Gregory A. Ator, M.D., FACS
A patient presenting with vague disequilibrium and occasional episodic vertigo is a common occurrence in the general otolaryngology clinic. Typical etiologies include status post head injury and the vestibulopathy of the elderly. These patients often have mild progressive symptoms without spontaneous resolution. Many patients, over time, will have resolution of their symptoms, but for the patient who continues to have symptoms, treatment is frequently required. Traditional treatment methods have relied upon medication such as Antivert® and Valium® and perhaps Cawthorne type exercises in an attempt to encourage central nervous system adaptation and rehabilitation. I will briefly describe vestibular physiology, as it relates to compensation, and discuss the design and efficacy of a program of vestibular rehabilitation.
The function of the vestibular system is to transduce head acceleration into a signal the brain can interpret. This information is used by the central nervous system (CNS) for gaze stabilization on the retina and posture control. Transduction is performed for rotational motion by the semicircular canals and for linear motion by the otolith organs. A spontaneous discharge rate is present in the nerve fibers arising from these sense organs and rotation or displacement is excitatory in one direction and inhibitory in the opposite direction. Any difference between the discharge rates of the bilateral symmetrical vestibular apparatus is perceived as motion.
After a unilateral vestibular insult, there is persistent asymmetry in the vestibular nerve discharge rates leading to the incorrect sensation of vertigo and motion. These static symptoms, present in the absence of motion, quickly resolve with restoration of symmetrical discharge rates in the vestibular nuclei. Symptoms brought about by head motion (dynamic) take longer to compensate and the remaining vestibular organ as well as the visual system and the somatosensory network work in concert to maintain posture and balance. In most cases by reliance on these and other inputs the CNS can adapt to the unilateral loss of input and near normal function in all aspects of daily living can be attained. The mechanisms for the static and dynamic aspects of vestibular compensation to a peripheral deficit are largely unknown. Several mechanisms have been proposed: commissural pathways between nuclei of the vestibular system, reactive synaptogenesis, cerebellum nuclei modifications, and denervation supersensitivity. The most likely mechanism for resolution of static symptoms is, however, that neurons of the vestibular nuclei have a spontaneous pacemaker activity which takes over after input is eliminated from the peripheral organ. The compensation mechanism is affected by external manipulations which are of therapeutic value. It is known that sedative medications may prolong the time course and decrease the extent of compensation while stimulants such as amphetamines accelerate compensation. Other external factors can also influence the compensation process. Visual input is important in dynamic compensation and animals deprived of visual input do not manifest dynamic compensation although this has no effect on static deficits. Somatosensory and visual dysfunction impair dynamic compensation. The best example is the diabetic with retinal and somatosensory disease who suffers a new onset vestibular deficit. Because of the existence of dysfunction in all three limbs of the posture and balance system, compensation will likely be very minimal. Exercise is important in vestibular compensation in that immobility has been demonstrated to prevent dynamic compensation from occurring.
The importance of exercise in vestibular rehabilitation is not new, having first been described by Cawthorne and Cooksey in 1946. They noted that patients who exercised early after a unilateral ablation did better and they did so faster than patients who did not exercise. This clinical observation in support of modern experimental evidence provides the basis for rehabilitation; CNS compensation is facilitated by exercises with visual and somatosensory stimulation. The first step in a rehabilitation program is an assessment which is typically performed by a physical or occupational therapist. The patient is questioned about symptoms and a objective clinical assessment of vestibular function is made by physical examination, rotatory function, and posturography. A specific, tailored program is developed to address the particular deficits. The treatment strategy relies on the following factors: balance retraining for postural control mechanisms; eye and head coordination with progressively more difficult visual tracking tests; habituation therapy; and a general conditioning program. Indications for rehabilitation therapy include patients with: movement induced dizziness or poor compensation after a unilateral vestibular injury; status post head injury; the elderly patient with vague disequilibrium; and poor compensation or recurrent symptoms after surgery.
Several large series have been published recently detailing results from vestibular rehabilitation programs. Horak and Shemway reported a prospective study of twentyfive subjects with a peripheral vestibular disorder and symptoms greater than six months duration. These patients were divided into three treatment groups. The first group underwent a tailored program of twice weekly outpatient exercises. The second group was given a regiment of general (Cawthorne) exercises. Finally, a third group was given medications such as Antivert® and Valium® only. The results are encouraging in that the
patients who were on medication alone showed no objective improvement on posturography scores, but in the patients who had a tailored vestibular exercise regiment, there was a statistically significant increase in the posturography scores indicating improvement in compensation. A subjective dizziness index also showed significant improvement with the vestibular exercise program while no improvement was seen with the general exercise program and approximately 50% improvement with the medication alone group.
A prospective study from Shepard et al at the University of Michigan of 98 patients with diagnoses including peripheral, central, and mixed etiologies. These patients participated in a tailored program with twice daily home therapy lasting ten to fifteen weeks. Results showed a reduction in symptoms scores in 87% with complete resolution of symptoms in 36%. Patients with head injury accompanied by postural problems, but with normal visual and somatosensory systems, and those with secondary gain did the worst. Patients with episodic motion dysfunction had the best prognosis for improvement with this protocol.
In summary, vestibular rehabilitation is a important treatment modality for patients with vestibular dysfunction who are not surgical candidates. An increasing proportion of our society, the elderly, are often prime candidates for vestibular rehabilitation therapy. It appears that patients with peripheral vertigo with classical symptoms, especially of an episodic variety will definitely benefit from a vestibular rehabilitation program but also patients with a vague disequilibrium and probable central etiology for this condition may also benefit from vestibular rehabilitation therapy.
A 39-year-old female had benign paroxysmal positional nystagmus, vertigo, and imbalance secondary to a mild blow to the head. She fell while downhill ski racing and hit her head (no loss of consciousness) but was able to continue her activities within several minutes. She was previously healthy, with no significant medical problems, led an active life, and continued employment as a nurse. Symptoms of vertigo, nausea, and disequilibrium progressed over two weeks post-injury and persisted for ten months. Neurologic examination was normal; CT and MRI were negative. Tests of horizontal vestibulo-ocular reflex control (caloric and rotary chair) were within normal limits. On ENG testing, the patient demonstrated a directionally fixed vertical oblique nystagmus and vertigo in the right Hallpike position. All other positional tests were normal. Symptoms progressed to the point of interfering with her work and she sought medical treatment. She received outpatient therapy twice a week for six weeks, and twice daily performed home exercises targeted at a variety of postural, gaze, and motion perception disabilities. In addition, she participated in a low-impact aerobics program several times a week. After six weeks of therapy, repeat platform posturography revealed that she had normal body sway during all six of the sensory organization tests and her complaints of dizziness had significantly decreased. She still had mild complaints (intensity two on a scale of zero to ten) in 12 positions. She continued with her exercises, and within six months she was vertigo-free in all positions and has remained so.
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