European Annals of Otorhinolaryngology, Head and Neck diseases 134 (2017) 171–175

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Review

Post-traumatic balance disorder

M. Elzière a,∗ , A. Devèze b , C. Bartoli c,d , G. Levy e
a
Service ORL, hôpital européen, 6, rue Désirée-Clary, 13003 Marseille, France
b
Service ORL, Ramsay générale de santé, hôpital Clairval, 13009 Marseille, France
c
UMR T24, IFSTTAR, laboratoire biomécanique appliqué, Aix-Marseille université, 13915 Marseille cedex, France
d
Service de médecine légale et droit de la santé, Aix-Marseille université, UFR médecine Timone, 27, boulevard Jean-Moulin, 13385 Marseille cedex 5, France
e
18, rue Gounod, 06000 Nice, France

a r t i c l e i n f o a b s t r a c t

Keywords: The causes of balance disorder are many and various, and the subjective syndrome of cranial trauma
Vertigo patients is diagnosed by elimination. Progress in otoneurologic functional exploration and brain imaging,
Balance disorder however, now generally allow this functional complaint to be given an objective basis. In recent years,
Cranial trauma
new diagnoses have improved recognition of such pathologies in the appraisal of corporal injury for
Appraisal
compensation purposes. The present article seeks to detail etiology and, by a review of the literature, to
Diagnostic decision-tree
determine factors liable to influence management and appraisal in particular.
© 2016 Elsevier Masson SAS. All rights reserved.

1. Introduction
Second to neck pain, balance disorder is the most frequent com-
plaint following cranial or neck trauma; instability is reported in
23–81% of cases in the first days post-trauma [1]. Progression is
often favorable, with symptom resolution within days or weeks.
On the other hand, balance disorder may also persist, becoming
disabling and sometimes preventing return to work. The balance
system involves various sensory receptors, including the 2 balance
organs, the eyes and somesthetic receptors. The balance organs
comprise 3 semicircular canals and an otolithic system composed
of utricle and saccule, the former coding for angular acceleration
and the latter for linear acceleration. Afferent information from the
various sensory receptors is integrated in the brain. If one receptor
emits faulty information, there will be discordance and ensuing bal-
ance disorder. Interview and clinical and paraclinical examination
are thus essential, to determine the origin of the balance disorder.
A range of audiovestibular examinations explore the various parts
of the inner ear [2]. Choice of examination and the performance
of the clinical examination, however, require good knowledge of
the etiologies underlying post-traumatic balance disorder. The ENT
physician should first rule out labyrinthine origin, but may also
refer the patient to other specialists such as a neurologist or oph-
thalmologist.
∗ Corresponding author.
E-mail addresses: melziere@gmail.com, drelziere@mesvertiges.com (M. Elzière).
The present article seeks to detail the various etiologies, both
labyrinthine and extra-labyrinthine, and, by means of a literature
review, to determine factors liable to influence management and
appraisal for compensation purposes in particular. We also present
the means at the practitioner’s disposal to identify malingerers.
2. Discussion
2.1. Vestibular etiologies
Benign paroxysmal positional vertigo (BPPV) is the principle
causal factor to be considered in post-traumatic balance disorder.
Classically, it is rotational, triggered by head movement. Patients
with BPPV, and especially BPPV of the semicircular canal, may also
complain of instability. Even minor cranial trauma may induce
BPPV [3]. Time to symptom onset is usually a few days, but cer-
tain reports found onset after several weeks or even months.
Post-traumatic forms frequently show recurrence and resistance
to therapeutic maneuvers [4]. Involvement is classically bilateral,
most frequently affecting the posterior semicircular canal [5]. Lat-
eral semicircular canal involvement is also possible. Anterior canal
involvement is very rare (3.2%) in idiopathic forms but classical
(27.3%) in post-traumatic forms [6]; incidence is underestimated,
as few physicians screen for it [7]. Videonystagmoscopic screening
of the 6 canals is recommended, using the Dix-Hallpike or modified
Dix-Hallpike maneuver; the Pagnini-McClure maneuver is used for
the lateral canal, consisting in positioning the patient supine and
imposing 90◦ head rotation on one side then the other; the Rose
maneuver is used for the anterior canal, with the patient supine and

http://dx.doi.org/10.1016/j.anorl.2016.10.005
1879-7296/© 2016 Elsevier Masson SAS. All rights reserved.
172 M. Elzière et al. / European Annals of Otorhinolaryngology, Head and Neck diseases 134 (2017) 171–175
the head in hyperextension. Videonystagmography (VNG) displays
positional nystagmus graphically, providing a complete written
record for the patient’s file. If obesity, multiple fracture or neck
stiffness prevent VNG, the patient should be referred to an otoneu-
rology team equipped with a dynamic Thomas Richard-Vitton
(TRV) chair [8]. Audiovestibular exploration is justifiable only for
recurrent BPPV or resistance to therapeutic maneuver. In post-
traumatic BPPV, however, audiometry seems indicated in case of
any atypic presentation: normal results argue for BPPV. Vestibular
work-up may be abnormal due to BPPV on the day of examination,
and results should be interpreted accordingly.
Temporal bone fracture should be suspected in case of high-
energy trauma and/or otorrhagia and/or Battle sign (retroauricular
ecchymosis). Auditory impairment and facial palsy should be
screened for systematically at interview and clinical examination.
Temporal CT distinguishes between 2 types of fracture. Extra-
labyrinthine or “longitudinal” fracture accounts for 80% of cases
and is caused by often lateral trauma. It often induces transmis-
sion hearing loss, due to hemotympanum and/or ossicle injury.
Vestibular work-up includes VNG, to detect any nystagmus (spon-
taneous, positional or revealed by Head Shaking Test [HST] or
nystagmus induced by bone vibration); the kinetic tests enable VNG
to quantify directional preponderance, which indicates imperfect
compensation, the importance of which in appraisal is well-known.
Subjective vertical visual deviation is a further argument for poor
compensation. The caloric reflex test and otolithic evoked poten-
tials (OEP) screen for vestibular injury and determine laterality,
and should be performed if otoscopy is normal (impedanceme-
try sometimes being contributive), or sufficiently late so as not to
be artifacted by hemotympanum. “Transverse” translabyrinthine
fracture, by often anterior or posterior impact, accounts for 20% of
temporal bone fractures; it induces sensorineural hearing loss or
complete deafness and/or facial palsy and/or cerebrospinal rhinor-
rhea. Given the seriousness of these conditions, vestibular function
should be assessed only after they have been treated.
Labyrinthine concussion is defined as sensorineural hearing
loss mainly affecting high frequencies, with or without vestibular
symptoms, following cranial trauma without labyrinthine frac-
ture. The concussion of the labyrinth causes micro-hemorrhage
[9]. Labyrinthine concussion should be considered in case of ves-
tibular impairment (e.g., hypovalence on caloric test) associated
with mainly high-frequency hearing loss, without bone lesion or
fracture on temporal CT. Clinical examination is, unfortunately,
poorly contributive. There is usually no spontaneous nystagmus,
although nystagmus may be revealed on HST. VNG may find uni-
lateral hypovalence and/or directional preponderance. As noted
above, audiometry often finds descending sensorineural hearing
loss predominating at 4000–8000 Hz [10]. Temporal CT is normal.
Cases of labyrinthine concussion have been reported with proven
contralateral labyrinth fracture, by bone-conducted pressure trans-
mission [11]. Progression is usually satisfactory within 5 days;
symptoms resolve spontaneously in most cases within a few weeks
to 2 months, but may persist or even worsen, in which case asso-
ciated cerebral concussion should be suspected. Balance disorder
associated to the auditory deficit is a factor of poor prognosis.
As a surgical treatment exists, perilymphatic fistula (PLF) should
be suspected in priority in case of post-traumatic balance disor-
der associated with auditory involvement. However, the typical
presentation of post-traumatic rapidly deteriorating sensorineural
hearing loss associated with vertigo triggered by pressure maneu-
vers is rare. PLF inducers multiple audiovestibular symptoms.
Diagnosis is based on a range of clinical and paraclinical findings,
requiring meticulous interview, appropriate audiovestibular tests
and high-quality imaging. At present there are, unfortunately, no
precise diagnostic tests, so that diagnosis is uncertain, and pos-
sibly late [12], complicating management, especially for expert
appraisal. A diagnostic scale, published in 2005, diagnoses PLF with
100% sensitivity and 70% specificity, based on clinical and paraclin-
ical data [13]; results should be regularly updated in the light of
other tests such as positional audiometry and electrocochleogra-
phy, which have proved contributive [14,15]. PLF consists in active
leakage of the labyrinthine fluid known as perilymph into the tym-
panum via the weak points of the oval and round windows [16].
Spontaneous PLF without evident trauma has been reported [17],
but traumatic etiologies are more frequent [12,18]. Symptom onset
is usually immediate, but the difficulty of diagnosis may cause
delay, and surgery may be implemented only some months or years
post-trauma. Audiometry may be normal, and in case of hearing
loss there is no specific profile. Positional pure-tone audiometry
completes auditory work-up, positioning the patient in left or right
lateral decubitus (depending on the affected ear) with renewed
auditory testing. It is considered positive in case of > 10 dB impair-
ment on ≥ 3 frequencies on change in position. Specificity is good
but sensitivity low; in some cases of pure vestibular involvement,
positional pure-tone audiometry can identify the affected ear. On
balance assessment, slightly fewer than half of patients with proven
PLF seem to show vestibular asymmetry on caloric testing [19].
Indirect signs (Tullio’s sign, instability or nystagmus triggered on
tragal pressure or Valsalva maneuver) should be screened for sys-
tematically, but lack sensitivity; a record of the tests should be
entered in the patient’s file. Asymmetric results on OEP [20] and
electrocochleography [21] contribute to diagnosis. Temporal CT
and brain MRI are highly contributive, but normal imaging does
not rule out PLF [22]. Apart from rare but pathognomic pneumo-
labyrinth, CT may show fluid filling one-third, two-thirds or all
of the round window recess: this is significant only if the rest of
the tympanum is well aerated. In the oval window, the position
of the footplate (dislocation, disorientation or fuzzy aspect) and
any adjacent fluid emission are screened for. Brain MRI is contribu-
tive to differential diagnosis, and should be prescribed ahead of
any surgery. Absence of nystagmus or of intraoperative perilymph
leakage in no way rules out diagnosis [18]. Depending on symp-
tom severity, surgery may be considered, consisting in filling the
windows with material. It is essential to inform the patient that sur-
gical exploration of the middle ear in case of doubt as to diagnosis
may not always succeed in providing proof of fistula, in which case
filling is performed “blindly”: i.e., systematically and preventively.
Filling the labyrinth windows may induce 5–10 dB transmission
hearing loss. Without pathognomic signs such as pneumolabyrinth
or in-vivo visualization of perilymph leakage, diagnosis is difficult
and controversial. Although prognosis seems correlated with early
treatment [23], there does not seem to be any deadline, as surgery
performed more than 10 months post-trauma in some cases pro-
vided functional benefit [24].
Otolithic disorder used to be undetectable, but new specific
paraclinical examinations now enable identification. Previously,
clinical examination failed to reveal otolithic disorder in these
patients with their particular complaints, now grouped together
as “otolithic syndrome”, defined by particular disorders such as a
sensation of sinking into the ground, walking on cotton wool, or
inebriation; onset is classically immediate on trauma, with symp-
toms that may last 6 weeks [25]. Animal studies demonstrated
otolith destruction following trauma, thus definitively proving the
existence of otolithic disorder [26]. Screening requires a subjective
visual vertical test and cervical or ocular OEPs. Asymmetric results
are significant, 72% of patients with post-traumatic instability
showing abnormal otolithic test results [27]. Vestibular rehabilita-
tion in otolithic syndrome [28,29], such as working on an inclined
plane or with otolithic stimulation, should be attempted, although
some cases of otolithic syndrome prove refractory.
It is established that minor cranial trauma may lead to decom-
pensation of previously asymptomatic inner ear deformity [30].
 M. Elzière et al. / European Annals of Otorhinolaryngology, Head and Neck diseases 134 (2017) 171–175
In such cases, temporal CT easily establishes etiologic diagnosis,
screening systematically for vestibular aqueduct dilation or semi-
circular canal dehiscence, among other signs.
Although rare, true Menière’s disease may be induced by
trauma, with histologic features identical to those of idiopathic
Menière’s disease [31]. Pure-tone and speech audiometry, electro-
cochleography, distortion-product otoacoustic emission phase-lag
and multifrequency impedancemetry are contributive [32]. Only 7
articles on the subject have been published since 1952.
2.2. Neurologic etiologies
Brain concussion or traumatic brain injury is secondary to
contusion or brain hemorrhage, mainly in the brainstem and/or
cerebellum. It is classified as mild, moderate or severe according to
Glasgow Score, initial loss of consciousness and/or post-traumatic
amnesia; these 3 factors are thus important elements in the inter-
view. Diffuse axonal lesions are secondary to shearing in the central
nervous system following sudden deceleration, and can be visual-
ized and demonstrated on MRI [33,34], using specific sequences:
susceptibility-weighted imaging and T2* gradient-recalled echo
[35]. Instability is frequent in mild concussion. Other symptoms
should be screened for: asthenia, headache, and concentration,
memory or mood disorder. A recent study demonstrated a par-
ticular entity, post-traumatic spatial disorientation, characterized
by instability in upright stance, alleviated by slow walking. Diffuse
axonal lesions and post-traumatic spatial disorientation show slow
and difficult recovery. Neuropsychological assessment may be pre-
scribed in case of cognitive disorder. Symptom duration is a matter
of debate, ranging from a few weeks to months or years; long-term
persistence is also possible.
Post-traumatic vestibular migraine is a well-established cause
of post-traumatic instability. Pathophysiology is controversial, but
management would seem to be the same as in other patients
with vestibular migraine. It should be systematically screened for
in interview, as treatment is available: vestibular physiotherapy,
anti-migraine drugs [36,37]. It is unfortunately little known and
probably underestimated: migraine attacks are classically without
vestibular symptoms, and diagnosis is difficult if headache is not
specifically screened for. Paraclinical assessment can confirm diag-
nosis, mainly by central signs on oculomotor tests on VNG, found
in 60% of cases, and abnormal kinetic test results, found in 75% of
cases [38].
Low cerebrospinal fluid pressure is an entity little known in the
medical and notably ENT community, and is probably underesti-
mated. It needs to be known and recognized, as there is effective
treatment: the Blood Patch, consisting in injection of autologous
blood into the lumbar peridural space, stopping the dural breach.
Low cerebrospinal fluid pressure should be considered in case
of post-traumatic balance disorder associated with orthostatic
headache occurring or worsening in upright posture and improv-
ing or ceasing in supine position. Other symptoms may be screened
for: edema, oculomotor disorder, etc. [39]. Brain and medullary
MRI is contributive, revealing pathognomic signs such as meningeal
breach or highly suggestive signs such as cerebellar tonsil descent,
pseudo-Chiari malformation aspect, or subdural fluid collection.
It may thus be useful to seek a neurologic opinion in case of post-
traumatic headache, cognitive disorder or any other sign suggesting
associated neurologic involvement.
2.3. Other etiologies
Cervical post-traumatic balance disorder is a very controversial
clinical entity, being difficult to study, unproven as yet in humans
but demonstrated in animal studies: ataxia and nystagmus were
triggered by local anesthetic injection in the neck [40].
173
There are, unfortunately, no specific sensitive tests to diagnose
balance disorder of cervical origin. Audiovestibular work-up should
be exhaustive, to rule out the previously discussed entities.
“Whiplash” consists in rapid acceleration–deceleration in the
cervical spine under frontal or dorsal impact, often concerning a
road accident. Impact is, by definition, not direct. Incidence has
risen with systematic seat-belt use. The mechanism leading to bal-
ance disorder consists in cervical proprioceptor overstimulation
due to hypertonicity in cervical gamma and orthosympathic fibers.
Secondary bone or soft-tissue lesions are known as whiplash-
associated disorder. The Quebec Task Force classified whiplash in
5 categories according to presence of neck pain, osteotendinous
signs, neurologic signs and fracture/distortion of the neck. Clinical
signs are non-specific. There is rarely initial loss of consciousness.
The presenting symptom is neck pain, leading to medical consulta-
tion and frequently neck X-ray and prescription of a Minerva brace.
Associated otolithic and semicircular canal involvement is proba-
bly underestimated. Unfortunately, few studies have focused on
the associated vestibular aspect. In whiplash with associated bal-
ance disorder, vestibular disorder should be assessed precisely, to
facilitate subsequent appraisal. Audiovestibular work-up should be
exhaustive, to rule out alternative etiologies.
Subjective syndrome of cranial trauma, also known as post-
concussion syndrome or psychogenic post-traumatic vertigo, is
perhaps the syndrome best known to medical appraisers, and the
most widely denounced. Given the etiologies described above, it
is clear that subjective syndrome of cranial trauma is a diagnosis
by elimination. We would stress that a minimum of audiovestibu-
lar functional exploration and imaging should be performed before
considering this diagnosis. Patients report diffuse, predominantly
posterior headache resistant to analgesia, dizziness, instability,
difficulty in concentration, sleep disorder, mood disorder and
asthenia. Symptoms resolve within 1 or 2 months in 50% of cases.
Exploration results as a whole are often normal. A slight directional
preponderance may be found on kinetic testing, but with no signs
of simulation on posturography.
Visuospatial disorder secondary to cervical afferent fiber lesion
may cause balance disorder [41]. It is therefore useful to screen sys-
tematically for visual and spatial perception complaints among the
complaints reported by patients with otolithic disorder or brain
concussion. Postural or visual instability, oscillopsia or impaired
distance judgment require orthoptic assessment, completed by a
dynamic visual acuity test to assess oscillopsia and VNG to analyze
and measure ocular saccade precision and latency. Other condi-
tions should be screened for: accommodation disorder, vergence,
photosensitivity, etc. Early diagnosis is essential, as detec-
tion 3 months post-trauma was associated with poor remission
[41].
The difficulty of assessing severity in post-traumatic balance
disorder lies in the subjective nature of the functional complaints.
Although undeniable, the “functional” component seems to be
overestimated by physicians.
We would stress the importance of clinical judgment in the
absence of any reliable tests. Dynamic posturography is useful in
some cases [42–47]. A scale of 9 criteria based on posturography
results was published in 2005; scores greater than 5 can con-
tribute to identifying patients with “non-physiological” behavior
[48]. Malingering is a kind of delusion based on an unjustified claim;
simulation consists in reporting imaginary disorders, to deliber-
ately mislead the observer; “oversimulation”, more characteristic
of our balance-disorder patients, consists in exaggerating a real
disorder secondary to a real, demonstrated lesion.
Having listed these various entities, we would stress the
important role of the ENT physician in managing patients with post-
traumatic balance disorder. A diagnostic decision-tree (Fig. 1) may
facilitate management. Medical appraisers, despite the subjective
174 M. Elzière et al. / European Annals of Otorhinolaryngology, Head and Neck diseases 134 (2017) 171–175

Management of post-traumac balance disorder

AUDIOMETRY and VNS

BPPV?
VNS
PLF?
abnormal Labyrinthine concussion?

Audiometry abnormal Audiometry and VNS

yes
normal
• With migraine criteria:
Temporal CT Headache? Post-traumac migraine?
• Posional:
CSF hypotension?

abnormal
normal no VESTIBULAR WORK-UP
abnormal
Temporal bone
PLF? Otolithic vergo?
fracture? normal
Labyrinthine concussion? PLF?
PLF ?
Post-traumac edema?
OPHTHALMOLOGIC/ORTHOPTIC WORK-UP

VESTIBULAR WORK-UP abnormal

normal
IMAGING, according to clinical context Visuospaal disorder?
(temporal CT/ brain MRI)

normal abnormal
Cervical origin? Decompensaon of inner ear deformity?
Post-traumac stress? Cerebral contusion?

Fig. 1. Diagnostic decision-tree for the management of post-traumatic balance disorder.

nature of the patients’ complaints, can more easily decide on the
existence of medical causes.
Current legislation in France distinguishes between unilateral
peripheral vestibular involvement, bilateral destructive peripheral
vestibular involvement and otolithic deficit in the scale used to
assess invalidity in BPPV.
3. Conclusion
In the interview and clinical examination, it is fundamental to
screen for the various entities implicated in post-traumatic bal-
ance disorder, which may be found in association, complicating
diagnosis. Audiovestibular exploration serves only to confirm clin-
ical suspicion and provide objective elements for the medical file.
Progress in functional exploration has considerably refined objec-
tive diagnosis of vestibular impairment. The PLF diagnostic scale
should be regularly updated, and balance disorder of cervical origin
should be better known. Likewise, progress in imaging may in the
future facilitate objective detection of early or late post-traumatic
lesions, enhancing recognition of this pathology for the purposes
of compensation for corporal injury.
Further research is needed concerning objective criteria of sim-
ulation, “oversimulation” and malingering, given the subjective
nature of the complaints.
The subjective syndrome in cranial trauma is at present a diag-
nosis by elimination. In the light of the recent literature, current
appraisal scales should be improved, with better recognition of
victims of cranial or cervical trauma presenting with secondary bal-
ance disorder. It would be useful in the future to try to harmonize
scales at a European level.
Disclosure of interest
The authors declare that they have no competing interest.
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