Antipsychotics/dopamine receptor agonists
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details of which have previously been published [see Reactions 1416 p10; 803075746].
Neuroleptic syndrome associated with catatonia: case report A 39-year-old woman with bipolar disorder who was receiving antipsychotics developed neuroleptic malignant syndrome (NMS) overlapping with catatonia. She was treated with dopamine receptor agonists and her malignant catatonia reappeared with the cessation of these agents [not all routes stated; durations of treatment to reaction onset not clearly stated]. The woman started treatment with daily clozapine 200mg, lithium 600mg, and pipamperone 80mg. She also received valproic acid. She was readmitted after a sudden relapse and her medication was adjusted by reducing the doses of pipamperone and valproic acid. She additionally received IM haloperidol which was titrated up to 7mg daily and also diazepam. Three days post-admission, she developed mild hyperthermia and leucocytosis. She showed tremulousness and generalised stiffness in her extremities, immobility, mutism, uncooperativeness, and extreme negativism. The woman’s psychopharmacological therapy was discontinued except for diazepam. She received paracetamol [acetaminophen] but there was no improvement. Her temperature rose the next day and tests revealed the following: creatine phosphokinase 2677 U/L, leucocytosis, potassium 2.93 mEq/L. She displayed tremors, generalised, significant rigidity, decreased intestinal peristalsis, and diaphoresis. She received supportive therapy, bromocriptine, diazepam and electroconvulsive therapy (ECT). She became worse after her first session of ECT with electrolyte imbalance and an increase in myoglobin levels. She was transferred to an ICU and hydrated. When she returned to the ward, SC apomorphine 24mg replaced bromocriptine. Approximately 2.5 weeks after her admission, she had a stable clinical status. She was treated with levodopa/carbidopa titrated up to 250/25mg three times a day, in addition to apomorphine and had further ECT. Over the next few weeks, she improved gradually with her clonic movements receding, her serum chemistries normalising, and her muscular stiffness turning into waxy flexibility. Her levodopa was gradually withdrawn, her dopamine agonists were reduced slowly; apomorphine was tapered off in 3 weeks. Her status worsened abruptly with an increase in temperature, rigidity, and leucocytosis. Apomorphine 15mg daily was reintroduced and within a few hours her temperature decreased and there was partial resolution of her clonic movements and rigidity. Ropinirole was added and lorazepam replaced diazepam. She had further ECT sessions which led to significant improvement in psychotic features, mood, and extrapyramidal and psychomotor symptoms. Clozapine was started at 37.5mg daily and increased progressively to 400mg daily. She continued to do well during the next 10 months after discharge on clozapine 150mg daily, lithium 450mg daily, and lorazepam. At last follow-up, she displayed mild affective lability, middle insomnia, and suspiciousness as residual symptom
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