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HCR240-Chapter33CerebrovascularDisorders1.pptx

Chapter 33

Cerebrovascular Disorders

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Copyright ©2020 F.A. Davis Company

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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