learning guide M6
Chapter 33
Cerebrovascular Disorders
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1
Neuroanatomy and Neurophysiology
Central nervous system (CNS)
Brain and spinal cord
PNS (peripheral nervous system)
Cranial nerves and spinal nerves
Spinal cord
Motor neurons descend
Sensory neurons ascend
Upper neurons: within the brain
Lower neurons: spinal cord
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Brain
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Neuroanatomy and Neurophysiology (continued_1)
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
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Neuroanatomy and Neurophysiology (continued_2)
Spinothalamic tract
Sensory neurons from periphery to brain
Cross over at some level spinal cord
Cerebral injury
Presentation often on opposite side of body
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Tracts
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Central Nervous System
Cerebrum
Upper most region of brain
Right and left hemisphere
Corpus callosum: connection
Categorical hemisphere
Language, sequential-analytic
L hemisphere in most
Representational hemisphere
Face recognition, music, visual-spatial
R hemisphere in most
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Central Nervous System (continued_1)
Speech and language center
Aphasia
Difficult to speak or understand language
Broca’s area
Speak language
Expressive aphasia
Wernicke’s area
Comprehend language
Receptive aphasia
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Brain (continued)
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Central Nervous System (continued_2)
Brainstem
Cranial 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 equilibrium
Atherosclerosis can affect blood flow to cerebellum
Vertebral-basilar insufficiency (VBI)
Can affect blood flow to cerebellum
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Cerebrovascular Circulation
R and L vertebral arteries
Feed posterior brain
Internal and external carotids
Internal carotid
Serves brain’s anterior and middle cerebral arteries
Anterior cerebral artery: frontal lobe
Middle cerebral artery: lateral cortex, 80% of brain’s tissue
Most strokes involve branch of this artery
Circle of Willis
Base of brain, provides collateral circulation
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Cerebrovascular Circulation (continued)
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Middle Cerebral Artery
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Circle of Willis
Base of brain
Formed by posterior cerebral artery and internal carotid
Common site for aneurysms (weakness in arterial wall)
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Cranial Nerves
12 pairs
Number I through XII
Either motor, sensory, or both
Brain injury, tumor, or stroke can disrupt cranial nerve functioning
Cranial nerve abnormalities may be a sign of increasing intracranial pressure
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Cerebral Metabolism
Brain
Most energy-consuming organ
20% of oxygen
Brain cells not capable of anaerobic metabolism
Irreversible damage may occur
Glucose for energy
Hypoglycemia and hypoxia affect brain functioning
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Epidemiology
Stroke
5th leading cause of death in U.S.
Often results in paralysis on one side of body
Because of rising number of elderly individuals, incidence of stroke increasing
Risk for African Americans greater
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Stroke Overview
Two types
Ischemic (85%)
Thrombus or embolus
Leads to cerebral infarction
Hemorrhagic (15%)
Rupture of cerebral artery
Transient ischemic attack (TIA)
Ischemic injury, “mini-stroke” (inaccurate label)
Disruption of cerebral circulation lasting less than 24 hours
No permanent injury, but can warn of future attacks
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Types of Strokes
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Ischemic Stroke
Most common in internal carotid and middle cerebral artery
Causes
Cerebral arteriosclerosis
Carotid stenosis
Atrial fibrillation
Stasis of blood leads to clot formation
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Ischemic Stroke (continued)
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Ischemia and Ischemic Penumbra
Cerebral ischemia 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 reperfusion is critical to recover cells
Cerebral edema may also develop in the area causing further damage
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Core Ischemia and Ischemic Penumbra
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Glutamate Toxicity
Cellular ion pumps begin to fail
Calcium ion influx results in release of glutamate, excitatory neurotransmitter
Glutamate opens Na+ and Ca++ channels
Ca++ influx activates degradative enzymes, causing further cell death
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Glutamate Toxicity (continued)
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Transient Ischemic Attacks (TIA’s)
Temporary and resolves
20%–25% of TIA’s progress to stroke
Neurological changes may go unnoticed by patient
Observable by bystanders
TIA may be resolved by time medical help is received
Interview of patient and observers is key
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Transient Ischemic Attacks (TIA’s) (continued)
Lacunar infarct
Small infarcts in brain due to occlusion of tiny blood vessels
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Hemorrhagic Stroke
Artery rupture results in bleeding
Causes
Hypertension: most common cause
Aneurysm rupture
Most common location: Circle of Willis
Subarachnoid hemorrhage
Arterial branch in subarachnoid space ruptures
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Hemorrhagic Stroke (continued_1)
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
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Hemorrhagic Stroke (continued_2)
Cerebral edema may occur, putting pressure on brain tissues
Pressure on brainstem causes alteration in HR, breathing, pupil dilation
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Hemorrhagic Stroke (continued_3)
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 symptoms
Eventually, immune response and scar tissue form
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Risk Factors for Stroke
Hypertension (HTN)
Hyperlipidemia
Diabetes
Smoking
Obesity
Lack of exercise
Atrial fibrillation
Oral contraceptives
Excess alcohol
Family history
Age 55+
Gender
Male risk is greater than female
Ethnicity
African American risk is greater than Caucasian
Sickle cell disease
Transient ischemic attack (TIA)
Amyloid accumulation
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Signs and Symptoms of Stroke
Ischemic and hemorrhagic strokes present with similar signs
Middle cerebral artery most common stroke location
Speech, motor, sensory deficits
Neurological deficits on one side of body
Slurred speech, loss of gag reflex, facial droop
Hemiparesis, hemiparalysis, loss of sensation
Vision loss
Some patients have disorientation, confusion
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SAH and VBI
Subarachnoid hemorrhage (SAH)
Presents differently than most hemorrhagic strokes
Sudden onset (“worst headache ever,” “thunderclap headache”)
Vertebrobasilar insufficiency (VBI)
Ischemia of vertebrobasilar circulation
Dizziness, vertigo, headache
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Diagnosis
Any sudden changes in neurological function should be assessed
No reliable clinical presentation to differentiate ischemic vs hemorrhagic stroke
1-sided symptoms and signs
Slurring speech, facial droop, hemiparalysis, etc., are key
Rule out other pathologies that may present similar to stroke
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Diagnosis (continued_1)
CT scans without contrast: acute phase
Identify or exclude hemorrhagic stroke
Treatment based on whether the stroke is ischemic or hemorrhagic
CT scan with dye may allow better visualization of ischemia
Magnetic resonance angiography (MRA)
Can distinguish between ischemic and hemorrhagic stroke
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