Posttraumatic Vertigo 

Updated: Jul 11, 2018
Author: Brian E Benson, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA 



Vertigo is a common symptom in individuals who have experienced blunt trauma of the head, neck, and craniocervical junction. Injuries that result from motor vehicle accidents, falls, assault, and contact sports may cause vertigo. The great variability of trauma mechanisms and impact forces results in multiple possible anatomic sites of injury to the vestibular system. The signs, symptoms, and treatment modalities for posttraumatic vertigo likewise vary according to the injured anatomic structures. However, no correlation between the mechanism of injury and a specific vestibular disorder has been shown.[1]

The most common vestibular pathologic condition associated with head trauma is benign paroxysmal positional vertigo (BPPV), which occurs in about 28% of individuals with head trauma.[2] Other less common vestibular disorders that result from head trauma include brainstem concussion or eighth nerve complex injury, posttraumatic Ménière syndrome or delayed endolymphatic hydrops, rupture of the round window membrane or perilymphatic fistula (PLF), and labyrinthine concussion.

Proper diagnosis of the exact vestibular disorder is the key to successful management. The focus of this article is limited to peripheral neurotologic injury and excludes the central causes of posttraumatic vertigo, which include postconcussion syndrome, whiplash injury syndrome, epileptic vertigo, diffuse axonal injury, posttraumatic migraine, and psychogenic vertigo.

An image depicting the Dix-Hallpike maneuver can be seen below.

Posttraumatic vertigo. The Dix-Hallpike maneuver. Posttraumatic vertigo. The Dix-Hallpike maneuver.


The entire vestibular system is potentially at risk following blunt trauma to the head and neck region. Radiologic and postmortem studies indicate that the pathophysiologic mechanisms that underlie these diverse vestibular injuries are sometimes unclear.

Benign paroxysmal positional vertigo

Of all the pathophysiologic mechanisms of posttraumatic vertigo, traumatic BPPV is the best understood. The underlying mechanisms of traumatic BPPV are the same as those of idiopathic BPPV and include the theories of canalolithiasis and cupulolithiasis. Canalithiasis is defined as the condition of particles residing in the canal portion of the semicircular canal (SCC).[3] These densities are considered to be free floating and mobile, causing vertigo by exerting a force. In contrast, cupulolithiasis refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating.

Brainstem concussion or eighth nerve complex injury

The eighth nerve complex is at risk for injury, even in cases of mild trauma, because of the shearing effect on the root entry zone of the nerve to the brainstem. This mechanism has been demonstrated in experimental models and in autopsy reports.

Posttraumatic Ménière syndrome or delayed endolymphatic hydrops

The mechanism of posttraumatic Ménière syndrome, aside from the disruption of the endolymphatic duct secondary to a temporal bone fracture, is thought to be caused by bleeding into the inner ear followed by a disturbance of fluid transport. One author found that trauma caused posttraumatic Ménière syndrome in 3% of 120 patients.[4] Other studies have also described trauma that causes endolymphatic hydrops without temporal bone fractures.[5]

Perilymphatic fistula

PLFs are abnormal communications between the inner ear and the middle ear. Although PLFs usually occur secondary to temporal bone fractures, leaks can occur through tears in the round window membrane or the ligamentous attachment of the stapes footplate to the rim of the oval window. Goodhill, who defined the exact pathophysiology of PLFs, highlighted 2 mechanisms for the rupture of the round or oval window: explosive and implosive.[6] The explosive mechanism theory postulates that head trauma results in a sudden increase in cerebrospinal fluid (CSF) pressure that is transmitted to the perilymphatic fluid, causing an explosive rupture of the membranes. The implosive mechanism occurs when external trauma applied to the tympanic membrane results in an implosive rupture of either membrane.

Cervical vertigo

The pathophysiologic mechanism of cervical vertigo is poorly understood. Although many theories exist, most authors suggest that cervical vertigo is due to vascular compression and alteration of sensory input to the vestibular system.

Labyrinthine concussion

The pathophysiology of labyrinthine concussion is poorly understood. However, posttraumatic vertigo that resolves spontaneously over time, after other diagnoses have been excluded, is known as labyrinthine concussion.



The incidence of vertigo in the United States, with even mild head injury, ranges from 15-78%. An Italian study of 3060 patients with BPPV found that 716 of them (23.4%) were clearly associated with a traumatic event.[7]  A smaller study, of 69 patients with chronic BPPV, found a history of head or neck trauma in 81% of the cohort.[8]


The causes of posttraumatic vertigo are not fatal, but they can be associated with significant morbidity. The amount of morbidity related to posttraumatic vertigo has not been well studied. Vertigo can cause further accidents and falls if not treated appropriately. In addition, some patients may no longer be able to work and may even have to claim disability.


No racial predilection has been shown to exist.


No sex predilection has been shown to exist.


Posttraumatic vertigo occurs in all age groups.




See the list below:

  • The patient should be asked exactly when and how the head or neck was injured and if a loss of consciousness occurred. If the patient was involved in a motor vehicle accident, the patient should be asked whether the airbag was deployed. One study found a significant incidence of vertigo and hearing disturbances after airbag deployment.[9] Available emergency room and hospital records should also be obtained.

  • Characterizing exactly what the patient means by "dizzy" is the most important step of the evaluation process. Vertigo is the illusion of movement in the absence of actual movement and is a specific symptom of a lesion of the inner ear, vestibular nuclei, or vestibular pathways. Characterizing the vertigo is also necessary for a precise diagnosis. The temporal relationship between the trauma and onset of symptoms is important. Momentary vertigo associated with rapid head movements suggests benign paroxysmal positional vertigo (BPPV), whereas vertigo that begins in a delayed fashion and lasts for several hours tends to occur in Ménière disease. Asking about associated symptoms such as hearing loss, tinnitus, nausea, and vomiting also helps to elucidate the diagnosis.

  • Although the symptomatology of vestibular injuries associated with head trauma may vary, some injuries may present similarly. For example, brainstem concussion and labyrinthine concussion can both cause acute vertigo that results in constant unsteadiness and worsens with darkness, fatigue, and motion. Further testing is necessary to differentiate between these 2 pathologies. BPPV is easily recognized based on the pattern of dizziness that is elicited only when the head is placed in certain positions. Ménière syndrome typically produces episodic whirling vertigo, often associated with nausea and vomiting, as well as with fluctuating hearing loss, tinnitus, and aural fullness. Onset of the symptoms of Ménière syndrome varies from immediately following the trauma to one year later. In posttraumatic Ménière syndrome, the vestibular symptoms often predominate.

  • Patients with perilymphatic fistulas (PLFs) present with symptoms similar to those of patients with Ménière syndrome; however, those symptoms can be differentiated based on the temporal relationship to the injury. Patients with PLFs are usually symptomatic within 24-72 hours after injury, whereas traumatic Ménière syndrome typically takes months to years to manifest. Patients with cervical vertigo can also have symptoms of tinnitus, as well as hearing loss and neck pain or tenderness with palpation.


See the list below:

  • A complete head and neck examination is necessary.

  • An otologic inspection is necessary to rule out disease of the external and middle ear. The Weber test and Rinne test are used to document sensorineural or conductive hearing losses.

  • A fistula test entails making a sensitive recording of eye movements while pressurizing each ear canal with a pneumatic otoscope and is almost always needed. A positive test is good grounds for surgical exploration. In window fistulae, very little nystagmus is produced, and a positive test may consist only of a slight nystagmus after pressurization.[10] In superior canal dehiscence, a strong nystagmus may be produced.

  • Examine the patient for the presence of spontaneous gaze and positional nystagmus.

  • Nasopharyngoscopy and indirect laryngoscopy are considered part of the neurotologic examination.

  • A cranial nerve examination is essential.

  • A vestibular and cerebellar assessment is made via past-pointing, rapid repetitive motion, Romberg, tandem walking, and cold-water caloric testing.

  • Administer the Dix-Hallpike maneuver.


See the list below:

  • Many mechanisms cause blunt trauma to the head. Motor vehicle accidents are responsible for half of all cases of mild head trauma, whereas assaults and falls account for the rest.[11]

  • Whiplash has also been implicated as a cause of posttraumatic vertigo.[12]



Diagnostic Considerations

These include the following:

  • Perilymph fistula

  • Cervical vertigo

  • Brainstem concussion

  • Labyrinthine concussion

Because of the high incidence of litigation associated with posttraumatic vertigo, most clinicians are cautious when making this diagnosis.

Differential Diagnoses



Laboratory Studies

See the list below:

  • Cochleovestibular

    • Standard audiometry (used to document present hearing acuity and, if loss is present, to determine whether it is sensorineural or conductive hearing loss)

    • Impedance audiometry or tympanometry (used to determine the status of the tympanic membrane and middle ear)

  • Electronystagmography or oculomotor testing (The standard ENG test battery is composed of saccadic, gaze, pursuit, optokinetic-eye movement, head-shake nystagmus, positional nystagmus, positioning nystagmus, and bithermal caloric tests. This testing battery is used to determine whether the vertigo is otologic or central in origin.)

    • Bithermal calorics

      • Barany introduced the caloric test in 1903. Since then, it has been the time-honored vestibular test in clinical neurotology. The caloric test remains the standard for evaluating unilateral vestibular deficit. However, it is a limited and nonphysiologic test of the vestibular system.

      • The traditional caloric test is performed with the patient lying with the head elevated; cold (30° C) and warm (44° C) water are used to irrigate each ear, 1 at a time. Cold irrigation is an inhibitory stimulus, and warm irrigation is excitatory. The direction of postcaloric nystagmus is determined by the quick phase direction and is easily remembered by using the mnemonic COWS: cold opposite and warm same (ie, quick phase away from or toward the irrigated ear).

      • The 3 most important findings from the caloric test are unilateral weakness, bilateral weakness, and failure of fixation suppression (FFS) of caloric-induced nystagmus. The first 2 abnormalities are due to peripheral vestibular disease, and the third is due to central cerebellar disease.

    • Rotary testing

      • Barany introduced rotational testing in 1907. In clinical practice, the rotation test lagged behind the caloric test. However, with the advancement of computer technology, rotational chair-test systems were developed in the late 1970s and continue to evolve. They are now used in several vestibular testing laboratories.

      • The test is used to evaluate the integrity of the vestibuloocular reflex (VOR) in the low- (0.1-0.32 Hz) or high-frequency (1-4 Hz) ranges. The measured parameters are VOR gain, phase (latency), and symmetry. The test is most useful in determining residual vestibular function and the degree of central vestibular compensation.

Imaging Studies

See the list below:

  • CT scan of the temporal bone

    • These scans are very useful for identifying temporal bone fractures.

    • Two kinds of fractures, longitudinal and transverse, are differentiated in relationship to the long axis of the petrous bone.

    • Transverse fractures extend through the inner ear and are more likely to cause vestibular symptoms.

  • MRI of the temporal bone and internal auditory canal, with and without contrast, can be obtained to rule out abnormal anatomy or lesions, which are important to exclude.


See the list below:

  • Dix-Hallpike maneuver

    • The patient sits upright on an examination table. The head is turned 45° such that the chin is toward the shoulder. The patient is then brought straight back rapidly into a head hanging position. This position is maintained for at least 30 seconds. See the image below.

      Posttraumatic vertigo. The Dix-Hallpike maneuver. Posttraumatic vertigo. The Dix-Hallpike maneuver.
    • The nystagmus characteristic of BPPV begins after a latency of 2-10 seconds, increases in amplitude over about 10 seconds, and decreases in velocity over the next 30 seconds.

    • Transient geotropic rotatory nystagmus (clockwise with left ear down, counterclockwise with right ear down)

    • Severe subjective vertigo

    • Fatigability

  • Epley maneuver (canalith repositioning maneuver)



Medical Care

The treatment is individualized to the diagnosis, as follows:

  • Brainstem concussion - Vestibular rehabilitation

  • Labyrinthine concussion – Vestibular suppressants and vestibular rehabilitation

  • Benign paroxysmal positional vertigo – The Epley maneuver and vestibular rehabilitation (See the image below.)

    Posttraumatic vertigo. The Epley maneuver. Posttraumatic vertigo. The Epley maneuver.
  • Posttraumatic Ménière disease - The same therapy as for the idiopathic type of the disease is used for a duration of 3 months, as follows:

    • Salt restriction

    • Diuretic

    • Niacin

    • The Meniett device, created by Xomed, is an FDA-approved class II device used for treatment of vertigo. It is a portable, low intensity, alternating pressure generator that is applied to the external auditory canal. It transmits pressure to the round window via a tympanostomy tube.

    • Transtympanic/intratympanic gentamicin injection by means of multiple delivery methods including low-dose therapy, titration, multiple daily dosing is also used. Chia et al performed a meta-analysis of different modalities of delivery for transtympanic gentamicin injections in 2004.[13] They found that low-dose therapy was the least effective in controlling symptoms, which is not surprising because of the lower amount of gentamicin used. However, hearing preservation was no better in this group than any other. The titration method exhibited the best results, and had the best hearing outcomes. Hearing loss was greatest for multiple daily dosing, but vertigo symptoms were not more improved in this group. Chia recommended titration therapy as a very useful method.

  • Perilymphatic fistula – Bed rest for at least 5 days and the avoidance of the Valsalva maneuver

  • Cervical vertigo - Vestibular rehabilitation and anti-inflammatory medications

Surgical Care

See the list below:

  • BPPV: Surgery is not a first-line treatment because it can have serious risks such as hearing loss and facial nerve damage. Surgical options include labyrinthectomy, posterior canal occlusion, singular neurectomy, vestibular nerve section. All have a high chance of vertigo control.

  • Brainstem concussion: No surgical options are available.

  • Labyrinthine concussion: Labyrinthectomy or vestibular nerve section are options.

  • Ménière disease: Endolymphatic shunt (success rate between 75-80%) and labyrinthectomy (success rate between 75-80%) are options.

  • Perilymphatic fistula: Middle ear exploration and tympanotomy and placement of soft tissue graft over the fistula are options.


An otolaryngologist should be consulted when conservative management fails. In addition, a neurologist should be consulted if vertigo of central origin is suspected.



Medication Summary

Acute vestibular symptoms caused by peripheral disorders may be temporarily ameliorated by antiemetics and vestibular suppressant drugs. Although vestibular neurochemistry is well understood, the treatment of vestibular disorders is primarily empirical. This is primarily the result of the lack of appropriate clinical trials that establish the efficacy, duration, and dosage of the drug.


Class Summary

The agents work as vestibulosuppressants and antiemetics by binding to specific receptor sites, which potentiates the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.

Diazepam (Valium)

Depresses all levels of CNS possibly by increasing activity of GABA.


Class Summary

These agents decrease symptoms by masking the vertigo. They dull the brain's response to the inner ear's signals.

Meclizine (Antivert, Antrizine)

Decreases the excitability of the middle ear labyrinth and blocks conduction in the middle ear vestibular-cerebellar pathways. Effects are associated with relief of nausea and vomiting.


Class Summary

These agents are useful in the treatment of nausea caused by vertigo.

Promethazine (Phenergan)

Antidopaminergic agent effective in the treatment of emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.



Further Outpatient Care

See the list below:

  • Close follow-up is essential for treatment of patients with posttraumatic vertigo.

  • Vestibular rehabilitation can help patients to cope with vertigo.


Treatment failures are most likely secondary to misdiagnosis. Posttraumatic vertigo can be treated successfully once the underlying cause is identified. The causes can be identified in most cases using the appropriate history, physical examination, and neurotological tests.


The prognosis depends on the diagnosis and the response to conservative therapy. A literature review by Aron et al suggested that symptom resolution rates in posttraumatic BPPV are comparable to those in nontraumatic BPPV. The investigators added, however, that multicanal involvement may be more prevalent in posttraumatic BPPV, leading to the need for more repositioning maneuvers in these patients than in those with the nontraumatic variety. They also stated that more studies are needed to prove their assertions, owing to a current lack of well-designed studies with adequate cohorts.[14]

A study by Prokopakis et al suggested that canalith repositioning procedures have less long-term efficacy in patients with BPPV who have suffered head trauma than in other patients with the condition. The study involved 965 patients, who were followed up at 48 hours and 7 days following their initial treatment and then every 6 months, for a mean total of 74 months. They were treated with variants of either the Epley maneuver or the barbecue roll maneuver, depending on whether they had posterior and anterior canal involvement or horizontal canal involvement, respectively. The investigators found that symptoms of benign paroxysmal positional vertigo recurred in 139 patients, with the recurrence rate being significantly greater in patients with head trauma, as well as in elderly patients and in those with a history of vestibular neuropathy.[15]

On the other hand, a retrospective study by Luryi et al did not find a traumatic etiology for BPPV to be linked to a greater risk for the condition’s recurrence.[16]