Disorders of neuromuscular transmission concern the neuromuscular junction. They may include
(See also summary of disorders of the peripheral nervous system) disorders of neuromuscular transmission affect the neuromuscular junction. They may include Postsynaptic receptors (eg. As in myasthenia gravis) presynaptic release of acetylcholine (z. B. botulism) breakdown of acetylcholine in the synapse are common features of these disorders (eg. As a result of medications or neurotoxic chemicals) fluctuating fatigue and muscle weakness without sensory deficits. Some diseases that other areas of the body mainly concern (eg. As stiff-person syndrome, Isaac’s syndrome) have neuromuscular manifestations. Lambert-Eaton syndrome Eaton-Lambert syndrome is due to the limited release of acetylcholine from presynaptic nerve endings. Botulism botulism, also due to a limited release of acetylcholine from presynaptic nerve terminals, produced by irreversible binding of the toxin produced by Clostridium botulinum spores to a specific receptor (synaptotagmin II) to the presynaptic cholinergic nerve terminal endings. The result is a pronounced weakness, sometimes to swallow with respiratory failure and difficulty. Other systemic symptoms may include: mydriasis, dry mouth, constipation, urinary retention and tachycardia by unrestrained activity of the sympathetic nervous system (anticholinergic syndrome). This systemic findings are absent in myasthenia gravis. Botulism a slight decrement However, a significant increment is reflected in the electromyography (EMG) at low frequency (2-3 Hz) repetitive nerve stimulation, after 10 s physical exertion or at fast (50 Hz) repetitive nerve stimulation. Drugs or toxic chemicals Cholinergic drugs, organophosphate insecticides, and most nerve gases (z. B. Sarin) block neuromuscular transmission by excessive effect of acetylcholine, which depolarizes the post-synaptic receptor. This results in miosis, abdominal cramps and Bronchorrhö myasthenieähnliche weakness (cholinergic syndrome). Aminoglycosides and polypeptide antibiotics decrease the presynaptic acetylcholine release and the sensitivity of the postsynaptic membrane to acetylcholine. At high serum levels these antibiotics can potentiate neuromuscular blockade in patients with latent myasthenia gravis. Long-term treatment with penicillamine can cause a reversible syndrome resembling clinical and electromyography of myasthenia gravis. Excessive magnesium gifts p.o. or iv (With blood levels by 8-9 mg / dl) may also induce severe muscle weakness, which is similar to a myasthenic syndrome. The treatment consists in the elimination of the drug or toxic chemical, and the supply of the required respiratory support and intensive care. Atropine 0.4-0.6 mg p.o. 3 times / day sets the bronchial reduced in patients with cholinergic excess. Higher doses (eg., 2-4 mg i.v. every 5 min) may be necessary in cases of poisoning with organophosphate insecticides or nerve gases.