Muscle fasciculations

Male rats exposed to 264 mg/m of methyl parathion by inhalation had 59% (range 53-61%) inhibition of blood (a combination of erythrocyte and plasma) cholinesterase 1 hour after exposure (EPA 1978e). These animals had typical cholinergic signs of toxicity salivation, exophthalmos, laerimation, spontaneous defecation and urination, and muscle fasciculation. Values for controls were not provided. Death was not correlated to the degree of eholinesterase inhibition in whole blood. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

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... 

Behavioral changes and muscle fasciculations in dogs exposed for 15 min to 1,1-dimethylhydrazine at 360 ppm (Weeks et al. 1963) served as the basis for... 

Key study Toxicity endpoint Weeks et al. 1963 1-h LC50 of 981 ppm in dogs reduced by a factor of three to 327 ppm as an estimate of a lethality threshold. Weeks et al. (1963) provided data showing that 15-min exposure of dogs at 36 100 ppm produced only minor, reversible effects (behavioral changes and mild muscle fasciculations)... 

Signs and Symptoms Symptoms include listlessness, stumbling, mild to severe incoordination (ataxia), and partial paralysis. Additionally, horses may exhibit weakness, muscle fasciculation, and cranial nerve deficits. Fever may or may not be present. 

Coma tncrease/decrease Pinpoint Hypersalivation, bradycardia, muscle fasciculation and tremors, hyperactive bowel sounds, diarrhea and urinary incontinence sometimes with smell of petroleum distillates (solvent) Organophosphate pesticides... 

Succinylcholine produces muscle fasciculation, which may result in myoglobinuria and postoperative muscle pain. The amount produced depends on the level of physical fitness. Succinylcholine causes contractions of extraocular muscles, posing the danger of transient elevated intraocular pressure. Succinylcholine may produce hyperkalemia in patients with large masses of traumatized or denervated muscle (e.g., spinal cord injury). Denervated muscle is especially sensitive to depolarizing drugs because of the increased number of AChRs on the sarcolemma (denervation supersensitivity). Succinylcholine also causes prolonged contraction of the diseased muscles of patients with myotonia or amyotrophic lateral sclerosis. 

Which of the following adjuvants to anesthesia has the potential to cause hyperkalemia, postoperative muscle pain, muscle fasciculation, and prolonged apnea and paralysis in genetically sensitive patients ... 

E. Succinylcholine is the only depolarizing neuromuscular blocking in widespread clinical use, particularly as an aid for intubation. Its administration may produce muscle fasciculation and postoperative muscle pain. It can produce hyperkalemia in patients with muscle damage or prolonged paralysis in patients with atypical plasma cholinesterase. 

Following the administration of succinylcholine, 0.75-1.5 mg/kg IV, transient muscle fasciculations occur over the chest and abdomen within 30 seconds, although general anesthesia and the prior administration of a small dose of a nondepolarizing muscle relaxant tends to attenuate them. As paralysis develops rapidly (< 90 seconds), the arm, neck, and leg muscles are initially relaxed followed by the respiratory muscles. As a result of succinylcholine s rapid hydrolysis by cholinesterase in the plasma (and liver), the duration of neuromuscular block typically lasts less than 10 minutes (Table 27-1). 

Problems with memory and concentration Nystagmus Emesis Increased deep tendon reflexes Increased tremor Muscle fasciculations Death... 

Somatic motor (nicotinic) Skeletal muscles Fasciculations, ataxia, paralysis... 

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