пятница, 24 июля 2009 г.
среда, 22 июля 2009 г.
четверг, 16 июля 2009 г.
Случаи нарушения функции печени при приёме страттеры
Reported cases of liver injury occurred within 120 days of initiation of atomoxetine in the majority of cases and some patients presented with markedly elevated liver enzymes [>20 X upper limit of normal (ULN)], and jaundice with significantly elevated bilirubin levels (>2 X ULN), followed by recovery upon atomoxetine discontinuation.
FDA
FDA
среда, 15 июля 2009 г.
диазепамовый тест
Надежным методом разграничения деперсонализации, депрессии и тревоги является диазепамовый тест (ДТ) . Он заключается в струйном (медленном) внутривенном введении раствора диазепама (седуксена). Обычная доза составляет 30 мг препарата, у пожилых и ослабленных больных иногда вводят 20 мг, при массивной деперсонализации дозу можно увеличить до 40 мг. Выделяют три основных типа ДТ. 1. Депрессивный: депрессивная симптоматика существенно не меняется, больной быстро засыпает или наступает выраженная сонливость. 2. Тревожный: быстро, часто «на игле», исчезает вся аффективная симптоматика (тревога, депрессия). Иногда наступает легкая эйфория. 3.Деперсонализационный (отставленный). В отличие от других вариантов ДТ, положительная реакция на тест наступает через 20-30 минут и выражается в исчезновении или частичной редукции деперсонализации: «все стало ярче, яснее», «появились какие-то чувства». У подавляющего большинства больных с острой деперсонализацией ДТ положительный, при хронической деперсонализации (продолжительностью многие месяцы или годы) – может выявиться неполный положительный эффект. В немногих случаях хронической деперсонализации положительная реакция на тест отсутствует. При депрессивно-деперсонализационном синдроме в нозологических рамках депрессивного расстройства возможны следующие ответы на ДТ: после редукции деперсонализации выявляется отчетливая депрессивная симптоматика или субдепрессия, иногда наступает эйфория или гипомания.
Ю.Л.Нуллер - Диагностика и терапия деперсонализационного расстройства.
Ю.Л.Нуллер - Диагностика и терапия деперсонализационного расстройства.
вторник, 14 июля 2009 г.
Антипсихотические свойства пропранолола
Propranolol in psychiatric illness.
Propranolol in chronic schizophrenia: a controlled study in neuroleptic-treated patients.
Propranolol in schizophrenia: a double blind, placebo controlled trial of propranolol as an adjunct to neuroleptic medication.
Does propranolol have an antipsychotic effect? A placebo-controlled study in acute schizophrenia.
Propranolol in chronic schizophrenia: a controlled study in neuroleptic-treated patients.
Propranolol in schizophrenia: a double blind, placebo controlled trial of propranolol as an adjunct to neuroleptic medication.
Does propranolol have an antipsychotic effect? A placebo-controlled study in acute schizophrenia.
понедельник, 13 июля 2009 г.
четверг, 9 июля 2009 г.
Treatment of Sexual Side Effects: Antidotes
Treatment of Sexual Side Effects: Antidotes
A variety of antidotes have been reported to treat SSRI-induced sexual dysfunction effectively; however, virtually all the data on these agents are derived from open case reports and case series. Insofar as sexual function improvement may be responsive to placebo effects, it is impossible to estimate the true efficacy of these antidotes.[27]
Most of these antidotes either have serotonin-blocking properties (especially 5HT-2 antagonistic effects) or augment catecholamine activity, especially that of dopamine. The antiserotonergic antidotes are cyproheptadine, buspirone, nefazodone, and mianserin. Medications enhancing dopaminergic tone include amantadine, bupropion, and stimulants, with yohimbine showing noradrenergic effects. Among the reported antidotes, the only 2 without antiserotonergic effects or catecholaminergic activity are gingko biloba and urecholine.
Cyproheptadine is an antihistamine with antiserotonergic properties that has been reported for over a decade to reverse antidepressant-induced sexual dysfunction. Only case reports and case series attest to its efficacy.[13,42-44] Effective doses range from 2mg to 16mg. In the most recent and largest case series, 12 of 25 patients described improvement in sexual function when treated with cyproheptadine (mean dose, 8.6mg).[13] Anorgasmia is the sexual side effect most often reported to be alleviated by cyproheptadine. Cyproheptadine is effective when taken either on an as-needed basis (typically, 1 to 2 hours before intercourse) or on a regular basis.
However, cyproheptadine's utility is often limited by its potential side effects. Excessive sedation and the reversal of the therapeutic effect of the antidepressant are major problems that limit its usefulness. Effectively treated depression and bulimic symptoms have been reported to reemerge soon after cyproheptadine was started.[42,45-48] This reversal of therapeutic effects is itself reversible upon discontinuation.
Buspirone is a serotonin-IA partial agonist typically prescribed to treat persistent anxiety. One case series reported that buspirone reversed both decreased sexual interest and orgasmic dysfunction caused by SSRIs.[49] Most patients using buspirone to treat sexual dysfunction take it daily. The dosage is the same as that used for anxiety (15mg to 60mg daily). The mechanism of action of buspirone in treating sexual dysfunction may be reduction of serotonergic tone via stimulation of presynaptic autoreceptors or the alpha-2 antagonist effects of one of buspirone's major metabolites, 1-pyrimidinylpiperazine.
Nefazodone and mianserin are antidepressants with strong postsynaptic blocking properties. In one case report, nefazodone 150mg taken 1 hour prior to sexual activity completely reversed sertraline-induced anorgasmia.[50] Mianserin, an antidepressant with 5HT-2 and alpha-2 adrenergic antagonist properties, is available in many countries but not in the US. It has been reported to reverse serotonin reuptake inhibitor-induced sexual dysfunction in 9 of 15 patients.[51] Mirtazapine is similar in its biological activity to mianserin and might also be effective in reversing sexual side effects. No case reports or case series have yet been published attesting to this, although clinicians have described such an effect. The putative capacity of mianserin and mirtazapine to reverse sexual side effects can be attributed either to their serotonergic activity or presynaptic alpha-2 activity.
Amantadine, a dopamine agonist, is used both as an antiviral agent and as a treatment for Parkinson's disease. It has been shown in a number of small case series to reverse anorgasmia.[13,52-54] Reported effective doses have ranged between 100mg to 400mg taken either on a daily or as-needed basis. In the most recent case series, 8 (42%) out of 19 patients with SSRI-induced sexual dysfunction improved with amantadine 200mg daily.[13] Given dopamine's consistent effect as a neurotransmitter involved in sexual arousal, a number of other dopamine agonists have been explored as treatments for sexual side effects.[2,55,56]
Bupropion is another commonly touted antidote for SSRI-induced sexual dysfunction.[57,58] It is assumed that the mechanism of action by which bupropion reverses sexual side effects is its weak dopamine agonism. The evidence for bupropion's efficacy is scant, except for unpublished, anecdotal reports, one case report,[57] and a case series[58] in which 31 (66%) of 47 patients showed improvement when bupropion was added to the regimen along with the serotonergic antidepressant. Most patients (18/31) with a successful outcome responded to as-needed use of bupropion 75mg to 150mg. Libido, arousal, and orgasmic difficulties were all effectively reversed. Fifteen percent of treated patients stopped taking bupropion because of its stimulation side effects. It is unclear whether bupropion doses need to be somewhat lower than usual when added to fluoxetine or paroxetine, to compensate for pharmacokinetic interactions resulting in increased bupropion levels.[59]
Stimulants, such as methylphenidate, D-amphetamine, and pemoline, are reported to reverse a variety of sexual side effects caused by SSRIs or MAOIs.[60-62] Low doses of 10mg-25mg of methylphenidate or D-amphetamine have been effective. One should add stimulants to an MAOI with extreme caution because of the risk of a hypertensive episode. However, use of an MAOI/stimulant combination has been shown to be safe in a case series.[63] SSRI/stimulant combinations show no similar risks.
Yohimbine is available with or without a prescription (and with unclear purity) in health food stores. It is an alkaloid from the bark of Corynanthe yohimbi (family, Rubiaceae) and has been used for decades to reverse erectile dysfunction.[64-66] Its efficacy in treating sexual dysfunction may be associated with its ability to block presynaptic alpha-2 adrenergic sites, leading to enhanced adrenergic tone.[65] A variety of sexual side effects have been reported to be alleviated by yohimbine in doses ranging from 2.7mg to 16.2mg daily, prescribed either on a regular 5.4mg 3 times daily basis or on an as-needed basis with single doses up to 16.2mg.[13,67-69] In the largest case series, 17 (81%) of 21 patients showed improvement of sexual side effects when treated with yohimbine (mean dose, 16.2mg).[12]
Typical side effects associated with yohimbine include anxiety, nausea, flushing, urinary urgency, and sweating. Yohimbine has been the subject of the only double-blind, placebo-controlled study to evaluate treatment of sexual dysfunction occurring as a drug side effect.[27] Unfortunately, the placebo effect was marked, showing a minimal drug-placebo difference with yohimbine given at a dose of 5.4mg 3 times daily. Yohimbine is also available in lower potency without a prescription. The purity, potency, and safety of these preparations, however, are unknown.
Bethanechol is a cholinergic agonist that has occasionally been useful in reversing sexual dysfunction associated with TCAs and MAOIs.[70-73] Typical doses are 10mg to 20mg as needed or 30mg to 100mg daily in a divided dose. Potential side effects with bethanechol include diarrhea, cramps, and diaphoresis. No reports have evaluated or suggested the efficacy of bethanechol for treating SSRI-induced sexual side effects.
Gingko biloba is an herbal extract reported to reverse a variety of sexual dysfunctions associated with antidepressants. Information about gingko's ability in this regard is derived from the experience of 1 clinician presenting a large case series.[74] The response rate was greater than 80%, with doses ranging from 60mg twice daily to 120mg twice daily (mean daily dose, 207mg). Reported side effects include gastrointestinal upset, lightheadedness, and stimulation effects. Because gingko may inhibit platelet-activating factor, caution should be used in considering its use by any patient with a bleeding diathesis. The mechanism by which gingko might alleviate sexual dysfunction is unknown.
http://www.medscape.com/viewarticle/430614_5
A variety of antidotes have been reported to treat SSRI-induced sexual dysfunction effectively; however, virtually all the data on these agents are derived from open case reports and case series. Insofar as sexual function improvement may be responsive to placebo effects, it is impossible to estimate the true efficacy of these antidotes.[27]
Most of these antidotes either have serotonin-blocking properties (especially 5HT-2 antagonistic effects) or augment catecholamine activity, especially that of dopamine. The antiserotonergic antidotes are cyproheptadine, buspirone, nefazodone, and mianserin. Medications enhancing dopaminergic tone include amantadine, bupropion, and stimulants, with yohimbine showing noradrenergic effects. Among the reported antidotes, the only 2 without antiserotonergic effects or catecholaminergic activity are gingko biloba and urecholine.
Cyproheptadine is an antihistamine with antiserotonergic properties that has been reported for over a decade to reverse antidepressant-induced sexual dysfunction. Only case reports and case series attest to its efficacy.[13,42-44] Effective doses range from 2mg to 16mg. In the most recent and largest case series, 12 of 25 patients described improvement in sexual function when treated with cyproheptadine (mean dose, 8.6mg).[13] Anorgasmia is the sexual side effect most often reported to be alleviated by cyproheptadine. Cyproheptadine is effective when taken either on an as-needed basis (typically, 1 to 2 hours before intercourse) or on a regular basis.
However, cyproheptadine's utility is often limited by its potential side effects. Excessive sedation and the reversal of the therapeutic effect of the antidepressant are major problems that limit its usefulness. Effectively treated depression and bulimic symptoms have been reported to reemerge soon after cyproheptadine was started.[42,45-48] This reversal of therapeutic effects is itself reversible upon discontinuation.
Buspirone is a serotonin-IA partial agonist typically prescribed to treat persistent anxiety. One case series reported that buspirone reversed both decreased sexual interest and orgasmic dysfunction caused by SSRIs.[49] Most patients using buspirone to treat sexual dysfunction take it daily. The dosage is the same as that used for anxiety (15mg to 60mg daily). The mechanism of action of buspirone in treating sexual dysfunction may be reduction of serotonergic tone via stimulation of presynaptic autoreceptors or the alpha-2 antagonist effects of one of buspirone's major metabolites, 1-pyrimidinylpiperazine.
Nefazodone and mianserin are antidepressants with strong postsynaptic blocking properties. In one case report, nefazodone 150mg taken 1 hour prior to sexual activity completely reversed sertraline-induced anorgasmia.[50] Mianserin, an antidepressant with 5HT-2 and alpha-2 adrenergic antagonist properties, is available in many countries but not in the US. It has been reported to reverse serotonin reuptake inhibitor-induced sexual dysfunction in 9 of 15 patients.[51] Mirtazapine is similar in its biological activity to mianserin and might also be effective in reversing sexual side effects. No case reports or case series have yet been published attesting to this, although clinicians have described such an effect. The putative capacity of mianserin and mirtazapine to reverse sexual side effects can be attributed either to their serotonergic activity or presynaptic alpha-2 activity.
Amantadine, a dopamine agonist, is used both as an antiviral agent and as a treatment for Parkinson's disease. It has been shown in a number of small case series to reverse anorgasmia.[13,52-54] Reported effective doses have ranged between 100mg to 400mg taken either on a daily or as-needed basis. In the most recent case series, 8 (42%) out of 19 patients with SSRI-induced sexual dysfunction improved with amantadine 200mg daily.[13] Given dopamine's consistent effect as a neurotransmitter involved in sexual arousal, a number of other dopamine agonists have been explored as treatments for sexual side effects.[2,55,56]
Bupropion is another commonly touted antidote for SSRI-induced sexual dysfunction.[57,58] It is assumed that the mechanism of action by which bupropion reverses sexual side effects is its weak dopamine agonism. The evidence for bupropion's efficacy is scant, except for unpublished, anecdotal reports, one case report,[57] and a case series[58] in which 31 (66%) of 47 patients showed improvement when bupropion was added to the regimen along with the serotonergic antidepressant. Most patients (18/31) with a successful outcome responded to as-needed use of bupropion 75mg to 150mg. Libido, arousal, and orgasmic difficulties were all effectively reversed. Fifteen percent of treated patients stopped taking bupropion because of its stimulation side effects. It is unclear whether bupropion doses need to be somewhat lower than usual when added to fluoxetine or paroxetine, to compensate for pharmacokinetic interactions resulting in increased bupropion levels.[59]
Stimulants, such as methylphenidate, D-amphetamine, and pemoline, are reported to reverse a variety of sexual side effects caused by SSRIs or MAOIs.[60-62] Low doses of 10mg-25mg of methylphenidate or D-amphetamine have been effective. One should add stimulants to an MAOI with extreme caution because of the risk of a hypertensive episode. However, use of an MAOI/stimulant combination has been shown to be safe in a case series.[63] SSRI/stimulant combinations show no similar risks.
Yohimbine is available with or without a prescription (and with unclear purity) in health food stores. It is an alkaloid from the bark of Corynanthe yohimbi (family, Rubiaceae) and has been used for decades to reverse erectile dysfunction.[64-66] Its efficacy in treating sexual dysfunction may be associated with its ability to block presynaptic alpha-2 adrenergic sites, leading to enhanced adrenergic tone.[65] A variety of sexual side effects have been reported to be alleviated by yohimbine in doses ranging from 2.7mg to 16.2mg daily, prescribed either on a regular 5.4mg 3 times daily basis or on an as-needed basis with single doses up to 16.2mg.[13,67-69] In the largest case series, 17 (81%) of 21 patients showed improvement of sexual side effects when treated with yohimbine (mean dose, 16.2mg).[12]
Typical side effects associated with yohimbine include anxiety, nausea, flushing, urinary urgency, and sweating. Yohimbine has been the subject of the only double-blind, placebo-controlled study to evaluate treatment of sexual dysfunction occurring as a drug side effect.[27] Unfortunately, the placebo effect was marked, showing a minimal drug-placebo difference with yohimbine given at a dose of 5.4mg 3 times daily. Yohimbine is also available in lower potency without a prescription. The purity, potency, and safety of these preparations, however, are unknown.
Bethanechol is a cholinergic agonist that has occasionally been useful in reversing sexual dysfunction associated with TCAs and MAOIs.[70-73] Typical doses are 10mg to 20mg as needed or 30mg to 100mg daily in a divided dose. Potential side effects with bethanechol include diarrhea, cramps, and diaphoresis. No reports have evaluated or suggested the efficacy of bethanechol for treating SSRI-induced sexual side effects.
Gingko biloba is an herbal extract reported to reverse a variety of sexual dysfunctions associated with antidepressants. Information about gingko's ability in this regard is derived from the experience of 1 clinician presenting a large case series.[74] The response rate was greater than 80%, with doses ranging from 60mg twice daily to 120mg twice daily (mean daily dose, 207mg). Reported side effects include gastrointestinal upset, lightheadedness, and stimulation effects. Because gingko may inhibit platelet-activating factor, caution should be used in considering its use by any patient with a bleeding diathesis. The mechanism by which gingko might alleviate sexual dysfunction is unknown.
http://www.medscape.com/viewarticle/430614_5
среда, 8 июля 2009 г.
ацетилцистеин и трихотилломания
Группе из 50 человек, страдающих трихотилломанией, предложили принять участие в 12-недельном исследовании, в котором половине из них давали таблетки, содержащие аминокислоту N-ацетилцистеин, а остальным — плацебо. Оказалось, спустя 12 недель, что среди людей, принимавших аминокислоты, значительно ослабла мания выдергивать у себя волосы, по сравнению с контрольной группой, сообщили специалисты.
Прием ацетилцистеина может уменьшать симптомы трихотилломании
Прием ацетилцистеина может уменьшать симптомы трихотилломании
вторник, 7 июля 2009 г.
четверг, 2 июля 2009 г.
Сравнение окскарбазепина и карбамазепина в терапии аффективных расстройств
In summary, the patient charts reviewed demonstrated that carbamazepine, as well as, oxcarbazepine are equally effective and tolerable as mood stabilizers.
Effectiveness and Tolerability of Carbamazepine vs. Oxcarbazepine as Mood Stabilizers
Effectiveness and Tolerability of Carbamazepine vs. Oxcarbazepine as Mood Stabilizers
Психоз после приёма валацикловира
METHOD: The patient presented with irritable mood and grandiose delusions 72 hours after starting valacyclovir for genital herpes. Valacyclovir treatment was stopped, and risperidone was initiated. RESULTS: The symptoms continued after stopping the valacyclovir, but improved with risperidone. DISCUSSION:There are reports of neuropsychiatric side effects with valacyclovir’s structural analogs in elderly patients with renal dysfunction. Clinicians should be aware that valacyclovir may induce psychosis with manic presentation in young, healthy patients without a psychiatric history.
Case Report
Case Report
Кататония при отмене клоназепама
BACKGROUND: Catatonia is a often a complex syndrome. It has been divided into categories of simple and malignant, with the latter being a more severe form involving autonomic instability and/or fever and having a higher mortality rate. OBJECTIVE: There have been only two cases presented in the literature postulating benzodiazepine-withdrawal as a possible trigger for malignant catatonia. Here, the authors present a case of catatonia likely caused by abrupt benzodiazepine discontinuation; they also discuss neurobiological mechanisms relating to catatonia. METHOD: The authors report on a 60-year-old man with a history of depression and posttraumatic stress disorder who was brought to the emergency department with acute confusion, grimacing, stereotypy, refusal of food and water, muscle rigidity, mutism, and extreme negativism. He had recently and abruptly discontinued all psychotropic medication. RESULTS: After administration of lorazapam, the patient was re-started on clonazepam, after which there was a complete and sustained resolution of catatonic symptoms and autonomic instability. CONCLUSION: Catatonia may result from a wide variety of etiologies. Catatonia due to benzodiazepine-withdrawal is a rare but serious condition that may be difficult to distinguish from other causes of catatonia. The mechanism by which catatonia may be precipitated by benzodiazepine-withdrawal is unknown, but likely involves a rapid decrease in GABA transmission in the central nervous system.
Case Report
Case Report
Антидепрессанты короткого действия в терапии БАР с быстрой сменой фаз
"I have found that in bipolar patients with extreme diurnal variation of mood (characterized by severe a.m.-hour depression followed by significant brightening in the evening), the non-time-release preparations of medications, such as bupropion and venlafaxine, given in low doses in the a.m. hours only can be very helpful and less likely to cause manic switching. Conversely, the long-acting preparations of the same medications tend to cause a reversal of diurnal variation, with improvement in the a.m. hours and agitation in the p.m. hours. It might turn out that short half-life reuptake inhibitors have a place in treating bipolar depression. Other relatively short-acting agents, such as atomoxetine, may also fall into this category."
The Use of Short Half-Life Antidepressants in the Treatment of Bipolar Depression
The Use of Short Half-Life Antidepressants in the Treatment of Bipolar Depression
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