Overview
Clinical Meaning
Anticholinergic toxidrome results from competitive antagonism of muscarinic acetylcholine receptors (M1 M5) in the central and peripheral nervous systems.
WHNP
WHNP
Anticholinergic toxidrome results from competitive antagonism of muscarinic acetylcholine receptors (M1-M5) in the central and peripheral nervous systems. Acetylcholine normally activates muscarinic receptors to produce parasympathetic effects: miosis, salivation, lacrimation, urination, defecation, GI motility, and bradycardia (via vagal tone). Blockade of these receptors produces the opposite effects—the classic presentation summarized by the mnemonic 'Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter, full as a flask.' Peripheral muscarinic blockade causes mydriasis (loss of pupillary constriction), anhidrosis (impaired thermoregulation leading to hyperthermia), tachycardia (loss of vagal tone), decreased GI motility (ileus), and urinary retention. Central muscarinic blockade produces agitation, hallucinations (often visual—'picking at the air'), delirium, myoclonus, and seizures. Common causative agents include antihistamines (diphenhydramine), tricyclic antidepressants, atropine, scopolamine, antipsychotics, jimsonweed (Datura stramonium), and antiparkinsonian agents (benztropine). The severity depends on the agent's central penetration and dose.
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