Chapter 446 Cerebrovascular Disease Flashcards
What is a Stroke or Cerebrovascular accident?
ABRUPT onset of a neuro deficit attributable to a FOCAL vascular cause
Neuro signs & symptoms last for >24h
Brain infarction is demonstrated
Why do neurologic symptoms manifest within seconds
Because neurons lack GLYCOGEN, so energy failure is rapid
TIA (Transient Ischemic Attack)
ALL neuro signs & symptoms resolve WITHIN 24h without evidence of brain infarction on brain imaging
The constellation of cognitive sequelae that ensues after widespread brain injury caused by global hypoxia-ischemia.
Hypoxic-ischemic encephalopathy
FOCAL ischemia or infarction is usually caused by? (2)
- Thrombosis of cerebral vessels themselves or 2. Emboli from a proximal arterial source or the heart.
How does INTRACRANIAL HEMORRHAGE produce neuro symptoms? (3)
- Mass effect on neural structures
- Toxic effects of blood itself
- Increasing intracranial pressure
Loss of the appreciation that something is wrong
Anosognosia
Other causes of sudden-onset neuro symptoms that may mimic stroke
Seizure
Intracranial tumor
Migraine
Metabolic encephalopathy
Migraine without head pain (term)
Acephalgic Migraine
Standard imaging modality to detect the presence or absence of intracranial hemorrhage
CT imaging of the brain
Cerebral blood flow = 0
How long before death of brain tissue occurs?
Within 4-10 minutes
Cerebral blood flow = <16-18 ml/100g tissue/minute
How long before infarction occurs?
Within an hour
Cerebral blood flow value that causes ischemia without infarction unless prolonged for several hours or days.
<20 ml/100g tissue/minute
Ischemic penumbra
Define.
The ischemic but reversibly dysfunctional tissue surrounding a core area of infarction.
Goal of revascularization therapies.
Saving the ischemic penumbra.
Focal cerebral infarction 2 distinct pathways.
- Necrotic pathway
- cellular cytoskeletal breakdown is rapid due to energy failure of the cell - Apoptotic pathway
- cells become programmed to die
How does ischemia produce necrosis?
By starving neurons of glucose and oxygen, which in turn results in failure of mitochondria to produce ATP.
- no ATP>membrane ion pumps stop functioning>neurons depolarize>rise of intracellular calcium
- cellular depolarization>glutamate release from synaptic terminals
How does excess extracellular glutamate produce neurotoxicity?
by activating postsynaptic glutamate receptors that increase neuronal calcium influx
How are free radicals produced?
Degradation of membrane lipids and mitochondrial dysfunction.
Free radicals cause catalytic destruction of membranes and likely damage other vital functions of cells.
First goal in the treatment of acute stroke
Prevent or reverse brain injury
Clinical finding/s that favor a dx of ISCHEMIC type of stroke (1)
Deficit that is maximal at onset or remits
Clinical finding/s that favor a dx of HEMORRHAGIC type of stroke (3)
More depressed level of consciousness
Higher initial BP
Worsening of symptoms after onset
Immediate goal in ischemic stroke
Optimize cerebral perfusion in the surrounding ischemic penumbra
When SHOULD blood pressure be lowered?
Malignant hypertension
Concomitant myocardial ischemia
BP >185/110mmHg and thrombolytic therapy is anticipated