Cases & Commentaries

Lethal Vertigo

Commentary By Joseph M. Furman, MD, PhD

The Case

A 64-year-old woman, with no prior medical
history, complained of sudden onset of severe vertigo and vomiting,
without headache. Her initial blood pressure in the emergency
department (ED) was 170/90 (at about 4:00 PM). Physical examination
was limited because the patient's vertigo dramatically worsened
when she opened her eyes. Neurological exam was grossly
normal—the patient could follow commands and there was no
focal weakness. A provisional diagnosis of labyrinthitis was made,
and prochlorperazine (Compazine) 10 mg IV was administered. An hour
later, however, the patient noted little improvement, and so
lorazepam 2 mg IV was given. An hour after that, the patient was
signed out to a second attending, who administered atropine 0.5 mg
IV. Four hours later, she was signed out to a third attending. At
that point (10:00 PM), the physician decided to hold her overnight
in the ED and admit her if she was not better in the morning. At
11:00 PM, the patient complained of a headache and was given
acetaminophen 650 mg by mouth. An hour later, the patient sustained
a cardiopulmonary arrest and could not be resuscitated.

Autopsy revealed that the patient had died of a
cerebellar hemorrhage. A subsequent review of the case indicated
that the death was potentially avoidable, had life-saving
neurosurgery been performed within the first few hours of her ED
presentation.

The Commentary

Vertigo is an illusory sensation of motion, of
self or surroundings, and can be rotational (ie, a spinning
sensation) or translational (ie, a sense of floating upward). The
causes of vertigo are many; the common denominator is an
abnormality in the vestibular system, which comprises the inner ear
labyrinth and the central nervous system (CNS) structures that
process signals from the labyrinth. Vertigo, unlike nonspecific
"dizziness," is never constant but rather occurs as either a single
episode or recurrent episodes. Vertigo can occur spontaneously (eg,
as the result of vestibular neuritis or Ménière's
disease), or can be provoked, as in benign paroxysmal positional
vertigo.(1) When severe,
vertigo is often accompanied by nausea and vomiting, as it was in
this case.

When patients experience vertigo for the first
time, especially if associated with nausea and vomiting, they
usually seek medical attention immediately, typically in an
emergency department. The causes of vertigo encountered in the ED
setting are given in the Table. Most
patients presenting to an ED with vertigo can be managed
conservatively with vestibular suppressants and antiemetics and
then sent home. A small percentage of patients with vertigo will
require admission to the hospital to treat dehydration with
intravenous fluids or for further management, such as for a
cerebellar infarction.(2) Rarely, as
in this case, vertigo represents the presenting symptom of a
life-threatening, treatable condition, such as a cerebellar
hemorrhage.(3)

What features of this case suggest that the CNS,
not the labyrinth, was the location of the abnormality?
Unfortunately, definitively localizing vertigo to the central
(brain) or peripheral (inner ear) portion of the vestibular system
is difficult and sometimes impossible since vertigo itself and most
associated signs and symptoms (eg, nausea, vomiting, and
diaphoresis) can be the same in both central and peripheral
vertigo. However, some signs and symptoms associated with vertigo
can point more specifically to the inner ear or to the brain. For
example, hearing loss and tinnitus suggest the inner ear, whereas
cranial nerve or cerebellar findings suggest a brain abnormality.
This patient did not present with any signs or symptoms that
definitively implicated the brain as the location for her vertigo.
However, several symptoms and signs, though not pathognomonic for a
central cause, are so highly suggestive of a CNS abnormality that
brain imaging should be obtained promptly when they accompany
vertigo. One such symptom is headache, even though it is an
inconsistent symptom of central vertigo and can sometimes be seen
in peripheral syndromes as well. In a patient with vertigo, an
inability to ambulate should also alert the treating physician that
a central process is highly likely, thus prompting immediate brain
imaging.(4) We have no
indication from the case record that the patient's gait was
evaluated (either initially or following treatment for vertigo and
nausea). Vertical nystagmus and horizontal direction-changing
nystagmus are definite central signs; unidirectional horizontal
nystagmus can be a peripheral or a central sign.

Given the stakes involved in missing a central
lesion, many evaluation centers now almost routinely perform brain
imaging for patients presenting with new-onset acute vertigo, even
in the absence of either definitive or suggestive CNS signs.
Although such imaging of patients with vertigo will rarely uncover
a structural abnormality, brain imaging is non-invasive and is the
only means of ruling out a life-threatening disorder. Although a
non-contrast computed tomography (CT) scan of the brain is adequate
for ruling out a life-threatening hemorrhage, magnetic resonance
imaging (MRI) is equally as reliable for this purpose.(5)
Additionally, MRI can uncover recent ischemic infarctions and, with
magnetic resonance angiography, arterial dissections.

What led to this patient's demise despite having
an easily diagnosed, treatable condition? Primarily, three
different physicians failed to seriously consider a central cause
of vertigo, as evidenced by what appears to be (i) the omission of
a complete neurologic examination by each examiner, and (ii) the
failure to obtain brain imaging by the third attending, despite the
presence of headache in a patient who had presented more than six
hours earlier with vertigo and who had been treated with three
different vestibular suppressants. Clinicians must never forget
that a peripheral localization for vertigo cannot be confirmed with
certainty. Rather, a peripheral localization is a diagnosis of
exclusion when there are no symptoms, signs, laboratory findings,
or evidence on imaging that point to a central process. Since the
cerebellum has numerous connections with central vestibular
structures, cerebellar lesions can masquerade as peripheral
vestibular disorders. That appears to have been the case here: this
patient's presenting symptom complex of vertigo, vomiting, and
visual intolerance were, in retrospect, all produced by a
cerebellar hemorrhage (the Figure, of a
cerebellar infarction, demonstrates the vascular anatomy), probably
because of involvement of the vestibulocerebellum—that is,
the flocculonodular lobe, which lies at the caudal extent of the
cerebellum.

Was a neurologic consultation necessary in this
case? Probably not. Had any one of the three attendings considered
obtaining a neurologic consultation, they probably would have done
so because they were seriously entertaining a central disorder.
That concern should have led them to assess the patient's gait and
obtain diagnostic brain imaging, with or without a formal
neurologic consultation.

An obvious "system failure" occurred in this
case, wherein a patient had three different attendings in the span
of six hours. In a busy emergency department, it is not reasonable
to expect each new attending to repeat a full neurologic
examination on each patient. However, when the presenting complaint
is vertigo, a focused neurologic examination can successfully
uncover a central abnormality, since the brain regions that can
cause vertigo are limited to the brain stem and cerebellum. Thus,
an abbreviated examination looking for an altered level of
consciousness, gaze palsy (6), or a
central (eg, vertical or horizontal direction-changing) type of
nystagmus, facial numbness or weakness, upper extremity
incoordination, or an ability to walk should suffice to rule out a
central abnormality. This type of focused examination requires only
a few minutes and should be routinely repeated when a patient with
vertigo is "handed off" to another provider. Lowering the room
lights to reduce vertigo can sometimes make it possible to examine
a patient's eye movements. Since a patient's condition may change
over the course of hours, this patient should have been examined
repeatedly, at least at hourly intervals, to make a diagnosis in a
timely fashion, even if multiple attendings had not been involved
in the case.

Take-Home Points

  • Most patients presenting to an ED with
    vertigo can be managed conservatively with vestibular suppressants
    and antiemetics and then sent home. Rarely, however, vertigo
    represents the presenting symptom of a cerebellar hemorrhage, which
    is a life-threatening, treatable condition.
  • In a patient with vertigo, a head CT or
    MRI is required if:
    • There is an associated headache;
    • The patient is unable to ambulate;
      or
    • Physical examination findings suggest a
      central cause.
  • A central process can be ruled out if
    all of the following are true:
    • There is no altered level of
      consciousness;
    • There is no gaze palsy;
    • There is no central (ie, vertical or
      direction-changing horizontal) nystagmus;
    • There is no facial numbness;
    • There is no upper extremity
      incoordination; and
    • The patient can walk.
  • A peripheral (ie, inner ear)
    localization for vertigo cannot be confirmed with certainty.
    Rather, a peripheral localization is a diagnosis of exclusion when
    there are no symptoms, signs, laboratory findings, or evidence on
    imaging for a central process.

Joseph
M. Furman, MD, PhD
Professor of Otolaryngology and Neurology
University of Pittsburgh School of Medicine

References

1. Furman JM, Cass SP. Vestibular disorders: a
case-study approach. 2nd ed. New York, NY: Oxford University Press,
Inc; 2003.

2. Huang CY, Yu YL. Small cerebellar strokes may
mimic labyrinthine lesions. J Neurol Neurosurg Psychiatry.
1985;48:263-5.[ go to PubMed ]

3. van der Hoop RG, Vermeulen M, van Gijn J.
Cerebellar hemorrhage: diagnosis and treatment. Surg Neurol.
1988;29:6-10.[ go to PubMed ]

4. Hotson JR, Baloh RW. Acute vestibular
syndrome. N Engl J Med. 1998;339:680-5.[ go to PubMed ]

5. Fiebach JB, Schellinger PD, Gass A, et al.
Stroke magnetic resonance imaging is accurate in hyperacute
intracerebral hemorrhage: a multicenter study on the validity of
stroke imaging. Stroke. 2004;35:502-6.[ go to PubMed ]

6. Kubo T, Sakata Y, Sakai S, Koizuka I,
Matsunaga T, Nogawa T. Clinical observations in the acute phase of
cerebellar hemorrhage and infarction. Acta Otolaryngol Suppl.
1988;447:81-7.[ go to PubMed ]

7. Alvord LS, Herr RD. ENG in the emergency room:
subtest results in acutely dizzy patients. J Am Acad Audiol.
1994;5:384-9.[ go to PubMed ]

Table

Table. Specific Diagnoses of 93 Patients
Presenting with Dizziness in an Emergency Room

Classification

Diagnosis

n

Central

Cerebellar infarct

2

Alcohol or drug toxicity

2

Brain tumor

1

Central nervous system concussion

1

Hepatic encephalitis

1

Hypertension

1

Hyponatremia

1

Multiple sclerosis

1

Pseudotumor

1

Total

11

Peripheral

Acute labyrinthitis

18

Peripheral vestibular disorder

17

Benign positional vertigo

7

Ménière's disease

4

Labyrinthine concussion

4

Cervical disorder

2

Serous otitis media

1

Total

53

Other

Hyperventilation

3

Psychogenesis

2

Malingering

1

Fumes intoxication

1

Cystitis

1

Migraine

1

Total

9

Unknown

Total

20

Reprinted with permission from The Journal of the
American Academy of Audiology.(7)

Figure

Figure. MRI of a Right Inferior Cerebellar
Infarction


The inset illustrates the vascular supply to the
inferior cerebellum, which is perfused by the medial and lateral
branches of the posterior inferior cerebellar artery (PICA) and the
anterior inferior cerebellar artery (AICA).

Reprinted with permission from The New England
Journal of Medicine.(4)