Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication

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Standard

Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication. / Oranje, Bob; Glenthøj, Birte Y.

I: Schizophrenia Bulletin, Bind 39, Nr. 3, 05.2013, s. 684-691.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Oranje, B & Glenthøj, BY 2013, 'Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication', Schizophrenia Bulletin, bind 39, nr. 3, s. 684-691. https://doi.org/10.1093/schbul/sbs071

APA

Oranje, B., & Glenthøj, B. Y. (2013). Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication. Schizophrenia Bulletin, 39(3), 684-691. https://doi.org/10.1093/schbul/sbs071

Vancouver

Oranje B, Glenthøj BY. Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication. Schizophrenia Bulletin. 2013 maj;39(3):684-691. https://doi.org/10.1093/schbul/sbs071

Author

Oranje, Bob ; Glenthøj, Birte Y. / Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication. I: Schizophrenia Bulletin. 2013 ; Bind 39, Nr. 3. s. 684-691.

Bibtex

@article{430e53da039f4e12ab7f77443665f0be,
title = "Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication",
abstract = "Background : Cognitive deficits form core features in schizophrenia. Several studies have shown improvements in prefrontal cognitive function by α ( 2 ) -agonists in schizophrenia. In the present study, it was investigated whether clonidine (an α ( 2 ) -adrenoceptor agonist) could normalize sensorimotor gating deficits in schizophrenia. Methods : In a double blind, placebo controlled, randomized, yet balanced, cross-over experiment, 20 male schizophrenia patients on stable medication were assessed in an auditory prepulse inhibition (PPI), sensitization, and habituation of the startle reflex paradigm on 5 occasions: once after oral administration of placebo and after a single dose of 25, 50, 75, and 150 µg of clonidine. Their results were compared with 20 age- and gender-matched healthy volunteers, who received no treatment. Results : In the placebo treatment, patients showed deficient PPI and sensitization, yet normal habituation compared with the controls. Except the highest dose, all dosages of clonidine significantly increased percentage PPI in the patients compared with placebo, to such levels that it no longer differed significantly from the healthy controls. However, none of the dosages increased sensitization or influenced habituation. Conclusions : This is the first study to show that even a single low dose of clonidine added to the medical treatment of patients with schizophrenia who are clinically stable on their antipsychotic medication not only significantly ameliorates their PPI deficits, but also normalizes them. The results have a potentially high clinical relevance for the medical treatment of schizophrenia.",
author = "Bob Oranje and Glenth{\o}j, {Birte Y}",
year = "2013",
month = may,
doi = "10.1093/schbul/sbs071",
language = "English",
volume = "39",
pages = "684--691",
journal = "Schizophrenia Bulletin",
issn = "0586-7614",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Clonidine Normalizes Sensorimotor Gating Deficits in Patients With Schizophrenia on Stable Medication

AU - Oranje, Bob

AU - Glenthøj, Birte Y

PY - 2013/5

Y1 - 2013/5

N2 - Background : Cognitive deficits form core features in schizophrenia. Several studies have shown improvements in prefrontal cognitive function by α ( 2 ) -agonists in schizophrenia. In the present study, it was investigated whether clonidine (an α ( 2 ) -adrenoceptor agonist) could normalize sensorimotor gating deficits in schizophrenia. Methods : In a double blind, placebo controlled, randomized, yet balanced, cross-over experiment, 20 male schizophrenia patients on stable medication were assessed in an auditory prepulse inhibition (PPI), sensitization, and habituation of the startle reflex paradigm on 5 occasions: once after oral administration of placebo and after a single dose of 25, 50, 75, and 150 µg of clonidine. Their results were compared with 20 age- and gender-matched healthy volunteers, who received no treatment. Results : In the placebo treatment, patients showed deficient PPI and sensitization, yet normal habituation compared with the controls. Except the highest dose, all dosages of clonidine significantly increased percentage PPI in the patients compared with placebo, to such levels that it no longer differed significantly from the healthy controls. However, none of the dosages increased sensitization or influenced habituation. Conclusions : This is the first study to show that even a single low dose of clonidine added to the medical treatment of patients with schizophrenia who are clinically stable on their antipsychotic medication not only significantly ameliorates their PPI deficits, but also normalizes them. The results have a potentially high clinical relevance for the medical treatment of schizophrenia.

AB - Background : Cognitive deficits form core features in schizophrenia. Several studies have shown improvements in prefrontal cognitive function by α ( 2 ) -agonists in schizophrenia. In the present study, it was investigated whether clonidine (an α ( 2 ) -adrenoceptor agonist) could normalize sensorimotor gating deficits in schizophrenia. Methods : In a double blind, placebo controlled, randomized, yet balanced, cross-over experiment, 20 male schizophrenia patients on stable medication were assessed in an auditory prepulse inhibition (PPI), sensitization, and habituation of the startle reflex paradigm on 5 occasions: once after oral administration of placebo and after a single dose of 25, 50, 75, and 150 µg of clonidine. Their results were compared with 20 age- and gender-matched healthy volunteers, who received no treatment. Results : In the placebo treatment, patients showed deficient PPI and sensitization, yet normal habituation compared with the controls. Except the highest dose, all dosages of clonidine significantly increased percentage PPI in the patients compared with placebo, to such levels that it no longer differed significantly from the healthy controls. However, none of the dosages increased sensitization or influenced habituation. Conclusions : This is the first study to show that even a single low dose of clonidine added to the medical treatment of patients with schizophrenia who are clinically stable on their antipsychotic medication not only significantly ameliorates their PPI deficits, but also normalizes them. The results have a potentially high clinical relevance for the medical treatment of schizophrenia.

U2 - 10.1093/schbul/sbs071

DO - 10.1093/schbul/sbs071

M3 - Journal article

C2 - 22750632

VL - 39

SP - 684

EP - 691

JO - Schizophrenia Bulletin

JF - Schizophrenia Bulletin

SN - 0586-7614

IS - 3

ER -

ID: 48454574