Color Atlas of Neurology
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Intracranial Pressure |
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ICP (mm Hg) |
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70 |
Compliance = V V/ V P |
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60 |
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50 |
Elastance = V P/ V V |
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40 |
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30 |
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VP |
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20 |
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V V |
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10 |
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Pressure-volume curve |
Volume |
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(green, compensation; |
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red, decompensation) |
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Communicating hydrocephalus |
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Sinus |
Venous sinus |
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thrombosis |
Subarach- |
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noid space |
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Brain |
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Obstructive |
Ventricular |
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hydrocephalus |
system |
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Etiology of hydrocephalus (right: normal state) |
Arteries |
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Supratentorial mass |
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Subfalcine herniation |
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Ventricular compression |
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Transtentorial |
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herniation |
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Edema of astrocytes/ |
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endothelial cells |
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Upward |
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Space-occupying lesion (mass) |
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posterior |
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fossa her- |
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niation |
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Trans en- |
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Infraten- |
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dothelial |
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torial mass |
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diffusion |
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Tonsillar |
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herniation |
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Pontomesencephalic |
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compression, |
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Open zonula |
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hemorrhages |
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occludens |
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(tight junction) |
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Astrocyte |
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Pinocytotic transport |
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Cerebral edema (left, vasogenic; right, cytotoxic) |
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Intracranial Pressure
163
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
164
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
3 Neurological Syndromes
!Brain Disorders
!Spinal Disorders
!Peripheral Neuropathies
!Myopathies
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
Stroke
Central Nervous System
A stroke is an acute focal or global impairment of brain function resulting from a pathological process (e. g. thrombus, embolus, vessel rupture) of the blood vessels. Its causes, in order of decreasing frequency, are ischemia (80%), spontaneous intracerebral or intraventricular hemorrhage (15%), and subarachnoid hemorrhage (5%). The signs and symptoms of stroke are usually not specific enough to enable identification of its etiology without further diagnostic studies. CT, MRI, cerebrovascular ultrasonography, ECG, and laboratory testing are usually needed.
Symptoms and Signs
The clinical manifestations of stroke persist, by definition, for more than 24 hours, and are often permanent, though partial recovery is common. The duration of symptoms and signs seems not to be correlated with the etiology of stroke.
Type of Deficit |
Clinical Manifestations |
Ischemia. A transient ischemic attack (TIA) differs from a stroke (by definition) in that its symptoms and signs resolve completely within 24 hours. The vast majority of TIAs resolve within one hour, and only 5% last longer than 12 hours. Patients with crescendo TIAs (a rapid succession of TIAs) have a high risk of developing a (completed) stroke, which can cause neurological deficits that are either minor (minor stroke) or major (disabling stroke, major stroke). A stuttering, fluctuating, or progressive course of stroke development (stroke in evolution) is uncommon.
Hemorrhage. Nontraumatic intracerebral hemorrhages usually cause acute neurological deficits that persist thereafter. If deficits worsen after the initial hemorrhage, the cause is either recurrent hemorrhage or a complication of the initial hemorrhage (cerebral edema, electrolyte imbalance, or heart disorder).
Weakness |
Acute hemi-, mono-, or quadriparesis/quadriplegia (ca. 80–90%); loss of coordination |
(pp. 46 ff, 70) |
and balance; hyperkinesia (during or after stroke), e. g. hemichorea, hemiballism, or |
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(rarely) dystonia |
Sensory loss |
Injury of postcentral cortex or subcortical area distal sensory (often also motor) defi- |
(pp. 70 ff, 106) |
cit in contralateral limbs. Paresthesiae and loss of stereognosis, graphesthesia, |
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topesthesia, and acrognosis are prominent |
Oculomotor and |
Conjugate horizontal eye movements, disjugate gaze, nystagmus, diplopia. Visual field |
visual disturbances |
defects (p. 82), transient monocular blindness (= amaurosis fugax) |
(pp. 70, 82 ff) |
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Headache (p. 182) |
May be caused by subarachnoid hemorrhage, temporal arteritis, venous sinus thrombo- |
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sis, arterial dissection, cerebellar hemorrhage, massive intracerebral hemorrhage (rare) |
Impairment of con- |
TIA and stroke generally do not impair consciousness (exception: brainstem stroke, |
sciousness (pp. 116, |
massive supratentorial stroke with bilateral cortical dysfunction) |
204) |
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Behavioral changes |
Aphasia, confusion (must be distinguished from aphasia), impairment of memory, neg- |
(p. 122 ff) |
lect, impaired affect control (compulsive crying and/or laughing), apraxia. Mental |
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changes, especially depression and anxiety disorders, are common after stroke |
Dysarthria and |
Severe dysarthria is often accompanied by coughing, difficulty chewing, and dysphasia. |
dysphagia (pp. 102, |
Pseudobulbar palsy loss of voluntary motor control (e. g., swallowing, speaking, |
130)tongue movement) with preservation of involuntary movements (e. g., yawning, coughing, laughing)
Dizziness (p. 58) |
Cerebellum, brainstem (vertigo, nausea, nystagmus) |
Epileptic seizures |
Simple partial, complex partial, or generalized tonic-clonic seizures may occur during |
(p. 192 ff) |
or after a stroke |
Respiratory disorders Hiccups (singultus) often occur in stroke, particularly in lateral medullary infarction.
(p. 150) Central hyperventilation is associated with a poor prognosis. Bihemispheric lesions may cause Cheyne–Stokes respiration (p. 118)
166Minor complications of stroke: Mild unilateral arm paresis, moderate sensory loss, mild dysarthria; these patients can care for themselves. Major complications: Aphasia, spastic hemiplegia, and hemianopsia; these patients generally need nursing care.
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
Stroke
Stroke
(right hemiplegia, aphasia, conjugate gaze deviation to left)
Persistent deficit
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Progressive deficit |
TIA |
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Time course |
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Territorial infarct |
Territorial infarct |
Territorial infarct |
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(anterior + middle cerebral a., CT) |
(anterior cerebral a., CT) |
(posterior inferior cerebellar a., CT) |
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Intracerebral hemorrhage |
Subarachnoid hemorrhage (CT) |
Aneurysm |
(brain stem, CT) |
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(internal carotid a., MRI) |
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Causes of stroke |
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Central Nervous System
167
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
Stroke: Ischemia
Stroke Syndromes: Carotid Artery
Territory
! Brachiocephalic Trunk
Brachiocephalic trunk occlusion by emboli from the aortic arch has the same clinical manifestations as internal carotid artery (ICA) occlusion. Patients with adequate collateral flow remain asymptomatic.
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! Common Carotid Artery (CCA) |
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System |
CCA occlusion is very rare and, even when it oc- |
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curs, is usually asymptomatic, because of an ade- |
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quate collateral supply. When symptoms do |
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Nervous |
occur, they are the same as those of ICA occlusion. |
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artery (MCA) more often than the anterior cere- |
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! Internal Carotid Artery (ICA) |
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Territorial infarcts affect the middle cerebral |
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Central |
bral artery (ACA). If the ICA is occluded and col- |
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lateral flow via the circle of Willis is inadequate, |
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extensive infarction occurs in the anterior two- |
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thirds of the hemisphere, including the basal |
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ganglia. Symptoms include partial or total blind- |
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ness in the ipsilateral eye, impairment of con- |
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sciousness (p. 116), contralateral hemiplegia |
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and hemisensory deficit, homonymous hemi- |
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anopsia, conjugate gaze deviation to the side of |
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the lesion, and partial Horner syndrome. ICA in- |
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farcts in the dominant hemisphere produce |
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global aphasia. The occipital lobe can also be af- |
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fected if the posterior cerebral artery (PCA) |
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arises directly from the ICA (so-called fetal |
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origin of the PCA). Border zone infarcts occur in |
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distal vascular territories with inadequate col- |
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lateral flow. They affect the “watershed” areas |
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between the zones of distribution of the major |
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cerebral arteries in the high parietal and frontal |
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regions, as well as subcortical areas at the inter- |
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face of the lenticulostriate and leptomeningeal |
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arterial zones. |
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Ophthalmic artery. Occlusion leads to sudden |
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blindness (“black curtain” phenomenon or cen- |
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tripetal shrinking of the visual field), which is |
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often only temporary (amaurosis fugax = tran- |
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sient monocular blindness). Thorough diagnostic |
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evaluation is needed, as the same clinical syn- |
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drome can be produced by other ophthalmo- |
168logical diseases (Table 22a, p. 372).
Anterior choroidal artery (AChA). Infarction in
the AChA territory, depending on its precise lo-
cation and extent, can produce contralateral motor, sensory, or mixed deficits, hemiataxia, homonymous quadrantanopsia (both upper and lower), memory impairment, aphasia, and hemineglect.
Anterior cerebral artery (ACA). Contralateral hemiparesis is usually more distal than proximal, and more prominent in the lower than in the upper limb (sometimes only in the lower limb). Infarction in the territory of the central branches of the ACA (A1 segment, recurrent artery of Heubner) produces brachiofacial hemiparesis, sometimes accompanied by dystonia. Bilateral ACA infarction (when the arteries of both sides share a common origin) and infarctions of the cortical branches of the ACA produce abulia (p. 120), Broca aphasia (dominant hemisphere), perseveration, grasp reflex, palmomental reflex, paratonic rigidity (gegenhalten), and urinary incontinence. Lesions in the superior and medial frontal gyri or the anterior portion of the cingulate gyrus cause bladder dysfunction. Disconnection syndromes due to lesions of the corpus callosum are characterized by ideomotor apraxia, dysgraphia, and tactile anomia of the left arm.
Middle cerebral artery (MCA). Main trunk (M1) occlusion produces contralateral hemiparesis or hemiplegia with a corresponding hemisensory deficit, homonymous hemianopsia, and global aphasia (dominant side) or contralateral hemineglect with limb apraxia (nondominant side). Occlusion of the posterior main branch produces homonymous hemianopsia or quadrantanopsia as well as Wernicke or global aphasia (dominant side) or apraxia and dyscalculia (nondominant side); central main branch occlusion produces contralateral brachiofacial weakness and sensory loss; anterior branch occlusion on the dominant side additionally produces Broca aphasia. Occlusion of peripheral branches produces monoparesis of the face, hand, or arm. Occlusions of the lenticulostriate arteries, depending on their precise location, produce (purely motor) hemiparesis/hemiplegia, or hemiparesis with ataxia (lacunar infarct, p. 172).
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
Stroke: Ischemia
Visual |
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Anterior |
Lenticulostriate |
Anterior/middle |
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Ophthalmic a. |
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distur- |
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cerebral a. |
arteries (end |
cerebral a. |
(amaurosis fugax) |
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bance |
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zone) |
(border zone) |
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Middle |
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cerebral a. |
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Internal carotid a. |
Middle/posterior cerebral a. |
Anterior choroidal a. |
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(brachiocephalic trunk, |
(border zone) |
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common carotid a.) |
Internal carotid a. |
Internal carotid a. (terminal branches) |
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(terminal branches) |
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Callosomarginal a. |
A. of central sul- |
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Middle |
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Frontopolar a. |
cus (rolandic a.) |
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cerebral a. |
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Pericallosal a. |
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Basal ganglia |
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A. of |
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angular |
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Anterior |
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gyrus |
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cerebral a. |
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Thalamus |
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Anterior |
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cerebral |
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Lenticulo- |
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a. |
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Temporal |
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striate a. |
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Ophthalmic a. |
aa. |
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Posterior |
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Internal |
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Anterior |
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cerebral a. |
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carotid a. |
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choroidal a. |
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Basilar a. |
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Internal carotid a. |
Vertebral a. |
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Internal carotid a. (branches) |
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Leptomeningeal arterial anastomoses |
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Terminal |
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branches |
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Central |
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Terminal branches |
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branches |
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Central |
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branches |
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Anterior cerebral a. |
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Middle cerebral a. |
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Central Nervous System
169
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
Stroke: Ischemia
|
Stroke Syndromes: Vertebrobasilar |
clusion causes impairment of consciousness |
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Territory |
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(ranging from somnolence to coma), mental |
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! Subclavian Artery |
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syndromes (hallucinations, confabulation, psy- |
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choses), quadriparesis, and oculomotor dis- |
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High-grade subclavian stenosis or occlusion |
orders (diplopia, vertical or horizontal gaze |
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proximal to the origin of the vertebral artery |
palsy). Apical BA occlusion (p. 359) is caused by |
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may cause a reversal of blood flow in the verte- |
cardiac or arterial emboli. Pontine infarction |
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bral artery, which worsens with exertion of the |
sparing the posterior portion of the pons (teg- |
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ipsilateral arm (subclavian steal). Rapid arm |
mentum) produces quadriplegia and mutism |
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fatigue and pain often result; less common are |
with preservation of sensory function and verti- |
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vertigo and other brain stem signs. The arterial |
cal eye movements (locked-in syndrome, pp. 120, |
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System |
blood pressure is measurably different in the |
359). |
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two arms. |
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Paramedian infarction in the BA territory usu- |
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! Vertebral Artery (VA) |
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ally affects the pons (pp. 72, 359 ff). |
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Dorsolateral infarction affects the cerebellum, |
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Nervous |
VA occlusion produces variable combinations of |
with a corresponding clinical picture. Occlusion |
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symptoms and signs, including homonymous |
of the labyrinthine artery (a branch of the AICA) |
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hemianopsia, |
dysarthria, |
dysphagia, |
unilateral |
produces rotatory vertigo, nausea, vomiting and |
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or bilateral |
limb paralysis with or |
without |
nystagmus. |
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Central |
sensory deficit, ataxia, drop attacks (due to |
! Posterior Cerebral Artery (PCA) |
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medullary ischemia), and impairment of con- |
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sciousness. Unilateral VA occlusion (e. g., due to |
PCA occlusion is rare and produces symptoms |
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dissection) can lead to infarction in the territory |
and signs similar to those of MCA infarction. |
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of the posterior inferior cerebellar artery. |
Unilateral occlusion of a cortical branch pro- |
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! Cerebellar Arteries |
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duces homonymous hemianopsia with sparing |
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of the macula (supplied by the MCA), while bi- |
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Large cerebellar infarcts can cause brain stem |
lateral occlusion produces cortical blindness |
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compression and hydrocephalus. |
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and, occasionally, Anton syndrome (p. 132). Cen- |
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Posterior inferior cerebellar artery (PICA). Dor- |
tral branch occlusion leads to thalamic infarc- |
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solateral medullary infarction produces (usually |
tion (p. 106; Dejerine–Roussy |
syndrome), re- |
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incomplete) |
Wallenberg |
syndrome |
(p. 361). |
sulting in transient contralateral hemiparesis, |
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Often, only branches to the cerebellum are af- |
spontaneous pain (“thalamic pain”), sensory |
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fected ( vertigo, headache, ataxia, nystagmus, |
deficits, ataxia, |
abasia, |
choreoathetosis, |
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lateropulsion). |
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“thalamic hand” (flexion of the metacar- |
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Anterior inferior cerebral artery (AICA). AICA oc- |
pophalangeal joints with hyperextension of the |
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clusion is rare. It produces ipsilateral hearing |
interphalangeal |
joints), and |
homonymous |
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loss, Horner syndrome, limb ataxia, and disso- |
hemianopsia. If branches to the midbrain are af- |
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ciated facial sensory loss, as well as contralateral |
fected, an ipsilateral CN III palsy results, accom- |
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dissociated sensory loss on the trunk and limbs |
panied by variable contralateral deficits includ- |
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(mainly the upper limbs) and nystagmus. |
ing hemiparesis/hemiplegia, (rubral) tremor, |
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Superior cerebellar artery (SCA). SCA occlusion |
ataxia, and nystagmus. Isolated hemihypesthe- |
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can produce ipsilateral Horner syndrome, limb |
sia is associated with thalamic lacunar infarc- |
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ataxia, dysdiadochokinesia, and CN VI and VII |
tion. |
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palsy, as well as contralateral hypesthesia and |
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hypalgesia. |
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! Basilar Artery (BA)
Basilar artery occlusion. Thrombotic occlusion
170of the BA may be heralded several days in advance by nonspecific symptoms (unsteadiness,
dysarthria, headache, mental changes). BA oc-
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
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Stroke: Ischemia |
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Ophthalmic |
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Medulla (dorsolateral branch) |
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a. |
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Basilar a. |
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External carotid a. |
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Internal |
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Vertebral a. |
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carotid a. |
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Subclavian a. |
Cerebellar hemisphere (medial branch) |
System |
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occlusion |
Posterior inferior cerebellar a. |
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Craniocervical collaterals |
Pericallosal a. |
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Caudate nucleus |
Nervous |
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(Example: subclavian steal) |
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Capsula interna |
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Putamen |
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Posterior cerebral a. |
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Superior cerebellar a. |
Central |
Middle |
Internal |
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V |
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cerebral a. |
capsule |
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VII, VIII |
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Anterior |
Caudate |
Anterior |
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cerebral |
nucleus |
cerebral a. |
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a. |
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Anterior |
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communicating a. |
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Ventricle |
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Posterior |
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Internal carotid a. |
Basilar a. |
inferior cerebellar a. |
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Anterior |
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Hypothalamus |
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inferior cerebellar a. |
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Posterior |
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communicating a. |
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Vertebrobasilar vessels |
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External capsule |
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Thalamus |
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Putamen |
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Vessels of basal ganglia |
Posterior cerebral a. |
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(schematic) |
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Central |
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Paramedian |
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branches |
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pontine |
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infarct |
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Terminal |
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Dorsolateral infarct |
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branches |
171 |
Basilar a. |
MRI (sagittal) |
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Posterior cerebral a. |
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Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.
Central Nervous System
172
Stroke: Pathogenesis of Infarction
! Risk Factors
The risk of stroke increases with age and is higher in men than in women at any age. Major risk factors include arterial hypertension (!140 mmHg systolic, !90 mmHg diastolic), diabetes mellitus, heart disease, cigarette smoking, hyperlipoproteinemia (total cholesterol
!5.0 mmol/l, LDL !3 mmol/l, HDL "0.9–1.2 mmol/l), elevated plasma fibrinogen, and obesity. Symptomatic or asymptomatic carotid artery stenosis, elevated plasma homocysteine levels, erythrocytosis, anti-phospholipid antibodies, alcohol abuse (#60 g of alcohol 75 cl of wine per day in men, #40 g in women). Drug abuse (amphetamines, heroin, cocaine), a sedentary lifestyle, and low socioeconomic status (unemployment, poverty) also increase the risk of stroke.
!Causes
Embolism (ca. 70%) is the most common cause of stroke. Emboli arise from local atheromatous lesions (atheromatous thromboembolism) on the walls of large arteries (macroangiopathy) of the brain or heart (cardiac embolism in atrial fibrillation, valvular heart disease, ventricular thrombus, and myxoma).
Thrombosis (ca. 25%). Occlusion of a small endartery (microangiopathy, small vessel disease) causes lacunar infarction. The cause is hyaline (lipohyalinosis)orproximalsclerosisofpenetrating arteries (lenticulostriate, thalamoperforating or pontine arteries, central branches). Causal factors include hypertension, diabetes, and blood– brain barrier disruption leading to deposition of plasma proteins in the arterial wall. Microan- giopathy-related hemodynamic changes sometimes cause hemodynamic infarction.
Rare causes (ca. 5%) include hematological diseases (e. g., coagulopathy, abnormal blood viscosity, anemia, leukemia) and arterial processes (dissection, vasculitis, migraine, fibromuscular dysplasia, moyamoya, vasospasm, amyloid angiopathy, and CADASIL = cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy).
! Infarct Types
infarcts in the subcortical periventricular region or brain stem. Classic lacunar syndromes include purely motor hemiparesis (internal capsule, corona radiata, pons), contralateral purely sensory deficit (thalamus, internal capsule), ataxic hemiparesis (internal capsule, corona radiata, pons), and dysarthria with clumsiness of one hand (= clumsy hand–dysarthria syndrome; internal capsule, pons). The presence of multiple supratentorial and infratentorial lacunes is termed the lacunar state (“état lacunaire”) and is clinically characterized by pseudobulbar palsy (p. 367), small-step gait (“marche à petit pas”), urinary incontinence, and affective disorders (compulsive crying). For leukoaraiosis, see p. 298.
Territorial infarcts are those limited to the distribution of the ACA, MCA, or PCA. With the exception of striatocapsular infarcts (internal capsule, basal ganglia), these infarcts are predominantly cortical. Embolic territorial infarcts often undergo secondary hemorrhage (“hemorrhagic conversion”).
End zone infarcts. Low-flow infarction in the subcortical white matter is due to extracranial high-grade vessel stenosis and/or inadequate collateral flow.
Border zone infarcts (p. 168) also result from hemodynamic disturbances due to microangiopathy. They are found at the interface (“watershed”) between adjacent vascular territories, and can be either anterior (MCA–ACA contralateral hemiparesis and hemisensory deficit, mainly in the lower limb and sparing the face, with or without aphasia) or posterior (MCA– PCA contralateral hemianopsia and cortical sensory deficit, with or without aphasia).
Global cerebral hypoxia/ischemia. The causes include cardiac arrest with delayed resuscitation, hemorrhagic shock, suffocation, and carbon monoxide poisoning. Global cerebral hypoxia/ischemia causes bilateral necrosis of brain tissue, particularly in the basal ganglia and white matter.
Lacunar infarcts (“small deep infarcts”). Lacunes are small ($1.5 cm in diameter), round or oval
Rohkamm, Color Atlas of Neurology © 2004 Thieme
All rights reserved. Usage subject to terms and conditions of license.