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Title Brain Attack Author: Peter Lapine Last modified by: Dr. Peter LaPine Created Date: 1/9/2002 11:25:05 PM Document presentation format – PowerPoint PPT presentation

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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.

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  • 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)

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  • Ischemicdeprived of blood
  • Sometimes called occlusive
  • Hemorrhagiccaused 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
Ischemic Stroke
  • 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

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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
Hemorrhages
  • Extracerebral hemorrhagesbleeding outside of the
    brain
  • Subarachnoid
  • subdural
  • extradural
  • Intracerebral hemorrhages
  • Within brain substance bleed

19
Intracerebral Hemorrhage
  • 90 occur in pts with high BP
  • Cause(s) hypertentionpressure on arterial walls
    or chronic hypertensionweakening of small
    penetrating arteries causing microaneurysms
  • Can cause snowball effect as the hemorrhage
    affects adjacent vessels

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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

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Berry Aneurysm
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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 familieshypothesis?

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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.

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

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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 dont invade brain
    substance
  • Can usually be completely removed
  • Symptoms are usually site specific

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

31
Other causes of brain impairment
  • Hydrocephalus enlargement of the cerebral
    ventricles
  • Obstructive hydrocephalus
  • IVPintraventricular 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

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

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Aphasias
  • Fluent
  • Wernickes
  • Conduction
  • Transcortical Sensory
  • NonFluent
  • Brocas
  • Transcortical Motor
  • Global
  • Other forms
  • Anomic
  • Alexia and Agraphia
  • Primary Progressive

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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

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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

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  • 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 recd 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---

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

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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

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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

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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.
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