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. 
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.  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.
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).  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.  Other studies have also described trauma that causes endolymphatic hydrops without temporal bone fractures. 
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.  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.
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.
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. 
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.
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