Stroke Flashcards
(40 cards)
Stroke تعريف
Acute neurological dysfunction occurring as a result of a vascular process, causing death or lasting damage
TRANSIENT ISCHEMIC ATTACK (TIA)
Transient episode of neurologic dysfunction caused by focal brain ischemia, lasting
between few minutes to 24 hrs, without acute infarction & without loss of consciousness.» high risk of developing stroke
Global Hypoxic/Ischemic encephalopathy due to
generalized decrease in cerebral blood flow
Features of global hypoxia: Selective Vulnerability of neurons in certain locations:
• Pyramidal cells in hippocampus
• Purkinje cells of the cerebellum
• Neurons in basal ganglia
• Cortical neurons especially in arterial boundary zones
Watershed (Borderzone) infarcts include:
- Boundary between anterior & middle cerebral arteries (Cerebral Convexities)
- Boundary between superior & posteriorcerebellar arteries (Posterior cerebellum)
- Necrosis few centimeters lateral to interhemispheric fissure.
Acute Global Hypoxic/Ischemic encephalopathy
after 12 hrs
layers 4-6 of cortex (RED NEURONS )
neutrophils
glial cell death
Subacute changes Global Hypoxic/Ischemic encephalopathy
24 hrs –2 weeks
tissue necrosis, macrophages & gliosis
Global Hypoxic/Ischemic encephalopathy
Repair after 2 weeks
irregular neuronal loss, gliosis & brain atrophy
Global Hypoxic/Ischemic encephalopathy outcomes depend on
Age, Duration of ischemia, Magnitude and rapidity of reduction of flow
Result of Global Hypoxic/Ischemic encephalopathy
varies from persistent neurological deficit to brain death → Deep coma & flat EE.
Focal brain necrosis due to complete and prolonged ischemia that affects all tissue
elements; neurons, glia, and vessels
INFARCTION (Focal Ischemia)
Risk factors of infarction
Family history of stroke: Genetic marker
Patients with TIA > increased Infarction in 5 years
Infarcts account for 80% of CVA
• Atherosclerosis
• Diabetes, Hypertension,age, hyperlipidemia
• Cardiac arrhythmias & Cardiomyopathy
• Hypercoagulable states
• Smoking
• Use of contraceptive pills
• Cerebral amyloid angiopathy
• Vasculitis: inflammatory or autoimmune
may lead to multiple small infarcts and more common
Embolism is more common than thrombosis
Other emboli are
fat, bone marrow, air, amniotic fluid
Histopathologic progression of CNS infarcts
1) EDEMA
2) “RED” NEURONS
3) POLYs(neutrophils)
4) MACROPHAGES (gitter cells) : clear damage , Can result in cyst and atrophy
5) GLIOSIS
Clinical picture of patient with INFARCTION (Focal Ischemia)
linked to site of infarction
• Contralateral hemiparesis
• Spasticity (UMNL)
• Loss of sensation
• Visual field abnormalities
• Aphasia (broca area in dominant hemisphere)
Mechanisms leading to infarction:
Thrombotic occlusion: Ischemic/ pale
• Embolic occlusion: hemorrhagic/ red
Thrombotic occlusion
Where
o Carotid bifurcation
o Origin of middle cerebral artery
o Basilar artery at either end
Embolic occlusion
Source + where
o Source: heart or atherosclerosis in carotid
o Middle Cerebral a. most affected
Traumatic vascular injuries
Epidural Hemorrhage
Subdural hemorrhage
Most occur with change head velocity e.g. boxers, battered baby & old age
Subdural hemorrhage or Epidural Hemorrhage
Subdural hemorrhage
Disruption of Bridging Veins from brain to dural sinuses, more over convexities
Subdural or epidural
Subdural
Which More common
Subdural
Patient has short LUCID interval followed by rapid loss of consciousness
Epidural or subdural
Epidural Hemorrhage