A 65-year-old patient on long-term neuroleptic therapy develops involuntary movements of the face, mouth, tongue, and limbs. Which diagnosis is most likely?

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Multiple Choice

A 65-year-old patient on long-term neuroleptic therapy develops involuntary movements of the face, mouth, tongue, and limbs. Which diagnosis is most likely?

Explanation:
Long-term dopamine receptor blockade from neuroleptics can lead to tardive dyskinesia, a movement disorder rooted in receptor changes in the basal ganglia. With prolonged exposure, dopamine D2 receptors become upregulated and supersensitive, producing involuntary, repetitive movements. The hallmark is orofacial and limb movements that develop after months to years of therapy—facial grimacing, lip smacking, tongue movements, and choreiform limb motions fit this pattern. This explains why an older patient on chronic antipsychotics is susceptible and why these movements can persist even after stopping the drug. Other disorders don’t fit as neatly. Parkinsonism from antipsychotics presents with slowed movements, rigidity, and tremor, not the characteristic choreiform, orofacial movements. Huntington’s disease is a genetic neurodegenerative disorder with chorea plus cognitive and psychiatric changes, typically without a clear link to antipsychotic exposure. Gilles de la Tourette’s syndrome features motor and vocal tics that begin in childhood, not as a late-onset consequence of long-term antipsychotic therapy. Managing tardive dyskinesia involves addressing the offending medication when possible, switching to a treatment with a lower risk of this side effect, and, for established cases, therapies like VMAT2 inhibitors to reduce the abnormal movements.

Long-term dopamine receptor blockade from neuroleptics can lead to tardive dyskinesia, a movement disorder rooted in receptor changes in the basal ganglia. With prolonged exposure, dopamine D2 receptors become upregulated and supersensitive, producing involuntary, repetitive movements. The hallmark is orofacial and limb movements that develop after months to years of therapy—facial grimacing, lip smacking, tongue movements, and choreiform limb motions fit this pattern. This explains why an older patient on chronic antipsychotics is susceptible and why these movements can persist even after stopping the drug.

Other disorders don’t fit as neatly. Parkinsonism from antipsychotics presents with slowed movements, rigidity, and tremor, not the characteristic choreiform, orofacial movements. Huntington’s disease is a genetic neurodegenerative disorder with chorea plus cognitive and psychiatric changes, typically without a clear link to antipsychotic exposure. Gilles de la Tourette’s syndrome features motor and vocal tics that begin in childhood, not as a late-onset consequence of long-term antipsychotic therapy.

Managing tardive dyskinesia involves addressing the offending medication when possible, switching to a treatment with a lower risk of this side effect, and, for established cases, therapies like VMAT2 inhibitors to reduce the abnormal movements.

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