Cerebrovascular Diseases
Transient Ischemic Attack
I. Epidemiology
Risk of stroke after transient ischemic attack (TIA)
4% to 8% in first month
12% in first year
24% to 29% in first 5 years
TIAs occur before:
25% to 50% of atherothrombotic infarcts
10% to 30% of cardioembolic infarcts
10% to 15% of lacunar infarcts
II. Clinical Features
Abrupt onset
Typically lasts 5 to 20 minutes (less than 24 hours by definition)
TIAs lasting longer than 1 hour are often associated with small areas of infarction.
Stroke
I. Epidemiology
More than 600,000 strokes occur per year.
Third leading cause of death in the United States
25% occur in people under age 65 years.
Modifiable risk factors (RR = relative risk of stroke)
Hypertension: RR is 1.9 in men and 1.7 in women with a 10 mmHg increase in blood pressure
Diabetes: RR is 1.5 to 3.0, depending on severity of the diabetes
Dyslipidemia: RR directly related to cholesterol and low-density lipoprotein
Atrial fibrillation: 5 × increased risk of stroke
Coronary artery disease: 2 × increased risk of stroke
Congestive heart failure: 4 × increased risk of stroke
Tobacco: RR is 1.7 but improves with smoking cessation
Nonmodifiable risk factors
Age: increasing risk with increasing age
Gender: increased risk in men
Race: increased risk in Blacks
II. Cerebral Blood Flow (CBF)
50 mL/100 g/min is normal
20 mL/100 g/min results in a change in electrophysiological activity
10 mL/100 g/min results in irreversible ischemia
Increasing CBF increases collateral blood flow.
Oxygen delivery equals the cerebral blood flow multiplied by the blood oxygen content.
Do2 = CBF × Cao2
III. Stroke Subtypes
Atherothromboembolic
Clinical criteria
Sudden, gradual, stepwise, or fluctuating
Absence of a cardioembolic source
Prior TIA in the same vascular distribution
Concurrent coronary or peripheral artery disease
Imaging
Computed tomography (CT): Bland or hemorrhagic infarct
Possible hyperdense artery
Magnetic resonance imaging (MRI): Bland or hemorrhagic infarct
Possible absent flow void
Acute infarction results in hyperintensity on diffusion-weighted images and hypointensity on the apparent diffusion coefficient (ADC) map.
Carotid ultrasound: stenosis >50% or ulcer >2 mm
Arteriography: stenosis >50% or ulcer >2 mm
Transcranial doppler (TCD): normal, collateralization, or absent flow
Cardioembolic
Clinical criteria
Sudden onset but may be stepwise/progressive
High risk—atrial fibrillation, prosthetic valve, left venticular thrombus, left atrial thrombus, dilated cardial myopathy, sick sinus syndrome, myocardial infarction (MI) in prior 4 weeks
Moderate risk—congestive heart failure, atrial flutter, mitral valve prolapse, atrial septal defect, patent foramen ovale, bioprosthetic valve, ventricular hypokinesis, MI between 4 and 6 weeks
Recent TIA/stroke in other vascular territories
Evidence of systemic embolization
Imaging
CT: Bland or hemorrhagic infarct
Possible hyperdense artery
May have infarctions in multiple vascular distributions.
MRI: Bland or hemorrhagic infarct
Possible absent flow void
May have infarctions in multiple vascular distributions.
Carotid ultrasound: various; stenosis typically <50%
Arteriography: may show occlusion of a vessel
Transesophageal echocardiography: may show thrombotic cause
TCD: normal, absent flow or distal occlusion
Lacunar
Clinical criteria
Abrupt or gradual onset
History of hypertension or diabetes mellitus
No cortical findings
Compatible with a lacunar syndrome
No evidence of embolic sources
Imaging
CT: infarct <1.5 cm
MRI: infarct <1.5 cm
TCD: normal or unrevealing
Note: Description of a stroke by cause and vascular distribution provides the most meaningful information about the stroke. The dichotomy between cortical and subcortical is not always so clear. These terms are frequently used, however.
Cortical—Stroke involves the cerebral hemispheric grey matter and often involves the underlying white matter. Cortical deficits depend on the vessel involved.
Middle cerebral artery—Contralateral hemiparesis and sensory loss (greater in the upper extremity and face), homonymous hemianopia, aphasia/aprosodia, gaze abnormalities, extinction, astereognosis, apraxia
Anterior cerebral artery—Contralateral hemiparesis and sensory loss (greater in the lower extremity), disconnection syndromes, behavioral disturbances (abulia, akinetic mutism)
Posterior cerebral artery—Contralateral homonymous hemianopia with macular sparing, preserved optokinetic nystagmus, cortical blindness, disconnection syndrome
Subcortical—Stroke involves the white matter as well as basal ganglia and brainstem nuclei. Cortical signs such as aphasia are typically absent.
Lacunar Syndromes
Pure sensory
Ventral posterior thalamus
Contralateral sensory loss
Pure motor
Posterior limb internal capsule, cerebral peduncle, pons, or hemispheric white matter
Contralateral weakness
Ataxic hemiparesis
Basis pontis but localizes poorly
Contralateral weakness and ataxia
Dysarthria, clumsy hand syndrome
Genu of the internal capsule
Contralateral clumsy hand and dysarthria
Thalamic dementia
Thalamus
Subcortical dementia
Sensorimotor
Thalamus and internal capsule
Contralateral sensory loss and weakness
Hemiballismus
Subthalamic nucleus
Contralateral hemiballismus
Status lacunaris
Multiple widespread lacunes
Parkinsonism, dementia
Claude syndrome
Midbrain tegmentum, red nucleus, cranial nerve (CN) III
Ipsilateral CN III palsy
Contralateral ataxia, tremor
Benedikt syndrome
Midbrain tegmentum, red nucleus, CN III, cerebral peduncle
Ipsilateral CN III palsy
Contralateral ataxia, tremor, and weakness
Weber syndrome
Ventral midbrain, CN III, cerebral peduncle
Ipsilateral CN III palsy
Contralateral weakness
Parinaud syndrome
Dorsorostral midbrain and posterior commisure
Paralysis of upgaze, convergence-retraction nystagmus, lid retraction, and light near dissociation
Nothnagel syndrome
Dorsal midbrain, brachium conjunctivum, CN III, medial longitudinal fasciculus
Ipsilateral ataxia, CN III palsy, and vertical gaze palsy
Raymond-Cestan syndrome
Mid pons, middle cerebellar peduncle, corticospinal tract
Ipsilateral ataxia
Contralateral weakness
One-and-a-half syndrome
Paramedian pontine reticular formation or CN VI and medial longitudinal fasciculus
Ipsilateral horizontal gaze palsy
Contralateral intranuclear ophthalmoplegia
Foville syndrome
Paramedian pontine reticular formation, CN VI and VII, corticospinal tract
Ipsilateral horizontal gaze palsy, CN VII palsy
Contralateral weakness, sensory loss, intranuclear ophthalmoplegia
Millard-Gubler syndrome
Ventral pons, CN VI and VII fascicles, and corticospinal tracts
Ipsilateral CN VI and VII palsy
Contralateral weakness
Raymond syndrome
Ventral pons, CN VI fascicles, and corticospinal tract
Ipsilateral CN VI palsy
Contralateral weakness
Babinski-Nageotte syndrome
Dorsolateral pontomedullary junction
Ipsilateral ataxia, facial sensory loss, Horner syndrome
Contralateral weakness, sensory loss in the body vertigo, vomiting, and nystagmus
Wallenberg syndrome
Dorsolateral medulla, restiform body, CN V, IX, and X
Ipsilateral ataxia, Horner syndrome, facial sensory loss
Contralateral loss of pain and temperature
Cestan-Chenais syndrome
Lateral medulla
Ipsilateral ataxia, Horner syndrome, facial sensory loss
Contralateral hemibody sensory loss and weakness
Avellis syndrome
Lateral medulla, CN IX and X, lateral spinothalamic tracts
Ipsilateral paralysis soft palate, vocal cords, posterior pharynx
Contralateral hemiparesis and sensory loss
Vernet syndrome
Lateral medulla, CN IX, X, and XI
Ipsilateral paralysis palate, sternocleidomastoid, decreased taste posterior tongue
Contralateral hemiparesis
Jackson syndrome
Lateral medulla, CN IX, X, XI, and XII
Ipsilateral paralysis palate, vocal cords, sternocleidomastoid, tongue
Contralateral weakness and sensory loss
Preolivary
Anterior medulla, CN XII, pyramid
Ipsilateral tongue weakness
Contralateral hemiparesis
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