cerebral hemispheres and cerebral vascular disease

stroke risk factors

HTN, smoking, afib, DM, high BMI, hypercholesteremia, family hx, cardiac disease, prior hx of stroke

stroke

rapidly developing clinical signs of focal disturbance of cerebral function lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin
may also occur in brainstem, cerebellum, and spinal cord

CNS perfusion

normally little more than is necessary to survive, little room for error, doesn’t take long to starve brain causing shut down and cell death

primary infarct zone

area supplied by vessel, where immediate cell death occurs - not going to regenerate
ischemic cascade initiated

penumbra

marginal zone
blood supply compromised, edema shuts down connections, potential cell death however can be recovered and have return of function
focus of medical interventions

stroke s/s

mostly unilat
hemiparesis, ataxia, hemianopsia, visual-perceptual deficits, aphasia, dysarthria, sensory and memory deficits, bladder control problems

neuro outcome factors

etiology: ischemic vs hemorrhagic
location, size (in cortex other areas can take up some of function however if in white matter tracts can’t do so)
rate and duration: tolerate short term better
glucose: high is bad
BP: avoid extremes
temp: high bad but low may be neuroprotective
collateral circulation

types of ischemic stroke

majority of strokes, inadequate blood supply
atherosclerotic, small artery (lacunar), cardiogenic (embolism), cryptogenic, other

types of hemorrhagic stroke

bleed into brain
intracerebral, subarachnoid

ischemic strokes

thrombus formation blocks blood flow, infarct develops 3-12 hours after ischemia
ischemic core (aka zone of infarction where cell death occurs), and ischemic penumbra (cells in critical condition)

thrombotic stroke

often preceded by TIA, blood clot forms locally, usually associated with an atherosclerotic plaque
HA present in 25-30% of cases

ischemic stroke event

5-10 min away from irreversible damage
regional blood flow mechanisms disrupted, vasogenic edema (cerebral peaks 48-72 hours after infarct) - compression effects

ischemic stroke event cellular level

cells become fragile
intracellular edema cytotoxic
anaerobic metabolism: H+ and lactic acid dangerous byproducts, metabolic acidosis
disrupt ion gradients: anoxic depolarization
excitotoxicity

excitotoxicity

cascade event, cells going through cell death cause contents to spill out affecting other cells which cause them to start to die
too much glutamate causes cell death due to overstimulation, upregulates Ca in target cell leading to self destruction

TIA

symptoms resolve in minutes to hours (<24), typically last 10 min or less
caused by minute emboli or partial thrombi with vasospasm
precedes 15% strokes, post is 90 day risk of stroke, often ignored

global ischemia

systemic drop in BP leads to global decrease in perfusion
watershed areas, hippocampus, and cerebellum most susceptible

watershed areas

boundaries between major cerebral blood vessel distribution
most distant aspect of supply for arteries, don’t get good blood supply from either vessel
affected 1st and most significantly with global ischemia

global ischemia deficits

proximal UE and LE weakness, transcortical aphasia, visual processing disturbance

embolic stroke

foreign material travels to and occludes a cerebral blood vessel
rapid onset, origin often cardiogenic (afib), most commonly MCA
determine origin to prevent further strokes, often put on blood thinners
fragile distal vessels may hemorrhage when blood flow returns

hemorrhagic strokes

rupture of small perforating vessels or aneurysms
commonly in lenticulostriate (HTN) or ACA (aneurysm)
surviving pts tend to recover better compared to ischemic stroke

hemorrhagic stroke concerns

volume lesion that can compress nervous tissue, blood can be toxic to brain tissue

lacunar infarcts

occlusion of small penetrating vessels cause small subcortical infarcts, associated with small vessel disease (HTN)

lacunar syndromes

pure motor hemiparesis, ataxic hemiparesis, pure sensory stroke, sensory and motor

AVM

congenital malformation from abnormal anastomoses between arteries and veins
onset of symptoms often between 10-30 yrs

medical tx for stroke

returning blood supply, directed at stroke event
CT to rule in/out hemorrhage
thrombolytic agents: t-PA if hemorrhage ruled out within 3 hours onset, heparin
cathetarization/angioplasty

preventing secondary damage from stroke

meds to control BP, blood sugar levels, fever, seizures
Ca channel blockers and NMDA receptor blockers

dominant hemisphere

hemisphere managing language, usually left
usually superior at logic/analytic tasks

left neglect

right brain pays attention to more of field than left, so left neglect is more severe

motor control and sensory

L: right side of body, sequencing movements
R: left side of body, sustaining movement/posture

language

L: processing and production of speech and writing, grammar, vocab, literal interpretation
R: processing nonverbal stimuli, contextual interpretation

academic

L: reading, performs calculations
R: mathematical reasoning, alignment of numerals in calculation, spatial relationships

emotions

L: positive emotions
R: negative emotions, perception of emotions

cognitive

L: detail oriented, processing info in a sequential, linear manner
R: whole picture, grasping overall organization, processing info in simultaneous manner, synthesizing info

functional mapping

cytoarchitectural organization: Brodman’s areas
lesions
direct stimulation under local anesthesia: identification of sensory areas
imaging studies and transcutaneous/transcranial stimulation of cortex