Peripheral polyneuropathy

Gilchrist MA, et al Toxic peripheral polyneuropathy. Morb Mart Weekly Rep 23 9-10,... 

Kornberg A, Segal R, Theitler J, Yona R, Kaufman S. Folic acid deficiency, megaloblastic anemia and peripheral polyneuropathy due to oral contraceptives. Isr J Med Sci 1989 25(3) 142-5. 

Su KP, Lee YJ, Lee MB. Severe peripheral polyneuropathy and rhabdomyolysis in lithium intoxication a case report. Gen Hosp Psychiatry 1999 21(2) 136-7. 

A delayed peripheral polyneuropathy, known as organophosphate-induced delayed neurotoxicity (OPIDN), from which recovery may be poor. 

Ben-Ami H, Pollack S, Nagachandran P, Lashevsky I, Yarnitsky D, Edoute Y. Reversible pancreatitis, hepatitis, and peripheral polyneuropathy associated with parenteral gold therapy. J Rheumatol 1999 26(9) 2049-50. 

Peripheral polyneuropathy as a result of chronic ammoniated mercury poisoning has been studied and followed over 2 years (60). 

A 36-year-old man developed peripheral polyneuropathy after chronic perianal use of an ammoniated mercury ointment. He had very high blood and urine mercury concentrations. Sural nerve biopsy showed mixed axonal degeneration/demyelination. His symptoms improved progressively over 2 years after withdrawal of the ointment, but neurophysiological recovery was incomplete. 

Deleu D, Hanssens Y, al-Salmy HS, Hastie 1. Peripheral polyneuropathy due to chronic use of topical ammoniated mercury. J Toxicol Clin Toxicol 1998 36(3) 233-7. 

None to abdominal pain, pancreatitis, eruptive xanthomas, peripheral polyneuropathy, high blood pressure, body mass index greater than 30 kg/m, or waist size greater than... 

Peripheral polyneuropathy due to chronic use of topical ammoniated mercury. J Toxicol Clin Toxicol 36 233-237. 

On 28 and 29 December 1994, 13 adult patients entered San Pedro Claver Clinic in Bogata with a loss of strength, muscular weakness and tingling in their legs. The doctors diagnosed peripheral polyneuropathy. All the patients came from a flower farm where in the previous eight days they have been exposed to a product. Karate, whose active ingredient is lambda-cyhalothrin. 

Glutamic acid and aspartic acid secretion is highly increased due to a specific tubular defect. This transport defect seems to be related to the glutamate transporter EAACl on chromosome 9p24 [12]. The few patients described showed neurological (external ophthalmoplegia, deafness, peripheral polyneuropathy), mental (oligophrenia) or no symptoms [13-15]. There is no treatment. 

Nutritional deficiencies—A number of alcohol-related neurological disorders are due to nutritional deficiencies— primarily the B vitamins, including thiamin. These deficiencies result from decreased taste for food, decreased appetite (alcohol is high in calories and suppresses the appetite), and malabsorption of nutrients due to the irritated lining of the stomach and small intestine. A common nutritional deficiency disorder, peripheral polyneuropathy, is characterized by weakness, numbness, partial paralysis of extremities, pain in the legs, and impaired sensory reaction and motor reflexes. This condition is reversible with adequate diet and supplemental thiamin and other B vitamins. 

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