CVA Flashcards
TIA
Transient ischemic attack
Temporary interruption of blood supply to brain
Symptoms last for a few mins to hours but do not last longer than 24
No residual deficits
Precursor to susceptibility for CI or MI
HTN and CVA
-Reducing diastolic by 5-6mm Hg can reduce risk by up to 40%
Homocysteine
High plasma levels w/ low folate and B6 associated w/ increase risk of heart disease which may increase stroke risk
Cigarette smoking
Increase risk by 50%
Associated w/ number per day
Alcohol
Direct dose rln w/ stroke
3+/day increase risk by 45%
Causes of CVA
Cerebral infarction 70%(thrombus or embolus occlusion)
Hemorrhage’s 20%(subarachnoid, subdural, intracerebral)
Thrombus usually form
Branching or curves in arteries
A-fib
Believed to cause thrombus formation
Embolic infarction
(Thrombus, tissue, fat, air, bacteria or foreign bodies)
Results are more damaging as no time for collateral circulation to develop
Heart is most common source of embolic material (atherothrombic disease)
Artery to artery embolism
from atherothrombic lesion in carotid or verterobasilar
Formation of a thromboemboli begins
Distal vessels of the artery
Micro vascular occlusion that progressively increase in number and continue to impair blood flow
Astroglial swelling
Earliest cell changes noted w/ single artery occlusion
Functioning is impaired when
Blood flow falls below 20mL/100mg
Neuronal death occurs when
The brain relieves less than 8-10mL/100mg/min
Complete cerebral circulatory arrest results in
irreversible cellular damage with a core area
of focal infarction
Cells that have 80-100% ischemia will die in a few min b/c they cant produce ATP ->activation of Ca -> chain rxn to cell death
Area surrounding the core
Ischemic penumbra - receives collateral circulation but is not able to sustain fx
Secondary response to ischemic CVA
Decreased perfusion relative to O2 requirements
Areas of altered metabolism distant from site
Decline in O2 metabolism of unaffected side from acute to subacute (delay of corpus callosum fiber degeneration)
Glutamate and secondary damage
Normal: glutamate is an excitatory NT
released into the EC space and is quickly reabsorbed
• If the cells that normally uptake compromised, excess glutamate depolarizes the post synaptic cells
• excess glutamate allows the influx of Ca++ ions
into the cells which begins the process of cell death
• Catabolic enzymes are activated by the release of the Ca++ ions
and damage the cells that support the neurons (glial cells)
The hypoxia triggers
Neurotoxin release —> cell death
Middle cerebral artery syndrome
-Supplies most of the lateral cortex and also frontal, temporal, and parietal lobes
- Contralateral hemiplegia and hemianesthesia (sensory loss) with greater involvement of the face and upper extremity than the lower extremity because of the somatotopic
organization of the cortex
Middle cerebral artery syndrome
– If the dominant hemisphere (~left) is involved, global aphasia (Broca’s and Wernicke’s aphasia) (loss of fluency, ability to name objects, comprehend auditory information, and repeat language)
– If the non-dominant hemisphere (~right) is involved,
deficits in spatial awareness/attention will be present /(Contralateral body and space >ipsilateral body and space)
– Homonomous hemianopsia if involvement of optic
radiations
Anterior cerebral artery syndrome
Uncommon and often a result of an embolus
– Supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobe)
– Results in contralateral hemiparesis and sensory loss with
greater involvement of the lower extremity than the
upper extremity and face because of the somatotopic
organization of the cortex
Collateral flow can compensate for the occlusion so
dysfunction can be minimal
– Primitive reflexes may be present (frontal release signs)
– Abulia (loss of desire to perform tasks or a delay in verbal and motor response if there is significant involvement of the frontal lobe (role in cognitive functioning and initiative)
Internal carotid artery syndrome
Supplies the MCA and the ACA
– Severity depends on the etiology, thrombus, or embolus of decreased blood flow
– If collateral circulation is present, the condition may be asymptomatic
– If collateral circulation is not present, extensive involvement resembling MCA and ACA manifestations may be present with possibility of coma and death
Posterior cerebral artery suplies
arises from terminal branches of the basilar artery and supplies the inferior and medial temporal lobes
– Also supplies the medial occipital cortex and most of the medial parietal cortex
– Also supplies a small portion of midbrain and most of the thalamus