Northeast Florida Medicine
Vol. 66, No. 1 2015
33
Otolaryngology
BPPV. Most of these cases will be recognized as vestibular
neuronitis. For anatomical reasons, the superior vestibular
nerve is thought to be more vulnerable to neuronitis.
13
Pa-
tients with this syndrome may complain bitterly of vertigo.
But, the prognosis for recovery is favorable. Symptoms will
last a shorter duration and fall risk is lower than when more
nerve branches are involved (Table 2). Additionally, the
risk for retro-labyrinthine tumor (vestibular schwannoma,
meningioma) is relatively low.
1
Points:
• vHIT and VEMP tests improve recognition of vestib-
ular syndromes and help predict recovery.
Chronic dizziness
Why is the passenger in a car driving down a winding road
more likely to become motion sick than the driver? Both are
exposed to the same visual, vestibular and proprioceptive in-
puts.The difference is that the driver is controlling the car and
can anticipate postural adjustments. In contrast, the passenger
has an imprecise idea of the car’s path and speed. They must
await the arrival of several streams of sensory information
and then react (organize the sensorium to estimate how the
car is or will be moving, develop and execute a motor plan
and monitor to determine if it was accurate). The reactive
process is more complex, time intensive and error prone than
the drivers’ task. Moreover, with uncertainty and fear (is the
car going to drive off a cliff?), there is a tendency to over-
weigh visual sensory information. Visual information takes
longer to process and is prone to ambiguities. Over-reliance
on vision can result is motion sickness.
Case #2:
An anxious 60-year-old woman presents with
chronic debilitating dizziness, spinning vertigo and fear of
falling. Her symptoms developed three years prior with a
severe disabling vertigo that lasted several days. The vertigo
gradually diminished, but never fully left her. She is constantly
dizzy, and feels better with her eyes closed. Headmovements
and complex visual scenes are particularly troubling. She has
been to several specialists with only marginal relief. She has
been treated for BPPV several times over the past three years.
These treatments initially helped, but symptoms continued.
She has also undergone several rounds of vestibular reha-
bilitation by competent physical therapists without relief.
Her audiological evaluationdemonstratednormal hearing;
vestibular evaluation demonstrated a right superior vestibu-
lar nerve deficit with signs of strong central compensation.
There was no BPPV noted. However, she resisted laying on
her right side for fear of re-provoking severe vertigo. Her
neurototologic evaluation was otherwise normal. She was
diagnosedwith prior vestibular neuronitis, quiet benign par-
oxysmal positional vertigo and chronic subjective dizziness.
Management involved three sequential goals:
1) Stabilize the unstable ear – monitor for and aggres-
sively treat BPPV.
2) Mitigate fear: Make any persistent dizziness sensa-
tions from chronic vestibulopathy predictable; Ensure the
patient understands that there is a benign reason for her
chronic symptoms; Include cognitive behavioral therapy
as a component of vestibular rehabilitation to address
dizziness induced anxiety.
3) Consider referral to psychiatry should symptoms
persist despite optimal management.
Comments:
It is likely that this patient experienced
frequent recurrences of BPPV. BPPV frequently develops
following a superior vestibular nerve based syndrome.
When present, vestibular output is unstable and vestibular
sensory information cannot be reliably re-registered with
the other senses. This often induces a visual over-reliance.
Even when BPPV has resolved, the brain may choose visual
over-reliance to register body sway. Such over-reliance will
result in an ambiguous sensorium, and may lead to a self-re-
inforcing perception of chronic dizziness, fear of falling,
catastrophic thinking and heightened anxiety.
14,15
When
this becomes habitual, the syndrome of chronic subjective
dizziness (CSD) has developed and may persist despite the
resolution of any vestibular deficit.
16,17
CSD can sometimes
be addressed through cognitive behavioral therapy and
vestibular rehabilitation that focuses on learning to move
into provocative positions or movements.
18,19
However in
some cases, psychotropicmedications may be needed. In this
case, the stratified approach of stabilizing vestibular output,
demonstrating vestibular compensation and addressing fear
reactions through cognitive behavioral therapy seemed to
be rational first steps in managing CSD. Ultimately, this
patient was referred to a psychiatrist specializing in chronic
subjective dizziness, and her symptoms did improve with the
addition of a Selective serotonin reuptake inhibitor (SSRI)
to her management plan.
Points:
• Before making the diagnosis of CSD, careful evalua-
tion to exclude unstable vestibular conditions such as
BPPV, perilymph fistula or superior canal dehiscence
is necessary.
• A cause for dizziness may not be
the
cause. In this case,
treating BPPV or the residual vestibular weakness did
not resolve dizziness complaints. Psycho-physiologic
interactions are real and need to be addressed to opti-
mize outcomes.
