Cerebrovascular Diseases



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








Bulbar vs. Pseudobulbar Signs



















































Bulbar


Pseudobulbar


Tongue



Size


Atrophy


Normal



Movement


Decreased


Slow



Fasciculation


Present


Absent


Speech


Flaccid


Spastic


Face


Weak


Weak


Emotional lability


Absent


Present


Jaw jerk


Absent


Present


Gag


Absent


Hyperactive


Extraocular movements


Decreased


Decreased

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Sep 8, 2016 | Posted by in NEUROLOGY | Comments Off on Cerebrovascular Diseases

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