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Cerebral Vascular Accident

Cerebral Vascular Accident. STROKE. Nonmodifiable Age- incidence ↑ with age until age 75. Race- higher in African Americans Gender- higher in men Heredity- family history increases risk. Potentially Modifiable

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Cerebral Vascular Accident

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  1. Cerebral Vascular Accident STROKE

  2. Nonmodifiable Age- incidence ↑ with age until age 75. Race- higher in African Americans Gender- higher in men Heredity- family history increases risk Potentially Modifiable Lifestyle- excessive alcohol, cigarette smoking, obesity, high fat diet, drug abuse. Pathologic conditions- cardiac disease, DM, HTN, migraine headaches, hypercoagulability states. RISK FACTORS FOR STROKES

  3. ETIOLOGY AND PATHO • Extra-cranial factors- related to the circulatory system. • Systemic blood pressure- <70 and >160 • cardiac output- when reduced by 30% cerebral blood flow is reduced. • Blood viscosity- anemia increases cerebral blood flow and polycythemia reduces it.

  4. INTRACRANIAL FACTORS • A. Metabolic factors • Increased CO2 and low O2 results in vasodilation to restore blood flow to normal. • CO2 is the most potent regulator of cerebral blood flow. • Increased Hydrogen ion concentration increases cerebral blood flow.

  5. Intracranial factors, cont’d • B. Blood vessels • The condition of the blood vessels supplying the brain is important!!! • Potential problems- congenital anomalies (tortuosity, coiling, kinking, and AV malformations). • The malformations interfere with cerebral blood flow and contribute to atherosclerotic disease • Collateral circulation develops • Circle of Willis

  6. Intracranial factors, cont’d • C. Intracranial pressure • ICP increases with an assault to brain. • Causes of ICP: stroke, neoplasms, inflammation, trauma, and hydrocephalus. • ICP compresses the brain and reduces cerebral blood flow, which may lead to infarct. • Both extracranial and intracranial factors may lead to stroke

  7. Atherosclerosis • An abnormal accumulation and infiltration of in the intima of the arteries. • Plaques develop in an area of high turbulence; which may later damage the plaque. • Platelets and fibrin aggregate or collect on the surface of the plaque. • Parts of the plaque breaks off and travel to a narrower distal artery • Cerebral infarct occurs.

  8. TYPES OF STROKE • Ischemic: Most common type of stroke! • Occurs due to decreased blood flow to an area of the brain due to partial or complete occlusion of and artery due to thrombosis. • This lack of blood, oxygen and nutrients to an area of the brain causes necrosis of cerebral tissue. • Two types: thrombotic and embolic • See Lewis, page 1648; table 55-1.

  9. Thrombotic stroke • Most common cause of cerebral infarct! • Cause: Due to formation of a blood clot or coagulation of blood that results in narrowing of blood vessel or occlusion. • 2/3 of strokes due to HTN or DM. (accelerate the atherosclerotic process) • May also be due to oral contraceptives, coagulation disorders, polycythemia, arteritis, chronic hypoxia and dehydration.

  10. Thrombotic Stroke • Thrombotic strokes are usually proceeded by prodromal episodes (warnings) called TIA’s (transient ischemic attacks). • TIA’s last from 5 to 30 minutes. • Include- paresis or decreased strength and motion of an extremity. • Aphasia or disturbance of language function, • Paralysis, mental confusion, or visual disturbances.

  11. Thrombotic stroke • The extent of the stoke depends on rapidity of onset, size of lesion, and presence collateral circulation. • There is a pattern to thrombotic stroke! • 1. single attack; symptoms occur over several hours • 2. intermittent progression toward a stroke over hours or days. • 3. partial stroke with permanent neuro deficits • 4. series of TIA’s followed by a stroke with permanent neuro deficits.

  12. Thrombotic stroke • Symptoms at 72 hours are usually due to resulting edema to tissues; symptoms improve after edema subsides (@ 2 weeks). • This type of stroke occurs during or after stroke.

  13. EMBOLIC STROKE • Cerebral embolism results from occlusion of cerebral artery by an embolus. • Necrosis and cerebral edema results. • Embolus is the second most common cause of stroke. • Most emboli originate in the endocardium with plaques or tissue breaking off and entering circulation.

  14. Embolic Stroke • Emboli are associated with heart conditions such as; • A fib • MI • Infective endocarditis • Rheumatic heart disease • Valvular prostheses • ASD

  15. Embolic stroke • Less common causes of emboli: • Air • Fat from long bone fracture • Amniotic fluid postpartum • tumors

  16. Embolic stroke • Prodromal warning less likely; single events • sudden onset • Most commonly related to head trauma • High rate of re-occurrence if cause is not treated.

  17. Hemorrhagic stroke • Intracerebral hemorrhage is bleeding within the brain caused by rupture of a blood vessel that lasts from minutes to days. • Most commonly caused by HTN • May be caused by brain tumors, trauma, thrombolytic drugs, and ruptured aneurysms.

  18. Hemorrhagic stroke • Blood within the closed area of the brain imposes pressure on the brain tissue and displaces brain tissue and decreases blood flow to brain. • Clinical manifestations depends on the site and amount of hemorrhage and resultant damage. • Poor prognosis; 70% die

  19. Subarachnoid stroke • Caused by aneurysms, AV malformations, trauma, and HTN. • May have prodromal symptoms if ballooning or dilation applies pressure to brain tissue. • May suddenly rupture, causing neuro changes • Majority of aneurysms are in the Circle of Willis

  20. Subarachnoid hemorrhage, cont’d • If aneurysm leaks, pt may have a headache! • Rupture of aneurysm causes pressure in subarachnoid space due to bleeding. Clinical manifestations: • Headache, lethargy, confusion, nausea, vomiting, fever, neck pain, and backaches, paralysis, coma and death. Massive hemorrhage is defines as 30 to 50 ml of blood. Watch for re-bleeding when clot starts to dissolve. (usually within first 2 weeks post rupture). Reduce activity and prevent straining.

  21. Temporal Development of CVA • Transient Ischemic Attacks (TIA’s)- • Brief episodes of neuro manifestations (less than 24 hours). • Leaves no residual effects • Three categories: • 1/3 never have another TIA • 1/3 will have more than one TIA • 1/3 will have a stroke WARNING SIGNS OF PROGRESSING CVA!

  22. TIA’s • s/s vary depending on the part of brain affected. • Treatment: • Medications such as aspirin, Persantine (dipyridamole), Ticlid, and anticoagulant medication. • Long term therapy post TIA • Surgical treatment- carotid endartarectomy, extra-cranial- intracranial bypass (EC-IC bypass), and transiluminal angioplasty.

  23. Reversible ischemic Neurologic Deficit • A neuro deficit which remains 24 hours after onset; but leaves no residual signs or symptoms. • Considered a completed stroke with minimal to no residual deficits

  24. Stroke –In- Evolution • A progressive stroke which develops over hours or days. • Characteristic of an enlarging intra-arterial thrombus. • A stepwise or intermittent progression of deterioration of neurological symptoms. • Manifestations do not resolve and leave residual damage.

  25. Completed Stroke • Neuro defects unchanged over 2 to 3 days. • Usually embolic in nature • Also called “stable stroke”. • Signals readiness for aggressive rehab therapy. (unless an aneurysm is involved).

  26. Clinical Manifestations • All deficits are directly related to area of brain that is involved. • See Lewis, page 1650, Table 55-2.

  27. Neuromotor Function • Destruction of motor neurons in the pyramidal pathway causes: • Mobility • Respiratory function • Swallowing and speech • Gag reflex • Self-care abilities

  28. Motor deficits • Loss of skilled voluntary movement (akinesia). • Impairment of integration of movements • Alterations in muscle tones • Alteration in reflexes • Initial hypo-reflexia which progresses to hyper-reflexia for most patients.

  29. Patterns of deficits • Contralateral deficits • A lesion on one side of the brain affects the motor function on the other side of the brain. • The arms and legs on the affected side may be weak or paralyzed to different degrees depending the degree of cerebral circulation compromised. • See Lewis, Page 1651; Table 55-5

  30. The affected shoulder tends to rotate internally; the hip rotates externally. • The affected foot is plantar flexed and inverted. • An initial period of flaccidity may lasts for several days to weeks. • Spasticity of muscles follows the flaccid stage and is related to interruption of upper neuron influence.

  31. Communication • Aphasia- total loss of comprehension and use of language due to damage to the dominant hemisphere (left hemisphere). • Dysphasia-dysfunction related to comprehension or use of language due to partial disruption or loss. • Non-fluent (minimal speech activity with slow speech that requires obvious effort) • Fluent- (speech is present, but contains little meaningful communication).

  32. Communication • Conductive aphasia- mixture of both expressive and receptive aphasia • Global aphasia- results from a massive lesion and there is virtual loss of all language ability.

  33. Communication, cont’d • Wernicke’s area damage • Receptive aphasia where neither the sound or speech or its meaning can be understood. • Impaired comprehension of both spoken and written language. Boca’s area damage Expressive aphasia (difficulty speaking and writing) Dysarthria- disturbance in muscular control of speech. (pronunciation, articulation, phonation) DOES NOT EFFECT COMPREHENSION OF LANGUAGE.

  34. Affect • May be unable to control emotions • May be depressed RT body image and loss of function • May be frustrated RT immobility and communication issues

  35. Intellectual Function • Memory and judgment may be impaired • Left-sided stroke patients are more cautious in judgment and movement. • Right-sided stroke patients more impulsive and move quicker.

  36. Spatial-Perceptual Alterations • Right sided stroke patient has more spatial-perceptual orientation issues: • Erroneous perception of self and illness (may deny illness or body parts). • Erroneous perception of self in space (may ignore affected side; can’t judge distances) • Agnosia or inability to recognize an object by sight, touch or hearing. • Apraxia or the inability to carry out learned sequential movements on command.

  37. Elimination • Most occur initially and are transient. • Frequent constipation DT immobility, weak abdominal muscles, dehydration, and diminished defecation reflexes. • Urinary and bowel elimination may be DT functional inabilities to express needs and manage clothing.

  38. Diagnostic Studies • CT Scan- indicate size and location of lesion, differentiates between infarct and hemorrhage, effectiveness of treatment, and evaluate the course of healing. • MRI- considered best method to differentiate between hemorrhage and infarct.

  39. Diagnostics • PET shows chemical activity and depicts extent if tissue damage. • DSA- IV or arterial injection of contrast material to visualize blood vessels. • TDA- transcranial doppler measures velocity of cerebral blood flow in the arteries, also detects micro-emboli. • LP may be done to detect blood or WBC’s (not done if increased ICP is suspected)

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