Thieme Mumenthaler, Neurology - part 3 pdf

farction in the basal ganglia, internal capsule, thalamus, brainstem, and (rarely) cerebral cortex. Arterioloscle- rosis isoftendirectlyvisiblebyreti- noscopy. Clinical examination of the heart and its rhythm may suggest the possibil- ity of cardiogenic embolism. A difference in blood pressure between the two arms should arouse suspicion of an aortic aneurysm, Takayasu’s arteritis, or subclavian steal syndrome. The presence of ecchymoses, pete- chiae, and other cutaneous lesions suggests that whatever process is un- derlying them has affected the brain as well. Deep venous thrombosis in an extremity may lead to paradoxical cerebral embolism in the presence of an anatomical right-to-left shunt. If the physical findings yield no evidence of atherosclerosis or cardiac disease, other types of vascular disease should be considered, particularly arterial dissection. Carotid artery dissection should be suspected when there is a Ta ble 2 .45 Initial ancillary studies for the patient with a focal neurologic deficit of acute onset Erythrocyte sedimentation rate Hemoglobin, hematocrit Leukocyte count (with differential count) Platelet count Sodium, potassium Glucose BUN, creatinine Syphilis serology Prothrombin time Urinalysis Serum osmolality ECG Chest radiograph history of cervical, facial, temporal, or orbital pain on one side, accompanied by ipsilateral Horner syndrome and contralateral hemiparesis or hemi- sensory syndrome. Carotid artery dissection may rarely cause ipsilateral cranial nerve deficits and thus mis- leadingly arouse suspicion of a brainstem process. Vertebral artery dissection presents with ipsilateral cervical and occipital pain and, as a ru le, with brainstem symptoms and signs (p. 193). Tenderness of the temporal arteries suggests the diagnosis of giant cell arteritis (temporal arteritis, polymyalgia rheumatica). Diagnostic Evaluation and Use of Ancillary Tests An acute, focal neurologic deficit is usually due to a cerebro vascular event. The differential diagnostic questions discussed above are usually rapidly answered with the ancillary tests listed in Table 2.45 and with a CT or MRI scan of the brain (cf. pp. 132, 133). An EEG is sometimes needed to distinguish TIAs from focal epileptic seizures. In the acute phase, the CT scan (p. 132) may reveal early signs of infarction, such as obscuration of the gray- white matter distinction, blurring the boundaries of the cerebral cortex and of the basal ganglia. The “dense artery sign” (Fig. 2.54), when it is seen, indi- cates thrombosis of an artery (855). The MRI scan (p. 137) may not reveal any sign of acute ischemia unless perfusion and diffusion images are ob- tained (265, 998, 999). Signs of arterial dissection, venous thrombosis, or venous sinusthrombosis should al- ways be looked for; they may be seen on either CT or MRI. If extra- or intracranial arterial disease is considered a diagnostic possi- 186 2DiseasesMainlyAffecting the Brain and its Coverings Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Fig. 2.54 Acute left hemisyndrome. CT scan. The acutethrombusinthe right middle cerebral artery is seen as a hyperdense line (“dense artery sign”). Parenchymal changes cannot yet be seen. bility in the individual case, the next step is cerebrovascular ultrasonogra- phy, or else MR or CT angiography (p. 136). If cardiogenic embolism is suspected on the basis of the clinical history , cardiac examination, and CT or MRI, the workup should include transthoracic or, possibly, transesophageal echocardiography (p. 146). If cardiac dysrhythmia is suspected, long-term ECG monitoring (Holter monitoring) should be performe d. If the cause of a stroke remains unclear, the aortic arch should also be considered as a possible source o f emboli and shouldbestudiedby transesophageal echocardiography (TEE). Further laboratory tests should be carried out, as delineated in Ta- ble 2.46.Ifthesefailtoprovide conclusive evidence for a final diagnosis, alumbarpuncture should be considered, as thismayprovideaclueto Ta ble 2 .46 Further laboratory studies for the patient with a focal neurologic deficit of acute onset Serum electrophoresis Antinuclear antibodies, rheumatoid factor Hemoglobin electrophoresis Anti-phospholipid antibodies Protein C, protein S, antithrombin III, and APC resistance (several weeks after the acute event) some of the rarer causes of stroke (e.g., vasculitis, basal meningitis). Conventional angiography (p. 140) is performed when endovascular ther- apy is to be provided, or for the con- firmation of an abnormal finding ob- tained by noninvasive means (ultra- sonography, MR or CTangiography). It may also be useful as part of the primary evaluation of younger patients with stroke of unclear etiology. Warning Signs and Speed of Progression Some 25–50% of atherothrombotic strokes are preceded by TIAs; for cardioembolic and lacunar strokes, the percentage is lower. Two-thirds of all strokes progress to their full symp- tomatic e xpressionwithinminutes, while one-third continue to progress after the patient arrives in the hospi- tal. Associated Symptoms, Temporal Course, and Complications (7) Headache. Headache rarely accompa- nies ischemic stroke but may be the leading symptom in cases of venous thrombosis, giant cell arteritis, arterial dissection, and intracerebral and subarachnoid hemor rhage. Disturbances of Cerebral Perfusion 187 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Seizures. Convulsions are common in cerebral venous thrombosis and venous sinus thrombosis. Focal seizures are seen in2%ofstrokepatientsover- all, more commonly in acutebrain hemorrhage and embolic stroke than in atherothrombotic stroke. Disturbance of consciousness. Con- sciousness isimpairedbymidbrain and diencephalic stroke, or when a hemispheric lesion (e.g., a large intracerebral hemorrhage, or a massively edematous infarct in the distribution of the middlecerebralartery) pro- duces masseffectleading t o a danger- ous elevation of intracranial pressure (p. 231). Cerebral edema, intracranial hypertension, hydrocephalus. Particularly when a younger patient suffers a very large stroke, the associated cerebral edema may exert sufficient mass effect to elevate the intracranial pressure dangerously, perhaps leading to brain herniation (p. 222). Infratento- rial strokes with mass effect may oc- clude the aqueduct or the pathways of CSF outflow from the fourth ventricle (foramina of Magendie and Luschka), and thereby produce hydrocephalus. Intracranial hypertension is the most common cause of death in the first few days after a stroke. Hemorrhagic transformation, sec- ondary hemorrhage. Ischemic strokes usually contain numerous petechial hemorrhages (302, 435), which rarely produce specific clinical signs, though they may become confluent and yield the radiologic picture of an infarct with hemorrhagic transformation. When an occluded vessel is reopened by endovascular thrombolysis, major hemorrhage may occur, leading to mass effect and clinical deterioration. Cardioembolic infarcts are more frequently hemorrhagic than atherothrombotic infarcts. As one might ex- pect, hemorrhageismorecommon when anticoagulants and fibrinolytic agents are administered. The larger the infarct, the more likely that there will b e an associated hemorrhage. Respiratory disturbances. These are a feature of medullary infarction and may present a critical problem. Cheyne-Stokes respirationsarealso seen in patients with a large hemispheric stroke. Respiratory disturbances such as sleep apnea syndrome are both a risk factor for, and a consequence of, stroke (70c). Dysphagia. Dysphagia intheafter- math of a stroke may lead to aspira- tion pneumonia. Myocardial infarction. One of the causes of stroke is cardiogenic embolism in the setting of acute myocardial infarction. Moreover, 40–60% of stroke patients have either overt or clinically silent ischemic heart disease. Cardiac dysrhythmia. Dysrhythmias are a frequent cause of stroke. They are also, rarely, a consequence of stroke, mostcommonlyafter medullary infarction. ST segment changes on ECG. Such changes are found in the setting of acute stroke affecting the insular cortex. They maymimic the ECG signs of acute myocardial infarction. Deep venous thrombosis. Not only bedridden patients, but also walking patients with a paretic limb or limbs, are at risk for deep venous thrombosis and pulmonary embolism. 188 2DiseasesMainlyAffecting the Brain and its Coverings Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Urinary tract infection. Urinary tract infection occurs frequently in patients with indwelling catheters. Decubitus ulcers. Bedridden patients, particularly those with poor nutri- tional status, are at risk for decubitus ulcers. Contractures, joint stiffness, reflex sympathetic dystrophy. Reduced motion across joints combined with elevated flexor tone in paretic limbs leads to joint stiffness, contractures, and trophic disturbances, such as pe- riarthropathy of the shoulder and reflex sympathetic dystrophy. Prognosis ofCerebral Infarction The prognosis depends on the type and etiology of stroke. In general, younger patients have a better prognosis, while impairment of consciousness in the initial phase of stroke is co rrelated with a poorer outcome. Lacunar infarction carries a low mortality (121). Six months after cerebral infarction (of any kind), ap- proximately 40 % of patients are handicapped, and 25% are dead. The risk of recurrent stroke is 10% in the first year, and 5%inthefollowing years (226). The risk of a cardiovascular event is also elevated (411). The clinical scales most commonly used for longitudinal study are the na- tional Institutes of Health Stroke Scale (NIHSS) and the Modified Rankin Scale (MRS) (see Appendix, p. 940 ff.). Specific Causes of Cerebrovascular Disease Atherosclerosis Frequency. Atherosclerosis is the most common disease affecting the cardiovascular system and the most common cause of death in the indus- trial world. It begins with micro- scopic intimal lesions and the accu- mulation of lipid-laden foam cells (fatty streaks).Later,theintima thick- ens and contains fibrous plaques, con- sisting of cholesterol crystals envel- oped in connective tissue. Fibrous plaques are found first in the aorta, later in the coronary and carotid arteries. Theydevelopfurther into complicated plaques, containing calcification, necrosis, and ulceration, which can cause stenosis, thrombosis, em- Ta ble 2 .47 Risk factors for atherosclerosis Family history of atherosclerosis of early onset (before age 55) Arterial hypertension* Cigarette smoking* Alcohol abuse* Diabetes mellitus* Hyperlipidemia:* Hypertriglyceridemia Low HDL-cholesterol level High LDL-cholesterol level Truncal obesity* Sleep apnea syndrome* Oral contraceptives with high estrogen content* Sedentary lifestyle* Elevated fibrinogen concentration* Elevated homocysteine concentration* Male sex Advanced age * Trea tabl e, modifiable, or preventable factors Disturbances of Cerebral Perfusion 189 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Atherosclerosis: Common Occasional Rare Fig. 2.55 Localization of atherosclerosis in the cerebral arteries. bolism, and vascular occlusion. Pa- tients with atherosclerosis of the arteries of the brain also have symp- tomatic or asymptomatic coronary artery disease in 40–60% of cases, oc- clusive peripheral vascular disease in 20%, and an asymptomatic abdomi- nal aortic aneurysm in 15%. Risk factors. The presenceandsever- ity of the risk factors listed in Ta- ble 2.47 largely determine whether atherosclerosis will develop. Some of these factors are present at birth or constitute independent diseases(e.g., diabetes mellitus, hypothyroidism), while others are related to lifestyle (e.g., smoking, obesity, sedentary habits). Sites of predilection. Atherosclerotic changes are most commonly found at vascular branch points and sites of curvature (Fig. 2.55), such as the ori- gins and bifurcations of the major ex- tracranial vessels (internal carotid artery, vertebral artery), the origin and bifurcation (or trifurcation) of the middle cerebral artery, and the proximal segments of the posterior cerebral artery. Involvement of the carotid siphon or of the vertebral artery at its loop around the atlas (V 3 segment) is usually found only in advanced atherosclerotic disease. Small arteries and arterioles. Small arteries and arterioles are frequently affected by arteriolosclerosis, which is characterized by hyalinization, fibrous hyperplasia, and necrosis of the vascular intima and media. Arterial hypertension is the main risk factor for arteriolosclerosis. Type of infarct. Thrombosis or arterio-arterial embolism due to atherosclerotic or arteriolosclerotic disease may produce either lacunar or territorial infarction, depending on the vessel affected. Risk of stroke. The risk of stroke is positively correlated with the degree of vessel narrowing, as is well known in the case of the internal carotid artery. The risk becomesclinically sig- nificant once a 60–70% stenosis is 190 2DiseasesMainlyAffecting the Brain and its Coverings Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. reached, which corresponds to a residual luminal diameter of approxi- mately 2 mm. Identification of persons at risk. Per- sons at risk for stroke shouldbeiden- tified in young adulthood so that ap- propriate health counseling can be given (cf. Treatment, p. 206). Subclavian steal syndrome. Subcla- vian steal syndrome is usually a man- ifestation of advanced atherosclerosis (412). If the subclavian artery is criti- cally stenotic or occluded proximal to the origin of the vertebral artery, there may be a reversal of flow in the vertebral artery, so that blood is still supplied to the arm. The blood flow- ing in the vertebralarteryisthusde- rived either from the contralateral vertebral artery or from the basilar artery, whence the name “subclavian steal” (187, 303). Subclavian steal is usually an incidental finding. It may manifest itself as a difference in blood pressure and in the intensity of the pulse in the two arms, or as a supra- clavicular bruit. The diagnosis is established by cerebrovascular ultraso- nography. Subclavian steal occasionally causes symptoms such as weakness, pain, or sensory disturbances when the arm is used, as well astransient vertebroba- silar symptoms, such as paroxysmal dizziness, diplopia, visual impairment, or unsteadiness of gait, which arise either spontaneously, or when the arm is used. The degree of collat- eral flow around the circle of Willis largely determines whether symptoms will be present. Causes of the subclavian steal syndrome other than atherosclerosis include arteritis (giant cell arteritis, Ta- kayasu’s disease) and mechanical in- fluences leading todissection and subsequent thrombosis of the subclavian artery (as in basketball players). Atheromatous plaques of the aortic arch and ascending aorta. Such plaques are a possible source of arterio-arterial emboli causing stroke. They are an expression of advanced atherosclerosis, and patients in whom they are found usually have multiple otherpossible etiologies for stroke. Pathological studies and two different ultrasound studies have shown that such plaques are an independent risk factor for stroke, particularly when thicker than 4–5 mm (24, 476). Cardiogenic Embolism Cardiogenic embolism is diagnosed as the cause of stroke when a cardiac disease or dysrhythmia producing emboli is found to be present and other causes of stroke have been ex- cluded (392). Typically, stroke due to cardiogenic embolism appears sud- denly, without further progression of the deficit; the initial neurologic symptoms may be accompanied by palpitations or retrosternal pain and often reflect involvement of only a small corticalarea,e.g.Wernicke’s dysphasia or isolatedhomonymous hemianopsia. Yet even a characteris- tic presentation cannot be taken as conclusive evidence that cardiogenic embolism, rather than atherosclerosis, is the etiology. CT and MRI usually reveal a single, smallterritorial infarct, though multiple infarcts or a single lacune are sometimes seen. Hemorrhagic transformation of the infarct is more common thaninthe case of stroke of atherosclerotic origin. Emboli arising from infectious endocarditis or atrial myxoma may Disturbances of Cerebral Perfusion 191 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. lead to the formation of cerebrovascular aneurysms, which are usually fusiform (643, 819). The diagnosis is generally established by echocardiography and Holter-ECG monitoring, which should be performed in all strokepatientswitha history of cardiac disease or an abnor- mality on clinical examination of the heart, and in all younger patients with stroke of undetermined cause. It has been shown that routine echocardiography and Holter monitoring in older patients with apparently normal cardiac status yield clinically rel- evant data in only 3% of cases, and such testing is therefore not recommended (293). Cardiac diseases associated with the production of emboli are listed in Table 2.48. Arterial Dissection Arterial dissection occurs in patients of both sexes, predominantly in early and mid-adulthood. The pathoana- tomical process involves detachment of the inner (intimal) layer of the vessel wallfromthetunicamedia.Thus, a“falselumen”between the two lay- ers comes into being, which commu- nicates with the true lumen through atearintheintima.Thefalselumen may be a conduitforblood flow alongside the true lumen, if there is a second, distal intimal tear through which the blood can exit; it may form asaccular aneurysm; or it may become thrombosed. Thrombosis, in turn, may lead to vessel stenosis or occlusion over a long segment, distal progression of thrombus, or arterio- arterial thromboembolism and stroke. Of all cases of dissection of the cerebral arteries, 80% affect the carotid artery, 20% the vertebral artery , and 25% more than onevessel (839). Intracranial arterialdissection is rare Ta ble 2 .48 Cardiac conditions predispos- ing to cerebral emboli (after 293) High risk: Atrial fibrillation Mitral stenosis Prosthetic heart valve Acute myocardialinfarction Left ventricular thrombus Atrial myxoma Infectious endocarditis Dilated cardiomyopathy Nonbacterial thrombotic endocarditis Aneurysm of atrial septum Low risk: Mitral valve prolapse Severe calcification of mitral annulus Patent foramen ovale Calcific aortic stenosis Left ventricular wall motion abnor- mality Mural aneurysm Spontaneous contrast on echocardio- gram in adults, but relatively common in children and adolescents (840). Factors including trauma,hypertension, and vasculopathy (such as fibro- muscular dysplasia and Marfan syndrome) predispose to arterial dissection, or are the immediate cause of it. Carotid artery dissection presents with unilateral cervical, temporal, or orbital pain, Horner syndrome, and neurologic deficits relating to the ipsilateral cerebral hemisphere. The patient may complain of pulsatile tinni- tus. The neurologic deficits are highly variable, ranging from an asymptomatic state to hemiplegia due to infarction in the territory of the middle cerebral artery. Lower cranial nerve deficits may appear, on the same side as the dissection—i.e., contralateral to the hemiparesis or other hemispheric signs. The appearance of crossed 192 2DiseasesMainlyAffecting the Brain and its Coverings Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Fig. 2.56 Dissection of the right vertebral artery. T1-weighted spin-echo image with fat suppression technique. The mural hematoma appears as a bright crescent surrounding the residual lumen. findings in the face and on the body may create the misleading impres- sion of a brainstem syndrome. Vertebral artery dissection causes ipsilateral cervical pain and vertebrobasi- lar stroke, most commonly infarction of the dorsolateral medulla (920). The manner of clinical presentation is variable, ranging from isolated pain in the neck or throat toamajorbrain- stem stroke due to basilar artery thrombosis. Arterial dissection can be diagnosed tentatively with ultrasound and de- finitively with MRI (918). Carotid artery dissection is typically seen as a stenosis or occlusion of the vessel near the skull base, in the absence of atheromatous changes of the vessel wall. In vertebral artery dissection, stenosis or occlusion is usually at the level of the loop around the atlas (V 3 segment). Spin-echo MRI may reveal a mural thrombus within the false lumen (Fig. 2.56). Residual flow in the vessel, if present, is seen as a flow void. Cerebral Infarction in Younger Patients The annual incidence of cerebral infarction roughly doubles with each decade: it is ca. 0.4% at age 45or55, 0.8% at age 65, 1.8 % at age 75, and 3.8% at age 85. Some 15% of all strokes affect patients under 65. The percentage of strokes due to atherosclerosis rises dramatically with age. In younger patients, the possible causes of stroke are numerous, as discussed above; the most common are cardiogenic emboli, dissection, and unknown (after a thorough diagnostic evaluation) (113, 332, 707). Practi- cally any of the etiologies listed in Ta- ble 2.44 may b e responsible. Young adults are particularly susceptible to stroke resulting from drug and alcohol abuse (485, 576, 887) or from hy- percoagulable states such as protein C, protein S, or antithrombin III defi- ciency, or resistance to activated protein C. Venous Thrombosis and Venous Sinus Thrombosis Thromboses of the cerebral veins and venous sinuses are somewhat more common in young women than in young men,butarestillrare overall (accounting for ca. 1% of cerebral ischemic events). The morecommonly involved structures are the superior sagittal and transverse sinuses, fol- lowed by the straight sinus, the cav- ernous sinus, and the cortical veins. The clinical manifestations include headache, focal or generalized seizures, papilledema, and sensory and motor deficits (126). Thrombosis may be due to intracranial and systemic infection, or to a noninfectious etiology. All diseasesassociated with thromboembolism are possible Disturbances of Cerebral Perfusion 193 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. Fig. 2.57 Thrombosis of the superior sagittal sinus. MRI of a 21-year- old woman. The cerebral venous sinusesusually appear dark in the spin- echo image (flow void). The sagittal T1-weighted image of thispatient reveals paucity of signal in the straight sinus (ar- rows). The thrombosed superior sagittal sinus (arrowheads), however, is iso- or hyperintense in comparison to the brain parenchyma. causes, in additiontogynecologic- obstetrical conditions in women and Beh ¸cet’s disease in men (26). Imaging studies reveal uni- or bilateral hemorrhagic infarction.Thrombosis is usually visible by contrast-enhanced CT, or by MRI (Figs. 2.57 and 2.58); MRI is the diagnostic method of choice. Binswanger Disease This disease mainly affects elderly hy- pertensives with multiple vascular risk factors; it may also be caused by conditions other than hypertension that cause small vessel disease, such as amyloid angiopathy or CADASIL (162) (see below). Its clinical manifestations include lacunar infarct syndromes, pseudobulbar and extrapyra- midal motor syndromes, apathy, lack of interest, and cognitive deficits that progress in stepwise fashion, with stable intervals in between. The neu- roradiologic and pathological findings include multiple lacunar infarcts in the basal ganglia, thalamus, pons, and white matter, aswellasbrainat- rophy (cf. Fig. 2.45). Amyloid A ngiopathy Cerebral amyloid angiopathy is a disease of old age (982).Rarefamilial forms (Icelandic and Dutch types) affect younger individuals. Pathology Amyloid deposits are found in small and middle-sized cerebral arteries, in the absence of systemic amyloidosis. Alzheimer-type lesions, including neuritic plaques and neurofibrillary tangles, are also seen (987). Clinical Manifestations Amyloid angiopathymanifestsitself either as progressive dementia or as recurrent lobar hemorrhage, producing acute, focal ne urologic deficits and ultimately l eading to multi- infarct dementia. 194 2DiseasesMainlyAffecting the Brain and its Coverings Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. a b Fig. 2.58a, b Thrombosis of the transverse sinus. A 59-year-old woman with un- usual right-sided headache and earache and a left hom- onymous visual field defect. a The T1-weighted spin- echo image shows the thrombus in the right transverse sinus as a bright structure. A small hemorrhage in the occipital lobe is also seen. b In the angiogram, only the left transverse sinus is seen. Disturbances of Cerebral Perfusion 195 Mumenthaler, Neurology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license. [...]... recanalization c Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license Disturbances of Cerebral Perfusion Fig 2.60a–f Middle cerebral artery occlusion Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license 205 206 2 Diseases Mainly Affecting the Brain and its Coverings | Stroke Prevention (61, 2 93, 35 2a, 637 )... prompt suspicion of an intracerebral hemorrhage (31 2, 635 ) > Drug abuse: The use of various illegal drugs may be complicated by intracerebral hemorrhage, particularly “crack” cocaine and amphetamines Hemorrhage is presumably due to a sudden elevation of blood pressure, or to drug-induced vasculitis Persons who abuse heroin in- Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms... types of systemic vasculitis affecting the CNS (pp 32 4 ff.) Necrotizing arteritis: > Isolated CNS vasculitis (p 32 6) > Giant-cell arteritis: – Cranial arteritis – Polymyalgia rheumatica – Takayasu’s arteritis > Periarteritis nodosa (p 32 4) > Wegener’s granulomatosis (p 32 6) > Lymphomatoid granulomatosis > Sarcoidosis (p 32 9) Autoimmune arteritis (p 32 7): > Systemic lupus erythematosus > Sjögren’s syndrome... if at all, then only by post hoc analysis (179c, 37 3, 37 3b) It is therefore not recommended for use in hours 4, 5, and 6 Selective intra-arterial thrombolysis: Selective intra-arterial thrombolysis may be performed at any time up to 6 hours from the onset of symptoms, in a center with an interventional neuroradiology team It has been shown that intra-arterial application of urokinase can reopen occluded... arteries The lesion is Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions of license 212 2 Diseases Mainly Affecting the Brain and its Coverings a b c d Fig 2.62a–d Arteriovenous malformation (unruptured) a Coronal, T2-weighted spin-echo image b Parasagittal, proton-density image of The feeding and draining vessels, and the same lesion part of the nidus, appear... possibly with signs of transtentorial herniation Table 2.53b 217 WFNS grading scale for subarachnoid hemorrhage (860b) WFNS grade Glasgow Coma Scale Focal neurologic deficit I 15 Absent II 13 14 Absent III 13 14 Present IV 7–12 Present or absent V 3 6 Present or absent WFNS: World Federation of Neurological Societies Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject to terms and conditions... (Table 2.52) ( 630 ) A low serum cholesterol level confers a mildly elevated risk of intracerebral hemorrhage, though it lowers the risk of ischemic stroke, as discussed above Clinical Manifestations Spontaneous intracerebral hemorrhage occurs more commonly in waking hours than during sleep (30 7) The typical presentation is the sudden appearance and rapid progres- Mumenthaler, Neurology © 2004 Thieme All... stroke First 3 hours after onset of symptoms: > Intravenous or intra-arterial thrombolysis > Aspirin, if thrombolysis is contraindicated First 6 hours after onset of symptoms: > Intra-arterial thrombolysis > Aspirin, if thrombolysis is contraindicated More than 6 hours after onset of symptoms: > Aspirin > Heparin: only in special circumstances (see Table 2.51) Mumenthaler, Neurology © 2004 Thieme All... medically and economically justified (166a, 38 3a) In patients who cannot tolerate aspirin or have no therapeutic response to it, clopidogrel is the best alternative The combination of aspirin with clopidogrel is more effective than either alone for cardiac patients, but has not been adequately tested in patients with cerebrovascular disease Mumenthaler, Neurology © 2004 Thieme All rights reserved Usage subject... dysfunction (The optimal dose is that corresponding to an INR of 2 3 for patients with nonvalvular atrial fibrillation, and 3 4 for patients with valvular atrial fibrillation.) All other patients may be treated with aspirin, and patients under 60 years of age with isolated atrial fibrillation can be treated by clinical follow-up alone (259, 39 0, 39 2a) Vasculitis is treated with immunosuppressive agents such . intra-arterial thrombolysis of the middle cerebral artery. a The T2-weighted spin-echo image appears normal and fails to reveal the ischemic area. b The diffusion-weighted image clearly reveals. Thrombosis of the transverse sinus. A 59-year-old woman with un- usual right-sided headache and earache and a left hom- onymous visual field defect. a The T1-weighted spin- echo image shows the thrombus. and unknown (after a thorough diagnostic evaluation) (1 13, 33 2, 707). Practi- cally any of the etiologies listed in Ta- ble 2.44 may b e responsible. Young adults are particularly susceptible to stroke