CHAPTER 1 INTRODUCTION

1.1

Background Disorders of the nervous system can occur at any time during the life span and can vary

from mild, self-limiting symptoms to devastating, life-threatening disorders. Meningitis is an infection of the meninges, the paper- thin membranes that cover and protect the brain and spinal cord, usually as a result of an infection of the CSF. While the term spinal meningitis is sometimes used, it is inaccurate. Because CSF circulates through the brain as well as the spinal canal, an infection of the fluid cannot be limited to the spinal area. While meningitis can strike anyone, it is most common in children, teens, and young adults. Meningitis strikes fear into the hearts of parents and health care workers because it often affects the youngest and most vulnerable people. Meningitis can cause a long list of symptoms. But it is best known for its triad of symptoms- fever, stiff neck, and impaired level of consciousness (such as confusion,fatigue, and irritability). Most people recover from meningitis. A few others are left with serious permanent problems, such as speech and learning disabilities, brain damage, deafness, or loss of fingers, toes, hands, and feet. Even with best medical care, some forms of meningitis kill one or two out of every ten people who get it. Meningitis is different from a disease such as Lyme disease, in which only one kind of bacterium is the culprit. Meningitis can be used by many kinds of dangerous microorganism. These microorganism include bacteria, viruses and fungi. The most dangerous type of bacterial meningitis may kill people within twenty-four hours after they start feeling sick. People with mwningitis by viruses usually are not as sick as those with bacterial meningitis. However, both types require prompt medical attention because only a doctor can tell the difference. Health care has made great strides over the past twenty years in the prevention and treatment of meningitis. Even though some forms of meningitis can be prevented with vaccination, its important to learn about meningitis so you can help protect yourself, your family, and your friends from this terrible disease. While meningitis is not as contagious (easily spread among people) as a cold or the flu, it can be passed by something as simple as sharing a cookie, a coke, or a kiss.

In the past, most cases of meningitis were in children younger than the age of 5, and most often the causative agent was Haemophilus influenza. Since 1990, a vaccine against H. influenza has become available and is administrated to most children in the United States and other countries as a series of injections, beginning in the second month of life. As result of this important intervention, the incidence of meningitis in children aged 1 month to 2 years has decreased 87 %. Because of the dramatic decline in H. influenza-type meningitis in this population, cases of bacterial meningitis overall in the United States have dropped 55 %. Meningitis now occurs mast commonly in adults ages 19 to 59. In this age group, the most common cause of bacterial meningitis is Streptococcus pneumonia (pneumococcal meningitis). The next greatest incidence is in children ages 2 to 18, and cause is most often Neisseria meningitides (meningococcal meningitis). In the neonate, the cause is most often group B streptococcus, in infants aged 1 to 23 months the cause are split almost equally between S. pneumonia and N.meningitides. while college students in general are no more likely to develop meningitis than other young adults of that age group, subgroups of college students are at increased risk. In particular, college freshman living in dormitories have a 6-fold greater risk of developing meningococcal meningitis than those not living in a dormitory. While most colleges now require vaccination against meningococcal meningitis, the vaccination is not effective against all strains.

1.2

Problem Formulation 1. What are the functions of the nervous system? 2. What are the two main divisons of the nervous system? How are these divisions subdivided? 3. What is the general structure of a neuron, and what are the functions of three different types of neurons? 4. What is meningitis disease? 5. What are types and classification of meningitis? 6. How is etiology of meningitis? 7. How does the Nursing Care Plan solve meningitis?

CHAPTER 2 NEUROLOGIC SYSTEM

2.1 Anatomy and Physiology of Nervous System The nervous system has three specific functions : 1. Sensory input. Sensory receptors present in skin and organ respond to external and internal stimuli by generating nerve impulses that travel to the brain spinal cord. 2. Integration .The brain and spinal cord sum up the data received from all over the body and send out nerve impulses. 3. Motor output. The nerve impulses from the brain and spinal cord go to the effectors, which are muscles and glands. Muscle contractions and gland secretions are responses to stimuli received by sensory receptors. The nervous system has two major divisions : the central nervous system and the peripheral nervous system. The central nervous system (CNS) includes the brain and spinal cord, which have a central location. They lie in the midline of the body. The peripheral nervous system (PNS) which is further divided into the somatic division and the autonomic division, includes all the cranial and spinal nerves. Nerves have a peripheral location in the body, meaning that they project out from the central nervous system. The divison between the central nervous system and the peripheral nervous system is arbitrary; the two systems work together as we shall see.

The nervous system approximately 10 million sensory neurons that send information about the internaland external environment to the brain and 500.000 motor neurons that control the muscles and glands. The brain itself contains more than 20 billion nerve cells that link the motor and sensory pathways, monitor the bodys processes, respond to the internal and external environment, maintain homeostasis, and direct all psychological, biologic, and physical activity, through complex chemical and electrical messages (Bradley, Daroff, Fenichel, and Marsden, 2000).

2.2

Cells of The Nervous System A view through a microscope reveals that the nervous system is made up of two types of

cells; neurons and neuroglial cells. Neurons are the cells that send information from one part of the body to another. Heat, sight, smell, and touch are some examples of the types of communication passed along by neurons. Neurons produce chemicals called neurotransmitters to send information from one

neuron to another. Neurons also use these chemical messengers to control how muscles flex and how the digestive system breaks down food. Neurons located in organs called sensory structures produce nerve impulse after they receive information from environment. Instead of responding to internal neurotransmitters, they react to chemicals, light, and pressure. Healthy sensory structures are able to send information from the environment to neurons. Damage to sensory structures does not usually affect how the signal stimulates the neurons. Rather, injury to these neurons interferes with how the signal is passed along to the brain. Most neurons release one neurotransmitter, although some neurons may also release a cotransmitter. Frequently, contransmitter, called neuromodulators, are a slightly different type of chemical than the neurotransmitter. Neuromodulators typically take longer to act than neurotransmitters, and may function to increase or decrease DNA transcription and protein synthesis. Neuromodulators often affect the response of a post-synaptic cell to a neurotransmitter, and are associated with long-term functions such as learning, mood, and development.

Table. Major Neurotransmitter

Neuroglial cells are the other type of cell that makes up the nervous system. They protect neurons and help them function. There is a different type of neuroglial cell for each function. The most common type of neuroglial cell is called a Schwann cell. These cells wrap around neurons, helping the neuron send faste impulses. Without Schwann cells, the nervous system would react very slowly, if at all. Aside from helping with impulses, scientist have discovered

that Scwhann cells also help damaged neurons heal. Other types of neuroglial cells protect neurons from disease and poisons. Neurons would quickly die without the assistance of these cells. Infectious microorganisms can damage neuroglial cells as well as neurons. Injury to neuroglial cells can impair neuron function and even lead to the death of neurons in the brain.

2.2.1 Neuron Structure Neurons vary in appearance, but all of them have just three parts : a cell body, dendrite (s), and an axon.

The cell body contains the nucleus as well as other organelles. The nucleus, which contains the genetic information of the neuron, orchestrates the production of the proteins, enzymes, and neurotransmitters required by the nerve for its proper function. Nerve cell bodies occurring in clustsers are called ganglia or nuclei. A cluster of cell bodies with the same function is called a center (eg, the respiratory center). The cell body delivers these substances as needed to the rest of the neuron. Although neural excitation typically begins with excitation to the dendrites, a cell body sometimes may be stimulated directly by incoming stimuli from other neurons and by chemical and electrical stimuli. The cell body delivers the electrical signal to the next segment, the axon. The dendrite is a branch-type structure with synapses for receiving electrochemical messages. The dendrites are the many short extensions that receives signals from sensory receptors or other neurons. At the dendrites, signals can resulting nerve impulses that are then conducted by an axon. Excitation of a neuron typically begins at the dendrite. The dendrite passes its excitation on to the adjacent segment, the cell body. The axon is a long projection that carries impulses away from the cell body. The axon is the portion of neuron thath conducts nerve impulses. Any long axon is also called a nerve

fiber.Long axons are covered by an insulating, lipid sheat,called myelin sheath formed from the membranes of tightly spiraled neuroglia. In the PNS, neuroglial cell called a neurolemmocyte (Schwann cell) performs this function, leaving gaps called neurofibril nodes (nodes of Ranvier). In the central nervous system, myelin is produced by a specialized type of cell, the oligodendrocytes. Myelin increases the velocity with which an electrical signal is transmitted down an axon, as described. Another type of neuroglial cell performs a similar function in the CNS. Axon terminals at the end of each main axon stem and collateral, the branching becomes extensive. These final divisions of the axon are called axon terminals. It is through axon terminals that an electrical signal is passed to the dendrites or the cell body of a second neuron. In the peripheral nervous system, the signal also may pass to a muscle or glandular cell. The synapse is the point of junction between two neurons. Neurons communicate with each other by releasing chemicals into the small cleft (synaptic cleft) separating one from the other. The chemical released from a particular neuron is called a neurotransmitter. Usually, a neurotransmitter is released from the axon terminal of one neuron, diffuses across the synaptic cleft, and binds to a receptor on the dendrite or cell body of the other neuron. The cell that releases the neurotransmitter is called the presynaptic neuron. The neuron that completes the synapse is called the postsynaptic neuron.

2.2.2 Types of Neurons Neurons can be classified according to their function and shape.

Motor neurons or efferent neurons take nerve impulses from the CNS to muscles or glands. Motor neurons are said to be multipolar because they have many dendrites and a single

axon. Motor neurons cause muscle fibers to contract or glands to secrete, and therefore they are said to innervate these structure. Sensory neurons or afferent neurons take nerve impulses from sensory receptors to the CNS. The sensory receptor, which is the distal end of the long axon of a sensory neuron, may be as simple as a naked nerve ending (a pain receptor), or it may be a part of a highly complex organ, such as the aye or ear. These neurons are the only type of nerve cell that do not have dendrites. Almost all sensory neurons have a structure that is termed unipolar. In unipolar neurons, the extension from the cell body divides into a branch that comes to the periphery and another that goes to the CNS. Because both branches are long and myelinated and transmit nerve impulses, it is now generally accepted to refer to them collectively as an axon. Interneurons , also known as association neurons, occur entirely within the CNS. Almost 99 % of all neurons in the body are interneurons. Interneurons, which are typically,convey nerve impulses between various parts of the CNS. Some lie between sensory neurons and motor neurons, and some take messages from one side of the spinal cord and vice versa. They also form complex pathways in the brain where processes accounting for thinking, memory, and language occur.

2.3

Central Nervous System The central nervous system, consisting of the brain and spinal cord, is composed of gray

matter and white matter. Gray matter is gray because it contains cell bodies and short, nonmyelinated fibers. White matter is white because it contains myelinated axons that run together in bundles called tracts.

2.3.1 Meninges and Cerebrospinal Fluid Both the spinal cord and the brain are wrapped in protective membranes known as meninges (sing., meninx). The outer meninx, the duramater, is though, white, fibrous connective tissue that lies next to the skull and vertebrae. The dural sinuses collect venous blood before it returns to the cardiovascular system. Bleeding into the space between the duramater and bone is called an epidural hematoma. The arachnoid consist of weblike connective tissue with thin strands that attach it to the piamater, the deepest meninx. The subarachnoid space is filled

with cerebrospinal fluid, a clear tissue fluid that forms a protective cushion around and within the CNS. The pia mater is very thin and closely follows the contours of the brain and spinal cord. Cerebrospinal fluid is stored within the central canal of the spinal cord and in the brains ventricles,which are interconnecting chambers that also produce cerebrospinal fluid. Normally, any excess cerebrospinal fluid drains away into the cardiovascular system. However, blockages can occur.

2.3.2 The Spinal Cord The spinal cord is a cylinder of nervous tissue that begins at the base of the brain and extends through a large opening in the skull called the foramen magnum. The spinal cord is protected by the vertebral column, which is composed of individual vertebrae. A cross section of the spinal cord shows a central canal, gray matter, and white matter. The central canal contains cerebrospinal fluid, as do the meninges that protect the spinal cord. The gray matter is centrally located and shaped like the letter H. Portions of sensory neurons and motor neurons are found there, as are interneurons that communicate with these two types of neurons. The white matter of the spinal cord contains ascending tracts taking information of the brain (primarily located posteriorly) and descending tracts taking information from the brain (primarily located anteriorly). Because the tracts cross just after they enter and exit the brain, the left side of the brain controls the right side of the body, and the right side of the brain controls the left side of the body.

Functions of the Spinal Cord The spinal cord provides a means of communication between the brain and the peripheral nerves that leave the cord. When someone touches your hand, sensory receptor generate nerve impulses that pass through sensory fibers to the spinal cord and up one of several ascending tracts to a sensory area of the brain. When you voluntarily move your limbs, motor impulses originating in the brain pass down one of several descending tracts to the spinal cors and out to your muscles by way of motor fibers. The spinal cord is also the center for thousands of reflex arcs : A stimulus cause sensory receptor to generate nerve impulses that travel in sensory neurons to the spinal cord. Interneurons integrate the incoming data and relay signals to motor neurons. A response to the stimulus occurs when motor axons cause skeletal muscles to contract. Each interneuron in the spinal cord has synapses with many other neurons, and therefore they send signals to several other interneurons in addition to motor neurons.

2.3.3

Anatomy of The Brain The brain is divided into three major areas : the cerebrum, the brain stem, and the

cerebellum. The cerebrum is composed of two hemispheres, the thalamus, the hypothalamus, and the basal ganglia. Additionally, connections for the olfactory (cranial nerve I) and optic (cranial nerve III) nerves are found in the cerebrum. The brain stem includes the midbrain, pons, medulla, and connections for cranial nerves II and IV through XII. The cerebellum is located under the cerebrum and behind the brain stem. The brain accounts for approximately 2% of the total body weight; it weights approximately 1.400 g in an average young adult (Hickey, 2003). In the elderly, the average brain weights approximately 1.200 g.

A.

Cerebrum The cerebrum consists of two hemispheres that are incompletely separated by the great

longitudinal fissure. This sulcus separates the cerebrum into the right and left hemispheres. The

two hemispheres are joined at the lower potion of the fissure by the corpus callosum. The outside surface of the hemispheres has a wrinkled appearance that is the result of many folded layers or convolutions called gyri, which increase the surface area of the brain, accounting for the high level of activity carried out by such a small-appearing organ. The external or outer portion of the cerebrum (the cerebral cortex) is made up of gray matter approximately 2 to 5 mm in depht; it contains billions of neurons, giving it a gray appearance. White matter makes up the innermost layer and is composed of nerve fibers and neuroglia that form tracts or pathways connecting various parts of the brain with one another (transverse and association pathways) and the cortex to lower portions of the brain and spinal cord (projection fibers). The cerebral hemispheres are divided into pairs of frontal, parietal, temporal, and occipital lobes. 1. Frontal- the largest lobe.it contains the motor and premotor areas. The major functions of this lobe are concentration, abstract thought, information storage or memory, and motor function. It also contains Brocas area is in the left frontal lobe, critical for motor control of speech. Many association areas in the frontal lobe receive information from throughout the brain and incorporate that information into thoughts, plans and behavior.The frontal lobe is also responsible in large part for an individuals affect, judgment, personality, and inhibitions. 2. Parietal- a predominantly sensory lobe. The primary sensory cortex, which analyzes sensory information and relays the interpretation of this information to the thalamus and other cortical areas, is located in the parietal lobe. The parietal lobe receives sensory input for touch and pain. It is also essential to an individuals awareness of the body in space, as well as orientation in space and spatial relations. 3. Temporal- contains the auditory receptive areas and includes Wernickes area, where language is interpreted. Contains a vital area called the interpretive area that provides integration of somatization, visual, and auditory areas and plays the most dominant role of any area of the cortex in cerebration. It is also involved in the interpretation of smell and is important for the formation and storage of memory. The hippocampus is part of the temporal lobe. 4. Occipital- the posterior lobe of the cerebral hemisphere is responsible for visual interpretation. The occipital lobe receives information that originated as signals in the retina of the eye.

The corpus callosum is a thick collection of nerve fibers that connects the two hemispheres of the brain and is responsible for the transmission of information from one side of the brain to the other. Information transferred includes sensation, memory, and learned discrimination. Right-handed people and some left-handed people have cerebral dominance on the left side of the brain for verbal, linguistic, arithmetical, calculating, and analytic functions. The nondominant hemisphere is responsible for geometric, spatial, visual, pattern, and musical functions. The dienchephalon structures lie deep between the cerebral hemispheres. The diencephalon includes the basal ganglia, the thalamus, and the hypothalamus. The basal ganglia are masses of nuclei located deep in the cerebral hemispheres that are responsible for control of fine motor movements, including those of the hands and lower extremities. The basal ganglia are composed of several structures that can be anatomically or physiologically separated, including the caudate nucleus, the putamen, and the globus pallidus. Virtually all projections to and from the basal ganglia go through the thalamus. Lesions of the basal ganglia cause repetitive movements, grimaces, and tremors, as seen with Huntingtons disease (chorea) and Parkinsons disease.

The thalamus lies on either side of the third ventricle and acts primarily as a relay station for all sensation except smell and in turn relays the information through numerous afferent tracts to the rest of the cerebral cortex. Function of the cerebral cortex depends on thalamic relay. All memory, sensation, and pain impulses also pass through this section of the brain. The hypothalamus is located anterior and interior to the thalamus. The hypothalamus lies immediately beneath and lateral to the lower portion of the wall of the third ventricle. The hypothalamus plays an important role in the endocrine system and neural organ responsible for maintaining homeostasis (constancy of the internal environment) because it regulates the pituitary secretion of hormones that influence metabolism, reproduction, stress response, and urine production. It works with the pituary to maintain fluid balance and maintans temperature regulation by promoting vasoconstriction or vasodilatation. The hypothalamus is the site of the hunger center and is involved in appetite control. It contains centers that regulate the sleep-wake cycle, blood pressure, aggressive and sexual behavior,and emotional responses. The hypothalamus also controls and regulates the autonomic nerveous sytem. The pituitary gland is located in the sella turcica at the base of the brain and is connected to the hypothalamus. The pituitary is a common site for brain tumors in adults; frequently they are detected by physical signs and symptoms that can be traced to the pituitary, such as hormonal imbalance or visual disturbances secondary to pressure on the optic chiasm. The posterior portion of each hemisphere (ie, the occipital lobe) is devoted to all aspects of visual perception. The lateral region, or temporal lobe, incorporates the auditory center. The midcentral zone, or parietal zone, is concerned with sensation; the anterior portion is concerned with voluntary muscle movements. The large area behind the forehead (ie, the frontal lobes) contains the association pathways that determine emotional attitudes and responses and contribute to the formation of thought processes. Damage to the frontal lobes as a result of trauma or disease is by no means incapacitating from the standpoint of muscular control or coordination, but it affects a persons personality, as reflected by basic attitude, sense of humor and propriety, selfrestaint, and motivations. The Limbic System. The limbic system is a diffuse grouping of neurons from different areas of the brain. Neurons in the limbic system include fibers from all lobes of the cerebrum and

extensive connections from the hypothalamus and thalamus. Midbrain (the pons, medulla oblongata, and mesencephalon) and hindbrain (cerebellum) areas also sends projections that contribute to the limbic system. The hippocampus is considered part of the limbic system and plays an important role in coding and consolidating memories. The amygdale, also considered part of the limbic system, is involved in the production of emotions, aggression, and sexual behavior. Learning and behavior are also influenced by several limbic system structures and connections. B. Brain Stem The brain stem consists of the midbrain, pons, and medulla oblongata. The midbrain connects the pons and the cerebellum with the cerebral hemispheres; it contains sensory and motor pathways and serves as the center for auditory and visual reflexes. Cranial nerves III and IV originate in the midbrain. The pons is situated in front of the cerebellum between the midbrain and the medulla and is a bridge between the twos halves of the cerebellum, and between the medulla and the cerebrum. Cranial nerves V through VIII connect to the brain in the pons. The pons contains motor and sensory pathways. Portions of the pons also control the heart, respiration, and blood pressure. The medulla oblongata contains motor fibers from the brain to the spinal cord and sensory fibers from the spinal cord to the brain. The medulla oblongata lies just superior to the spinal cord, and it contains tracts that ascend or descend between the spinal cord and higher brain centers.Most of these fibers cross, or decussate, at this level. Cranial nerves IX through XII connect to the brain in the medulla. The medulla oblongata contains a number of reflex centers for regulating heartbeat, breathing, and vasoconstriction. It also contains the reflex centers for vomiting, coughing, sneezing, hiccupping, and swallowing.

C.

Cerebellum The cerebellum is separated from the cerebral hemispheres by a fold of duramater, the

tentorium cerebella. The cerebellum has both excitatory and inhibitory actions and is largely responsible for coordination of movement. It also controls fine movement, balance, position sense (awareness of where each part of the body is), and integration of sensory input. The cerebellum receives sensory input from the eyes, ears, joints, and muscles about the present position of body parts. It also receives motor input from the cerebral cortex about where these parts should be located. After integrating this information, the cerebellum sends motor impulses by way of the brain stem to the skeletal muscles. In this way, the cerebellum maintains posture and balance. It also ensures that all of the muscles work together to produce smooth, coordinated voluntary movements. 2.4 Peripheral Nervous System The peripheral nervous system (PNS) lies outside the central nervous system and is composed of nerves and ganglia. Nerves are bundles of myeilinated axons. Ganglia (ganglion) are swellings associated with nerves that contain collections of cell bodies. As with muscles, connective tissue separates axons at various levels of organization. The PNS is subdivided into the somatic system and the autonomic system. The somatic system serves the skin, skeletal muscles, and tendons. It includes nerves that take sensory information from external sensory receptors to the CNS and motor commands away from the CNS to the skeletal muscles. The autonomic system, with a few exceptions, regulates the activity of cardiac and smooth muscles and glands. 2.4.1 Types of Nerves The cranial nerves are attached to the brain, and the spinal nerves are attached to the spinal cord. A. Cranial Nerves

Humans have 12 pairs of cranial nerves. By convention, the pairs of cranial nerves are referred to by roman numerals. Most of the cranial nerves belong to the somatic system. Some of

these are sensory nerve. That is, they contain only sensory fibers. Some are motor nerves, containing only motor fibers and others are mixed nerves, so called because they contain both sensory and motor fibers. Cranial nerves are largely concerned with the head, neck, and facial regions of the body. However, the vagus nerve (X),which has branches to most of the internal organs, is a part of the autonomic system. B. Spinal Nerves

Humans have 31 pairs of spinal nerves. One each pair is on either side of the spinal cord. The spinal nerves are grouped because they are at either cervical, thoracic, or lumbar regions of the vertebral column. The spinal nerves are designated according to their location in relation to the vertebrae because each passes through an intervertebral foramen as it leaves the spinal cord.

Many spinal nerves carry fibers that belong to either the somatic or the autonomic system. However, the spinal nerves are called mixed nerves because they contain both sensory fibers that conduct impulses to the spinal cord from sensory receptors and motor fibers that conduct impulses away from the cord to effectors. The sensory fibers enter the cord via the posterior root, and the motor fibers exit by way of the anterior root. The cell body of a sensory neuron is in a posterior (dorsal)- root ganglion. Each spinal nerve serves the particular region of the body in which it is located .

2.4.2 Subdivided of The PNS A. The Autonomic Nervous System Autonomic nerve fibers leave the spinal cord and innervate smooth and cardiac muscle and the endocrine and exocrine glands. Autonomic nerves fibers are considered involuntary because there is little conscious control over their function. These two divisions of the autonomic nervous system, the sympathetic and parasympathetic. Sympathetic and parasympathetic nerves innervate many of the same organs but typically cause opposite responses. The cell bodies of these neurons lie in the brain or spinal cord. In both divisions of the autonomic system, two nerve fibers participate in the efferent pathway. 1. The sympathetic nervous system. The first fibers of the sympathetic nerves, called the preganglionic fibers, leave from the thoracic or lumbar regions of the spine. Soon after leaving the spine, a preganglionic fiber joins other preganglionic fibers to form an autonomic ganglion. At this point, the preganglionic fiber synapses on the second nerve fiber of the system, the postganglionic fiber, and releases acetylcholine, which causes the postganglionic fiber to fire an action potential. From the autonomic ganglia, the postganglionic fiber travels to its target organ, the muscle or gland. The sympathetic postganglionic fiber usually releases the neurotransmitter norepinephrine. Target organ receptors for norepinephrine are called adrenergic receptors. 2. The parasympathetic nervous system. The fibers of the parasympathetic nervous system leave the brain in the cranial nerves or leave the spinal cord from the sacral area. The preganglionic fiber of the parasympathetic system is typically long and travels to an autonomic ganglion located near the target organ. Preganglionic parasympathetic nerves release acetylcholine that then stimulates the postganglionic fiber. The parasympathetic postganglionic fiber then travels a short distance to its target tissue, a muscle or a gland. This nerve also releases acetylcholine. Preganglionic acetylcholine receptors for sympathetic and parasympathetic fibers are called nicotinic receptors. Postganglionic acetylcholine receptors are called muscarinic receptors. These names relate to the experimental stimulation of the receptors by nicotine and muscarine (a mushroom poison).

B.

The Somatic Nervous System Somatic nerves of the peripheral nervous system consist of efferent motor neurons that

leave the brain or spinal cord and synapse directly on skeletal muscle cells. Motor neurons are large myelinated nerves that release acetylcholine at the neuromuscular junction. Acetylcholine binds to receptors on a specialized area of the muscle cell, called the end plate. Binding of acetylcholine causes the muscle cell to reach threshold, resulting in an action potential and the opening of calcium channels (gates) in the membrane. This leads to an increase in intracellular calcium and contraction of the skeletal muscle fiber. There are no inhibitory motor neurons.

CHAPTER III MENINGITIS

3.1

Introduction of Meningitis The meninges (dura, archnoid, and pia meter)are the coverings surrounding the brain.

The purpose of meninges is to protect the brain and spinal cord from invading organism. Meningitis is the inflammation of the meningeal coverings of the brain and spinal cord, most commonly due to bacterial or viral cause, although it can also be caused by fungus, protozoa, or toxic exposure. Infection and inflammation (caused by pathogens releasing toxins) can progress rapidly due to the circulating CSF around the brain and spinal cord. Bacterial meningitis is the most common and is typically due to Streptococcus pneumonia (pneumococcal), Neisseria meningitides (meningococcal), or Haemophilus influenza. The incidence of H. influenza meningitis infections has decreased since the vaccine against H. influenza began to be used routinely in infants in the early 1900s. Other organisms that can cause bacterial meningitis include Staphylococcus aureus, Escherichia coli and Pseudomonas. Organis typically travel either through the bloodstream to the central nervous system or enter by direct contamination (skull fracture or extension from sinus infections). The body is normally home to many types of microorganisms that live on the skin and the inner mucous membrane surfaces of the digestive system, reproductive tract, respiratory system and urinary tract. Bacterial meningitis is more common in colder months when upper respiratory tract infections are more common. People in close living conditions, such as prisons, military barracks, or college dorms are at greater risk for outbreaks of bacterial meningitis due to likelihood of transmission. Viral meningitis may follow other viral infections, such as mumps, herpes simplex or zoster, enterovirus and measles. Viral meningitis is often a self-limiting illness. The pathogens that cause meningitis are very attracted to the nervous system and must overcome many barriers to get there (invade the CNS). The pathogens usually colonize and multiply in the nasopharyngeal area, break into the bloodstream, and then break through the blood-brain barrier. In addition, the pathogen must be able to survive the bodys natural immune response and the inflammatory response as well. These pathogens are very determined.

Patients who are immunocompromised have an increased risk for contracting a fungal meningitis. This may travel from bloodstream to the central nervous system or by direct contamination. Cryptococcus neoformans may be the causative organism in the patients. Diseases that are difficult to predict and that appear without warning cause what scientists call silent outbreaks. The term outbreaks refers to the rapid spread of a disease among many people living within a certain area. Almost all cases of meningitis were confirmed across the metropolitan area.

3.2

Pathophysiology Meningeal infections generally originate in one of two ways : through the bloodstream as

consequence of other infections, or by direct extension, such as might occur after a traumatic injury to the facial bones, or secondary to invansive procedures. N.meningitidis concentrates in the nasopharynx and is transmitted by secretion or aerosol contamination. Bacterial or meningococcal meningitis also occurs as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS) and as a complication of Lyme disease.S.pneumoniae the most frequent causative agent bacterial meningitis associated with AIDS (Rosenstein, Perkins, Stephens et al.,2001). Once the causative organism enters the bloodstream,it crosses the blood-brain barrier and causes an inflammatory reaction in the meninges. Independent of the causative agent,inflammation of the subarachnoid space and piamater occurs. Since there is little room for expansion within the cranial vault,the inflammation may cause increased intracranial pressure. Cerebrospinal fluid (CSF) flows in the subarachnoid space, where inflammatory cellular material from the affected meningeal tissue enters and accumulates in the subarachnoid space,thereby increasing the CSFcell count (Coyle, 1999). Some bacteria that cause meningitis, especially meningococci, shed bubbles of poisonous endotoxin as they circulate in the blood. The bubbles seem to act as decoys, making it difficult for the immune system to identify the bacteria. Antibiotics have no effect on endotoxin. In fact, bacteria release even more endotoxin as they die, making the patient even sicker. Endotoxin has two major effects on the body. First, it weakens the myocardium, leading to decreased cardiac output, systemic hypoxia and shock. Second, endotoxin leads to disseminated intravascular coagulation.

As white blood cells engulf the bacteria, endotoxin makes them sticky, causing them to adhere to and damage the linings of the blood vessels. The body tries to repair the damaged blood vessels, but endotoxin disrupts clotting mechanisms. Tiny blood clots form in vessels all over the body. The vessels walls disintegrate, letting blood leak into surrounding tissue and damaging organs, such as the kidneys and lungs. The distinctive petechial rash of meningococcal sepsis results from bleeding under the skin. Unlike rashes caused by other diseases (for example, measles), the rash caused by meningococcal infection doesnt blanch when pressed. The prognosis for bacterial meningitis depends on the causative organism,the severity of the infection and illness,and the timeliness of treatment. In acute fulminant presentations there may be adrenaldamage, circulatory collapse, and widespread hemorrhages (WaterhouseFriderichsen syndrome).this syndrome is the result of endothelial damage and vascular necrosis caused by the bacteria. Complications include visual impairment,deafness,seizures,paralysis, hydrocephalus,and septic shock. Bacterial meningitis still has a significant mortality rate and these patients need to be managed in the hospital. Some patients will have permanent neurologic effects following the acute episode. Viral meningitis is typically self-limiting. Fungal meningitis often occurs in patients who are immunocompromised. Patients who are have comorbidities or are eldery have greater difficulty with the symptoms of meningitis.

3.3

Types and Classification of Meningitis

3.3.1 Viral Meningitis One of the most common, but least dangerous, forms of meningitis is a viral meningitis in the spring and fall seasons. Viral meningitis will normally clear up by itself without complications. Viral meningitis is sometimes called aseptic meningitis when doctors attempt but fail to produce a positive identification of the underlying virus. Nearly every aseptic meningitis is caused by a virus. The condition generally lasts 7 to 10 days and although serious, is rarely fatal in people with normal immune systems. Many different viruses can cause meningitis, including herpes simplex types 1 and 2, mumps, influenza, Epstein-Barr, measles, rubella, and polio, among other. The most common causes of viral meningitis are enteroviruses. These viruses normally live in the intestines. Enteroviruses like Coxsackie and Echovirus are often the cause of viral meningitis. Since many

people who have it do not get sick enough to seek medical attention, it is difficult to know how wide-spread viral meningitis might be. In populations where vaccinations are common, some of these causes of meningitis are rare. Other viruses that may cause meningitis include those spread by mosquitoes, ticks and other insects. 3.3.2 Fungal Meningitis Fungi can also cause meningitis. Candida, Histoplasma, Coccidioides, and Cryptococcus fungi have all been responsible for meningitis infections. Most cases of fungal meningitis occur in people who are already sick with a disease like AIDS, which has suppressed their immune systems and the loss of immunity associated with aging. The fungi that cause meningitis are found in the environment and are spread on air currents. Healthy people will not develop meningitis from breathing in these particles. Several of these fungi are found in soil, and others, like Candida, are found everywhere, including on human skin and inside the intestine. The most common fungal meningitis is cryptococcal meningitis due to Cryptococcus neofarmans.in Africa, cryptococcal meningitis is estimated to be the most common cause of meningitis and it accounts for 20-25 % of AIDS-related deaths in Africa. Meningitis caused by Coccidiodes immitis is called coccidiodal meningitis. If left untreated, it is usually fatal. This fungus lives in the soil.

3.3.3 Bacterial Meningitis The most common form, can be community acquired or associated with prior infection. Other causes include injury, facial or basilar skull fractures, shunt occlusion /malfunction, craniotomy, otitis media, sinusitis, or bacteremia (e.g., endocarditis, pneumonia). Streptococcus pneumonia, a gram-positive cocci, has been the leading cause of adult meningitis in United States. Pneumococcal meningitis occurs in crowded conditions and is spread seasonally (fall and winter). This organism is not prevalent as a cause of meningitis since the development of Pneumovax and Prevnar vaccines. Pneumococcal meningitis may occur following an upper respiratory tract infection (URI) or nasopharyngeal colonization with pneumococcal strain, is a complication of conditions associated with CSF leaks, is associated with asplenia and is more prevalent in immunocompromised persons and in older adults.

Neisseria meningitidis, is a gram-negative cocci, is the second leading cause of meningitis in adults. Infection is more likely to occur in patients with complement component deficiencies (e.g., conginetal or associated with nephritic syndrome, hepatic failure, systemic lupus erythematosus, multiple myeloma). Haemophilus influenza,a gram-negative bacilli, is the most common cause in children. However it may affect adults. Predisposing factors include URIs, hypogammaglubulinemia, diabetes mellitus, alcoholism, and head trauma. Listeria monocytogenes, a gram-positive bacilli, is being seen more frequently as a cause of meningitis, especially in immunocompromised patients and those of extreme ages. Outbreaks have been linked to consumption of contaminated dairy products, undercooked chicken, fish, and meats. Gram-negative species (E.Coli. Klebsiella, Proteus, and Pseudomonas) are increasing in prevalence as a nosocomial cause secondary to trauma or neurosurgical procedurs. Spontaneous gram-negative meningitis is found in older adults, the immunocompromised, or persons with underlying conditions such as cirrhosis, diabetes, malignancy, or splenectomy. The urinary tract is the usual portal of entry of bacteria. Other microbes : Mycobacterium pneumonia, B. burgdorferi, and Treponeme pallidum are also associated with meningitis. Other surgical procedures complicated by gram-negative infections are ventriculoperitoneal shunts, craniofacial repair, ventriculostomy, hypophysectomy, reservoir insertion, and myelography. The types of bacteria that cause bacterial meningitis vary according to the infected individual's age group.

In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and bacteria that normally inhabit the digestive tract such as Escherichia coli (carrying the K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics.

Older children are more commonly affected by Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination).

In adults, Neisseria meningitidis and Streptococcus pneumoniae together cause 80% of bacterial meningitis cases. Risk of infection with Listeria monocytogenes is increased in persons over 50 years old. The introduction of pneumococcal vaccine has lowered rates of pneumococcal meningitis in both children and adults. Recent skull trauma potentially allows nasal cavity bacteria to enter the meningeal space.

Similarly, devices in the brain and meninges, such as cerebral shunts, extraventricular drains or Ommaya reservoirs, carry an increased risk of meningitis. In these cases, the persons are more likely to be infected with Staphylococci, Pseudomonas, and other Gram-negative bacteria. These pathogens are also associated with meningitis in people with an impaired immune system. An infection in the head and neck area, such as otitis media or mastoiditis, can lead to meningitis in a small proportion of people. Recipients of cochlear implants for hearing loss risk more a pneumococcal meningitis. Tuberculous meningitis, which is meningitis caused by Mycobacterium tuberculosis, is more common in people from countries where tuberculosis is endemic, but is also encountered in persons with immune problems, such as AIDS. Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system. Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is a skull fracture, particularly fractures that affect the base of the skull or extend towards the sinuses and petrous pyramids. Approximately 59% of recurrent meningitis cases are due to such anatomical abnormalities, 36% are due to immune deficiencies (such as complement deficiency, which predisposes especially to recurrent meningococcal meningitis), and 5% are due to ongoing infections in areas adjacent to the meninges.

3.3.4 Parasitic Meningitis A parasitic meningitis is more common in underdeveloped countries and usually is caused by parasites found in contaminated water, food, and soil. A parasitic cause is often assumed when there is a predominance of eosinophils (a type of white blood cell) in the CSF. The most common parasities implicated are Angiostrongylus cantonensis, Gnathostoma spinigerum, Schistosoma as well as the conditions cysticercosis, taxocariasis, baylisascariasis, paragonimiasis, and a number of rare infections and noninfective conditions. 3.3.5 Non-infectious Meningitis Non-infectious meningitis may develop as a complication of another illness (e.g., mumps, tuberculosis, syphilis ). A break in the skin and/ or bones in the face or skull (caused by birth defect, brain surgery, head injury) can allow bacteria to enter the body. Meningitis may occur as the result of several non-infectious causes : spread of cancer to the meninges (maglinant or neoplastic meningitis) and certain drugs (mainly non-steroidal, anti inflammatory drugs, antibiotics and intravenous immunoglobulins). It may also be caused by several inflammatory conditions, such as systemic lupus erythematosus, and certain forms of vasculitis (inflammatory conditions of the blood vessel wall), such as Behcets disease. Epidermoid cysts and dermoid cysts may cause meningitis by releasing irritant matter into subarachnoid space. Mollarets meningitis is a syndrome of recurring episodes of aseptic meningitis. It is thought to be caused by herpes simplex virus type 2. Rarely, migraine may cause meningitis, but this diagnosis is usually only made when other causes have been eliminated.

3.4

Etiology of Meningitis Meningitis is a particularly dangerous infection because of the very delicate nature of the

brain. Brain cells are some of the only cells in the body that, once killed, will not regenerate themselves. Therefore, if enough brain tissue is damaged by an infection, serious, life-long handicaps will remain. In order to learn about meningitis, it is important to have a basic understanding of the anatomy of the brain. The meninges are three separate membranes, layered together, which encase the brain and spinal cord:

The dura is the toughest, outermost layer, and is closely attached to the inside of the skull.

The middle layer, the arachnoid, is important because of its involvement in the normal flow of the cerebrospinal fluid (CSF), a lubricating and nutritive fluid that bathes both the brain and the spinal cord.

The innermost layer, the pia, helps direct blood vessels into the brain. The space between the arachnoid and the pia contains CSF, which helps insulate the brain from trauma. Many blood vessels course through this space. CSF, produced within specialized chambers deep inside the brain, flows over the surface

of the brain and spinal cord. This fluid serves to cushion these relatively delicate structures, as well as supplying important nutrients for brain cells. CSF is reabsorbed by blood vessels located within the meninges. A careful balance between CSF production and reabsorption is important to avoid the accumulation of too much CSF. Because the brain is enclosed in the hard, bony case of the skull, any disease that produces swelling will be damaging to the brain. The skull cannot expand at all, so when the swollen brain tissue pushes up against the skull's hard bone, the brain tissue becomes damaged and may ultimately die. Furthermore, swelling on the right side of the brain will not only cause pressure and damage to that side of the brain, but by taking up precious space within the tight confines of the skull, the left side of the brain will also be pushed up against the hard surface of the skull, causing damage to the left side of the brain as well. Another way that infections injure the brain involves the way in which the chemical environment of the brain changes in response to the presence of an infection. The cells of the brain require a very well-regulated environment. Careful balance of oxygen, carbon dioxide, sugar (glucose), sodium, calcium, potassium, and other substances must be maintained in order to avoid damage to brain tissue. An infection upsets this balance, and brain damage can occur when the cells of the brain are either deprived of important nutrients or exposed to toxic levels of particular substances. The cells lining the brain's tiny blood vessels (capillaries) are specifically designed to prevent many substances from passing into brain tissue. This is commonly referred to as the

blood-brain barrier. The blood-brain barrier prevents various substances that could be poisonous to brain tissue (toxins), as well as many agents of infection, from crossing from the blood stream into the brain tissue. While this barrier is obviously an important protective feature for the brain, it also serves to complicate treatment in the case of an infection by making it difficult for medications to pass out of the blood and into the brain tissue where the infection is located. 3.5 Clinical Appearance A complete neurologic examination should be performed to establish the patients baseline neurologic function. One or more tests for meningitis usually are positive. Examination of associated systems (head, eye, ear, nose, and throat and pulmonary ) provides additional data. Bacterial meningitis presents with classic symptoms of fever, altered mental status, headache, and nuchal rigidity. Immediate diagnosis and isolation of the organism are paramount in this life threatening disease. Delay in obtaining necessary information needed to diagnosis and threat the underlying organism will increase more morbidity and mortality. A. History and Risk Factors a. History of presents illness 1. Times courses for symptoms development. 2. Recent infection (respiratory/ ear) 3. Recent trauma to the head. 4. Exposure of the meningitis. 5. Use of antibiotics. 6. Petechial or ecchymotic rash. 7. Ear or nose drainage. b. Medical / social history 1. Drug allergies. 2. Past medical history. 3. Recent surgical procedure. 4. Immune compromising condition. 5. IV drug use 6. HIV status or risk behaviors

3.5.1 Assessment Meningitis

7. Travel to endemic meningococcal area B. Vital Sign a. BP, HR, and RR changes : may further alter cerebral tissue perfusion. Monitored, rhythm, and death of respiration for changes or abnormal breathing patterns. b. Hipertermia : may be associated with injury or irritation of the hipotalamic temperature regulating center, presents of blood on the CSF, or infection. Elevated temperature increases the metabolic needs of the brain, potentially leading to increased blood flow to the area, with concomitant cerebral hyperemia. C. Observations

Level of consciousness (LOC): when assessing LOC it is important to not use subjective term such as stupor or lethargy but rather to assess and communicate clearly the description patients of the spontaneous activity response, response to verbal stimuli and reaction to painfull stimuli, and how this differs from previous assessment. Assess for an acute changes in mental status or fluctuation in mental status ; voriuos scale can be used that include LOC and other key indicators. Examples are the Richmond Agitation and Seadtion Score (RASS) and GCS.

Pupillary changes: Examine puppils for size (In mm), shape, simetry, reactivity, contriction, consensual response, and accommodation. Pupillary abnormalitys can indicate unilateral or bilateral brain disfunction, interruption of sympathetic or parasympathetic pathways, damage in the brainstem, cranial nerve damage, and herniation.

Clinical Presentation a. S.pneumoniae: The classic presentation of pneumococcal meningitis is fewer, headache, meningismus, and altered mental status that prograsses quickly to coma. Nuchal regality an Kernig or Brudzinski sign. Nousea, fomitting, profuse sweats, weakness, myalgia, seizures, and cranial nerve palsies also may be present. b. N. meningitidis : Patients may quickly deteriorate, beginning with fever and early macular erythematous rash that progresses rapidly to petechial and purpuric states, conjunctival petechiae, and aggressive behavior. Dysfunctions of cranial nerves VI, VII,

and VIII and aphasia, ventriculitis, subdural empyema, cerebral venous thrombosis, and disseminated intravascular coagulation (DIC) may occur. c. H. influenza : The most distinguishing sign is early development of deafness, which can occur within 24 to 36 hours after onset. A morbilliform or petechial rash may be present. d. L. monocytogenes : Seizures and focal deficits such as ataxia, cranial nerve palsies, and nystagmus are seen early in the course of infection. Conclusive diagnosis may require serology testing. e. Gram negative species : In older adults, fever may be absent or low grade and headache may not be reported. Meningeal signs may be subtle, but confusion, severe mental status changes, and pneumonia are commonly reported. Nuchal rigidity in older adults must be differentiated from degenerative changes of the cervical spine. f. B. burgdorferi : The symptoms of meningitis may be preceded by symptoms of Lyme disease, which occur in three stages. The first stage is a bulls eye rash within a few days of the tick bite followed by headache, stiff neck, lethargy, irritability, and changes in mental status, especially memory loss. Stage two , weeks to months after the tick deficits, mental status changes, peripheral neuropathies, and myalgias. In the last or third stage , arthritic types of symptoms and brain parenchymal changes are apparent. g. Acute meningitis with negative Gram stain : Fever and neck stiffness are the most frequent findings. The Gram stain for bacteria is negative, but CSFWBC count elevated. Symptoms are similliar to those for other types of meningitis. h. M. tuberculosis : A slow-onset process that causes neurologic damage before treatment is sought. Symptoms include headache, lethargy, confusion, nuchal rigidity, cranial nerve abnormalities, SIADH, weight loss, and night sweats. Kernig and Brudzinki sign are present. The chest radiographic results may be clear, and purified protein derivative (PPD) may be nonreactive. i. Cryptococcus neoformans : Because the infection is subacute, fever and headache may have a subtle pattern lasting for weeks while other symptoms of meningitis accur, including positive meningeal signs, alterations in mental status (e.g hyperactivity, bizarre behavior, emotional lability, poor judgment), photophobia, focal cranial nerve deficits, nausea, vomiting and rarely seizures.

j. Aseptic meningitis syndrome : Fever, headache, stiff neck, fatigue, anorexia, and altered LOC are seen several hours after ingestion of causative drug. Severity varies with amount of drug taken and previous exposure. CSF glucose may be slightly elevated. D. Functional Assesment 1. Assess motor function and sensory responses a. Motor : Assess motor movement in extremities related to strength, symmetry of movement and coordination. Assess for abnormal motor movements unilaterally and bilaterally, such as decorticate posturing, decerebrate posturing, or flaccidity. Motor deficits (weakness or paralysis) are caused by injury or edema to the primary motor cortex and corticospinal (pyramidal) tracts. b. Sensory : Assess perception of touch, proprioception, pain, temperature, and vibration. Superficial and deep reflexes are tested on symmetrical side of the body and compared noting the strength of contraction. Sensory deficits occur when the primary sensory cortex, the sensory association areas of the parietal lobe, or spinothalamic tracts are injured or edematous. 2. Assess for cranial nerve impairment : Cranial nerve deficits may improve as cerebral edema resolves or may be permanent. Nursing assessment of cranial nerve dysfunction is important. E. Screening Labwork 1. CSF analysis : Evaluates the color, WBC count, differential, glucose content, and protein level. 2. Complete blood count, electrolytes, and coagulation studies : Evaluate for anemia, hypo or hyperglycemia; potential for hemorrhage or infection.

3.5.2 Diagnostic Tests Bacterial meningitis presents with classic symptoms of fever, altered mental status, headache, and nuchal rigidity. Immediate diagnosis and isolation of the organisms are paramount in this life-threatening disease. Delay in obtaining the necessary information needed to diagnosis and treat the underlying organism will increase morbidity and mortality.

Diagnostic Tools 1. In patients with suspected acute bacterial meningitis for whom there is no clinical contraindication, the CSF is collected through lumbar puncture and examined for white blood cells and microorganism sensitivity. Elevated protein, elevated neutrophils, and low glucose in the CSF indicate meningitis. 2. Laboratory studies for viral meningitis are not indicated (e.g., normal glucose, elevated lymphocytes). 3. Rapid diagnostic of CNS infection is essential. This is especially true of meningitis. CT scan and MRI may be used to evaluate the degree of swelling and sites of necrosis. CT is very rapid and is most useful in emergency situations. 4. Corticosteroid (dexamethasone) therapy to reduce inflammation appears to be beneficial for the adjuvant treatment of most adults with suspected pneumococcal meningitis.

3.5.3 Collaborative Management Care Priorities 1. Control Priorities a. Antibiotic therapy: There are two major caveats to treating bacterial meningitis. First, the bactericidal agent must be effective against the organism and second, the agent must achieve a bacteriodical effect within the CSF. Only IV antibiotics should be used, expect for fifampin which is useful as synergistic agent. b. Rapid sterilization of the CSF via appropriate pharmacologic thingerapy (Table 7-4) : Prophylaxis, using appropriate antimicrobials for people to N. meningitidis (rimfampin or spiramycin) or H. influenza meningitis, is recommended. 2. Rapid inflammation with adjunctive pharmacologic therapies: Dexamethasone may decrase inflammation by reducing cytokines produced by bacterial products. In recent study result, improvement in outcome, decrease in neurologic sequelae, and reduction in mortality with the use of dexamethasone have been reported. Recommended dosing is 0.15 mg/kg ever 6 hours for 4 days. Start dose with or just prior to first antibiotic dose.

Table . Common Drug Therapy For The Management of Meningitis Causative agent Bacterial Meningitis S. pneumonia Gram-positive cocci Penicillin (PCN), ceftriaxone, cefotaxime, vancomycin with ceftriaxone if beta-lactam resistance; chloramphenicol for PCN allergies H. influenza Gram-negative bacilli Cefotaxime or ceftriaxone, add rifampin if pharyngeal colonization N. meningitides Gram-negative cocci Penicillin G, add rifampin, fluoroquinolones, or chepalosporin if pharyngeal colonization; alternative is third generation chepalosporin (cefotaxime) L. monocytogenes Gram-positive bacilli Penicillin G or ampicillin with gentamycin for synergy; if allergi to PCN, the trimethoprimsulfamethoxazole M. tuberculosis Acid-fast bacteria Isoniazid, rifampin, ethambutol, pyrazinamide B. burgdorferi Fungal C. neofarmans Fungus Amphotericin B + flucytosine, fluconazole, or itraconazole Cocci Gram-positive Vancomycin + penicillin G + aminoglycosides Spirochete Ceftriaxone or penicillin G Characteristic Therapy

Gram-negative Bacilli Gram- positive

Penicillin G

Ampicillin, penicillin + aminoglycosides

P. aeruginosa, Klebsiella, E. coli, Citrobacter, Acinetrobacter, Enterobacter, Serratia marcescens

Gram-negative

High doses of third-generation cephalosporins + aminoglycosides

3. Maintain fluid and electrolyte balance: Overhydration and underhydration can lead to adverse effects. Research supports the use of IV maintance fluids over fluid restriction during the first 48 hours of treatment of bacterial meningitis. Electrolyte imbalance should be corrected. 4. Provide adequate nutrition: Oral feeding should be encouraged when possible. Enteral or parenteral feeding may be initiated. Parenteral nutrition is used if enteral feeding is not tolerated. Hydration should be maintained. Several nutrients can help strengthen the immune system, possibly helping to prevent meningitis or build up the immune system after meningitis has been treated, though scientific studies have not examined these nutrients specifically for meningitis. 5. Control seizures with anticonsulvant therapy : used prophylactically or if seizures occur. Seizures increase metabolic rate and cerebral blood flow, which may cause deterioration in patients with cerebral edema and intracranial hypertension. 6. Maintain normothermia/ control fever : helps prevents intracranial hypertension associated with increased metabolic rate. Fever should be controlled by antipyretics such as acetaminophen or use of other cooling measures such as tepid baths. 7. Prevent infection : Vaccines are currently avalaible for meningitis prophylaxis, including the following : (1) influenza type B (Hib), given as a childhood immunization; (2) bacillus Calmette-Guerin (BCG), used for tuberculosis, also prevents tuberculosis meningitis; (3) pneumococcal vaccine recommended for those who are chronically ill and adults over 65 years of age, and (4) N.meningitides vaccine for specific or combined prophylaxis for five

investigational subgroups. The CDC guidelines recommend Transmission- Based Precautions be implemented until effectiveness of antimicrobial treatment is established. 8. Facilititate mobility : Physical therapy (PT), occupational therapy (OT), and speech therapy should be initiated as soon as patient is stable, to minimize physical and cognitive complications. 9. Monitor neurologic function at least every 2 to 4 hours, changes in mental status, level of consciousness, pupil reactions, speech, facial kovement symmetry, and signs of increased intracranial pressure. 10. Respiratory isolation (until pathogen identified and for 24 hours after antibiotics started). 11. Evaluate the need for support services : Evaluate the need for home health care, support groups, and social services.

CHAPTER 4 CONCLUSION 4.1 Conclusion The nervous system permits sensory input, performs integration and stimulates motor output. The nervous system is divided into the central nervous system (brain and spinal cord) and the peripheral nervous system (somatic and autonomic nervous system). The CNS lies in the midline of the body, and the PNS is located peripherally to the CNS. The CNS, consisting of the spinal cord and brain, is protected by the meninges and the cerebrospinal fluid. The PNS, in the somatic system, cranial nerves take impulses to and/or from the brain. Spinal nerves take impulses to and from the spinal cord. The autonomic nervous system controls the functioning of internal organs. The autonomic nervous system consisting of the sympathetic divion and the parasympathetic divion. Nervous tissue contains neurons and neuroglia. Each type of neuron (motor, sensory, and interneuron) has three parts (dendrites, cell body, and axon). Neuroglia support, protect, and nourish the neurons. The diverse group of neurologic disorders that make up infectious and autoimmune disorders. Infectious processes of the nervous system sometimes cause death permanent dysfunction.The infectious disorders of the nervous system include meningitis. Meningitis as a serious inflammation of the meninges, the thin, membranous covering of the brain and the spinal cord. Meningitis is most commonly caused by infection (by bacteria, viruses, or fungi), although it can also be caused by bleeding into the meninges, cancer, diseases of the immune system, and an inflammatory response to certain types of chemotherapy or other chemical agents. The most common infectious causes of meningitis vary according to an individuals age, habits, living environment, and health status. The nurse who cares for patients with these disorders must have clear understanding of the pathologic processes and the clinical outcomes. Some of the issues nurses must help patients and families confront include adaptation to the effects of the disease, potential changes in family dynamics, and possibly end of life issue.The clinical manifestations, assessment, and diagnostic finding as well as the medical and nursing management are related to the specific infectious process.

BIBLIOGRAPHY

Baird, Marianne Saunorus. 2005. Manual of Critical Care Nursing, Fifth Edition. St.Louis, Missouri : Elsever Mosby. Page : 644. Brunner and Suddarths Textbook of Medical-Surgical Nursing. Pages: 1821-1833, 1943-1945. Corwin, Elizabeth J. 2008. Handbook of Pathophysiology, Third Edition.Ohio : Lippincott Williams & Wilkins. Pages: 186-242. Goldsmith, Connie.2008. Meningitis. Minneapolis: Lerner Publishing Group,Inc.Pages :8-9. Kneib, Martha.2005. Meningitis, First Edition. New York : The Rosen Publishing Group,Inc. Mader, Sylvia.S. 2004. Understanding Human Anatomy and Physiologi, Fifth Edition. The McGraw-Hill Companies. Pages: 144-158. Shmaefsky, Brian., Hilary Babcock. 2010.Meningitis, Second Edition. New York : Infobase Publishing.

PAPER ENGLISH IN NURSING NEUROLOGIC SYSTEM MENINGITIS

By :
1. 2. 3. 4. 5. 6. 7. 8. 9. Hannik Rahmaningrum Nasischa Ayu Wardhanie Rega Setiananda Haiva Dwi Puspha Nur Indra Gebyar Hafit S. Dyah Khusnul Fadhilah Qamila Anindita Jen Riko Dewantoro Dimas Hadi Prayoga (131211132061) (131211132062) (131211133007) (131211133008) (131211133016) (131211133017) (131211133025) (131211133026) (131211133034)

NURSING FACULTY AIRLANGGA UNIVERSITY SURABAYA 2013

PREFACE

All praise to Allah who has given blessing and guidance, so we can complete this paper about Neurogical System with Meningitis well. We wanna say thank for all of you who have helped and supported in making this paper. We hope this paper can be brought the advantages to all especially for students of the Nursing Faculty, Airlangga University. We realize this paper still further from perfectly , thus we expect the critism and suggestion for improving this paper. Hopefully this paper can be utilized and useful to expand the knowledges readers.

Surabaya, May 2013

Authors