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cerebrovascular disorders - Coggle Diagram
cerebrovascular disorders
neuroanatomy and neurophysiology
central nervous system (CNS): bran and spinal cord
peripheral nervous system (PNS): cranial nerves and spinal nerves
spinal cord: motor neurons descend, sensory neurons ascend
upper neurons: within the brain
lower neurons: spinal cord
corticospinal tract: upper motor neurons that descend into spinal cord, contralateral (cross over, 80%), ipsilateral (remain on same side, 20%), decussation (brainstem area of crossover)
corticobulbar tract: run parallel to corticospinal tract
spinothalamic tract: sensory neurons from periphery to brain, cross over at some level spinal cord
cerebral injury: presentation often on opposite side of the body
CNS
cerebrum: uppermost region of brain, right and left hemisphere, corpus callous (connection)
categorical hemisphere: language, sequential-analytic (L hemisphere in most)
representational hemisphere: face recognition, music, visual-spatial (R hemisphere in most)
speech and language center
aphasia: difficult to speak or understand language
broca's area: speak language, expressive aphasia
wercicke's area: comprehend language, receptive aphasia
brainstem
crainial nerves originate
midbrain: auditory and visual responses, motor movement
pons: arousal, sleep
medulla oblongata: HR, respiratory function
cerebellum
smooth movement
ataxic gait: uncoordinated walking
posture and equalibrium
atherosclerosis can affect blood flow to cerebellum
vertebral-basilar insufficiency (VBI): can affect blood flow to cerebellum
brain
parts:
cerebrum
thalamus
hypothalamus
pituitary gland
brainstem: pons, medulla
spinal cord
cerebellum
functions:
motor region
sensorimotor region
speech
sensory region
hearing
vision
brainstem controls vital functions: consciousness, heart rate, respiratory rate, blood pressure
cerebellum: balance and coordination
strokes
ischemic
most common in internal carotid and middle cerebral artery
causes: cerebral arteriosclerosis, carotid stenosis, atrial fibrillation (stasis of blood leads to clot formation)
may develop gradually (if completely occluded: neurons in core area of ischemia suffer irreversible infarction within minutes)
ischemic penumbra: perimeter of ischemic zone (less perfusion but not irreversible damage, rapid repercussion is critical to recover cells
cerebral edema may also develop in the area causing further damage
transient ischemic attacks
temporary and resolves (20-25% of TIAs progress to stroke)
neurological changes may go unnoticed by patient (observable by bystanders, may be resolved by time medical help is received, interview of patient and observers is key)
lacunar infarct (small infarcts in brain due to occlusion of tiny blood vessels
hemorrhagic stroke
artery rapture results in bleeding
causes: hypertension (most common), aneurysm rupture (mostly in circle of willis), subarachnoid hemorrhage (arterial branch in subarachnoid space ruptures)
blood flows into brain, compresses, and displaces brain tissue
blood causes vasospasm of adjacent blood vessels
blood released is toxic to surrounding cells
anoxic encephalopathy (lack of oxygen delivery causes decreased level of consciousness)
cerebral edema may occur, putting pressure on brain tissues (pressure on brainstem causes alteration in HR, breathing, pupil dilation
cushing's triad: pressure on brainstem
bradypnea or irregular respirations, bradycardia, hypertension
if hemorrhage is large, hematoma and clot form; may expand in first 24 hours, worsening the original symptoms (immune response and scar tissue form)
risk factors
hypertension
hyperlipidemia
diabetes
smoking
obesity, lack of exercise
atrial fibrillation
oral contraceptives
excess alcohol
family history
age 55+
gender (male is higher risk
ethnicity (African American highest risk)
sickle cell disease
TIA
amyloid accumulation