OBJECTIVE: To report a case of catatonic schizophrenia treated with memantine that resulted in a rapid reduction of catatonic symptoms. CASE SUMMARY: A 68-year-old male with catatonic schizophrenia presented with bizarre and catatonic behavior manifested by mutism, waxy flexibility, immobility, staring, nonresponsiveness to verbal commands, grimacing, rigidity, and posturing. During the course of his hospitalization, he was treated with memantine up to 10 mg/day. The catatonia responded rapidly and significantly to memantine. DISCUSSION: Few treatment options are available for the management of catatonia. Lorazepam is generally the agent that has been used most often and has had varying degrees of success. Our report adds to a recently published case that also suggested that memantine might be useful for the management of catatonic behaviors in a patient with schizophrenia. While its mechanism of action is unknown, it has been thought that glutamate antagonists, such as memantine, may be beneficial in catatonic schizophrenia due to a glutamatergic dysfunction present in catatonic patients. It also has been hypothesized that there is a decrease in gamma-aminobutyric acid released to the supplementary motor areas, resulting in less glutamate inhibition. This results in a net effect of glutamatergic hyperfunction in the striatum, which may produce catatonia. Based on this hypothesis, memantine would be beneficial as an N-methyl-D-aspartic acid antagonist to decrease the amount of glutamate in the striatum and thereby relieve symptoms of catatonia. However, these potential benefits must be weighed against recently reported adverse reactions associated with memantine use, namely, psychosis and seizures. CONCLUSIONS: Memantine produced a rapid and significant reduction in catatonic symptoms in our patient with catatonic schizophrenia.
OBJECTIVE: To report a case of catatonic schizophrenia treated with memantine that resulted in a rapid reduction of catatonic symptoms. CASE SUMMARY: A 68-year-old male with catatonic schizophrenia presented with bizarre and catatonic behavior manifested by mutism, waxy flexibility, immobility, staring, nonresponsiveness to verbal commands, grimacing, rigidity, and posturing. During the course of his hospitalization, he was treated with memantine up to 10 mg/day. The catatonia responded rapidly and significantly to memantine. DISCUSSION: Few treatment options are available for the management of catatonia. Lorazepam is generally the agent that has been used most often and has had varying degrees of success. Our report adds to a recently published case that also suggested that memantine might be useful for the management of catatonic behaviors in a patient with schizophrenia. While its mechanism of action is unknown, it has been thought that glutamate antagonists, such as memantine, may be beneficial in catatonic schizophrenia due to a glutamatergic dysfunction present in catatonicpatients. It also has been hypothesized that there is a decrease in gamma-aminobutyric acid released to the supplementary motor areas, resulting in less glutamate inhibition. This results in a net effect of glutamatergic hyperfunction in the striatum, which may produce catatonia. Based on this hypothesis, memantine would be beneficial as an N-methyl-D-aspartic acid antagonist to decrease the amount of glutamate in the striatum and thereby relieve symptoms of catatonia. However, these potential benefits must be weighed against recently reported adverse reactions associated with memantine use, namely, psychosis and seizures. CONCLUSIONS:Memantine produced a rapid and significant reduction in catatonic symptoms in our patient with catatonic schizophrenia.