среда, 27 мая 2009 г.

Long-term findings for the novel antipsychotic agent asenapine did not confirm any advantage over second-generation antipsychotics for negative symptoms of schizophrenia...Extrapyramidal symptoms were "slightly" higher at 10.4% with asenapine compared with 4.1% with olanzapine. Prolactin, hepatic enzymes, lipids, glucose, and the QTC interval were similar or better with asenapine.
New Drug No Better for Negative Schizophrenia Symptoms

Конфабуляторная гипермнезия

Confabulatory hypermnesia, or severe false memory syndrome

рисперидон и паксил в терапии тревожных расстройств с паническими атаками

We can identify no difference in the efficacy of paroxetine and low-dose risperidone in the treatment of panic attacks. Low-dose risperidone appears to be tolerated equally well as paroxetine. Low-dose risperidone may be an effective treatment for anxiety disorders in which panic attacks are a significant component.
A comparison of low-dose risperidone to paroxetine in the treatment of panic attacks: a randomized single-blind study.

пятница, 22 мая 2009 г.

взаимодействие психотропных лекарственных средств

An Overview of Psychotropic Drug-Drug Interactions

+Clinically relevant drug interactions with antiepileptic drugs

Cytochrome P450 Enzymes and Psychopharmacology

Cytochrome P450 Enzymes and Psychopharmacology

эндокринные эффекты нормотимиков

Both seizures and antiepileptic drugs may induce disturbances in hormonal system. Regarding endocrine effects of anticonvulsants, an interaction of these drugs with gonadal, thyroid, and adrenal axis deserves attention. Since majority of antiepileptic drugs block voltage dependent sodium and calcium channels, enhance GABAergic transmission and/or antagonize glutamate receptors, one may expect that similar neurochemical mechanisms are engaged in the interaction of these drugs with synthesis of hypothalamic neurohormones such as gonadotropin-releasing hormone (GnRH), thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone (CRH) and growth hormone releasing hormone (GHRH). Moreover some antiepileptic drugs may affect hormone metabolism via inhibiting or stimulating cytochrome P-450 iso-enzymes. An influence of antiepileptic drugs on hypothalamic-pituitary-gonadal axis appears to be sex-dependent. In males, valproate decreased follicle-stimulating hormone (FSH) and luteinizing hormone (LH) but elevated dehydroepiandrosterone sulfate (DHEAS) concentrations. Carbamazepine decreased testosterone/sex-hormone binding globulin (SHBG) ratio, whereas its active metabolite--oxcarbazepine--had no effect on androgens. In females, valproate decreased FSH-stimulated estradiol release and enhanced testosterone level. On the other hand, carbamazepine decreased testosterone level but enhanced SHBG concentration. It has been reported that carbamazepine, oxcarbazepine or joined administration of carbamazepine and valproate decrease thyroxine (T4) level in patients with no effect on thyrotropin (TSH). While valproate itself has no effect on T4, phenytoin, phenobarbital and primidone, as metabolic enzyme inducers, can decrease the level of free and bound thyroxine. On the other hand, new antiepileptics such as levetiracetam, tiagabine, vigabatrine or lamotrigine had no effect on thyroid hormones. With respect to hormonal regulation of metabolic processes, valproate was reported to enhance leptin and insulin blood level and increased body weight, whereas topiramate showed an opposite effect. In contrast to thyroid and gonadal hormones, only a few data concern antiepileptic drug action in HPA axis. To this end, no effect of antiepileptic drugs on adrenocorticotropic hormone (ACTH)/cortisol circadian rhytmicity was found. Valproate decreased CRH release in rats, whereas lamotrigine stabilized ACTH/cortisol secretion. Moreover, felbamate was found to inhibit stress-induced corticosterone release in mice. Interestingly, recent data suggest that felbamat and some other new antiepileptic drugs may inhibit transcriptional activity of glucocorticoid receptors. Summing up, the above data suggest that traditional antiepileptic drugs may cause endocrine disturbances, especially in gonadal hormones.
Endocrine effects of antiepileptic drugs

+ Effects of antiepileptic drugs on immune system

среда, 20 мая 2009 г.

коррекция побочных эффектов психотропных средств

...And then one interesting approach, which may be a little counterintuitive, is to add a small amount of mirtazapine (Remeron). The reason for this is that mirtazapine, which works by stimulating the 5-HT1 receptor and blocking presynaptic autoreceptors, actually blocks two of the serotonin receptors that we think are involved in a lot of serotonergic side effects: 5-HT2 and 5-HT3.
Managing Side Effects of Psychotropics

вторник, 19 мая 2009 г.

Кортиколиберин-дексаметазоновый тест

Кортиколиберин-дексаметазоновый тест имеет большую специфичность в отношении депрессивных больных по сравнению с дексаметазоновым тестом. Если специфичность дексаметазонового теста не превышала 50%, то, по данным зарубежных авторов, специфичность кортиколиберин-дексаметазонового теста составляет 80-90% (11).

Тест состоит в том, что вечером больной получает дексаметазон - синтетический глюкокортикоид, по принципу обратной связи тормозящий активность гипоталамо-гипофизарно-надпочечниковой оси. На следующий день в 15.00 больному внутривенно вводят кортиколиберин, стимулирующий выброс АКТГ. В норме уровень кортизола и АКТГ остаётся очень низким, т.к. после подавления дексаметазоном ГГН-ось какое-то время не реагирует на стимуляцию. У пациентов с депрессией уровень кортизола и АКТГ резко возрастает через час после введения кортиколиберина, то есть подавление дексаметазоном оказывается недостаточным. Это отмечается в 90% случаев, что делает этот тест достаточно убедительным.
Я.А.Кочетков. - Депрессия и гипоталамо-гипофизарно-надпочечниковая система: новые стратегии изучения

понедельник, 18 мая 2009 г.

Cognitive Symptoms in Schizophrenia Recognizing and Treating Cognitive Deficits in Schizophrenia

Cognitive Symptoms in Schizophrenia Recognizing and Treating Cognitive Deficits in Schizophrenia

Cause of schizophrenia identified

we have shown that 25 per cent of people who have schizophrenia have lost 80 per cent of a protein in their brain known as muscarinic M1 receptor.
Cause of schizophrenia identified

''Виагра'' помогла принимающим антидепрессанты женщинам

Известное средство для лечения эректильной дисфункции силденафил (“Виагра”) может помочь и некоторым женщинам. По данным американских исследователей, регулярный прием препарата способствует нормализации сексуальной функции у пациенток, принимающих антидепрессанты.
''Виагра'' помогла принимающим антидепрессанты женщинам

воскресенье, 17 мая 2009 г.

A randomized, crossover comparison of herbal medicine and bromocriptine against risperidone-induced hyperprolactinemia in patients with schizophrenia.

Hyperprolactinemia is a common adverse effect that occurs as a result of antipsychotic therapies, which often results in discontinuation. Empirical evidence has shown that some herbal medicines have suppressive effects on prolactin (PRL) hyperactivities. This study was designed to compare the herbal preparation called Peony-Glycyrrhiza Decoction (PGD) with bromocriptine (BMT), a dopamine agonist widely used for PRL-secreting disorders, in the treatment of risperidone-induced hyperprolactinemia. Twenty schizophrenic women who were under risperidone maintenance treatment, diagnosed with hyperprolactinemia (serum PRL levels >50 mug/L), and currently experiencing oligomenorrhea or amenorrhea were selected for the study. Subjects were randomized to additional treatment with PGD (45 g/d) followed by BMT (5 mg/d) or BMT followed by PGD at the same doses for 4 weeks each, with an interval of 4-week washout period between 2 treatment sessions. The severity of psychotic symptoms, adverse events, serum PRL, estradiol, testosterone, and progesterone levels were examined at baseline and end point. Peony-Glycyrrhiza Decoction treatment produced a significant baseline-end point decrease in serum PRL levels, without exacerbating psychosis and changing other hormones, and the decreased amplitudes were similar to those of BMT (24% vs 21%-38%). Moreover, there was a significantly greater proportion of patients during PGD treatment than BMT treatment showing improvements on adverse effects associated with hyperprolactinemia (56% vs 17%, P = 0.037). These results suggest that the herbal therapy can yield additional benefits while having comparable efficacy in treating antipsychotic-induced hyperprolactinemia in individuals with schizophrenia.
http://www.ncbi.nlm.nih.gov/pubmed/18480682

Шизофрения и эстрогены

The oestrogen protection hypothesis proposes that oestrogen has a protective effect against onset of schizophrenia. In support of this: Epidemiological studies have shown that young women are less likely to develop schizophrenia than men of the same age, and women are more likely to develop late-onset schizophrenia after menopause. Clinical studies have shown higher psychotic symptoms in perimenopausal women, and women at the low oestrogen phase of the menstrual cycle. Animal studies provide further evidence in support of the oestrogen protection hypothesis. Three randomised double-blind placebo-controlled trials and an open-label study showed that adding oestradiol to women's usual antipsychotic medications was associated with significant abatement of schizophrenia symptoms. A small study of men with schizophrenia who received oral oestradiol valerate also showed a significant abatement in psychotic symptoms. Although oestrogen appears to be a useful treatment for schizophrenia, further research is required to determine the correct dose and duration of use of oestradiol. New types of oestrogen compounds may provide a safer, non-feminising approach for the treatment of schizophrenia.
Oestrogen--a new treatment approach for schizophrenia?

пятница, 15 мая 2009 г.

омега-3 эйкозапентаеновая кислота

Sixty outpatients with a diagnosis of major depressive disorder based on DSM-IV criteria and a score >or=15 in the 17-item Hamilton Depression Rating Scale (HDRS) were randomly allocated to receive daily either 1000 mg EPA or 20 mg fluoxetine, or their combination for 8 weeks...
In the present 8 week trial EPA and fluoxetine had equal therapeutic effects in major depressive disorder. EPA + fluoxetine combination was superior to either of them alone.
Comparison of therapeutic effects of omega-3 fatty acid eicosapentaenoic acid and fluoxetine, separately and in combination, in major depressive disorder

эффективность ДПДГ-психотерапии

Shifting eye therapy successfully treats trauma

прозак и рыбы

Fish caught near wastewater treatment plants serving five major U.S. cities had residues of pharmaceuticals in them, including medicines used to treat high cholesterol, allergies, high blood pressure, bipolar disorder and depression
Study: Range of Pharmaceuticals in Fish Across US

One of Klaine's graduate students, Kristen Gaworecki, is looking at Prozac. She exposed bass to the drug, though at higher levels than those found in surface water, and found the fish had no desire to eat. They also behaved abnormally--swimming vertically as opposed to horizontally or with their backs out of the water
Prozac In Water Makes Fish Swim Weirdly And Not Eat

The purpose of this study was to determine if realistic environmental concentrations of fluoxetine can alter the behavior of Betta splendens. Five fish were given 0.54µg of fluoxetine and four fish were used as controls. After the study concluded, the experimental fish did reduce their aggressiveness significantly (p-value = .002). This reduced aggression could be
reducing the reproductive output of male Betta splendens.
THE EFFECTS OF FLUOXETINE ON AGGRESSIVE BEHAVIORS IN SIAMESE FIGHTING FISH

Клептомания

Additionally, there is some suggestion that selective serotonin reuptake inhibitors, the treatment of choice for obsessive compulsive disorder,may lack efficacy for kleptomania. Instead, other medications (lithium, anti-epileptics, and opioid antagonists) have shown early promise
in treating kleptomania. Evidence suggests that theremay be subtypes of kleptomania that aremore likeOCD, whereas others have more similarities to addictive and mood disorders.
Understanding and Treating Kleptomania:NewModels and New Treatments

терапия деперсонализации

For example, a number of studies suggest that opioid receptor antagonists such as naltrexone and naloxone are useful in at least a subgroup of patients. In spite of initial expectations, the use of lamotrigine as a sole medication has not been found useful. However, open-label trials suggest that its use as an add-on treatment with selective serotonin reuptake inhibitors (SSRIs) is beneficial in a substantial number of patients. Similarly, the use of clonazepam, particularly in conjunction with SSRI antidepressants, appears to be beneficial in patients with high levels of background anxiety.
Depersonalization disorder: pharmacological approaches

Two recent controlled medication trials, one with lamotrigine and one with fluoxetine, failed to show efficacy. There is some evidence for dysregulation of endogenous opioid systems in depersonalization, and a few studies have suggested that opioid antagonists may have efficacy in the treatment of dissociation and depersonalization symptoms. In this prospective open treatment trial, 14 subjects were recruited and treated with naltrexone for 6 weeks to a maximum dose of 100 mg/d (first 7 subjects) or 10 weeks to a maximum dose of 250 mg/d (next 7 subjects). Mean naltrexone dose was 120 mg/d. There was an average 30% reduction of symptoms with treatment, as measured by 3 validated dissociation scales. Three patients were very much improved, and 1 patient was much improved with naltrexone treatment.
An open trial of naltrexone in the treatment of depersonalization disorder


среда, 13 мая 2009 г.

Future Treatments for Depression, Anxiety, Sleep Disorders, Psychosis, and ADHD

Список разрабатываемых ЛС.
Future Treatments for Depression, Anxiety, Sleep Disorders, Psychosis, and ADHD

Абилифай и акатизия

Remission rates were significantly greater with adjunctive aripiprazole than placebo (25.4% vs 15.2%; P = 0.016) as were response rates (32.4% vs 17.4%; P The Efficacy and Safety of Aripiprazole as Adjunctive Therapy in Major Depressive Disorder: A Second Multicenter, Randomized, Double-Blind, Placebo-Controlled Study



Adverse events (AEs) that occurred in >= 10% of patients with adjunctive placebo or adjunctive aripiprazole were akathisia (4.5% vs. 23.1%), headache (10.8% vs. 6.0%), and restlessness (3.4% vs. 14.3%).

The Efficacy and Safety of Aripiprazole as Adjunctive Therapy in Major Depressive Disorder: A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study

вторник, 12 мая 2009 г.

Genetic and Clinical Predictors of Sexual Dysfunction in Citalopram-Treated Depressed Patients

These hypothesis-generating analyses suggest the potential for glutamatergic treatment targets for sexual dysfunction during major depressive episodes.

http://www.nature.com/npp/journal/v34/n7/abs/npp20094a.html

Narcolepsy linked to immune system

But the association is not the final piece of the puzzle, Mignot says. Even with all of the known genetic risk factors, including the newly discovered version of the T cell receptor gene, a person has only a 1.5 percent chance of developing narcolepsy, he says. That suggests that, while narcolepsy is probably an autoimmune disorder, further genetic and environmental triggers and risk factors remain to be found.

http://sciencenews.org/view/generic/id/43455/title/Narcolepsy_linked_to_immune_system

пятница, 8 мая 2009 г.

галлюцинаторный "взрыв в голове"

Case 1
A 48-year-old man was seen in December 2006. For the past several months about three to four times a month, he had been having attacks of a peculiar sensation in the head likened to the noise of an exploding bomb only at night while going off to sleep. The 'explosion' would wake him up and disappear completely the moment he woke up.

There was no headache and no associated symptoms such as nausea, vomiting or any visual sensation. For the past 3 months, the frequency of these sensations had increased and had been occurring nearly daily at the time of consultation. The noise occurred only once during every night, after which he could go off to sleep. His past medical history had been unremarkable and he had never suffered from any significant headache problem. General physical and neurological examination had been unremarkable. Magnetic resonance imaging (MRI) of brain with contrast had been normal. He was prescribed Flunarazine 10 mg daily. At 6 months' follow-up he had much improved and noticed the exploding head symptom only on two occasions.

Case 2
A 65-year-old man was seen in February 2007. He was hypertensive and diabetic (both well controlled on oral medication) and had been having infrequent attacks of International Headache Society migraine headache (every 2–4 months) without aura since the age of 15 years. For the past 4 months prior to consultation, every 2–3 weeks, he had been awakened while going off to sleep only during taking a daytime nap by a sudden exploding (like a bomb bursting) noise in his head lasting for only few moments.

This noise was always accompanied with jerky elevation of his right arm and a queer sensation in the right side of his chest (not arm) and again lasting only momentarily. He felt quite well on waking up and could go off to sleep again. These were never accompanied by any visual flashes and never occurred during sleep at night. These sensations were very different from his migraine headaches, which lasted for several hours and the noises were not accompanied by any nausea or vomiting.

Physical examination was normal and his blood presswure in the clinic was 136/80 mmHg. He had already had a MRI of brain with contrast, MR angiography of brain and two interictal sleep EEG recordings performed before consultation with the author, all of which were normal. A video EEG with daytime sleep recording was performed, but no event could be captured.

Кофеиновый психоз

[The patient reported drinking less than one case of beer annually. However, ~7 years before presentation, he had sharply increased his consumption of coffee from 10–12 cups/day to ~36 cups/day, a change in coffee consumption corroborated by his wife who made much of the coffee for him at home]

http://mbldownloads.com/0309CNS_Hedges.pdf

понедельник, 4 мая 2009 г.

Relationships between thyroid hormone and antidepressant responses to total sleep deprivation in mood disorder patients.

Acute removal of the sleep-related break on the hypothalamic-pituitary-thyroid axis remains a promising candidate for the mechanism of sleep deprivation-induced improvement in mood in depressed patients.

Фантомный синдром беспокойных ног

Bilateral restless legs affecting a phantom limb, treated with dopamine agonists

Lithium levels in drinking water and risk of suicide

Lithium levels in drinking water and risk of suicide

Hallucinations in the Context of Varenicline Withdrawal

"Mr. A" was a 43-year-old, well-educated, healthy man with no current or previous medical or psychiatric history, including no past alcohol dependence or drug abuse. Notably, his family history was positive for schizophrenia, with one brother suffering from the illness. The patient reported smoking 10 cigarettes daily for more than 20 years. Varenicline was administered at a dose of 0.5 mg once daily for an initial period of 3 days, followed by 0.5 mg twice daily for the next 4 days. The drug was then administered at a dose of 1.0 mg twice daily.

The patient reported headaches shortly after starting varenicline. However, he was able to stop smoking after 2 weeks of treatment and therefore reduced the dose of the drug during the third week of treatment, taking only 0.5 mg once daily for 4 days. He then discontinued treatment. After taking the last tablet of varenicline on the following day, the patient began experiencing symptoms of derealization. His symptoms then progressed to visual hallucinations of unknown, distressing people who he "shooed" away. At that point, Mr. A suspected that he was having a "realistic dream." He also perceived that he had a conversation with a deceased rock star while being conscious that the person in question was actually dead. He became distressed and presented to his general practitioner, and he was started on quetiapine (50 mg at bedtime) for 10 days. The symptoms of hallucinosis rapidly disappeared. When interviewed by a psychiatrist 1 month later, the patient showed no symptoms of any psychiatric disorder, and he was not taking any medication. He had also managed to remain smoke-free.

http://ajp.psychiatryonline.org/cgi/content/short/166/5/619-a?rss=1