Fasciculations and convulsions

Onset is rapid and the eyes and respiratory system are most affected. Low-level exposure causes tightness of the chest, rhinorrhea and salivation. Dimming of vision due to miosis, eye pain and headache then follow. On examination, the pupils are constricted and the conjunctivae hyperaemic. These effects may last several hours after cessation of exposure and the headache and visual problems several days. In severe cases, salivation and rhinorrhea are more marked, and wheezing and dyspnea are prominent. Other effects, such as abdominal pain, vomiting, involuntary defecation and micturition, weakness, fasciculation and convulsion, follow depending on the degree of systemic absorption. Death may occur from respiratory failure. 

Intravenous diazepam (adult 10-20 mg child 1-5 mg) is useful in controlling apprehension, agitation, fasciculation and convulsions the dose may be repeated as required. In some experimental studies, the addition of diazepam to an atropine and oxime regimen has increased survival further (Marrs, 2004). 

Glasgow scale E2M4V2) with profuse oral secretions, sweating, cyanosis, muscle fasciculations and convulsions, and was intubated. Organophosphate poisoning was not suspected at first, and he was treated with dopamine and isoprenaline to increase blood pressure and heart rate and with phenytoin to control the convulsions, but all of these treatments were without effect. At 3.5 h after exposure, he was treated with 2 mg IV of atropine, which immediately increased both heart rate and blood pressure, and 10 mg IV of diazepam, which controlled the convulsions. He was maintained on continuous IV atropine (3 mg day-1) and mechanical ventilation, and 9 days after exposure he became alert and was extubated. The authors stressed the importance of systemic atropine for treating the bradycardia produced by the VX. 

Intoxicated patients on medication normally have one or several recurrent cholinergic crises (LeBlanc etal., 1986 Menzel and Wessel, 1966 Merrill and Mihm, 1982). In these crises, more severe symptoms, such as fasciculations and convulsions, are often preceded by increased anxiety or restlessness (Barr, 1964,1966 Hopmann and Wanke, 1974 Menzel and Wessel, 1966 Stoeckel and Meinecke, 1966). It has been suggested that such symptoms should be used as indications for the use of an anticonvulsant and that such prophylactic treatment of the cholinergic crisis would ensure less damage to the brain and the muscles. Accordingly, diazepam administration at doses of 5-10 mg intravenously has been recommended in cases of OP poisoning accompanied by anxiety and restlessness, in the absence of convulsions, (Johnson and Vale, 1992 Marrs, 2004). 

Moderately affected patients presented with respiratory distress and fascicula-tions (there was difficulty in distinguishing between fasciculations and convulsions). 

Similarly, convulsive seizures and a sustained epileptic state persisted after stomach contents were pumped and activated charcoal and anticonvulsive medication were administered in a 43-year-old man who ingested approximately 260 mg/kg endosulfan (Boereboom et al. 1998). At 4 days after exposure, the man was pronounced brain dead, and autopsy revealed cerebral hernia from massive cerebral edema. Eight additional accidental and/or intentional cases of acute poisoning with endosulfan resulting in adverse neurological effects have been reported in more recent studies, six by Blanco-Coronado et al. (1992), one by Lo et al. (1995), and one by Pradhan et al. (1997) two out of the eight resulted in death. Tonic-clonic convulsions were seen in the Blanco-Coronado et al. (1992) cases, whereas Lo et al. (1995) reported the development of muscle fasciculations and episodes of convulsions in their case. In the case reported by Pradhan et al. (1997), the patient had consumed about 75 mL of hquid endosulfan (35% w/v). In this case, in addition to tonic-clonic seizures and myoclonic jerks, the patient developed... 

With severe intoxication by all routes, an excess of acetylcholine at the neuromuscular junctions of skeletal muscle causes weakness aggravated by exertion, involuntary twitchings, fasciculations, and eventually paralysis. The most serious consequence is paralysis of the respiratory muscles. Effects on the central nervous system include giddiness, confusion, ataxia, slurred speech, Cheyne-Stokes respiration, convulsions, coma, and loss of reflexes. The blood pressure may fall to low levels, and cardiac irregularities, including complete heart block, may occur. ... 

Intraspecies 10 - A broad spectrum of effects were seen, including behavioral effects, hyperactivity, fasciculations, tremors, convulsions, and vomiting. The mechanism of toxicity is uncertain and susceptibility among individuals regarding these effects may vary. This variability was especially demonstrated in dogs wherein responses varied from one of extreme severity (vomiting, tremors, convulsions, and death) to no observable effects. Therefore, a factor of 10 was applied. A factor of 10 was also applied because experiments by Weeks et al. (1963) indicated that dogs had been previously stressed (auditory stimuli), which may have affected their response to dimethylhydrazine. Based upon these data, it was assumed that humans may be equally variable in their response to dimethylhydrazine. 

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