- Email: [email protected]
P.8.070 Escitalopram in the treatment of premenstrual dysphoric disorder
P8 Other topics
$636
research. Only randomised controlled trials were included. Study participants were of either sex and any age with a diagnosis of personality disorders. Two reviewers independently extracted data, using a standardised form. The total number of randomised patients, the number of patients who completed the study and the number of patients who responded were considered for the efficacy analysis. In the tolerability analysis, the number of patients failing to complete the study and the number of patients complaining side-effects was extracted. Data were analysed using STATA 8.0 and RevMan 4.2. Results: The literature search yielded more than 600 references. After removing studies not meeting inclusion criteria and duplicates, a total of 76 articles were assessed. O f these, 39 randomised clinical trials were included. These studies were grouped according to the outcome measure into the following three groups: (1) studies assessing pharmacological interventions for improving cognitive symptoms; (2) studies assessing pharmacological interventions for improving emotional dysregulations; (3) studies assessing pharmacological interventions for improving impulsivebehavioural symptoms. The overall estimate of the efficacy of pharmacological interventions in these three domains will be presented using both Peto Odds Ratio and Relative Risk with a 95% Confidence Interval. Additionally, the tolerability profiles of these interventions will be analysed and discussed. Conclusion: This systematic review will highlight whether there are effective pharmacological interventions in the treatment of patients with personality disorders. The benefit of these interventions will be analysed by diagnostic category and length of follow-up.
period of 60 min SDs were elicited with NMDA repetitively and latency to the appearance of SD was measured, 30 s increase in latency relative to control was considered 100% inhibition; Population spikes (PS) were recorded from CA1 of hippocampal slices prepared from male Wistar rats (120 160 g) using conventional extracellular recording techniques. Schaffer collaterals were stimulated (0.1 ms) to evoke 80% of the maximal PS amplitude. Concentration-response curves were calculated using sigmoidal curve fitting to logistic equation. Results: NMDA (100 ~tM) at a Mg2+ concentration of 1 mM, elicited SD in the chicken retina with a latency of 15 20s. Deramciclane (up to 100 ~tM) did not influence significantly the effect of NMDA. When lower concentration of NMDA (50 ~tM) and Mg2+ (0.33 mM) were applied, deramciclane inhibited the NMDA-evoked SD in a concentration-dependent manner. In addition, this inhibition seemed to be use-dependent, i.e. during consecutive elicitations of SD, higher inhibition was achieved by the same concentrations of deramciclane (inhibition changed from the initial 33.3±2.4% to 88.3±3.4% at 70raM, mean ± S.E.M., n 4). Similar results were obtained in patch clamp experiments: deramciclane (50 ~tM) inhibited NMDA current in a use-dependent manner, and the inhibitory effect increased when deramciclane was added repetitively. Deramciclane did not inhibit population spikes in the hippocampus up to 100 ~tM. Conclusions: Our results showed that deramciclane at higher micromolar concentrations negatively modulated NMDA receptor function in retinal spreading depression as well as NMDA current in telecephalon neurons in vitro. This inhibitory action seems to differ from that of 'classical' receptor antagonists and may contribute to the anxiolytic properties of deramciclane.
References [1] Lieb K., Zanarini M.C., Schmahl C., Linehan M.M., Bohus M., 2004. Borderline personality disorder. Lancet 364, 453 61. [2] Sanislow C.A. & McGlashan T.H., 1998. Treatment outcome of personality disorders. Can J Psychiatry 43, 237 250.
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•
E. Eriksson 1 *, H. Nissbrandt 1, K. S6rvik 2, S. Sinclair3, C. Ysander 2, B.M. Mattson 1 , A. Ekman 1 , J. Bothmer4.
Deramciclane (EGIS-3886) negatively modulates N-methyI-D-aspartate receptor function in vitro
S. Kert6sz*, M. Vegh, G. Kapus, G. Kovfics, G. L6vay. EGIS Pharmaceuticals Ltd., Division of Preclinical Research, Budapest, Hungaty Introduction: Deramciclane is a novel compound that is proved
to be anxiolytic in preclinical as well as in clinical studies. Deramciclane has an axiolytic profile differs from that of the benzodiazepines. Deramciclane has a direct effect on serotonergic receptors (antagonist at 5HT2A and an inverse agonist at 5HT2C receptor) and it has been demonstrated to show inhibitory potency at N-methyl-D-aspartate (NMDA) receptors as well. Our purpose was to investigate the NMDA antagonist properties of deramciclane in vitro. Methods: Whole cell patch clamp recordings on primary cultures of embryonic telencephalon neurons. NMDA (100 ~tM) and glycine (1 ~tM) were prepared with the bath solution, recordings were made by glass micropipette at resistance between 4.5 5.5MOhm at room temperature, membrane potential was held at 70mV; Spreading depression (SD) in the chicken retina: retinas of 5 7 day-old Shaver redbrow chickens were used. The eyes were enucleated and cut along the equatorial plane. Posterior parts (retinas) were placed in carbogenated Ringer solution and maintained at room temperature (23 24°C). After an equilibrium
Escitalopram in the treatment of premenstrual dysphoric disorder
] University of G6teborg, Pharmacology, Valby-Copenhagen, Sweden; 2University of G6teborg, Institute of Clinical Neuroscience, Sweden; 3Liikarttuset, Sweden; eLundbeck GmbH & Co, Clinical Research, Germany Purpose: Escitalopram, the most selective serotonin reuptake
inhibitor available, has shown to be efficacious in the treatment of major depression, panic disorder, generalised anxiety disorder, and social anxiety disorder. The current study was designed to evaluate the efficacy and tolerability of intermittent dosing (luteal phase only) with 10 and 20 mg escitalopram in the treatment of premenstrual dysphoric disorder (PMDD). Methods: A total of 158 patients with a diagnosis of PMDD, confirmed during two cycles of prospective self-rating of their symptoms (baseline), were treated for 3 cycles in this singlecentre, randomised, double-blind, placebo-controlled 3-arm fixed dose study. The primary measure of efficacy was the relative median change from baseline in the mean of the luteal VAS rating (0 100mm) for the four key psychological symptoms, i.e., irritability, tension, affective lability, and depressed mood. Results: The patients had a baseline severity of approximately 50 mm in the mean luteal VAS key psychological symptom score (49 mm, 51 mm, and 53 mm for the placebo, escitalopram 10 mg and 20 mg groups, respectively). At endpoint, both escitalopram treatment groups showed superior improvements on the relative median change in the key psychological symptom score versus the
P8 Other topics placebo group [86% decrease for the 10mg escitalopram group (p <0.01) and 94% decrease for the 2 0 m g escitalopram group (p < 0.001) versus 69% decrease for the placebo group], with escitalopram 2 0 m g being more efficacious than 10mg (p < 0.01). Escitalopram reached its maximal effect in the first treatment cycle, and this effect was maintained during the following treatment cycles. The reduction of the key symptom of PMDD, irritability, was 86% (escitalopram 10mg, p < 0.01), 92% (escitalopram 20 mg, p < 0.001), and 56% (placebo). The percentage of subjects achieving remission (defined as at least 80% reduction in the irritability score) was 30% (placebo), 60% (escitalopram 10mg) and 80% (escitalopram 20mg). The most frequent adverse event was nausea with an incidence of 44% and 45% in the escitalopram 10 mg and 20 mg groups, respectively, versus 12% in the placebo group; most adverse events were rated as mild or moderate in severity. Adaptation of patients to nausea within a treatment cycle and from one treatment cycle to another was marked. The withdrawal rates due to adverse events were 6% (placebo), 13% (escitalopram 10 mg) and 6% (escitalopram 20 mg). C o n c l u s i o n s : Intermittent treatment with escitalopram 10 and 20 mg/day was effective and well tolerated in the treatment of PMDD.
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Effects of the metabotropic glutamate receptor subtype5 blockade on inhibitory avoidance in rats
I. Stankova 1 *, M. Genkova-Papazova2, t3. Petkova 2, N. Changarova 2, M. Lazarova 2, K. Ossowska 3. ]Institute of
Physiology, Bulg. Acad. Sci., Lab. of CArS Pharmacology, Sofia, Bulgaria; 2Institute of Pharmacology, Bulg. Acad. Sci., Lab. CArS Pharmacology, Bulgaria; 3Inst. Pharmacol., Polish Acad. Sci, Neuro-psychopharmacology, Poland Pharmacological evidence strongly implicates that the neurotransmitter glutamate plays a major role in learning and memory. Although the involvement of ionotropic glutamate receptors has been proven, the role of the newly characterised metabotropic glutamate receptors (mGluRs) is still uncertain. We tested whether intraperitoneal administration of the non competetive mGluR5 antagonist MPEP (2-methyl-6-(phenylethynyl)pyridine) injected prior to, immediately after or 30 minutes after training affects acquisition and/or retrieval of the inhibitory stepdown and active shuttle-box avoidance in rats. Experiments were carried out on mature male Wistar rats (10 rats per group) weighing 1 8 0 ~ 0 0 g. Punishment reinforced active (shuttle-box) and inhibitory avoidance (step-down) were used to follow up the changes in memory. In step-down situation rats were trained in 6 consecutive training sessions and retention was tested 3h, 24h and 7 days after training. Percentage of rats remaining on the platform for at least 30 s was recorded. Learning criterion was reached when the animal remained on the platform for at least 30 s. The number of rats reaching the learning criterion was calculated in percentage. Data were analysed by the X2criterion. By the shuttle-box method rats were trained in one session with 50 trials and retention testing with 30 trials was given 24 h. and 7 days later. The number of avoidances was given in percentage. Data were analyzed by two-way ANOVA and posthoc comparissons were made using Kolmogoroff-Smirnoff test. Our present data strongly suggest that the blockade of mGluR5 by the selective antagonist MPEP, injected before or after training, impairs memory consolidation of inhibitory and active avoidance paradigm without affecting acquisition. These results are
$637
in agreement with previous data of Packard et al. (2001) and Schulz et al. (2001), showing that pre- and posttraining blockade of mGluR5 by MPEP task-dependent impairs retention of some different learning paradigms. According to Riedel et al., (2003) metabotropic glutamate receptors (mGluRs) may contribute little to the stage of acquisition, but memory formation appears to require them through the modulation of consolidation and/or recall. In conclusion, the present data show that the selective mGluR5 anatagonist MPEP impairs retention of an inhibitory avoidance paradigm and support the involvement of mGluR5 in memory consolidation stage.
References [1] Riedel, G., Platt, B., Micheau, J., 2003. Glutamate receptor fuction in learning and memory. Behav Brain Research 140, 140, 1 47. [2] Packard, M., Vecchioli, S., Scbxoeder, J., Gasbarri, A., 2001. Taskdependent role for dorsal striatum metabotropic glutamate receptors in memory. Learn Mem 8, 9(~103. [3] Schulz, B., Fendt, M., Gasparini, E, Lingenhohl, K., Kuhn, R., Koch, M., 2001. The metabotropic glutamatr receptor antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) blocks fear conditioning in rats. Neuropharmacology 41, 1 7.
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Effects of pretreatment with ibuprofen in post-electroconvulsive therapy headache
L. Jarosch-von Schweder 1 *, L. Pedersen 2, W. Stuen Leira 2.
]Department of Neuroscience, Research Department, Trondheim, Notway," 2Alesund Hospital, Psychiatry Department, Norway S t a t e m e n t o n the p u r p o s e o f the study: ECT is a well known treatment for severe depression. However patients do experience side effects like headcache related to electroonvulasive therapy [1]. Commonly patients are treated well after the course of ECT with analgesics and narcotics. Some have reported pretreatment with NSAIDs to reduce post-ECT headache [2] and there are also other option tried as profylaxis treatment. The aim of our study is to determine wether ibuprofen reduce post- ECT headache or reduce its severity. We also want to investigate if there are a possible effect of Ibuprofen preatment on seizure duration during electroconvulsive therapy. M e t h o d s used: Patients admitted to the psychiatric units in Aalesund hospital and St. Olavs hospital, Trondheim who are receiving ECT along their hospitalization are participating in the study. Patients are randomly assigned to receive either 600mg ibuprofen 90 min prior to ECT or placebo orally, blinded to patient, physician and treatment team. Patients will be asked about their headache with a visual analuoge scale (VAS) [3] 2 hours prior to and within 2 hours after treatment, 2-month, 6-month and 1 year follow-up. S u m m a r y o f results a n d statistical a s s e s s m e n t s : Preliminary results will be in october 2005. C o n c l u s i o n : If giving ibuprofen prior to ECT reduce the severity or prevent the onset of ECT-related headache we could consider giving ibuprofen prior to ECT to patients who can tolerate it. Wether ibuprofen affects seizure duration are worth further examination.
References [1] Fink M., 2001, Convulsive therapy: a review of the first 55 years. Journal of Affective Disorders 63, issue 1 3, 1 15. [2] Leung M., Hollander Y., Brown GR. 2003. Pretreatment with ibuprofen to prevent electroconvulsive-therapy induced headache. J Clin Psychiatry 64, 551 553.
$636
research. Only randomised controlled trials were included. Study participants were of either sex and any age with a diagnosis of personality disorders. Two reviewers independently extracted data, using a standardised form. The total number of randomised patients, the number of patients who completed the study and the number of patients who responded were considered for the efficacy analysis. In the tolerability analysis, the number of patients failing to complete the study and the number of patients complaining side-effects was extracted. Data were analysed using STATA 8.0 and RevMan 4.2. Results: The literature search yielded more than 600 references. After removing studies not meeting inclusion criteria and duplicates, a total of 76 articles were assessed. O f these, 39 randomised clinical trials were included. These studies were grouped according to the outcome measure into the following three groups: (1) studies assessing pharmacological interventions for improving cognitive symptoms; (2) studies assessing pharmacological interventions for improving emotional dysregulations; (3) studies assessing pharmacological interventions for improving impulsivebehavioural symptoms. The overall estimate of the efficacy of pharmacological interventions in these three domains will be presented using both Peto Odds Ratio and Relative Risk with a 95% Confidence Interval. Additionally, the tolerability profiles of these interventions will be analysed and discussed. Conclusion: This systematic review will highlight whether there are effective pharmacological interventions in the treatment of patients with personality disorders. The benefit of these interventions will be analysed by diagnostic category and length of follow-up.
period of 60 min SDs were elicited with NMDA repetitively and latency to the appearance of SD was measured, 30 s increase in latency relative to control was considered 100% inhibition; Population spikes (PS) were recorded from CA1 of hippocampal slices prepared from male Wistar rats (120 160 g) using conventional extracellular recording techniques. Schaffer collaterals were stimulated (0.1 ms) to evoke 80% of the maximal PS amplitude. Concentration-response curves were calculated using sigmoidal curve fitting to logistic equation. Results: NMDA (100 ~tM) at a Mg2+ concentration of 1 mM, elicited SD in the chicken retina with a latency of 15 20s. Deramciclane (up to 100 ~tM) did not influence significantly the effect of NMDA. When lower concentration of NMDA (50 ~tM) and Mg2+ (0.33 mM) were applied, deramciclane inhibited the NMDA-evoked SD in a concentration-dependent manner. In addition, this inhibition seemed to be use-dependent, i.e. during consecutive elicitations of SD, higher inhibition was achieved by the same concentrations of deramciclane (inhibition changed from the initial 33.3±2.4% to 88.3±3.4% at 70raM, mean ± S.E.M., n 4). Similar results were obtained in patch clamp experiments: deramciclane (50 ~tM) inhibited NMDA current in a use-dependent manner, and the inhibitory effect increased when deramciclane was added repetitively. Deramciclane did not inhibit population spikes in the hippocampus up to 100 ~tM. Conclusions: Our results showed that deramciclane at higher micromolar concentrations negatively modulated NMDA receptor function in retinal spreading depression as well as NMDA current in telecephalon neurons in vitro. This inhibitory action seems to differ from that of 'classical' receptor antagonists and may contribute to the anxiolytic properties of deramciclane.
References [1] Lieb K., Zanarini M.C., Schmahl C., Linehan M.M., Bohus M., 2004. Borderline personality disorder. Lancet 364, 453 61. [2] Sanislow C.A. & McGlashan T.H., 1998. Treatment outcome of personality disorders. Can J Psychiatry 43, 237 250.
•
•
E. Eriksson 1 *, H. Nissbrandt 1, K. S6rvik 2, S. Sinclair3, C. Ysander 2, B.M. Mattson 1 , A. Ekman 1 , J. Bothmer4.
Deramciclane (EGIS-3886) negatively modulates N-methyI-D-aspartate receptor function in vitro
S. Kert6sz*, M. Vegh, G. Kapus, G. Kovfics, G. L6vay. EGIS Pharmaceuticals Ltd., Division of Preclinical Research, Budapest, Hungaty Introduction: Deramciclane is a novel compound that is proved
to be anxiolytic in preclinical as well as in clinical studies. Deramciclane has an axiolytic profile differs from that of the benzodiazepines. Deramciclane has a direct effect on serotonergic receptors (antagonist at 5HT2A and an inverse agonist at 5HT2C receptor) and it has been demonstrated to show inhibitory potency at N-methyl-D-aspartate (NMDA) receptors as well. Our purpose was to investigate the NMDA antagonist properties of deramciclane in vitro. Methods: Whole cell patch clamp recordings on primary cultures of embryonic telencephalon neurons. NMDA (100 ~tM) and glycine (1 ~tM) were prepared with the bath solution, recordings were made by glass micropipette at resistance between 4.5 5.5MOhm at room temperature, membrane potential was held at 70mV; Spreading depression (SD) in the chicken retina: retinas of 5 7 day-old Shaver redbrow chickens were used. The eyes were enucleated and cut along the equatorial plane. Posterior parts (retinas) were placed in carbogenated Ringer solution and maintained at room temperature (23 24°C). After an equilibrium
Escitalopram in the treatment of premenstrual dysphoric disorder
] University of G6teborg, Pharmacology, Valby-Copenhagen, Sweden; 2University of G6teborg, Institute of Clinical Neuroscience, Sweden; 3Liikarttuset, Sweden; eLundbeck GmbH & Co, Clinical Research, Germany Purpose: Escitalopram, the most selective serotonin reuptake
inhibitor available, has shown to be efficacious in the treatment of major depression, panic disorder, generalised anxiety disorder, and social anxiety disorder. The current study was designed to evaluate the efficacy and tolerability of intermittent dosing (luteal phase only) with 10 and 20 mg escitalopram in the treatment of premenstrual dysphoric disorder (PMDD). Methods: A total of 158 patients with a diagnosis of PMDD, confirmed during two cycles of prospective self-rating of their symptoms (baseline), were treated for 3 cycles in this singlecentre, randomised, double-blind, placebo-controlled 3-arm fixed dose study. The primary measure of efficacy was the relative median change from baseline in the mean of the luteal VAS rating (0 100mm) for the four key psychological symptoms, i.e., irritability, tension, affective lability, and depressed mood. Results: The patients had a baseline severity of approximately 50 mm in the mean luteal VAS key psychological symptom score (49 mm, 51 mm, and 53 mm for the placebo, escitalopram 10 mg and 20 mg groups, respectively). At endpoint, both escitalopram treatment groups showed superior improvements on the relative median change in the key psychological symptom score versus the
P8 Other topics placebo group [86% decrease for the 10mg escitalopram group (p <0.01) and 94% decrease for the 2 0 m g escitalopram group (p < 0.001) versus 69% decrease for the placebo group], with escitalopram 2 0 m g being more efficacious than 10mg (p < 0.01). Escitalopram reached its maximal effect in the first treatment cycle, and this effect was maintained during the following treatment cycles. The reduction of the key symptom of PMDD, irritability, was 86% (escitalopram 10mg, p < 0.01), 92% (escitalopram 20 mg, p < 0.001), and 56% (placebo). The percentage of subjects achieving remission (defined as at least 80% reduction in the irritability score) was 30% (placebo), 60% (escitalopram 10mg) and 80% (escitalopram 20mg). The most frequent adverse event was nausea with an incidence of 44% and 45% in the escitalopram 10 mg and 20 mg groups, respectively, versus 12% in the placebo group; most adverse events were rated as mild or moderate in severity. Adaptation of patients to nausea within a treatment cycle and from one treatment cycle to another was marked. The withdrawal rates due to adverse events were 6% (placebo), 13% (escitalopram 10 mg) and 6% (escitalopram 20 mg). C o n c l u s i o n s : Intermittent treatment with escitalopram 10 and 20 mg/day was effective and well tolerated in the treatment of PMDD.
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Effects of the metabotropic glutamate receptor subtype5 blockade on inhibitory avoidance in rats
I. Stankova 1 *, M. Genkova-Papazova2, t3. Petkova 2, N. Changarova 2, M. Lazarova 2, K. Ossowska 3. ]Institute of
Physiology, Bulg. Acad. Sci., Lab. of CArS Pharmacology, Sofia, Bulgaria; 2Institute of Pharmacology, Bulg. Acad. Sci., Lab. CArS Pharmacology, Bulgaria; 3Inst. Pharmacol., Polish Acad. Sci, Neuro-psychopharmacology, Poland Pharmacological evidence strongly implicates that the neurotransmitter glutamate plays a major role in learning and memory. Although the involvement of ionotropic glutamate receptors has been proven, the role of the newly characterised metabotropic glutamate receptors (mGluRs) is still uncertain. We tested whether intraperitoneal administration of the non competetive mGluR5 antagonist MPEP (2-methyl-6-(phenylethynyl)pyridine) injected prior to, immediately after or 30 minutes after training affects acquisition and/or retrieval of the inhibitory stepdown and active shuttle-box avoidance in rats. Experiments were carried out on mature male Wistar rats (10 rats per group) weighing 1 8 0 ~ 0 0 g. Punishment reinforced active (shuttle-box) and inhibitory avoidance (step-down) were used to follow up the changes in memory. In step-down situation rats were trained in 6 consecutive training sessions and retention was tested 3h, 24h and 7 days after training. Percentage of rats remaining on the platform for at least 30 s was recorded. Learning criterion was reached when the animal remained on the platform for at least 30 s. The number of rats reaching the learning criterion was calculated in percentage. Data were analysed by the X2criterion. By the shuttle-box method rats were trained in one session with 50 trials and retention testing with 30 trials was given 24 h. and 7 days later. The number of avoidances was given in percentage. Data were analyzed by two-way ANOVA and posthoc comparissons were made using Kolmogoroff-Smirnoff test. Our present data strongly suggest that the blockade of mGluR5 by the selective antagonist MPEP, injected before or after training, impairs memory consolidation of inhibitory and active avoidance paradigm without affecting acquisition. These results are
$637
in agreement with previous data of Packard et al. (2001) and Schulz et al. (2001), showing that pre- and posttraining blockade of mGluR5 by MPEP task-dependent impairs retention of some different learning paradigms. According to Riedel et al., (2003) metabotropic glutamate receptors (mGluRs) may contribute little to the stage of acquisition, but memory formation appears to require them through the modulation of consolidation and/or recall. In conclusion, the present data show that the selective mGluR5 anatagonist MPEP impairs retention of an inhibitory avoidance paradigm and support the involvement of mGluR5 in memory consolidation stage.
References [1] Riedel, G., Platt, B., Micheau, J., 2003. Glutamate receptor fuction in learning and memory. Behav Brain Research 140, 140, 1 47. [2] Packard, M., Vecchioli, S., Scbxoeder, J., Gasbarri, A., 2001. Taskdependent role for dorsal striatum metabotropic glutamate receptors in memory. Learn Mem 8, 9(~103. [3] Schulz, B., Fendt, M., Gasparini, E, Lingenhohl, K., Kuhn, R., Koch, M., 2001. The metabotropic glutamatr receptor antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) blocks fear conditioning in rats. Neuropharmacology 41, 1 7.
•
Effects of pretreatment with ibuprofen in post-electroconvulsive therapy headache
L. Jarosch-von Schweder 1 *, L. Pedersen 2, W. Stuen Leira 2.
]Department of Neuroscience, Research Department, Trondheim, Notway," 2Alesund Hospital, Psychiatry Department, Norway S t a t e m e n t o n the p u r p o s e o f the study: ECT is a well known treatment for severe depression. However patients do experience side effects like headcache related to electroonvulasive therapy [1]. Commonly patients are treated well after the course of ECT with analgesics and narcotics. Some have reported pretreatment with NSAIDs to reduce post-ECT headache [2] and there are also other option tried as profylaxis treatment. The aim of our study is to determine wether ibuprofen reduce post- ECT headache or reduce its severity. We also want to investigate if there are a possible effect of Ibuprofen preatment on seizure duration during electroconvulsive therapy. M e t h o d s used: Patients admitted to the psychiatric units in Aalesund hospital and St. Olavs hospital, Trondheim who are receiving ECT along their hospitalization are participating in the study. Patients are randomly assigned to receive either 600mg ibuprofen 90 min prior to ECT or placebo orally, blinded to patient, physician and treatment team. Patients will be asked about their headache with a visual analuoge scale (VAS) [3] 2 hours prior to and within 2 hours after treatment, 2-month, 6-month and 1 year follow-up. S u m m a r y o f results a n d statistical a s s e s s m e n t s : Preliminary results will be in october 2005. C o n c l u s i o n : If giving ibuprofen prior to ECT reduce the severity or prevent the onset of ECT-related headache we could consider giving ibuprofen prior to ECT to patients who can tolerate it. Wether ibuprofen affects seizure duration are worth further examination.
References [1] Fink M., 2001, Convulsive therapy: a review of the first 55 years. Journal of Affective Disorders 63, issue 1 3, 1 15. [2] Leung M., Hollander Y., Brown GR. 2003. Pretreatment with ibuprofen to prevent electroconvulsive-therapy induced headache. J Clin Psychiatry 64, 551 553.