Classification of Stroke



Figure 7-1
Reversible cerberal vasoconstriction syndrome. A 58-year-old female that presented with acute severe headache and vision changes. Axial FLAIR image (a) shows T2 hyperintense lesions in the bilateral parieto-occipital and right frontal lobes. Time of flight MRA (b) showed multifocal areas of irregularity and narrowing




  • Treatment: corticosteroids, calcium channel blockers (verapamil)





    • Fibromuscular Dysplasia (FMD)



      • Nonatherosclerotic, noninflammatory vasculopathy of medium and large arteries, most commonly in middle third of ICA


      • Bilateral involvement common


      • Hyperplasia of arterial wall with loss of elastic layer


      • Associated with cerebral aneurysms and arterial dissections


      • Seen most often in CNS and renal arteries


      • Women > men


      • Clinical Presentation: most often asymptomatic. May present with renovascular hypertension . Neurological symptoms include headaches, tinnitus, vertigo, transient ischemic attack (TIA), Horner syndrome (in case of carotid dissection)


      • Type I: hyperplasia of media



        • Most common, ~80 %


        • String of beads, aka “medial fibroplasia”: alternating foci of luminal stenosis with aneurysmal outpouchings


      • Type II: hyperplasia of intima



        • Smooth arterial narrowing


        • <10 % of FMD cases


      • Type III: hyperplasia of subadventitia



        • Rarest


        • Diverticulations along one side of arterial wall


      • Treatment: unclear. Antiplatelet agents often used in symptomatic patients, surgery rarely indicated


    • Cerebral Amyloid Angiopathy (CAA)



      • Amyloid beta deposits in leptomeningeal, middle, and small cortical arteries, leading to small infarcts and lobar hemorrhages (Fig. 7-2)

        A330798_1_En_7_Fig2_HTML.jpg


        Figure 7-2
        Cerebral amyloid angiopathy. A 79-year-old female with multiple parenchymal lobar hemorrhages as seen on CT (top left). Corresponding MRI (top right) showed areas of susceptibility with surrounding edema suggestive of acute lobar bleeds. A previous MRI from a year prior (bottom row) shows classic peripheral distribution of multiple punctate parenchymal bleeds (Images courtesy of Dr. Ajay Malhotra)


      • Amyloid deposits stain + with Congo Red, show green birefringence under polarized light (Fig. 7-3)

        A330798_1_En_7_Fig3_HTML.jpg


        Figure 7-3
        Cerebral amyloid angiopathy. Low magnification view (a) demonstrating amorphous eosinophilic material deposited in arterial walls (blue arrow). Immunohistochemical study (b) showing deposition of Aβ-amyloid peptide within several blood vessels (Images courtesy of Dr. Anita Huttner)


      • Familial Cerebral Amyloid Angiopathy : rare AD disorder of small arteries predisposes to ischemic and hemorrhagic strokes.


      • Dutch variety: autosomal dominant, mutation in amyloid precursor protein (APP), mainly affects elderly, vascular deposits contain B-amyloid peptide


      • Icelandic variety: affects younger people, and vascular deposits contain cystatin C


    • Cerebral Autosomal Dominant Arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL )



      • Due to NOTCH3 (chromosome 19p) mutation, leading to impaired function and apoptosis of vascular smooth muscle cells


      • Early onset (mean age 37 years) of TIA symptoms or stroke, high prevalence of migraine and depression, progressive dementia, and leukoencephalopathy


      • MRI: multiple subcortical ischemic strokes, micro-hemorrhages, characteristic FLAIR hyperintensities in bilateral anterior temporal lobes and external capsules


      • Vessel walls become fibrotic, hyalinized, and basophilic. PAS-positive granules are deposited in the media (seen in skin biopsy).


    • Sneddon Syndrome



      • Focal cerebral infarcts with livedo racemosa, headaches, seizures, progressive encephalopathy


      • Livedo racemosa: fixed reddish-blue lesions in a reticular pattern on legs and body


      • Associated with antiphospholipid syndrome


      • Occurs commonly in middle-aged women


    • Hyperhomocysteinemia



      • Elevated levels most commonly result from inability to convert homocysteine to methionine (requires folate derivatives)


      • Plasma homocysteine concentrations of 15–100 μmol/L


      • Associated with dietary deficiency in B6, B12, and folate


    • Homocystinuria



      • Most commonly caused by autosomal recessive deficiency in cystathione β-synthase, a key enzyme in degradation of homocysteine


      • Plasma homocysteine concentrations of ≥ 100 μmol/L


      • Causes stroke, mental retardation, lens and skeletal abnormalities in children


    • Kohlmeier-Degos disease



      • Also known as malignant atrophic papulosis


      • Rare progressive vasculopathy involving skin, intestines, and CNS


      • Skin exam reveals papular lesions with depressed white center


      • Commonly affects white males 20–30 years old






        Inflammatory Vasculopathy (Vasculitis)




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        Oct 7, 2017 | Posted by in NEUROLOGY | Comments Off on Classification of Stroke

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