Parkinsonism or catatonia: That’s the question

Dear Sir, We read with interest the article by Dr. Jha, which describes a patient with catatonia syndrome, presumably due to extrapontine myelinolysis (EPM).[1] Psychiatry and neurology literature have both included the use of the term catatonia since 1874, and the exact pathophysiology and precise neurotransmitter abnormalities remain incompletely understood.[2] Moreover, due to the lack of a clear definition and the absence of a standardized description of the individual motor features, catatonia is often misdiagnosed. Patients with severe Parkinson's disease (PD) and dementia with Lewy bodies (DLB) exhibiting severe akinetic-rigid features and cognitive dysfunction may fulfill the diagnostic criteria of catatonia. In the case described by Dr. Jha, there were mild signal abnormalities in the basal ganglia. The majority of symptoms/signs described in the case (i.e., mutism, immobility, rigidity, negativism, staring, and drooling of saliva) can be observed in severe parkinsonism of any etiology. "Waxy flexibility" is controversial and often overlaps with rigidity.[3] The author mentioned that the absence of cogwheeling and tremors was the basis for distinguishing catatonic rigidity and parkinsonian rigidity. The distinction between catatonic and parkinsonian rigidity based solely on the absence of cogwheeling and tremor is less than conclusive, as these features are not definitive of parkinsonism. Therefore, in the absence of video documentation, it may become hard for the readers of this report to accept the diagnosis of catatonia. If catatonia was the initial diagnosis, why was levodopa preferred over benzodiazepines, especially when the latter has been historically considered the most effective treatment option for catatonia?[4] It is possible and more likely that the patient had parkinsonism in the context of EPM, which has been reported.[5-7] The patient's complete improvement with levodopa further supports this alternative hypothesis to the one presented by the author. We believe that a more careful clinical evaluation, inclusion of a video, and advanced imaging techniques (i.e.,Positron Emission Tomography (PET), Dopamine active Transporter (DaT) scans) could clarify the phenomenology to be more specifically aligned with parkinsonism rather than catatonia. Acknowledgement Nil. Author contribution (1) Research Project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution; (3) Manuscript Preparation: A. Writing of the First Draft, B. Review and Critique. AL: 1A, 1B, 1C, 3A AJE: 1A, 1B, 1C, 3B MSO: 1A, 1B, 1C, 3B Ethics statement We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines. Conflicts of interest There are no conflicts of interest. Financial support and sponsorship Nil.