Pub Date : 2012-01-23DOI: 10.2174/1876523801205010018
H. Hori, T. Teraishi, D. Sasayama, Takashi Fujii, K. Hattori, M. Ishikawa, H. Kunugi
Earlier studies have used the dexamethasone (DEX) suppression test (DST) to investigate the hypothalamic- pituitary-adrenal (HPA) function in schizophrenia, although the findings are controversial. Recently there has been an increased interest in the role of dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) in HPA axis function. Several studies have investigated basal DHEA(S) levels and cortisol/DHEA(S) ratios in schizophrenia patients, while no attempts have been made to investigate DHEA(S) level in response to the DEX administration. We aimed to compare the post- DEX cortisol and DHEAS levels and the cortisol/DHEAS ratio between schizophrenia patients and healthy controls. Here we administered the DST to 43 patients with schizophrenia and 37 age- and sex-matched healthy controls. Plasma cortisol levels, serum DHEAS levels, and cortisol/DHEAS ratio after administration of 0.5 mg of DEX were compared between the two groups. Schizophrenia patients showed significantly higher cortisol level and cortisol/DHEAS ratio than controls, while DHEAS levels were not significantly different between groups. These results suggest that besides the cortisol level, cortisol/DHEAS ratio as assessed with the DST might reflect abnormal HPA axis function in schizophrenia.
{"title":"Elevated Cortisol Level and Cortisol/DHEAS Ratio in Schizophrenia as Revealed by Low-Dose Dexamethasone Suppression Test","authors":"H. Hori, T. Teraishi, D. Sasayama, Takashi Fujii, K. Hattori, M. Ishikawa, H. Kunugi","doi":"10.2174/1876523801205010018","DOIUrl":"https://doi.org/10.2174/1876523801205010018","url":null,"abstract":"Earlier studies have used the dexamethasone (DEX) suppression test (DST) to investigate the hypothalamic- pituitary-adrenal (HPA) function in schizophrenia, although the findings are controversial. Recently there has been an increased interest in the role of dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) in HPA axis function. Several studies have investigated basal DHEA(S) levels and cortisol/DHEA(S) ratios in schizophrenia patients, while no attempts have been made to investigate DHEA(S) level in response to the DEX administration. We aimed to compare the post- DEX cortisol and DHEAS levels and the cortisol/DHEAS ratio between schizophrenia patients and healthy controls. Here we administered the DST to 43 patients with schizophrenia and 37 age- and sex-matched healthy controls. Plasma cortisol levels, serum DHEAS levels, and cortisol/DHEAS ratio after administration of 0.5 mg of DEX were compared between the two groups. Schizophrenia patients showed significantly higher cortisol level and cortisol/DHEAS ratio than controls, while DHEAS levels were not significantly different between groups. These results suggest that besides the cortisol level, cortisol/DHEAS ratio as assessed with the DST might reflect abnormal HPA axis function in schizophrenia.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"20 1","pages":"18-24"},"PeriodicalIF":0.0,"publicationDate":"2012-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68144849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-01-23DOI: 10.2174/1876523801205010009
E. Stone, Yan Lin, Yasmeen Sarfraz
A long standing problem with antidepressant drugs is their delayed onsets of action which has made them unsatisfactory in the rapid treatment of serious depressions involving agitated and suicidal behavior. Two new approaches to this problem involve the glutamatergic antagonist, ketamine, recently reviewed, and the acute inhibition of central stress circuits, which is the subject of the present review. The rationale behind stress-circuit inhibition comes from the findings that both clinical and experimental depressions are accompanied by increased neural activity in the stress network together with inhibited activity in regions underlying active motivated behaviors, and that both changes are reversed by effective antidepressant treatment. It has been shown further that direct pharmacological inhibition of central noradrenergic stress nuclei produces immediate reversal of depressive-like passive as well as sickness behaviors. Dipivalyl-6-fluoronorepinephrine (dp6FNE), a brain-permeable pro-drug of 6FNE, a full agonist at inhibitory brain � - adrenoceptors in brainstem noradrenergic stress nuclei, has been developed and found in preliminary studies to cause rapid reversal of both passivity and anhedonia as well as anxiolysis without significant hypoactivity in the open field. Low doses of agonists of glucocorticoid and 5HT1A autoreceptors, which respectively inhibit the hypothalamic-pituitary- adrenal axis and serotonergic stress systems, may also share these effects as well as potentiate the actions of dp6FNE. Anti-stress effects may also be involved in the rapid therapeutic effects found with intracerebral administration of first generation antidepressants and may prove helpful in potentiating the therapeutic actions of stimulants.
{"title":"Toward the Rapid Treatment of Depression by Selective Inhibition of Central Stress Circuits","authors":"E. Stone, Yan Lin, Yasmeen Sarfraz","doi":"10.2174/1876523801205010009","DOIUrl":"https://doi.org/10.2174/1876523801205010009","url":null,"abstract":"A long standing problem with antidepressant drugs is their delayed onsets of action which has made them unsatisfactory in the rapid treatment of serious depressions involving agitated and suicidal behavior. Two new approaches to this problem involve the glutamatergic antagonist, ketamine, recently reviewed, and the acute inhibition of central stress circuits, which is the subject of the present review. The rationale behind stress-circuit inhibition comes from the findings that both clinical and experimental depressions are accompanied by increased neural activity in the stress network together with inhibited activity in regions underlying active motivated behaviors, and that both changes are reversed by effective antidepressant treatment. It has been shown further that direct pharmacological inhibition of central noradrenergic stress nuclei produces immediate reversal of depressive-like passive as well as sickness behaviors. Dipivalyl-6-fluoronorepinephrine (dp6FNE), a brain-permeable pro-drug of 6FNE, a full agonist at inhibitory brain � - adrenoceptors in brainstem noradrenergic stress nuclei, has been developed and found in preliminary studies to cause rapid reversal of both passivity and anhedonia as well as anxiolysis without significant hypoactivity in the open field. Low doses of agonists of glucocorticoid and 5HT1A autoreceptors, which respectively inhibit the hypothalamic-pituitary- adrenal axis and serotonergic stress systems, may also share these effects as well as potentiate the actions of dp6FNE. Anti-stress effects may also be involved in the rapid therapeutic effects found with intracerebral administration of first generation antidepressants and may prove helpful in potentiating the therapeutic actions of stimulants.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"5 1","pages":"9-17"},"PeriodicalIF":0.0,"publicationDate":"2012-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68144840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2012-01-01DOI: 10.2174/1876523801205010001
Devon L Graham, Nicole R Herring, Tori L Schaefer, Katherine D Holland, Charles V Vorhees, Michael T Williams
The abuse of drugs such as methamphetamine (MA), 3,4-methylenedioxymethamphetamine (Ecstasy, MDMA), and 5-methoxydiisopropyltryptamine (5-MeO-DIPT; Foxy) is global. Symptoms from taking these drugs include tachycardia, agitation, hyperpyrexia, and sometimes seizures. We compared the EEG effects of these drugs in male Sprague-Dawley rats (~300 g) implanted with cortical electroencephalographic (EEG) electrodes prior to testing. Animals received four subcutaneous injections of MA, MDMA, or Foxy (10 mg/kg each as freebase, administered every 2 h), or saline as these doses produce lasting effects on learning, memory, and monoamines. EEG tracings were recorded before, during, and after treatment. Animals receiving MDMA showed no significant EEG abnormalities or myoclonus. MA treatment resulted in myoclonic activity and in brief (<10 s) EEG epileptiform activity in ~50% of the rats. Longer seizure activity (10 s to 5 min) was recorded in some MA-treated rats following the third and fourth doses. The onset of myoclonic activity following Foxy treatment occurred shortly after the first dose. All rats receiving Foxy showed seizures by the second dose and this continued throughout the treatment regimen. The results show that binge doses of MA and MDMA, which mimic the neurochemical changes seen in chronic users, increase EEG abnormalities after MA but not after MDMA. While the neurochemical effects of Foxy are not known in humans, this drug causes severe EEG abnormalities and overt seizures in 100% of tested animals.
{"title":"Electroencephalographic and convulsive effects of binge doses of (+)-methamphetamine, 5-methoxydiisopropyltryptamine, and (±)-3,4-methylenedioxymethamphetamine in rats.","authors":"Devon L Graham, Nicole R Herring, Tori L Schaefer, Katherine D Holland, Charles V Vorhees, Michael T Williams","doi":"10.2174/1876523801205010001","DOIUrl":"https://doi.org/10.2174/1876523801205010001","url":null,"abstract":"<p><p>The abuse of drugs such as methamphetamine (MA), 3,4-methylenedioxymethamphetamine (Ecstasy, MDMA), and 5-methoxydiisopropyltryptamine (5-MeO-DIPT; Foxy) is global. Symptoms from taking these drugs include tachycardia, agitation, hyperpyrexia, and sometimes seizures. We compared the EEG effects of these drugs in male Sprague-Dawley rats (~300 g) implanted with cortical electroencephalographic (EEG) electrodes prior to testing. Animals received four subcutaneous injections of MA, MDMA, or Foxy (10 mg/kg each as freebase, administered every 2 h), or saline as these doses produce lasting effects on learning, memory, and monoamines. EEG tracings were recorded before, during, and after treatment. Animals receiving MDMA showed no significant EEG abnormalities or myoclonus. MA treatment resulted in myoclonic activity and in brief (<10 s) EEG epileptiform activity in ~50% of the rats. Longer seizure activity (10 s to 5 min) was recorded in some MA-treated rats following the third and fourth doses. The onset of myoclonic activity following Foxy treatment occurred shortly after the first dose. All rats receiving Foxy showed seizures by the second dose and this continued throughout the treatment regimen. The results show that binge doses of MA and MDMA, which mimic the neurochemical changes seen in chronic users, increase EEG abnormalities after MA but not after MDMA. While the neurochemical effects of Foxy are not known in humans, this drug causes severe EEG abnormalities and overt seizures in 100% of tested animals.</p>","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"5 ","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4435606/pdf/nihms688199.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33321741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-11-25DOI: 10.2174/1876523801104010036
R. Penning, L. D. Haan, J. Verster
This study examined the relationship between consumption of caffeinated beverages and alcohol, and effects on next day hangover severity. In 2010, a survey funded by Utrecht University was conducted among N=549 Dutch students. Beverages consumed on their latest drinking session that produced a hangover were recorded. Hangover severity was scored using the Acute Hangover Scale. No significant correlation between caffeine use and hangover severity was found. Subjects who mixed alcohol with colas consumed significantly more alcohol than those who drank alcohol alone (p=0.001), or mixed alcohol with energy drinks (p=0.001). Future studies with larger sample sizes should confirm these findings.
{"title":"Caffeinated drinks, alcohol consumption and hangover severity","authors":"R. Penning, L. D. Haan, J. Verster","doi":"10.2174/1876523801104010036","DOIUrl":"https://doi.org/10.2174/1876523801104010036","url":null,"abstract":"This study examined the relationship between consumption of caffeinated beverages and alcohol, and effects on next day hangover severity. In 2010, a survey funded by Utrecht University was conducted among N=549 Dutch students. Beverages consumed on their latest drinking session that produced a hangover were recorded. Hangover severity was scored using the Acute Hangover Scale. No significant correlation between caffeine use and hangover severity was found. Subjects who mixed alcohol with colas consumed significantly more alcohol than those who drank alcohol alone (p=0.001), or mixed alcohol with energy drinks (p=0.001). Future studies with larger sample sizes should confirm these findings.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"4 1","pages":"36-39"},"PeriodicalIF":0.0,"publicationDate":"2011-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68144548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-08-18DOI: 10.2174/1876523801104010025
B. Dean, S. Boer, E. Scarr, J. Um, M. Udawela, T. Boom, I. Reinieren, J. Cilia, Mark D Hill, Andrea M. Bradford, Declan Jones, J. Gartlon
There are well validated rodent paradigms of schizophrenia which are based on environmental manipulation (e.g. altered rearing conditions) or drug challenges. These manipulations induce behavioural changes in rodents that are thought to involve neuronal circuitry similar to the ones that are affected by the pathophysiology of the disorder. This study has investigated whether three such rodent paradigms (isolation rearing, neonatal PCP treatment or sub-chronic PCP treatment) are associated with changes in muscarinic receptors (CHRMs) or ionotropic glutamate receptors, some of which have been reported to be altered in the CNS of subjects with schizophrenia. ( 3 H)pirenzepine (CHRM1), ( 3 H)4DAMP (CHRM1/CHRM3), ( 3 H)MK801 (NMDA receptors) and ( 3 H)kainate (kainate receptors; KAR) binding were measured using in situ radioligand binding and autoradiography. Isolation rearing caused widespread decreases in ( 3 H)4DAMP (p = 0.01) and ( 3 H)kainate binding (p = 0.03). Neonatal PCP caused widespread increases in ( 3 H)4DAMP binding (p <0.0001), whereas sub-chronic PCP treatment caused widespread decreases in the binding of that radioligand (p < 0.002) and widespread increases in (3H)MK801 binding (p < 0.0001). There were no changes in ( 3 H)pirenzepine binding to CHRM1 receptors in any paradigm or no significant within region changes in the binding of any radioligand. In conclusion, in the absence of any changes in CHRM1 receptors, our ( 3 H)4DAMP and the binding of (3H)MK801 data would suggest that different rodent paradigms cause variable changes in levels of CHRM3 and KAR in the rat CNS. Our data raises the possibility that such changes may, in part, modulate the behavioural differences that have been observed after isolation rearing, neonatal PCP treatment or sub-chronic PCP treatment.
{"title":"Levels of Ionotropic Glutamate and Muscarinic Receptors in Three Animal Models of Schizophrenia","authors":"B. Dean, S. Boer, E. Scarr, J. Um, M. Udawela, T. Boom, I. Reinieren, J. Cilia, Mark D Hill, Andrea M. Bradford, Declan Jones, J. Gartlon","doi":"10.2174/1876523801104010025","DOIUrl":"https://doi.org/10.2174/1876523801104010025","url":null,"abstract":"There are well validated rodent paradigms of schizophrenia which are based on environmental manipulation (e.g. altered rearing conditions) or drug challenges. These manipulations induce behavioural changes in rodents that are thought to involve neuronal circuitry similar to the ones that are affected by the pathophysiology of the disorder. This study has investigated whether three such rodent paradigms (isolation rearing, neonatal PCP treatment or sub-chronic PCP treatment) are associated with changes in muscarinic receptors (CHRMs) or ionotropic glutamate receptors, some of which have been reported to be altered in the CNS of subjects with schizophrenia. ( 3 H)pirenzepine (CHRM1), ( 3 H)4DAMP (CHRM1/CHRM3), ( 3 H)MK801 (NMDA receptors) and ( 3 H)kainate (kainate receptors; KAR) binding were measured using in situ radioligand binding and autoradiography. Isolation rearing caused widespread decreases in ( 3 H)4DAMP (p = 0.01) and ( 3 H)kainate binding (p = 0.03). Neonatal PCP caused widespread increases in ( 3 H)4DAMP binding (p <0.0001), whereas sub-chronic PCP treatment caused widespread decreases in the binding of that radioligand (p < 0.002) and widespread increases in (3H)MK801 binding (p < 0.0001). There were no changes in ( 3 H)pirenzepine binding to CHRM1 receptors in any paradigm or no significant within region changes in the binding of any radioligand. In conclusion, in the absence of any changes in CHRM1 receptors, our ( 3 H)4DAMP and the binding of (3H)MK801 data would suggest that different rodent paradigms cause variable changes in levels of CHRM3 and KAR in the rat CNS. Our data raises the possibility that such changes may, in part, modulate the behavioural differences that have been observed after isolation rearing, neonatal PCP treatment or sub-chronic PCP treatment.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"4 1","pages":"25-35"},"PeriodicalIF":0.0,"publicationDate":"2011-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68145029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-08-01DOI: 10.2174/1876523801104010018
S. Flaisher-Grinberg, H. Einat
The development of appropriate models for bipolar disorder (BPD) is a critical step in the efforts to further study the underlying pathology of the disorder and develop novel treatments. One approach to achieve better models is to develop a battery of tests for the different behavioral domains of the disease. Previous work examined ways to model reward-related behaviors in the context of BPD with some success. Because disregulation of the reward system is one of the hallmarks of BPD the present study was designed to evaluate the possibility of using amphetamine-induced conditioned place preference (CPP) as an additional method to model the reward seeking behavioral domain in BPD. To evaluate the pharmacological (predictive) validity of amphetamine-i nduced CPP for BPD, the study examined the effects of the prototypic mood stabilizer lithium in a biased (black/white) amphetamine-induced CPP paradigm. To delineate generalized effects of drugs, animals were also tested for locomotor activity at the end of the CPP paradigm. As expected, amphetamine pairing resulted in the development of CPP, evidenced by an increase in the time spent in the paired compartment from pre-conditioning to post-conditioning sessions. Lithium had no effects on the expression of CPP or on locomotor activity. The results suggest that amphetamine-induced CPP lacks pharmacological validity and it is therefore not a good choice as a model for the reward-seeking domain of BPD. Additional tests should be explored as suitable modes for this important component of the disorder.
{"title":"Amphetamine-Induced Conditioned Place Preference and Modeling Domains of Bipolar Disorder","authors":"S. Flaisher-Grinberg, H. Einat","doi":"10.2174/1876523801104010018","DOIUrl":"https://doi.org/10.2174/1876523801104010018","url":null,"abstract":"The development of appropriate models for bipolar disorder (BPD) is a critical step in the efforts to further study the underlying pathology of the disorder and develop novel treatments. One approach to achieve better models is to develop a battery of tests for the different behavioral domains of the disease. Previous work examined ways to model reward-related behaviors in the context of BPD with some success. Because disregulation of the reward system is one of the hallmarks of BPD the present study was designed to evaluate the possibility of using amphetamine-induced conditioned place preference (CPP) as an additional method to model the reward seeking behavioral domain in BPD. To evaluate the pharmacological (predictive) validity of amphetamine-i nduced CPP for BPD, the study examined the effects of the prototypic mood stabilizer lithium in a biased (black/white) amphetamine-induced CPP paradigm. To delineate generalized effects of drugs, animals were also tested for locomotor activity at the end of the CPP paradigm. As expected, amphetamine pairing resulted in the development of CPP, evidenced by an increase in the time spent in the paired compartment from pre-conditioning to post-conditioning sessions. Lithium had no effects on the expression of CPP or on locomotor activity. The results suggest that amphetamine-induced CPP lacks pharmacological validity and it is therefore not a good choice as a model for the reward-seeking domain of BPD. Additional tests should be explored as suitable modes for this important component of the disorder.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"4 1","pages":"18-24"},"PeriodicalIF":0.0,"publicationDate":"2011-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68145013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-07-28DOI: 10.2174/1876523801104010010
H. D. Özgüven, B. Baskak, O. Oner, C. Atbaşoğlu
The objective of this study is to compare the course of metabolic effects of olanzapine and quetiapine, two atypical antipsychotics with similar structure and receptor binding affinities but clinically observed different metabolic ef- fects. This 6 week, single blind, randomized, controlled study was carried out during a structured treatment protocol in a female inpatient service, thus enabled to control effects of energy expenditure and other life style related factors. Subjects were randomly assigned into olanzapine (n=15) and quetiapine (n=15) groups. Weight and calorie intake (CI) were meas- ured daily. Symptom severity and serum leptin levels (SLL) were measured biweekly. Serum lipids were measured at baseline and 6th week. Olanzapine treatment was associated with more severe weight gain (F=11.2, p<0.01), increase in CI (F=8.1, p<0.01) and a more disturbed lipid profile than quetiapine. The course of SLL were similar between the groups (F=1.39, p=0.26). Weight, CI and SLL changed in a similar pattern within the groups but the patterns were different for each drug, suggesting that the two drugs have different mechanisms for weight change. The explanation probably involves different affinities for 5HT2C receptors leading to different patterns of CI which we propose as possible targets of inter- vention to manage antipsychotic induced weight gain.
{"title":"Metabolic Effects of Olanzapine and Quetiapine: A Six-Week Randomized,Single Blind, Controlled Study","authors":"H. D. Özgüven, B. Baskak, O. Oner, C. Atbaşoğlu","doi":"10.2174/1876523801104010010","DOIUrl":"https://doi.org/10.2174/1876523801104010010","url":null,"abstract":"The objective of this study is to compare the course of metabolic effects of olanzapine and quetiapine, two atypical antipsychotics with similar structure and receptor binding affinities but clinically observed different metabolic ef- fects. This 6 week, single blind, randomized, controlled study was carried out during a structured treatment protocol in a female inpatient service, thus enabled to control effects of energy expenditure and other life style related factors. Subjects were randomly assigned into olanzapine (n=15) and quetiapine (n=15) groups. Weight and calorie intake (CI) were meas- ured daily. Symptom severity and serum leptin levels (SLL) were measured biweekly. Serum lipids were measured at baseline and 6th week. Olanzapine treatment was associated with more severe weight gain (F=11.2, p<0.01), increase in CI (F=8.1, p<0.01) and a more disturbed lipid profile than quetiapine. The course of SLL were similar between the groups (F=1.39, p=0.26). Weight, CI and SLL changed in a similar pattern within the groups but the patterns were different for each drug, suggesting that the two drugs have different mechanisms for weight change. The explanation probably involves different affinities for 5HT2C receptors leading to different patterns of CI which we propose as possible targets of inter- vention to manage antipsychotic induced weight gain.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"4 1","pages":"10-17"},"PeriodicalIF":0.0,"publicationDate":"2011-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68145004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-04-29DOI: 10.2174/1876523801104010008
M. Bucur, P. Jeczmien
Pregabalin is a drug used in UK for the following conditions: peripheral and central neuropathic pain, adjunctive therapy for partial seizures with or without secondary generalization and generalized anxiety disorder. Drugs used to treat anxiety disorders very often do have sexual side effects (e.g. SSRIs, SNRIs, and Benzodiazepines). Patients with generalized anxiety disorder can have an impaired libido due to the direct effect of anxiety. Since mid 2009, when we first started prescribing Pregabalin for patients with a diagnosis of Generalized Anxiety Disorder, two male patients reported enhanced libido after having started treatment with Pregabalin. It would be argued that the Pregabalin mechanism of action might be responsible for these changes. An extensive search of the medical literature conducted in 2010 failed to retrieve any relevant published studies or case reports that comment on the impact of Pregabalin on increased libido. Pregabalin is a drug used in the treatment of neuropathic pain, partial seizures and generalized anxiety disorder. Pregabalin inhibits the release of the excess excitatory neurotransmitters, presumably by binding to the alpha 2 delta proteins of the widely distributed voltage dependent calcium channels in spine and brain. This mechanism is responsible for the anxyolitic, anticonvulsant and antinocioceptive effect. (1) Libido is the term used to describe sexual desire or the psychic and emotional energy related to sexuality. In the accepted sense, libido refers specifically to the mental manifestations of the sexual instinct. (2) Drugs used to treat anxiety disorders very often do have sexual side effects. Patients with generalized anxiety disorder can have an impaired libido due to the direct effect of anxiety. Since 2009, when we have started prescribing Pregabalin for community patients with Generalized Anxiety Disorder, two patients self reported enhanced libido shortly after having started treatment with Pregabalin. The first case is a 42-year-old gentleman who has a diagnosis of Alcohol Dependence, Narcissistic Personality Disorder associated with Generalized Anxiety Disorder. His only pharmacological treatment was Pregabalin 150mg (twice daily) and Quetiapine 50mg (twice daily). Pregabalin was introduced three weeks before he reported increased libido. He was in a stable relationship with a lady he met four years ago. Although he was off work for about 6 months, no significant life events were identified since he started Pregabalin. The above pharmacological treatment was the mainstay of his management plan when he self- reported increased libido.
{"title":"Pregabalin and Libido- Case Reports","authors":"M. Bucur, P. Jeczmien","doi":"10.2174/1876523801104010008","DOIUrl":"https://doi.org/10.2174/1876523801104010008","url":null,"abstract":"Pregabalin is a drug used in UK for the following conditions: peripheral and central neuropathic pain, adjunctive therapy for partial seizures with or without secondary generalization and generalized anxiety disorder. Drugs used to treat anxiety disorders very often do have sexual side effects (e.g. SSRIs, SNRIs, and Benzodiazepines). Patients with generalized anxiety disorder can have an impaired libido due to the direct effect of anxiety. Since mid 2009, when we first started prescribing Pregabalin for patients with a diagnosis of Generalized Anxiety Disorder, two male patients reported enhanced libido after having started treatment with Pregabalin. It would be argued that the Pregabalin mechanism of action might be responsible for these changes. An extensive search of the medical literature conducted in 2010 failed to retrieve any relevant published studies or case reports that comment on the impact of Pregabalin on increased libido. Pregabalin is a drug used in the treatment of neuropathic pain, partial seizures and generalized anxiety disorder. Pregabalin inhibits the release of the excess excitatory neurotransmitters, presumably by binding to the alpha 2 delta proteins of the widely distributed voltage dependent calcium channels in spine and brain. This mechanism is responsible for the anxyolitic, anticonvulsant and antinocioceptive effect. (1) Libido is the term used to describe sexual desire or the psychic and emotional energy related to sexuality. In the accepted sense, libido refers specifically to the mental manifestations of the sexual instinct. (2) Drugs used to treat anxiety disorders very often do have sexual side effects. Patients with generalized anxiety disorder can have an impaired libido due to the direct effect of anxiety. Since 2009, when we have started prescribing Pregabalin for community patients with Generalized Anxiety Disorder, two patients self reported enhanced libido shortly after having started treatment with Pregabalin. The first case is a 42-year-old gentleman who has a diagnosis of Alcohol Dependence, Narcissistic Personality Disorder associated with Generalized Anxiety Disorder. His only pharmacological treatment was Pregabalin 150mg (twice daily) and Quetiapine 50mg (twice daily). Pregabalin was introduced three weeks before he reported increased libido. He was in a stable relationship with a lady he met four years ago. Although he was off work for about 6 months, no significant life events were identified since he started Pregabalin. The above pharmacological treatment was the mainstay of his management plan when he self- reported increased libido.","PeriodicalId":88752,"journal":{"name":"The open neuropsychopharmacology journal","volume":"4 1","pages":"8-9"},"PeriodicalIF":0.0,"publicationDate":"2011-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68144954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2011-04-14DOI: 10.2174/1876523801104010005
M. Raja, A. Azzoni
Acute pancreatitis is a very rare complication of clozapine treatment. We report a new case of symptomatic pancreatitis subsequent to starting of clozapine treatment. In this case, the diagnosis of pancreatitis can be considered de- finitive and the etiological link between clozapine and pancreatitis highly likely. Recovery was not complete. In a 10-year period, we treated 363 cases (196 patients) with clozapine. We diagnosed clozapine-associated pancreatitis only in this pa- tient. However, we did not check amylase and lipase plasma levels in all patients and possibly missed several cases of pancreatitis. We suggest monitoring pancreatic enzymes routinely, at least in the first months of clozapine therapy. Between 2 and 5% of cases of acute pancreatitis are drug related (1). Drugs cause pancreatitis either by a hypersensi- tivity reaction or by the generation of a toxic metabolite. The autodigestion by proteolytic enzymes activated in pancreas rather than in the intestinal lumen is the suspected patho- genic mechanism. Rechallenge tests, consistent case reports, animal experiments, data on the incidence in drug trials pro- vide evidence of a definite association with pancreatitis for didanosine, valproic acid, aminosalicylates, estrogen, cal- cium, anticholinesterases, and sodium stibogluconate. An association with pancreatitis is likely, but not definitely proven, for thiazide diuretics, pentamidine, ACE inhibitors, asparaginase, vinca alkaloids, nonsteroidal anti- inflammatory drugs, and clozapine (2). In a pharmacovigi- lance study of spontaneously reported adverse events (3), 192 patients developed pancreatitis during antipsychotic treatment. Most cases of pancreatitis occurred within 6 months after the start of antipsychotics. Of the reports of pancreatitis associated with antipsychotics, 40%, 33%, 16%, and 12% were in patients receiving clozapine, olanzapine, risperidone, and haloperidol, respectively. In 50% of the patients receiving haloperidol, an atypical antipsychotic was listed as a concomitant drug. Valproate was administered concomitantly in 23% of patients.
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Pub Date : 2011-02-03DOI: 10.2174/1876523801104010001
Etievant Adeline
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