Hemorrhagic stroke, 431
Ischemic stroke, 434.91
Stroke/brain attack, 434.91
Transient ischemic attack, 436
I. Definition
A. Classic definition: sudden or rapid onset of neurologic deficit caused by focal ischemia that lasts for a few minutes and resolves completely within 24 hours
B. Recently proposed revision of classic definition: brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour and no evidence of acute infarction
II. Etiology/incidence/prevalence
A. Incidence is 160/100,000; prevalence is 135/100,000.
B. Carotid or vertebral artery disease
C. Cardiac emboli as seen in arrhythmia (atrial fibrillation), myocardial infarction, congestive cardiomyopathy, and valvular disease
D. Hematologic causes
1. Red blood cell (RBC) disorders
a. Increased sludging
b. Decreased cerebral oxygenation such as in severe anemia
c. Polycythemia, sickle cell anemia
2. Platelet disorders
a. Thrombocytosis
b. Thrombocytopenia
4. Increased viscosity/hypercoagulable conditions
a. Antiphospholipid antibody syndrome (e.g., lupus anticoagulant, anticardiolipin antibody)
b. Oral contraceptive use
c. Antithrombin III deficiency
d. Protein S and C deficiency
e. Tissue-type plasminogen activator (t-PA) and plasminogen deficiencies
f. Patients particularly at risk for a hypercoagulable state
i. Older than age 45
ii. History of thrombolytic event
iii. History of spontaneous abortion
iv. Related autoimmune conditions (e.g., lupus)
v. Stroke of unknown cause
vi. Family history of thrombotic events
E. Intracranial causes
1. Brain tumor
2. Focal seizure
3. Hemorrhage
a. Subdural hematoma (SDH)
b. Subarachnoid hemorrhage (SAH)
c. Intra cerebral hemorrhage (ICH), which may cause cerebrovascular dysfunction due to leakage of blood outside the normal vessels
F. Subclavian steal syndrome
1. Localized stenosis or occlusion of a subclavian artery proximal to the source of the vertebral artery, so that blood is stolen from that artery
2. Blood pressure is significantly lower in the affected arm than in the opposite arm.
G. Others
1. Transient hypotension
2. Osteophytes that cause compression of neck vessels
3. Kinking of neck vessels during rotation of the head
4. Cocaine abuse
5. Hypoglycemia
III. Risk factors
A. TIA: Individuals are at risk for stroke in the months, as well as the years, immediately after the initial TIA; therefore, proper treatment of attacks is important. Approximately one third of stroke patients have a history of TIA.
B. Hypertension
C. Cardiac disease, such as the following:
1. Mitral valve disease
2. Anterior wall myocardial infarction
4. Arrhythmia (e.g., atrial fibrillation)
D. Smoking
E. Obesity
F. Hyperlipidemia
G. Elevated homocysteine levels in the elderly
H. Advanced age
I. Diabetes
J. Alcohol and recreational drug abuse
IV. Clinical manifestations
A. Carotid artery syndrome
1. Ipsilateral monocular blindness (amaurosis fugax) described as similar to a shade coming down over one eye
2. Paresthesia/weakness of contralateral arm, leg, and face (may be episodic)
3. Dysarthria, transient aphasia
4. Ipsilateral, vascular-type headache
5. Carotid bruit may be present.
6. Microemboli, hemorrhage, and exudate may be visualized in the ipsilateral retina.
B. Vertebrobasilar artery syndrome
1. Visual disturbance bilaterally (blurred vision, diplopia, complete blindness)
2. Vertigo, ataxia, tinnitus
3. Nausea and/or vomiting
4. Sudden loss of postural tone in all extremities while consciousness remains intact (drop attacks)
5. Dysarthria
6. Perioral or facial paresthesia
7. Acute confusional state
V. Diagnostics/laboratory findings
A. Laboratory evaluation should include the following:
1. Complete blood count (CBC), platelet count, prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR) to detect these conditions:
a. Anemia
b. Polycythemia
c. Leukemia
d. Thrombocytopenia
e. Hypercoagulopathy
2. Anticardiolipin antibodies (immuno globulin [Ig]G, IgM, IgA) and assay for lupus anticoagulant for suspected antiphospholipid antibody syndromes
3. Assays for antithrombin III, proteins S and C, plasminogen, and t-PA
5. Sedimentation rate, to detect these conditions:
a. Vasculitis
b. Infective endocarditis
c. Hyperviscosity
d. Giant cell arteritis
6. Lipid profile
a. Detects hyperlipidemia
7. In selected patients, antinuclear antibody (ANA), Venereal Disease Research Laboratory test (VDRL), and toxicology screen
8. Homocysteine level
a. An amino acid
b. Elevated plasma level associated with increased risk of vascular events
B. Computed tomography (CT) scan of the head
1. May reveal “silent” ischemia or ischemic images, as well as hemorrhage or infarct and SDH
2. 10% to 20% of patients with TIAs have an infarct in the territory relevant to their symptoms.
C. Magnetic resonance imaging (MRI), particularly diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI)
1. More sensitive than CT scan to early pathologic changes of ischemic infarction because of its excellent detection of brain edema
2. MRI is also preferred for the detection of lacunar or vertebrobasilar TIAs, or when vascular territory is not well defined.
D. Single photon emission computed tomography (SPECT)
1. Injection with 99mTc-labeled agent
2. Multiple views of emission projection data
3. Essentially, a VQ (ventilation/quantification) scan of the brain
E. Duplex ultrasonography
1. 85% sensitivity and 90% specificity
2. Useful in identifying hemodynamically significant carotid stenosis
F. Magnetic resonance angiography (MRA)
1. Alternative to ultrasound studies
2. No contrast medium is needed.
3. Can be obtained at the same time as an MRI scan
4. Good means for assessment of extracranial and intracranial vessels
G. Carotid Doppler ultrasound has limited usefulness.
H. Echocardiography and a 24-hour Holter monitor are used to evaluate for a cardiac source of emboli.
J. Cerebral angiography for patients whose symptoms suggest involvement of the carotid circulation and who are candidates for carotid endarterectomy (CEA)
K. Chest x-ray for enlarged heart
L. Blood cultures to monitor for infective endocarditis
M. Temporal artery biopsy to detect giant cell arteritis
N. Cardiac enzymes to detect an acute myocardial infarction
O. Electroencephalography (EEG) indicated in patients suspected of having a seizure disorder associated with stroke, as well as an underlying toxic-metabolic disorder that may cause seizure activity
VI. Management
A. Address the following underlying risk factors:
1. Hyper tension (HTN)
2. Diabetes mellitus (DM)
3. Obesity
4. Hyperlipidemia
5. Smoking
B. Carotid TIAs
1. Greater than 70% obstruction: CEA is indicated for those who are a good surgical risk.
2. Less than 30% obstruction: Surgery is not indicated.
3. Recently, carotid angioplasty and stenting (CAS) has emerged as an alternative in high-risk surgical patients, or when CEA is contraindicated for technical or medical reasons.
C. Anticoagulation if caused by a cardioembolic event
1. May prevent recurrent cardioembolic events
2. Begin with heparin (loading dose of 5000-10,000 units for those not at risk for hemorrhagic transformation and maintenance infusion of 1000-2000 units/hour).
3. Target PTT should be 1.5 times control.
4. Follow with warfarin (Coumadin), 5-15 mg PO (per os; by mouth), which is indicated for the following:
a. TIA caused by embolism arising from a mural thrombus after a myocardial infarction (MI)
b. TIA caused by embolus in patients with mitral stenosis or prosthetic heart valves
c. Recurrent TIAs despite platelet antiaggregant agents
d. INR of 2 to 3 is considered therapeutic.
D. Antiplatelet therapy is useful for patients who are not candidates for surgery or warfarin therapy (those with gastrointestinal [GI] bleeding, bleeding tendencies, or severe hypertension, elderly patients who fall frequently, or uncooperative patients).
2. Clopidogrel (Plavix)
a. Antiplatelet agent that is a chemical relative of ticlopidine (Ticlid)
b. Causes far fewer adverse hematologic effects
c. May cause thrombotic thrombocytopenia purpura (TTP) during the first 2 weeks of treatment
d. Indicated for secondary prevention of ischemic stroke, MI, and other vascular events in patients who cannot tolerate ASA, or in patients who were taking ASA at the time of the event
e. Dosage is 75 mg/day PO.
3. Combined dipyridamole (Persantine) (200 mg extended release) and ASA (25 mg immediate release)
a. Available as fixed-dose formulation under the trade name Aggrenox
b. Both drugs suppress platelet aggregation but do so through different mechanisms.
c. Combination treatment is more effective than either drug alone.
d. Recommended dose is 2 capsules daily—1 in the morning and 1 at night.
e. Significantly more expensive than ASA therapy: approximately $90/month versus $3/month for ASA therapy alone
STROKE/BRAIN ATTACK
I. Definition
A. Rapid onset of a neurologic deficit involving a certain vascular territory and lasting longer than 24 hours
B. A stroke-in-evolution is an enlarging infarction manifested by neurologic defects that increase over 24 to 48 hours.
C. Stroke is the leading cause of disability and the third leading cause of death in the U.S.
D. Stroke can be classified as ischemic and hemorrhagic.
E. 80% of strokes are caused by blood clots that produce ischemic areas in the brain; remaining strokes are caused by intracerebral hemorrhage.
II. Etiology and risk factors
A. Same as for TIA
B. Cocaine-related stroke is increasingly common.
C. Women who use oral contraceptives and who smoke are at high risk.
D. Hyperlipidemia raises the risk of ischemic stroke.
E. Low cholesterol increases the risk of hemorrhagic stroke.
I. Etiology
A. Caused by a thrombus (30%)
1. Progression of symptoms over hours to days
2. Patients often have a history of TIA.
3. This often occurs during the night while the patient is sleeping; the patient may completely infarct and may be unarousable in the morning.
4. Patient may awaken with a slight neurologic deficit that gradually progresses.
5. Predisposing factors
a. Atherosclerosis
b. HTN
c. DM
d. Arteritis
e. Vasculitis
f. Hypotension
g. Trauma to the head and neck
B. Caused by embolism (25%)
1. Very rapid onset
2. History of TIA uncommon
3. Patient is usually involved in an activity when symptoms occur.
4. Predisposing factors
a. Atrial fibrillation
b. Mitral stenosis and regurgitation
c. Endocarditis
d. Mitral valve prolapse
II. Clinical manifestations (depend on the cerebral vessel involved)
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A. Middle cerebral artery
1. Hemiplegia (involves upper extremity and face more often than lower extremity)
2. Hemianesthesia
3. Hemianopia (blindness of half the field of vision)
4. Eyes may deviate to the side of the lesion.
5. Aphasia if dominant hemisphere is involved
6. Occlusions of various branches of the middle cerebral artery may cause different findings (involvement of the anterior division may cause expressive aphasia, and involvement of the posterior branch may produce receptive aphasia).
B. Anterior cerebral artery
1. Hemiplegia (lower extremity more often than upper extremity)
2. Primitive reflexes (such as thumb sucking)
3. Urinary incontinence
4. Bilateral anterior infarction may cause behavioral changes and disturbance in memory.
