Post-traumatic vertigo immediately follows head trauma in most cases implying end organ damage in the absence of other central nervous system signs. The interval between injury and onset of symptoms can, however, be days or even weeks. The mechanism for the delay of symptoms is uncertain but includes hemorrhage into the labyrinth, with later development of serous labyrinthitis. Another mechanism for delayed post-traumatic positional vertigo is cupulolithiasis in which the calcareous deposits (otoconia) of a damaged organ of the labyrinth are displaced to a sensitive region of the posterior canal making it more susceptible to stimulation in certain head positions. In posttraumatic vertigo, the symptoms may be those of general peripheral vestibulopathy or benign positional vertigo. Generally, the prognosis is good with symptoms gradually resolving within weeks to months. As pointed out by Baloh and colleagues, disabling persistent positional vertigo unresponsive to medical therapy, occurs more commonly than was previously recognized. The vast majority of patients respond to exercise therapy, as described below, and rarely need selective section of the nerve to the posterior semicircular canal.

Drug Toxicity 

Patients with dizziness produced by vestibulotoxic drugs are presumed or documented to have persistent injury to the peripheral end organ. Among the agents causing such end organ injury are the aminoglycosides. Streptomycin and gentamycin are most detrimental to the vestibular end organ; kanamycin, tobramycin, and neomycin cause more damage to the auditory end organ. Patients usually report progressive unsteadiness, particularly when visual input is diminished, as happens at night or in a darkened room. Vestibular testing documents a progressive bilateral loss of vestibular function. The aminoglycosides are concentrated in the endolymph and perilymph, thus the hair cells are exposed to high concentrations of the drugs. Extreme caution should be used in patients with renal disease because most of these agents are primarily eliminated by the kidney. This type of end organ toxicity should be contrasted with that produced by the large group of drugs with widespread reversible central and peripheral nervous system effects such as anticonvulsants and hypnotics (See section on Systemic Causes of Dizziness). The non-toxic drugs listed cause transient disequilibration which subsides with cessation of the medication.
A brand NEW chapter has been posted (current date 1-23-98) concentrating entirely on toxicity to the hearing and balance system: Drug Induced Vestibulocochlear Toxicity

Meniere's Syndrome 

Meniere's syndrome is characterized by attacks of severe vertigo, tinnitus, fluctuating hearing loss and ill-described aural sensations of fullness with spontaneous recovery in hours to days. Initially, the patient develops a sensation of fullness and pressure along with decreased hearing and tinnitus in a single ear. This is followed by severe vertigo, which reaches peak intensity within minutes and slowly subsides over hours. There is persistent sense of disequilibration for days after an acute episode. Occasionally, sufferers from Meniere's syndrome experience such severe attacks that they suddenly fall to the ground. Consciousness is not lost in such episodes, although awareness of surroundings may be altered by the intensity of the accompanying sensation and nausea which has been called Tumarkin's crisis. The most consistent pathological finding in Meniere's syndrome is an increase in the volume of the endolymphatic fluid and distention of the canals, hence the term endolymphatic hydrops. Although some specific causes such as bacterial, viral, and syphilitic infections may lead to the same pathological changes and symptoms, the majority of cases are idiopathic. Meniere's disease usually develops between the ages of thirty and fifty and is slightly more common in women than in men. The prognosis is for progressive reduction in hearing along with increasing frequency of attacks. Some patients stabilize with no subsequent attacks of severe vertigo, but they are left with residual hearing loss. Fifty percent of Meniere's patients become bilateral. The hearing loss often progresses to a moderate degree of deficit and then stabilizes.

Other Peripheral Vestibular Conditions 

Many other disorders affect the peripheral labyrinth, including acute otitis media, chronic ear infection, hereditary degenerative disorders of the end organ, and local tumors. Conditions such as a vertebrobasilar transient ischemic attack (TIA) or focal ischemic stroke of the end organ, particularly in an elderly patient, are often cited as a cause of vertigo. Such isolated involvement is difficult to document, and vertebrobasilar insufficiency should not be diagnosed without associated brainstem symptoms and signs. Please see discussion of central causes of vertigo, below, for further discussion of brain stem ischemia.