Central nervous system dysfunction

Hereditary deficiency of phosphoglycerate kinase (PGK) is associated with hereditary hemolytic anemia and often with central nervous system dysfunction and/or myopathy. The first case, reported by Kraus et al. (K24), is a heterozygous female, and the results are not so clear. The second family, reported by Valentine et al. (V3), is a large Chinese family, whose pedigree study indicates that PGK deficiency is compatible with X-linked inheritance. To date, 22 families have been reported (04, T25, Y3). Nine of these have manifested both symptoms five have shown only hemolysis seven have shown the central nervous system dysfunction and/or myopathy but without hemolysis and one case, PGK Munchen, is without clinical symptoms (F5). PGK II is an electrophoretic variant found in New Guinea populations (Y2). Red blood cell enzyme activity, specific activity, and the kinetic properties of this polymorphic variant are normal. 

Rabbit 0.04 mg/kg BW After 16 weeks, central nervous system dysfunction 20... 

Diseases mediated through ion channel receptors include cardiovascular disease, hypertension, and central nervous system dysfunctions. A voltagegated ion channel is a key to the treatment of cystic fibrosis (see Exhibit 2.4). 

Hollander, E., Schiffman, E., Cohen, B., Rivera-Stein, M.A., Rosen, W., Gorman, J.M., Fyer, A.J., Papp, L., and Liebowitz, M.R. (1990) Signs of central nervous system dysfunction in obsessive-compulsive disorder. Arch Gen Psychiatry, 47 27-32. 

Hollander E, Schiffman E, Cohen B, et al Signs of central nervous system dysfunction in obsessive-compulsive disorder. Arch Gen Psychiatry 47 27-32, 1990b Hollander E, Mullen L, DeCaria CM, et al Obsessive compulsive disorder, depression, and fluoxetine. J Clin Psychiatry 52 418-422, 1991 Hollander E, De Caiia CM, Nitescu A, et al Serotonergic function in OCD. Arch Gen Psychiatry 49 21-28, 1992... 

In college, I had studied central nervous system dysfunction and knew that psycholexia is a condition in which a person has difficulty attaching meaning to printed symbols. I experienced a similar condition after the psilocybin began to take effect. 

The neuroleptics can produce a variety of other symptoms of central nervous system dysfunction, including abnormal electroencephalogram (EEG) findings, an increased frequency of seizures, respiratory depression, and disturbances of body temperature control (Davis, 1980 Davis et al., 1975). Endocrine disorders, especially in females, may also be of central... 

The presentation of neuroleptic malignant syndrome with clozapine can be different from that associated with traditional neuroleptic drugs (SEDA-28, 66), and the authors of a recent report have pointed out the differential diagnosis with heat stroke, a medical emergency with the two cardinal features of raised core body temperature (40° C) and central nervous system dysfunction, which is fatal in up to 50% of cases (205). 

Marcondes MC, Burudi EM, Huitron-Resendiz S, Sanchez-Alavez M, Watry D, Zandonatti M, Henriksen SJ, Fox HS (2001) Highly activated CD8(+) T cells in the brain correlate with early central nervous system dysfunction in simian immunodeficiency virus infection. J Immunol 167 5429-5438. 

In hypobetalipoproteinenia the plasma LDL level is decreased (10-20% of normal), but that of HDL is normal, and that of VLDL is mildly lowered. Of 23 affected individuals from the four known affected families, one had central nervous system dysfunction and fat malabsorption. The others had mild or no pathological changes. The disease is inherited as an autosomal dominant trait. The benign nature of this condition is in sharp contrast with the seriousness of hyperbetalipoproteinemia. In the latter, LDL cholesterol concentrations are two to six times normal, and patients are predisposed to premature atherosclerosis. In another form of hypobetalipoproteinemia, the patient synthesized apo B-48 and secreted chylomicrons but did not produce apo B-lOO or secrete VLDL. 

M18. Melamed, E., Reches, A., and Hershko, C., Reversible central nervous system dysfunction in folate deficiency. J. Neurol. Sci. 25, 93-98 (1975). 

Valciukas JA, Lilis R, Fischbein A, et al Central nervous system dysfunction due to lead exposure. Science 201 465-467,1978b Whitfield CL, Ch ien LT, Whitehead JD Lead encephalopathy in adults. Am J Med 52 289-298, 1972... 

Low level chronic exposme to mercury vapour can also affect the peripheral nervous system, leading to pol)meuropathy (reduced sensory and motor nerve function) and neuropsychological symptoms of stress and behaviour problems. Longer exposures, around 15 years, have been shown in several studies to lead to alterations in pulse rate, blood pressure, memory, sleep disturbance and EEGs, probably as a result of kidney and CNS (central nervous system) dysfunction. 

Bll. Berman, P. H., Balis, M. ., and Dancis. J., Diagnostic test for congenital hyperuricemia with central nervous system dysfunction. /. Lab. Clin. Med. 7, 1247-1253 (1968). 

L4. Lesch, M., and Nyhan, W. L., A familial disorder of uric acid metabolism and central nervous system dysfunction. Amer. J. Med. 36, 561-570 (1964). 

J. E., Correlation between central nervous system dysfunction and biochemical defects. /. Amer. Med. Ass. 202, 103 (1967). 

The mechanisms by which PTH might impair central nervous system function are only partially nnderstood. The increased calcium content in such diverse tissues as skin, cornea, blood vessels, brain, and heart in patients with hyperparathyroidism suggests that PTH may somehow facilitate the entry of Ca into such tissues. The finding of increased calcium in the brains of both dogs and humans with either acute or chronic renal disease and secondary hyperparathyroidism is consistent with the conception that part of the central nervous system dysfunction and EEG abnormalities found in acute renal failure or chronic renal failure may be due in part to a PTH-mediated increase in brain calcium. Calcium is essential for the function of neurotransmission in the central nervous system and for a large number of intracellular enzyme systems. Thus, increased brain calcium content could disrupt cerebral function by interfering with any of these processes (Rasmussen, 1986). It is also possible that PTH itself may have a detrimental effect on the central nervous system. 

A 2-month-old boy bom to a mother taking valproate had typical dysmorphic features characteristic of fetal valproate syndrome [342 ]. He had a distinctive facial appearance, a cluster of minor and major anomalies, central nervous system dysfunction, a persistent left superior vena cava draining into a dilated coronary sinus, and mild pulmonary hypertension. 

Central nervous system dysfunction. Acute effects of exposure to acrylonitrile generally involve the central nervous system. Symptoms of acrylonitrile exposure include headache, nausea, dizziness, and general weakness. The animal studies cited above suggest possible carcinogenic effects of acrylonitrile on the central nervous system, since rats exposed by either inhalation or ingestion have developed similar CNS tumors. 

The deficiencies of cystathionine )5-synthase (CBS), sulfite oxidase, and methylenetetrahydrofolate reductase (MTHFR) may all result in central nervous system dysfunction, in particular mental retardation [1-3]. Defects of CBS and sulfite oxidase both cause dislocated lenses of the eyes, but the phenotypes are different otherwise. The manifestations of CBS deficiency, the most common of these disorders, and MTHFR deficiency range from severely affected to asymptomatic patients both may cause vascular occlusion. Deficiency of sulfite oxidase is clinically uniform, but genetically heterogeneous, and functional deficiency of the enzyme can result from several inherited defects of molybdenum cofactor biosynthesis [2, 4]. Hereditary folate malabsorption and defects of cobalamin transport (transcobala-min II deficiency) or cobalamin cofactor biosynthesis (cblC-G diseases) may cause megaloblastic anemia, in addition to CNS dysfunction [3, 5, 6]. 

Rosenbloom, F. M., Kelley, W. N., Miller, J. M., Henderson, J. F. and Seegmiller, J. E. 1967. Inherited disorder of purine metabolism Correlation between central nervous system dysfunction and biochemical defects. J.A.M.A. 202 175-177. 

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