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Arquivos de Neuro-Psiquiatria

Print version ISSN 0004-282X

Arq. Neuro-Psiquiatr. vol.41 no.3 São Paulo Sept. 1983

http://dx.doi.org/10.1590/S0004-282X1983000300011 

Polineuropatia por Parathion: estudo clinico, eletrofisiológico e histológico de um caso

 

Polyneuropathy caused by Parathion: clinical, eletrophysiological and histological study of a case

 

 

José L. AlonsoI;  Açucena AtallaII; Maria J. CavaliereII;  Sonia M. GagiotiII; Maria A. A. LorentiIII

IMédico responsável pelo Setor de Eletromiografia. Clínica Neurológica e Serviço de Anatomia Patológica do Hospital do Servidor Público Estadual de São Paulo
IIBióloga do Setor de Patologia Experimental. Clínica Neurológica e Serviço de Anatomia Patológica do Hospital do Servidor Público Estadual de São Paulo
IIIMédica da Clínica Neurológica. Clínica Neurológica e Serviço de Anatomia Patológica do Hospital do Servidor Público Estadual de São Paulo

 

 


RESUMO

Estudamos um paciente com quadro clínico rebelde, produzido por intoxicação pelo Parathion. Foi observado um fenômeno miotônico transitório, não descrito na literatura revisada. A constatação de cifras de AchE eritrocitária baixas e de colinesterase plasmática normais, indicou que era portador de déficit congênito de AchE, esclarecendo-se a evolução crônica do seu quadro. O fenômeno miotônico associado ao quadro clínico, eletrofisiológico, histológico e bioquímico fazem deste paciente um modelo clínico, de etiologia conhecida, da discutida síndrome de Isaacs.


SUMMARY

A case of 38 year old man who worked with organochlorinated and Parathion during 5 years is reported. His follow-up was up to 2 years. The onset of the disease was characterized by cholinergic signs, headache, loss of weight, trembling, miokimias, fasciculations, ataxia, myotonic phenomena (in hands only) and motor sensitive peripheral polyneuropathy (affecting the lower limbs symmetrically). Low concentrations of blood cholinesterases confirmed the etiology. Myotonic phenomena disappeared spontaneuosly 6 months after the initial observation. One year later, the concentration of erytrocyte acetilcholinesterase was found to be low and plasma cholinesterase was normal, suggesting that the patient was carrier of a congenital deficiency of acetilcholinesterase. in literature relationship between myotonia and intoxication due to organophosphorus was not found. The whole clinical picture, cholinergic symptoms, transitory myotonic phenomena and spontaneous motor activity could be explained by an excess of acetilcholine. Eletromyography (EMG) in the first observation showed neuromuscular transmission blocking characterized by deficiency or absence of voluntary activity, unexcitability of fibular nerves, with fibrilations and positive peaks as described previously with Mipafox (another organophosphorus agent). During 2 years of observation numerous end-plates potentials of muscular fibres persisted in the EMG. A progressive increase in voluntary activity showed by unit motor potential of almost normal amplitude and very increased duration was observed. No potentials of reinnervation were noted. The results of EMG were explained as disturbances of neuromuscular transmission associated with moderate signs of denervation The Eaton-Lambert's test and the stimulation of a single unit motor potential confirmed disorder of neuromuscular synapses. The histochemistry of brachial biceps showed scattered atrophic and angulated type I and II fibres. Teased-fibres preparations showed nerve fibres with B, C, and G alterations as defined by Dyck et al. indicating axonal degeneration. These results were according to velocity of sensitive conduction. The conduction velocity of fibular nerves was strongly delayed during all the evolution indicating serious disorders of motor nerves myelin. We think that intoxication by organophosphorus should not be expressed as an identical alteration of both motor and sensitive nerves. The association of myotonic phenomena with such clinical, electrophysiological and histological picture is characteristic of the Isaac's syndrome model with known etiology.


 

 

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Trabalho realizado, com auxílio da Fundação de Amparo à Pesquisa do Estado de São Paulo na Clínica Neurológica e no Serviço de Anatomia Patológica do Hospital do Servidor Público Estadual de São Paulo.
Agradecimento - À Dra. Rosa Gaeta da Seção de Toxicologia e Higiene Comparada do Instituto Biológico de São Paulo, pela realização das dosagens de colinesterases no sangue; ao Dr. Flávio Rodrigues Puga, da mesma instituição, pelas dosagens de colinesterase eritrocitária e plasmática e da cromatografia de fase gasosa no plasma.
Trabalho realizado, com auxílio da Fundação de Amparo à Pesquisa do Estado de São Paulo na Clínica Neurológica e no Serviço de Anatomia Patológica do Hospital do Servidor Público Estadual de São Paulo.
Setor de Eletromiografia - Hospital do Servidor Público - Caixa Postal 8570 -01000 São Paulo, SP - Brasil.

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