Muscle fasciculations, acetylcholinesterase

Nerve agents are organophosphorus (OP) compounds that inhibit acetylcholinesterase (AChE) extremely rapidly, which results in an accumulation of acetylcholine (ACh), leads to muscle fasciculations and paralysis, and finally results in death (Dacre, 1984). There are several strategies available to verify an exposure to nerve agents. It is not... 

IMS is clearly a separate clinical entity from acute cholinergic crisis and delayed neuropathy. The acute cholinergic crisis usually emerges within a few minutes to a few hours and is due to acetylcholinesterase (AChE) inhibition resulting in acetylcholine accumulation at the synapses in the nervous system and at the neuromuscular junctions. Patients acutely poisoned with OPs exhibit muscle fasciculations. 

Cholinomimetic dmgs (carbamate, organophosphate inhibitors of acetylcholinesterase) Anxiety, agitation, seizures, coma, bradycardia or tachycardia, pinpoint pupils, salivation, sweating, hyperactive bowel, muscle fasciculations, then paralysis Support respiration. Treat with atropine and pralidoxime. Decontaminate... 

Succinylcholine, similar to acetylcholine, interacts with the cholinergic receptors at the end plate region of the muscle, resulting in depolarization of the chemically excitable membrane. This, in turn, creates local action potentials, spreading them to and depolarizing the adjacent excitable membranes, finally culminating in a muscle contraction, or fasciculation, which is an uncoordinated muscle contraction. However, unlike acetylcholine, succinylcholine is not metabolized by acetylcholinesterase, and hence causes persistent depolarization of the end plate. The continuous presence of succinylcholine leads to inexcitability of the membrane adjacent to the end plate, resulting in... 

Acetylcholine is broken down by the acetylcholinesterase enzyme to choline and acetate. The time required for hydrolysis of acetylcholine is less than a millisecond. If the enzyme is depleted or inhibited, then excessive acetylcholine accumulation in the body can cause toxicity. Symptoms are salivation, lacrimation, urination, diarrhea, muscle tremor, and fasciculation. 

V 1 1 IM/IV. Diffuses away from endplate, hydrolyzed by plasma pseudocholinesterase and acetylcholinesterase. T intraocular pressure (contraindicated open eye wounds) and gastric pressure (caution reflux during intubation), dysrhythmias. Postoperative muscle pain (myoglobin release and hyperkalemia). May trigger malignant hyperthermia. 1. Fasciculations in chest and abdomen 2. Neck, arms, legs 3. Facial, phaiynx, larynx 4. Respiratory muscles Effects not reversed by acetylcholinesterase inhibitors. Effects are poorly reversed by electrical stimulation. 

As described above, acetylcholine carries the signal across the gap between nerves and nerve to muscle. If acetylcholine lingered in the synaptic gap it would continually stimulate the acetylcholine receptor and the enzyme acetylcholinesterase degrades the acetylcholine. Anatoxin-a(S) inhibits acetylcholinesterase preventing the removal of acetylcholine and nerve and muscle cells become hyperexcited. Mice injected intraperitoneally with anatoxin-a(S) excessively salivate and exhibit lacrimation, urinary incontinence, defecation, convulsion, fasciculation, and die by respiratory arrest. By this route, the toxin has an LD50 approaching 50 pg kg... 

---