Peripheral motor and sensory nerve conduction studies in haemodialysis patients. A study of 54 patients.

Peripheral motor and sensory nerve conduction velocities were studied prospectively in 54 chronic haemodialysis patients. The most sensitive parameters for the detection of polyneuropathy were the deep peroneal nerve motor conduction velocity, the sural nerve sensory conduction velocity and the H-reflex latency and H-index of the S1 roots. All patients examined were found to present at least one abnormal nerve conduction parameter. In the present study the side of the arteriovenous shunt had no statistically significant effect on the sensory and motor nerve conduction velocities in the upper extremities. There was a significant correlation between H-reflex latency and H-reflex index, and between H-reflex latency and sural nerve sensory conduction velocity.

Intermediate syndrome in organophosphorus poisoning: a prospective study.

OBJECTIVES: To estimate the frequency of the intermediate syndrome in organophosphorus-poisoned patients, and examine its relationship to cholinesterase inhibition and electromyographic findings. Muscle biopsies were available in some patients. DESIGN: A 3-yr prospective study. SETTING: University teaching hospital intensive care unit. PATIENTS: Consecutive patients with acute organophosphorus poisoning (n = 19). MEASUREMENTS AND MAIN RESULTS: We determined the frequency of the intermediate syndrome in poisonings with various organophosphates, duration of (acetyl) cholinesterase inhibition and metabolite excretion, evolution of alterations on repetitive nerve stimulation, type and frequency of muscle lesions. A total of eight of 19 patients developed an intermediate syndrome. In some patients, short relapses of muscarinic symptoms superimposed on the intermediate syndrome. Agents such as methylparathion, fenthion, and dimethoate carry a high risk, but we also noted a prolonged intermediate syndrome in an ethyl-parathion-poisoned patient. Prolonged and severe cholinesterase inhibition occurred during the intermediate syndrome in all patients, and metabolite excretion was prolonged. As the intermediate syndrome evolved, repetitive nerve stimulation initially demonstrated decrement, then increment, and finally, normal responses. Necrotic fibers were noted in muscle biopsies, but these fibers were too sparse to explain severe muscle weakness and were similar in patients with and without the intermediate syndrome. No patients developed delayed neuropathy. CONCLUSIONS: The intermediate syndrome is not rare. Although it is more likely to occur with some organophosphates, it is not confined to a few distinct compounds. This syndrome coincides with prolonged cholinesterase inhibition, and is not due to muscle fiber necrosis. When viewed together, the clinical and electromyographic features are best explained by combined pre- and postsynaptic dysfunction of neuromuscular transmission. The intermediate syndrome is not related to an incipient delayed neuropathy.

Intermediate syndrome due to prolonged parathion poisoning.

A parathion-poisoned patient with prolonged cholinesterase inhibition due to impaired hepatic metabolism and urinary excretion is reported. An intermediate syndrome characterized by respiratory paresis, weakness in the territory of several motor cranial nerves and of proximal limb and neck flexor muscles, persisted for 3 weeks. During this whole period, cholinesterase remained markedly reduced. Serial EMGs with repetitive nerve stimulation pointed to a combined pre- and postsynaptic disorder of neuromuscular transmission. Electron microscopy of an intercostal muscle biopsy showed focal degeneration at the poorly branched postsynaptic folds, and was considered to be nonspecific.

The intermediate syndrome in organophosphate poisoning: presentation of a case and review of the literature.

A dimethoate-poisoned woman gradually developed a moderately severe cholinergic crisis that was readily treated by atropine. After being symptom-free for nearly two days, she suffered from sudden life-threatening respiratory paresis and weakness of the facial, extraocular, neck flexor and proximal limb muscles. Muscarinic symptoms were absent. Cholinesterase inhibition was severe, and EMG revealed marked decrements at low rates of repetitive nerve stimulation, and increments at a high rate. The clinical course was compatible with the Intermediate Syndrome. This syndrome seems due to persistent cholinesterase inhibition presumably leading to combined pre- and postsynaptic impairment of neuromuscular transmission. Inadequate pralidoxime therapy is proposed but not established as contributory. Prolonged monitoring of respiratory function in patients poisoned by particular organophosphate agents is mandatory.

Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning.

A prolonged type of organophosphate toxicity, previously characterized as the Intermediate Syndrome, has been recognized in 6 out of 7 prospectively studied patients poisoned by insecticide containing parathion and methyl parathion in equal proportions. The clinical characteristics included respiratory paresis, weakness in the territories of several motor cranial nerves, neck flexors and proximal limb muscles, and depressed tendon reflexes, all lasting for several days or weeks. Electromyography in the early stages disclosed diverse types of impaired neuromuscular transmission. EMG normalization preceded clinical recovery. Severe plasma butyrylcholinesterase and erythrocyte acetylcholinesterase inhibition persisted along with the occurrence of Intermediate Syndrome-related symptoms. We conclude that combined parathion and methyl parathion poisoning is more likely to induce Intermediate Syndrome than parathion poisoning alone. The mechanisms underlying this difference remain obscure. The Intermediate Syndrome shows clinical and electromyographic hallmarks of combined postsynaptic impairment of neuromuscular transmission.

The neurophysiologic examination in organophosphate ester poisoning. Case report and review of the literature.

A 65-year-old woman who has been admitted after organophosphate-induced poisoning (Fenthion), develops pareses as a result of neuromuscular junctional dysfunction 7 days post-exposure. These findings are consistent with an intermediate syndrome, which may appear within 24 to 96 hours of exposure and subsides after 5 to 18 days. Delayed polyneuropathy develops within 1 to 3 weeks and abates after 6 to 12 months. A distal axonopathy can be demonstrated. Several authors have attempted EMG monitoring of pesticide-workers in agricultural and industrial settings. The electrophysiologic examination is an important diagnostic adjunct in the development and course of muscle paresis following organophosphate-ester poising.

Postsynaptic neuromuscular dysfunction in organophosphate induced intermediate syndrome.

A 65-year-old Caucasian female developed an intermediate syndrome seven days after an acute cholinergic crisis, caused by the ingestion of fenthion. Cholinesterase activity in the blood, plasma and red cells was monitored daily by the method according to Nenner and serial serum fenthion levels were measured by capillary gas chromatography. Electromyographic studies showed fade on tetanic stimulation by means of surface electrodes at 20 Hz of the left M. abductor digiti quinti at day 7, which could no longer be observed at day 19. Fade on low-frequency stimulation and post-tetanic facilitation were both absent. A biopsy of the N. suralis was normal. A biopsy of the M. tibialis anterior revealed a limited rhabdomyolysis with a very weak staining for cholinesterase. It is hypothesized that the pathophysiologic process underlying the syndrome is the result of a time-confined phenomenon, which includes both changes in the postsynaptic structures by a desensitization process and a gradually restoring ratio of acetylcholine to acetylcholinesterase. This hypothesis is suggested by the similarity in the EMG-findings of this patient and those in myasthenia gravis, which is known to be characterized by a postsynaptic transmission defect.