GABA(A)-NMDA Hypothesis and Pharmacotherapy of Catatonia.
- Author:
Sung Woong SHIN
1
Author Information
1. ChookRyeong Evangelian Hospital, Namyangju, Korea. sswjyj4@gmail.com
- Publication Type:Review
- Keywords:
Catatonia;
Schizophrenia;
GABA;
NMDA;
Pharmacotherapy
- MeSH:
Amantadine;
Benzodiazepines;
Bipolar Disorder;
Catatonia;
Cooperative Behavior;
Depressive Disorder, Major;
gamma-Aminobutyric Acid;
Humans;
Inpatients;
Memantine;
N-Methylaspartate;
Neurotransmitter Agents;
Prevalence;
Schizophrenia
- From:Korean Journal of Psychopharmacology
2008;19(5):247-255
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Catatonia is a pathological condition in which the patient shows inappropriate motor, behavioral and affective responses to external stimuli. Catatonia can be observed in major depressive disorder, bipolar disorder, schizophrenia, and other conditions. Although the overall prevalence of catatonia has decreased dramatically, nearly 10% of schizophrenic inpatients still exhibit catatonic symptoms that are divided into immobility, abnormal repetitive behaviors and extreme emotional responses. Although numerous pharmacotherapies have been investigated for catatonia, benzodiazepine remains the treatment of choice. NMDA receptor antagonists such as amantadine and memantine have emerged as promising alternatives. As an effort to explain catatonia, 'GABA-NMDA collaboration model' has been proposed. According to this model, functional impairment of GABA-ergic orbitofrontal cortex can lead to disinhibition of subcortical motor system which utilize NMDA as neurotransmitter. This model was able to explain many aspects of catatonia.
