Neuroleptic Malignant Syndrome in a Patient with Autism Spectrum Disorder: Case Report

Neuroleptic Malignant Syndrome (NMS) and Malignant Catatonia (MC) are conditions with significant overlap and are classically characterized by autonomic dysfunction, rigidity, bradyreflexia, posturing, lead-pipe rigidity in the former and waxy flexibility in the latter, stereotyping, an increase in creatinine kinase, and/or leukocytosis. Onset after inciting factor ranges from days to weeks, as does resolution with appropriate treatment. The overlap in symptomatology with Autism spectrum disorder (ASD) presents a formidable diagnostic challenge in a situation that must be parsed out with alacrity and accuracy. An 18-year-old male with a history of ASD, developmental delay with limited verbal use (functional age of approximately 5 years), and intermittent explosive disorder initially presented to an outside inpatient psychiatry hospital for worsening agitation that had spanned several weeks. At the outside facility trazodone, haloperidol, and clonazepam were added to his usual home regimen of valproic acid and escitalopram. Over the course of the next two weeks, he developed lethargy, tachycardia, and hypertensive emergency at which point he was transferred to our medical center’s Emergency Department. Due to concern over infection vs NMS/MC, an initial treatment plan consisted of: strict avoidance of all antipsychotics, scheduled acetaminophen for antipyretic care, 100 cc/hr IV fluids for rhabdomyolysis, a respiratory PCR panel, blood cultures, lorazepam 2 mg IV q6h, valproic acid 250 mg IV BID PRN for agitation, and discontinuation of patient’s home escitalopram. As patient was scoring positively for catatonia per Bush-Francis rating scale with scores of up to 20 and notable for marked tremulousness, myoclonic movements, rigidity with negativism, waxy flexibility, gegenhalten, and fever, the psychiatry service recommended starting a bromocriptine trial of 2.5 mg PO every 8 hours due to worry for progression to NMS/MC due to the antipsychotics he had received at the outside psychiatric facility. After down-titrating the bromocriptine dose as his symptoms resolved and up-titrating to doses as high as 7.5 mg every 6 hours when fever and concern for lead-pipe rigidity developed over a week after his symptoms had initially resolved, after nearly a month our patient was able to successfully be titrated down to a home regimen of lorazepam 1 mg at bedtime for the next 6 months. What made this case particularly unique (other than NMS/MC and ASD sharing many characteristics) were the many logistical hurdles that had to be navigated: first, our institution does not have an in-house Medicine-Psychiatry floor or electroconvulsive therapy (ECT), the definitive treatment for NMS/MC; second, there were neither adult nor pediatric inpatient Medicine-Psychiatry facilities in our state equipped with ECT that were willing to accept our patient as a transfer due to his developmental and physiological age, respectively. This case demonstrates the significant overlap in NMS/MC and ASD, illustrates the importance of recognizing these parallels so that appropriate treatment may be initiated (e.g., knowing one’s patient very well before making the decision to treat catatonia presenting as agitation in ASD with antipsychotics), and brings to light the stark reality of logistical challenges in medicine. Our patient’s symptoms resolved with bromocriptine and lorazepam and he tolerated the taper without complications.