“Brain Attack”

1. “Brain Attack” Cerebrovascular Accident Or “Stroke”

2. Stroke • Generic term for temporary or permanent disturbance of brain function due to vascular disruption (Brookshire) • Also called cerebrovascular accident (CVA) • 3rd leading cause of death in the USA; about 500,000 per year----150,000 die from stroke • 80% of pts. Survive for at least 1 mo. Post; about 1/3 of those are alive 10 years post.

3. The Five Most Common Stroke Symptoms Include: • Sudden numbness or weakness of face, arm or leg, especially on one side of the body • Sudden confusion, trouble speaking or understanding • Sudden trouble seeing in one or both eyes • Sudden trouble walking, dizziness, loss of balance or coordination • Sudden severe headache with no known cause

4. Other Important but less Common Stroke Symptoms Include: • Sudden nausea, fever and vomiting distinguished from a viral illness by the speed of onset (minutes or hours vs. several days) • Brief loss of consciousness or period of decreased consciousness (fainting, confusion, convulsions or coma)

5. Uncontrollable Stroke Risk Factors Include:AgeThe chances of having a stroke go up with age. Two-thirds of all strokes happen to people over age 65. Stroke risk doubles with each decade past age 55.Uncontrollable Stroke Risk FactorsGenderMales have a slightly higher stroke risk than females. But, because women in the United States live longer than men, more stroke survivors over age 65 are women.RaceAfrican-Americans have a higher stroke risk than most other racial groups.Family history of stroke or TIARisk is higher for people with a family history of stroke or TIA.Personal history of diabetes People with diabetes have a higher stroke risk. This may be due to circulation problems that diabetes can cause. In addition, brain damage may be more severe and extensive if blood sugar is high when a stroke happens. Treating diabetes may delay the onset of complications that increase stroke risk. However, even if diabetics are on medication and have blood sugar under control, they may still have an increased stroke risk simply because they have diabetes.

6. Coronary Heart Disease and High Cholesterol High cholesterol can directly and indirectly increase stroke risk by clogging blood vessels and putting people at greater risk of coronary heart disease, another important stroke risk factor. A cholesterol level of more than 200 is considered "high." Cholesterol is a fatty substance in the blood that our bodies make on their own, but we also get it from fat in the foods we eat. Certain foods (such as egg yolks, liver or foods fried in animal fat or tropical oils) contain cholesterol. High levels of cholesterol in the blood stream can lead to the buildup of plaque on the inside of arteries, which can clog arteries and cause heart or brain attack. Sleep Disordered Breathing - Sleep ApneaSleep apnea is a major cardiovascular and stroke risk factor increasing blood pressure rates which may cause stroke or heart attack. Studies also indicate that people with sleep apnea develop dangerously low levels of oxygen in the blood while carbon dioxide levels rise, possibly causing blood clots or even strokes to occur. Diagnosing sleep apnea early may be an important stroke prevention tool. Personal history of stroke or TIA People who have already had a stroke or TIA are at risk for having another. After suffering a stroke, men have a 42 percent chance of recurrent stroke within five years, and women have a 24 percent chance of having another stroke. TIAs are also strong predictors of stroke because 35 percent of those who experience TIAs have a stroke within five years.

7. Lifestyle Factors that Increase Stroke Risk Include: • SmokingSmoking doubles stroke risk. Smoking damages blood vessel walls, speeds up the clogging of arteries by deposits, raises blood pressure and makes the heart work harder. • AlcoholExcessive consumption of alcohol is associated with stroke in a small number of research studies. Its specific role in stroke has not yet been determined or proven. Recent studies have also suggested that modest alcohol consumption (one 4 oz. glass of wine or the alcohol equivalent) may protect against stroke by raising levels of a naturally occurring "clot-buster" in the blood. • WeightExcess weight puts a strain on the entire circulatory system. It also makes people more likely to have other stroke risk factors such as high cholesterol, high blood pressure and diabetes.

8. The Impact of Stroke Risk Factors

10. Most strokes occur in the 7th decade • 85% of survivors return to prestroke-living environment (with some residual impairment) • 15 % require institutional care (Greenberg, Aminoff, and Simon, 1993)

11. Ischemic—”deprived of blood” • Sometimes called “occlusive” • Hemorrhagic—”caused by bleeding” • Loss of blood flow for 3-5 minutes causes necrosis of the CNS • Infarct---death of tissue caused by interruption of blood supply

12. Thrombotic Artery is gradually occluded by a plug of material the collects in a given site Uncommon in smaller arteries Usually in areas of disturbance like twists and bends in an artery Atherosclerosis: Greek “hard paste” Embolic Artery is suddenly occluded by material that moves thought he vascular system to occlude an artery Often a fragment from a thrombosis Atrial fibrillation is a common cause Ischemic Stroke

13. Transient Alchemic Attack (TIA) • Temporary disruptions of circulation, e.g, less than 24 hours in length • Quickly developing: • Sensory disturbances, limb weakness, slurred sph., visual complaints, dizziness, confusion, or mild aphasia

14. RIND and PRINDs • “Reversible ischemic neurologic deficits” (less than 24 hours) • Partially reversible ischemic neurologic deficits (longer than 24 hours but leave minor deficits after a few days • TIAs sometimes called “small strokes”

15. Greenberg et al. (1993) • 1/3 of pts who have TIAs or RINDs will within 5 years have a stroke that leaves them with permanent neurologic deficits

16. Hypofusion • Insufficient blood flow to the brain and the brain stem • Diaschisis---disruption of brain function in regions AWAY from the site of injury (but connected by neural pathways (“within system”) • Edema, decreased blood flow, neurotransmitters and diaschisis help diffuse impairment of brain function!

17. Hemorrhagic stroke(cerebral hemorrhage) • Caused by disruption of a cerebral blood vessel • Due to weakness of the vessel wall, by traumatic injury to the vessel or (rarely) by extreme fluctuation in BP

18. Extracerebral hemorrhages—bleeding outside of the brain Subarachnoid subdural extradural Intracerebral hemorrhages Within brain substance bleed Hemorrhages

19. Intracerebral Hemorrhage • 90% occur in pts with high BP • Cause(s): hypertention—pressure on arterial walls or chronic hypertension—weakening of small penetrating arteries causing “microaneurysms” • Can cause “snowball effect” as the hemorrhage affects adjacent vessels

20. Aneurysm • “Pouches” formed in arterial walls • berry or saccular, term depends upon the shape • Nearly 50% of extracerebral aneurysms occur in the arteries at the base of the brain (vertebrals, basilar, internal carotid and Circle of Willis • Most are due to injury to MCA and ACA • 2-3% occur in the posterior cerebral artery

21. Berry Aneurysm

22. Arteriovenous Malformation • Arteriovenous malformation • Collections of dilated, thin-walled vein connected to a tangled mass of equally thin-walled arteries. • Usually present at birth; most will not live to 60s-70s without a hemorrhage. • Symptoms include headaches and CNS symptoms • Can be removed surgically or vessel is tied off

23. AVF • Greatest risk is the potential for rupture and subsequent hemorrhage

24. Intracranial Tumors • Primary site: point of origin • Secondary site: originated elsewhere and moved • Relocation of tumor = metastasis---”mets” • Primary tumors: usually cerebrum and cerebellum • Occur at any age, most commonly age 25-50 • MAY run in families—hypothesis?

25. Herniation Syndromes • Masses the force movement of brain substance (or brain stem) • Tumors: course is deterioration of function • Early stage = lower intracranial pressure = causes nonspecific alterations of cognition ( forgetfulness, drowsiness, blurred or double vision, vertigo, lightheadedness, etc.

27. Intracranial tumors, cont. • Inc. IC pressure = increased sig. Symptoms: e.g., lethargy, stupor, bifrontal and bioccipital headaches (unaffected by analgesic meds), vomiting, imbalance.

28. Symptoms Determined by Cell Type and Growth Rate • Gliomas: most common form---2 particular types are astrocytoma and glioblastoma multiforme • Astrocytoma: usually benign, slow growth, 5-6 year development • Glioblastoma Mul.: a most malignant and rapidly growing intracranial mass • Develops in 3-12 mo.—average postsurgical survival is only 6-9 months

29. More IC Tumors--Primary • Meningioma: arise from the ________?? • Most benign of all, very slow growing, well-defined margins, usually don’t invade brain substance • Can usually be completely removed • Symptoms are usually site specific

30. Secondary Intracranial tumors • Metastatic carcinoma---cells have migrated—usually passed by bloodstream • Prognsosis is poor: mean survival rate: 2-6 mo. • Primary sources of Met. CA are: • Breast—most frequent occurrence • Lung • Pharynx/larynx---least frequent occurrence.

31. Other causes of brain impairment • Hydrocephalus –enlargement of the cerebral ventricles • Obstructive hydrocephalus • IVP—intraventricular shunt---VP shunt • Infections: abscesses and meningitis • brain abscess –introduction of bacteria, fungus or parasites into brain tissue from infection site somewhere in the body • 40% of sources are nasal sinuses, ME and mastoid cells

32. Viral infections • 2 common sources: • General infections (mumps/measles) and viruses transmitted by bites (animal or insect) • Equine encephalitis and rabies • Progression depends on the virus • Slow: Jakob-Creutzfeld v. (Bovine Spongiform Encephalitis) • Rapid: AIDs • Tx is palliative: tx. Vital signs, nutrition, fluid balance to help system rid virus

33. Toxemia • Due to substances invading the NS that inflame or poison nerve tissue • May result from: drug overdoses or interactions, bacterial toxins (tetanus, botulism, diphtheria) or heavy metal poisoning (lead and mercury)----WTC??? • TX is to remove the substance

34. Metabolic and Nutritional Disorders • Metabolic: rarely cause specific communication disorders • Severe hypoglycemia can cause cerebral dysfunction • Nutritional: rare in the USA • Wernicke’s Encephalopathy: thiamine deficiency, usually associated with alcoholism • Paralysis of eye muscles, incoordination, poor gait, mental confusion

35. Fluent Wernicke’s Conduction Transcortical Sensory NonFluent Broca’s Transcortical Motor Global Other forms: Anomic Alexia and Agraphia Primary Progressive Aphasias

37. Post Stroke Considerations • Acute therapy • Focuses on preservation of life and preventing further expansion of injury due to the stroke • Chronic Therapy • Rehabilitation with goal to reestablish the most normal lifestyle as possible

38. Acute Therapy • After ischemic stroke, the area of infarction is surrounded by tissue that will either recover or die: the ischemic penubra • Routine tx have been vasodilators: inc. cerebral blood flow and to inc. arterial pressure (to increase blood into the area of infarct, and; • Corticosteroids used to reduce swelling of the brain

39. These “neuroprotective” measures have not been protective; most medical (acute) treatments for ischemic stroke have been limited to preservation of life • Until 1995: National Institute of Neurological Disorders and Stroke (NINCDS) study on t-PA

40. Tissue Plasminogen Activator “t-PA” • A clot-buster: delivered intravenously; breaks up the clot allowing blood flow to return to the deprived area of the brain • NINCDS found pts who rec’d t-PA within 3 hours of symptom onset have better recovery at 3 months post onset • Negative finding: after 36 hours there was in an increased incident of intracerebral hemorrhage (6.4%) • Mortality of t-PA group was lower after 3 months post

41. 1996, t-PA approved • For acute ischemic stroke, if • Administered within 3 hours of stroke; • No sign of intracerebral hemorrhage as confirmed by CT; • No previous stroke or head trauma in 3 mo prior to dose; • No major surgery in past 14 days before stroke; • No hx of subarachnoid or intracranial hemorrhage; • No hx of hypertension • No hx of GI or urinary tract hemorrhage, and---

42. No history of anticoagulant meds • Heparin and Coumadin (Warfarin)

43. IF criteria for t-PA were not met? • Tx requires identification of etiology or locating the blockage in the internal carotid or heart • If carotid: tx of etiology is to remove thrombus via Carotid Endarterectomy (CAE), or via antiplatlets, e.g., aspirin • If heart (cardiogenic): Coumadin or Heparin are administered

44. Chronic Therapy: “Rehabilitation” • Begins when pt is medically stable; initial goal: ambulate, communicate and ADLs • 2nd goal: stimulate sph production and language use via social interactions

45. Rehabilitation team • Physiatry,nursing, social services, psychology and, PT, OT, SLP and vocational tx • Settings: rehabilitation unit (inpatient), SNF, outpatient clinic, or at home. • Rehab unit qualifier: pt must be able to handle 3 hours of activity per day • BBA of 1997? Fiduciary Cap.

46. American Heart Association • 6 major areas of stroke rehab: 1: handle concurrent illnesses and complaints 2: maximize independence 3: maximize psychosocial coping of family 4: promote reintegration 5: improve quality of life 6: prevent recurrent vascular events

47. Primary Indicator of Recovery? • Severity of neurological impairment. • The more severe the damage and subsequent impairments, the longer the hospital stay, the more complicated the treatment plan, the longer the recovery process • Degree of communication impairment: global aphasia or hemineglect tend to perform poorly in rehab

48. Contraindicators of Rehabilitation • Psychiatric Disorders; • Dementias, Apathy Syndrome, Negative Symptom Complex • Not a functional loss: these conditions have less ambition, less motivation, poor effort to succeed, etc.