NEUROLOGIC ASPECTS OF
DIZZINESS
Dizziness is a generic term as used by
patients for a feeling of unsteadiness or disorientation. In some cases the cause may be emotional,
manipulative or psychiatric. In others
a metabolic change may mimic symptoms as in hyperventilation. This outline concerns the neurologic causes
of dizziness. Vertigo is an illusion that self or the
environment is moving, and indicates inner ear or brain disease. Presyncope implies
a feeling of faintness or sensory disturbance caused by a transient or
progressive decrease in cerebral blood flow.
There is no hallucination of movement associated with presyncope. Multisensory deficit produces unsteadiness
in diabetics and elderly. Psychogenic
causes may mimic vertigo. Romberg testing can help differentiate a cause.
The cochlea and semicircular canals send
messages about movement to the vestibular nucleus in the brain stem. The brain stem sends this message to the
temporal lobe where it reaches consciousness.
Vertigo from inner ear
malfunction is rarely dangerous.
Vertigo from brain stem disease is rarely benign. Information from vision, vestibular
system, nuchal musculature and proprioception is integrated in the cerebellum
to produce equilibrium.
1. Inner
Ear Nystagmus: The inner ear sends a false message of
falling to the brain. The eyes drift
slowly towards the direction of the fall (primary phase). The intact cerebral cortex responds by
moving the eyes back quickly, resulting in repetitive jerky movements. Inner ear nystagmus is horizontal or
rotatory - never vertical. This
nystagmus can be suppressed by visual fixation and is fatigueable. It is a result of brain stem deviation and
cortical correction. It cannot occur in
coma.
The
patient activates fluid in the posterior semicircular canal by moving the head
back. Vertigo lasts only a few seconds,
has a latency of a few seconds, and tends to fatigue with repetition. It tends to be self-limiting, but can
persist or recur. Diagnosis and determination of the affected side is done
using the Dix-Hallpike maneuver.
Once
the affected side is determined, the Epley maneuver is
used to attempt repositioning of the
offending otolith crystals to a less sensitive part of the inner ear.
Caused
by accumulation of endolymph distending semicircular canals. This is continuous with the inner ear.
Attacks
of hearing loss, tinnitis and vertigo can last hours to days and tend to recur.
These
are isolated attacks of vertigo only lasting several days. Previously presumed to be viral, but the
cause is not known.
2. Brain Stem Vertigo: Almost always associated with other neurologic symptoms from the
brain stem (double vision, weakness, paresthesiae, incoordination). Ataxic nystagmus is displayed. Nystagmus beats in direction of gaze. It can be vertical. Eyes do not move in tandem. Nystagmus is enhanced by visual
fixation. Nystagmus without vertigo
is always CNS. In intranuclear
ophthalmoplegia only one eye moves when the patient looks to one side
· Posterior Circulation TIA or
Stroke
Posterior
circulation fills with clot. Occurs in
older patients with recurrent dizzy spells.
Risk factors for stroke exist, or patient may have known
atherosclerosis, heart disease, neck bruits or arrhythmia predisposing to
vascular pathology. Other brain stem
symptoms usually associated. Difference
in arm BP can imply subclavian stenosis leading to this mechanism. CT or MRI shows evidence of current or past
stroke.
Uncommon
condition presenting in patients with severe untreated hypertension. Sudden violent vertigo, vomiting, posterior
headache, diplopia, ataxia, decreasing level of consciousness, deviation of
eyes, slurred speech. CT or MRI in
acute stage may show hemorrhage but not infarct. Refer to a neurosurgeon.
Younger
patient with brain stem vertigo. Vertigo rare in first attack.
Multiple lesions in vestibular nucleus on MRI. If this is inconclusive, triple evoked potentials may show
evidence of asymptomatic lesions.
This
is caused by transient decrease in global cerebral blood flow. There is dizziness but not vertigo. Compensatory adrenergic symptoms
(tachycardia, hypertension, sweating, vasoconstriction, pallor). Usually benign and vasovagal. Can progress to syncope. Can imply serious disease such as coronary
disease, hypovolemia, aortic stenosis
or arrhythmia.
1. Audio Digest Family Practice April 28,
2002. Demystifying Dizziness. Dr John Edmeads.
2. http://www.vertigone.com/hallpike.htm
3. http://www.tchain.com/otoneurology/disorders/bppv/epley/fifth.html
4. Audio Digest Family Practice December 5,
1988. Dizziness/Preoperative
Examination. Dr. Gregory L. Henry
prepared
by N.J. Bosomworth, MD, CCFP
not
peer reviewed
1.
The
patient is seated with the head in neutral position
2.
The head
is rotated 45 degrees to one side.
3.
The
patient is briskly taken to the supine position with the head rotated. Vertigo is reproduced if this is the
affected side.
4.
The
patient is returned to the sitting head-neutral position.
1.
The
patient is seated with the head in neutral position.
2.
The
head is rotated 45 degrees to the affected side determined by the Dix-Hallpike
maneuver.
3.
The
patient is briskly taken to the supine position with the head rotated. Remain in this position 30-60 sec. Vertigo will result.
4.
The
head is rotated 45 degrees to the other side and held 30-60 seconds. Vertigo will result.
5.
The
patient is rolled 45 degrees to the same side as (4) with the neck rotated the
same 45 degrees. The face will be
directed to the floor. This is held 30
seconds. Vertigo will result.
6.
The
patient is returned to the sitting position with the head inclined forward for
1 minute.
7.
The
maneuver can be repeated 2 or 3 times
if tolerated.
8.
If
this is successful, recurrence is about 30%.
1.
In
end organ disease, patient falls toward the lesion and the environment tends to
move away from the involved side.
2.
If
results poor with eyes open, generally a cerebellar problem
3.
If
results good with eyes open and poor with eyes closed, suspect a proprioceptive
problem.