TY  - JOUR
AU  - Sweeney, Ryan
AU  - La Rosa, Alvaro J
AU  - Sheade, Nina
AU  - Olson-Marszewski, Rachael C.
AU  - Bergren, Ryan
AU  - Meresh, Edwin
PY  - 2020
DA  - 2020/04/01
TI  - Catatonia Following Cessation of Topiramate in a Patient with Prader-Willi Syndrome: Case Report and Review of Literature
JO  - OBM Neurobiology
SP  - 054
VL  - 04
IS  - 02
AB  - Case studies have associated catatonia with withdrawal from benzodiazepines and clozapine, both of which have been shown to increase GABA activity. Long-term use of GABAergic medications could result in GABAA downregulation and sudden discontinuation of the GABAergic drug could lead to a GABA hypoactive state which could predispose the patient to catatonia5. The anticonvulsant topiramate, is known to increase brain GABA activity6. Prader-Willi syndrome (PWS) is a genetic imprinting disorder characterized by lack of expression of genes in the paternal chromosome 15q11-q13, resulting in neonatal hypotonia, small hands and feet, almond-shaped eyes, hypogonadism, short stature, excessive hunger, obesity, diabetes, and sometimes behavioral phenotypes, including catatonic symptoms, stereotypies, compulsive self-injury, excessive sleepiness or unresponsiveness, and psychosis7-8. Prader-Willi syndrome (PWS) is associated with catatonia and is linked to GABA system abnormalities9-11. A reduction in GABA transmission could be responsible for the neuropsychiatric complication like catatonia12. We report a case of PWS who developed catatonia after cessation of Topiramate.
SN  - 2573-4407
UR  - https://doi.org/10.21926/obm.neurobiol.2002054
DO  - 10.21926/obm.neurobiol.2002054
ID  - Sweeney2020
ER  -