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Original Article

Pineal Calcification and its Relationship to the Fatigue of Multiple Sclerosis

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Pages 95-103 | Received 25 Jul 1992, Published online: 07 Jul 2009
 

Abstract

Fatigue is one of the most common clinical features of multiple sclerosis (MS) and is a frequent cause of disability. The pathogenesis of fatigue remains obscure. It may result from impaired propagation of action potentials in areas of demyelination. Other contributors may be mental depression, immobility, and physical disability. The fatigue of MS may be relieved by diverse pharmacological drugs such as amantadine and pemoline, but the mechanisms by which these agents act to ameliorate fatigue are unknown. Attention has been focused recently on the relationship between MS and the pineal gland and evidence has been presented to implicate the pineal gland and melatonin in the pathogenesis of the disease. To investigate this relationship further, we studied in 47 MS patients (mean age: 41.6 ± 9.9 yrs; mean duration of illness: 13.6 ± 12.6 yrs) the association between fatigue and incidence of pineal calcification (PC) on CT scan, which is thought to reflect past secretory activity of the gland. For comparison, we also evaluated the incidence of choroid plexus calcification (CPC) in these patients. The sample included 20 patients who experienced ongoing, debilitating fatigue during the course of the disease. 27 patients who did not complain of fatigue served as controls. The two groups were not distinguishable with respect to age, sex, age of onset, chronicity, course (relapsing-remitting vs. chronic progressive), and severity of the disease (ambulatory vs. immobile), as well as the incidence of affective illness. The incidence of PC was found to be significantly lower in fatigued patients compared to controls (70% vs. 96.3%; p <. 01), while the incidence of CPC did not differ between the groups. As PC was statistically unrelated to CPC, these findings imply a specific association between the fatigue of MS and PC. Furthermore, since the process of PC has been linked to past secretory activity of the gland, our findings add further support implicating the pineal gland and melatonin secretion in the pathogenesis of MS and provide an indirect evidence that the fatigue of MS is associated with alterations in pineal melatonin functions. If confirmed by further studies, our findings suggest that employment of major synchronizers of melatonin circadian rhythms such as bright light, sleep, or external magnetic fields may be beneficial for the treatment of fatigue in MS.

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