Archives of Mental Health (Jan 2015)

Role of amantadine in catatonic schizophrenia

  • Swaroop R S Achary,
  • Samrat Kar,
  • Pavankumar C M Reddy,
  • Sharbandh V Raj

Journal volume & issue
Vol. 16, no. 1
pp. 100 – 102

Abstract

Read online

Background: Catatonia is a neuropsychiatric syndrome most commonly characterized by mutism, stupor, refusal to eator drink, posturing, and excitement or hypo kinesis. The concept of catatonia was first described by Karl Kahlbaum in1874. Although the introduction of antipsychotics has reduced the incidence of catatonia, it is still not uncommon and itsdetection rate can be significantly improved by using a standardized rating scale. The prevalence of catatonia is unknown.Catatonia is likely underdiagnosed by psychiatrists and other physicians. It has been reported that the use of amantadinein patients of catatonia, who do not respond to lorazepam has shown effective results because of its N-methyl-D-aspartate receptor (NMDA) antagonistic property. There is a dearth of studies documenting the usefulness of amantadinein catatonia. Case description: Mr. A, a 25 year old male person presented to the psychiatric with the chief complaints of decreasedinteraction with others, poor personal care, appearing sad and bemused, staying aloof, having low appetite and maintainingmundane posters for prolonged time since seven to eight days. The patient was diagnosed as having catatonic schizophreniaas per the International Classification of Diseases Research and Diagnostic Criteria 10th revision (ICD-10 RDC). BuschFrancis Catatonia Rating Scale was applied to assess the severity of catatonia symptoms. The initial score on day one wastwenty one. Patient who was unresponsive to inj. lorazepam in the dosage of 8-12mg/day by day eight had shown asignificant improvement on adding amantadine 20mg/day by 12th day. Discussion: Amantadine has N-methyl-D-aspartate receptor (NDMA) receptor antagonist activity, in addition to dopamineagonist activity and its potential efficacy in catatonia may be due to the blockade of hyperglutaminergic excitotoxicity toneurons and decreasing the free radical formation. Conclusion:

Keywords