A 67-year-old man with a 5-year history of Parkinson disease has been stable on levodopa/carbidopa 25/100 mg four times daily for the past 2 years. Due to a pharmacy dispensing error, he receives only placebo tablets instead of his morning and midday doses. Within 24 hours of medication interruption, he develops acute worsening of tremor and rigidity. On presentation to the emergency department, his temperature is 39.3°C, blood pressure is 152/95 mmHg, and heart rate is 118 bpm. Physical examination reveals generalized lead-pipe rigidity, diaphoresis, and dark urine. Laboratory studies show creatine kinase of 1,400 U/L and myoglobinuria. Serum creatinine is elevated at 1.8 mg/dL (baseline 0.9 mg/dL). Mental status is alert and oriented with no evidence of confusion or agitation. Which of the following best explains the pathophysiology of his acute clinical presentation?

1. A)Acute dopamine agonist toxicity from the accumulated levodopa metabolite
2. B)Dopamine depletion in the basal ganglia leading to severe hyperkinetic movement disorder
3. C)Acute withdrawal of dopaminergic therapy resulting in dopamine depletion in the basal gangliaGABARITO
4. D)Neuroleptic malignant syndrome secondary to unmasking of endogenous dopamine-blocking activity
5. E)Carbidopa accumulation causing cholinergic excess and increased acetylcholinesterase inhibition