The Experts below are selected from a list of 17709 Experts worldwide ranked by ideXlab platform
Michael W Jann - One of the best experts on this subject based on the ideXlab platform.
-
Haloperidol and reduced Haloperidol plasma concentrations after a loading dose regimen with Haloperidol decanoate
Progress in Neuro-psychopharmacology & Biological Psychiatry, 1996Co-Authors: Michael W Jann, F C Wei, Hsinnan Lin, C Piaochien, Wenho ChangAbstract:1. Haloperidol and reduced Haloperidol plasma levels were measured in schizophrenic patients who received both oral (10 mg, N=16 and 20 mg, N=4) and depot Haloperidol treatment 2. Patients were of Asian ethnicity and were safely and effectively converted from oral to depot therapy using a loading dose regimen using a 100 mg weekly injection interval for 4 weeks, biweekly for one month and then monthly. 3. Significant correlations were found for plasma Haloperidol and reduced Haloperidol levels and reduced Haloperidol/Haloperidol ratios between oral and depot therapy in these non-smoking patients. 4. A loading dose regimen is needed due to the long elimination half-life of decanoate of 26 days otherwise steady-state condition will not occur until 34 months of therapy. 5. Patients were maintained on monthly depot treatment for 40 weeks after the loading dose regimen and only one patient relapsed during treatment despite dosage increases. 6. The formation of reduced Haloperidol remained consistent for oral and depot Haloperidol treatment.
-
disposition of Haloperidol and reduced Haloperidol plasma levels after single dose Haloperidol decanoate administration
Human Psychopharmacology-clinical and Experimental, 1995Co-Authors: Wenho Chang, Dongjuiing Juang, Shihku Lin, Jinding Huang, Yw Francis Lam, Michael W Jann, Chingpiao ChienAbstract:A single dose of Haloperidol decanoate 100 mg was administered to 15 schizophrenic patients. Blood samples were obtained prior to injection, 1 h, 3 h, 6 h, 8 h, 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, one week, two weeks, three weeks and four weeks post-injection. Haloperidol and its reduced metabolite, reduced Haloperidol, plasma levels were assayed by HPLC with electrochemical detection. The pharmacokinetic parameters of Haloperidol were determined. The mean time of maximal (Tmax) plasma levels for Haloperidol was 5·73 ± 0·80 days. The Haloperidol plasma levels showed a biexponential decline with an elimination half-life of 15·78 ± 5·90 days. Reduced Haloperidol was rapidly formed from the Haloperidol. The Tmax of reduced Haloperidol was 7·00 ± 2·35 days. The mean ratio reduced Haloperidol/Haloperidol was 0·155 ± 0·111. Since the Tmax occurs at approximately six days, a weekly loading dose of Haloperidol decanoate is feasible during the transition from oral to depot therapy.
-
prolonged Haloperidol and reduced Haloperidol plasma concentrations after decanoate withdrawal
Schizophrenia Research, 1993Co-Authors: Wenho Chang, Dongjuiing Juang, Shihku Lin, Li Chin Chen, Chih Hsien Yang, Ching Paio Chien, Y Franics W Lam, Michael W JannAbstract:Abstract Haloperidol and reduced Haloperidol plasma concentrations were measured in twelve schizophrenic patients upon cessation of Haloperidol decanoate (HLD) treatment. Each patient received HLD 100 mg every 4 weeks for five injections. After the fifth injection, HLD was discontinued.Haloperidol and reduced Haloperidol plasma concentrations were obtained prior to cessation and at weeks 1, 3, 4, 5, 7, 9, 11, and 13 post-injection. Haloperidol and reduced Haloperidol plasma concentrations were assayed by HPLC. Both Haloperidol and reduced Haloperidol plasma concentrations were detectable 13 weeks post HLD discontinuation. Maximal Haloperidol plasma concentrations were observed at one week post cessation and gradually declined. The mean elimination half-life for Haloperidol was 27.4 ± 8.6 days (range 19.0– 47.0 days). Reduced Haloperidol plasma concentrations declined very slowly. Our results show that both Haloperidol and reduced Haloperidol plasma concentrations can remain for extended time periods after HLD is discontinued.
-
reduced Haloperidol Haloperidol ratios after oral Haloperidol and decanoate administration in schizophrenics
Progress in Neuro-psychopharmacology & Biological Psychiatry, 1993Co-Authors: Chang Wehho, Yw Francis Lam, Lin Shihku, Juang Dongjuiing, Chen Lichen, Yang Chihhsien, Hu Weiherng, Chien Chingpiao, Michael W JannAbstract:Abstract 1. Haloperidol and reduced Haloperidol plasma concentrations were measured in thirteen stable schizophrenic patients that received both oral Haloperidol and Haloperidol decanoate. 2. Significant correlations between reduced Haloperidol/Haloperidol ratios from oral Haloperidol and Haloperidol decanoate occurred at week two and week 16, respectively. 3. The formation of RH was consistent during Haloperidol decanoate treatment.
Shrinivas K Kulkarni - One of the best experts on this subject based on the ideXlab platform.
-
differential striatal levels of tnf α nfκb p65 subunit and dopamine with chronic typical and atypical neuroleptic treatment role in orofacial dyskinesia
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2008Co-Authors: Mahendra Bishnoi, Kanwaljit Chopra, Shrinivas K KulkarniAbstract:Abstract Long term use of typical neuroleptics such as Haloperidol may be limited by unwanted motor side effects like tardive dyskinesia characterized by repetitive involuntary movements, involving the mouth, face and trunk. Atypical neuroleptics, such as clozapine and risperidone are devoid of these side effects. However the precise mechanisms of the neuronal toxicity induced by Haloperidol are poorly understood. It is possible that typical and atypical antipsychotic differently affects neuronal survival and death and that these effects considerably contribute to the differences in the development of TD. The aim of the present study is to investigate the role of TNF-α and NFκB on the toxicity induced by chronic Haloperidol administration in an animal model of tardive dyskinesia. Rats were treated for 21 days with: Haloperidol (5 mg/kg), clozapine (5 and 10 mg/kg), risperidone (5 mg/kg) or saline. Orofacial dyskinetic movements and total locomotor activity was evaluated. Striatal levels of dopamine were measure by HPLC/ED whereas striatal levels of TNF-α and NFκB p65 subunit were measured by ELISA technique. Haloperidol increased orofacial dyskinetic movements and total locomotor activity (on day 22) ( P ≤ 0.05). Clozapine and risperidone also increased the orofacial dyskinetic movements but that significantly less than Haloperidol ( P ≤ 0.05). Differential effect of Haloperidol and atypical neuroleptics on striatal dopamine levels and striatal levels of TNF-α and NFκB p65 subunit was found out. Haloperidol significantly decreased the striatal dopamine levels whereas clozapine and risperidone did not. Haloperidol but not clozapine and risperidone significantly increased the levels of TNF-α and NFκB p65 subunit ( P ≤ 0.05). The present study suggests the impossible involvement of striatal TNF-α and NFκB p65 subunit in Haloperidol-induced orofacial dyskinesia in rats, an animal model for human tardive dyskinesia.
-
possible mechanism of action in melatonin attenuation of Haloperidol induced orofacial dyskinesia
Pharmacology Biochemistry and Behavior, 2003Co-Authors: Pattipati S Naidu, Pushpinder Kaur, Rajat Sandhir, Amanpreet Singh, Shrinivas K KulkarniAbstract:Abstract Tardive dyskinesia (TD) is a late complication of prolonged neuroleptic treatment characterized by involuntary movements of the oral region. In spite of high incidence and much research, the pathophysiology of this devastating movement disorder remains elusive. Chronic treatment with neuroleptics leads to the development of abnormal oral movements in rats, referred to as vacuous chewing movements (VCMs). VCMs in rats are widely accepted as an animal model of TD. Rats chronically treated with Haloperidol (1.5 mg/kg ip) significantly developed VCMs and tongue protrusions. Melatonin dose-dependently (1, 2, and 5 mg/kg) reversed the Haloperidol-induced VCM and tongue protrusions frequencies. Biochemical analysis reveals that chronic Haloperidol treatment significantly induced lipid peroxidation and decreased the forebrain glutathione (GSH) levels in the rats. Chronic Haloperidol-treated rats also showed decreased levels of antioxidant defense enzymes, superoxide dismutase (SOD), and catalase. Coadministration of melatonin (1, 2, and 5 mg/kg) along with Haloperidol significantly reduced the lipid peroxidation and restored the decreased GSH levels by chronic Haloperidol treatment, and significantly reversed the Haloperidol-induced decrease in forebrain SOD and catalase levels in rats. However, a lower dose of melatonin (1 mg/kg) failed to reverse chronic Haloperidol-induced decreases in forebrain GSH, SOD, and catalase levels. In conclusion, melatonin could be screened as a potential drug candidate for the prevention or treatment of neuroleptic-induced orofacial dyskinesia.
-
possible involvement of prostaglandins in Haloperidol induced orofacial dyskinesia in rats
European Journal of Pharmacology, 2001Co-Authors: Pattipati S Naidu, Shrinivas K KulkarniAbstract:Abstract Dopaminergic abnormality is one of the pathological mechanisms involved in the pathophysiology of tardive dyskinesia, a late complication of neuroleptic treatment. Prostaglandins modulate the dopamine release in the striatum, the principle area involved in the pathophysiology of tardive dyskinesia. Rats were chronically treated with Haloperidol (HPD) (1.5 mg/kg) for a period of 21 days, to induce orofacial dyskinesia. Behavioural assessment of orofacial dyskinesia was done 24 h after the last dose of Haloperidol. Catalepsy was induced in rats by acute treatment with Haloperidol (1 mg/kg), and catalepsy was scored for the next 4 h. Chronic Haloperidol treatment induced profound vacuous chewing movements in rats. Indomethacin, a nonselective cyclooxygenase inhibitor dose-dependently (5–20 mg/kg) suppressed the vacuous chewing movements count in Haloperidol-treated animals. In conclusion, the results of the present study infer that prostaglandins might play a significant role in the Haloperidol-induced vacuous chewing movements, and prostaglandin synthesis inhibitors can serve as novel drug candidates for the treatment of tardive dyskinesia.
Joao Rocha - One of the best experts on this subject based on the ideXlab platform.
-
ebselen attenuates Haloperidol induced orofacial dyskinesia and oxidative stress in rat brain
Pharmacology Biochemistry and Behavior, 2005Co-Authors: Roselei Fachinetto, Gilson Zeni, Joao RochaAbstract:Haloperidol-induced orofacial dyskinesia is an animal model of tardive dyskinesia whose pathophysiology has been related to basal ganglia oxidative stress. In this study the authors examined whether ebselen, an antioxidant organochalcogen with glutatione peroxidase-like activity, changes the behavioral and neurochemical effect of sub-chronic Haloperidol administration. Haloperidol administered (12 mg/kg/week, sc) for 4 weeks caused a significant increase in vacuous chewing movements (VCMs), tongue protrusion (TP) and the duration of facial twitching (FT) observed in 4 weekly evaluations (p < 0.05). Ebselen (30 mg/kg, ip), administered every other day, along with Haloperidol (12 mg/kg/week, sc) once weekly, reversed the increase of VCMs and FT in four weekly evaluations (p < 0.05), while TP frequency was reverted in the 2nd, 3rd, and 4th week. After the treatments and behavioral observation, biochemical parameters in segments of the brain were analyzed. Haloperidol significantly increased the thiobarbituric acid-reactive species (TBARS) levels in the cortex, striatum and subcortical parts of the brain. The co-administration of ebselen reversed the effect of Haloperidol on TBARS production in cortex and striatum. The results of the present study clearly indicate that ebselen has a protective role against Haloperidol-induced orofacial dyskinesia and reverses the increase in TBARS production caused by Haloperidol administration. Consequently, the use of ebselen as a therapeutic agent for the treatment of tardive dyskinesia should be considered.
-
high fat diet increases the incidence of orofacial dyskinesia and oxidative stress in specific brain regions of rats
Pharmacology Biochemistry and Behavior, 2005Co-Authors: Roselei Fachinetto, Daniele Cristina Wondracek, Caroline Wagner, Verônica B Brito, Juliano Ferreira, Cristina W Nogueira, Joao RochaAbstract:Abstract Haloperidol-induced orofacial dyskinesia (OD) is a putative animal model of tardive dyskinesia (TD) whose pathophysiology has been related to free radical generation and oxidative stress. Schizophrenic patients have been reported to eat a diet higher in fat than the general population and dietary fat intake can lead to an increase in oxidative stress in animal models. The objective of this study was to determine whether association of ingestion of a high fat diet with prolonged Haloperidol treatment could lead to OD and oxidative stress in the rat brain. Haloperidol decanoate administration (38 mg/kg, IM, which is equivalent to 1 mg/kg/day) monthly for a period of 6 months to rats fed previously with a high fat and normo fat diets (6 months) caused a increase in vacuous chewing (VCM) and duration of facial twitching (FT). Haloperidol caused a reduction in body weight gain and the loss of body weight occurred after 4 months of treatment with Haloperidol. The effects on body weight were more accentuated in HF diet group. HF diet ingestion was associated with an increase in TBARS levels in cerebellum and cerebral cortex (regardless of Haloperidol treatment). A significant diet × Haloperidol treatment interaction in striatum, subcortical parts and the region containing the substantia nigra was observed for TBARS. In fact, Haloperidol caused an increase in TBARS levels of these regions only in rats fed with the HF. These results indicate that a high fat diet caused a transitory increase in Haloperidol-induced OD in rats and this in part can be related to the Haloperidol-induced oxidative stress in brain structures involved with OD.
Wenho Chang - One of the best experts on this subject based on the ideXlab platform.
-
Haloperidol and reduced Haloperidol plasma concentrations after a loading dose regimen with Haloperidol decanoate
Progress in Neuro-psychopharmacology & Biological Psychiatry, 1996Co-Authors: Michael W Jann, F C Wei, Hsinnan Lin, C Piaochien, Wenho ChangAbstract:1. Haloperidol and reduced Haloperidol plasma levels were measured in schizophrenic patients who received both oral (10 mg, N=16 and 20 mg, N=4) and depot Haloperidol treatment 2. Patients were of Asian ethnicity and were safely and effectively converted from oral to depot therapy using a loading dose regimen using a 100 mg weekly injection interval for 4 weeks, biweekly for one month and then monthly. 3. Significant correlations were found for plasma Haloperidol and reduced Haloperidol levels and reduced Haloperidol/Haloperidol ratios between oral and depot therapy in these non-smoking patients. 4. A loading dose regimen is needed due to the long elimination half-life of decanoate of 26 days otherwise steady-state condition will not occur until 34 months of therapy. 5. Patients were maintained on monthly depot treatment for 40 weeks after the loading dose regimen and only one patient relapsed during treatment despite dosage increases. 6. The formation of reduced Haloperidol remained consistent for oral and depot Haloperidol treatment.
-
disposition of Haloperidol and reduced Haloperidol plasma levels after single dose Haloperidol decanoate administration
Human Psychopharmacology-clinical and Experimental, 1995Co-Authors: Wenho Chang, Dongjuiing Juang, Shihku Lin, Jinding Huang, Yw Francis Lam, Michael W Jann, Chingpiao ChienAbstract:A single dose of Haloperidol decanoate 100 mg was administered to 15 schizophrenic patients. Blood samples were obtained prior to injection, 1 h, 3 h, 6 h, 8 h, 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, one week, two weeks, three weeks and four weeks post-injection. Haloperidol and its reduced metabolite, reduced Haloperidol, plasma levels were assayed by HPLC with electrochemical detection. The pharmacokinetic parameters of Haloperidol were determined. The mean time of maximal (Tmax) plasma levels for Haloperidol was 5·73 ± 0·80 days. The Haloperidol plasma levels showed a biexponential decline with an elimination half-life of 15·78 ± 5·90 days. Reduced Haloperidol was rapidly formed from the Haloperidol. The Tmax of reduced Haloperidol was 7·00 ± 2·35 days. The mean ratio reduced Haloperidol/Haloperidol was 0·155 ± 0·111. Since the Tmax occurs at approximately six days, a weekly loading dose of Haloperidol decanoate is feasible during the transition from oral to depot therapy.
-
prolonged Haloperidol and reduced Haloperidol plasma concentrations after decanoate withdrawal
Schizophrenia Research, 1993Co-Authors: Wenho Chang, Dongjuiing Juang, Shihku Lin, Li Chin Chen, Chih Hsien Yang, Ching Paio Chien, Y Franics W Lam, Michael W JannAbstract:Abstract Haloperidol and reduced Haloperidol plasma concentrations were measured in twelve schizophrenic patients upon cessation of Haloperidol decanoate (HLD) treatment. Each patient received HLD 100 mg every 4 weeks for five injections. After the fifth injection, HLD was discontinued.Haloperidol and reduced Haloperidol plasma concentrations were obtained prior to cessation and at weeks 1, 3, 4, 5, 7, 9, 11, and 13 post-injection. Haloperidol and reduced Haloperidol plasma concentrations were assayed by HPLC. Both Haloperidol and reduced Haloperidol plasma concentrations were detectable 13 weeks post HLD discontinuation. Maximal Haloperidol plasma concentrations were observed at one week post cessation and gradually declined. The mean elimination half-life for Haloperidol was 27.4 ± 8.6 days (range 19.0– 47.0 days). Reduced Haloperidol plasma concentrations declined very slowly. Our results show that both Haloperidol and reduced Haloperidol plasma concentrations can remain for extended time periods after HLD is discontinued.
Roselei Fachinetto - One of the best experts on this subject based on the ideXlab platform.
-
ebselen attenuates Haloperidol induced orofacial dyskinesia and oxidative stress in rat brain
Pharmacology Biochemistry and Behavior, 2005Co-Authors: Roselei Fachinetto, Gilson Zeni, Joao RochaAbstract:Haloperidol-induced orofacial dyskinesia is an animal model of tardive dyskinesia whose pathophysiology has been related to basal ganglia oxidative stress. In this study the authors examined whether ebselen, an antioxidant organochalcogen with glutatione peroxidase-like activity, changes the behavioral and neurochemical effect of sub-chronic Haloperidol administration. Haloperidol administered (12 mg/kg/week, sc) for 4 weeks caused a significant increase in vacuous chewing movements (VCMs), tongue protrusion (TP) and the duration of facial twitching (FT) observed in 4 weekly evaluations (p < 0.05). Ebselen (30 mg/kg, ip), administered every other day, along with Haloperidol (12 mg/kg/week, sc) once weekly, reversed the increase of VCMs and FT in four weekly evaluations (p < 0.05), while TP frequency was reverted in the 2nd, 3rd, and 4th week. After the treatments and behavioral observation, biochemical parameters in segments of the brain were analyzed. Haloperidol significantly increased the thiobarbituric acid-reactive species (TBARS) levels in the cortex, striatum and subcortical parts of the brain. The co-administration of ebselen reversed the effect of Haloperidol on TBARS production in cortex and striatum. The results of the present study clearly indicate that ebselen has a protective role against Haloperidol-induced orofacial dyskinesia and reverses the increase in TBARS production caused by Haloperidol administration. Consequently, the use of ebselen as a therapeutic agent for the treatment of tardive dyskinesia should be considered.
-
high fat diet increases the incidence of orofacial dyskinesia and oxidative stress in specific brain regions of rats
Pharmacology Biochemistry and Behavior, 2005Co-Authors: Roselei Fachinetto, Daniele Cristina Wondracek, Caroline Wagner, Verônica B Brito, Juliano Ferreira, Cristina W Nogueira, Joao RochaAbstract:Abstract Haloperidol-induced orofacial dyskinesia (OD) is a putative animal model of tardive dyskinesia (TD) whose pathophysiology has been related to free radical generation and oxidative stress. Schizophrenic patients have been reported to eat a diet higher in fat than the general population and dietary fat intake can lead to an increase in oxidative stress in animal models. The objective of this study was to determine whether association of ingestion of a high fat diet with prolonged Haloperidol treatment could lead to OD and oxidative stress in the rat brain. Haloperidol decanoate administration (38 mg/kg, IM, which is equivalent to 1 mg/kg/day) monthly for a period of 6 months to rats fed previously with a high fat and normo fat diets (6 months) caused a increase in vacuous chewing (VCM) and duration of facial twitching (FT). Haloperidol caused a reduction in body weight gain and the loss of body weight occurred after 4 months of treatment with Haloperidol. The effects on body weight were more accentuated in HF diet group. HF diet ingestion was associated with an increase in TBARS levels in cerebellum and cerebral cortex (regardless of Haloperidol treatment). A significant diet × Haloperidol treatment interaction in striatum, subcortical parts and the region containing the substantia nigra was observed for TBARS. In fact, Haloperidol caused an increase in TBARS levels of these regions only in rats fed with the HF. These results indicate that a high fat diet caused a transitory increase in Haloperidol-induced OD in rats and this in part can be related to the Haloperidol-induced oxidative stress in brain structures involved with OD.
