Memantine-Induced Sialorrhea: A Rare Adverse Reaction and Review of Pathophysiological Mechanisms.

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Memantine is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist widely utilized in the management of moderate-to-severe neurocognitive disorders, specifically Alzheimer's disease. While its common adverse effects, such as dizziness, headache, and confusion, are well documented, parasympathetic or motor-related side effects such as drooling are not listed in the standard prescribing information and remain rarely reported in clinical practice. We present a case of a 68-year-old man with a primary diagnosis of moderate-to-severe major neurocognitive disorder due to Alzheimer's disease who developed pronounced daytime drooling immediately following the initiation of oral memantine therapy. Before starting the medication, the patient had no history of excessive drooling, dysphagia, parkinsonism, or recent changes to his baseline medication regimen. Within 24 hours of taking the initial 5 mg dose, he began experiencing significant pooling of saliva, requiring frequent wiping of the mouth. A clinical evaluation revealed no facial asymmetry, resting tremor, rigidity, or signs of acute neurological deficits. Due to the strong temporal relationship between the drug administration and the onset of symptoms, memantine was promptly discontinued. The patient experienced a complete resolution of symptoms within a day of the final dose, representing a positive dechallenge. Application of the Naranjo Adverse Drug Reaction Probability Scale yielded a score of 5, indicative of a probable adverse drug reaction. This phenomenon may be driven by off-target antagonism at alpha-7 nicotinic acetylcholine receptors or the modulation of central glutamatergic signaling within the brainstem salivatory nuclei, leading to localized parasympathetic dysregulation or subclinical impairment of automatic swallowing. This case emphasizes the importance of clinical vigilance when initiating memantine. It highlights that new-onset drooling should prompt clinicians to consider a reversible, drug-induced etiology, though it should not preclude appropriate neurological evaluation to rule out acute pathology.

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