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Clinical Presentation of

Cerebrovascular Disease
David Griesemer, MD
Department of Neurosciences
Medical University of South Carolina
Presentation Outline
Stroke from the patients perspective
Definition of transient ischemic attacks
Classic presentations of stroke types
Focus on lacunar strokes
Prevention pearls
Diagnostic pitfalls
The Patient Perspective
Stroke Statistics
15% of adults > age 50 cannot name a
single symptom of stroke

13 hours after onset of symptoms is the
median time to presentation

58% of stroke patients dont present during
the first 24 hours after onset

52% of stroke patients in the ED are
unaware that they are experiencing a stroke
Stroke Knowledge
MYTHS

Cant prevent stroke
Cant treat stroke
Stroke affects the heart
Stroke affects the elderly
Recovery happens for a
few months after stroke

FACTS

Stroke is preventable
Stroke is treatable
Stroke is a brain attack
Stroke affects anyone
Stroke recovery occurs
throughout life
Stroke Symptoms
Sudden numbness or weakness of face, arm or leg,
especially on one side of the body

Sudden confusion, trouble understanding or
speaking

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 Symptoms
Sudden nausea, fever and vomiting,
distinguished from a viral illness by rapid onset
(minutes or hours vs. days)

Brief loss of consciousness or period of
decreased consciousness
(fainting, confusion, convulsions or coma)
The Three Rs for Brain Attack
Reduce risk

Recognize symptoms

Respond by calling 911
TIA: The First Clue
Transient Ischemic Attack
Sudden, focal neurologic deficit lasting less
than 24 hours, confined to an area of the
brain or eye perfused by a specific artery.

Based on assumption that TIAs do not
cause infarction or other permanent brain
injury.

Time criterion is arbitrary.
Problems with TIA Definition
Most TIAs last seconds to 10 minutes, with
symptoms lasting greater than 1 hour in only 25%
of patients

Less than 15% of patients with symptoms lasting
> 1 hour resolve within 24 hours

Following TIAs, evidence of infarction is found in
20% by CT imaging and almost 50% with MRI

The 24-hour rule leads to complacency and delay.
Tissue Definition of TIA
A TIA is a brief episode of neurologic
dysfunction caused by focal brain or retinal
ischemia, with clinical symptoms typically
lasting less than one hour, and without
evidence of acute infarction.

Parallel to distinction between angina and
myocardial infarction (i.e. depends on the
absence of tissue injury rather than the
resolution of symptoms)

Advantages
Acknowledges that transient neurologic
symptoms may cause permanent brain injury

Supports rapid intervention to diagnose and
treat acute brain ischemia

More accurately reflects the presence or
absence of brain infarction

Avoids assigning an arbitrary time criterion to
define TIA
TIA - Differential Diagnosis
Anxiety (panic attack)
Hyperventilation
Neuropathy (focal)
Neuropathy (ischemic)
Vertigo
Disequilibrium
Migraine
Orthostatic hypotension
Syncope
Arrhythmias (ischemia)
Seizures
Conversion disorder
TIA v. Dizziness
Isolated symptom unlikely to be
ischemic (true also for blurred vision or
diplopia)

Evidence of brainstem dysfunction
Ataxia or nystagmus
Cranial nerve abnormality
Contralateral corticospinal tract abnormality

TIA v. Migraine
Onset in middle age
Aura without headache
Dysfunction in periaqueductal gray region of
brainstem, not vascular

Progressive visual scintillation affecting both
eyes
Stereotypic episodes or positive family history,
especially with familial hemiplegic migraine
Stroke: The Initial Symptoms
Clinical Presentations of Stroke
Focal ischemia (85%)
Embolism
Thrombosis

Hemorrhage (15%)
Epidural
Subdural
Intraparenchymal
Cerebral Ischemia
Embolism

Abrupt onset
Small vascular area
Focal deficit
Pure aphasia
Pure hemianopia
Acute CT normal
High recurrence risk
Thrombosis
Preceded by TIAs
Abrupt onset
Large vascular area
More complex symptoms


Acute CT normal


Cerebral Hemorrhage
Epidural hemorrhage
Smooth onset
Arterial origin
Mass effect causes
coma over hours
Similar (but slower
in evolution) to
hemorrhage in
basal ganglia
Subdural hemorrhage
Smooth onset
Venous origin
May be recurrent
Fluctuating, falsely
localizing signs
Remember Lacunar Strokes
Lacunar Strokes
15 20% of ischemic strokes
Small penetrating branches of circle of
Willis, MCA, or vertebrobasilar artery
Atherothrombotic or lipohyalinotic
occlusion
Infarct of deep brain structures
Basal ganglia, cerebral white matter,
thalamus, pons, and cerebellum
From 3 mm to 2 cm
Presentation of Lacunar Stroke
Risk factors
Diabetes
Hypertension
Polycythemia

Variable course progressing over days
Fluctuating; progressing in steps; or remitting
Preceded by TIAs in 25%
Without headache or vomiting
Lacunar Stroke Syndromes
Well-defined syndromes
Pure motor hemiparesis (with dysarthria)
Pure sensory stroke (loss or paresthesias)
Dysarthria-clumsy hand (with contralateral
face and tongue weakness)
Ataxia-hemiparesis (contralateral face and
leg weakness)
Isolated motor-sensory stroke
Lacunar Stroke Outcome
Management
Long-term blood pressure control
Empiric anti-platelet therapy
Omega-3 oil 1 gm TID to improve viscosity

Prognosis
Good recovery of function
Other lacunes develop
Prevention Pearls
Reducing Primary Risk - 1
Obstructive sleep apnea
Homocysteine folate, B6, B12
Hypertension morning BP surge
Smoking 50% risk reduction in 1 yr
Hyperlipidemia statins
Migraine triptans
Drugs cocaine, ephedra, PPA

Reducing Primary Risk - 2
Asymptomatic carotid stenosis
Endarterectomy for > 60% stenosis
Risk reduction for 3% to 1% per year
Benefit related to surgical risk
Nonvalvular atrial fibrillation
Aspirin for patients < 65 years, healthy
Warfarin for patients > 65 years or
having other stroke risk factors
Reducing Secondary Risk
Reducing risk of recurrence
TIA with ipsilateral carotid stenosis
endarterectomy for > 70% stenosis
Cardiogenic embolism warfarin
Lacunar infarcts aspirin, dipyridamole
Cryptogenic infarcts (40% embolic)
anticoagulation?
Reducing Risk in Children
Sickle cell disease
Screen with transcranial doppler q 6 mo
Transfusion therapy for 2 abnormal studies
Congenital heart disease
Arterial dissections (trauma)
Prothrombotic disorders
Mitochondria disorders (MELAS)
Medical Evidence


www.jr2.ox.ac.uk/bandolier/knowledge.html
Decreasing Salt Intake
Reducing salt intake by 3 g per day
lowers blood pressure; the effect is
doubled with a 6 gm/day reduction
and tripled with a 9 gm/d reduction.

Reduction in stroke risk parallels
reduction in salt intake.
Using Statins
Pooled results after 5 years
Pravastatin or Simvastatin 40 mg/day
Changes in cholesterol levels
Total cholesterol decreased 20%
LDL cholesterol decreased 28%
HDL cholesterol increased 5%
Triglycerides decreased 13%
Using Statins
Reducing LDL cholesterol by 1 mmol/L
22% stroke reduction in patients with
known vascular disease

6% stroke reduction in patients without
known vascular disease

28% reduction in thromboembolic stroke

Diagnostic Pitfalls
Practical Guidance

Goldszmidt and Caplan, Stroke Essentials,
Physicians Press, 2003

www.physicianspress.com

Pitfall #1
Basing treatment on brain imaging alone
without a vascular work-up.

A left frontal stroke caused by tight carotid
stenosis requires revascularization, but the
same stroke caused by atrial fibrillation
requires warfarin.
Pitfall #2
Basing work-up and treatment on the
temporal course of stroke.

Intervention should focus on the vascular lesion.
In fact, the same vascular lesion could cause
TIA, evolving stroke, or completed stroke.
Pitfall #3
Overlooking a mimic of TIA or stroke.

19% of patients diagnosed with stroke in ED
have an imitator of stroke

Common confounders
Seizures
Systemic infection
Brain tumor
Toxic-metabolic encephalopathy

Pitfall #4
Mistaking the time of symptom onset for
patients who wake up with stroke.

Strokes are painless and do not wake people up.
Because of risk of late thrombolysis, onset time
should be assumed to be when they were last
awake.

Diffusion-weighted MRI may be helpful in determining
benefit/risk of thrombolytic therapy.
Pitfall #5
Failing to investigate intracranial as well
as extracranial circulations.

Emboli or thrombi can come from anywhere in the
carotid or vertebrobasilar. Carotid duplex imaging
does not investigate the intracranial circulation.

Transcranial doppler or MRA can non-invasively
detect intracranial lesions,l more common in
African-American and Asian patients.
Pitfall #6
Failing to distinguish severe carotid
stenosis from total occlusion.

Severe stenosis may require urgent surgery; total
occlusion usually requires medical therapy.
Neither carotid duplex imaging nor MRA can
fully distinguish between the two. Conventional
angiography is the test of choice.
Pitfall #7
Failing to check spinal fluid in patients with
suspected subarachnoid hemorrhage.

CT has 90% sensitivity for subarachnoid blood on
day of onset, but sensitivity decreases over time.
Also, small hemorrhages can be missed.
For patients with suspected SAH who have a
negative CT, lumbar puncture is needed.
Pitfall #8
Considering only embolism in stroke patients
with atrial fibrillation.

More than 25% of ischemic strokes in patients with AF
have causes other than cardiogenic embolism (e.g.
aortic arch atheroma and intrinsic vascular disease).

Other interventions, such as carotid revascularization,
may be required.
Pitfall #9
Overtreating hypertension in acute stroke.

Because autoregulation is lost in ischemic brain,
aggressive lowering of BP may cause infarct
extension.
Treat BP > 200/120 in absence of thrombolytics or
> 180/115 with thrombolytics
Pitfall #10
Failing to adequate evaluate the heart.

Silent myocardial infarction and arrhythmias are
common complications of stroke.

MI occurs in 20% of patients with acute stroke.
It is a common cause of death at 1 4 weeks.

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