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31 Cards in this Set

  • Front
  • Back
Astrocytes
main cells responsible for repair and scar formation in the brain
→Gliosis (fibrosis of the brain)
Oligiodendrocytes
forms myelin in the CNS
Acute neuronal injury
red neurons
→hypoxia/ischemia
→cell death
Chronic neuronal injury
progressive neurologic disease
astrocytes hypertrophy and become hyperplastic → gliosis
Rosenthal fibers
Astrocytes → eosinophilic structures in long standing gliosis
Corpora amylacea
degenerative change in astrocytes with increasing age
Cerebral vascular disease
abnormality of the brain resulting from pathological blood vessels:
thrombosis, embolism, hemorrhage
usually due to atherosclerosis, embolism, hypertension, ruptured aneurysm
Hypoxia
decreased oxygen supply
Ischemia
decreased blood supply
Encephalopathy
disease of the brain involving structure alteration
Global cerebral ischemia
diffuse hypoxia/ischemia, encephalopathy
low flow state, hypotention, hypoperfusion
resulting in edematous brain with white gyri and narrow sulci
poor demarcation between grey and white matter
Global cerebral ischemia
12-24 hours
acute neuronal change (red neurons), neutrophils, microvacuolization, nuclear pyknosis (shrinking) and karyorrhexis (fragmentation)
Global cerebral ischemia
24 hours - 2 weeks
tissue necrosis, reactive gliosis, macrophages, vascular proliferation
Global cerebral ischemia
2 weeks and on
repair, necrotic tissue removal, gliosis
Ischemic pathogensis
Ischemia → overstimulation of glutamate receptors → uncontrolled Ca++ influx → apoptosis
Cerebral infarction
oculsion of arterial supply to the brain
→ localized ischemia
Transient Ischemic Attack
cerebral infarction
→ reversal of neurological functions by removal of oclusion

loss of function depends on influenced arteries
may last from seconds to hours and may have many attacks

neuro exam between attacks are normal
Artherosclerosis
arterial degeneration
Cerebral thrombosis
stationary occlusion of blood vessels secondary to atherosclerosis

most commonly: origin of middle cerebral a. and end of basilar a. (carotid bifurcations)

frequently associated with hypertension and diabetes
Thrombotic infarction
pale infarcts (non-hemorrhagic)
softening and swelling of brain
→ liquefied tissue leaving fluid filled cavities

may be preceded many brief transient ischemic attacks
most commonly during sleep

Tx: anti-coagulants
Embolic infarction
Red infacts (hemorrhagic)
most commonly from thrombus within heart due to fat, tumor cells, fibrocartilage, amniotic fluid

most frequently in the middle cerebral a.

→strokes
Hemorrhagic infarcts
Red infarcts
usually embolic
hemorrhages because of reperfusion to damaged vessels directly after removal of occlusion
Lacunar infarct
secondary to hypertention
small branches of cerebral arteries occluded
may be asymptomatic
leaves small cavity (lacune) after softened tissue is removed
Intracranial hemorrhages
due to chronic hypertension
cerebral arteries degenerated
hemorrhage may damage brain tissue and compress vascular structures
→ edema, ischemia
Intracerebral hemorrhage
(intraparenchymal)
hypertension→atherosclerosis→necrosis of arteries
middle age to elderly
rupture of small intraparenchymal vessel
putamen, thalamus, pons
Charcot Bouchard aneurysm
intracerebral hemorrhage
chronic hypertension
micro-aneurysm → vascular rupture
espically in basal ganglia
Lobar Hmorrhage
Hypertensive hemorrhage in subcortical white matter
symptoms varies with location
Pontine Hemorrhage
Coma → death within 48 hours
pinpoint pipils
impaired horizontal eye movemnt
Cerebellar hemorrhage
headache, dizziness, vomitting, disequillibrium
Subarachnoid hemorrhage
congential, atherosclerotic, hypertensive, embolic, infections, traumatic

most frequently saccular (berry) aneurysm of anterior part of circle of willis
blood in subarachnoid space causes high pressure → severe sudden headache
usually when patient is active during sex or straining stool
Arteriovenous malformation
common cause of subarachnoid hemorrhage
arteries connect with veins without capillary bed
males age 10-30
seizures, strokes, ischemia

evidence of prior hemorrhage: greatly enlarged blood vessels separated by gliotic tissue