STROKE

WHAT IS STROKE?
• Sudden onset of neurologic deficit from
vascular mechanism:
– 85% are ischemic
– 15% are primary hemorrhages (subarachnoid and
parenchymal)
• TRANSIENT ISCHEMIC ATTACK
- Ischemic disease that resolves rapidly
- 24 hour is commonly used boundary between TIA and
stroke whether or not a new infarction has occurred
- Most TIA last between 5-15 minutes
• Stroke is the leading cause of neurologic
disability in adults; 200,000 deaths anually in
US.
In the PHILIPPINES

Source: Department of Health

 Pathophysiology
Ischemic stroke is most often due to embolic occlusion of
large cerebral vessels; source of emboli may be heart, aortic
arch, or other arterial lesions such as carotid arteries.
 CLASSIFICATION BASED ON
ETIOLOGY ICTUS SEVERITY
(TIME FROM
STROKE
ONSET)
• ISCHEMIC (80- • Hyperacaute (0-6 • Mild (NHISS 0-5)
85%): h) • Moderate (NIHSS
atherothrombotic • Acute (6-72 h) 6-21)
, embolic (cardiac • Subacute (3 days • Severe (NIHSS
or artery-to- to 3 weeks) >22)
artery), or lacunar • Chronic (>3
• Hemorrhagic (10- weeks)
15%)
• Small, deep ischemic lesions are most often
related to intrinsic small-vessel disease
(lacunar strokes).
• Hemorrhages most frequently result from
rupture of aneurysms or small vessels within
brain tissue.
• If blood flow is restored prior to significant cell
death, the patient may experience only
transient symptoms.
 Clinical Features
ISCHEMIC STROKE
- abrupt and dramatic onset of focal neurologic
symptoms
- patients are rarely in pain and may loose
appreciation that something is wrong (anosognosia).
- symptoms reflect the vascular territory involved.
- transient monocular blindness ( amaurosis
fugax)
LACUNAR SYNDROMES (small vessel strokes)
most common are:
- pure motor hemiparesis of face, arm and
leg (internal capsule or pons)
- pure sensory stroke (ventral thalamus)
- ataxic hemiparesis (pons and internal
capsule)
- dysarthria – clumsy hand ( pons or genu
of internal capsule)
INTRACRANIAL
HEMORRHAGE
- vomiting and
drowsiness occur in
some cases, and
headache in about one-
half.
- signs and symptoms
are often not confined
to a single vascular
territory.
- hypertension-
related is the most
common etiology
Hypertensive hemorrhages typically occur in the
following locations:
• Putamen: contralateral hemiparesis often with
homonymous hemianopsia
• Thalamus: hemiparesis with prominent
sensory deficit.
• Pons: quadriplegic, “pinpoint pupils” impaired
horizontal eye movements
• Cerebellum: headache, vomiting, gait ataxia
A neurologic deficit that evolves
gradually over 5-30 minutes
strongly suggest intracerebral
bleeding.
 Deep venous thrombosis prophylaxis
Physical ， occupational ， speech therapy
Evaluate for rehab ， discharge planning
Secondary prevention based on disease
 Treatment
• IMAGING: after initial stabilization, an
emergency non contrast head CT scan is
necessary to differentiate ischemic from
hemorrhagic stroke.

– With large hemorrhagic strokes, ct abnormalities

are usually evident within the first few hours
ACUTE ISCHEMIC STROKE
Treatment designed to reverse or lesses
tissue infarction include:
• Medical support
• Thrombolysis and cardiovascular techniques
• Antiplatelet agents
• Anticoagulation
• Neuroprotection
 Medical support
• Optimize perfusion in ischemic penumbra
surrounding the infarct
 BP should never be lowered precipitously
 Intravascular volume should be maintained with isotonic
fluids as volume restriction is rarely helpful. Osmotic therapy
with mannitol may be necessary to control edema in large
infarcts, but isotonic volume must be replaced to avoid
hypovolemia
 In cerebellar infarction (or hemorrhage) rapid deterioration
can occur from brainstem compression and hydrocephalus,
requiring neurosurgical intervention.
Thrombolysis and endovascular techniques

• Ischemic deficits of <3 hour duration, with no

hemorrhage by CT criteria, may benefit from
thrombolytic therapy with IV recombinant
tissue activator
• Ischemic stroke from large-vessel intracranial
occlusion results in high rates of morbidity ad
mortality; patients with such occlusions may
benefit from intraarterial thrombolysis (<6 h
duration) or embolectomy (<8 h duration)
 Acute intracerebral hemorrhage
• Noncontrast head CT will confirm diagnosis
• Rapidly identify and correct any coagulopathy
• Stuporous or comatose patients generally are
treated presumptively for elevated ICP.
Primary and secondary prevention of stroke

Risk factors
ATHEROSCLEROSIS is a systemic disease
affecting arteries throughout the body. Multiple
factors including hypertension, diabetes,
hyperlipidemia, and family history influence
stroke and TIA risk.
 Antiplatelet agents
• Inhibits the formation of intraarterial platelet
aggregates.
• ASPIRIN (50-325 mg/d) inhibits thromboxane
A2
 Carotid revascularization
• CAROTID ENDARTERECTOMY
– Benefits many patients with symptomatic severe
(>70%) carotid stenosis; the relative risk reduction
is 65%.
– Endovascular stenting is an emerging option.