POST-TRAUMATIC VERTIGO

Medicine and Health Rhode Island, Oct 2004 by Friedman, Jules M

The incidence of dizziness and dysequilibrium following head and/or neck injury lies between 40-60%, even following mild or moderate head injuries not requiring acute hospitalization. Accordingly, most practitioners should have a fairly extensive experience with this large outpatient group. Yet, in spite of their familiarity with this common problem, many clinicians routinely use a diagnostic approach which is not pathophysiologically based and a treatment approach which is often confined to attempts at providing symptomatic relief with vestibular suppressants. Indeed, the tendency to attribute most post-traumatic dizziness to the post-concussion syndrome without diagnostic consideration of specific vestibular pathologies has been the cause of a significant and largely unnecessary increase in morbidity in this population. What follows is a review of those specific pathologies which, taken together, cause the great proportion of post-traumatic symptoms and which should rightly form the basis for a diagnostic and management approach.

TEMPORAL BONE FRACTURE

Fractures of the temporal bone occur in the more severe cases of head injury and have a number of clinical and radiological manifestations. They represent what should be an easily identifiable subgroup of head trauma patients discharged from acute hospitals in whom residual vestibular and/or auditory system symptoms can be expected to occur in high incidence (upwards of 95% in certain types of fractures). These symptoms commonly persist well beyond the period of acute hospitalization, and as such will most often require active (and possibly long-term) management by outpatient primary and specialty caregivers.1

Basal skull fractures may be of two kinds depending upon the relationship of the fracture line to the long axis of the petrous bone. These fractures can be well demonstrated on thin section temporal bone CT. Eighty percent are longitudinal and twenty percent are transverse. As longitudinal fractures run thru the axis of the middle ear, they often produce tympanic membrane tears with otorrhagia, and conductive or mixed hearing loss. They also can cause facial palsies. Given that the fracture line does not directly involve the inner ear, vestibular symptoms are somewhat less common in this type of fracture, but they can often occur due to concurrent labyrinthine concussion, perilymphatic fistula, or benign paroxysmal positional vertigo (see below). Transverse fractures extend thru the inner ear and produce damage to cochlear and/or vestibular labyrinthine neural structures directly with or without hemorrhage. They often produce hemotympanum and sensorineural hearing loss, and less commonly facial palsies. They also can be complicated by CSF leak and/or meningitis. Vestibular symptoms consist acutely of severe vertigo and ataxia (and possibly vegetative symptoms), which progressively improves due to CNS compensation, but in most cases persists to some degree well into the outpatient course. The nature of these persistent vestibular symptoms depends also upon the possible concurrent presence of a perilymphatic fistula, BPPV or the development of delayed hydrops (see below).

Successful outpatient management of the post-traumatic vertigo in this group of patients involves judicious restraint in the use of symptomatic treatment with vestibular suppressants (so as not to interfere with the development of CNS compensation), early resort to vestibular rehabilitation as the mainstay of treatment, and vigilance in detecting the concurrent existence or development of BPPV, perilymphatic fistula or delayed hydrops. Ongoing follow-up, including serial exams and timely utilization of vestibular laboratory diagnostic studies should be routine in patients not demonstrating progressive, if not rapid, recovery.

In spite of all such efforts, however, a small but significant percentage of patients with uncomplicated temporal bone fracture (estimates vary from 10-30% depending upon severity criteria) will remain with some degree of vestibular symptomatology indefinitely due to incomplete CNS compensation. This is the likely prognosis for those patients whose recovery during vestibular rehabilitation plateaus for two months in the absence of any other concurrent treatable vestibular post-traumatic pathology. In such cases, liberal use of vestibular suppressants long term remains the only option.

LABYRINTHINE CONCUSSION

Blunt head injury can concuss the membranous labyrinth against the otic capsule (much as the brain is concussed against the skull in cerebral concussion). This results in acute hypofunction of some portion of the vestibular neural substrate within the affected labyrinth. As labyrinthine concussions and transverse temporal bone fractures both produce acute unilateral (or asymmetrical) vestibular hypofunction, their clinical manifestations and course are much the same. There is the acute onset of vertigo and ataxia whose severity is proportional to the degree of hypofunction and there is some variable degree of associated vegetative symptomatology. Symptoms are most severe at the time of the head injury and invariably improve but with a temporal profile which can vary from days to months, with a minority of patients having some degree of residual symptomatolgy which persists indefinitely. There are, however, some differences which can be seen between labyrinthine concussions and fractures. Concussions are somewhat more likely to produce reversible neural insults which can result in a very abbreviated course of recovery. They are less likely to produce associated perilymphatic fistulas and to lead to the development of delayed hydrops, but are more likely to be associated with coexistent BPPV (perhaps because fractures more often result in complete ablation of all vestibular function), and hearing loss is a less common accompaniment. Although radiological confirmation of involvement of vestibular structures is necessarily absent in uncomplicated concussions, several types of vestibular diagnostic studies are now available to confirm and quantify the severity of these lesions and even to measure the degree of CNS compensation. Outpatient management considerations are otherwise the same for labyrinthine concussions as described above for fractures.