Taylor

Danette

C.

Vertigo.

Edisi

29

Januari

2014.

Diunduh

dari:

http://www.medicinenet.com/vertigo_overview/article.htm, 1 Juli 2015.

Medical Author:
Charles Patrick Davis, MD, PhD

Doctor's View on Vertigo Causes

Comment by Charles P. Davis, MD, PhD
What is vertigo?
Vertigo is the sensation of dizziness. About 40% of patients over age 40 report vertigo as a
symptom, some of which report chronic vertigo intermittently for years. Many patients have
vertigo that is mild and resolves quickly without medical intervention. However, in some
patients, vertigo episodes may lead to dangerous falls. Unfortunately, there are many causes of
vertigo. Vertigo is sometimes accompanied by nausea and vomiting. The elderly are more
susceptible to complications like falls when vertigo occurs.
Vertigo causes
Most causes of vertigo originate in the brain or inner ear. Some causes are relatively benign
while others are not. The most common form of vertigo is benign paroxysmal positional vertigo
(BPPV). Some people refer to this as motion sickness. It is triggered by sudden head movements,
mild dehydration, or simply by standing up quickly. Some people develop BPPV after drinking
alcoholic beverages. Vertigo may be caused by inflammation of the inner ear (labyrinthitis or
vestibular neuritis) due to a bacterial or viral inner ear infection. Migraine headaches can also
trigger vertigo. Most cases of BPPV and labyrinthitis resolve spontaneously or can be treated.
Meniere's disease (tinnitus, hearing loss, vertigo) is usually intermittent but the cause is not
known. The symptoms may respond to treatment. More serious causes of vertigo are low blood
pressure, acoustic neuromas (tumors of ear nerve tissue), bleeding into the brain, loss of blood to
the brain (from complications of arteriosclerosis or neck trauma that compromises blood vessels
that supply blood to the brain), and multiple sclerosis.
Diagnosis of the underlying problems that lead to vertigo symptoms is the best way to approach
vertigo treatment

Vertigo Overview (cont.)

Medical Author:
Danette C. Taylor, DO, MS, FACN
Medical Editor:
Benjamin Wedro, MD, FACEP, FAAEM
What is vertigo?

Vertigo is a sense of rotation, rocking, or the world spinning, experienced even when someone is
perfectly still.
Many children attempt to create a sense of vertigo by spinning around for a time; this type of
induced vertigo lasts for a few moments and then disappears. In comparison, when vertigo
occurs spontaneously or as a result of an injury it tends to last for many hours or even days
before resolving.
Sound waves travel through the outer ear canal until they reach the ear drum. From there, sound
is turned into vibrations, which are transmitted through the inner ear via three small bones -- the
incus, the malleus, and the stapes -- to the cochlea and finally to the vestibular nerve, which
carries the signal to our brain. Another important part of the inner ear is the collection of
semicircular canals. These are positioned at right angles to each other, and are lined with
sensitive cells to act like a gyroscope for the body. This distinctive arrangement, in combination
with the sensitivity of the hair cells within the canals, provides instantaneous feedback regarding
our position in space.

Picture of the outer and inner structures of the ear.

What causes vertigo?

There are a number of different causes of vertigo. Vertigo can be defined based upon whether the
cause is peripheral or central. Central causes of vertigo arise in the brain or spinal cord while
peripheral vertigo is due to a problem within the inner ear. The inner ear can become inflamed
because of illness, or small crystals or stones found normally within the inner ear can become
displaced and cause irritation to the small hair cells within the semicircular canals, leading to
vertigo. This is known as benign paroxysmal positional vertigo (BPPV).
Meniere's disease, vertigo associated with hearing loss and tinnitus (ringing in the ear), is caused
by fluid buildup within the inner ear; the cause of this fluid accumulation is unknown. Head
injuries may lead to damage to the inner ear and be a cause of vertigo. Infrequently, strokes
affecting certain areas of the brain, multiple sclerosis, or tumors may lead to an onset of vertigo.
Some patients with a type of migraine headache called basilar artery migraine may develop
vertigo as a symptom.
What are the risk factors for vertigo?

Head injuries may increase the risk of developing vertigo, as can different medications, including
some antiseizure medications, blood pressure medications, antidepressants, and even aspirin.
Anything that may increase your risk of stroke (high blood pressure, heart disease, diabetes, and
smoking) may also increase your risk of developing vertigo. For some people, drinking alcohol
can cause vertigo.
Studies of the incidence of vertigo find that between 2% to 3% of a population is at risk of
developing BPPV; older women seem to have a slightly higher risk of developing this
condition. Continue Reading
Medically Reviewed by a Doctor on 5/1/2015

What are the signs and symptoms of vertigo?

The symptoms of vertigo include a sense of spinning or moving. These symptoms can be present
even when someone is perfectly still. Movement of the head or body, like rolling over in bed, can
escalate or worsen the symptoms. The symptoms are different from lightheadedness or a sense of
fainting. Many people experience associated nausea or vomiting.
Physical examination often shows signs of abnormal eye movements, called nystagmus. Some
patients experience imbalance in association with the vertigo. If imbalance lasts for more than a
few days, or if the vertigo is accompanied by weakness or incoordination of one side of the body,
the suspicion of stroke or other problem of the brain is much higher. In those cases, prompt
evaluation is recommended.

How is vertigo diagnosed?

During an evaluation for vertigo, the health care professional may obtain a full history of the
events and symptoms. This includes medications that have been taken (even over-the-counter
medications), recent illnesses, and prior medical problems (if any). Even seemingly unrelated
problems may provide a clue as to the underlying cause of the vertigo.
After the history is obtained, a physical examination is performed. This often involves a full
neurologic exam to evaluate brain function and determine whether the vertigo is due to a central
or peripheral cause. Signs of nystagmus (abnormal eye movements) or incoordination can help
pinpoint the underlying problem. The Dix-Hallpike test is done to try to recreate symptoms of
vertigo; this test involves abruptly repositioning the patient's head and monitoring the symptoms
which might then occur. However, not every patient is a good candidate for this type of
assessment, and a physician might instead perform a "roll test," during which a patient lies flat
and the head is rapidly moved from side to side. Like the Dix-Hallpike test, this may recreate
vertigo symptoms and may be quite helpful in determining the underlying cause of the vertigo.
If indicated, some cases of vertigo may require an MRI or CT scan of the brain or inner ears to
exclude a structural problem like stroke. If hearing loss is suspected, audiometry may be ordered.
Hearing loss is not seen with BPPV or other common causes of vertigo. Electronystagmography,
or electrical evaluation of vertigo, can help distinguish between peripheral and central vertigo,
but is not routinely performed. Continue Reading

What is the treatment for vertigo?

Some of the most effective treatments for peripheral vertigo include particle repositioning
movements. The most well-known of these treatments is the Epley maneuver or canalith
repositioning procedure. During this treatment, specific head movements lead to movement of
the loose crystals (canaliths) within the inner ear. By repositioning these crystals, they cause less
irritation to the inner ear and symptoms can resolve. Because these movements can initially lead
to worsening of the vertigo, they should be done by an experienced health care professional or
physical therapist.
Cawthorne head exercises, or vestibular rehabilitation habituation exercises, are a series of eye
and head movements which lead to decreased sensitivity of the nerves within the inner ear and
subsequent improvement of vertigo. These simple movements need to be practiced by the patient
on a regular basis for best results.
Medications may provide some relief, but are not recommended for long-term use. Meclizine is
often prescribed for persistent vertigo symptoms, and may be effective. Benzodiazepine
medications like diazepam (Valium) are also effective but may cause significant drowsiness as a
side effect. Other medications may be used to decrease nausea or vomiting. It is should be
recognized that medications can provide symptomatic relief, but are not considered "cures" for
vertigo.

Are home remedies effective for treating vertigo?

While several suggestions for treatment of vertigo can be found, most of these are ineffective.
Many cases of vertigo resolve spontaneously within a few days, which may promote the belief
that a certain home remedy has been beneficial in resolving the symptoms.
The vestibular rehabilitation exercises (Cawthorne head exercises) or modified Epley maneuvers
are meant to be done on a regular basis by patients, and may lead to marked improvements in
vertigo. Continue Reading
Can vertigo be prevented?

Controlling risk factors for stroke may decrease the risk of developing central vertigo. This
includes making sure that blood pressure, cholesterol, weight, and blood glucose levels are in
optimal ranges. To decrease symptoms of vertigo in cases of Meniere's disease, controlling salt
intake may be helpful. If peripheral vertigo has been diagnosed, then performing vestibular
rehabilitation exercises routinely may help prevent recurrent episodes.
As most cases of vertigo occur spontaneously, it is difficult to predict who is at risk; as such,
complete avoidance or prevention may not be possible. However, maintaining a healthy lifestyle
will decrease the risks of experiencing this condition.
What is the prognosis for vertigo?

Most patients with peripheral vertigo can find substantial relief with treatment; it has been
suggested that the Epley maneuver in cases of BPPV can benefit as many as 90% of affected
patients. Although recurrence of BPPV may be more than 15% in the first year after an episode,
it is unlikely that vertigo will persist beyond a few days. When vertigo persists, evaluation for
any underlying structural problems of the brain, spinal canal, or inner ear may be necessary.

Central Vertigo
http://emedicine.medscape.com/article/794789-overview
Keith A Marill, MD Faculty, Department of Emergency Medicine, Massachusetts
General Hospital; Assistant Professor, Harvard Medical School
Keith A Marill, MD is a member of the following medical societies: American
Academy of Emergency Medicine, Society for Academic Emergency Medicine
Updated: Oct 08, 2014

Background
Central vertigo is vertigo due to a disease originating from the central nervous system (CNS). In
clinical practice, it often includes lesions of cranial nerve VIII as well. Individuals with vertigo
experience hallucinations of motion of their surroundings.
Central vertigo may be caused by hemorrhagic or ischemic insults to the cerebellum (see the
image below), the vestibular nuclei, and their connections within the brain stem. Other causes
include CNS tumors, infection, trauma, and multiple sclerosis.[1, 2]

CT scan of a patient with an acute spontaneous

cerebellar hemorrhage. The hemorrhage in the right lobe of the cerebellum is partly
obscured by bony artifact.

Vertigo due to acoustic neuroma is also included in the broader category of central vertigo. An
acoustic neuroma develops within the eighth cranial nerve, usually within the course of the
internal auditory canal, yet it often expands into the posterior fossa with secondary effects on
other cranial nerves and the brain stem.

Pathophysiology
The brainstem, cerebellum, and peripheral labyrinths are all supplied by the vertebrobasilar
arterial system. Thus, the central and peripheral ischemic vertigo syndromes overlap.
Vertebrobasilar arterial system

The basilar artery is formed from the 2 vertebral arteries within the cranium at the level of the
medulla. The artery has 3 branches on each side that supply the cerebellum. The posterior
inferior cerebellar artery branches from the vertebral artery, while the anterior inferior cerebellar
artery and the superior cerebellar artery branch from the basilar artery.
All 3 of the cerebellar arteries may have branches that supply brainstem tissue. A labyrinthine
artery on each side branches from the basilar artery and supplies the labyrinth and associated
structures via the internal auditory canal. In approximately two thirds of people, the basilar artery

ends by bifurcating into the posterior cerebral arteries, with small posterior communicating
arteries connecting to the internal carotid system in the circle of Willis.
Arterial occlusion and ischemic infarction

Arterial occlusion and ischemic infarction can result from cardioembolism, embolism of plaque
from a vertebral artery, or local arterial thrombosis. One or both vertebral arteries, the basilar
artery, or any of the smaller branches may be occluded. Even complete occlusion of a large
artery may not result in death because of anastomotic retrograde flow via the circle of Willis and
posterior communicating arteries.
Temporary vertebrobasilar ischemia may present as migraine syndrome or transient ischemic
attacks (TIAs). While less common than cerebellar infarction, spontaneous cerebellar
hemorrhage is an important life-threatening cause of vertigo associated with hypertensive
vascular disease and anticoagulation.[3]
Multiple sclerosis

Multiple sclerosis is a demyelinating disease of the CNS. The course generally waxes and wanes,
with varying neurologic symptoms and signs. Isolated vertigo may be the initial symptom in
approximately 5% of cases. This disease is discussed in detail in the relevant article (see Multiple
Sclerosis).
Acoustic neuromas

Acoustic neuromas are Schwann cell tumors that usually originate on the vestibular division of
the eighth cranial nerve in the proximal internal auditory canal.[4] Usually unilateral in
development, bilateral acoustic neuromas do occur in young adults, although rarely, in
association with neurofibromatosis type 2. If untreated, an acoustic neuroma may expand into the
cerebellopontine angle and compress facial and other cranial nerves.[5] If it compresses the
brainstem, ataxia, gait disturbances, spasticity, and weakness from long-tract effects may result.
See the image below.

CT scan of a patient with a large acoustic neuroma on

the right side of the brainstem. The scan was performed after injection of
intravenous contrast, which is critical for identifying tumors with CT imaging.
Other causes

Isolated vertigo due to CNS infection, such as a microabscess, or temporal lobe seizures is rare
and is not discussed in this article. Vertigo and dizziness are common complications of head and
neck trauma. Traumatic central vertigo may be caused by petechial hemorrhages in the vestibular
nuclei of the brainstem. These may result from shearing forces on the brainstem.[6]

Epidemiology
Frequency

United States
Approximately 500,000 people have strokes each year. About 85% of these strokes are ischemic,
and 1.5% of ischemic strokes affect primarily the cerebellum. Ratio of ischemic to hemorrhagic
cerebellar strokes is 3-5:1.[7] Up to 10% of patients with an isolated cerebellar infarction present
with only isolated vertigo and imbalance.[8] Incidence of multiple sclerosis ranges from 1080/100,000 per year, depending on the latitude. About 3000 cases of acoustic neuroma are
diagnosed each year in the United States.

Mortality/Morbidity

Vascular injuries and infarcts in the posterior circulation can cause severe permanent debilitating
disease. The excellent recovery typical of acute vertigo caused by peripheral disease should not
necessarily be expected in central vertigo.

A study of the rate and predictors of CNS disease in emergency department

patients with dizziness, vertigo, or imbalance found that most cases were
benign, although a substantial fraction of patients had serious neurologic
disease. Of 907 patients experiencing dizziness (mean age, 59 years; 58%
women [n=529]), 49 (5%) had a serious neurologic diagnosis, including 37
cerebrovascular events. Dizziness was often caused by benign conditions,
such as peripheral vertigo (294 patients [32%]) or orthostatic hypotension
(121 patients [13%]). [9]

In one series, cerebellar infarctions had mortality rates of 7% and 17% when
associated with the superior cerebellar artery and posterior inferior cerebellar
artery distributions, respectively. [10] Infarctions in the latter distribution are
associated more commonly with a mass effect and compression of the brain
stem and the fourth ventricle. In another series of patients with cerebellar
infarction and mass effect, mortality rate was 17% despite aggressive
neurosurgical and medical management. [11]

In one series of 94 patients, 20 presented with a Glasgow Coma Scale (GCS;

see the Glasgow Coma Scale calculator) score less than 8, indicating
significantly impaired consciousness. Mortality rate in the remaining patients
who presented with GCS score higher than 8 was 20%.

Acoustic neuroma has a low rate of mortality once diagnosed. The tumor
often may be removed with preservation of facial nerve function, but
unilateral hearing loss is common.

Sex

Incidence of cerebrovascular disease is slightly higher in men than in women. In one series of
patients with cerebellar infarction, the ratio of men to women was about 2:1. Multiple sclerosis is
about twice as common in women as in men.
Age

Incidence of stroke increases with age. The mean age of patients with cerebellar infarction in one
series was 65 years, with half of the cases occurring in those aged 60-80 years.[7] In one series,
the mean age of patients with cerebellar hematoma was 70 years.[3

Causes
See the list below:

Positional vertigo: abrupt onset of vertigo associated with a change in

position suggests benign positional vertigo, a form of peripheral vertigo.

Cranial nerve deficits

o

Symptoms related to derangement of cranial nerves other than the

eighth nerve suggest involvement of the brainstem and/or cerebellum.

As the cerebellar arteries supply areas of the dorsal brain stem,

cerebellar infarcts also may involve the trigeminal, facial, and other
cranial nerve nuclei. Mass effect due to edema, acute hemorrhage, or
an acoustic neuroma also can cause cranial nerve deficits.

Facial nerve dysfunction, most commonly manifested as weakness or

twitching in the periorbital area, is seen in 10% of patients with
acoustic neuroma.[5]

Crossed findings (ie, when the patient has signs on one side of the face
and sensory and [less commonly] motor signs on the other side of the
body) clearly suggest brainstem involvement.

This includes the classic lateral medullary infarction (Wallenberg

syndrome) consisting of ipsilateral limb ataxia, Horner
syndrome, palatal weakness, facial hypesthesia to pain and
temperature, and contralateral hypesthesia to pain and
temperature in the limbs and trunk.

Crossed findings result from unilateral lesions of the brainstem

involving cranial nerve nuclei and long tracts from higher brain
centers that have yet to cross to the other side of the CNS.

TIAs: Recurrent transient symptoms lasting a few minutes suggest TIAs.

Acute cerebellar disease

o

Loss of balance and difficulty maintaining posture, standing, and

walking suggest cerebellar disease. These symptoms occur in 50-75%
of patients with cerebellar infarction or hemorrhage. [3]

Occipital headache and difficulty with speech are also common

complaints with acute cerebellar disease.

Caudal cerebellar infarction: A prospective study of 24 patients aged 50-75

years with isolated vertigo lasting longer than 48 hours found that 6 (25%) of
the patients had a caudal cerebellar infarction. [15] Infarcts of the medial
branch of the posterior inferior cerebellar artery territory appear to be the
most common cerebellar cause of isolated vertigo and imbalance.

Cerebrovascular disease: A recent history of drop attacks, cranial nerve

deficits, or transient vertigo should raise suspicion for cerebrovascular
disease of the posterior circulation.

Basilar artery occlusion: In one study of basilar artery occlusion, 4 of

53 (8%) patients had prodromal symptoms consisting only of vertigo
and nausea.[16]

Vertebral artery occlusion: Thirty-seven of 85 (44%) patients who

presented with either basilar or bilateral distal vertebral artery
occlusion had prodromal symptoms that cleared in the 2 months prior
to admission.[16]

Cardiovascular risk factors

o

The risk of stroke in patients with atrial fibrillation is highest in the first
year after onset in patients not receiving anticoagulation.

Diabetes mellitus, hyperlipidemia, and cigarette smoking are also

important risk factors.

Mnire disease and acoustic neuroma

o

Chronic high- and low-frequency hearing loss with associated tinnitus,

which fluctuates over time, suggests Mnire disease.

Associated auditory symptoms suggest that vertigo has a peripheral

origin, though exceptions exist.

Hearing loss, often with associated tinnitus, is the most common early
symptom of acoustic neuroma.[5]

Multiple sclerosis: In younger patients, recent history of neurologic deficits,

particularly weakness and/or numbness in one or more limbs (lesions in time
and space) or unilateral visual loss, should raise suspicion for multiple
sclerosis.

Emergency Department Care

First, distinguish true vertigo from disequilibrium and other forms of dizziness. Ascertaining this
history from patients sometimes requires patience and persistence. Once the presence of vertigo
or disequilibrium has been confirmed, consider a central cause. Evaluate on the basis of a careful
history and physical examination and liberal use of imaging studies of the posterior fossa.

Therapy usually targets the etiology of the symptoms. However, a variety of

medications may be used to reduce symptoms of central vertigo, including
antihistamines and benzodiazepines.

Regardless of the vertigo's etiology, attempt to alleviate the patient's

suffering.

Place intravenous lines to rehydrate patients.

Allow patients to lie still in bed as desired.

Administer parenteral medicines for symptomatic relief.

If clinical and radiologic evaluation suggest an acute ischemic stroke,

consider thrombolytic therapy after thorough evaluation and consultation.
o

Thrombolytic therapy is administered with an intra-arterial catheter

close to the clot[18] , or intravenously, if within 3 hours of the onset of
symptoms and no other contraindications exist.[19]

Prior to using thrombolytic therapy, consider several issues, especially

the risk of intracerebral bleeding. Emergency physicians should be
familiar with contraindications such as major surgery within the
previous 10 days, severe hypertension, evidence of acute bleed or
edema on CT scan, and rapidly improving symptoms.

The decision to administer thrombolytic therapy preferably is made

with direct neurologic consultation and only after the patient has
received a thorough explanation of the procedure and given informed
consent. This therapy is discussed further in other articles (see Stroke,
Ischemic and Thrombolytic Therapy).

Lethargic patients or those with altered level of consciousness require

vigilance and close supervision, including direct visual, ECG, and pulse
oximetry monitoring.

Do not administer anticoagulant medicine, including aspirin, until intracranial

hemorrhage has been ruled out by imaging.

Imaging studies should be performed expeditiously, and the patient never

should be left unattended by clinical personnel in the imaging suite.

Patients with altered consciousness and a deteriorating course in the ED may

require emergent interventions to minimize edema and brainstem
compression.

As the posterior fossa is a relatively small and nonexpandable space,

hemorrhage or edema can lead to rapid compression and compromise
of vital medullary functions, obstructive hydrocephalus, or herniation of
the medullary tonsils.

Invasive actions may include endotracheal intubation to protect the

airway, control breathing, and allow therapeutic hyperventilation.

Consider elevating the head of the bed, performing diuresis with

mannitol or furosemide, and administering dexamethasone.

Preliminary evidence suggests that recombinant activated factor VII may be

useful for acute hemorrhagic stroke when administered within 4 hours of
symptom onset.[20] The data supporting the use of this therapy for
hemorrhagic cerebellar stroke is too limited thus far to make a therapeutic
recommendation, but further results are expected to clarify its utility and
adverse effect profile.

Medication Summary
Patients with depressed mental status may have documented or suspected increased intracranial
pressure (ICP). Administer diuretics or corticosteroids to decrease pressure while planning more
definitive actions. Administer this therapy preferably in consultation with a neurosurgeon.

H1- receptor antagonists

Class Summary

These agents may suppress vestibular responses through an effect in the CNS; however, the
mechanism remains unknown. Some investigators believe this action is mediated primarily by
central anticholinergic activity.
Dimenhydrinate (Dramamine, Dimetabs, Dymenate, Triptone)

A 1:1 salt of 8-chlorotheophylline and diphenhydramine, thought to be particularly

useful in treatment of peripheral vertigo. Diminishes vestibular stimulation and
depresses labyrinthine function through central anticholinergic activity.
Diphenhydramine (Benadryl, Bydramine, Hyrexin)

Used for treatment and prophylaxis of vestibular disorders.

Promethazine hydrochloride (Phenergan)

Used for symptomatic treatment of nausea in vestibular dysfunction.

An antidopaminergic agent effective in treatment of vertigo, blocks postsynaptic mesolimbic
dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.

Benzodiazepines
Class Summary

Centrally, these agents inhibit vestibular responses, presumably by potentiating inhibitory GABA
receptors.
Diazepam (Valium, Diastat, Diazemuls)

Probably most commonly used benzodiazepine to treat vertigo. Highly lipophilic and undergoes
rapid redistribution after administration. Duration of effects in CNS relatively short, which may
make it relatively less desirable.
Lorazepam (Ativan)

Sedative hypnotic in benzodiazepine class that has short time to onset and relatively long halflife.
Depresses all levels of CNS, including limbic and reticular formation, probably through
increased action of GABA, a major inhibitory neurotransmitter.

Diuretics
Class Summary

Diuretic agents are used as a temporary measure to lower ICP until definitive intervention is
performed.
Mannitol (Osmitrol)

Nonreabsorbable solute, decreases water reabsorption in water-soluble portions of nephron.

Reduces reabsorption of sodium chloride as well. Perhaps more importantly, does not cross
blood-brain barrier. Creates osmotic gradient, drawing water from brain into intravascular
compartment. Used to lower ICP in variety of conditions.

Initially assess for adequate renal function in adults by administering test dose of 200 mg/kg IV
over 3-5 min. Should produce a urine flow of at least 30-50 mL/h over 2-3 h.
In children, assess by administering same test dose and rate. Should produce a urine flow of at
least 1 mL/kg/h over 1-3 h.
Furosemide (Lasix)

Loop diuretic that blocks transport of sodium, potassium, and chloride in thick ascending limb of
loop of Henle in kidney. May enhance effect of mannitol and produce greater and more sustained
decrease in ICP.

Corticosteroids
Class Summary

These agents are used to decrease brain edema associated with intracranial tumors.
Dexamethasone (Decadron)

Preferred corticosteroid for this purpose because it demonstrates high glucocorticoid potency and
minimal mineralocorticoid activity.

Prognosis
See the list below:

Prognosis for patients with central vertigo depends on the underlying disease
and is highly variable.

Neurosurgical advancements have improved the prognosis for many serious

conditions. This magnifies the importance of identifying these patients in the
emergency setting.

The prognosis of infarction of the basilar or vertebral arteries is poor. In one

series, 45% of patients presented in coma. Importantly, half of the patients in
this series had prodromal symptoms, including vertigo, which cleared
completely in the 6 months prior to the stroke.[16]

The prognosis for patients with spontaneous cerebellar hemorrhage is poor.

Neurologic deterioration in these patients is associated independently with a
hematoma in the central vermian area of the cerebellum and with secondary
hydrocephalus.[3]