Never Sedate a Vertigo Patient

Immediate relief cannot balance the permanent damage to CNS compensating mechanism, says expert

So, the number one thing is, never, ever sedate a patient in this condition (vertigo)."

    This is as clear and as emphatic as Dr. Herman Kingma could get as he presented current concepts on the pathophysiology, diagnosis, and treatment of balance disorders during Solvay Pharma's recent Vertigo Teaching Day. He explained that the immediate relief derived from sedation cannot balance the permanent damage to the central nervous system's compensating mechanism, which is responsible for restoring vestibular function and balance.

    The problem with vertigo, said the secretary general of the International Society for Posture and Gait Research, is that it is very difficult and time-consuming to diagnose with precision. He noted that very often, the physician is confronted with a patient who complains of dizziness that is hard to classify whether of vestibular or other origin. Even if the physician is able to determine the problem with a complex and long history-taking, vestibular diagnostic tests are still necessary--and even these do not yield pinpoint accuracy.

    But the bigger problem, he noted, is that very little is really known about the etiology and pathophysiology of vestibular disorders to accurately tell what really goes on in the system that causes the problem. Said Dr. Kingma: "That's why in our current state of patient management, we do trial and error. We try to treat the symptoms as much as we can, and try one therapy after another to make the most of [treatment]. We have problems at all levels. We have a problem in defining the disease. We have a problem in the diagnosis. So we have a problem in defining the correct therapy. We have a problem in defining the efficacy of treatment and we find it very difficult to set the right indication area."

Three Functions

    Dr. Kingma said understanding vertigo requires a thorough understanding of how the vestibular system works. He outlined its three primary functions.

    First, it gives spatial orientation--"to let us know where we are in space, how we move, and how we stand." The vestibular system uses all sensory information from various senses to know what occurs within the environment. Based on the interpretation in the brain, it tries to learn what is happening around. Explained Dr. Kingma: "Apparently even if all senses are available, it is difficult to know whether it is you or the environment that moves. So, if you lose a part of your labyrinthine function, it means that your ability to know how and where you are in space is compromised. A labyrinthine loss implies a reduction of spatial orientation abilities--not only vertigo--which makes it more complicated."

    Second, it enables us to control balance. The labyrinth regulates muscle tone, specifically the extensor postural muscles, to make sure the person does not fall or lose balance. A sudden decrease of labyrinthine function causes a person to fall down. But this regulation of muscle tone is induced by the detection of gravity. The vestibular system also interacts with balance control to regulate the center of mass or gravity, which is the basic support of the body.

    Third, it stabilizes visual image during head movements. Image stabilization refers to the maintenance of the focusing ability of the retina on a visual image. Vestibular oto-reflexes correct fast movements by automatically calculating how fast an image moves throughout the visual field, which eventually controls the eye velocity via the oculomotor muscles.

    Dr. Kingma pointed to three problems associated with labyrinthine dysfunction. One of these, gaze stabilization, presents a very important reflex that can be measured easily in the clinic. These three functions require three modalities to be evaluated in the clinic. "You also have to consider the reserved capacity of the labyrinth, which helps overcome balance problems through learning and rehabilitation," he said. The simplest reflex is the vestibular oto-reflex where the labyrinth senses the motion of the head. The information goes from the canals to the statolith system to the vestibular nucleus, going to the oculomotor nucleus that crosses the optic nerve, which then controls the extra ocular muscles. To stabilize the whole image on the retina, reduction of the velocity of the image occurs within the brain.

    Post rotatory reaction occurs during excessive acceleration and rotation. This can be counteracted by the memory within the brain, which uses this information to control eye movements and other labyrinthine functions. Memory retained in the brain controls post-rotational reactions, thus vertigo and other labyrinthine symptoms can be unlearned.

Epley Maneuver

    Dr. Kingma explained that in labyrinthine disorders, the pathology arises in the vestibular nerve or the labyrinth, which induces central compensation for the body to achieve faster, optimal recovery.

    Vestibulospinal tests, like the Romberg test, are confirmatory in acute loss of vestibular function. These tests, however, have limited sensitivity and specificity. Force platforms and multi-directional moving platforms can measure balance and postural movements. Dynamic postugraphy can also determine the difference between patients with a labyrinthine deficit and healthy subjects. Dr. Kingma said it is also necessary to measure the canal function and vestibulo-ocular reflex at different frequencies. Labyrinthine loss is detected if the velocity of the eye reflex is not consistent with the velocity of the head movements induced by high sound frequencies. The faster the head shakes, the slower is the eye reflex.

    He admitted, however, that results from these tests are not always clinically relevant and helpful. And management is facilitated by simply helping the patient describe the disorder's behavioral patterns. The question, "when did it start?" as opposed to "what is your complaint?" will take the diagnosis farther since the description of vertigo-like symptoms is precisely what the patient finds so difficult to point out.

    Dr. Kingma demonstrated a simple way of looking for balance problems in a patient--the modified Epley maneuver. This positional test is composed of simple head and arm rotary movements performed at varying speeds to help the physician localize the origin of the balance disorder (whether labyrinthine or central) and identify the impaired sensory function.

    The Epley manuever will also help the physician weed out the inapplicable from the probable causes of the dysfunction based on the orientation of the vertigo canals at the time they experience stimulation. It serves as a simple treatment procedure as well. Through the controlled positionings, miniscule clogs that disrupt the vestibular balance are liberated.

Therapeutic Modalities

    Pharmacotherapy presents an important challenge since patients expect a strong action with fast alleviation of symptoms and minimal adverse reactions. Dr. Kingma said betahistine HCl (Serc) reduces the vestibulo-ocular reflex by about 50 percent, a result that is reproducible in most studies. Betahistine presents the first-line treatment for all types of labyrinthine problems. The problem of dose dependency arises since the medication works at different levels in the brain. However, it has been shown that dose dependency tapers off and reaches a plateau as treatment progresses.

    Dr. Kingma stressed that direct administration of a sedating agent will only provide temporary relief to the sensory conflicts and cause irreversible damage to the central compensating mechanism. He said adjunctive drugs like beta-receptor blockers and anti-epileptic drugs are for vestibular epileptic and chronic vertigo. Neurectomy is also suggested, but the potential damage is worse than the result. Ototoxic agents like injected gentamycin can also be of help, but dose-related complications occur and toxicity presents a formidable adverse reaction, he added.

    He noted other drugs like cinnarazine, flunarizine, piracetam, prochlorperazine, cyclizine, and dimenhydrinate are less efficient and act slow. They also have a strong sedating effect that will counteract the central nervous system's bid to restore symmetric sensitivity after a loss of function within the peripheral vestibular system. Sedation will interfere with neoplasticity, which relies on the unimpeded movement of sensory input to the peripheral vascular lesion site.

    Dr. Kingma stressed that direct administration of a sedating agent will only provide temporary relief to the sensory conflicts and cause irreversible damage to the central compensating mechanism. On the other hand, stimulating the vestibular system will restore the functionality of the impaired labyrinth side by encouraging the development of new synapses and reprogramming of neural connections. Since betahistine stimulates (neuroplasticity) instead of sedating, it serves as a more appropriate solution to spatial disorientation.

    Structurally similar to histamine, betahistine acts within four hours, lasting for about eight hours with a mechanism of action by competitive antagonism on the histamine receptors found within the vestibular nuclei and on the cerebral circulation.

     Dr. Kingma said adverse reactions are minimal and it is generally well-tolerated. More importantly, betahistine doesn't interfere with the vestibular adaptation response, with no psychomotor effects, and effectively reduces the frequency, duration and severity of vertigo and other associated symptoms such as tinnitus and deafness.