A fascinating new video case just dropped in Tremor and Other Hyperkinetic Movements, and what resonated with me was how an extraordinarily common and generally well-tolerated medication, lansoprazole, can precipitate a movement disorder that could easily be misdiagnosed. Kumar and Sharma describe a 62-year-old man who developed jerking of the arms and head beginning approximately six hours after his first 15-mg dose of lansoprazole; examination revealed both positive and negative myoclonus, including asterixis, and the movements completely disappeared within two days of stopping the drug. Watching the accompanying video is particularly instructive because, at first glance, many practitioners might label these movements as “tremor.” This is exactly why phenomenology matters. Tremor is an oscillatory, generally rhythmic movement, whereas myoclonus consists of sudden, brief, shock-like movements that may result from muscle contraction (positive myoclonus) or an interruption of ongoing muscle activity (negative myoclonus); asterixis is an important form of negative myoclonus. Jerky appearing tremor can be myoclonus. The teaching point is to resist naming every shaking or jerking movement a tremor and instead ask: Is it rhythmic or irregular? Is there a sudden muscle contraction or a brief lapse in posture? Is the movement stimulus-sensitive, action-induced, positional, or present at rest? The differential diagnosis should include tremor, myoclonus, asterixis, dystonic movements, dyskinesia, tics, seizures and functional movement disorders, followed by a careful search for metabolic, toxic and medication-related causes. In this case, blood counts, electrolytes, toxicology testing, kidney and liver function were unrevealing, while the striking temporal relationship to lansoprazole and rapid resolution after withdrawal supported an idiosyncratic drug reaction. Although PPIs are considered quite safe, neurological complications have occasionally been reported, and PPIs can also produce hypomagnesemia, another potential pathway to neurological symptoms. Perhaps the most practical lesson is one we repeatedly encounter in movement disorders: before ordering another scan or adding another medication, define the phenomenology and review the medication list, including seemingly innocuous drugs and anything that was recently started, stopped or dose-adjusted. Sometimes the diagnosis is hiding in plain sight in the medicine cabinet. tremorjournal.org/articles/1… @tremorjournal

One of the practical pearls I took away from Susan Fox's excellent Aspen Course lecture this morning was how important it is to quickly distinguish neuroleptic malignant syndrome (NMS), serotonin syndrome, and malignant hyperthermia, because although they can all present with fever, autonomic instability, and altered mental status, the triggers and examination findings are different. NMS should come to mind after dopamine blockade or abrupt withdrawal of dopaminergic therapy and is characterized by lead-pipe rigidity and a slower evolution. Serotonin syndrome, in contrast, is usually linked to serotonergic medications and stands out because of hyper-reflexia, clonus, and myoclonus, often developing rapidly after a medication change or overdose. Malignant hyperthermia is a different entity altogether, typically occurring after exposure to volatile anesthetics or succinylcholine in genetically susceptible individuals and requiring immediate recognition and treatment. My biggest takeaway was that the medication history, timing of symptom onset, and a careful neurological examination remain our most powerful diagnostic tools when every minute counts.