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.