerebral hemispheres is displaced through the tentorium, resulting in significant pressure on the upper brainstem. Upward, or cerebellar, herniation occurs when either a large mass or an increased pressure in the posterior fossa is present and the cerebellum is displaced in an upward direction through the tentorial opening. This also causes significant upper brainstem compression. Tonsillar herniation occurs when increased pressure develops in the posterior fossa. In this form of herniation, the cerebellar tonsils are displaced in a downward direction through the foramen magnum, causing compression on the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum. Another aspect of the intracranial anatomy that has a significant role in TBI is the irregular surface of the skull underlying the frontal and temporal lobes. These surfaces contain numerous ridges that can cause injury to the inferior aspect of the frontal lobes and the temporal lobes as the brain glides over these irregular ridges following impact. Typically, these ridges cause cerebral contusions. The roof of the orbit has many ridges, and, as a result, the inferior frontal lobe is one of the most common sites of traumatic cerebral contusions. Laboratory Studies After the patient has been stabilized and an appropriate neurologic examination has been conducted, the diagnostic evaluation may begin. Patients with TBI do not require any additional blood tests beyond the standard panel of tests obtained in all trauma patients. A urine toxicology screen and an assessment of the blood alcohol level are important for any patient who has an altered level of consciousness because any central nervous system depressant can impair consciousness. Imaging Studies

Skull radiographs Once an important part of the head injury evaluation, skull radiographs have been replaced by CT scans and are rarely used in patients with closed head injury. Skull radiographs are occasionally used in the evaluation of penetrating head trauma, and they can help provide a rapid assessment of the degree of foreign body penetration in nonmissile penetrating head injuries (eg, stab wounds). Skull radiographs are sometimes used in patients with gunshot wounds to the head to screen for retained intracranial bullet fragments. CT scan A CT scan is the diagnostic study of choice in the evaluation of TBI because it has a rapid acquisition time, is universally available, is easy to interpret, and is reliable. When first introduced more than 25 years ago, CT scans of the brain required almost 30 minutes to complete. This acquisition time has decreased steadily; the current generation of ultrafast CT scanners can perform a head CT scan in less than 1 minute, faster than the time required to enter patient's demographic data into the scanner. The standard CT scan for the evaluation of acute head injury is a noncontrast scan that spans from the base of the occiput to the top of the vertex in 5-mm increments. Three data sets are obtained from the primary scan, as follows: (1) bone windows, (2) tissue windows, and (3) subdural windows. These different types of exposure are necessary because of the significant difference in exposure necessary to visualize various intracranial structures. The bone windows allow for a detailed survey of the bony anatomy of the skull, and the tissue windows allow for a detailed survey of the brain and its contents. The subdural windows provide better visualization of intracranial hemorrhage, especially those hemorrhages adjacent to the brain (eg, subdural hematomas). Each intracranial structure has a characteristic density, which is expressed in Hounsfield units. These units are defined according to a scale that ranges from (-) 1000 units to (+) 1000 units. Air is assigned a density of (-) 1000 units, water is assigned a density of 0 units, and bone has a density of (+) 1000 units. On this scale, CSF has a density of (+) 4 to (+) 10 units, white matter has a density of (+) 22 to (+) 36 units, and gray matter has a density of (+) 32 to (+) 46 units. Extravascular blood has a density of (+) 50 to (+) 90 units, and calcified tissue and bone have a density of (+) 800 to (+) 1000 units. When reviewing a CT scan, using a systematic approach and following this same protocol each time are important. Consistency is much more important than the specific order used.

First, examine the bone windows for fractures, beginning with the cranial vault and then examining the skull base and the facial bones. Next, examine the tissue windows for the presence of (1) extra-axial hematomas (eg, epidural hematomas, subdural hematomas), (2) intraparenchymal hematomas, or (3) contusions. Next, survey the brain for any evidence of pneumocephalus, hydrocephalus, cerebral edema, midline shift, or compression of the subarachnoid cisterns at the base of the brain. Finally, examine the subdural windows for any hemorrhage that may not be visualized easily on the tissue windows. Skull fractures may be classified as either linear or comminuted fractures. Linear skull fractures are sometimes difficult to visualize on the individual axial images of a CT scan. The scout film of the CT scan, which is the equivalent of a lateral skull x-ray film, often demonstrates linear fractures. The intracranial sutures are easily mistaken for small linear fractures. However, the sutures have characteristic locations in the skull and have a symmetric suture line on the opposite side. Small diploic veins, which traverse the skull, may also be interpreted as fractures. Comminuted fractures are complex fractures with multiple components. Comminuted fractures may be displaced inwardly; this is defined as a depressed skull fracture. Extra-axial hematomas include epidural and subdural hematomas. Epidural hematomas are located between the inner table of the skull and the dura. They are typically biconvex in shape because their outer border follows the inner table of the skull and their inner border is limited by locations at which the dura is firmly adherent to the skull. Epidural hematomas are usually caused by injury to an artery, although 10% of epidural hematomas may be venous in origin. The most common cause of an epidural hematoma is a linear skull fracture that passes through an arterial channel in the bone. The classic example of this is the temporal epidural hematoma caused by a fracture through the course of the middle meningeal artery. Epidural hematomas, especially those of arterial origin, tend to enlarge rapidly. Subdural hematomas are located between the dura and the brain. Their outer edge is convex, while their inner border is usually irregularly concave. Subdural hematomas are not limited by the intracranial suture lines; this is an important feature that aids in their differentiation from epidural hematomas. Subdural hematomas are usually venous in origin, although some subdural hematomas are caused by arterial injuries. The classic cause of a posttraumatic subdural hematoma is an injury to one of the bridging veins that travel from the cerebral cortex to the dura. As the brain atrophies over time, the bridging veins become more exposed and, as a result, are more easily injured. Occasionally, the distinction between a subdural and an epidural hematoma can be difficult. The size of an extra-axial hematoma is a more important factor than whether the blood is epidural or subdural in location. In addition, a mixed hematoma with both a subdural and an epidural component is not uncommon.

Intra-axial hematomas are defined as hemorrhages within the brain parenchyma. These hematomas include intraparenchymal hematomas, intraventricular hemorrhages, and subarachnoid hemorrhages. Subarachnoid hemorrhages that occur because of trauma are typically located over gyri on the convexity of the brain. The subarachnoid hemorrhages that result from a ruptured cerebral aneurysm are usually located in the subarachnoid cisterns at the base of the brain. Cerebral contusions are posttraumatic lesions in the brain that appear as irregular regions, in which highdensity changes (ie, blood) and low-density changes (ie, edema) are present. Frequently, 1 of these 2 types of changes predominates within a particular contusion. Contusions are most often caused by the brain gliding over rough surfaces, such as the rough portions of the skull that are present under the frontal and temporal lobes. CT scans may be used for classification and for diagnostic purposes. Marshall et al published a classification scheme that classifies head injuries according to the changes demonstrated on CT scan images.[4] This system defines 4 categories of injury, from diffuse injury I to diffuse injury IV.

In diffuse injury I, evidence of any significant brain injury is lacking. In diffuse injury II, either no midline shift or a shift of less than 5 mm is present and the CSF cisterns at the base of the brain are widely patent. In addition, no high-density or mixed-density lesions (contusions) of greater than 25 mL in volume are present. In diffuse injury III, a midline shift of less than 5 mm is present, with partial compression or absence of the basal cisterns. No high- or mixed-density lesions with a volume greater than 25 mL are present. Diffuse injury IV is defined as midline shift greater than 5 mm with compression or absence of the basal cisterns and no lesions of high or mixed density greater than 25 mL MRI MRI has a limited role in the evaluation of acute head injury. Although MRI provides extraordinary anatomic detail, it is not commonly used to evaluate acute head injuries because of its long acquisition times and the difficulty in obtaining MRIs in persons who are critically ill. However, MRI is used in the subacute setting to evaluate patients with unexplained neurologic deficits. MRI is superior to CT scan for helping identify diffuse axonal injury (DAI) and small intraparenchymal contusions. DAI is defined as neuronal injury in the subcortical gray matter or the brainstem as a result of severe rotation or deceleration. DAI is often the reason for a severely depressed level of consciousness in patients who lack evidence of significant injury on CT scan images and have an ICP that is within the reference range. Magnetic resonance angiography may be used in some patients with TBI to assess for arterial injury or venous sinus occlusion. Angiography Once a common diagnostic study in persons with acute head injury, angiography is rarely used in the evaluation of acute head injury today. However, conventional angiography has been the screening and diagnostic modality of choice for identifying blunt cerebrovascular injuries (BCVI) in trauma patients.[5] Before the development of the CT scan, cerebral angiography provided a reliable means for demonstrating the presence of an intracranial mass lesion. Angiography in used in acute head injury only when a vascular injury may be present. This includes patients with unexplained neurologic deficits, especially in the setting of temporal bone fractures, and patients with clinical evidence of a potential carotid injury (eg, hemiparesis, Horner syndrome). Goodwin et al found that conventional angiography is more accurate than 16- or 64-slice CT angiography as a screening tool for BCVI in trauma patients.[5]In a prospective study, 158 patients underwent CT angiography (16-slice or 64-slice) at the time of injury assessment, followed 24-48 hours later with conventional angiography of the cerebral vasculature. CT angiography detected only 13 true cerebrovascular injuries (40.6%) in 12 patients, whereas conventional angiography identified 32 injuries in 27 patients.[5] For detection of cerebrovascular injury, CT angiography had a sensitivity of 0.97 (95% confidence interval [CI], 0.92-0.99) and a specificity of 0.41 (95% CI, 0.22-0.61). A study by Emmett et al confirmed that angiography is the criterion standard for BCVI diagnosis, but that CT angiography should be added as a screening criterion in order to capture BCVI that goes unrecognized in asymptomatic trauma patients.[6] Other Tests Initial clinical evaluation The initial evaluation of patients with TBI involves a thorough systemic trauma evaluation according to the advanced trauma life support (ATLS) guidelines. Once this has been completed and the patient is stable from a cardiopulmonary standpoint, attention may be directed to a focused head injury evaluation. The evaluation of the spine for potential injury is critically important in patients with TBI because approximately 10% of those with severe head injuries have a concomitant spine injury. Many of these injuries are cervical spine injuries.

Attempt to obtain a thorough history of the mechanism of the trauma and the events immediately preceding the trauma. Specific information, such as the occurrence of syncope or the onset of a seizure prior to a fall or a motor vehicle accident, prompts a more extended evaluation of the etiology of such an event. Because many patients with TBI have altered levels of consciousness, the history is often provided by family members, police officers, paramedics, or witnesses. Neurologic assessment After sufficient information has been obtained regarding patient history, appropriate physical and neurologic examinations are performed. The neurologic assessment begins with ascertaining the GCS score. This is a screening examination and does not substitute for a thorough neurologic examination. In addition to determining the GCS score, the neurologic assessment of patients with TBI should include the following:

Brainstem examination Pupillary examination, ocular movement examination, corneal reflex, gag reflex Motor examination Sensory examination Reflex examination Many patients with TBI have significant alterations of consciousness and/or pharmaceuticals present that limit the scope of the neurologic examination. When such factors limit the neurologic examination, noting their presence is important. Pupillary examination A careful pupillary examination is a critical part of the evaluation of patients with TBI, especially in patients with severe injuries. When muscle relaxants have been administered to a patient, the only aspect of the neurologic examination that may be evaluated is the pupillary examination. Several factors can alter the pupillary examination results. Narcotics cause pupillary constriction (meiosis), and medications or drugs that have sympathomimetic properties cause pupillary dilation (mydriasis). These effects are often strong enough to blunt or practically eliminate pupillary responses. Prior eye surgery, such as cataract surgery, can also alter or eliminate pupillary reactivity. Proper assessment of the pupillary response requires the use of a strong light source to override any of the potential factors that may affect pupillary reaction. Each pupil must be assessed individually, with at least 10 seconds between assessment of each eye to allow consensual responses to fade prior to stimulating the opposite eye. A normal pupillary examination result consists of bilaterally reactive pupils that react to both direct and consensual stimuli. Bilateral small pupils can be caused by narcotics, pontine injury (due to disruption of sympathetic centers in the pons), or early central herniation (mass effect on the pons). Bilateral fixed and dilated pupils are secondary to inadequate cerebral perfusion. This can result from diffuse cerebral hypoxia or severe elevations of ICP preventing adequate blood flow into the brain. Pupils that are fixed and dilated usually indicate an irreversible injury. If due to systemic hypoxia, the pupils sometimes recover reactivity when adequate oxygenation is restored. A unilateral fixed (unresponsive) and dilated pupil has many potential causes. A pupil that does not constrict when light is directed at the pupil but constricts when light is directed into the contralateral pupil (intact consensual response) is indicative of a traumatic optic nerve injury. A unilateral dilated pupil that does not respond to either direct or consensual stimulation usually indicates transtentorial herniation. Unilateral constriction of a pupil is usually secondary to Horner syndrome, in which the sympathetic input to the eye is disrupted and the pupil constricts due to more parasympathetic than sympathetic stimulation. In patients with TBI, Horner syndrome may be caused by an injury to the sympathetic chain at the apex of the lung or a carotid artery injury. A unilateral constricted pupil can be caused by a unilateral brainstem injury, but this is quite rare. A core optic pupil is a pupil that appears irregular in shape. This is caused by a lack of coordination of contraction of the muscle fibers of the iris and is associated with midbrain injuries. Ocular movement examination When the patient's level of consciousness is altered significantly, a loss of voluntary eye movements often occurs and abnormalities in ocular movements are frequently present. These abnormalities can provide specific clues to the extent and location of injury.

Ocular movements involve the coordination of multiple centers in the brain, including the frontal eye fields, the paramedian pontine reticular formation (PPRF), the medial longitudinal fasciculus (MLF), and the nuclei of the third and sixth cranial nerves. In patients in whom voluntary eye movements cannot be assessed, oculocephalic and oculovestibular testing may be performed. Oculocephalic testing Oculocephalic testing (doll's eyes) involves observation of eye movements when the head is turned from side to side. This maneuver helps assess the integrity of the horizontal gaze centers. Before performing oculocephalic testing, the status of the cervical spine must be established. If a cervical spine injury has not been excluded reliably, oculocephalic testing should not be performed. When assessing oculocephalic movements, the head is elevated to 30 from horizontal and is rotated briskly from side to side. A normal response is for the eyes to turn away from the direction of the movement as if they are fixating on a target that is straight ahead. This is similar to the way a doll's eyes move when the head is turned; this is the origin of the term doll's eyes. If the eyes remain fixed in position and do not rotate with the head, this is indicative of dysfunction in the lateral gaze centers and is referred to as negative doll's eyes. Some patients may have negative doll's eyes and normal oculovestibular reflexes. Oculovestibular testing Oculovestibular testing, also known as cold calorics, is another method for assessment of the integrity of the gaze centers. Oculovestibular testing is performed with the head elevated to 30 from horizontal to bring the horizontal semicircular canal into the vertical position. Oculovestibular testing requires the presence of an intact tympanic membrane; this must be assessed before beginning the test. In oculovestibular testing, 20 mL of ice-cold water is instilled slowly into the auditory canal. If is no response occurs within 60 seconds, the test is repeated with 40 mL of cold water. When cold water is irrigated into the external auditory canal, the temperature of the endolymph falls and the fluid begins to settle. This causes an imbalance in the vestibular signals and initiates a compensatory response. Cold-water irrigation in the ear of an alert patient results in a fast nystagmusaway from the irrigated ear and a slow compensatory nystagmus toward the irrigated side. If warm water is used, the opposite will occur; the fast component of nystagmus will be toward the irrigated side, and the slow component will be away from the irrigated side. This is the basis for the acronym COWS, which stands for cold opposite, warm same. This refers to the direction of the fast component of nystagmus. As the level of consciousness declines, the fast component of nystagmus fades gradually. Thus, in unconscious patients, only the slow phase of nystagmus may be evaluated. A normal oculocephalic response to cold-water calorics (ie, eye deviation toward the side of irrigation) indicates that the injury spares the PPRF, the MLF, and third and sixth cranial nerve nuclei. This means that the level of injury must be rostral to the reticular activating system in the upper brainstem. If a unilateral frontal lobe injury is present, the eyes are deviated toward the side of injury prior to caloric testing. Cold-water irrigation of the opposite ear results in a normal response to caloric testing (ie, eye deviation toward the irrigated side) because the injury is in the frontal region and spares the pontine gaze centers. When a pontine injury is present, the eyes often deviate away from the side of injury. In this situation, cold-water irrigation of the contralateral ear does not cause the gaze to deviate toward the irrigated ear because an injury has occurred at the level of the pons and the pontine gaze centers are compromised. A dysconjugate response to caloric testing suggests an injury to either the third or sixth cranial nerves or an injury to the MLF, resulting in an internuclear ophthalmoplegia. If caloric testing causes a skew deviation, in which the eyes are dysconjugate in the vertical direction, this indicates a lesion in the brainstem. The exact location of injury that results in skew deviation is not known. Motor examination After completing the brainstem examination, a motor examination should be performed. A thorough motor or sensory examination is difficult to perform in any patient with an altered level of consciousness.

When a patient is not alert enough to cooperate with strength testing, the motor examination is limited to an assessment of asymmetry in the motor examination findings. This may be demonstrated by an asymmetric response to central pain stimulation or a difference in muscle tone between the left and right sides. A finding of significant asymmetry during the motor examination may be indicative of a hemispheric injury and raises the possibility of a mass lesion. Sensory examination Performing a useful sensory examination in patients with TBI is often difficult. Patients with altered levels of consciousness are unable to cooperate with sensory testing, and findings from a sensory examination are not reliable in patients who are intoxicated or comatose. Peripheral reflex examination A peripheral reflex examination can be useful to help identify gross asymmetry in the neurologic examination. This may indicate the presence of a hemispheric mass lesion. Other factors Notably, Ley et al have suggested that diabetic patients with moderate-to-severe TBI are increased risk of mortality, with the likely contributing factor being insulin deficiency.[7] Intracranial hypertension (ICH) and cerebral hypoperfusion (CH) are secondary insults in patients with TBI that are hard to predict. Stein et al conducted a study to determine whether cytokine levels are indicative of impending ICH or CH in patients with severe TBI. They found that interleukin 8 (IL-8) shows the most promise as a potential biomarker of impending ICH and CH. Results showed higher serum IL-8 levels in patients with poor neurologic outcome and a moderate correlation between serum IL-8 levels with ICH and CH and between cerebrospinal fluid (CSF) levels of IL-8 and cerebral perfusion pressure (CPP).[8] Medical Therapy The treatment of head injury may be divided into the treatment of closed head injury and the treatment of penetrating head injury. While significant overlap exists between the treatments of these 2 types of injury, some important differences are discussed. Closed head injury treatment is divided further into the treatment of mild, moderate, and severe head injuries. Mild head injury Most head injuries are mild head injuries. Most people presenting with mild head injuries will not have any progression of their head injury; however, up to 3% of mild head injuries progress to more serious injuries. Mild head injuries may be separated into low-risk and moderate-risk groups. Patients with mild-to-moderate headaches, dizziness, and nausea are considered to have low-risk injuries. Many of these patients require only minimal observation after they are assessed carefully, and many do not require radiographic evaluation. These patients may be discharged if a reliable individual can monitor them. Patients who are discharged after mild head injury should be given an instruction sheet for head injury care. The sheet should explain that the person with the head injury should be awakened every 2 hours and assessed neurologically. Caregivers should be instructed to seek medical attention if patients develop severe headaches, persistent nausea and vomiting, seizures, confusion or unusual behavior, or watery discharge from either the nose or the ear. Patients with mild head injuries typically have concussions. A concussion is defined as physiologic injury to the brain without any evidence of structural alteration. Concussions are graded on a scale of I-V. A grade I concussion is one in which a person is confused temporarily but does not display any memory changes. In a grade II concussion, brief disorientation and anterograde amnesia of less than 5 minutes' duration are present. In a grade III concussion, retrograde amnesia and loss of consciousness for less than 5 minutes are present, in addition to the 2 criteria for a grade II concussion. Grade IV and grade V concussions are similar to a grade III, except that in a grade IV concussion, the duration of loss of consciousness is 5-10 minutes, and in a grade V concussion, the loss of consciousness is longer than 10 minutes. As many as 30% of patients who experience a concussion develop postconcussive syndrome (PCS). PCS consists of a persistence of any combination of the following after a head injury: headache, nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances. Fixed neurologic deficits are not part of PCS, and any patient with a fixed deficit requires careful evaluation. PCS usually lasts 2-4 months. Typically, the symptoms peak 4-6 weeks following the injury. On occasion, the symptoms of PCS last for a year or longer. Approximately 20% of adults with PCS will not have returned to full-time work 1 year after the initial injury, and some are disabled permanently by PCS. PCS tends to be more severe in children than in adults. When PCS is severe or persistent, a multidisciplinary approach to treatment may be necessary. This includes social services, mental health services, occupational therapy, and pharmaceutical therapy.

After a mild head injury, those displaying persistent emesis, severe headache, anterograde amnesia, loss of consciousness, or signs of intoxication by drugs or alcohol are considered to have a moderate-risk head injury. These patients should be evaluated with a head CT scan. Patients with moderate-risk mild head injuries can be discharged if their CT scan findings reveal no pathology, their intoxication is cleared, and they have been observed for at least 8 hours. Moderate and severe head injury The treatment of moderate and severe head injuries begins with initial cardiopulmonary stabilization by ATLS guidelines. The initial resuscitation of a patient with a head injury is of critical importance to prevent hypoxia and hypotension. In the Traumatic Coma Data Bank study, patients with head injury who presented to the hospital with hypotension had twice the mortality rate of patients who did not present with hypotension. The combination of hypoxia and hypotension resulted in a mortality rate 2.5 times greater than if neither of these factors was present. Once a patient has been stabilized from the cardiopulmonary standpoint, evaluation of their neurologic status may begin. The initial GCS score provides a classification system for patients with head injuries but does not substitute for a neurologic examination. After assessment of the coma score, a neurologic examination should be performed. If a patient has received muscle relaxants, the only neurologic response that may be evaluated is the pupillary response. After a thorough neurologic assessment has been performed, a CT scan of the head is obtained. The results of the CT scan help determine the next step. If a surgical lesion is present, arrangements are made for immediate transport to the operating room. Fewer than 10% of patients with TBI have an initial surgical lesion. Although no strict guidelines exist for defining surgical lesions in persons with head injury, most neurosurgeons consider any of the following to represent indications for surgery in patients with head injuries: extra-axial hematoma with midline shift greater than 5 mm, intra-axial hematoma with volume greater than 30 mL, an open skull fracture, or a depressed skull fracture with more than 1 cm of inward displacement. In addition, any temporal or cerebellar hematoma that is larger than 3 cm in diameter is considered a high-risk hematoma because these regions of the brain are smaller and do not tolerate additional mass as well as the frontal, parietal, and occipital lobes. These high-risk temporal and cerebellar hematomas are usually evacuated immediately If no surgical lesion is present on the CT scan image, or following surgery if one is present, treatment of the head injury begins. The first phase of treatment is to institute general measures. Once appropriate fluid resuscitation has been completed and the volume status is determined to be normal, intravenous fluids are administered to maintain the patient in a state of euvolemia or mild hypervolemia. A previous tenet of head injury treatment was fluid restriction, which was believed to limit the development of cerebral edema and increased ICP. Fluid restriction decreases intravascular volume and, therefore, decreases cardiac output. A decrease in cardiac output often results in decreased cerebral flow, which results in decreased brain perfusion and may cause an increase in cerebral edema and ICP. Thus, fluid restriction is contraindicated in patients with TBI. Another supportive measure used to treat patients with head injuries is elevation of the head. When the head of the bed is elevated to 20-30, the venous outflow from the brain is improved, thus helping to reduce ICP. If a patient is hypovolemic, elevation of the head may cause a drop in cardiac output and CBF; therefore, the head of the bed is not elevated in hypovolemic patients. In addition, the head should not be elevated (1) in patients in whom a spine injury is a possibility or (2) until an unstable spine has been stabilized. Sedation is often necessary in patients with traumatic injury. Some patients with moderate head injuries have significant agitation and require sedation. In addition, patients with multisystem trauma often have painful systemic injuries that require pain medication, and many intubated patients require sedation. Short-acting sedatives and analgesics should be used to accomplish proper sedation without eliminating the ability to perform periodic neurologic assessments. This requires careful titration of medication doses and periodic weaning or withholding of sedation to allow periodic neurologic assessment. The use of anticonvulsants in patients with TBI is a controversial issue. No evidence exists that the use of anticonvulsants decreases the incidence of late-onset seizures in patients with either closed head injury or TBI. Temkin et al demonstrated that the routine use of Dilantin in the first week following TBI decreases the incidence of early-onset (within 7 d of injury) seizures but does not change the incidence of late-onset seizures.[9] In addition, the prevention of early posttraumatic seizures does not improve the outcome following TBI. Therefore, the prophylactic use of anticonvulsants is not recommended for more than 7 days following TBI and is considered optional in the first week following TBI. After instituting general supportive measures, the issue of ICP monitoring is addressed. ICP monitoring has consistently been shown to improve outcome in patients with head injuries. ICP monitoring is indicated for any patient with a GCS score less than 9, any patient with a head injury who requires prolonged deep sedation or pharmacologic relaxants for a systemic condition, or any patient with an acute head injury who is undergoing extended general anesthesia for a nonneurosurgical procedure. ICP monitoring involves placement of an invasive probe to measure the ICP. Unfortunately, noninvasive means of monitoring ICP do not exist, although they are under development. ICP may be monitored by means of an intraparenchymal monitor, an intraventricular monitor (ventriculostomy), or an epidural monitor. These devices measure ICP by fluid manometry, strain-gauge technology, or fiberoptic technology.

Intraparenchymal ICP monitors are devices that are placed into the brain parenchyma to measure ICP by means of fiberoptic, strain-gauge, or other technologies. The intraparenchymal monitors are very accurate; however, they do not allow for drainage of CSF. Epidural devices measure ICP via a strain-gauge device placed through the skull into the epidural space. This is an older form of ICP measurement and is rarely used today because the other technologies available are more accurate and more reliable. A ventriculostomy is a catheter placed through a small twist drill hole into the lateral ventricle. The ICP is measured by transducing the pressure in a fluid column. Ventriculostomies allow for drainage of CSF, which can be effective in decreasing the ICP. A risk of symptomatic hemorrhage exists with ventriculostomy placement, and Bauer et al report from a retrospective study that an international normalized ratio (INR) of 1.2-1.6 is an acceptable range for emergent ventriculostomy placement in patients with TBI.[10] Once an ICP monitor has been placed, ICP is monitored continuously. No absolute value of ICP exists for which treatment is implemented automatically. In adults, the reference range of ICP is 0-15 mm Hg. The normal ICP waveform is a triphasic wave, in which the first peak is the largest peak and the second and third peaks are progressively smaller. When intracranial compliance is abnormal, the second and third peaks are usually larger than the first peak. In addition, when intracranial compliance is abnormal and ICP is elevated, pathologic waves may appear. Lundberg described 3 types of abnormal ICP waves, A, B, and C waves. [11]Lundberg A waves, known as plateau waves, have a duration of 5-20 minutes and an amplitude of 50 mm Hg over the baseline ICP. After an episode of A waves dissipates, the ICP is reset to a baseline level that is higher than when the waves began. Lundberg A waves are a sign of severely compromised intracranial compliance. The rapid increase in ICP caused by these waves can result in a significant decrease in CPP and may lead to herniation. Lundberg B waves have a duration of less than 2 minutes, and they have an amplitude of 10-20 mm Hg above the baseline ICP. B waves are also related to abnormal intracranial compliance. Because of their smaller amplitude and shorter duration, B waves are not as deleterious as A waves. C waves, known as Hering-Traube waves, are low-amplitude waves that may be superimposed on other waves. They may be related to increased ICP; however, C waves can also occur in the setting of normal ICP and compliance. When treating elevated ICP, remember that the goal of treatment is to optimize conditions within the brain to prevent secondary injury and to allow the brain to recover from the initial insult. Maintaining ICP within the reference range is part of an approach designed to optimize both CBF and the metabolic state of the brain. Treatment of elevated ICP is a complex process that should be tailored to each particular patient's situation and should not be approached in a "cookbook" manner. Many potential interventions are used to lower ICP, and each of these is designed to improve intracranial compliance, which results in improved CBF and decreased ICP. Acute treatment of increased intracranial pressure The Monro-Kellie doctrine provides the framework for understanding and organizing the various treatments of elevated ICP. In patients with head injuries, the total intracranial volume is composed of the total volume of the brain, the CSF, intravascular blood volume, and any intracranial mass lesions. The volume of one of these components must be reduced to improve intracranial compliance and to decrease ICP. The discussion of the different treatments of elevated ICP is organized according to which component of intracranial volume they affect. The first component of total intracranial volume to consider is the blood component. This includes all intravascular blood, both venous and arterial, and comprises approximately 10% of total intracranial volume. Elevation of the head increases venous outflow and decreases the volume of venous blood within the brain. This results in a small improvement in intracranial compliance and, therefore, has only a modest effect on ICP. The second component of intracranial vascular volume is the arterial blood volume. Hypocapnia is capable of reducing cerebral blood flow 4% for each mm Hg change in PaCO2. The control mechanism is probably extravascular pH changes in fluid bathing cerebral resistor vessels, which alter smooth muscle intracellular calcium concentrations. This may be reduced by mild-to-moderate hyperventilation, in which the PCO2 is reduced to 30-35 mm Hg. This decrease in PCO2 causes vasoconstriction at the level of the arteriole, which decreases blood volume enough to reduce ICP. The effects of hyperventilation have a duration of action of approximately 48-72 hours, at which point the brain resets to the reduced level of PCO2. This is an important point because once hyperventilation is used, the PCO2 should not be returned to normal rapidly. This may cause rebound vasodilatation, which can result in increased ICP. Below a PaCO2 of 25-30 Torr, CBF falls much less rapidly, presumably because of severe enough vasoconstriction to induce hypoxemia in brain tissues, limiting oxygen delivery. PaCO2 tensions less than 25 Torr are sufficient to change brain metabolism into anaerobic, which increases acidosis. Low arterial O 2 tensions influence CBF but to a lesser degree than PaCO2. No measurable changes in CBF occur during hypoxemia until the PaO2 drops below 50 Torr, at which time CBF gradually increases. In addition to reducing CBF, the resultant respiratory alkalosis may reverse local tissue acidosis, which develops in cerebral edema, benefiting cellular respiration and restoring autoregulation. Within 48-72 hours, renal mechanisms for handling bicarbonate excretion compensate for altered PaCO2 tensions, thereby normalizing cerebral pH and returning CBF to baseline values. There are 3 paradoxes to hyperventilation therapy for the control of ICP.

Since cerebral vasospasm is a serious concern in subarachnoid hemorrhage (SAH), attempts to create further vessel constriction by hyperventilation in order to decrease concomitant cerebral edema are rarely indicated unless the amount of edema is clinically emergent. Vessels in the damaged area of the brain have lost their autoregulatory control. While unaffected brain regions would vasoconstrict normally to the stimulus of decreased PaCO2, damaged areas might vasodilate in response to diminished cerebral blood flow. This can create a reverse steal phenomenon, where blood and nutrients are diverted away from normal areas of the brain and into damaged areas. This diversion would feed the increased metabolic requirement of damaged tissues, but the sum total eff ect may cause more harm to the rest of the brain. In addition, the increased hydrostatic pressure combined with the capillary permeability damage might, in some cases, paradoxically increase ICP in damaged areas. Sudden increases in PaCO2, as a result of ventilator changes, often result in dramatic increases in CBF, and rapid deteriorations in the patients condition. During hyperventilation, the cerebr al bicarbonate level gradually adjusts to offset the lower level of CO2, maintaining normal pH. If the pCO2 is allowed to rise suddenly, the excess CO2rapidly crosses the blood-brain barrier, but the bicarbonate level in the brain increases much less rapidly. The result is cerebral acidosis, with attendant cerebral vascular dilatation, increased cerebral blood volume, and elevated ICP, usually resistant to further hyperventilation. Unfortunately, little objective evidence exists that treatment by hypocapnia has significantly improved mortality or survival. At best, it seems to be a temporary stop-gap measure until some other curative measure, such as surgery, might be attempted. Patients with the most prompt response to hyperventilation generally have the best prognosis for recovery. No evidence exists that hyperventilation therapy produces benefit in hypoxemic-anoxic encephalopathy. CSF represents the third component of total intracranial volume and accounts for 2-3% of total intracranial volume. In adults, total CSF production is approximately 20 mL/h or 500 mL/d. In many patients with TBI who have elevated ICP, a ventriculostomy may be placed and CSF may be drained. Removal of small amounts of CSF hourly can result in improvements in compliance that result in significant improvements in ICP. The fourth and largest component of total intracranial volume is the brain or tissue component, which comprises 85-90% of the total intracranial volume. When significant brain edema is present, it causes an increase in the tissue component of the total intracranial volume and results in decreased compliance and increased ICP. Treatments of elevated ICP that reduce total brain volume include diuretics, perfusion augmentation (CPP strategies), metabolic suppression, and decompressive procedures. Diuresis and brain edema Diuretics are powerful in their ability to decrease brain volume and, therefore, to decrease ICP. Mannitol, an osmotic diuretic, is the most common diuretic used. Mannitol is a sugar alcohol that draws water out from the brain into the intravascular compartment. It has a rapid onset of action and a duration of action of 2-8 hours. Mannitol is usually administered as a bolus because it is much more effective when given in intermittent boluses than when used as a continuous infusion. The standard dose ranges from 0.25-1 g/kg, administered every 4-6 hours. Because mannitol causes significant diuresis, electrolytes and serum osmolality must be monitored carefully during its use. In addition, careful attention must be given to providing sufficient hydration to maintain euvolemia. The limit for mannitol is 4 g/kg/d. At daily doses higher than this, mannitol can cause renal toxicity. Mannitol should not be given if the patient's serum sodium level is greater than 145 or serum osmolality is greater than 315 mOsm. Other diuretics that sometimes are used in patients with TBI include furosemide, glycerol, and urea. Mannitol is preferred over furosemide because it tends to cause less severe electrolyte imbalances than a loop diuretic. Interestingly, mannitol and furosemide have a synergistic effect when combined; however, this combination tends to cause severe electrolyte disturbances. Urea and glycerol have also been used as osmotic diuretics. Both of these compounds are smaller molecules than mannitol and, as a result, tend to equilibrate within the brain sooner than mannitol; therefore, they have a shorter duration of action than mannitol. Urea has the additional problem that it can cause severe skin sloughing if it infiltrates into the skin. Hypertonic saline (3%) has generated some interest in the treatment of intracranial hypertension secondary to brain edema because it is thought to be less disruptive to fluid and electrolyte balance than other diuretic agents. Boluses of mannitol can generate a dramatic diuresis, resulting in rapid intravascular depletion and potential kidney damage. Mannitol can cause as much as 1500 cc of fluid to diurese in the space of 2 hours, as intravascular fluid depletion occurs, hematocrit can rise, blood viscosity can increase, and cloning is enhanced. This makes the area of brain irritation much more amenable to stroke. Saline 3% or 7.5% administered in continuous infusion generates a more predictable and gentle osmotic flow of brain intracellular water into the interstitial space. The maximum effect occurs after the end of infusion and is visible over 4 hours. Hypertonic saline hydroxyethyl starch (HS-HES) seems to effectively lower ICP but does not increase CPP as much as does mannitol. Therapeutically, the limits of serum sodium and osmolality are in the range of 155-320. More research is needed to elucidate the exact method of action of hypertonic saline and the contraindications. Other supportive treatments While awaiting possible operative therapy, other supportive treatments are as follows:

Early extraventricular drainage of CSF is sometimes of value in controlling brain edema if there is a suspicion that the ventricles will progressively diminish in size because edema cannot be cannulated from a burr hole. Coughing and straining increase venous pressure, restricting drainage and backing up blood into the head, thereby increasing ICP. Neuromuscular paralysis may decrease ICP by preventing sudden changes related to coughing or straining and by promoting systemic venous pooling that increases venous drainage from the head. Any other restrictions to jugular blood drainage, such as a kinked neck from positioning in bed, increase ICP by retarding jugular drainage, transmitting pressure back into the brain. Trying to differentiate a drug-induced coma from an increased ICPinduced coma with a trial of naloxone (Narcan) is contraindicated, as it invariably induces agitation if the stupor is narcotic induced. Agitation increases catecholamine response, increases cardiac output, and increases blood flow to the head, thereby increasing hydrostatic pressure and ICP. Decreased serum protein (albumin) from malnutrition causes a decreased serum osmolality compared to the osmolality in the surrounding tissues. This allows intravascular water to flow along the increased osmotic gradient into the tissues, increasing edema. Hyperalimentation should be initiated as soon as possible if the course is likely to be protracted. Boutique intravenous stabilizing cocktails have been said to maintain homeostasis of intravascular and extravascular fluid compartments, avoiding rapid fluid shifts that might adversely affect cerebral metabolism and edema. Composed of an albumin, bicarbonate, and Lasix solution, the albumin increases intravascular colloid content, resisting fluid flow into the brain substance, the bicarbonate buffers pH changes, and the Lasix tends to promote a stable, consistent urine output, resisting intravascular fluid changes from renal compensations. This may be useful in diffuse brain edema to protect against further damage from vascular compartment shifts, but body physiology probably adapts to it rapidly, thereby limiting its effect. These cocktails have not been proven to be effective as a treatment of SAH since they tend to promote diuresis and intravascular depletion. Management of cerebral perfusion pressure CPP management involves artificially elevating the blood pressure to increase the MAP and the CPP. Because autoregulation is impaired in the injured brain, pressure-passive CBF develops within these injured areas. As a result, these injured areas of the brain often have insufficient blood flow, and tissue acidosis and lactate accumulation occur. This causes vasodilation, which increases cerebral edema and ICP. When the CPP is raised to greater than 65-70 mm Hg, the ICP is often lowered because increased blood flow to injured areas of the brain decreases the tissue acidosis. This often results in a significant decrease in ICP. Metabolic therapies are designed to decrease the cerebral metabolic rate, which decreases ICP. Metabolic therapies are powerful means of reducing ICP, but they are reserved for situations in which other therapies have failed to control ICP. This is because metabolic therapies have diffuse systemic effects and often result in severe adverse effects, including hypotension, immunosuppression, coagulopathies, arrhythmias, and myocardial suppression. Metabolic suppression may be achieved through drug therapies or induced hypothermia. Barbiturates are the most common class of drugs used to suppress cerebral metabolism. Barbiturate coma is typically induced with pentobarbital. A loading dose of 10 mg/kg is administered over 30 minutes, and then 5 mg/kg/h is administered for 3 hours. A maintenance infusion of 1-2 mg/kg/h is begun after loading is completed. The infusion is titrated to provide burst suppression on continuous electroencephalogram monitoring and a serum level of 3-4 mg/dL. Typically, the barbiturate infusion is continued for 48 hours, and then the patient is weaned off the barbiturates. If the ICP again escapes control, the patient may be reloaded with pentobarbital and weaned again in several days. Hypothermia may also be used to suppress cerebral metabolism. The use of mild hypothermia involves decreasing the core temperature to 34-35C for 24-48 hours and then slowly rewarming the patient over 2-3 days. Patients with hypothermia are also at risk for hypotension and systemic infections. Another treatment that may be used in patients with TBI with refractory ICP elevation is decompressive craniectomy. In this surgical procedure, a large section of the skull is removed and the dura is expanded. This increases the total intracranial volume and, therefore, decreases ICP. Which patients benefit from decompressive craniectomy has not been established. Some believe that patients with refractory ICP elevation who have diffuse injury but do not have significant contusions or infarctions will benefit from decompressive craniectomy. Management of elevated ICP involves using a combination of treatments. Each patient represents a slightly different set of circumstances, and treatment must be tailored to each patient. Although no rigid protocols have been established for the treatment of head injury, many published algorithms provide treatment schemas. The American Association of Neurologic Surgeons published a comprehensive evidence-based review of the treatment of TBI, called theGuidelines for the Management of Severe Head Injury. In these guidelines, 3 different categories of treatments, standards, guidelines, and options are outlined. Standards are the accepted principles of management that reflect a high degree of clinical certainty. Guidelines are a particular strategy or a range of management options that reflect a high degree of clinical certainty. Options are strategies for patient management for which clinical certainty is unclear. Penetrating trauma The treatment of penetrating brain injuries involves 2 main aspects. The first is the treatment of the TBI caused by a penetrating object. Penetrating brain injuries, especially from high-velocity missiles, frequently result in severe ICP elevations. This aspect of penetrating brain injury treatment is identical to the treatment of closed head injuries. The second aspect of penetrating head injury treatment involves debridement and removal of the penetrating objects. Penetrating injuries require careful debridement because these wounds are frequently dirty. When objects penetrate the brain, they introduce pathogens into the brain from the scalp surface and from the surface of the penetrating object.

Penetrating injuries may be caused by high-velocity missiles (eg, bullets), penetrating objects (eg, knives, tools), or fragments of bone driven into the brain. Bullet wounds are treated with debridement of as much of the bullet tract as possible, dural closure, and reconstruction of the skull as needed. If the bullet can be removed without significant risk of neurologic injury, it should be removed to decrease the risk of subsequent infection. Penetrating objects, such as knives, require removal to prevent further injury and infection. If the penetrating object either is near or traverses a major vascular structure, an angiogram is necessary to assess for potential vascular injury. When the risk of vascular injury is present, penetrating objects should be removed only after appropriate access has been obtained to ensure that vascular control is easily achieved. Penetrating brain injuries are associated with a high rate of infection, both early infections and delayed abscesses. Appropriate debridement and irrigation of wounds helps to decrease the infection rate. Some of the risk factors for infection following penetrating brain injury include extensive bony destruction, persistent CSF leak, and an injury pathway that violates an air sinus. Late-onset epilepsy is a common consequence of penetrating brain injuries and can occur in up to 50% of patients with penetrating brain injuries. No evidence exists that prophylactic anticonvulsants decrease the development of late-onset epilepsy. During the Vietnam War, prophylactic anticonvulsants were used, and the rate of late-onset epilepsy was not different from that of previous wars, when prophylactic anticonvulsants were not used. Complications Functional deficits resulting from TBI are common and can be divided into 2 categories, as follows: systemic complications and neurologic complications. The systemic complications of TBI are typical of any severe injury and depend on the types of intensive treatments used. Be aware of the complications of intensive care treatment when considering systemic complications of head injury. The neurologic complications of TBI include focal neurologic deficits, global neurologic deficits, seizures, CSF fistulae, hydrocephalus, vascular injuries, infections, and brain death. Focal neurologic deficits Focal neurologic deficits are quite common following TBI. Cranial nerves are affected often because of their anatomic location at the base of the brain. When the brain shifts within the skull as it undergoes either acceleration or deceleration forces, significant force is often placed on the entire brain and the cranial nerves. The cranial nerves are tethered at their exit sites from the skull, and, as a result, they may be stretched when the brain shifts as a result of acceleration or deceleration forces. In addition, the cranial nerves are very susceptible to injury as they course through narrow bony canals and grooves. The cranial nerves that are injured most commonly in patients with TBI are cranial nerves I, IV, VII, and VIII. Anosmia caused by traumatic injury to the first cranial nerve occurs in 2-38% of patients with TBI. It is more common in those with frontal fractures and in those with posttraumatic rhinorrhea. Posttraumatic anosmia improves slowly, and as many as one third of patients do not show any improvement in olfaction. Injuries to the fourth cranial nerve, the trochlear nerve, are also quite common. This nerve is often injured in patients with head trauma because it has the longest intracranial course of the cranial nerves. Injury to the trochlear nerve causes a positional diplopia, in which those affected experience diplopia when they look down and toward the eye in which the trochlear nerve is injured. As a result, to compensate, the head is tilted up and away from the side of the injury. Trochlear nerve injuries resolve fully in approximately two thirds of those with unilateral injury and in one fourth of those with bilateral injuries. Facial nerve injuries often occur with head injuries in which the temporal bone is fractured. From 10-30% of persons with longitudinal fractures of the temporal bone and 30-50% of those with transverse fractures of the temporal bone have either acute or delayed facial nerve injury. Immediate facial nerve injury suggests direct injury to the nerve, while delayed injury suggests progressive edema within the nerve. In severely injured patients, a delay in the diagnosis of facial nerve injuries occurs frequently because facial nerve function is difficult to assess in obtunded patients. Cochlear nerve injury (cranial nerve VIII) is also a common occurrence in patients with head injury, especially in patients with temporal bone fractures. In addition, vestibular disorders, including vertigo, dizziness, and tinnitus, are extremely common in patients with head injuries. Hydrocephalus Hydrocephalus is a common late complication of TBI. Posttraumatic hydrocephalus may present as either ventriculomegaly with increased ICP or as normal pressure hydrocephalus. In patients with increased ICP secondary to posttraumatic hydrocephalus, the typical signs of hydrocephalus are often observed and include headaches, visual disturbances, nausea/vomiting, and alterations in the level of consciousness. Normal pressure hydrocephalus usually manifests as memory problems, gait ataxia, and urinary incontinence. The diagnosis of normal pressure hydrocephalus may be difficult to make in patients with TBI because they often have memory difficulties and gait abnormalities secondary to their head injury. In addition, as many as 86% of patients with TBI demonstrate some degree of ventriculomegaly on follow-up CT scan images. This ventriculomegaly is often secondary to diffuse brain atrophy, and radiographic features rarely help make the distinction between atrophy and normal pressure hydrocephalus. Any patient who develops neurologic deterioration weeks to months following TBI should be evaluated for the possibility of normal pressure hydrocephalus. When CT scan findings cannot help distinguish between normal pressure hydrocephalus and ventriculomegaly secondary to brain atrophy, a high-volume lumbar puncturetap test is performed to ascertain if CSF drainage would improve the patient's neurologic condition.

Seizures Posttraumatic seizures are a frequent complication of TBI and are divided into 3 categories. Early seizures occur within 24 hours of the initial injury, intermediate seizures occur 1-7 days following injury, and late seizures occur more than 7 days after the initial injury. Posttraumatic seizures are very common in those with a penetrating cerebral injury, and late seizures occur in as many as half of these patients. Cerebrospinal fluid fistulae Cerebrospinal fistulae, either in the form of rhinorrhea or otorrhea, may occur in as many as 5-10% of patients with TBI. They may present either immediately or in a delayed fashion and are more frequent in patients with basilar skull fractures. Approximately 80% of acute cases of CSF rhinorrhea resolve spontaneously within 1 week. A 17% risk of meningitis exists when CSF rhinorrhea is present. Prophylactic antibiotics have not been demonstrated to decrease this meningitis risk, although very few studies have examined this issue. More than 95% of acute episodes of CSF otorrhea resolve spontaneously within 1 week, and CSF otorrhea is complicated by meningitis in fewer than 4% of cases. When acute CSF fistulae do not resolve spontaneously, a lumbar subarachnoid drain may be placed for several days in an attempt to divert CSF and allow the fistula to close. If this fails, radiographic dye is introduced into the subarachnoid space via lumbar puncture (metrizamide cisternogram), and a high-resolution CT scan is performed in an attempt to identify the origin of the CSF fistula. A craniotomy is performed, and the fistula site is repaired. Delayed CSF fistulae may occur from 1 week after the initial injury to years later. These delayed fistulae are more difficult to treat and frequently require surgical intervention. Vascular injuries Vascular injuries are uncommon sequelae of TBIs. Arterial injuries that may occur following head trauma include arterial transactions, thromboembolic phenomena, posttraumatic aneurysms, dissections, and carotid-cavernous fistulae (CCF). Arterial occlusions secondary to transactions or thromboembolism following closed head injuries are uncommon occurrences. Posttraumatic intracranial aneurysms, which are also rare, differ from congenital aneurysms because the posttraumatic aneurysms tend to be located distally, as opposed to the congenital aneurysms, which are typically proximal in location. Arterial dissections are more common than the aforementioned arterial injuries and should be considered if significant injury has occurred to the petrous portion of the temporal bone, through which the carotid artery passes, or when an unexplained neurologic deficit is present. A cerebral angiogram is often necessary to help exclude arterial injury in these cases. Posttraumatic CCF occur when the internal carotid artery is injured within the cavernous sinus, resulting in a direct connection between the carotid artery and the veins of the cavernous sinus. This overloads the venous system and results in chemosis and proptosis on the affected side. Other signs of CCF include diplopia, ophthalmoplegia, visual disturbances, and headaches. Some high-risk fistulae may cause intracerebral hemorrhage. CCF are treated with endovascular balloon occlusion of the fistula origin. Specific intracranial venous injuries are uncommon following TBI if one excludes the injury to the bridging veins, which are the most common source of subdural hematomas. Depressed skull fractures overlying any of the major intracranial venous sinuses may cause injury to the sinus. When these venous sinus injuries require treatment, substantial, and sometimes life-threatening, blood loss can occur. A second type of venous injury following TBI involves venous sinus thrombosis. Although very rare following head injury, this is a potentially life-threatening injury because the impaired venous drainage often causes severe ICP elevations and venous infarction. The treatment of venous sinus thrombosis is anticoagulation, which presents significant risk in those with acute head injuries. If the thrombosis progresses despite systemic anticoagulation, direct intracranial intravenous thrombolysis is necessary. Infections Intracranial infections are another potential complication of TBI. In uncomplicated closed head injury, infection is uncommon. When basilar skull fractures and/or CSF fistulae are present, the risk of infection is increased. In addition, if a patient has had a ventriculostomy for ICP monitoring, the risk of infection is also increased, for either a ventriculitis or meningitis. Other intracranial infections, such as subdural or epidural empyema and intraparenchymal abscesses, are rare following closed head injury. As one would expect, the incidence of infection in penetrating cerebral injuries and open depressed skull fractures increases. Diagnosis of brain death Brain death protocols have evolved to become very specific and sensitive. Brain death is a diagnosis of what is, not what might be, and must be proven rather than insinuated.

Initially, for an accurate diagnosis of brain death, there must be clear evidence of an acute, catastrophic, irreversible brain injury, and any reversible conditions that may obfuscate the clinical assessment must be excluded. Subsequently, the physical examination must show complete unresponsiveness, absent motor responses, absent brainstem reflexes, and apnea. Further confirmatory studies, such as EEG or cerebral blood flow studies, may be ordered if there is any ambiguity in the clinical evaluation. A typical brain death protocol may be summarized as follows:

Confirm that the patient is in a coma. Evaluate the patient for seizure activity and decerebrate or decorticate movements. Test for motor response to painful stimulation. Test for pupillary response to light. Test for corneal reflex. Test for oculocephalogyric reflex (dolls head reflex). Test for vestibulo-ocular reflex (caloric test). Test for upper and lower airway stimulation (eg, pharyngeal and endotracheal suction). Test for gag reflex. Perform apnea test. This test should be the last test and should be conducted after two clinical examinations (separated by the mandatory observation period) have confirmed the absence of brainstem functions. The patient is disconnected from the ventilator while oxygenation of the lungs is continued passively. On the basis of calculation (whereby PaCO 2 is assumed to rise 4 mm Hg in the first minute and 3 mm Hg every minute thereafter), the patient is allowed to build up to a PaCO 2 of 60 mm Hg or more without becoming hypoxic. If there is no respiratory effort, the apnea test is considered confirmatory. Consider an EEG. The EEG should show electrocerebral silence for at least 30 minutes and must conform to established criteria for brain death. If the cause of death cannot be determined with absolute accuracy, consider cerebral angiography. The absence of intracranial arterial circulation, as demonstrated by four-vessel angiography, confirms brain death. Brain death and life support In earlier times, it could be said that a person was dead when pulseless and apneic. Today, this view no longer suffices. Death is more a process than an event. Lack of blood flow to the brain leads to loss of consciousness within seconds, but other functions of the brain may persist for much longer. Other somatic organs may take hours to stop functioning, and connective tissues can take days to die. The evolution of life-support systems capable of prolonging death indefinitely necessitated a more accurate definition of death, which arrived in 1968 with the formulation of the Harvard criteria for the working definition of death. In essence, these criteria considered the irreversible loss of brain function, rather than whole-body metabolic cessation, to be indicative of death. When the Harvard criteria were met, death was inevitable, even with continuing treatment. The Harvard criteria objectified the progression of disease, thereby making it possible for clinicians to predict death accurately even on somatic life support. In 1981, the Presidents Commission established brain death as a criterion for determining death, not simply for predicting t he inevitability of death. The Uniform Determination of Death Act (UDDA) made brain death and cardiopulmonary collapse criteria for death in most states. Under the UDDA, death is pronounced at the time the criteria are met, and families may not demand continuing mechanical ventilation or other forms of ICU life support (except in the states of New York and New Jersey, both of which have conscience clauses). The controversy surrounding death Providers and ethicists continue to disagree on the question of whether whole-brain death is equivalent to death. These factions do, however, agree asserted that there is only one real definition of deathirreversible cessation of the integrated functioning of the organism as a whole. However, an ambiguous portion of the Dead Do nor Rule has muddied the water, stating an individual who has sustained either irreversible cessation of circulatory and respiratory functions or irreversible cessation of all functions of the entire brain is dead. The connections between cardiovascular and neurologic criteria are tenuous, and the criteria mean different things to different people at different times. For example, the criterion of irreversible cessation of all circulatory and respiratory function does not imply the cessation of brain function. Conversely, the criterion of irreversible cessation of all brain function does not imply the cessation of circulation and respiration. It appears, then, that the definition of death does not require the permanent cessation of the functioning of the organism as a whole but, rather, cessation of only certain functions. Ethicists maintain that the criteria used to fulfill the definition of death should be both necessary and sufficient. This is not an easy standard to meet. For example, loss of consciousness is necessary for death, but it is not sufficient. Loss of heartbeat and breathing is sufficient for death, but it is not necessary if whole-brain death is present. Moreover, the UDDA does not require that every brain cell be dead for brain death to be declaredonly those cells that contribute to the integration of the organism as a whole.

This argument is far too convoluted to adequately explore here, but other interesting wrinkles abound. In the modern, digital sense, death can be conceived as the irreversible loss of the structural information that encodes personal identity. Brains and bodies can appear dead but can be restored to function (eg, cold water drowning, brief periods of normothermic ischemia). As such, these people are not dead because the essence of death is irreversibility. In fact, the irreversible loss of life is the dictiona ry definition of death. Is life necessarily dependent upon continuous dynamic function? Is a tobacco mosaic virus dead if a researcher removes its constituent parts and shakes them in solution, following which they selfassemble into a viable virus? These 21st century revelations suggest that any meaningful definition of death must satisfy an information-theoretic criterion. In other words, does the patient contain enough undamaged informational structure to interpret his or her working state from his or her current nonfunctioning state? The technology to transform from one state to another state does not currently exist, but, at the current rate of knowledge accumulation, it will in the future, and that knowledge will radically redefine our definition of life and death. Outcome and Prognosis The outcome of TBI is related to the initial level of injury. While the initial GCS score provides a description of the initial neurologic condition, it does not correlate tightly with outcome. Various methods have been used in an attempt to predict the outcome of TBI, and these are beyond the scope of this discussion. However, one simplified model uses 3 factors, that is, age, motor score of the GCS, and pupillary response (ie, normal, unilateral unresponsive pupil, bilateral unresponsive pupils), to provide a probability of outcome. The Traumatic Coma Data Bank analyzed 780 patients with head injuries and identified 5 factors that correlated with a poor outcome, as follows: (1) age older than 60 years, (2) initial GCS score of less than 5, (3) presence of a fixed dilated pupil, (4) prolonged hypotension or hypoxia early after injury, and (5) presence of a surgical intracranial mass lesion. An examination of the Crash Injury Research Engineering Network database found a significantly higher mortality rate among elderly motor vehicle accident victims (age >60 years) compared to their younger counterparts.[12] Many methods exist for evaluating the outcome of TBI. A simple and commonly used method is the Glasgow outcome scale. This divides outcome into 5 categories, as follows: (1) good, (2) moderate disability, (3) severe disability, (4) vegetative, and (5) dead. The scale can be divided further into good outcomes (eg, good plus moderate disability) and poor outcomes (eg, severe disability, vegetative, dead). Future and Controversies The most significant controversy today in the treatment of TBI is the minimum desirable CPP to achieve in the patient with a head injury. Previously, a CPP of 79 mm Hg was considered the minimum; however, many now believe that a CPP of 60 mm Hg is sufficient. Further controversy also exists as to whether elevated ICP or decreased CPP is a more important prognostic factor. This is an important distinction because it directs the main goals of therapy in severely injured patients. If ICP elevations are considered a more important factor, then efforts may be directed at lowering ICP as a primary goal and improving CPP as a secondary goal. If one considers CPP to be the more important factor, then the primary goal of treatment should be to maintain an appropriate CPP.

http://emedicine.medscape.com/article/433855-overview#showall

Traumatic brain injury From Wikipedia, the free encyclopedia See also: Brain injury (disambiguation) Traumatic brain injury Classification and external resources

CT scan showing cerebral contusions,hemorrhage within the hemispheres, subdural hematoma, and skull fractures[1] ICD-10 ICD-9 S06 800.0-801.9, 803.0804.9, 850.0-854.1 5671

DiseasesDB

MedlinePlus 000028 eMedicine MeSH med/2820 neuro/153ped/929 D001930

Traumatic brain injury (TBI), also known as intracranial injury, occurs when an external force traumatically injures the brain. TBI can be classified based on severity, mechanism (closed or penetrating head injury), or other features (e.g., occurring in a specific location or over a widespread area). Head injury usually refers to TBI, but is a broader category because it can involve damage to structures other than the brain, such as the scalp and skull. TBI is a major cause of death and disability worldwide, especially in children and young adults. Males sustain traumatic brain injuries more frequently than do females. Causes include falls, vehicle accidents, and violence. Prevention measures include use of technology to protect those suffering from automobile accidents, such as seat belts and sports or motorcycle helmets, as well as efforts to reduce the number of automobile accidents, such as safety education programs and enforcement of traffic laws. Brain trauma can be caused by a direct impact or by acceleration alone. In addition to the damage caused at the moment of injury, brain trauma causes secondary injury, a variety of events that take place in the minutes and days following the injury. These processes, which include alterations in cerebral blood flow and the pressure within the skull, contribute substantially to the damage from the initial injury.

TBI can cause a host of physical, cognitive, social, emotional, and behavioral effects, and outcome can range from complete recovery to permanent disability or death. The 20th century saw critical developments in diagnosis and treatment that decreased death rates and improved outcome. Some of the current imaging techniques used for diagnosis and treatment include CT scans computed tomography and MRIs magnetic resonance imaging. Depending on the injury, treatment required may be minimal or may include interventions such as medications, emergency surgery or surgery years later. Physical therapy, speech therapy, recreation therapy, occupational therapy and vision therapy may be employed for rehabilitation. Contents [hide]

1 Classification
o o

1.1 Severity 1.2 Pathological features

2 Signs and symptoms 3 Causes 4 Mechanism

o o

4.1 Physical forces 4.2 Primary and secondary injury

5 Diagnosis 6 Prevention 7 Treatment

o o

7.1 Acute stage 7.2 Chronic stage

8 Prognosis 9 Complications 10 Epidemiology

o o

10.1 Mortality 10.2 Demographics

11 History 12 Research 13 References 14 Cited texts 15 External links Classification Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile.[2] Brain function is temporarily or permanently impaired and structural damage may or may not be detectable with current technology.[3] TBI is one of two subsets of acquired brain injury (brain damage that occur after birth); the other subset is non-traumatic brain injury, which does not involve external mechanical force (examples include stroke and infection).[4][5] All traumatic brain injuries are head injuries, but the latter term may also refer to injury to other parts of the head. [6][7][8] However, the terms head injury and brain

injury are often used interchangeably.[9] Similarly, brain injuries fall under the classification of central nervous system injuries[10] and neurotrauma.[11] In neuropsychology research literature, in general the term "traumatic brain injury" is used to refer to non-penetrating traumatic brain injuries. TBI is usually classified based on severity, anatomical features of the injury, and the mechanism (the causative forces). [12] Mechanism-related classification divides TBI into closed and penetrating head injury.[2] A closed (also called nonpenetrating, or blunt)[6] injury occurs when the brain is not exposed.[7] A penetrating, or open, head injury occurs when an object pierces the skull and breaches thedura mater, the outermost membrane surrounding the brain.[7] Severity Severity of traumatic brain injury[13]

GCS

PTA

LOC

Mild

1315

<1 day

030 minutes

Moderate

912

>1 to <7 >30 min to days <24 hours

Severe

38

>7 days

>24 hours

Brain injuries can be classified into mild, moderate, and severe categories. [12] TheGlasgow Coma Scale (GCS), the most commonly used system for classifying TBI severity, grades a person's level of consciousness on a scale of 315 based on verbal, motor, and eye-opening reactions to stimuli.[14] It is generally agreed that a TBI with a GCS of 13 or above is mild, 912 is moderate, and 8 or below is severe.[3][8][15] Similar systems exist for young children.[8] However, the GCS grading system has limited ability to predict outcomes. Because of this, other classification systems such as the one shown in the table are also used to help determine severity. A current model developed by the Department of Defense and Department of Veterans Affairs uses all three criteria of GCS after resuscitation, duration of post-traumatic amnesia (PTA), and loss of consciousness (LOC).[13] It also has been proposed to use changes that are visible on neuroimaging, such as swelling, focal lesions, or diffuse injury as method of classification.[2] Grading scales also exist to classify the severity of mild TBI, commonly called concussion; these use duration of LOC, PTA, and other concussion symptoms.[16] Pathological features Main article: Focal and diffuse brain injury

CT scan Spread of the subdural hematoma (single arrows), midline shift(double arrows) Systems also exist to classify TBI by its pathological features.[12] Lesions can be extra-axial, (occurring within the skull but outside of the brain) or intra-axial (occurring within the brain tissue).[17] Damage from TBI can be focal or diffuse, confined to specific areas or distributed in a more general manner, respectively.[18] However, it is common for both types of injury to exist in a given case.[18] Diffuse injury manifests with little apparent damage in neuroimaging studies, but lesions can be seen with microscopy techniques post-mortem,[18][19] and in the early 2000s, researchers discovered that diffusion tensor imaging (DTI), a way of processing MRI images that shows white matter tracts, was an effective tool for displaying the extent of diffuse axonal injury.[20][21] Types of injuries considered diffuse include edema (swelling) and diffuse axonal injury, which is widespread damage to axons including white matter tracts and projections to the cortex.[22][23] Types of injuries considered diffuse include concussion and diffuse axonal injury, widespread damage to axons in areas including white matter and thecerebral hemispheres.[22] Focal injuries often produce symptoms related to the functions of the damaged area.[10]Research shows that the most common areas to have focal lesions in non-penetrating traumatic brain injury are the orbitofrontal cortex (the lower surface of the frontal lobes) and the anterior temporal lobes, areas that are involved in social behavior, emotion regulation, olfaction, and decision-making, hence the common social/emotional and judgment deficits following moderate-severe TBI.[24][25][26][27]Symptoms such as hemiparesis or aphasia can also occur when less commonly affected areas such as motor or language areas are, respectively, damaged.[28][29] One type of focal injury, cerebral laceration, occurs when the tissue is cut or torn.[30] Such tearing is common in orbitofrontal cortex in particular, because of bony protrusions on the interior skull ridge above the eyes.[24] In a similar injury, cerebral contusion (bruising of brain tissue), blood is mixed among tissue.[15] In contrast, intracranial hemorrhage involves bleeding that is not mixed with tissue.[30] Hematomas, also focal lesions, are collections of blood in or around the brain that can result from hemorrhage. [3] Intracerebral hemorrhage, with bleeding in the brain tissue itself, is an intra-axial lesion. Extra-axial lesions include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraventricular hemorrhage.[31] Epidural hematoma involves bleeding into the area between the skull and the dura mater, the outermost of the three membranes surrounding the brain.[3] In subdural hematoma, bleeding occurs between the dura and the arachnoid mater.[15] Subarachnoid hemorrhage involves bleeding into the space between the arachnoid membrane and the pia mater.[15] Intraventricular hemorrhage occurs when there is bleeding in the ventricles.[31] Signs and symptoms

Unequal pupil size is potentially a sign of a serious brain injury.[32] Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected. [33] Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right.[7] Symptoms are also dependent on the injury's severity. With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes.[34] Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing,[35]lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.[34] Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking.[34] Mild TBI symptoms may also be present in moderate and severe injuries.[34] A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken, dilation of one or both pupils, slurred speech, aphasia (word-finding difficulties), dysarthria (muscle weakness that causes disordered speech), weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation.[34]Common long-term symptoms of moderate to severe TBI are changes in appropriate social behavior, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning. [27][36][37][38][39]Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI.[40]Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved with appropriate rehabilitation.[39][41][42][43] When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly.[44] Signs of increased ICP include decreasing level of consciousness, paralysis or weakness on one side of the body, and a blown pupil, one that fails to constrict in response to light or is slow to do so.[44] Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP.[3] Anisocoria, unequal pupil size, is another sign of serious TBI.[32] Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.[3] Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them.[45] Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat,[45] and irritability.[3] Causes The most common causes of TBI in the U.S. include violence, transportation accidents, construction, and sports. [35][46] Motor bikes are major causes, increasing in significance in developing countries as other causes reduce.[47] The estimates that between 1.6 and 3.8 million traumatic brain injuries each year are a result of sports and recreation activities in the US.[48] In children aged two to four, falls are the most common cause of TBI, while in older children traffic accidents compete with falls for this position.[49] TBI is the third most common injury to result from child abuse.[50] Abuse causes 19% of cases of pediatric brain trauma, and the death rate is higher among these cases. [51] Domestic violence is another cause of TBI,[52] as are work-related and industrial accidents.[53] Firearms[7] and blast injuries from explosions[54] are other causes of TBI, which is the leading cause of death and disability in war zones. [55] According to Representative Bill Pascrell (Democrat, NJ), TBI is "the signature injury of the wars in Iraq and Afghanistan." [56] There is a promising technology called activation database guided EEG biofeedback which has been documented to return a TBI's auditory memory ability to above the control group's performance [57] [58] Mechanism

Physical forces

Ricochet of the brain within the skull may account for the coup-contrecoup phenomenon.[59] The type, direction, intensity, and duration of forces all contribute to the characteristics and severity TBI. [2] Forces that may contribute to TBI include angular, rotational, shear, andtranslational forces.[30] Even in the absence of an impact, significant acceleration or deceleration of the head can cause TBI; however in most cases a combination of impact and acceleration is probably to blame.[30] Forces involving the head striking or being struck by something, termed contact orimpact loading, are the cause of most focal injuries, and movement of the brain within the skull, termed noncontact or inertial loading, usually causes diffuse injuries.[12] The violent shaking of an infant that causes shaken baby syndrome commonly manifests as diffuse injury.[60] In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage.[30] Shock waves caused by penetrating injuries can also destroy tissue along the path of a projectile, compounding the damage caused by the missile itself.[15] Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup injury, respectively).[59] When a moving object impacts the stationary head, coup injuries are typical,[61] while contrecoup injuries are usually produced when the moving head strikes a stationary object. [62] Primary and secondary injury

MRI scan showing damage due to brain herniation after TBI[1] Main article: Primary and secondary brain injury A large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event; [63] rather than improving after being hospitalized, some 40% of TBI patients deteriorate.[64] Primary brain injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this deterioration; rather, it is caused by secondary injury, a complex set of cellular processes and biochemical cascades that occur in the minutes to days following the trauma.[65] These secondary processes can dramatically worsen the damage caused by primary injury[55] and account for the greatest number of TBI deaths occurring in hospitals.[32] Secondary injury events include damage to the bloodbrain barrier, release of factors that cause inflammation, free radical overload, excessive release of the neurotransmitterglutamate (excitotoxicity), influx of calcium and sodium ions into neurons, and dysfunction ofmitochondria.[55] Injured axons in the brain's white matter may separate from their cell bodies as a result of secondary injury,[55] potentially killing those neurons. Other factors in secondary injury are changes in the blood flow to the brain; ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); cerebral edema (swelling of the brain); and raised intracranial pressure (the pressure within the skull).[66] Intracranial pressure may rise due to swelling or a mass effect from a lesion, such as a hemorrhage.[44] As a result, cerebral perfusion pressure(the pressure of blood flow in the brain) is reduced; ischemia results.[32][67] When the pressure within the skull rises too high, it can cause brain death or herniation, in which parts of the brain are squeezed by structures in the skull.[44] A particularly weak part of the skull that is vulnerable to damage causing extradural haematoma is the pterion, deep in which lies the middle meningeal artery which is easily damaged in fractures of the pterion. Since the pterion is so weak this type of injury can easily occur and can be secondary due to trauma to other parts of the skull where the impact forces spreads to the pterion. Diagnosis

CT scan showing epidural hematoma (arrow) Diagnosis is suspected based on lesion circumstances and clinical evidence, most prominently a neurological examination, for example checking whether the pupils constrict normally in response to light and assigning a Glasgow Coma Score.[15] Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments to give. [68] The preferred radiologic test in the emergency setting is computed tomography (CT): it is quick, accurate, and widely available.[69] Followup CT scans may be performed later to determine whether the injury has progressed.[2]

Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected outcome in the long term. [15] It is more useful than CT for detecting injury characteristics such as diffuse axonal injury in the longer term.[2] However, MRI is not used in the emergency setting for reasons including its relative inefficacy in detecting bleeds and fractures, its lengthy acquisition of images, the inaccessibility of the patient in the machine, and its incompatibility with metal items used in emergency care.[15] Other techniques may be used to confirm a particular diagnosis. X-rays are still used for head trauma, but evidence suggests they are not useful; head injuries are either so mild that they do not need imaging or severe enough to merit the more accurate CT.[69] Angiographymay be used to detect blood vessel pathology when risk factors such as penetrating head trauma are involved.[2] Functional imaging can measure cerebral blood flow or metabolism, inferring neuronal activity in specific regions and potentially helping to predict outcome.[70] Electroencephalography and transcranial doppler may also be used. The most sensitive physical measure to date is the quantitative EEG which has documented an 80% to 100% ability in discriminating between normals and traumatic brain injured subjects. [71] [72] Neuropsychological assessment can be performed to evaluate the long-term cognitive sequelae and to aid in the planning of therehabilitation.[68] Instruments range from short measures of general mental functioning to complete batteries formed of different domain-specific tests. Prevention

Protective sports equipment such as helmets can help to protect athletes from head injury. Since a major cause of TBI are vehicle accidents, their prevention or the amelioration of their consequences can both reduce the incidence and gravity of TBI. In accidents, damage can be reduced by use of seat belts, child safety seats[48] and motorcycle helmets,[73] and presence of roll bars and airbags.[30] Education programs exist to lower the number of crashes.[68] In addition, changes to public policy and safety laws can be made; these include speed limits, seat belt and helmet laws, and road engineering practices.[55] Changes to common practices in sports have also been discussed. An increase in use of helmets could reduce the incidence of TBI.[55] Due to the possibility that repeatedly "heading" a ball practicing soccer could cause cumulative brain injury, the idea of introducing protective headgear for players has been proposed.[74] Improved equipment design can enhance safety; softer baseballs reduce head injury risk.[75] Rules against dangerous types of contact, such as "spear tackling" in American football, when one player tackles another head first, may also reduce head injury rates.[75] Falls can be avoided by installing grab bars in bathrooms and handrails on stairways; removing tripping hazards such as throw rugs; or installing window guards and safety gates at the top and bottom of stairs around young children.[48] Playgrounds with shock-absorbing surfaces such as mulch or sand also prevent head injuries.[48] Child abuse prevention is another tactic; programs exist to prevent shaken baby syndrome by educating about the dangers of shaking children.[51]Gun safety, including keeping guns unloaded and locked, is another preventative measure.[76] Studies on the effect of laws that aim to control access to guns in the United States have been insufficient to determine their effectiveness preventing number of deaths or injuries.[77] Recent clinical and laboratory research by neurosurgeon Julian Bailes, M.D., and his colleagues from West Virginia University, has resulted in papers showing that dietary supplementation with omega-3 DHA offers protection against the biochemical brain damage that occurs after a traumatic injury. [78] Rats given DHA prior to induced brain injuries suffered smaller increases in two key markers for brain damage (APP and caspase-3), as compared with rats given no DHA.[79] The potential for DHA to provide prophylactic benefit to the brain against traumatic injury appears

promising and requires further investigation. The essential concept of daily dietary supplementation with DHA, so that those at significant risk may be preloaded to provide protection against the acute effects of TBI, has tremendous public health implications.[80] Treatment It is important to begin emergency treatment within the so-called "golden hour" following the injury.[81] People with moderate to severe injuries are likely to receive treatment in an intensive care unit followed by a neurosurgical ward.[82] Treatment depends on the recovery stage of the patient. In the acute stage the primary aim of the medical personnel is to stabilize the patient and focus on preventing further injury because little can be done to reverse the initial damage caused by trauma. [82] Rehabilitation is the main treatment for the subacute and chronic stages of recovery.[82] International clinical guidelines have been proposed with the aim of guiding decisions in TBI treatment, as defined by an authoritative examination of current evidence.[2] Acute stage Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center.[44][83] Both during transport and in hospital the primary concerns are ensuring proper oxygen supply, maintaining adequate cerebral blood flow, and controlling raised intracranial pressure (ICP),[3] since high ICP deprives the brain of badly needed blood flow[84]and can cause deadly brain herniation. Other methods to prevent damage include management of other injuries and prevention ofseizures.[15][68] Neuroimaging is helpful but not flawless in detecting raised ICP.[85] A more accurate way to measure ICP is to place a catheter into aventricle of the brain,[32] which has the added benefit of allowing cerebrospinal fluid to drain, releasing pressure in the skull.[32]Treatment of raised ICP may be as simple as tilting the patient's bed and straightening the head to promote blood flow through the veins of the neck. Sedatives, analgesics and paralytic agents are often used.[44] Hypertonic saline can improve ICP by reducing the amount of cerebral water (swelling), though it is used with caution to avoid electrolyte imbalances or heart failure.[2] Mannitol, an osmoticdiuretic,[2] was also studied for this purpose,[86][87][88] but such studies have been heavily questioned.[89] Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures, but may cause hypovolemia(insufficient blood volume).[32] Hyperventilation (larger and/or faster breaths) reduces carbon dioxide levels and causes blood vessels to constrict; this decreases blood flow to the brain and reduces ICP, but it potentially causes ischemia[3][32][90] and is, therefore, used only in the short term.[3] Endotracheal intubation and mechanical ventilation may be used to ensure proper oxygen supply and provide a secure airway.[68]Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal blood pressure. Failing to maintain blood pressure can result in inadequate blood flow to the brain.[15] Blood pressure may be kept at an artificially high level under controlled conditions by infusion of norepinephrine or similar drugs; this helps maintain cerebralperfusion.[91] Body temperature is carefully regulated because increased temperature raises the brain's metabolic needs, potentially depriving it of nutrients.[92] Seizures are common. While they can be treated with benzodiazepines, these drugs are used carefully because they can depress breathing and lower blood pressure. [44] TBI patients are more susceptible to side effects and may react adversely or be inordinately sensitive to some pharmacological agents.[82] During treatment monitoring continues for signs of deterioration such as a decreasing level of consciousness. [2][3] Traumatic brain injury may cause a range of serious coincidental complications which include cardiac arrhythmias[93] and neurogenicpulmonary edema.[94] These conditions must be adequately treated and stabilised as part of the core care for these patients. Surgery can be performed on mass lesions or to eliminate objects that have penetrated the brain. Mass lesions such as contusions or hematomas causing a significant mass effect (shift of intracranial structures) are considered emergencies and are removed surgically.[15] For intracranial hematomas, the collected blood may be removed using suction or forceps or it may be floated off with water.[15] Surgeons look for hemorrhaging blood vessels and seek to control bleeding.[15] In penetrating brain injury, damaged tissue is surgically debrided, and craniotomy may be needed.[15] Craniotomy, in which part of the skull is removed, may be needed to remove pieces of fractured skull or objects embedded in the brain.[95] Decompressive craniectomy (DC) is performed routinely in the very short period following TBI during operations to treat hematomas; part of the skull is removed temporarily (primary DC). [96] DC performed hours or days after TBI in order to control high intracranial pressures (secondary DC) has not been shown to improve outcome in some trials and may be associated with severe side effects.[2][96]

Chronic stage

Physical therapy will commonly include muscle strength exercise. Once medically stable, patients may be transferred to a subacute rehabilitation unit of the medical center or to an independent rehabilitation hospital.[82] Rehabilitation aims to improve independent function at home and in society and to help adapt to disabilities [82] and has demonstrated its general effectiveness, when conducted by a team of health professionals who specialise in head trauma.[97] As for any patient with neurologic deficits, amultidisciplinary approach is key to optimising outcome. Physiatrists or neurologists are likely to be the key medical staff involved, but depending on the patient, doctors of other medical specialties may also be helpful. Allied health professions such as physiotherapy,speech and language therapy, cognitive rehabilitation therapy, and occupational therapy will be essential to assess function and design the rehabilitation activities for each patient. Treatment of neuropsychiatric symptoms such as emotional distress and clinical depression may involve mental health professionals such as therapists, psychologists, andpsychiatrists, while neuropsychologists can help to evaluate and manage cognitive deficits.[82] After discharge from the inpatient rehabilitation treatment unit, care may be given on an outpatient basis. Community-based rehabilitation will be required for a high proportion of patients, including vocational rehabilitation; this supportive employment matches job demands to the worker's abilities. [98] People with TBI who cannot live independently or with family may require care in supported living facilities such as group homes.[98] Respite care, including day centers and leisure facilities for the disabled, offers time off for caregivers, and activities for people with TBI.[98] Pharmacological treatment can help to manage psychiatric or behavioral problems.[99] Medication is also used to control post-traumatic epilepsy; however the preventive use of anti-epileptics is not recommended.[100] In those cases where the person is bedridden due to a reduction of consciousness, has to remain in a wheelchair because of mobility problems, or has any other problem heavily impacting self-caring capacities, caregiving and nursing are critical. The most effective research documented intervention approach is the activation database guided EEG biofeedback approach which has shown significant improvements in memory abilities of the TBI subject which are far superior than traditional approaches (strategies, computers, medication intervention). Gains of 2.61 standard deviations have been documented. The TBI's auditory memory ability was superior to the control group after the treatment. [57] Prognosis Prognosis worsens with the severity of injury.[101] Most TBIs are mild and do not cause permanent or long-term disability; however, all severity levels of TBI have the potential to cause significant, long-lasting disability.[102] Permanent disability is thought to occur in 10% of mild injuries, 66% of moderate injuries, and 100% of severe injuries. [103] Most mild TBI is completely resolved within three weeks, and almost all people with mild TBI are able to live independently and return to the jobs they had before the injury, although a portion have mild cognitive and social impairments.[76] Over 90% of people with moderate TBI are able to live independently, although a portion require assistance in areas such as physical abilities, employment, and financial managing.[76] Most people with severe closed head injury either die or recover enough to live independently; middle ground is less common.[2] Coma, as it is closely related to severity, is a strong predictor of poor outcome.[3] Prognosis differs depending on the severity and location of the lesion, and access to immediate, specialised acute management. Subarachnoid hemorrhage approximately doubles mortality.[104] Subdural hematoma is associated with worse outcome and increased mortality, while people with epidural hematoma are expected to have a good outcome if they receive surgery quickly.[68] Diffuse axonal injury may be associated with coma when severe, and poor outcome. [2] Following the acute stage, prognosis is strongly influenced by the patient's involvement in activity that promotes recovery, which for most patients requires access to a specialised, intensive rehabilitation service.

Medical complications are associated with a bad prognosis. Examples are hypotension (low blood pressure), hypoxia (low blood oxygen saturation), lower cerebral perfusion pressures and longer times spent with high intracranial pressures.[2][68] Patient characteristics also influence prognosis. Factors thought to worsen it include abuse of substances such as illicit drugs and alcohol and age over sixty or under two years (in children, younger age at time of injury may be associated with a slower recovery of some abilities).[68] Complications Main article: Complications of traumatic brain injury

The relative risk of post-traumatic seizures increases with the severity of traumatic brain injury.[105]

A CT of the head years after a traumatic brain injury showing an empty space where the damage occurred marked by the arrow. Improvement of neurological function usually occurs for two or more years after the trauma. For many years it was believed that recovery was fastest during the first six months, but there is no evidence to support this. It may be related to services commonly being withdrawn after this period, rather than any physiological limitation to further progress. [2] Children recover better in the immediate time frame and improve for longer periods.[3] Complications are distinct medical problems that may arise as a result of the TBI. The results of traumatic brain injury vary widely in type and duration; they include physical, cognitive, emotional, and behavioral complications. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a

state of alertness to interact with their surroundings),[106]and minimally conscious state (in which patients show minimal signs of being aware of self or environment).[107][108] Lying still for long periods can cause complications includingpressure sores, pneumonia or other infections, progressive multiple organ failure,[82] anddeep venous thrombosis, which can cause pulmonary embolism.[15] Infections that can follow skull fractures and penetrating injuries include meningitis and abscesses.[82]Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke.[82] Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), myoclonus (shock-like contractions of muscles), and loss of movement range and control (in particular with a loss of movement repertoire).[82] The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas.[103] People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma).[109] People may lose or experience altered vision, hearing, or smell.[3] Hormonal disturbances may occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients. Development of diabetes insipidus or an electrolyte abnormality acutely after injury indicate need for endocrinologic work up. Signs and symptoms of hypopituitarism may develop and be screened for in adults with moderate TBI and in mild TBI with imaging abnormalities. Children with moderate to severe head injury may also develop hypopituitarism. Screening should take place 3 to 6 months, and 12 months after injury, but problems may occur more remotely.[110] Cognitive deficits that can follow TBI include impaired attention; disrupted insight, judgement, and thought; reduced processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking.[111] Memory loss, the most common cognitive impairment among head-injured people, occurs in 2079% of people with closed head trauma, depending on severity.[112] People who have suffered TBI may also have difficulty with understanding or producing spoken or written language, or with more subtle aspects of communication such as body language.[82] Post-concussion syndrome, a set of lasting symptoms experienced after mild TBI, can include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression.[3] Multiple TBIs may have a cumulative effect.[108] A young person who receives a second concussion before symptoms from another one have healed may be at risk for developing a very rare but deadly condition calledsecond-impact syndrome, in which the brain swells catastrophically after even a mild blow, with debilitating or deadly results. About one in five career boxers is affected by chronic traumatic brain injury (CTBI), which causes cognitive, behavioral, and physical impairments.[113] Dementia pugilistica, the severe form of CTBI, affects primarily career boxers years after a boxing career. It commonly manifests as dementia, memory problems, and parkinsonism (tremors and lack of coordination).[114] TBI may cause emotional, social, or behavioral problems and changes in personality. [115][116][117][118] These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, problems with social judgment, and impaired conversational skills.[115][118][119] TBI appears to predispose survivors to psychiatric disorders including obsessive compulsive disorder, substance abuse, dysthymia, clinical depression, bipolar disorder, and anxiety disorders.[120] In patients who have depression after TBI, suicidal ideation is not uncommon; the suicide rate among these persons is increased 2- to 3-fold.[121] Social and behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, poor social judgment, and changes in personality. [115][117][118][122] TBI also has a substantial impact on the functioning of family systems[123] Caregiving family members and TBI survivors often significantly alter their familial roles and responsibilities following injury, creating significant change and strain on a family system. Typical challenges identified by families recovering from TBI include: frustration and impatience with one another, loss of former lives and relationships, difficulty setting reasonable goals, inability to effectively solve problems as a family, increased level of stress and household tension, changes in emotional dynamics, and overwhelming desire to return to pre-injury status. In addition, families may exhibit less effective functioning in areas including coping, problem solving and communication. Psychoeducation and counseling models have been demonstrated to be effective in minimizing family disruption [124] Epidemiology

Causes of TBI fatalities in the US[125] TBI is a leading cause of death and disability around the globe[126] and presents a major worldwide social, economic, and health problem.[2] It is the number one cause of coma,[127]it plays the leading role in disability due to trauma,[68] and is the leading cause of brain damage in children and young adults.[7] In Europe it is responsible for more years of disability than any other cause.[2] It also plays a significant role in half of trauma deaths.[15] Findings on the frequency of each level of severity vary based on the definitions and methods used in studies. A World Health Organization study estimated that between 70 and 90% of head injuries that receive treatment are mild,[128] and a US study found that moderate and severe injuries each account for 10% of TBIs, with the rest mild. [64] The incidence of TBI varies by age, gender, region and other factors.[129] Findings of incidence and prevalence in epidemiological studies vary based on such factors as which grades of severity are included, whether deaths are included, whether the study is restricted to hospitalized people, and the study's location. [7] The annual incidence of mild TBI is difficult to determine but may be 100600 people per 100,000.[55] Mortality In the US, the mortality (death rate) rate is estimated to be 21% by 30 days after TBI.[83] A study on Iraq War soldiers found that severe TBI carries a mortality of 30 50%.[55] Deaths have declined due to improved treatments and systems for managing trauma in societies wealthy enough to provide modern emergency and neurosurgical services.[92] The fraction of those who die after being hospitalized with TBI fell from almost half in the 1970s to about a quarter at the beginning of the 21st century.[68] This decline in mortality has led to a concomitant increase in the number of people living with disabilities that result from TBI.[130] Biological, clinical, and demographic factors contribute to the likelihood that an injury will be fatal.[125] In addition, outcome depends heavily on the cause of head injury. In the US, patients with fallrelated TBIs have an 89% survival rate, while only 9% of patients with firearm-related TBIs survive.[131] In the US, firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls.[125] Of deaths from firearms, 75% are considered to be suicides.[125] The incidence of TBI is increasing globally, due largely to an increase in motor vehicle use in low- and middle-income countries.[2] In developing countries, automobile use has increased faster than safety infrastructure could be introduced.[55] In contrast, vehicle safety laws have decreased rates of TBI in high-income countries,[2] which have seen decreases in traffic-related TBI since the 1970s.[47] Each year in the United States about two million people suffer a TBI[13] and about 500,000 are hospitalized.[129] The yearly incidence of TBI is estimated at 180250 per 100,000 people in the US,[129] 281 per 100,000 in France, 361 per 100,000 in South Africa, 322 per 100,000 in Australia, [7] and 430 per 100,000 in England.[53] In the European Union the yearly aggregate incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000.[2]

Demographics TBI is present in 85% of traumatically injured children, either alone or with other injuries.[132] The greatest number of TBIs occur in people aged 1524.[5][30] Because TBI is more common in young people, its costs to society are high due to the loss of productive years to death and disability. [2] The age groups most at risk for TBI are children ages five to nine and adults over age 80, [101] and the highest rates of death and hospitalization due to TBI are in people over age 65. [102] The incidence of fall-related TBI in First World countries is increasing as the population ages; thus the median age of people with head injuries has increased.[2] Regardless of age, TBI rates are higher in males.[30] Men suffer twice as many TBIs as women do and have a fourfold risk of fatal head injury, [101] and males account for two thirds of childhood and adolescent head trauma.[133] However, when matched for severity of injury, women appear to fare more poorly than men. [84] Socioeconomic status also appears to affect TBI rates; people with lower levels of education and employment and lower socioeconomic status are at greater risk.[7] History

The Edwin Smith Papyrus Head injury is present in ancient myths that may date back before recorded history. [134]Skulls found in battleground graves with holes drilled over fracture lines suggest thattrepanation may have been used to treat TBI in ancient times.[135] Ancient Mesopotamiansknew of head injury and some of its effects, including seizures, paralysis, and loss of sight, hearing or speech. [136] The Edwin Smith Papyrus, written around 16501550 BC, describes various head injuries and symptoms and classifies them based on their presentation and tractability. [137] Ancient Greek physicians including Hippocrates understood the brain to be the center of thought, probably due to their experience with head trauma. [138] Medieval and Renaissance surgeons continued the practice of trepanation for head injury.[138] In the Middle Ages, physicians further described head injury symptoms and the term concussion became more widespread.[139] Concussion symptoms were first described systematically in the 16th century by Berengario da Carpi.[138] It was first suggested in the 18th century that intracranial pressure rather than skull damage was the cause of pathology after TBI. This hypothesis was confirmed around the end of the 19th century, and opening the skull to relieve pressure was then proposed as a treatment. [135] In the 19th century it was noted that TBI is related to the development of psychosis.[140] At that time a debate arose around whetherpost-concussion syndrome was due to a disturbance of the brain tissue or psychological factors.[139] The debate continues today.

Phineas Gage carrying the rod that caused his TBI Perhaps the first reported case of personality change after brain injury is that of Phineas Gage, who survived an accident in which a large iron rod was driven through his head, destroying one or both of his frontal lobes; numerous cases of personality change after brain injury have been reported since.[24][26][27][36][37][41][141][142] The 20th century saw the advancement of technologies that improved treatment and diagnosis such as the development of imaging tools including CT and MRI, and, in the 21st century, diffusion tensor imaging (DTI). The introduction of intracranial pressure monitoring in the 1950s has been credited with beginning the "modern era" of head injury.[92][143] Until the 20th century, the mortality rate of TBI was high and rehabilitation was uncommon; improvements in care made during World War I reduced the death rate and made rehabilitation possible.[134] Facilities dedicated to TBI rehabilitation were probably first established during World War I.[134] Explosives used in World War I caused many blast injuries; the large number of TBIs that resulted allowed researchers to learn about localization of brain functions.[144] Blast-related injuries are now common problems in returning veterans from Iraq & Afghanistan; research shows that the symptoms of such TBIs are largely the same as those of TBIs involving a physical blow to the head.[145] In the 1970s, awareness of TBI as a public health problem grew,[146] and a great deal of progress has been made since then in brain trauma research,[92] such as the discovery ofprimary and secondary brain injury.[135] The 1990s saw the development and dissemination of standardized guidelines for treatment of TBI, with protocols for a range of issues such as drugs and management of intracranial pressure.[92] Research since the early 1990s has improved TBI survival;[135] that decade was known as the "Decade of the Brain" for advances made in brain research.[147] Research No medication to halt the progression of secondary injury exists,[55] but the variety of pathological events presents opportunities to find treatments that interfere with the damage processes.[2] Neuroprotection, methods to halt or mitigate secondary injury, have been the subject of great interest for their ability to limit the damage that follows TBI. However, clinical trials to test agents that could halt these cellular mechanisms have met largely with failure.[2] For example, interest existed in hypothermia, cooling the injured brain to limit TBI damage, but clinical trials showed that it is not useful in the treatment of TBI.[92] In addition, drugs such as NMDA receptor antagoniststo halt neurochemical cascades such as excitotoxicity showed promise in animal trials but failed in clinical trials.[92] These failures could be due to factors including faults in the trials' design or in the insufficiency of a single agent to prevent the array of injury processes involved in secondary injury.[92] Recent research has gone into monitoring brain metabolism for ischaemia, in particular the parameters of glucose, glycerol, and glutamate through microdialysis[citation needed].

Developments in technologies may provide doctors with valuable medical information. For example, work has been done to design a device to monitor oxygenation that could be attached to a probe placed into the brainsuch probes are currently used to monitor ICP.[92] Research is also planned to clarify factors correlated to outcome in TBI and to determine in which cases it is best to perform CT scans and surgical procedures.[148] Hyperbaric oxygen therapy (HBO) has been evaluated as an adjunctive treatment following TBI, concluding a Cochrane review stating that its use could not be justified.[149] HBO for TBI has remained controversial as studies have looked for improvement mechanisms, [150][151][152] and further evidence shows that it may have potential as a treatment.[153][154] http://en.wikipedia.org/wiki/Traumatic_brain_injury

TRAUMATIC BRAIN INJURY Definition By Mayo Clinic staff Traumatic brain injury occurs when an external mechanical force causes brain dysfunction. Traumatic brain injury usually results from a violent blow or jolt to the head or body. An object penetrating the skull, such as a bullet or shattered piece of skull, also can cause traumatic brain injury. Mild traumatic brain injury may cause temporary dysfunction of brain cells. More serious traumatic brain injury can result in bruising, torn tissues, bleeding and other physical damage to the brain that can result in long-term complications or death. Symptoms By Mayo Clinic staff Traumatic brain injury can have wide-ranging physical and psychological effects. Some signs or symptoms may appear immediately after the traumatic event, while others may appear days or weeks later. Mild traumatic brain injury The signs and symptoms of mild traumatic brain injury may include:

Loss of consciousness for a few seconds to a few minutes No loss of consciousness, but a state of being dazed, confused or disoriented Memory or concentration problems Headache Dizziness or loss of balance Nausea or vomiting

Sensory problems, such as blurred vision, ringing in the ears or a bad taste in the mouth Sensitivity to light or sound Mood changes or mood swings Feeling depressed or anxious Fatigue or drowsiness Difficulty sleeping Sleeping more than usual Moderate to severe traumatic brain injuries Moderate to severe traumatic brain injuries can include any of the signs and symptoms of mild injury, as well as the following symptoms that may appear within the first hours to days after a head injury:

Loss of consciousness from several minutes to hours Profound confusion Agitation, combativeness or other unusual behavior Slurred speech Inability to awaken from sleep Weakness or numbness in fingers and toes Loss of coordination Persistent headache or headache that worsens Repeated vomiting or nausea Convulsions or seizures Dilation of one or both pupils of the eyes Clear fluids draining from the nose or ears Children's symptoms Infants and young children with brain injuries may lack the communication skills to report headaches, sensory problems, confusion and similar symptoms. In a child with traumatic brain injury, you may observe:

Change in eating or nursing habits Persistent crying and inability to be consoled Unusual or easy irritability Change in ability to pay attention Change in sleep habits Sad or depressed mood Loss of interest in favorite toys or activities When to see a doctor Always see your doctor if you or your child has received a blow to the head or body that concerns you or causes behavioral changes. Seek emergency medical care if there are any signs or symptoms of traumatic brain injury following a recent blow or other traumatic injury to the head. The terms "mild," "moderate" and "severe" are used to describe the effect of the injury on brain function. A mild injury to the brain is still a serious injury that requires prompt attention and an accurate diagnosis. Causes By Mayo Clinic staff Traumatic brain injury is caused by a blow or other traumatic injury to the head or body. The degree of damage can depend on several factors, including the nature of the event and the force of impact. Injury may include one or more of the following factors:

Damage to brain cells may be limited to the area directly below the point of impact on the skull. A severe blow or jolt can cause multiple points of damage because the brain may move back and forth in the skull. A severe rotational or spinning jolt can cause the tearing of cellular structures. A blast, as from an explosive device, can cause widespread damage. An object penetrating the skull can cause severe, irreparable damage to brain cells, blood vessels and protective tissues around the brain. Bleeding in or around the brain, swelling, and blood clots can disrupt the oxygen supply to the brain and cause wider damage. Common causes Common events causing traumatic brain injury include the following:

Falls. Falling out of bed, slipping in the bath, falling down steps, falling from ladders and related falls are the most common cause of traumatic brain injury overall, particularly in older adults and young children.

Vehicle-related collisions. Collisions involving cars, motorcycles or bicycles and pedestrians involved in such accidents are a common cause of traumatic brain injury. Violence. About 10 percent of traumatic brain injuries are caused by violence, such as gunshot wounds, domestic violence or child abuse. Shaken baby syndrome is traumatic brain injury caused by the violent shaking of an infant that damages brain cells. Sports injuries. Traumatic brain injuries may be caused by injuries from a number of sports, including soccer, boxing, football, baseball, lacrosse, skateboarding, hockey, and other high-impact or extreme sports. Explosive blasts and other combat injuries. Explosive blasts are a common cause of traumatic brain injury in active-duty military personnel. Although the mechanism of damage isn't well understood, many researchers believe that the pressure wave passing through the brain significantly disrupts brain function. Traumatic brain injury also results from penetrating wounds, severe blows to the head with shrapnel or debris, and falls or bodily collisions with objects following a blast. Risk factors By Mayo Clinic staff The people most at risk of traumatic brain injury include:

Children, especially newborns to 4-year-olds Young adults, especially those between ages 15 and 24 Adults age 75 and older Complications By Mayo Clinic staff Several complications can occur immediately or soon after a traumatic brain injury. Severe injuries increase the risk of a greater number of complications and more-severe complications. Altered consciousness Moderate to severe traumatic brain injury can result in prolonged or permanent changes in a person's state of consciousness, awareness or responsiveness. Different states of consciousness include:

Coma. A person in a coma is unconscious, unaware of anything and unable to respond to any stimulus. This results from widespread damage to all parts of the brain. After a few days to a few weeks, a person may emerge from a coma or enter a vegetative state. Vegetative state. Widespread damage to the brain can result in a vegetative state. Although the person is unaware of his or her surroundings, he or she may open his or her eyes, make sounds, respond to reflexes, or move. It's possible that a vegetative state can become permanent, but often individuals progress to a minimally conscious state. Minimally conscious state. A minimally conscious state is a condition of severely altered consciousness but with some evidence of self-awareness or awareness of one's environment. It is often a transitional state from a coma or vegetative condition to greater recovery. Locked-in syndrome. A person in a locked-in state is aware of his or her surroundings and awake, but he or she isn't able to speak or move. The person may be able to communicate with eye movement or blinking. This state results from damage limited to the lower brain and brainstem. This rarely occurs after trauma.

Seizures Some people with traumatic brain injury will have seizures within the first week. Some serious injuries may result in recurring seizures, called post-traumatic epilepsy. Fluid buildup Cerebrospinal fluid may build up in the spaces in the brain (cerebral ventricles) of some people who have had traumatic brain injuries, causing swelling and increased pressure in the brain. Infections Skull fractures or penetrating wounds can tear the layers of protective tissues (meninges) that surround the brain. This can enable bacteria to enter the brain and cause infections. An infection of the meninges (meningitis) could spread to the rest of the nervous system if not treated. Blood vessel damage Several small or large blood vessels in the brain may be damaged in a traumatic brain injury. This damage could lead to a stroke, blood clots or other problems. Nerve damage Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

Paralysis of facial muscles Damage to the nerves responsible for eye movements, which can cause double vision Damage to the nerves that provide sense of smell Loss of vision Loss of facial sensation Swallowing problems Cognitive problems Most people who have had a significant brain injury will experience changes in their thinking (cognitive) skills. Traumatic brain injury can result in problems with many skills, including:

Memory Learning Reasoning Problem solving Speed of mental processing Judgment

Attention or concentration Multitasking Organization Decision making Beginning or completing tasks Communication problems Language and communications problems are common following traumatic brain injuries. These problems can cause frustration, conflict and misunderstanding for people with a traumatic brain injury, as well as family members, friends and care providers. Communication problems may include:

Difficulty understanding speech or writing Difficulty speaking or writing Difficulty deciphering nonverbal signals Inability to organize thoughts and ideas Inability to use the muscles needed to form words (dysarthria) Problems with changes in tone, pitch or emphasis to express emotions, attitudes or subtle differences in meaning Trouble starting or stopping conversations Trouble with turn taking or topic selection Trouble reading cues from listeners Trouble following conversations Behavioral changes People who've experienced brain injury often experience changes in behaviors. These may include:

Difficulty with self-control Lack of awareness of abilities Risky behavior Inaccurate self-image Difficulty in social situations

Verbal or physical outbursts Emotional changes Emotional changes may include:

Depression Anxiety Mood swings Irritability Lack of empathy for others Anger Insomnia Changes in self-esteem Sensory problems Problems involving senses may include:

Persistent ringing in the ears Difficulty recognizing objects Impaired hand-eye coordination Blind spots or double vision A bitter taste or a bad smell Skin tingling, pain or itching Trouble with balance or dizziness Degenerative brain diseases A traumatic brain injury may increase the risk of diseases that result in the gradual degeneration of brain cells and gradual loss of brain functions. These include:

Alzheimer's disease, which primarily causes the progressive loss of memory and other thinking skills Parkinson's disease, a progressive condition that causes movement problems, such as tremors, rigidity and slow movements Dementia pugilistica most often associated with repetitive blows to the head in career boxing which causes symptoms of dementia and movement problems

Tests and diagnosis By Mayo Clinic staff Because traumatic brain injuries are usually emergencies and because consequences can worsen swiftly without treatment, doctors usually need to assess the situation rapidly. Glasgow Coma Scale This 15-point test helps a doctor or other emergency medical personnel assess the initial severity of a brain injury by checking a person's ability to follow directions and move their eyes and limbs. The coherence of speech also provides important clues. Abilities are scored numerically. Higher scores mean milder injuries. Information about the injury and symptoms If you observed someone being injured or arrived immediately after an injury, you may be able to provide medical personnel with information that's useful in assessing the injured person's condition. Answers to the following questions may be beneficial in judging the severity of injury:

How did the injury occur? Did the person lose consciousness? How long was the person unconscious? Did you observe any other changes in alertness, speaking, coordination or other signs of injury? Where was the head or other parts of the body struck? Can you provide any information about the force of the injury? For example, what hit the person's head, how far did he or she fall, or was the person thrown from a vehicle? Was the person's body whipped around or severely jarred? Imaging tests

Computerized tomography (CT). A CT scan uses a series of X-rays to create a detailed view of the brain. A CT scan can quickly visualize fractures and uncover evidence of bleeding in the brain (hemorrhage), blood clots (hematomas), bruised brain tissue (contusions) and brain tissue swelling. Magnetic resonance imaging (MRI). An MRI uses powerful radio waves and magnets to create a detailed view of the brain. Doctors don't often use MRIs during emergency assessments of traumatic brain injuries because the procedure takes too long. This test may be used after the person's condition has been stabilized. Intracranial pressure monitor Tissue swelling from a traumatic brain injury can increase pressure inside the skull and cause additional damage to the brain. Doctors may insert a probe through the skull to monitor this pressure. Treatments and drugs By Mayo Clinic staff

Mild injury Mild traumatic brain injuries usually require no treatment other than rest and over-the-counter pain relievers to treat a headache. However, a person with a mild traumatic brain injury usually needs to be monitored closely at home for any persistent, worsening or new symptoms. He or she also may have follow-up doctor appointments. The doctor will indicate when a return to work, school or recreational activities is appropriate. It's best to avoid physical or thinking (cognitive) activities until symptoms have stopped. Most people return to normal routines gradually. Immediate emergency care Emergency care for moderate to severe traumatic brain injuries focuses on making sure the person has an adequate oxygen and blood supply, maintaining blood pressure, and preventing any further injury to the head or neck. People with severe injuries may also have other injuries that need to be addressed. Additional treatments in the emergency room or intensive care unit of a hospital will focus on minimizing secondary damage due to inflammation, bleeding or reduced oxygen supply to the brain. Medications Medications to limit secondary damage to the brain immediately after an injury may include:

Diuretics. These drugs reduce the amount of fluid in tissues and increase urine output. Diuretics, given intravenously to people with traumatic brain injury, help reduce pressure inside the brain. Anti-seizure drugs. People who've had a moderate to severe traumatic brain injury are at risk of having seizures during the first week after their injury. An anti-seizure drug may be given during the first week to avoid any additional brain damage that might be caused by a seizure. Additional anti-seizure treatments are used only if seizures occur. Coma-inducing drugs. Doctors sometimes use drugs to put people into temporary comas because a comatose brain needs less oxygen to function. This is especially helpful if blood vessels, compressed by increased pressure in the brain, are unable to deliver the usual amount of nutrients and oxygen to brain cells. Surgery Emergency surgery may be needed to minimize additional damage to brain tissues. Surgery may be used to address the following problems:

Removing clotted blood (hematomas). Bleeding outside or within the brain can result in a collection of clotted blood (hematoma) that puts pressure on the brain and damages brain tissue. Repairing skull fractures. Surgery may be needed to repair severe skull fractures or to remove pieces of skull in the brain. Opening a window in the skull. Surgery may be used to relieve pressure inside the skull by draining accumulated cerebral spinal fluid or creating a window in the skull that provides more room for swollen tissues. Rehabilitation Most people who have had a significant brain injury will require rehabilitation. They may need to relearn basic skills, such as walking or talking. The goal is to improve their abilities to perform daily activities. Therapy usually begins in the hospital and continues at an inpatient rehabilitation unit, a residential treatment facility or through outpatient services. The type and duration of rehabilitation varies by individual, depending on the severity of the brain injury and what part of the brain was injured. Rehabilitation specialists may include:

Physiatrist, a doctor trained in physical medicine and rehabilitation, who oversees the entire rehabilitation process Occupational therapist who helps the person learn, relearn or improve skills to perform everyday activities Physical therapist, who helps with mobility and relearning movement patterns, balance and walking Speech and language pathologist, who helps the person improve communication skills and use assistive communication devices if necessary Neuropsychologist or psychiatrist, who helps the person manage behaviors or learn coping strategies, provides talk therapy as needed for emotional and psychological well-being, and prescribes medication as needed Social worker or case manager, who facilitates access to service agencies, assists with care decisions and planning, and facilitates communication among various professionals, care providers and family members

Rehabilitation nurse, who provides ongoing rehabilitation care and services and who helps with discharge planning from the hospital or rehabilitation facility Traumatic brain injury nurse specialist, who helps coordinate care and educates the family about the injury and recovery process Recreational therapist, who assists with leisure activities Vocational counselor, who assesses the ability to return to work and appropriate vocational opportunities, and provides resources for addressing common challenges in the workplace Prevention By Mayo Clinic staff Follow these tips to reduce the risk of brain injury:

Seat belts and airbags. Always wear a seat belt in a motor vehicle. Small children should always sit in the back seat of a car and be secured in child safety seats or booster seats that are appropriate for their size and weight. Alcohol and drug use. Don't drive under the influence of alcohol or drugs, including prescription medications that can impair the ability to drive. Helmets. Wear a helmet while riding a bicycle, skateboard, motorcycle, snowmobile or all-terrain vehicle. Also wear appropriate head protection when playing baseball or contact sports, skiing, skating, snowboarding or riding a horse. Preventing falls The following tips can help older adults avoid falls around the house:

Install handrails in bathrooms Put a nonslip mat in the bathtub or shower Remove area rugs Install handrails on both sides of staircases

Improve lighting in the home Keep stairs and floors clear of clutter Get regular vision checkups Get regular exercise Preventing head injuries in children The following tips can help children avoid head injuries:

Install safety gates at the top of stairs Keep stairs clear of clutter Install window guards to prevent falls Put a nonslip mat in the bathtub or shower Use playgrounds that have shock-absorbing materials on the ground Make sure area rugs are secure Don't let children play on fire escapes or balconies http://www.mayoclinic.com/health/traumatic-brain-injury/DS00552

CRANIOCEREBRAL TRAUMA Divisions of Trauma 1. Divided into three groups based upon the nature of the injury. 1. Closed head injuries 2. Depressed fracture of the skull 3. Compound fracture of the skull (direct contact with cerebral tissue) 2. Concussion -- loss of consciousness following head injury: may be momentary or prolonged and full recovery may or may not occur. 1. Damage due to head movement swirling forces and shear forces. 2. Damage begins at surface and progresses inward. 3. If severe enough to reach brain stem on diencephalon, loss of consciousness will occur. 4. Direct area damage also contrecoup injury w*hich is greater in closed head injury. 3. Contusion or lacerations -- bruising or tissue injury most common with Penetiating injuries where loss of consciousness is less likely to occur. 4. Recovery 1. Coma 2. Stupor 3. PTA

4. Confusion 5. PCS TOP

Complications of head injury 1. Subdural hemorrhage - arachnoid - normal 2. Extradural hemorrhage - due to tear in meningeal arteries or dural sinus 15% 1. relatively rare (3%) 2. usually pt. recovers consciousness and then suffers a relapse into coma with development of hemiplegia 3. with more severe injuries - may not have lucid interval 4. may develop after several weeks 5. fixed - dilated pupil may be present 6. most fatal complication - mortality 100% in untreated and over 50% in treated cases 7. death usually occurs within 12 to 72 hours 8. Rx - evacuation and repair 3. Subdural hemorrhage (1 to 10%) 1. always secondary to head trauma 2. blood not absorbed in CSF but is encapsulated by dura 3. fibroblasts invade clot from dura 4. newly formed capillaries enter the clot and absorb 5. causes dural thickening - with large clot may cause subdural cyot with calcification 6. clot may cause contralateral compression thus confusing effects 7. symptoms develop within first few days 8. frequently bilateral 4. Subdural Hygroma - excessive collection of subdural fluid 5. Intracerebral Hemorrhage 6. Infections 1. extradural 2. subdural abscess 3. meningitis 4. brain abscess 7. Rhinorrhea - cribraform plate injury TOP

Sequelae of head injuries 1. Seizures - develop several months later 1. 2.5 to 40% incidence 2. 5% with closed head injury 3. 30 to 40% with penetrating head injury 2. Psychoses and mental disturbances

3. Intracerebral hemorrhage 4. Subarachnoid Hemorrhage 1. blood in cerebral spinal fluid 5. Trauma consequences 1. Concussion 2. Contusions & lacerations 3. Complications of skull fractures TOP

Basic Information regarding TBI

Statistics o In 1977, approximately 10 million head injuries o 1.5 million severe including concussions, intercranial injuries, and fractures. o 90% are less than 44 years old o Leading cause of death between 4 - 44 years. Type of injuries: o Work injuries - 3%; o Auto Accidents- 12%; o Play (kids) injuries - 42%; o Injuries at home - 44%;

Mechanics of Traumatic Brain Injury

Contusion - bruise o effect of pressure Concussion o Transient loss of consciousness due to mechanical forces to the brain o Shear force o Centrifugal forces (Ommya and Gennerali) o Most severe at surface (Cortex) causing cognitive impairment. o If severe, damage may extent down into the midbrain, causing an acute memory deficit (post- traumatic amnesia). o If even more severe, extend down into brainstem - Coma. Initial hospital records very important o Clarify source of data

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Neuropsych vs CT Scan and EEG

Percent who appear impaired o EEG: 28% mild, 72% severe o CT Scan: 26% mild, 45% severe o Neuropsychological battery: 87% mild, 89% severe

Neuropsychology is most important for the mild injury

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Post-Concussion Symptoms

Symptoms often confused with cognitive impairment Actually reflect interaction of cognitive and emotional factors Good guide to recovery o Number o Intensity o Change over time

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Outcome Measures

Pre-Injury Factors o Pre-injury level o Age o Education/Occupation o Personality o Emotional Adjustment Neurological Factors o Severity - Cognitive Impairment Post-Injury Factors o Post-Concussion Symptoms o Pain o Family Support o Compensation o Stress o Expectancy

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Severity Determination Post-Traumatic Amnesia Length PTA Russell 35 Alternate Cognitive Recovery Full Recovery

< 5 min 5-60 min 1-24 hrs 1-7 days 8-28 days > 28 days TOP

Mild Mod Severe V Sev V Sev

Minim V mild Mild Mod Severe V Sev

1 mo 1-3 mo 3-6 mo 6-12 mo 12-24 mo +24 mo

1 mo 3 mo 1 yr 1-2 yrs Residual Residual

Minor Head Injury

Definition o Coma < 20 minutes o Hospitalization < 72 hours o Glasgow Coma Scale > 12 Problem with Definition o No Lower Limits o Leads to misclassification of individuals who sustain no neurological trauma Redefine - some PTA or neurological symptoms

Consequences of Mild Head Injury

Cognitive Impairment o Recovery Mild = 3 mo Mod.= 1 yr Post-Concussion Symptoms o Minor = 78% of cases. Symptoms last approximately 3 months o Severe = 24% of cases. Symptoms last approximately 1 year. Percentage of patients who return to work by 1 year o Mild = 90% o Mod.= 80% RECOVERY figure

A Model of Recovery to Maximize the Rehabilitation of Individuals with Head Trauma By Charles J. Long Ph.D. THE JOURNAL OF HEAD INJURY VOL 11, NO. 3 1991 (pp18-28)

In recent years, health care professionals have made tremendous strides in understanding the effects of head injury. In spite of this understanding, it is often difficult to communicate this information to the survivors and their family; and, without effective communication, it is difficult to elicit their maximum effort during rehabilitation. The purpose of this article is to outline methods for enhancing this communication and, by outlining various models, to assist in improving the rehabilitation process. A further advantage of a model of recovery is to allow more effective communication with other health care professionals as well as to objectify one's own perception of the patient's progress. TOP

THE NATURE OF HEAD INJURY It is important to understand the nature of head trauma, as this provides necessary information about both the severity of the injury and the sequence and rate of recovery. Such understanding enhances the ability to plan appropriate treatment and rehabilitation strategies and to counsel the head inured survivors and their family. With this in mind, a brief review of the mechanisms of head injury will be presented (Long & Webb, 1983; Long & Williams, 1988).< P> Functional Systems of the Brain: Perhaps the best way to understand the effects of head injury is to consider the simplified view of the functional systems of the brain as depicted in Figure 1 and outlined in Table 1. As you can see in this figure and table, the brain can be viewed as composed of three separate but interconnected systems: brain stem, diencephalon, and cortical system. A brief discussion of these three systems will serve to clarify the effects of head injury and the process of recovery. Although these three systems function in many other ways and are highly interconnected in the way that they process information, this over-simplified view of brain function will provide a better understanding of changes in behavior following head injury. 3 Systems figure Table 1. Outline of the three functional systems of the brain. CORTICAL SYSTEM INFORMATION PROCESSING MODALITY (Vision, Audition, Somatosensory) MATERIAL (Verbal/Non-Verbal) PREFRONTAL CORTEX (Planning and Regulation) DIENCEPHALON (Limbic System) AROUSAL EMOTION MOTIVATION MEMORY CONSOLIDATION BRAIN STEM ACTIVATION (Cortical Desynchronization)

SHIFTING ATTENTION HABITUATION PERCEPTION Brain Stem: The brain stem and related structures at the base of the brain, between the brain and spinal cord, represent the oldest structures in the brain. This system has many important functions. It receives input from sensory systems and relays this information through the thalamus to activate the cortex. This activation is essential for the cortex to function. In elementary terms, it might be thought of as the volume control for the higher systems. Specifically, when it does not sufficiently activate the cortex, perception is not possible; and no amount of stimulation will be perceived by the higher systems. In addition, it causes the person to attend to incoming stimuli. It is particularly sensitive to novel stimuli and plays an important role in allowing the person to quickly shift attention to such stimuli. When input is constant, the person will habituate (i.e., they will cease to notice the stimuli). Based on these functions, it is clear that this system is essential for the function of higher systems. It does not work like an on or off switch; rather, it works across a broad range. With variation in its level of activity, the person varies from being highly alert to asleep (or unconscious). When damaged, the higher systems cannot perceive stimuli; the individuals are unresponsive and do not attend to stimuli in their environment. They are in a coma. Dencephalon: This system, along with other structures, makes up the middle part of the brain and receives input from the brain stem, sensory systems, and the higher systems. It maintains behavioral arousal, and its basic function is to monitor input to the body and determine those stimuli that have significance or high survival value. Stimuli that cause pain directly influence this system, and conditions are established to move the individual away from painful stimuli. In like manner, it is involved in moving us toward stimuli which are important (e.g., things which we desire or which are necessary for survival). This system therefore plays an important role in emotion and motivation. It is also essential for converting memories from temporary to long-term storage (called memory consolidation). Damage to this system can alter emotion and motivation; and, more specifically, it can impair memory consolidation. When the latter occurs, the individuals may retain old, pre-injury memories, but they will not be able to maintain new memories over time (i.e., from minute to minute of day to day). Memory consolidation, while appearing to be quite different from emotion and motivation, fits into the same process in that it is important for us to remember things that are significant for our survival (Long, 1984). Thus, we tend to remember things that allow us to get what we need to survive and to avoid things that are not helpful in this regard. Memory consolidation varies according to the importance of stimuli. We tend to remember very important or unusual things (whether they are positive or negative) and tend not to remember more neutral things. During recovery from head injury, some pieces of information will be recalled but others will not. These recollections are most likely related to the emotional significance of the stimuli. Cortical System: The third system includes the cortex and its associated components. This system, the most complex and most specialized in function, is concerned with information processing. This system receives the sensory information from our receptors and processes it through various stages of complexity. The dominant hemisphere of the brain (usually the left hemisphere) is concerned with language processing, and the non-dominant hemisphere (usually the right hemisphere) deals with non-language or spatial processing. Damage to this system directly affects cognitive processing by increasing the processing time, making perception difficult, and disrupting the individual's ability to interpret new information. Direct damage to this system will impair both information processing and specific memories because both processing and memory are dependent upon the functions of different areas of the cortex and related systems (Williams & Long, 1987, 1988). The most anterior region (the prefrontal cortex) is concerned with planning, formulating complex motor responses to the environment, and orienting the receptors to enhance sensory input. In addition to formulating plans, this system is important in directing the individual's behavior toward these plans or goals. Damage to this region impairs the individual's ability to sustain attention or to concentrate on a task. They have trouble with both developing a plan and with breaking down a problem into the necessary steps to carry out the plan. In addition, they lose the ability to monitor their activities. Thus, they are easily distracted from their pursuit of a goal and tend not to be aware of such problems. TOP

CONTUSION/CONCUSSION A blow to the head may cause a contusion (bruise) to the brain, which is usually focal, and it may or may not result in unconsciousness. However, a concussion is a brief loss of consciousness, usually resulting from a mechanical force. A concussion most frequently relates to different forces which occur when the head is mobile (Ommaya & Gennarelli, 1974). According to Ommaya and Gennarelli's research, what happens at impact is that the head is mobile and is thrown forward, backward, or to the side. More specifically, the skull is thrown forward, but the brain tends to lag behind because of inertia. The head pivots at the neck; thus, when the head is suddenly thrown forward, the maximum effect of the inertia (or resistance) is at the point between the skull and the cortex where the forces are greatest. The brain stem is least affected since it is closest to the pivot point and moves the least distance. The effect is that the skull suddenly moves and the brain resists, causing shear forces. These shear forces are maximum at the surface of the brain (the cortex). Using this model, it is easy to see that even a mild injury (in which there is no loss of consciousness) can result in some damage to the cortex and lead to problems in cognitive functioning for a time after the accident. The likelihood of such damage is even easier to understand when you consider that the brain is specialized for transmission of information, has little internal structural support, and is dependent on the skull and other structures to support and protect it. If the forces are greater, the shear forces radiate down into the mid part of the brain (the diencephalon) and result is impaired memory consolidation, affecting the storage of new memories. If the shear forces are even greater, they radiate further down to the brain stem; damage to this region results in unconsciousness. These findings have been demonstrated in studies with both humans and animals (Gennarelli, Thibault, Adams, Graham, Thompson, & Marcincin 1982). Ommaya & Gennarelli's model is extremely helpful in understanding both the effects of head injury and the process of recovery. TOP

THE PROCESS OF RECOVERY Brain Stem: As can be seen from the above, the brain stem is usually the least affected and will therefore be the first to recover. The first stage of recovery, then, is the regaining of consciousness since that is a function of the brain stem. Also, using this model, it is clear that even after the recovery of consciousness there is a period of impaired memory consolidation called post-traumatic amnesia. This results from damage to the mid-part of the brain, and the individual loses the ability to store and retrieve new information. As a result, when head-injured individuals regain consciousness, they may recognize people and remember their past, but they won't remember new facts from hour to hour or from day to day. This, of course, is quite different from the typical television portrayal where the person has been unconscious for three weeks, wakes up, and says, "Gee, where have I been? I'd like to have ham and eggs for breakfast." Other than on TV, the only way that happens is with an injury that doesn't cause shear forces. For example, an impact may rupture a vessel and put pressure on the brain stem. In this case, the rest of the brain hasn't been affected to the extent outlined above, and the body may resolve the clot on the brain stem. When the brain stem regains function in this case, the rest of the brain, not being significantly damaged, is able to function normally. Diencepalon: Patients with very severe head injury may have little or no memory. As they recover, however, their memory returns from very early memories to more recent ones. That is, their memory begins to recover from the distant past toward the time of the accident. This is referred to as shrinking retrograde amnesia and apparently relates to the fact that, as facts are stored, they are associated with old memories or built upon existing memories. Early stored memories are recovered before more recent ones because early memories serve as the foundation upon which newer memories are associated or built. The most common problem with memory following head injury does not involve retrograde amnesia but, rather, to impaired memory consolidation. This relates to the fact that, even after recovery of brain stem functions, the diencephalon (hippocampus, hypothalamus, etc.) remains impaired. Since this system is essential for storing new memories, the person may recall early experiences but not be able to retain current events or have memories of things since the accident. With recovery, therefore, patients first regain consciousness and then memory consolidation,which results in recovery from post-traumatic amnesia. A frequent question relates to whether survivors will ever regain these lost memories. While they will regain their preciously stored memories, they will not regain any memory for the period of 5 to 15 minutes before the accident until they regain memory consolidation after their accident. This is due to the fact that the brain is not able to store information during this time; and, since the information is not stored, it is not available for later recall.

It is not anatomically possible to suffer severe damage to the brain that will destroy all personal memories and not destroy other memories as well. Head injury survivors who can walk, talk, and function without apparent impairment, but who cannot recall who they are, who their family is, or anything of their life from birth to the accident, most likely have emotional factors playing an important role. This is because the parts of the brain that remember how to move a hand or leg, the parts that remember what speech sounds mean, and the parts that can interpret visual images would also be damaged to some extent. While the period of memory loss before the accident (retrograde amnesia) may be very long at first, it shrinks over time and usually is no longer than 5 to 15 minutes in most cases. The time for which no memories are stored and, thus cannot be recalled, is the period from 5 minutes before the accident until the time the individual recovers memory consolidation. Cortex: Finally, head-injury survivors are left with a fairly long period of recovery of cognitive function, (i.e., those functions carried out by the cortex). The duration of unconsciousness can be used as a guide for severity of closed head injury, although the best measure is the duration of post-traumatic amnesia. This will be specifically addressed later. In most cases there are more than shear forces operating. For example, people may strike their head on an object and receive a contusion; and this force may be great enough to cause the brain to fly toward the impact, leaving a vacuum on the opposite side. The effects of this type of injury are referred to as a contra cou injury (injury on the side opposite the primary impact). In addition, there are several predominant bony ridges in the skull which encases the brain. If the brain is suddenly thrown forward, it may be forced across these ridges, and frequently this results in direct injury to the temporal and frontal lobes. This type of injury will cause greater problems in functioning than would occur with only shear-force type injury. In specific cases, individuals might experience posttraumatic seizures with this type of injury and most certainly would have some areas of more specific deficits. In addition to these variations, small vessels may rupture and cause focal areas of damage. TOP

DEVELOPING AN AWARENESS OF THE CONSEQUENCES OF HEAD INJURY Our own early awareness of the effects of head injury on cognitive functions occurred quite by chance. We were investigating cognitive functioning in patients with temporal lobe seizures and their performance was compared with that of patients that we assumed were normal controls (i.e., people who had normal neurological exams and were found to have normal CAT scans and EEGS). It was surprising to find that 50% of the patients considered normal on the CAT scan, EEG, and the neurological exam were impaired on the neuropsychological test battery. In reviewing these cases, however, 60% were found to have a history of head injury that was sufficient for them to seek medical attention. The implication of this is that even a head injury that does not produce prolonged unconsciousness can result in impaired cognitive functioning. Also, although CAT scan and EEGs may be interpreted as normal, cognitive functions may take quite some time to recover. The advantage of the neuropsychological assessment is that it does not focus on the tissue damage resulting from an injury but on the functional consequences of the injury (i.e., the impaired cognitive functions secondary to damage to the brain). Further research indicated that, of the majority of patients with mild and moderate injuries who were tested during the -early course of their recovery, only 28% showed impairment on the EEG and 26% on CAT scan. In contrast, on the neuropsychological assessments which were given at the same time, 87% of these patients demonstrated some form of cognitive impairment. As the severity of the injuries increased, the differences between these tests were less pronounced (Long & Gouvier, 1982). Despite these findings, neurosurgeons complain that, while insurance companies will allow numerous CAT or MRI scans, these same companies often won't approve a neuropsychological assessment. Unfortunately, this can create obstacles in providing a thorough and accurate treatment strategy for survivors of head injury. Regardless of the assessment procedure, the major problem is one of clearly and successfully communicating to the survivor, family, and physician where the individual is in the course of recovery, the severity of the injury, and what to expect in terms of recovery. TOP

A MODEL OF RECOVERY

Figure 2 represents a model that outlines the various stages of recovery from head injury (Long, Gouvier & Cole, 1984). The vertical axis on this figure refers to the level of cognitive functioning. It may decline from the pre-injury level to coma. Coma is the lowest level of cognitive functioning in a living person. The horizontal axis refers to the time course of recovery, varying from a few minutes to many years. Viewing this figure from left to right affords a view of the sequence of recovery across time. The initial decline from the pre-injury level to coma (in cases of more severe head injury) is the period of retrograde amnesia which is usually measured in minutes. Figure 2. Diagrammatic representation of level of cortical functioning as a function of time since head trauma: (A) premorbid level, (B) retrograde amnesia, (C) coma, (D) post-traumatic amnesia, (E) recovery of cognitive functions, (F) final level of recovery (Long & Webb, 1983). The effect of the trauma suddenly lowers the level of cognitive functioning from the pre-injury level. In cases of mild head injury, the cognitive functioning of the individual may not be reduced to the level of post-traumatic amnesia. However, as the severity of the forces increases, the degree of cognitive decline also increases. In cases of severe head injury, recovery progresses from a period of coma, stupor, and post-traumatic amnesia. Finally, they regain memory consolidation only to find themselves functioning at a level of impaired cognitive functioning. It is clear from this figure that the period of recovery from impaired cognitive functioning is much longer than the period of coma and post traumatic amnesia. In many cases, it is this prolonged period of recovery of cognitive functioning that is most problematic. On the surface, the individuals appear to be functioning at their pre-injury level; however, they are not. They may be slower in their responses, more distractible, more irritable, prone to fatigue, and have headaches, dizziness, etc. Furthermore, the survivors and/or families may be unaware of the potential problems confronting them. They may be continually frustrated by their inability to perform at the level they expect and, as a result, may make poor decisions. They may go back to work or school too early or attempt to take on too much. The role of the neuropsychologist is to help patients and their family understand the nature of the injury, where they are in the recovery process, what barriers are present to impede their recovery, and the time period that should elapse before they attempt to make important decisions (Long & Williams, 1988; Long & Schmitter, 1990a,b). This model aids this process in the following ways. First the survivor's level of cognitive functioning is assessed by neuropsychological and/or other testing. These test results need to be communicated to those involved. When communicating to a family, a survivor, or to another professional, it is inadequate to merely relay test results, such as intellectual functioning, speed of processing, etc. No one is particularly interested in that. What attorneys want to know is how does the present level of functioning compare with abilities prior to the injury. In almost all cases, this has to be estimated. Likewise, what families and physicians want to know is how long will recovery take and how long will it take to reach some specified point in recovery. This also must be estimated from experience with similar individuals with head injury. What does become clear is that no matter how accurately cognitive functions are measured, they must invariably be compared with some estimated starting or end point to answer most questions. To do this, relatively accurate estimates of the pre-injury level of functioning must be made. In addition, to predict time to recovery to some specified level, one must also be able to estimate the severity of the injury. These points will be discussed below. Pre-injury Level of Functioning: Regardless of the assessment procedure, the major problem is one of clearly and successfully communicating to the survivor, family, and physician where the individual is in the course of recovery, the severity of the injury, and what to expect in terms of recovery. Normally, the neuropsychologist needs to understand the individual's pre-injury level of functioning. This often remains an unknown, and perceptions may be distorted. Often, when asked how the survivor performed before his injury, the family may say, " Well, he was a brilliant student," while school records indicate that this may have not been the case. This distorted perception of level of functioning before injury can create problems in accurately perceiving the individuals' status after head injury. In other words, if the survivors and/or their family perceives the pre-injury level of function in a distorted manner, then their perceptions of current functioning will be further distorted by this comparison. In estimating pre-injury level of functioning, it is important to obtain as much information as possible from different sources. This estimation can be greatly enhanced if the neuropsychologist has access to school grades, work history, and information from family members. Typically, however, one does not have direct access to this information, or the access is limited, and they must exercise professional judgment based on past experience with similar individuals. Attempts at developing a more accurate predictive formula have met with little success (Bolter, Gouvier, Veneklasen, & Long, 1982). Determination of Severity of Injury: The severity of the injury must also be considered. Generally, recovery time and severity of injury increase in proportion to the duration of coma and post-traumatic amnesia. Coma, however, tends to be too short, and is usually not evaluated sufficiently to provide a reliable measure. For this reason, the duration of post traumatic amnesia (i.e., the period of time from the injury to the time when memory becomes relatively stable) is considered to be the best measure of severity of injury (see table 2). Length of post-traumatic amnesia can be established by asking the individual such things as: "When did the accident occur? What is the first thing that you remember after the accident?" By careful interview, the time when memory became relatively stable can be established. This is certainly not a perfect method; however, with some careful discussion it is possible to get a fairly reasonable idea of the duration of post-traumatic amnesia.

Severity Table Table 2. Post traumatic amnesia (PTA) as a measure of severity of injury (modified from Russell, 1932, and Bond, 1983). Mild Head Injury: Post-traumatic amnesia of less than one day indicates a mild injury. This does not mean that there is no cognitive impairment. In fact, most of these individuals have cognitive weaknesses and require one to three months for full recovery. These individuals need to be advised in terms of how to plan and manage their time in order to avoid overdoing it during this period. The professional needs to be able to explain this possibility and assist the individual in developing strategies for minimizing stress. Moderate Head Injury: Post-traumatic amnesia (PTA) duration of one to seven days is considered a moderate head injury. Such an injury typically requires three to eleven months before early recovery. Severe and Very Severe Head Injury: Severe head injury involves a PTA duration of eight to twenty-eight days. Recovery from severe injury may require twelve to twenty-four months. With PTA duration of over twenty-nine days, the injury is considered very severe and maximum recovery often takes over two years. Duration of post-traumatic amnesia helps the professional to get an idea of the time span needed for the head-injury patient to recover. The age of the individual as well must also be considered. The older one is at the time of injury, the longer the time required for recovery. Conversely, the younger one is, the more likely this process may be speeded up. So, when does recovery time end? Technically, it may go on to infinity; but, as noted in Figure 2, it is rapid at first and gradually slows over time. Which things are likely to improve the most: Those things that are being slowed down or impaired by some barrier or some limitation. Once the professional understands the individual's pre-injury level of functioning, and obtains a measure of the severity of injury, treatment planning can be more effective. If an individual appears to be 30% below the pre-injury level, and it appears that is about where he or she should be on the recovery curve, it may be concluded that this individual does not have any significant emotional problems, probably has a good family support system, an not much can be done to speed recovery. On the other hand, if an individual is 30% below the pre-injury level, and this is much below what would be expected within these parameters, other factors should be taken into account. At this point, one should evaluate the individual's personality, talk to the family, and attempt to identify barriers to recovery. If the barriers are identified and strategies are developed to work around them, then recovery time should be reduced. Other things being equal, the extent of the final recovery decreases as a function of the severity of head injury. For survivors of mild and many survivors of moderate head injury, cognitive functions will recover to the level they were before the injury. Survivors of severe and very severe head injury are more likely to retain residual weaknesses or impairments, requiring them to learn compensatory strategies (Jones & Long, 1990). Of course, things are never equal and, as you will learn, there are many barriers which can greatly limit the recovery of less severely injured survivors. An example of potential barriers can be seen in the story of a young man with a moderate head injury who attempted to return to school. Before his injury, he was a B student. However, when he attempted to take 18 hours the semester after his head injury, he was making all Fs. His neurosurgeon couldn't understand the reason for such problems, because the young man's CAT scan appeared normal. His family thought he wasn't applying himself, and he was getting very depressed. This young man had post-traumatic amnesia of 18 days, indicating a severe head injury; and his return to school was only 0- months since his injury. The results of a neuropsychological evaluation revealed that he was functioning at a level estimated to be 30% below his pre-injury level. The recovery curve outlined above was used to explain his estimated pre-injury level, his current level, and what this 30 % reduction in cognitive abilities meant in terms of his ability to function at that point in his recovery. It was explained that taking on too much too soon and working long hours inefficiently was delaying his recovery by increasing his frustration and leading to depression. He was advised to take only one course. This was not agreeable with him and it was concluded that he could function best if he attempted to take 2 or 3 courses and dropped one or two if the schedule proved to be too difficult. Following this advice, he registered for three courses, ended up dropping one, and received B and a C in his remaining two classes. He was off for the summer and by the fall semester was able to function near his pre-injury level. Expectancy: The above experience is an example of the need for head injury survivors to understand their level of cognitive functioning and to plan accordingly. While this sounds rather simple, it is not. The difficulty is due primarily to the fact that we each have an expectancy regarding our performance. This expectancy is developed over a long period of time and is based on past experience. Head injury survivors and, in many cases, their families are operating on expectancies which do not take into account the sudden and often dramatic change in cognitive functioning which alters the individual's ability to perform. If the professional can identify the barriers and then effectively communicated them to the survivors and/or their family, many potential problems can be avoided.

Further examples can be seen in the cases of two young ladies, both 25 years of age and both severely injured. The mother of the first young woman reported frustration with the rehabilitative system. As a result, she traveled the country, talked to representatives of numerous rehabilitation programs both in the United States and in England, and finally put together a program for her daughter. Fourteen months after her accident, the daughter returned to work, and we had a chance to test her about 6 or 7 times during the rehabilitation period. She made an amazing recovery. She was exceptional before her head injury, and she also had an exceptional social support system. The other girl's situation was totally different. There was turmoil in her home environment. There was no father in the home. She and her mother didn't agree on very much. And she didn't get along with her brothers and sisters. In addition, she didn't have the insurance or the finances to stay in a rehabilitation program, which she really needed. We tested this young woman over a period of four years and never observed any recovery in her. Social Support Systems: As can be seen from the above illustrations, the degree to which the survivors have a good social support system is the degree to which they can function in the home environment and do well. Other resources are needed in proportion to how severely that home support is degraded. For example, in many situations a single parent has to work to support the family; as a result, the parent cannot stay at home, and it's not desirable for the survivor to be left alone all day. Thus, how much need there is for rehabilitation is a function of the severity of the injury, where the person is in the recovery process, and the barriers that must be faced. Family support systems vary widely; but, with training, families can modify the extent to which they provide support. Many families need advice and counsel; they also need information as to what works and what doesn't. As was shown previously, this is something that they are not likely to develop on their own. The use of diagrams and demonstrations often helps these individuals better understand the recovery process and the time period involved. The time factor is especially significant. Denial: A common element in the family's perception of head trauma is denial. Often, when it becomes apparent that the head-injury patient is not going to die, family members unrealistically expect the survivor to eventually leave the hospital and return home essentially the same as he or she was prior to the injury. Such denial can be adaptive, as it is an important defense against stress; but, if used excessively, it will distort the family's perception of the actual situation. It is very important that this not happen. The family needs to have an accurate picture as to where the survivor is in the process of recovery, what times are expected for recovery, and what barriers exist. Only by having a reasonably accurate perception of these things can the family respond realistically and facilitate the recovery process. Eventually, with time and hard work, recovery stabilizes. Hopefully functioning reaches the same level it was before that injury. If it does, this generally reflects that the survivor is using a different part of the brain, accomplishing the same tasks in different ways. The most important thing about this process is not how much of the individual's brain was damaged but, rather, how well he or she learns to use what remains. As Symonds said in the early part of this century, " It is not only the kind of injury that matters, but the kind of head that is injured that determines recovery of function" (Symonds, 1939). In other words, all things being equal, the higher functioning the patient is before the injury, the better the recovery. Someone who could not play the piano well before a head injury will not be able to play it well afterwards. TOP

Pre-existing factors: Everyone has strengths, weaknesses, habits, attitudes, fears, and desires. Those that were present before the injury are likely to be present after the injury; and, in many cases, they may be exaggerated. These preexisting problems can serve as barriers to recovery, and family therapy may be very important in resolving such issues. As noted in the third example above, problems that existed before an injury are likely to be increased after the injury. These problems will produce additional stresses on all involved. This is due to the fact that the family sees the survivor regress and function at a more immature level; becoming impulsive, demanding, and dependent in areas where he or she may have been independent before his or her injury. If there were preexisting problems in the family, they will almost invariably be increased. Everyone becomes frustrated, and this frustration further adds to the stress. It is for these reasons that almost everyone needs family therapy, to some extent, to aid in the process of recovery.

Mental Regression: Mental regression refers to the fact that, with development, we become mobile, verbal, and independent to varying degrees. A head injury regresses this development. Initially, it may be total (to the point that the survivor has to relearn walking, talking, and self care skills). There is almost always a dependency on the family for transportation. In addition, survivors become more impulsive; they speak or act first and think about the consequences later. They may also lose the ability to sustain attention, plan, and develop the necessary steps to carry out the plan. In addition, they have memory weaknesses which further complicate the picture. In many ways the process of recovery can be viewed as going through the whole process of development all over again, hopefully at a faster rate than before. Parents of young children and young adults can be aided by helping them determine at what mental age the survivor appears to be functioning and then advising the parent to treat the survivor as they would have at that age. For example, 18 year olds who sustain a severe head injury and return home after hospitalization and brief rehabilitation will not be able to drive. They will be dependent upon the family to transport them everywhere. They also will be more impulsive and may curse, without thinking, or say things to upset others. In short, the family concludes that these 18 year olds are functioning much like they were at 12 years of age. In this case, the family should be encouraged to treat these teenagers as if they really were 12; and hopefully, with time and effort, they will quickly progress to 13 or above. One problem with this strategy is that the survivor may act 18 at one time and 6 at another. This variability relates to fatigue or stress. The family needs to be aware of the time of day or the period of time involved in an activity and understand how to modify their behavior appropriately. This approach works particularly well with young children (Long, 1987). Invariably one family member becomes the primary caregiver. These individuals may find themselves caught in the middle; they must deal with the immaturity and frustration from the survivor, an they also are bombarded with advice and criticism from the rest of the family. In terms of priorities, the needs of the primary caregiver should come first. If they can't function effectively, then the whole system breaks down. They need support and understanding from the rest of the family; and, if they don't get it, they need to seek adequate professional help for the whole family. Post-Concussion Symptoms: A very important source of information (particularly later in the process of recovery or with less severe head injuries) is post-concussion symptoms (Long & Novack, 1986; Novack, Daniel, & Long, 1983, 1985; Wood, Novack, & Long, 1984). These refer to headaches, dizziness, fatigue, irritability, memory weaknesses, etc. It is interesting that these symptoms are most likely seen later in recovery or with mild head injury. However, they occur at this time because they relate to the interaction between neurological damage and situational stress. Neurological damage alone may not cause such symptoms; rather, they become more pronounced when the individual attempts to take on more and, as a result, experiences more stress (Long & Haban, 1986). Post-concussion symptoms can serve as a valuable guide to the overall functioning of the individual. If none are experienced, it is likely that the survivor is not doing much. On the other hand, if symptoms increase in number and/or frequency, then this usually indicates that he or she is taking on too much. Monitoring post concussion symptoms can provide valuable information as the effect that the injury and the situation is having on the survivor at any given time. Some symptoms are expected, but too many indicate that the individual needs to readjust their schedule. TOP

Future Research: The future of head injury research looks exciting. After many years of a general lack of knowledge about the nature of head injury and the lack of funds, government agencies have been made aware of the magnitude of the problem and research regarding treatment of head injury is now being actively supported and encouraged. Biochemical studies of conditions causing secondary damage to the body following head injury hold promise of significantly reducing the effects of head injury and also enhancing the time of recovery. Early transportation and treatment in trauma centers continues to improve patient outcome. Certainly all of the effects that are due to secondary damage may be identified and corrected, and this alone appears to hold great promise. Even so, there remain many concerns with regard to head injury. One of these relates to the families' early needs. The best resource for this are other survivors and their families. Hopefully trauma centers will become aware of this and have survivors and/or their families available to talk to families of new head injury survivors. This would provide a vital source of support because the neurosurgeon would not be able to provide much exact information at that point in their recovery anyway.

Another area that needs to be developed is the use of home health care to provide head trauma services. They have a very good model. They can train family members to do nursing and provide physical therapy. Having these needs met by family members would be cost effective; professional who would simply come back once every week or two to monitor the process. In cases where family members are unable to be trained or provide home care, then available inpatient resources become more desirable. This is especially true for stressful home environments such as those previously discussed. TOP

NON-ORGANIC FACTORS INFLUENCING RECOVERY Often when recovery is discussed, the focus is on the nature and severity of the injury. Families are often advised that the individual had X amount of head injury or that CT or MRI scan revealed a certain amount of organic damage, and this should translate into X amount of recovery. It doesn't. This is because the individuals' organic status is reflected in their cognitive function; and this may have been either good or bad before the injury. However, that is only one factor that will influence their behavior. Another is stress: how the individuals deal with stress, and how effectively they cope. These factors interact. Not all survivors have to deal with the same amount of stress. This will be affected by a number of factors, including the circumstances of the accident. For instance, a man who has an accident at work will probably have much less stress than a man who gets hit by a car driven by his wife (as she ran off with his car and money but left the kids and the bills). The stress in these two cases is quite different. Finally, the kind of occupational status the individual has is important. Consider, for instance, a young 21 year old who works in a parts warehouse and part of his job requirements is to know every number for every part. After a severe head injury, he is unlikely to be able to function in that environment. If he's smart enough, he may do well in many other environments; but his prior job will add significant stress. The results is a reduction in his occupational status. Social, vocational, educational, and cognitive factors, plus the amount of stress and how the individual deals with it, all complicate the situation (Long & Webb, 198; Long, Gouvier, & Cole, 1984). Neurological factors are only part of the story. Primary pre- and post-trauma factors that influence Post Trauma Behavior are: Situational (perceived) Stress Personality (Stress Management) Organic Status Occupational Status The trauma often caused the following changes: Increased Stress Reduced Stress Management Neurological Damage (Impaired Cognitive Functions_ Reduced Occupational Status http://neuro.psyc.memphis.edu/neuropsyc/np-dx-traum.htm

Traumatic Brain Injury

March, 2011

A traumatic brain injury (TBI) is defined as a blow to the head or a penetrating head injury that disrupts the normal function of the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain. Mild cases may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma, or even death. Prevalence About 1.7 million cases of TBI occur in the United States every year. Approximately 5.3 million people live with a disability caused by TBI in the United States alone. Incidence and Demographics

Annual direct and indirect TBI costs are estimated at $48 to $56 billion. There are about 235,000 hospitalizations for TBI every year, which is more than 20 times the number of hospitalizations for spinal cord injury. Among children ages 14 and younger, TBI accounts for an estimated 2,685 deaths, 37,000 hospitalizations, and 435,000 emergency room visits. Every year, 80,000 to 90,000 people experience the onset of long-term or lifelong disabilities associated with TBI. Males represent 78.8 percent of all reported TBI accidents, and females represent 21.2 percent. National statistics estimate between 50 and 70 percent of TBI accidents are the result of a motor vehicle crash. Sports and recreational activities contribute to about 21 percent of all traumatic brain injuries among American children and adolescents. The mortality rate for TBI is 30 per 100,000, or an estimated 50,000 deaths in the United States annually. Of those who die, 50 percent do so within the first two hours of their injury. Deaths from head injuries account for 34 percent of all traumatic deaths. Beginning at age 30, the mortality risk after head injury begins to increase. Persons age 60 and older have the highest

death rate after TBI, primarily because of falls, which have a rising incidence in this age group. Sources: Centers for Disease Control and Prevention, Traumatic Brain Injury (TBI): Incidence and Distribution, 2004. Traumatic Brain Injury Model System, University of Alabama at Birmingham, Introduction to Brain Injury Facts and Stats, February, 2000 TBI Symptoms Symptoms vary greatly depending on the severity of the head injury, but may include any of the following:

Vomiting Lethargy Headache Confusion Paralysis Coma Loss of consciousness Dilated pupils Vision changes (blurred vision or seeing double, not able to tolerate bright light, loss of eye movement, blindness) Cerebrospinal fluid (CSF) (which may be clear or blood-tinged) coming out of the ears or nose Dizziness and balance problems Breathing problems Slow pulse Slow breathing rate, with an increase in blood pressure Ringing in the ears, or changes in hearing Cognitive difficulties Inappropriate emotional responses Speech difficulties (slurred speech, inability to understand and/or articulate words) Difficulty swallowing Body numbness or tingling

Droopy eyelid or facial weakness Loss of bowel control or bladder control If a TBI is suspected, call 911 immediately or take the person to an emergency room. Surgical Lesions When discussing TBI, the term "mass lesion" is often used. This refers to an area of localized injury that may cause pressure within the brain. The most common mass lesions related to TBI are hematomas and contusions. A hematoma is a blood clot within the brain or on its surface. Hematomas may occur anywhere within the brain. An epidural hematoma is a collection of blood between the dura mater (the protective covering of the brain) and the inside of the skull. A subdural hematoma is a collection of blood between the dura mater and the arachnoid layer, which sits directly on the surface of the brain. A cerebral contusion is bruising of brain tissue. When examined under a microscope, cerebral contusions are comparable to bruises in other parts of the body. They consist of areas of injured or swollen brain mixed with blood that has leaked out of arteries, veins, or capillaries. Contusions are seen most commonly at the base of the front parts of the brain, but they may occur anywhere. An intracerebral hemorrhage (ICH) describes bleeding within the brain tissue, which may be related to other brain injuries, especially contusions. The size and location of the hemorrhage helps determine whether it can be removed surgically. Subarachnoid hemorrhage (SAH) is caused by bleeding into the subarachnoid space. It appears as diffuse blood spread thinly over the surface of the brain, and is seen commonly after TBI. Most cases of SAH associated with head trauma are mild. Hydrocephalus may result from severe traumatic SAH. Diffuse Injuries TBI can produce microscopic changes that cannot be seen on CT scans and that are scattered throughout the brain. This category of injuries is called diffuse brain injury, which may occur with or without an associated mass lesion. Diffuse axonal injury refers to impaired function and gradual loss of some axons, which are the long extensions of a nerve cell that enable such cells to communicate with each other even if they are located in parts of the brain that are far apart. If enough axons are injured in this way, then the ability of nerve cells to communicate with each other and to integrate their function may be lost or greatly impaired, possibly leaving a patient with severe disabilities. Another type of diffuse injury is ischemia, or insufficient blood supply to certain parts of the brain. It has been shown that a decrease in blood supply to very low levels may occur commonly in a significant number of TBI patients. This is crucial because a brain that has just undergone a traumatic injury is especially sensitive to even slight reductions in blood flow. Changes in blood pressure during the first few days after head injury can also have an adverse effect. Skull Fractures No treatment is required for most linear skull fractures, which are simple breaks or "cracks" in the skull. Of greater concern is the possibility that forces strong enough to cause a skull fracture may also have caused some damage to the underlying brain. Fractures of the base of the skull are problematic if they cause injury to nerves, arteries, or other structures. If a fracture extends into the sinuses, there may be leakage of cerebrospinal fluid (CSF) from the nose or ears. Most leaks will stop spontaneously. Sometimes, however, it may be necessary to insert a lumbar drain, which is a long, thin, flexible tube that is inserted into the CSF space in the spine of the lower back. This provides an alternate route for CSF drainage so that the dural tear that is responsible for the CSF leak in the base of the skull has time to seal. Depressed skull fractures are those in which part of the bone presses on or into the brain. These may require surgical treatment. The damage caused by depressed skull fractures depends upon the region of the brain in which they are located and also upon the possible coexistence of any associated diffuse brain injury. Diagnosis Like all trauma patients, persons with TBI need to undergo a systematic yet rapid evaluation in the emergency room. Cardiac and pulmonary function is assessed first. Next, a quick examination of the entire body is performed, followed by a complete neurological examination. The neurological examination includes an assessment utilizing the Glasgow Coma Scale (GCS). In addition to the GCS, the ability of the pupils to become smaller in bright light is also tested. In patients with large mass lesions or with high intracranial pressure (ICP), one or both pupils may be very wide or "blown". The presence of a wide or dilated pupil on only one side suggests that a large mass lesion may be present on the same side as the dilated pupil. Brainstem reflexes including gag and corneal (blink) may also be tested. Radiological Tests A computed tomography scan (CT or CAT scan) is the gold standard for the radiological assessment of a TBI patient. A CT scan is easy to perform and is an excellent test for detecting the presence of blood and fractures, which are the most crucial lesions to identify in medical trauma cases. Plain x-rays of the skull are recommended by some as a way to evaluate patients with only mild neurological dysfunction. However, most centers in the United States have readily available CT scanning, which is a more accurate test. For this reason, the routine use of skull x-rays for TBI patients has declined. Magnetic resonance imaging (MRI) is not commonly used for acute head injury because it takes longer to perform MRI than CT scanning. MRI is not as practical for acute trauma because it is difficult to transport an acutely-injured patient from the emergency room to the MRI scanner. However, after a patient has been stabilized, MRI may demonstrate the existence of lesions that were not detected on the CT scan. This information is generally more useful for determining prognosis than for influencing treatment. Surgical Treatment Many patients with moderate or severe head injuries are taken directly from the emergency room to the operating room. In many cases, surgery is performed to remove a large hematoma or contusion that is significantly compressing the brain or raising the pressure within the skull. After surgery, these patients are usually observed and monitored in the intensive care unit (ICU).

Other head-injured patients may not go to the operating room immediately, but instead are taken from the emergency room to the ICU. Contusions or hematomas may enlarge over the first hours or days after head injury, so some patients are not taken to surgery until several days after an injury. Delayed hematomas may be discovered when a patient's neurological exam worsens or when their ICP increases. On other occasions, a routine follow-up CT scan that was ordered to determine if a small lesion has changed in size indicates that the hematoma or contusion has enlarged significantly. In many cases, removing the lesion before it enlarges and causes neurological damage may be the safest approach for the patient. At surgery, the hair over the affected part of the head is usually shaved. After the scalp incision is made, the bone that is removed is usually taken out in a single piece or flap, which is then replaced after surgery. Sometimes, however, the bone may be shattered or heavily contaminated. In these cases, the contaminated or shattered fragments may be removed and not replaced. The dura mater is carefully cut to reveal the underlying brain. After any hematoma or contusion is removed, the neurosurgeon ensures that the area is not bleeding. He or she then closes the dura, replaces the bone, and closes the scalp. If the brain is very swollen, some neurosurgeons may decide not to replace the bone until the swelling decreases, which may take up to several weeks. The neurosurgeon may elect to place an ICP monitor or other types of monitors if these were not already in place. The patient is then returned to the ICU for observation and additional care. Medical Treatment At the present time, there is no medication or "miracle treatment" that can be given to prevent nerve damage or promote nerve healing after TBI. The primary goal in the ICU is to prevent any secondary injury to the brain. The "primary insult" refers to the initial trauma to the brain, whereas the "secondary insult" is any subsequent development that may contribute to neurological injury. For example, an injured brain is especially sensitive and vulnerable to decreases in blood pressure that might otherwise be well tolerated. One way of avoiding secondary insults is to try to maintain normal or slightly elevated blood pressure levels. Likewise, increases in ICP, decreases in blood oxygenation, increases in body temperature, increases in blood glucose, and many other disturbances can potentially worsen neurological damage. The prevention of secondary insults is a major part of the ICU management of head-injured patients. Various monitoring devices may assist healthcare personnel in caring for the patient. Placement of an ICP monitor into the brain itself can help detect excessive swelling of the brain. One commonly used type of ICP monitor is a ventriculostomy, which is a narrow, flexible, hollow catheter that is passed into the ventricles, or fluid spaces in the center of the brain, to monitor ICP and to drain CSF if ICP increases. Another commonly used type of intracranial pressure monitoring device involves placement of a small fiberoptic catheter directly into the brain tissue. Additional catheters may be added that measure brain temperature and brain tissue oxygenation. Placement of an oxygen sensor into the jugular vein can detect how much oxygen in the blood is arising from the brain and can indicate how much oxygen the brain is using. This may be related to the degree of brain damage. Many other monitoring techniques are currently under investigation to see if they can help to improve outcome after head injury or provide other critical information about caring for TBI patients. Outcome One of the most widely used systems to classify outcome from head injury is the Glasgow Outcome Scale (GOS). Patients with mild head injury (usually defined as GCS score on admission of 1315) tend to do well. They may experience headaches, dizziness, irritability, or similar symptoms, but these gradually improve in most cases. Patients with moderate head injuries fare less well. Approximately 60 percent will make a positive recovery, and an estimated 25 percent will be left with a moderate degree of disability. Death or a persistent vegetative state will be the outcome in about 7 to 10 percent of cases. The remainder of patients will have a severe degree of disability. The group comprised of severely head-injured patients has the worst outcomes. Only 25 to 33 percent of these patients have positive outcomes. Moderate disability and severe disability each occur in about a sixth of patients, with moderate disability being slightly more common. About 33 percent of these patients do not survive. The remaining few percent remain persistently vegetative. The above statistics apply to patients with so-called closed head injuries. For penetrating head injuries, which today are caused most commonly by handguns, outcomes follow a different pattern. More than 50 percent of all patients with gunshot wounds to the head who are alive upon arrival at a hospital do not survive because their initial injuries are so severe. However, most of the remaining patients tend to do fairly well, largely because their injuries are relatively mild (GCS score of 13-15). Relatively few patients suffer injuries of intermediate severity (GCS score of 9-12) from gunshot wounds, but it is this group that has the most variability in outcomes. Despite its usefulness, the GOS is not a good tool with which to measure subtle emotional or cognitive problems. Several months after a severe head injury, patients who have a good score on the GOS may in fact have significant neuropsychological disabilities. Tremendous effort is being directed into finding better ways to evaluate these problems, into improving the quality of prehospital, acute, and rehabilitative care, and into research to learn more about the effects of head injury and potential treatment options. Table 1: Glasgow Coma Scale SCALE VALUE BEST MOTOR RESPONSE BEST VERBAL RESPONSE BEST EYE OPENING RESPONSE 6 Obeys Commands Oriented -5 Localizes stimulus Oriented -4 Withdraws from stimulus Conversant, but confused Eyes open spontaneously 3 Flexes arm States recognizable words or phrases Eyes open to voice 2 Extends arm Makes unintelligible sounds Eyes open to painful stimulus 1 No response No response Remain closed Table 2: Glasgow Outcome Scale OUTCOME SCORE DESCRIPTION Good Recovery (GR) 5 Minor disabilities, but able to resume normal life. Moderate Disability (MD) 4 More significant disabilities, but still able to live independently. Can use public transportation, work in an assisted situation, etc. Severe Disability (SD) 3 Conscious, but dependent upon others for daily care. Often institutionalized. Persistent Vegetative State (PVS) 2 Not conscious, though eyes may be open and may "track" movement. Death (D) 1 Self-explanatory.

Sources: Teasdale G, Jennett B. Assessment of coma and impaired consciousness. Lancet 1974; 81-84. Teasdale G, Jennett B. Assessment and prognosis of coma after head injury. Acta Neurochir 1976; 34:45-55. Rehabilitation Once head-injured patients leave the acute-care hospital, some may benefit from a rehabilitation program. Prime candidates for rehabilitation are patients that had less severe initial injuries, or those that have started to show significant improvement. In some cases, further recovery may be expedited by transfer to a rehabilitation hospital or to the rehabilitation service of a large hospital. For more severely injured patients or for those whose recovery is slow, constant vigilance is required to prevent the gradual onset of problems with joint mobility, skin integrity, respiratory status, infection, and many other physiological functions. Patients with moderate or mild injuries, as well as severely injured patients who have improved sufficiently, may be candidates for outpatient therapy. Regardless of the setting, most head-injury rehabilitation centers emphasize compensatory strategies, which essentially help patients learn to reach the maximum level of function allowed by their impairments. The concept of cognitive retraining, which presumes that at least some of the brain's cognitive capacity can be restored by constant repetition of certain simple tasks, is more controversial but is also emphasized at many centers. Another major goal of head injury rehabilitation is working with patients' families to educate them about what they can realistically expect and how they can best help their injured family member. General Head Injury Prevention Tips

Wear a seatbelt every time you drive or ride in a motor vehicle. Never drive while under the influence of drugs or alcohol or ride as a passenger with anybody else who is under the influence. Keep firearms unloaded in a locked cabinet or safe, and store ammunition in a separate, secure location.

Remove hazards in the home that may contribute to falls. Secure rugs and loose electrical cords, put away toys, use safety gates, and install window guards. Install grab bars and handrails if you are frail or elderly. Sports and Recreation Head Injury Prevention Tips

Buy and use helmets or protective head gear approved by the ASTM for specific sports 100 percent of the time. Supervise younger children at all times, and do not let them use sporting equipment or play sports unsuitable for their age. Do not let them use playgrounds with hard surface grounds. Follow all rules and warning signs at water parks, swimming pools, and public beaches. Do not dive in water less than 12 feet deep or in above-ground pools. Check the depth and check for debris in the water before diving. Wear appropriate clothing for the sport. Do not wear any clothing that can interfere with your vision. Do not participate in sports when you are ill or very tired. Obey all traffic signals and be aware of drivers when cycling or skateboarding. Avoid uneven or unpaved surfaces when cycling, skateboarding, or in-line skating. Perform regular safety checks of sports fields, playgrounds and equipment. Discard and replace sporting equipment or protective gear that is damaged.

Never slide head-first when stealing a base. Glossary of Terms Agnosia failure to recognize familiar objects even though the sensory mechanism is intact. Agraphia the inability to express thoughts in writing. Alexia the inability to read. Amnesia lack of memory about events occurring during a particular period of time. Anosmia loss of the sense of smell. Anoxia a condition in which there is an absence of oxygen supply to an organ's tissues although there is adequate blood flow to the tissue. Aphasia loss of the ability to express oneself and/or to understand language. Arachnoid Middle layer of membranes covering the brain and spinal cord. Ataxia shaky and unsteady movements that result from the brain's failure to regulate the body's posture and the strength and direction of movements. Axon the nerve fiber that carries an impulse from the nerve cell to a target, and also carries materials from the nerve terminals back to the nerve cell. Brain Stem the stemlike part of the brain that connects to the spinal cord. Closed Head Injury impact to the head from an outside force, without any skull fracture or displacement.

Concussion a disruption, usually temporary, of neurological function resulting from a head injury or violent shaking. Cerebrospinal fluid (CSF) a clear fluid surrounding the brain and spinal cord. Contusion a bruise; an area in which blood that has leaked out of blood vessels is mixed with brain tissue. Coup-Contrecoup Injury contusions that are both at the site of the impact and on the complete opposite side of the brain. Depressed skull fracture a break in the bones of the head in which some bone is pushed inward, possibly pushing on or pressing into the brain. Diplopia a condition in which a single object appears as two objects; also called double vision. Dura mater the outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and the spinal cord. Dysarthria speech that is characteristically slurred, slow, and difficult to understand. Edema collection of fluid in the tissue causing swelling. Epidural located on or outside the dura mater, the outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain. Hemiplegia paralysis of one side of the body as a result of injury to neurons carrying signals to muscles from the motor areas of the brain or spinal cord. Hemiparesis weakness, paralysis or loss of movement on one side of the body. Hemianopsia loss of part of one's visual field in one or both eyes. Hydrocephalus a condition in which excess CSF builds up within the ventricles (fluid-containing cavities) of the brain and may cause increased pressure within the head. Hypoxia a condition in which there is a decrease of oxygen to the tissue despite adequate blood flow to the tissue. Intraparenchymal inside the parenchyma of the brain. Ischemia a reduction of blood flow that is thought to be a major cause of secondary injury to the brain or spinal cord after trauma. Locked-in Syndrome a rare neurological condition in which a person cannot physically move any part of the body except the eyes. Open head injury trauma to the brain resulting in loss of consciousness due to the penetration of the brain by a foreign object such as a bullet. Subarachnoid hemorrhage Blood in, or bleeding into, the space under the arachnoid membrane, most commonly from trauma or from rupture of an aneurysm. Subcortical the region beneath the cerbral cortex. Subdural the area beneath the dura covering the brain and spinal cord. Vasospasm spasm of blood vessels which decreases their diameter. Ventricles (brain) four natural cavities in the brain which are filled with CSF. http://www.aans.org/en/Patient%20Information/Conditions%20and%20Treatments/Traumatic%20Brain%20Injury.aspx

What is Traumatic Brain Injury? Traumatic brain injury (TBI), a form of acquired brain injury, occurs when a sudden trauma causes damage to the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. A person with a mild TBI may remain conscious or may experience a loss of consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking. A person with a moderate or severe TBI may show these same symptoms, but may also have a headache that gets worse or does not go away, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation. Is there any treatment? Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible. Because little can be done to reverse the initial brain damage caused by trauma, medical personnel try to stabilize an individual with TBI and focus on preventing further injury. Primary concerns include insuring proper oxygen supply to the brain and the rest of the body, maintaining adequate blood flow, and controlling blood pressure. Imaging tests help in determining the diagnosis and prognosis of a TBI patient. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures or spinal instability. For moderate to severe cases, the imaging test is a computed tomography (CT) scan. Moderately to severely injured patients receive rehabilitation that involves individually tailored treatment programs in the areas of physical therapy, occupational therapy, speech/language therapy, physiatry (physical medicine), psychology/psychiatry, and social support. What is the prognosis? Approximately half of severely head-injured patients will need surgery to remove or repair hematomas (ruptured blood vessels) or contusions (bruised brain tissue). Disabilities resulting from a TBI depend upon the severity of the injury, the location of the injury, and the age and general health of the individual. Some common disabilities include problems with cognition (thinking, memory, and

reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (expression and understanding), and behavior or mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness). More serious head injuries may result in stupor, an unresponsive state, but one in which an individual can be aroused briefly by a strong stimulus, such as sharp pain; coma, a state in which an individual is totally unconscious, unresponsive, unaware, and unarousable; vegetative state, in which an individual is unconscious and unaware of his or her surroundings, but continues to have a sleep-wake cycle and periods of alertness; and a persistent vegetative state (PVS), in which an individual stays in a vegetative state for more than a month. What research is being done? The National Institute of Neurological Disorders and Stroke (NINDS) conducts TBI research in its laboratories at the National Institutes of Health (NIH) and also supports TBI research through grants to major medical institutions across the country. This research involves studies in the laboratory and in clinical settings to better understand TBI and the biological mechanisms underlying damage to the brain. This research will allow scientists to develop strategies and interventions to limit the primary and secondary brain damage that occurs within days of a head trauma, and to devise therapies to treat brain injury and improve long-term recovery of function. http://www.ninds.nih.gov/disorders/tbi/tbi.htm