Nervous system lesions

B, Thiamin Coenzyme in pyruvate and a-ketoglutarate, dehydrogenases, and transketolase poorly defined function in nerve conduction Peripheral nerve damage (beriberi) or central nervous system lesions (Wernicke-Korsakoff syndrome)... 

Central sleep apnea (CSA less than 10% of all apneas) is characterized by repeated episodes of apnea caused by temporary loss of respiratory effort during sleep. It may be caused by autonomic nervous system lesions, neurologic diseases, high altitudes, and congestive heart failure. 

Valade MP. 1952. [Central nervous system lesions in chronic experimental poisoning with gaseous hydrocyanic acid]. Bull Acad Natl Med (Paris) 136 280-225. (French)... 

Vitamin E-deficiency diseases are well known among laboratory and farm animals and can be a considerable problem in animal husbandry. Thus, the vitamin was discovered because its absence from the diet causes pregnant female rats to resorb their foetuses [25], and male rats to suffer testicular degeneration [26]. In the rabbit muscular dystrophy occurs, and in sheep and cattle similar muscular degeneration also is the principle sign of vitamin E deficiency [27], In the chick given high levels of linoleic acid and no vitamin E an acute central nervous system lesion called encephalomalacia occurs... 

Thiamin was the first of the vitamins to be demonstrated to have a clearly defined metabolic function as a coenzyme indeed, the studies of Peters group in the 1920s and 1930s laid the foundations not only of nutritional biochemistry but also of modern metabolic biochemistry and neurochemistry. Despite this, the mechanism by which thiamin deficiency results in central and peripheral nervous system lesions remains unclear in addition to its established coenzyme role, thiamin regulates the activity of a chloride transporter in nerve cells. 

In general, a relatively acute deficiency is involved in the central nervous system lesions of the Wernicke-Korsakoff syndrome, and a high-energy intake, as in alcoholics, is also a predisposing factor. Dry beriberi is associated with a more prolonged, and presumably less severe, deficiency, with a generally low food intake, whereas higher carbohydrate intake and physical activity predispose to wet beriberi. 

Torsteinsdottir, S., Geoigsson, G., Gisladottir, E., Rafnar, B., Palsson, P. A., and Petursson, G., Pathogenesis of central nervous system lesions in visna cell-mediated immunity and lymphocyte subsets in blood, brain, and cerebrospinal fluid, Ann. N.Y. Acad. Sci., 724, 159, 1994. 

Less common etiologies include central nervous system lesions that physically compress the pituitary stalk and interrupt tonic hypothalamic dopamine secretion, resulting in hyperprolactinemia. Increased thyroid-releasing hormone (TRH) concentrations in hypothyroidism can stimulate prolactin secretion and cause hyperprolactinemia. During conditions of renal or liver compromise, the... 

Goedert, M., Fine, A., Hunt, S.P. and Ullrich, A. (1986) Nerve growth factor mRNA in peripheral and central rat tissues and in human central nervous system lesion effects in the... 

Klein, R., Smeyne, R.J., Worst, W., Long, L.K., Auerbach, B.A., Joyner, A.L. and Barbacid, M. (1993) Targeted disruption of the trkB neurotrophin receptor gene results in nervous system lesions and neonatal death. Cell 75 113-122. 

Jellinger K (1977) Human central nervous system lesions following radiation therapy. Zentralbl Neurochir 38 199-200... 

Yokoyama, M., E. G. Trams, and R. 0. Brady Sphingolipid antibodies in sera of animals and patients with central nervous system lesions. J. Immunol. 90, 372 (1963). 

While peripheral neuritis and acute cardiac beriberi with lactic acidosis occur in thiamin deficiency associated with alcohol abuse, the more usual presentation is as the Wernicke—Korsakoff syndrome, due to central nervous system lesions. Initially there is a confused state, Korsakoff s psychosis, which is characterized by confabulation and loss of recent memory, although memory for past events may be unimpaired. Later, clear neurological signs develop — Wernicke s encephalopathy. This is characterized by nystagmus and extraocular palsy. Post-mortem examination shows characteristic brain lesions. 

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