Hiroshi Kimura1, Nobuhisa Kanahara2, Naoya Komatsu3, Minoru Ishige4, Katsumasa Muneoka5, Masayuki Yoshimura6, Hiroshi Yamanaka7, Tomotaka Suzuki8, Hideki Komatsu9, Tsuyoshi Sasaki1, Tasuku Hashimoto1, Tadashi Hasegawa1, Akihiro Shiina10, Masatomo Ishikawa1, Yoshimoto Sekine11, Tetsuya Shiraishi1, Hiroyuki Watanabe12, Eiji Shimizu13, Kenji Hashimoto14, Masaomi Iyo1. 1. Department of Psychiatry, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan. 2. Department of Psychiatry, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan; Division of Medical Treatment and Rehabilitation, Center for Forensic Mental Health, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan. Electronic address: kanahara@faculty.chiba-u.jp. 3. Department of Psychiatry, Dowa-kai Chiba Hospital, 2-508 Hasama-cho, Funabashi-shi, Chiba 274-0822, Japan. 4. Department of Psychiatry, Satsuki-kai Sodegaura-satsukidai Hospital, 5-21 Nagaura-ekimae, Sodegaura-shi, Chiba 299-0246, Japan. 5. Department of Psychiatry, Gakuji-kai Kimura Hospital, 6-19 Higashihon-machi, Chuou-ku, Chiba-shi, Chiba 260-0004, Japan. 6. Department of Psychiatry, Doujin-kai Kisaradzu Hospital, 2-3-1 Iwane, Kisaradzu-shi, Chiba 292-0061, Japan. 7. Department of Psychiatry, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan; Department of Psychiatry, Chiba Psychiatric Medical Center, 5 Toyosuna, Mihama-ku, Chiba-shi, Chiba 261-0024, Japan. 8. Department of Psychiatry, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan; Department of Psychiatry, Koutoku-kai Sato Hospital, 948-1 Kunugizuka, Nanyo-shi, Yamagata 999-2221, Japan. 9. Department of Psychiatry, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan; Department of Psychiatry, Choshi-Kokoro Clinic, 1-48-8 Shinsei-cho, Choshi-shi, Chiba 288-0056, Japan. 10. Department of Psychiatry, Chiba University Hospital, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan. 11. Division of Medical Treatment and Rehabilitation, Center for Forensic Mental Health, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan; Department of Psychiatry, Choshi-Kokoro Clinic, 1-48-8 Shinsei-cho, Choshi-shi, Chiba 288-0056, Japan. 12. Department of Psychiatry, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan; Department of Psychiatry, Asahi Hosipital, I-1326, Asahi-shi, Chiba 289-2511, Japan. 13. Department of Cognitive Behavioral Physiology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan. 14. Division of Clinical Neuroscience, Center for Forensic Mental Health, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba-shi, Chiba 260-8670, Japan.
Abstract
OBJECTIVE: Dopamine supersensitivity psychosis (DSP) is considered to be one cause of treatment-resistant schizophrenia (TRS). The authors investigated the efficacy of risperidone long-acting injections (RLAI) in patients with TRS and DSP. METHOD: This is a multicenter, prospective, 12-month follow-up, observational study that included unstable and severe TRS patients with and without DSP. 115 patients with TRS were recruited and divided into two groups according to the presence or absence of DSP which was judged on the basis of the clinical courses and neurological examinations. RLAI was administered adjunctively once every 2weeks along with oral antipsychotics. We observed changes in scores for the Brief Psychiatric Rating Scales (BPRS), Clinical Global Impression-Severity of Illness (CGI-S), Global Assessment of Functioning Scale (GAF), and Extrapyramidal Symptom Rating Scale (ESRS) during the study. Of the assessed 94 patients, 61 and 33 were categorized into the DSP and NonDSP groups, respectively. RESULTS: While baseline BPRS total scores, CGI-S scores and GAF scores did not differ, the ESRS score was significantly higher in the DSP group compared with the NonDSP group. Treatment significantly reduced BPRS total scores and CGI-S scores, and increased GAF scores in both groups, but the magnitudes of change were significantly greater in the DSP group relative to the NonDSP group. ESRS scores were also reduced in the DSP group. Responder rates (≥20% reduction in BPRS total score) were 62.3% in the DSP group and 21.2% in the NonDSP group. CONCLUSIONS: It is suggested that DSP contributes to the etiology of TRS. Atypical antipsychotic drugs in long-acting forms, such as RLAI, can provide beneficial effects for patients with DSP. CLINICAL TRIALS REGISTRATION: UMIN (UMIN000008487).
OBJECTIVE:Dopamine supersensitivity psychosis (DSP) is considered to be one cause of treatment-resistant schizophrenia (TRS). The authors investigated the efficacy of risperidone long-acting injections (RLAI) in patients with TRS and DSP. METHOD: This is a multicenter, prospective, 12-month follow-up, observational study that included unstable and severe TRS patients with and without DSP. 115 patients with TRS were recruited and divided into two groups according to the presence or absence of DSP which was judged on the basis of the clinical courses and neurological examinations. RLAI was administered adjunctively once every 2weeks along with oral antipsychotics. We observed changes in scores for the Brief Psychiatric Rating Scales (BPRS), Clinical Global Impression-Severity of Illness (CGI-S), Global Assessment of Functioning Scale (GAF), and Extrapyramidal Symptom Rating Scale (ESRS) during the study. Of the assessed 94 patients, 61 and 33 were categorized into the DSP and NonDSP groups, respectively. RESULTS: While baseline BPRS total scores, CGI-S scores and GAF scores did not differ, the ESRS score was significantly higher in the DSP group compared with the NonDSP group. Treatment significantly reduced BPRS total scores and CGI-S scores, and increased GAF scores in both groups, but the magnitudes of change were significantly greater in the DSP group relative to the NonDSP group. ESRS scores were also reduced in the DSP group. Responder rates (≥20% reduction in BPRS total score) were 62.3% in the DSP group and 21.2% in the NonDSP group. CONCLUSIONS: It is suggested that DSP contributes to the etiology of TRS. Atypical antipsychotic drugs in long-acting forms, such as RLAI, can provide beneficial effects for patients with DSP. CLINICAL TRIALS REGISTRATION: UMIN (UMIN000008487).
Authors: Marc De Hert; Jan Sermon; Paul Geerts; Kristof Vansteelandt; Joseph Peuskens; Johan Detraux Journal: CNS Drugs Date: 2015-08 Impact factor: 5.749