STROKE
„ Stroke is an injury to
the brain caused
by occlusion or rupture of a cerebral
artery
„ Third most common cause of death &
most leading cause of adult disability
„ Challenges of stroke prevention & care
are particularly compelling for
geriatricians
„ Most significant risk factor for stroke is
AGE
Prof. DAHAB
Stroke
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MAJOR CATEGORIES OF
STROKE
ISCHEMIC STROKE: Results
from thrombosis (65%) or
embolism (25%)
2. HAEMORRHAGIC STROKE: Due
to intracerebral hemorrhage
(95%) or subarachnoid
hemorrhage (5%)
1.
Prof. DAHAB
Stroke
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MODE OF ONSET
THROMBOTIC: variable onset,
preceded by TIA’s ± step-wise
(stroke in evolution)
„ EMBOLIC: Sudden with maximal
deficit from start
„ INTRACEREBRAL HGE: Sudden
onset + ⇑ BP & during activity
„ SAH: Sudden crushing headache
proceeds to coma
„
Prof. DAHAB
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MAJOR CLINICAL SYNDROMES
OF STROKE
„MCA
„ACA
„PCA
„ICA
„VBA
Prof. DAHAB
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MCA
„ Contra
lateral hemiplegia +
hemilyposthene.
„ Contra lateral homonymous
hemiaropia
„ APHASIA (dominant hemisphere)
„ AFFECTIVE DISTURBANCE (non
dominant hemisphere)
„ NEGLECT: Failure to respond to
contra lateral stimuli
Prof. DAHAB
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ACA
„ Contra
lateral leg/foot
paralysis
„ Gait disturbances
„ Ideomotor apraxia
„ Preservation
„ Urinary incontinence
Prof. DAHAB
Stroke
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PCA
„ Contra
lateral hemiparesis &
hemihypothesia
„ Contralateral homonymus
hemianopia
„ Memory impairment
„ Dyslexia
„ Brain stem signs: 3rd, cranial
nerve palsy ± ataxia
Prof. DAHAB
Stroke
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ICA
„ Transient
monocular blindness
„ Homonymus hemianopia
„ Aphasia (dominant hemisphere)
„ Neglect (non-dominant
hemisphere)
„ Signs of MCA, ACA, ± PCA
ischemia
Prof. DAHAB
Stroke
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VBAs
– Ipsilateral cerebellar ataxia ±
nystagmus
– Nausea & vomiting ± vertigo
– Contralateral hemiplegia &
hemihyposthesia
– Intranuclear opthalmoplegia ±
deafness
– “Locked-in” syndrome (conscious
+ quadriplegia)
Prof. DAHAB
Stroke
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LACUNAR SYNDROMES
„ Pure
motor hemiparesis
„ Pure sensory stroke
„ Dysartheria / clumsy hand
syndrome
„ Hemichorea / hemiballismus
„ Homolateral ataxia & crural
paresis
Prof. DAHAB
Stroke
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STROKE AETIOLOGY
„
„
„
„
„
THROMBOTIC: Atherosclerotic plague ±
polycythemia.
EMBOLIC: Cardiac source or
atherosclerotic plagues
INTRACEREBRAL HGE: Rupture penetrating
vessels by HTN or hemorrhagic conversion
of infarct
SUBARACHNOID HGE: Cerebral aneurysm
± AVM
LACUNAR STROKE: AGE, DM & HTN
Prof. DAHAB
Stroke
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DD of TIAs or STROKE
„
„
„
„
„
„
„
„
„
„
Seizures
Syncope
Migraine
Subdural hematoma
Brain tumor
Hypoglycemia
Demyelinating disease
Brain abscess
Encephalitis
Panic attacks
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Non-Modifiable Risk Factors
„Age
„Male
„Africans
„Hereditary
Prof. DAHAB
Stroke
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MODIFIABLE RISK
FACTORS
„ Hypertension
„ AF
„ DM
„ Smoking
„ Hyperlipidemia
4 times
16 times
4 times
2 times
& physical inactivity (uncertain)
Prof. DAHAB
Stroke
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OTHER POTENTIAL RISK
FACTORS
„Atrial septal aneurysm
„Patent foramen ovale
„Aortic arch atheroma
„Anticardiolipin antibodies
„Chronic inflammation
Prof. DAHAB
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OPTIONS for PRIMARY
PREVENTION
„Coronary
artery disease
„HTN
„DM
„Hyperlipidemia
„Tobacco
abuse
„Obesity
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ANTICOAGULATION in
PRIMARY PREVENTION?
„ Cardiac
source for embolic stroke
e.g. AF ⇒ Warfarin
„ People over 75 share in
decreased risk of embolization
„ Antiplatelet therapy with aspirin
325 mg daily ⇒ ⇓ Risk of stroke
with AF ⇒ Half efficacy than
Warfarin
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Initial management of
acute stroke
„
„
„
„
Rapid clinical evaluation ⇒ Thrombolytic
therapy: tissue-type plasminogen activator
<3 hours
Emergency ECG, chest X-ray, CBC,
bleeding profile, ESR & ABG
Distinguish hge from infarction ASAP ⇒
noncontrast CT & urgent interpretation
Diffusion-weighted MRI & perfusion imaging
⇒ detect within min the territory
undergoing ischemia
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Initial management of acute
stroke (Cont’d)
„
„
„
BP should not lowered unless >220/120 or
heart failure in ischemic infarction
whereas in hgic stroke, lower it to average
TTT of hypoglycemia or hyperglycemia
>180 mg%, O2 for hypoxemia, monitor for
cerebral edema & seizures
Stroke units: save lives & improves
outcome. They should be used if available
Prof. DAHAB
Stroke
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THROMBOLYTIC
TREATMENT
„
„
1.
2.
3.
4.
5.
Stroke recognition : pt + family +
emergency services
Should be offered if:
Diagnosis of acute ischemic stroke
Interval between onset & TTT <3 hours
Acute focal neurological deficit
Neurologist is consulted & participates in the
treatment
Brain CT Scan is obtained & interpreted by
expertise
Prof. DAHAB
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THROMBOLYTIC TREATMENT
(Cont’d)
„ SHOULD
NOT BE OFFERED IF:
1.Time
of onset is unclear
2.BP > 185/110
3.CT Scan shows evidence of hge
4.Neurologic deficits improve
spontaneously
5.Risk for hge
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TIA’s: DIAGNOSIS &
MANAGEMENT
„ TIA’S
are warning signs of stroke.
Management prevents disability &
death
„ Rate of stroke after TIA is 50% in 2
yrs, 70% of them in the 1st year.
„ Risk is very high for stroke in the
first 10 days after TIAs ⇒ URGENT
EVALUATION
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DIAGNOSTIC WORK-UP
„
„
„
„
„
„
„
„
„
Based on age, presentation, risk factors & intent
to treat
Head CT
Noninvasive carotid artery evaluation
TCD
MRI & MRA
Coagulopathy tests: protein C & S, antiphospholipid
Abs, antithrombin III deficiency
LP in suspected SAH with nondiagnostic CT
Early angiography for aneurysm repair
PET & SPECT
Prof. DAHAB
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ROLE OF ANTICOAGULATION
„
„
„
„
„
Preventing recurrent cardioembolic stroke
AF, recent MI, valvular disease, patent FO
Heparin for 48 hrs before replaced by
Warfarin
Aspirin alone ⇓ risk of further AF emboli
Anticoagulation is of no benefit in
completed stroke
Prof. DAHAB
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ROLE OF NEURO-PROTECTIVE
AGENTS
„ Potential
role in interrupting the
cascade of molecular events leading to
neuron death
„ Ca Ch. Blockers, glutamate
antagonists, Na Ch. Blockers, glycine
antagonists, Opioid antagonists &
antioxidants / free radical scavengers
„ Little evidence in ⇓ size of infarction
& improving outcome
Prof. DAHAB
Stroke
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COMPLICATIONS OF ACUTE
STROKE
„
„
„
„
„
„
„
DVT
Pulmonary embolism
Aspiration pneumonia
Urinary tract infection
Decubitus ulcers
Neurologically: Cerebral edema + seizures
+ hgic transformation
Brain stem herniation: TTT by
hyperventilation, osmotic therapy or even
surgery. Steroids are not effective.
Prof. DAHAB
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CAROTID ENDARTERECTOMY
„ Decreases
risk of subsequent stroke
„ Confirmed stenosis >70%
„ No benefit in patients with <50 %
„ Consider surgical skill
„ 50-70% : individualized decision
(ulcerated plaque)
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Stroke
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Carotid Endarterectomy
„⇑
risk of complications with ⇑
age
„ Safe & effective as for
general population
„ In prohibitive surgery ⇒ TTT
with antiplatelet agents
Prof. DAHAB
Stroke
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MEDICAL THERAPY
agents: Aspirin ⇒ 25% ⇓ risk
„ Optimal dose: ranging from 30mg-1300mg
„ Ticlopidine & Clopidogrel: Two other
platelet antiaggregants for 2ry prevention
of stroke proved to be more effective than
Aspirin
„ Warfarin for prevention is unclear
„ Dipyridamol & sulfinpyrazone ⇒ no effect
„ Antiplatelet
Prof. DAHAB
Stroke
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REHABILITATION AFTER
STROKE
„ Great
proportion of patients survive
with substantial neurologic
impairment
„ Goal of rehabilitation is not cure but
rather adaptation to functional
handicap
„ To maximize function in the service
of enhancing quality of life
„ Physiatrist, physical therapist,
occupational therapist and/or speech
therapist
Prof. DAHAB
Stroke
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REHABILITATION AFTER STROKE
(Cont’d)
„
„
„
Mild deficits do not need specialized
rehabilitation services whereas patient
who are stuporous, immobile, cognitively
impaired or severely ill derive little benefit
Success of rehabilitation efforts depends
on neurological deficit, cognition, patient
& family goals, social & psychological
support
Age is not a factor for rehabilitation
outcome
Prof. DAHAB
Stroke
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DEPRESSION AFTER STROKE
„ Mood
disturbances are common due to
physical & psychological factors
„ Depression plays a critical role in
patient’s recovery. Prevalence : 25%
to 50% (under-diagnosed)
„ TTT with SSRI’s e.g. Sertraline,
Paroxetine & Flextime
„ Delirium with agitation & emotional
incontinence distress patient, family &
caregivers
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maggodd@yahoo.com
Thank you
Prof. DAHAB
Stroke
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Stroke
Prof. Magdy Dahab, MD
Azhar University
May 11th, 2006