CNS 2 Flashcards

1
Q

Reduction or cessation of blood flow to a localized area of brain due to partial or complete arterial occlusion
clinical manifestations depend on the anatomic location of the lesion
Causes: thrombosis, embolism, inflammatory lesions

A

Focal Cerebral Ischemia

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2
Q
  • evident at 48 hours as pale, soft regions of edematous brain, with neutrophilic infiltration; tissue then liquefies, and a fluid-filled cavity containing macrophages is lined by reactive glia
  • Acute: red neuron, cerebral edema, neutrophilic infiltration
  • Subacute: liquefactive necrosis, influx of macrophages, reactive gliosis with neovascularization
  • Healed: tissue loss surrounded by residual gliosis
A

Nonhemorrhagic infarcts (bland or anemic infarcts)

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3
Q

exhibit blood extravasation and resorption

A

Hemorrhagic infarcts

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4
Q
  • ## occurs with generalized reduction of cerebral perfusion or decreased oxygen carrying capacity of the bloodclinical outcome varies with the severity and length of the insult
  • Neurons are most sensitive to ischemia
    + Pyramidal layer of hippocampus (CA1: Sommer sector)
    + Cerebellar Purkinje cells
    +
    Pyramidal cells of cerebral cortex
A

Global Cerebral Ischemia

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5
Q
  • occur in the regions of the brain or spinal cord that lie at the most distal reaches of the arterial blood supply
  • usually develop after severe hypotensive episodes and are most commonly seen in patients resuscitated after cardiac arrest
A

Border zone (“watershed”) infarcts

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6
Q

Gross
- Edematous and swollen brain: widening of the gyri and narrowing of the sulci
Microscopic
- Early changes: dead red neurons
Subacute changes: tissue necrosis, influx of macrophages, vascular proliferation, and reactive gliosis
- Repair: removal of necrotic tissue, loss of normal CNS architecture, and gliosis
- Laminar necrosis in cerebral neocortex

A

Global Cerebral Ischemia

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7
Q
  • involves spontaneous rupture of a small intraparenchymal vessel
  • “ganglionic hemorrhages” occurs in basal ganglia and thalamus
  • “lobar hemorrhages” occurs in cerebral hemispheres
  • Hypertension is the risk factor most commonly associated with deep brain parenchymal hemorrhages; occur in the putamen, thalamus, pons, and rarely the cerebellar hemispheres
  • Cerebral amyloid angiopathy (CAA) is the risk factor most commonly associated with lobar hemorrhages
A

INTRAPARENCHYMAL HEMORRHAGE

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8
Q
  • Most common cause: ruptured saccular “berry” aneurysm
  • Saccular aneurysm: most common intracranial aneurysm
    + Most common location: anterior circulation (90%)
  • Associated with ADPKD, Ehlers-Danlos syndrome type IV, NF Type 1, Marfan syndrome, fibromuscular dysplasia, CoA
  • Clinical manifestation: “worst headache of my life” and syncope
  • Lesions are a few millimeters to 2 to 3 cm in diameter with a red, shiny, translucent wall. At the aneurysm neck, the muscular wall and intimal elastic lamina are absent or fragmentary; the sac wall is composed of only thickened hyalinized intima
A

SUBARACHNOID HEMORRHAGE

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9
Q

Classification of Vascular Malformations that is enlarged tangled vessels with intervening brain tissue
as its common location is in the vessels of the subarachnoid space and brain

A

AV Malformation

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10
Q

Classification of Vascular Malformations that is Enlarged vessels without intervening brain tissue
as its common location are in Cerebellum, pons, and subcortical regions

A

Cavernous malformation

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11
Q

Classification of Vascular Malformations that is Small, thin-walled vessels with intervening brain tissue
as its common location are in the pons

A

Capillary telangiectasia

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12
Q

Classification of Vascular Malformations that is Ectatic venous channels
as its common location are variable

A

Developmental venous anomalies (venous angiomas)

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13
Q

is caused by multi-focal vascular disease of several types, including

(1) cerebral atherosclerosis,
(2) vessel thrombosis or embolization from carotid vessels or from the heart, and
(3) cerebral arteriolosclerosis from chronic hypertension.

A

vascular dementia

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14
Q

When the pattern of injury preferentially involves large areas of the subcortical
white matter with myelin and axon loss, the disorder is referred to as

A

Binswanger disease (subcortical white matter dementia)

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