There is, nonetheless, a type of vestibular concussion accompanying closed head trauma that may leave the patient with imbalance or positional vertigo. Otolaryngologists are familiar with a syndrome resulting from a perilymph fistula after traumatic injury. The trauma may be minor, even forceful coughing, sneezing, or lifting; some cases are a result of chronic ear infection or cholesteatoma. Disruption of the oval or round windows causes a leak of perilymph into the middle ear. Vertigo and nystagmus can be induced by pressure in the external ear canal (the fistula test). If enough perilymph migrates to the middle ear, a conductive hearing loss may also be detected. Superior canal dehiscence, in which loud sounds induce brief vertigo and nystagmus (Tullio phenomenon) is another result of perilymphatic fistula, as discussed earlier. A perilymph fistula may be pronounced enough to also cause low pressure of the spinal fluid with the characteristic enhancement of the dura on MRI.
Vertigo of Brainstem Origin
Reference was made above to the occurrence of vertigo and nystagmus with lower and upper brainstem lesions. In these cases, vestibular nuclei and their connections are implicated. Auditory function is nearly always spared, because the vestibular and cochlear fibers diverge upon entering the brainstem at the junction of the medulla and pons. The vertigo of brainstem origin, as well as the accompanying nausea, vomiting, nystagmus, and disequilibrium, is generally more protracted but less severe than with labyrinthine lesions, but one can think of exceptions to this statement. Nevertheless, with brainstem lesions, one often observes marked nystagmus without the slightest degree of vertigo—which does not happen with labyrinthine disease. The nystagmus of brainstem origin may be unior bidirectional, purely horizontal, vertical or rotary, and is characteristically worsened by attempted visual fixation. In contrast, nystagmus of labyrinthine origin is unidirectional when the head is in a single position, usually with a rotary component, and past pointing and falling are in the direction of the slow phase; purely vertical nystagmus does not occur, and a purely horizontal nystagmus without a rotary component is unusual. Furthermore, labyrinthine nystagmus is inhibited by visual fixation and reverses direction with changes in the position of the head; nystagmus of brainstem origin generally displays none of these features. Either may have a positionalor movement-induced worsening, but this finding is more prominent in labyrinthine disease. Table 14-2 summarizes these findings.
The central localization of vertigo is confirmed mainly by finding signs of involvement of other structures within the brainstem (cranial nerves, sensory and motor tracts, etc.). Furthermore, Newman-Toker and colleagues have devised a combination of the head impulse test, nystagmus, and skew deviation (termed by them “HINTS”) that dependably differentiates central from peripheral; causes of and are particularly useful in emergency room diagnosis of vertigo.
Vertigo is a prominent symptom of ischemic attacks and of brainstem infarction occurring in the territory of the vertebrobasilar arteries, particularly the Wallenberg syndrome of lateral medullary infarction.
On the other hand, our colleague C.M. Fisher had pointed out that vertigo as the sole manifestation of brainstem ischemia from basilar arterial disease is rare. Unless other symptoms and signs of a brainstem disorder appear contemporaneously or soon after the vertigo, one can usually postulate an aural origin and nearly always exclude vascular disease of the brainstem. However, we have encountered rare patients with repeated brief attacks of vertigo that later proved to be caused by basilar artery stenosis, but in whom only a few episodes were associated with signs of brainstem disease such as dysarthria, facial numbness, or diplopia. In other words, frequent and sudden episodes of vertigo lasting a minute or so may infrequently be related to transient brainstem ischemia.