Static Compensation for Peripheral Vestibular Lesions

Vertigo of acute onset is accompanied by nystagmus and a variety of neurovegetative symptoms, such as nausea and vomiting. This symptom complex is a result of a persistent asymmetry of vestibular input, often seen after ablative surgical procedures or with acute insults to the peripheral system. The acute or static phase of recovery is mediated by tonic rebalancing of the resting activity in the vestibular nuclei. These changes minimize side-to-side discrepancies between the tonic firing rates in the second-order neurons originating in the nuclei and occur without the need of head movement or vision.^14–18 This activity generally provides relief from the most intense symptoms of vertigo and vomiting within 24 to 72 hours. Nevertheless, the patient continues to experience considerable dysequilibrium, because the system is unable to respond appropriately to the dynamic aspects of vestibular input produced by normal head movements. Thus, even after the intense vertigo has been controlled, continued motion-provoked vertigo is common until dynamic compensation is achieved.

Dynamic Compensation

To eliminate persisting dysequilibrium and residual motion-provoked vertigo after a vestibular lesion, the system must adjust to produce accurate responses to head movements. The dynamic compensation phase seems to be accomplished by reorganization of brainstem and cerebellar pathways, without modulating the neural input to the vestibular nuclei from the peripheral system.¹⁴ This process is much slower than static compensation and typically requires reprogramming of eye movements and postural control responses to head movements. The necessary reprogramming is accomplished by exposure to stimuli that challenge both the gaze stabilization and postural control systems. Because of the brainstem commissural pathways connecting the vestibular nuclei, appropriate central vestibular responses can be produced from inputs arriving from one functioning labyrinth. This feature of the compensation process is critical to recovery after extensive pathologic insults or ablative vestibular surgery, such as labyrinthectomy or vestibular nerve section. As discussed next, three major areas are active in the process of dynamic compensation: adaptation, habituation, and sensory substitution.

Adaptation is the neurologic mechanism that allows for long-term changes in the neuronal response to head movement-provoked gaze stabilization. The neural signals that induce the adaptation are generated primarily by “retinal slip” of the visual image on the retina. This phenomenon is generated by a disordered VOR response, when a head movement produces a perceived motion of a stable object in the visual environment. The resulting error signal can lead to fairly prompt and long-term changes in the functional performance of the VOR.⁴ This process of adaptation produced by retinal slip seems to be context-dependent, so that specific adjustments must be made for movements of different frequency, directions of head movement, eye position in the orbit, and distances from the visual target.^3,19 The complexity of the adaptation process helps explain why residual symptoms are almost unavoidable even in a fairly well-compensated patient. Postural stability also is improved by reducing abnormal visual influences on postural control mechanisms secondary to retinal slip.

Habituation is the long-term reduction of a response to a noxious stimulus resulting from repeated exposure to the stimulus.²⁰ This phenomenon seems to be context-dependent and does not generalize well from one head movement to another. This mechanism is essential for a variety of conditions that can produce sensitivity to head movement or motion in the visual surroundings. Although peripheral asymmetry is one common cause of these symptoms, other common causes are central lesions, anxiety disorders, and migraine disorders.⁵ Although the adjustments produced by habituation are made fairly quickly and are reasonably accurate, the central system requires consistency in the inputs to use them properly for habituation. For this reason, it is essentially impossible to “compensate” for an unstable vestibular lesion such as Meniere’s disease.

The primary goals of both adaptation and habituation are to produce gaze stability and postural stability in both static and dynamic situations. The response frequency ranges for gaze and postural stability are very different. To achieve gaze stability, the responsible mechanisms must function properly in a range from static position (no motion) up to movements that correlate with head motions as quick as 10 Hz. Postural stability is predominantly a task that requires responsiveness only below 4 Hz.^21,22

In addition to adaptation and habituation, another critical component of dynamic compensation involves sensory substitution. This process requires the adoption of alternate strategies for gaze and postural control, in order to replace the compromised sensory function. For example, the patient with bilateral loss of peripheral vestibular function becomes dependent primarily on visual or proprioceptive inputs to maintain postural stability. Although these mechanisms may need to be fostered in a therapeutic setting, many patients will have developed some of these out of necessity before coming for evaluation. Although sensory substitution may be helpful, it may be maladaptive in some environmental settings. For example, a patient may be overly dependent on vision and therefore cannot use proprioceptive and residual vestibular inputs to successfully navigate in darkness. In addition to the common substitution of visual and proprioceptive inputs, some of the other mechanisms that may be invoked in the setting of vestibular loss include (1) activation of the cervico-ocular reflex, which is not particularly active in healthy persons¹⁰; (2) use of the smooth pursuit tracking system¹¹; and (3) use of anticipatory or corrective saccades. Patients with both unilateral and bilateral vestibular deficits use corrective saccades to adjust for the reduction of VOR-induced eye movements after head movement. With central preprogramming through exposure to specific eye-head coordinated movements, these eye movements can be applied automatically to help maintain gaze stability when the VOR is deficient.^7,8

Research findings suggest that initial central vestibular compensation for a peripheral lesion can be enhanced by head movement but is delayed by inactivity.^23–26 It also is hampered by central vestibular dysfunction of any cause.²⁷ Medications that typically are used for acute symptoms of vertigo, such as meclizine, scopolamine, and benzodiazepines, all cause sedation and central nervous system depression. Although they may provide helpful symptomatic relief during the initial stages of an acute labyrinthine crisis, their effects are potentially counterproductive with respect to vestibular compensation, especially with use over extended periods.^24,28 In addition, chronic anxiety or other psychiatric disorders may delay or disrupt the compensation process.^29,30

Although remarkably reliable, vestibular compensation seems to be a somewhat fragile, energy-dependent process. Even after it is apparently complete, periods of symptomatic relapse may occur because of decompensation. A period of inactivity, extreme fatigue, change in medications, general anesthesia or an intercurrent illness may trigger these relapses. A relapse of vestibular symptoms in this setting does not imply ongoing, progressive, or new labyrinthine dysfunction.

These features of vestibular compensation suggest that avoidance of movements and body positions that provoke vertigo, as well as the traditional practice of prescribing vestibular suppressants, may be inappropriate. Because the stimulus for recovery seems to be repeated exposure to the sensory conflicts produced by movement, the patient’s medications should be discontinued once the acute symptoms are resolved, and an active program geared toward recovery should be encouraged. For most affected persons, recovery will be rapid and nearly complete. For some, the symptoms of vestibular dysfunction may persist. Although the latter patients are candidates for vestibular rehabilitation programs, starting a formal vestibular rehabilitation program as early as possible for patients whose symptom presentation suggests a high likelihood of benefit from such programs can help to avoid the persistence of symptoms.

Role of the Clinical History

A complete neuro-otologic history probably is the single most important component of the diagnostic evaluation of the patient with a balance disorder. Balance function study results must be interpreted in light of the presenting symptoms and medical history.³¹ In general, the information sought should include the onset of symptoms and their characteristics at that time, the progression of symptoms over time, the nature and duration of typical spells, any predisposing factors in the medical history, and use of medications or other management strategies. Complicating features of anxiety, depression, or excessive dependence on medications should be addressed. Some effort should be extended to identify the degree of disability produced by the patient’s vestibular complaints with respect to his or her professional and social activities. The stability and commitment of the patient’s psychological support system also should be assessed.

Ongoing complaints after a peripheral vestibular insult indicate that compensation is incomplete. The history and presenting symptoms are used to determine whether these continuing sensations may be a result of a fluctuating or progressive labyrinthine disorder. In the case of the unstable lesion, poor compensation results because the central nervous system cannot react to unpredictable peripheral inputs. In the history, an unstable periphery is suspected if symptoms are spontaneous in onset. In the stable cases, the symptoms are much more likely to be consistently provoked by head or eye movements. It is the patients with stable lesions who are most likely to benefit from vestibular and balance rehabilitation. The patients in the group with unstable lesions may have VBRT as part of their management, but it is not likely to be the primary modality of treatment.

Role of Vestibular Testing

The most traditional purpose of balance function studies is site-of-lesion localization addressing the sensory inputs, motor output elements, and neural pathways that may be involved in producing the reported symptoms. Balance function studies also may assess the patient’s functional ability to use sensory input systems in an integrated fashion, as in maintenance of stance before and after induced sway and coordination of head and eye movements during gaze activities. The third assessment goal is to evaluate, in a limited manner, the current degree of physiologic and functional compensation.³²

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