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pg=headct

A CT cross-section through a patient's brain shows an intraparenchymal hemorrhage (arrow), meaning blood within the substance of the brain. Also shown is a subarachnoid hemorrhage (arrowhead), or blood surrounding the surface of the brain; and edema (asterisk), or swelling of the brain.

Bleeding within the brain (a hemorrhagic stroke, arrows). The blood is white, and there is slightly darker than normal areas surrounding this, due to local brain swelling (edema). G = normal brain gray matter W = normal brain white matter (darker on CT scans than gray matter) Arrows = blood

http://www.medscape.com/viewarticle/452843_2

Neuroimaging of Stroke: A Review: Computed Tomography

Andrew R. Xavier, MD, Adnan I. Qureshi, MD, Jawad F. Kirmani, MD, Abutaher M. Yahia, MD, and Rohit Bakshi, MD, Departments of Neurology and Neurosurgery, University at Buffalo, State University of New York, and the Department of Imaging Services, Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, Kaleida Health, Buffalo, NY

Computed Tomography

Computed tomographic (CT) images of the brain are produced by scanning a collimated beam of x-rays through the brain in thin, sequential slices. The x-ray output is counted, analyzed, and reconstructed for clinical interpretation. The newer generation scans use spiral technology, where the imaging is performed in a continuous helical fashion instead of the conventional slice-by-slice method. CT scanning is still the preferred method for imaging hyperacute stroke. It is widely available, can be performed on patients who have a pacemaker or are on a ventilator, and can be performed quickly on confused, delirious patients. In addition, interpretation in the hyperacute stroke setting is fairly straightforward without the need for special training.
Hyperacute Infarct

In cases of hyperacute stroke (0-6 h), CT is usually not sensitive in the identification of cerebral infarction.[1] But, it is quite sensitive in identifying various forms of acute intracranial hemorrhage and other gross lesions that would preclude the use of thrombolytic therapy (Fig. 1).[2] In the first 24 hours, CT signs of infarction are sulcal effacement with loss of gray-white differentiation in superficial cortical infarction[3] and hypodensity of the basal ganglia[4, 5] in cases of deep cerebral infarction (Fig. 2). The presence of these early changes spread over a large area (>1/3 of the parent arterial territory) is often associated with large infarctions and a relative contraindication to the use of thrombolytic therapy in a patient who would otherwise qualify for that therapy.[6-9] At a minimum, the presence of extensive CT abnormalities in a patient presenting in the first 3 hours for possible thrombolysis should necessitate a careful review of the time of stroke onset. A hyperdense large vessel, described in cases of middle cerebral artery (MCA) stroke[10] is often suggestive of a persistent large vessel occlusion with poor prognosis ("hyperdense MCA" or "dense MCA" sign) (Fig. 3).[11] The presence of this sign is not a contraindication for intravenous thrombolysis,[6] but is an indicator that a large clot burden may be present, and supplemental recanalization strategies might have to be considered. Recent advances in CT technology provide additional data that are helpful in the management of stroke patients. Two such promising techniques are CT angiography and perfusion CT. CT angiography (CTA) is a 3-dimensional reconstruction of the cerebral vasculature from source images showing contrast material in the cerebral vessels shortly after an intravenous contrast bolus. It is a fairly sensitive technique in identifying large vessel occlusions.[12-16] It can be also used to track patients with large vessel occlusions, who have undergone recanalization procedures. A normal CTA can potentially be used to exclude patients from further aggressive recanalization procedures. The contrast saturation in a slice of brain following a rapid intravenous injection of high volume contrast is used to

construct perfusion CT images. The perfusion deficit gives a rough estimate of the extent of microvasculature hypoperfusion and hypometabolism and includes the cerebral infarction and the surrounding ischemic penumbra.[17-20]

Figure 1. A noncontrast CT scan (left, middle) and fast FLAIR MRI (right) was obtained 3 hours after the onset of a patient's severe headache. The CT shows hyperdensities (arrows) in the basal cisterns and left sylvian and frontal cortical sulci, consistent with acute subarachnoid hemorrhage. FLAIR-MRI shows bilateral hyperintense frontal and parietal sulci (arrow), consistent with acute subarachnoid hemorrhage. The MRI abnormalities are more conspicuous and more widespread than shown by CT.

Figure 2. An 89-year-old woman presented with slurred speech and confusion 12 hours before the performance of the initial noncontrast CT scan (left). Note the subtle asymmetry of findings. There is

early hypodensity of the left posterior putamen (arrowhead) and peri-insular cortex (arrow) as compared with the contralateral side. Twenty-four hours after the initial scan, repeat CT (right) shows clear hypodensity involving the entire main stem middle cerebral artery territory with mild associated mass effect. The findings are diagnostic of an acute middle cerebral artery stroke.

Figure 3. Noncontrast CT scan is shown of a patient who presented 8 hours after onset of left-sided weakness and aphasia. Note the tubular hyperdensity (arrow) suggestive of acute clot in the left middle cerebral artery. This is accompanied by hypodensity of the ipsilateral temporal lobe in the middle cerebral artery territory (arrowhead). Compare these abnormalities to the contralateral (right) side of the brain. Taken together, these findings are highly suggestive of acute stroke. Acute Infarct

In the acute period (6-24 h), the changes of ischemia become more apparent on the noncontrast CT scan. The loss of gray-white interface, sulcal effacement, hypodensity of basal ganglia, and hypodensity of the insular cortex become prominent (Fig. 3). The vascular distribution of the infarct becomes increasingly clear during this stage. In severe cases, edema and mass effect can appear at this stage.
Subacute and Chronic Infarct

During the subacute period (1-7 d), there is increasing edema and mass effect with lateral and vertical shift of infarcted tissue in cases of infarction involving large vessel territories. Edema and mass effect peak at 1 to 2 days and then decline. The edema surrounding the infarcts caused by occlusions of the deep, perforating branches are much more modest, with little, if any, associated mass effect. The first 1 to 2 days are also when hemorrhagic transformation peaks; this is noted in about 5 to 40% of all ischemic strokes.[21-25] When hemorrhagic transformation occurs, it is usually in the form of petechial hemorrhages and is clinically not significant but, in a minority, particularly in those who received thrombolytic or

anticoagulant medication, it could take the form of a frank parenchymal hematoma with clinical deterioration (Fig. 4).[8, 22, 24] Contrast scans performed during this period have a characteristic "gyral enhancement" pattern.[26] Chronic infarctions are characterized by marked hypodensity and lack of mass effect on CT scans; the density is similar to cerebrospinal fluid (CSF) (Fig. 5).

Figure 4. Two patients with subacute hemorrhagic stroke. Patient 1 received intra-arterial urokinase treatment for a hyperacute stroke associated with internal carotid artery occlusion. After urokinase treatment, the patient developed increased function of the left side. Two days later, noncontrast CT was performed and is shown. Note the hematoma, seen as a round hyperdensity, in the right subcortical region (arrowhead). There is a completed subacute middle cerebral artery infarction. Patient 2 (right) obtained noncontrast CT scan 36 hours after stroke onset. Note the subtle linear and patchy hyperdensities (arrow) in the anterior and medial aspects of the operculofrontal infarction. The hyperdensities are consistent with petechial hemorrhagic transformation of infarction.

Figure 5. CT scans were obtained for two patients with chronic infarctions. Note the marked hypodensity of each lesion with similar density similar to cerebrospinal fluid and how each conforms to a known vascular distribution - central sulcal middle cerebral artery stroke and posterior cerebral artery occipital stroke. Intracranial Hemorrhage

Imaging of intracranial hemorrhage is fairly straightforward with CT,[27] where image contrast is determined by tissue density. Acute blood clots have a high density and appear hyperdense,[28] often strikingly so, when compared with the surrounding brain tissue. (Figure 1, Figure 4, Figure 6) Acute subarachnoid hemorrhage (SAH) appears as a high density in the subarachnoid spaces (Fig. 1).[29, 30] The severity of SAH on CT is usually graded using the system described by Fisher,[31] and the CT findings are important predictors of clinical outcome.[32, 33] The CT findings of SAH may be subtle (Fig. 1), particularly in the subacute stage.[34, 35] Findings may only include a mild hydrocephalus, diffuse sulcal effacement, and subtle hyperdensities in the CSF spaces. Acute and subacute intraparenchymal hemorrhage is comparatively much easier to identify on CT as it has excellent contrast as compared with the surrounding brain tissue (Figure 4, Figure 6). The location of the hemorrhage often gives a clue to the underlying pathophysiology. [36] Hemorrhages due to chronic hypertension are commonly situated in the putamen,[37] thalamus, pons, cerebellum,[38] caudate,[39] and the subcortical white matter/gray-white junction.[40] It is controversial whether Charcot-Bouchard aneurysms are the primary underlying pathology in these cases. The location, size, and intraventricular extension correlate well with clinical severity and can predict clinical outcome.[32, 41] In cases of amyloid angiopathy, the hemorrhages are usually large, superficial, lobar, and prone to recur (Fig. 6).[42-44] In the setting of anticoagulation, thrombolysis, or systemic coagulopathy, hemorrhages are often multiple, large, and associated with fluid-fluid levels due to impaired clotting ability.[35, 45, 46] Another common cause of nontraumatic intracranial hemorrhage is hemorrhagic transformation of cerebral infarction (described above) (Fig. 4). In patients who received intra-arterial thrombolysis treatment, extravasations

(focal intraparenchymal extravasations) of the angiographic dye commonly occur during the procedure and may be confused with hemorrhagic transformation.[47, 48]

Figure 6. Patient 1 is a 97-year-old woman who presented with acute onset coma. The noncontrast CT scan (left) shows a large acute intraparenchymal frontal lobar hemorrhage with severe mass effect. Patient 2 is a 75-year-old man who presented with lethargy. The noncontrast CT scan (right) shows an acute intraparenchymal occipital lobar hemorrhage (arrowhead) with mild to moderate mass effect. Autopsy of both patients showed widespread cerebral amyloid angiopathy.
http://emedicine.medscape.com/article/1916662-overview

Hemorrhagic Stroke in Emergency Medicine

Author: David S Liebeskind, MD; Chief Editor: Rick Kulkarni, MD

Background
The terms intracerebral hemorrhage (ICH) and hemorrhagic stroke are used interchangeably in this discussion and are regarded as separate entities from hemorrhagic transformation of ischemic stroke. Intracerebral hemorrhage accounts for 10-15% of all strokes and is associated with higher mortality rates than cerebral infarctions.[1] Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke. Previous literature indicates that only 8-18% of strokes were hemorrhagic. (See Etiology.)

Although a 2010 retrospective review from a stroke center found that 40.9% of 757 strokes were hemorrhagic,[2] nonetheless, the authors stated that the increased percentage of hemorrhagic stroke may be due to improvement of computed tomography (CT) scanning availability and implementation, unmasking a previous underestimation of the actual percentage (see Workup), or it may be due to an increase in therapeutic use of antiplatelet agents and warfarin causing an increase in the incidence of hemorrhage (see Treatment and Management).[2] Patients with hemorrhagic stroke present with similar focal neurologic deficits but tend to be more ill than patients with ischemic stroke. Patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension; however, none of these findings reliably distinguishes between hemorrhagic stroke and ischemic stroke. (See Clinical Presentation.) An intracerebral hemorrhage is shown in the CT scan below.

Axial noncontrast computed tomography scan of the brain in a 60-yearold male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of the hemorrhage.

Anatomy
Knowledge of cerebrovascular arterial anatomy and the territories supplied by each is useful in determining which vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate another diagnosis, such as venous infarction. The cerebral hemispheres are supplied by 3 paired major arteries, the anterior, middle, and posterior cerebral arteries. The anterior and middle cerebral arteries comprise the anterior circulation and arise from the supraclinoid internal carotid arteries. The posterior cerebral arteries arise from the basilar artery and form the posterior circulation, which also supplies the thalami, brainstem, and cerebellum. The angiograms in the images below demonstrate some of the circulation involved in hemorrhagic strokes.

Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).

Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the Sylvian

point. Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries. The image below shows the supratentorial vascular territories of the major cerebral arteries.

The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes, insula, and basal ganglia. The anterior cerebral artery (blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.

Approach Considerations
Brain imaging is a crucial step in a patient's evaluation and must be obtained on an emergent basis. Brain imaging aids in making the diagnosis of hemorrhage, and it may identify complications such as intraventricular hemorrhage, brain edema, or hydrocephalus. Either NCCT scanning or magnetic resonance imaging (MRI) of the brain is the modality of choice. Imaging has greatly evolved in the past 2 decades, and advanced CT and magnetic resonance neuroimaging techniques have been developed for improved physiologic imaging of acute stroke. These techniques allow clinicians to assess for the core infarct size and to characterize cerebral blood volume and cerebral blood flow to identify potentially salvageable tissue at risk for infarction (ie, ischemic penumbra). Some examples of these techniques include diffusion-weighted MRI (DWI) and perfusion imaging of acute stroke with magnetic resonance and CT scanning. CT scanning and magnetic resonance angiography (MRA) can give useful information regarding large-vessel occlusion, which is an important consideration, as intraarterial interventions for acute ischemic stroke are available. Although the sensitivity of CT scanning and MRI for large-vessel occlusion is conceivably similar, CT angiography (CTA) may be more practical for several reasons. For example, its more rapid image acquisition makes CTA less susceptible to motion artifacts, more accurate at depicting vascular anatomy, and more sensitive for stenosis, occlusion, vascular malformations, and aneurysms. Imaging with CT studies has multiple logistic advantages for patients with acute stroke; it is able to more rapidly acquire images than magnetic resonance studies, allowing for assessment with an examination that includes NCCT, CTA, and CT perfusion in less than 10 minutes. Expedient acquisition is of the utmost importance in acute stroke imaging because of the narrow window of time available for definitive ischemic stroke treatment with pharmacologic agents and mechanical devices. CT studies can also be performed in patients who are unable to tolerate a magnetic resonance examination or who have contraindications to MRI, including pacemakers, aneurysm clips, or other ferromagnetic materials in their bodies. Additionally, CT examination is more easily accessible for patients who require special equipment for maintaining and monitoring life support. Ultrasonography has multiple uses in the workup of stroke patients. This examination is usually performed on a nonemergent basis to evaluate cerebrovascular ischemic disease preoperatively or in the acute setting after evaluation with CT scanning or MRI. Transthoracic and transesophageal echocardiography (TTE and TEE, respectively) may also be used in assessing for cardioembolic disease and patent foramen ovale or, more acutely, to exclude thoracic aortic dissection. Conventional angiography is the gold standard in evaluating for cerebrovascular disease, as well as for disease involving the aortic arch and great vessels in the neck, and for providing less invasive endovascular interventions. This modality can be performed to clarify equivocal findings or to confirm and treat disease seen on MRA, CTA, transcranial Doppler, or neck ultrasonograms. Angiography is also useful in preoperative evaluation for hemodynamically significant or flow limiting lesions and to confirm the presence of trickle flow versus occlusion seen on

ultrasonography when considering carotid endarterectomy. Angiography is also more sensitive than MRA for detecting ulceration and is superior to both MRA and CTA for detecting vasculitis. Angiography allows for endovascular treatment with intraarterial thrombolytic therapy or mechanical thrombectomy in acute stroke and for stenting of patients with arterial stenosis intracranially or in the neck. It can also be used to characterize and treat aneurysms and vascular malformations using stents and embolic agents, such as coils or other embolic material.
Hypertension

The most common etiology of primary hemorrhagic stroke (intracerebral hemorrhage) is hypertension, with at least two thirds of patients with primary intraparenchymal hemorrhage reported to have preexisting or newly diagnosed hypertension. Hypertensive small-vessel disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymal hemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons.

Axial noncontrast computed tomography scan of the brain in a 60-yearold male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral

ventricle with intraventricular extension of the hemorrhage. Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance image (middle image) redemonstrates the hemorrhage with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.

Aneurysms and subarachnoid hemorrhage

The most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of an intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most frequently encountered intracranial type being the berry aneurysm or saccular aneurysms. Aneurysms may less commonly be related to altered hemodynamics associated with

arteriovenous malformations, collagen vascular disease, polycystic kidney disease, septic emboli, and neoplasms. Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen and is thought to arise from capillary or venous rupture. It has a less severe clinical course and, in general, better prognosis. Berry aneurysms are most commonly isolated lesions that form due to a combination of hemodynamic stresses and acquired or congenital weakness in the vessel wall. Saccular aneurysms typically occur at vascular bifurcations, with more than 90% occurring in the anterior circulation. These include the junction of the anterior communication arteries and anterior cerebral arteriesmost commonly, the MCA bifurcationthe supraclinoid internal carotid artery at the origin of the posterior communicating artery, and the bifurcation of the internal carotid artery (ICA). The pathologic effects of subarachnoid hemorrhage (SAH) on the brain are multifocal. SAH results in elevated intracranial pressure and impairs cerebral autoregulation. This, in combination with acute vasoconstriction, microvascular platelet aggregation, and loss of microvascular perfusion are also seen, resulting in profound reduction in blood flow and cerebral ischemia.[9] See the images below.

Noncontrast computed tomography (CT) scanning was performed emergently in a 71-year-old male who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT scan (le image) ft demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. There is diffuse loss of gray-white differentiation. The fluid-attenuated inversion-recovery (FLAIR) image (right) demonstrates high signal throughout the cortical sulci, basilar cisterns and in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage, owing to the suppression of high cerebrospinal fluid signal lending to greater conspicuity of subarachnoid hemorrhage compared with conventional magnetic resonance image

sequences. The patient above subsequently underwent a computed tomographic angiography examination and subsequent cerebral angiography. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery injection.

Balloon-assisted coil embolization was performed. Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.

Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing petechial hemorrhage or more frank intraparenchymal hematoma.[6, 7, 10] To see complete information on Reperfusion Injury in Stroke, please go to the main article by clicking here. Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days post ictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.[6, 8, 11] Hemorrhagic transformation is also more likely following administration of tissue plasminogen activator (tPA) and with noncontrast CT scans demonstrating areas of hypodensity.[12, 13, 10] See the image below.

Noncontrast computed tomography scan (left) obtained after a 75year-old male was admitted for cerebrovascular accident demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right) with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.

Vascular malformations and amyloid angiography

The remaining cases of spontaneous intraparenchymal hemorrhage may be secondary to vascular malformations (eg, arteriovenous malformations and cavernous malformations) or amyloid angiopathy