Reactions Weekly | 2021
Loxapine/risperidone
Abstract
Neuroleptic malignant syndrome: case report A 17-year-old boy developed atypical neuroleptic malignant syndrome following neuroleptic treatment with loxapine and risperidone for type 1 bipolar disorder [not all routes and duration of treatment to reaction onset stated]. The boy was admitted for an inaugural episode of delusional mania with catatonia related to his bipolar disorder. His medical history was significant for a neurodevelopmental disorder impacting communication, intelligence and learning. However, he did not have any family history. On day 1, he was admitted for psychomotor acceleration. Therefore he started receiving IM loxapine 50mg in 2 doses at H0 and H12 [sic], with oral loxapine 25mg at H24 [sic]. A localised contracture appeared at day 2, which was resistant to unspecified anticholinergics stabiliser. Therefore, he was transferred to a hospital. At day 6, he had persistent psychomotor instability associated with muscle stiffness, tremors and profuse sweats, without hyperthermia. His contact was impaired. Based on these findings, he was initially diagnosed with catatonia. Consequently, the boy’s loxapine was stopped, and treatment with lorazepam was initiated. The blood test demonstrated inflammatory syndrome, rhabdomyolysis and decreased TSH (hypothyroidism). Clinical development was marked by the onset of hypoxemic respiratory distress with clinical signs such as dyspnea, polypnea, cyanosis and crackling and paraclinical as bilateral alveolositial syndrome in favour of acute pulmonary oedema. Therefore, he underwent resuscitation for 24 hours. Thereafter, his TSH level normalised at 48 hours, and protein kinase C decreased to 50%, which normalised at day 11. No infectious or metabolic aetiology is found. Therefore, he was suspected with neuroleptic malignant syndrome secondary to neuroleptic treatment with loxapine. Thereafter, he was discharged home on day 30, without treatment. At 7 months, he had a second episode of psychomotor agitation associated with insomnia and mood exaltation with the delusional syndrome. No triggering factors were found. He was then admitted again at child psychiatry and treatment with lorazepam was started. Thereafter, he was initiated on risperidone 0.25mg due to the persistence of delusional elements at day 2. On the next day, contact was again impaired (mutism), and he had several febrile peaks as well his BP was elevated. Sinus tachycardia and fine tremors of the extremities were noted. He had a cough associated with moderate polypnoea. Based on these findings, the diagnosis of recurrence of neuroleptic malignant syndrome related to risperidone therapy was considered. Therefore, the boy’s treatment with risperidone was discontinued following its single administration. On day 3 rhabdomyolysis and a decrease in TSH were noted. Because of the persistence of catatonic elements, the lorazepam dose was increased. Thereafter, he improved clinically, and blood flow was fully normalised on day 15. A new lumbar puncture with anti-NMDA antibody research was negative, and a brain MRI was normal. He was subsequently treated with carbamazepine and then lithium salts to achieve satisfactory thymic efficiency and stability.