Chapter 17

Neurologic Emergencies

Stroke & TIA

Devin R. Harris, MD MHSc CCFP(EM)

Stroke is the fourth leading cause of death in Canada and is the leading cause of
disability. Each year, there are between 40,000 to 50,000 strokes and 16,000
people die from stroke in Canada. Currently, there are approximately 300,000
Canadians living with a disability from stroke.

A stroke results from any disease process that disrupts vascular blood flow to a
distinct region of the brain. It is caused by the interruption of the flow of blood to
the brain (an ischemic stroke) or the rupture of blood vessels in the brain (a
hemorrhagic stroke).

The treatment of stroke in the emergency department is a medical emergency as

certain therapies need to be given within a very short time window.

STROKE TYPES
Ischemic Stroke (80%)

Ischemic stroke can be divided into three major categories:

1. Thombotic Stroke (75%)
 Caused by clot formation in a blood vessel
 Most common cause is atherosclerotic disease. Other causes
include vasculitis, dissection, polycythemia and hypercoagulable
states

2. Embolic Stroke (20%)

 Caused by intravascular material from a proximal source being
released and then occluding a distal vessel
 Most common sources of emboli are the heart and major vessels
(aorta, carotid arteries, and vertebral arteries)
 Cardiac sources of emboli include valvular vegetations, mural
thrombi (due to atrial fibrillation, myocardial infarction, or
dysrhythmia), paradoxical emboli (due to atrial or ventricular septal
defect) or cardiac tumours (myxomas).

3. Systemic hypoperfusion (5%)

 Most commonly due to cardiac pump failure (myocardial infarction
or dysrhythmias)
 Leads to a more generalized or diffuse injury pattern; in border
zones or “watershed” regions at the periphery of major vascular-
 supply territories (for example, where the anterior cerebral artery
meets the middle cerebral artery territory)
Hemorrhagic Stroke (20%)

Although hemorrhagic stroke comprise only one of every five strokes, they have
a mortality rate of 30 to 50% at one month and occur in younger patients.

Hemorrhagic stroke can be divided into two types:

1. Intracerebral hemorrhage (ICH) (67%)
 Bleeding into the brain parenchyma
 Risk factors: increasing age, history of prior stroke, Asian or black
race, smoking, alcohol abuse
 The majority of ICH’s are associated with chronic hypertension
 Also associated with amyloidosis

2. Subarachnoid hemorrhage (SAH) (33%)

 Bleeding into the subarachnoid space
 Sudden release of blood at systemic arterial pressure leads to
direct cellular damage and a rapid increase in intracranial pressure
 Most common cause is berry aneurysm rupture; arteriovenous
malformations are another common cause.

CLINICAL FEATURES
History

Often, the etiology of the stroke can be predicted based on the patient’s
demographics and past medical history. Younger patients are more likely to
have a hemorrhagic stroke than older patients. Hypertension, coronary artery
disease and diabetes suggest an atherosclerotic cause for stroke. Atrial
fibrillation, valvular replacement or a recent myocardial infarction suggest an
embolic cause.

Time of onset of symptoms is extremely important to determine. It is imperative

to determine “time last seen well” as acute therapies for stroke depend on the
accurate assessment of the onset of deficits. Any fluctuations or improvement in
symptoms should be documented. Other complaints such as headache,
vomiting or recent trauma should be recorded. Headache occurs in the majority
of patients with hemorrhage but only in 10 to 20 percent of those with ischemic
stroke. Recent neck trauma may suggest a carotid dissection.

Physical Examination
General

A detailed neurologic examination should never occur without prior stabilization

of a patient’s ABC’s. A primary survey should occur and any immediate threats
to life should be dealt with appropriately and urgently.
The vital signs of the patient should be examined carefully. A Glasgow Coma
Score (GCS) should be documented with every stroke patient. Elevated blood
pressure may indicate a primary cause of the patient’s symptoms (hypertension
causing stroke; hypertensive encephalopathy) or as a consequence of increased
ICP (Cushing’s response – elevated blood pressure and bradycardia).
Neurologic deficits can occur due to hypoglycaemia so a rapid glucose
determination should occur.

Neurologic Examination

The goal of the neurologic examination is to localize the brain lesion (where is
the lesion, what is the lesion?) and to rule out other neurologic disease
processes. The neurologic examination can be divided into the following areas:

1. Level of consciousness (LOC)

 Part of the primary survey
 Can be evaluated by asking simple questions and by having the
patient follow simple commands
 Patients may be alert, drowsy (requires minor stimulation to obey),
lethargic (requires repeated or painful stimulation to obey), or
obtunded (no response or posturing)

2. Cranial Nerves

3. Visual Assessment
 Evaluate visual fields and extraocular movements

4. Language
 Determination of dysarthria (disturbance in articulation due to
paralysis or incoordination of muscles used for speech) or aphasia
(disturbance in processing language).
 Aphasia may be receptive (comprehension) or expressive
(communicating thoughts) or both

5. Sensory
 Sensory deficits and neglect should be evaluated by pinprick
testing and double-simultaneous extinction (touch the patient’s right
and left limbs individually and then simultaneously)

6. Cerebellar Function
 Finger-to-nose testing, heel-to-shin testing, rapid alternating
movements can be tested.
 If the patient can stand, perform a Romberg test

7. Gait
  Not always possible to perform in the stroke patient
Stroke Syndromes

Once a complete history and physical have been performed, it is important to

integrate physical findings with brain anatomy and function to determine the
anatomic location of the lesion and the possible vessels that may be involved.
Certain patients may present with classic patterns:

Ischemic Stroke Syndromes

1. Anterior cerebral artery infarct

 Contralateral leg weakness greater than arm weakness
 Patients may perseverate with speech or motor actions and respond
slowly

2. Middle cerebral artery infarct

 The most common stroke presentation
 Contralateral weakness and numbness variably affecting the face and
arm greater than the leg
 If the dominant hemisphere is involved (left hemisphere in right-handed
patients and 80% of left-handed patients), aphasia is often present
 If the nondominant hemisphere is involved, inattention, neglect or
extinction on double-simultaneous stimulation may be present
 Homonymous hemianopsia and gaze preference toward the side of the
infarct may also be found

3. Posterior cerebral artery infarct

 Patients may be unaware of their deficits until tested
 Motor involvement is minimal; may have visual cortex abnormalities
 Light-touch and pinprick may be significantly reduced

4. Vertebrobasilar syndrome
 The posterior circulation supplies blood to the brainstem, cerebellum
and visual cortex
 Findings may include dizziness, vertigo, diplopia, dysphagia, ataxia,
cranial nerve palsies, and limb weakness
 Hallmark is “crossed neurologic deficits” (ipsilateral cranial nerve
deficits with contralateral motor weakness)

5. Basilar artery occlusion

 This is a devastating condition – presents with severe quadriplegia,
coma and the “locked-in syndrome”

6. Cerebellar infarct
 Patients may present with a “drop attack” – sudden inability to walk or
stand
  Findings include vertigo, headache, nausea, vomiting and neck pain
 At risk of developing significant edema and increased brainstem
pressure

7. Lacunar infarcts
 Pure motor or pure sensory deficits that are due to infarction of small
penetrating arteries
 Commonly associated with chronic hypertension

8. Arterial dissection
 May be associated with trauma or neck injury
 May occur in the carotid (anterior) and vertebral (posterior) circulation

Hemorrhagic Stroke Syndromes

1. Intracerebral hemorrhage
 May be clinically indistinguishable from cerebral infarction (above
syndromes)
 More commonly lethargic and may have significant hypertension
 Often associated with headache, nausea and vomiting
 Bleeding often localized to (in order of frequency): putamen, thalamus,
pons, or cerebellum

2. Subarachnoid hemorrhage
 Sudden onset of severe constant headache (worst headache of their
life) that is often occipital or nuchal; often with straining
 May have had a “sentinel hemorrhage” – a severe headache lasting for
a few days prior to the event that brought them to the emergency
department
 Vomiting common; may have decreased level of consciousness

Differential Diagnosis

Although stroke is the most common cause of unilateral weakness, other

diagnoses must be considered – the so-called “stroke mimics.” It is essential to
rule these out prior to instituting acute stroke therapies.

Most common:
 Postictal paralysis (Todd’s paralysis)
 Systemic infections
 Tumours
 Toxic-metabolic disturbances (hypoglycaemia, diabetic ketoacidosis,
hyperosmotic coma, Wernicke’s encephalopathy)
Other causes:
 Bell’s palsy, epidural/subdural hematoma, complicated migraine,
labyrinthitis, Meniere’s disease, drug toxicity

Diagnostic Tests

All patients with suspected stroke should undergo rapid laboratory testing and
imaging.

Laboratory Tests
 CBC with platelet count – identifies polycythemia, thrombocytosis or
thrombocytopenia
 INR, PTT – rule out coagulopathy or excessive anticoagulation with
warfarin
 Glucose – should be determined early, ideally by paramedical personnel.
If hypoglycaemic, 50% dextrose should be administered immediately.

Electrocardiogram (ECG)
 Atrial fibrillation and acute myocardial infarction are associated with up to
60% of all cardioembolic strokes

Computed tomography (CT)

 Initial scan should be noncontrast
 Can differentiate between ischemic infarction and hemorrhagic infarction;
can also determine other causes for the neurologic deficits
 Identifies almost all ICH greater than 1 cm and 95% of SAH
 Most ischemic stroke will not be seen prior to 6 hours after onset of
symptoms

Lumbar puncture
 Required in all patients in whom SAH is suspected but who have a normal
CT scan

Other tests
 Depending on clinical scenario, patients may necessitate:
o Echocardiogram – mural thrombus, tumour, valvular vegetation
o Carotid duplex – to detect carotid stenosis
o Magnetic resonance imaging (MRI) – good to detect very early
ischemia; poor at differentiating ischemia from hemorrhage
o CT angiogram / MR angiogram – to detect intravascular occlusion
or sources of hemorrhage
Treatment – Ischemic Stroke
General Treatment

Common to all emergency department patients, attention should first be given to

the patient’s ABC’s. Stroke patients should be placed on oxygen and hooked up
to a cardiac monitor, the head of the bed slightly elevated, and intravenous lines
established.

Intravenous fluids should be given judiciously to prevent cerebral edema, unless

there is hypotension, which should be treated aggressively. Normal saline is the
preferred intravenous fluid – hyperglycemia has been associated with worse
stroke outcomes. Patients with fever should be promptly treated with an
antipyretic.

The management of blood pressure is controversial. In general, frequent

monitoring of blood pressure in hypertensive stroke patients is necessary and
only persistent, severe hypertension (defined as > 220 systolic or > 130 diastolic)
should be treated. Large reductions in blood pressure may result in converting a
reversible area of injury in the brain, to an area of infarction. Labetolol or sodium
nitroprusside should be used.

Seizures should be treated, if they occur, with benzodiazepines then with a

loading dose of phenytoin. Seizures should not be treated prophylactically.

All patients with stroke symptoms should not receive any by mouth (NPO) until
their swallowing status has been assessed. They are at risk of aspiration.

If your hospital has a stroke team, the stroke team should be activated either pre-
hospital or when the patient arrives in the emergency department. Neurology
should be consulted on all acute (less than 3 hours) stroke patients.

Specific Treatments

1. Thrombolysis
 Some evidence that stroke can be treated (reduce morbidity) if given
within 3 hours of neurologic deficit onset
 Patients who present under 3 hours since onset of symptoms need
rapid assessment, rapid CT scanning and rapid administration of
thombolytics
 Exclusions: minor or improving stroke symptoms; previous ICH;
seizure; low or high glucose; GI or GU bleeding within 21 days; recent
MI; major surgery within 14 days; blood pressure > 185 systolic or >
110 diastolic; previous stroke within 90 days; previous head injury
 within 90 days; on oral anticoagulants (or INR > 1.7); platelet <
100,000; proliferative diabetic retinopathy
 Dose: rt-PA 0.9 mg/kg; 10% given as a bolus with the remaining 90%
given over 60 minutes; maximum dose 90 mg.
 CT scan should be interpreted by a neurologist or radiologist; rt-PA
should be given by a neurologist
 All patients given rt-PA should be admitted to an intensive care unit or
a neurology intensive care unit for monitoring

2. Platelet inhibitors
 After CT scan to rule out hemorrhage, all patients should be
considered for a platelet inhibitor acutely
 Best evidence for acetylsalicylic acid (ASA) – no difference between
low dose (80 mg) vs. high dose (1000 mg)
 Also can consider: Dipyridamole (200 mg) or clopidogrel (300 mg)

3. Anticoagulants
 No evidence for anticoagulants (heparin or coumadin) to treat ischemic
thrombotic stroke
 Excellent evident to treat patients who have atrial fibrillation and
presumed embolic stroke – timing of anticoagulation is controversial.
Consultation is necessary.
 Also may be considered in recurrent TIA’s, high grade carotid artery
stenosis and vertebrobasilar infarction

Treatment – Hemorrhagic Stroke

Again, all patients should be evaluated with respect to their ABC’s and should be
resuscitated and stabilized.

Intracerebral Hemorrhage
 Blood pressure should be maintained less than 220 / 120 as per published
recommendations. Use labetolol or nitroprusside.
 Treat increased intracranial pressure with standard measures (mannitol,
furosemide; hyperventilation is controversial)
 Urgent neurosurgical consultation – surgical intervention is warranted for
some cases

Subarachnoid Hemorrhage
 Blood pressure should be maintained at “prehemorrhage levels” due to a
high risk of rebleeding – treat blood pressure aggressively
 Vasospasm may occur 2 days to 3 weeks after aneurysm rupture –
prescribe nimodipine 60 mg PO QID for all patients
 Urgent neurosurgical consultation
TRANSIENT ISCHEMIC ATTACK (TIA)

A transient ischemic attack (TIA) is an acute onset of brief focal neurological

impairment or deficit due to a temporary disruption of blood supply to a region of
the brain. This diagnosis has been traditionally defined as a neurologic symptom
that resolves within 24 hours; however, due to advances in imaging and acute
treatment for stroke, it has been proposed to define TIA as lasting less than one
hour, without evidence of acute infarction.

Transient ischemic attack is a significant warning symptom for impending

ischemic stroke. A recent study estimated the 90-day risk of recurrent stroke to
be 10.5%, with half of these strokes occurring within the first two days after a
TIA. Therefore, TIA’s should be investigated and treated urgently.

History and Physical Examination

Patients who present after a TIA should be evaluated in the same manner
described above. Timing of the event and symptoms during the event (motor
weakness, speech difficulties, dizziness) should be determined; patients should
also be questioned if this is a recurrent event. A cardiovascular exam should be
performed, specifically to listen for carotid bruits and to assess heart rate (regular
vs. irregular). A complete neurological exam should be performed to determine if
the patient has residual deficits.

Investigations
 Laboratory: CBC, electrolytes, glucose, INR, PTT
 Electrocardiogram
 CT scan
 Carotid Doppler ultrasound – not necessarily needs to be performed in
the emergency department, but should be ordered
 Echocardiogram – consider in patients who have a history of MI

Treatment
 All patients should be prescribed an antiplatelet agent – aspirin is first-line.
If on aspirin, consider adding a second antiplatelet agent
 Patients with atrial fibrillation and a TIA need to be anticoagulated
 Blood pressure and lipid status should be determined at some point after
a TIA, but this does not need to be done in the emergency department

Disposition
 Some centers admit all TIA patients for urgent evaluation
 Consultation and admission should be considered for patients with atrial
fibrillation, recurrent TIA events, vertrobasilar symptoms, or significant
comorbidities.
 If discharged (and available), should be referred to a stroke prevention
clinic or neurologist for follow up.