Transcript Document 7417067

“Brain Attack”
Cerebrovascular Accident
Or
“Stroke”
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.
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
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)
Uncontrollable Stroke Risk Factors Include:
Age
The 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 Factors
Gender
Males 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.
Race
African-Americans have a higher stroke risk than most other
racial groups.
Family history of stroke or TIA
Risk 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.
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 Apnea
Sleep 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.
Lifestyle Factors that Increase Stroke Risk Include:
•Smoking
Smoking 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.
•Alcohol
Excessive 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.
•Weight
Excess 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.
The Impact of Stroke Risk Factors
• 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)
• 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
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
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
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”
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
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!
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
Hemorrhages
• Extracerebral
hemorrhages—
bleeding outside of the
brain
– Subarachnoid
– subdural
– extradural
• Intracerebral
hemorrhages
– Within brain substance
bleed
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
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
Berry Aneurysm
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
AVF
• Greatest risk is the
potential for
rupture and
subsequent
hemorrhage
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?
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.
Intracranial tumors, cont.
• Inc. IC pressure = increased sig. Symptoms:
e.g., lethargy, stupor, bifrontal and
bioccipital headaches (unaffected by
analgesic meds), vomiting, imbalance.
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
More IC Tumors--Primary
• Meningioma: arise from the ________??
– Most benign of all, very slow growing, welldefined margins, usually don’t invade brain
substance
– Can usually be completely removed
– Symptoms are usually site specific
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.
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
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
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
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
Aphasias
• Fluent
– Wernicke’s
– Conduction
– Transcortical Sensory
• NonFluent
– Broca’s
– Transcortical Motor
– Global
• Other forms:
– Anomic
– Alexia and Agraphia
– Primary Progressive
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
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
• 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
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
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---
• No history of anticoagulant meds
– Heparin and Coumadin (Warfarin)
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
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
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.
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
Primary Indicator of Recovery?
1) 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
2) Degree of communication impairment:
global aphasia or hemineglect tend to
perform poorly in rehab
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.