Why do neurologists miss catatonia in neurology emergency? A case series and brief literature review.

Catatonia is a well-described clinical syndrome characterized by features that range from mutism, negativism and stupor to agitation, mannerisms and stereotype. Causes of catatonia may range from organic brain disorders to psychiatric conditions. Despite a characteristic syndrome, catatonia is grossly under diagnosed. The reason for missed diagnosis of catatonia in neurology setting is not clear. Poor awareness is an unlikely cause because catatonia is taught among conditions with deregulated consciousness like vegetative state, locked-in state and akinetic mutism. We determined the proportion of catatonia patients correctly identified by neurology residents in neurology emergency. We also looked at the alternate diagnosis they received to identify catatonia mimics. Twelve patients (age 22-55 years, 7 females) of catatonia were discharged from a single unit of neurology department from 2007 to 2017. In the emergency department, neurology residents diagnosed none of the patients as catatonia. They offered diagnosis of extrapyramidal syndrome in 7, meningitis in 2, and conversion reaction, acute psychosis/encephalopathy and non-convulsive status epilepticus in one each. Their final diagnosis at discharge was catatonia due to general medical condition in 6 (progressive supranuclear palsy in 2, post-status epilepticus, uremic encephalopathy, glioblastoma multiforme and tuberculous meningitis in one each), catatonia due to major depression in 4, schizophrenia and idiopathic catatonia in one each. Extrapyramidal syndrome appeared as common mimic of catatonia. The literature reviewed also revealed the majority of organic catatonia secondary to causes that are usually associated with extrapyramidal features. Therefore, we suggest that neurologists should consider catatonia in patients presenting with extrapyramidal syndromes.

Immune response to different fractions of Taenia solium cyst fluid antigens in patients with neurocysticercosis.

The immunopathogenesis of neurocysticercosis (NCC) largely remains unknown. We analyzed the immune response to different fractions of Taenia solium cyst fluid antigens in patients with NCC. Lymphocytes were separated from 48 patients with NCC-related active epilepsy and 30 healthy controls. T. solium (isolated from pig muscles) antigens (crude lysate, CL; cyst wall, CW and cyst fluid, CF) at 20 µg/well concentrations were used to stimulate the cells in a lymphocyte transformation test (LTT). Only CF antigen stimulated cell proliferation significantly greater than control (p<0.001), hence cyst fluid antigens were further studied. The CF antigens were electro-blotted on nitrocellulose membrane (NC), cut at 0.5 cm distance and particulate antigens were prepared. A total of 12 fractions, designated F1 to F12 according to molecular weight were tested in-vitro for LTT. After 72 h of stimulation by the different fractions, Th1 (IL-1ß, TNF-α, IL-2) and Th2 (IL-4, IL-10) cytokine responses were determined in culture supernatants by ELISA. Low molecular weight fractions F1 through F4 (Mol. wt.<25 kDa) were found to be potent inducers of cytokines. Fractions F1, F3 and F4 induced the production of Th1 (IL-1ß, TNF-α, IL-2), whereas F2 induced the production of Th2 (IL-4 and IL-10) cytokine. The study shows that the low molecular weight fractions of CF antigens are immuno-dominant. Most of these fractions (F1, F3, F4) induce strong Th1 immune response except F2 which induces Th2 response. Further studies are needed to identify the different antigens present in these fractions to determine the molecules responsible for the immune response.