The pineal gland, cataplexy, and multiple sclerosis

Abstract

Since the discovery of melatonin as the principal hormone of the pineal gland in 1963, scientists have come to recognize that melatonin is a "master hormone" involved in the control of circadian rhythms and other biological functions. Although little is known about the influence of the pineal gland on motor control, important clues may be obtained by considering the pattern of melatonin secretion during the sleep cycles and particularly during rapid eye movement (REM) sleep when melatonin plasma levels are at their lowest. Since REM sleep is characterized by the occurrence of profound atonia which results in an almost complete paralysis of striated muscles, it is suggested that there might be a causal relationship between inhibition of melatonin secretion during REM sleep and the development of REM sleep atonia. This relationship is supported by the findings that melatonin regulates the activity of brainstem serotonin (5-HT) neurons which characteristically cease to fire during REM sleep and which faciliate the development of REM sleep atonia. Moreover, as the muscular atonia of REM sleep is physiologically and pharmacologically indistinguishable from cataplexy, it is possible that the pineal gland also influences to the development of cataplexy. Cataplexy is an ancillary symptom of narcolepsy and also occurs in multiple sclerosis (MS). In fact, it is believed that several of the neurological symptoms experienced by patients with MS such as weakness in the legs, feeling of collapsing knees, paroxysmal sudden falling, weakness in the neck, extreme fatigue, intermittent paresthesias, slurring of speech and intermittent blurring of vision, which often are exacerbated by stress and other emotional influences, may reflect the manifestations of cataplexy. Thus, several of the clinical features of MS may reflect a dissociated state of wakefulness and sleep and may improve by the administration of anticataplectic drugs.