Hyperactive catatonia in autism and schizoaffective disorder: diagnostic pitfalls and pharmacological insights
A. Mitrea1, D. Lambert1, M. Kosel1,2
1Geneva University Hospitals (HUG), Division of Developmental Mental Health, Geneva, Switzerland, 2University of Geneva, Faculty of Medicine, Geneva, Switzerland
Background: Catatonia is a severe psychomotor syndrome frequently associated with psychotic and mood disorders, and may be under-recognized when overlapping with obsessive-compulsive or neurodevelopmental symptoms. Pharmacological response can provide crucial diagnostic and therapeutic guidance, particularly in treatment-resistant presentations.
Aims & Objectives: The aim of this case report is to describe a severe episode of hyperactive catatonia occurring in a patient with autism spectrum disorder (ASD) and schizophrenia conceptualized as schizoaffective disorder. A major objective is to highlight the diagnostic challenge of identifying catatonia in an autistic patient, in whom baseline stereotypies, communication difficulties, and behavioral rigidity may obscure acute catatonic phenomena. An additional objective is to explore the role of baseline psychotropic treatment reduction, particularly mood-stabilizing medication, as a potential trigger for catatonia within a mixed affective episode, and to emphasize the diagnostic value of zolpidem responsiveness in this complex clinical context.
Method: This longitudinal inpatient case report is based on detailed clinical observation, repeated psychiatric assessments, sequential psychopharmacological interventions as well as extensive blood testing. The 61 year-old patient, known for ASD and a long-standing psychotic disorder initially diagnosed as schizophrenia, was hospitalized for severe behavioral disorganization and insomnia. Clinical assessment focused on changes from baseline functioning, with particular attention to psychomotor signs, affective instability, and vital signs. Medication adjustments included antipsychotics, benzodiazepines, and a zolpidem challenge test. Acute organic causes were systematically excluded through metabolic, inflammatory, and genetic investigations. Diagnostic hypotheses were continuously re-evaluated based on clinical evolution and treatment response.
Results: The patient developed a severe catatonic syndrome dominated by hyperactive and positive features, which could initially mimic a decompensation of her previously diagnosed obsessive–compulsive disorder, including mutism alternating with agitation, verbigeration, motor stereotypies, psychomotor ambivalence, posturing, echolalia, and paramimias. Distinguishing catatonia from baseline autistic stereotypies was also particularly challenging, as repetitive movements and limited verbal output were part of the patient’s premorbid functioning. However, the acute onset, fluctuating psychomotor presentation, qualitative change from baseline behaviors, and striking responsiveness to GABAergic agents supported a diagnosis of catatonia.
The clinical picture emerged following a reduction of baseline psychotropic treatment, retrospectively identified as a likely precipitating factor in a patient with underlying mood instability, supporting the hypothesis of a mixed affective episode within a schizoaffective disorder. Symptoms persisted despite antipsychotic treatment and showed only partial improvement under low-dose benzodiazepines. A zolpidem challenge test produced a rapid and striking, though transient, remission of catatonic symptoms, including restoration of contact, disappearance of posturing and agitation, and improved behavioral organization. After lorazepam adjustment, the clinical course stabilized with reduced psychomotor variability.
Discussion & Conclusions: This case emphasizes the clinical heterogeneity of catatonia and the risk of misattributing catatonic stereotypies to obsessive–compulsive phenomena. The dramatic but transient response to zolpidem supports its role as a valuable diagnostic probe in complex catatonic presentations, particularly when standard treatments yield equivocal responses. Early identification and targeted treatment of catatonia are essential to reduce somatic risks and to allow a more accurate assessment of underlying psychotic or mood disorders. Pharmacological challenge tests may therefore serve as crucial tools in treatment-resistant psychiatric syndromes.
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