Новые стратегии лечения депрессий у пациентов с гепатитом C

Novel Treatment Strategies for Depression in Patients With Hepatitis C

Ларазидон: сравнение эффективности доз

Table 1. Comparison of Symptom Reduction

Intervention	PANSS Positive Score Change	PANSS Negative Score Change
Placebo	-5.4	-3.6
Lurasidone 40 mg	-7.7	-6.0
Lurasidone 120 mg	-7.7	-5.2
Olanzapine	-9.3	-6.2

Lurasidone, a novel antipsychotic agent submitted for review to the Food and Drug Administration, with high binding affinities for D2, 5-HT-7, 5-HT-2A, and 5-HT-1A receptors, and is being studied as an antipsychotic with reduced likelihood of causing weight gain, central nervous system depression, and orthostatic hypotension. The multi-center, phase 3 Program to Evaluate Antipsychotic Response to Lurasidone (PEARL 2) trial was conducted to evaluate the efficacy of 2 doses of lurasidone in the treatment of individuals experiencing an acute exacerbation of schizophrenia.

Lurasidone: A Novel, Weight-Neutral Antipsychotic Agent

Антипсихотики: галоперидол - оланзапин

Antipsychotics A-Z: Haloperidol - Olanzapine

Оланзапина памоат

In this well-designed study, depot olanzapine provided clinically significant prevention of psychotic relapse in outpatients treated with 3 dosing regimes. The highest dose was slightly more effective than the lowest dose but had a greater side effect burden. Injections of 405 mg every 4 weeks, more convenient and possibly safer than injections every 2 weeks, were effective and well tolerated. Because of the risk for postinjection sedation and delirium in approximately 7 injections in 10,000, a 3-hour postinjection observation period is required on the warning label approved by the FDA in December 2009. Given this and the risk for metabolic adverse effects, use of long-acting OP requires careful patient selection.

Recent Research in Antipsychotic Therapy

Ламотриджин и ЭСТ

OBJECTIVE:: To evaluate the effect of lamotrigine (LMT) on electroconvulsive therapy (ECT)-induced seizures. METHODS:: Charts of all patients receiving LMT while undergoing an ECT course from July 2001 through May 2009 were reviewed. Apart from demographic variables, data collection consisted of diagnosis, indication for ECT, index or continuation ECT, electrode placement, stimulus dose, motor and electroencephalographic seizure duration, LMT dose, and number of restimulations. The stimulus dose and the seizure duration of ECT treatments with concurrent LMT (>/=200 mg/d) were compared with the stimulus dose and seizure duration of ECT treatments without concurrent LMT. RESULTS:: Lamotrigine was used by 19 patients (16 women, 3 men) during 289 treatment sessions. Eleven patients had ECT treatments with and without LMT, of which 8 were at a dosage of 200 mg/d or higher. Analyses did not reveal a significant difference in seizure duration and stimulus dose. Missed seizures, however, occurred more frequently during ECT treatments with concurrent LMT. CONCLUSIONS:: In all patients, seizures of adequate duration could be elicited. The combination was well tolerated. Therapeutic doses of LMT do not seem to have a clinically significant influence on the length of ECT-induced seizures nor on the stimulus dose.

Concurrent Use of Lamotrigine and Electroconvulsive Therapy.

Concurrent use of lamotrigine with ECT in bipolar depression seems safe, did not interfere with routine ECT practice, and allowed for transition to maintenance pharmacotherapy.

Combined Use of Lamotrigine and Electroconvulsive Therapy in Bipolar Depression: A Case Series

OBJECTIVES: To review the literature on the concurrent use of electroconvulsive therapy (ECT) and anticonvulsant drugs (AC) and to provide recommendations to guide clinical practice. METHODS: A MEDLINE search (1985-2006) was performed, using the terms "electroconvulsive therapy," "anticonvulsants," "epilepsy," "carbamazepine," "gabapentin," "lamotrigine," "topiramate," and "valproate," supplemented by manual searches of guidelines and textbooks on ECT. RESULTS: To date, no prospective, randomized and controlled trials examining outcome and safety of the AC-ECT combination have been published. Existing data are from case reports on the use of ECT for psychiatric conditions that are simultaneously treated with AC, and from case reports of patients treated with ECT and AC for epilepsy or for psychiatric conditions with comorbid epilepsy. Apart from an occasional difficulty in eliciting seizures, no severe adverse effects or complications are reported. CONCLUSIONS: The literature that is currently available indicates that ECT can be safely and effectively administered to patients treated with various AC. There is, however, no evidence to combine the 2 treatment modalities to augment therapeutic efficacy.

Anticonvulsants during electroconvulsive therapy: review and recommendations.

Временные обрывы маниакального состояния вестибулярной стимуляцией

Caloric vestibular stimulation is a common clinical procedure, routinely employed during testing of vestibulocochlear nerve function. The procedure involves stimulation of vestibular afferents by the application of cooled water to the tympanic membrane. Vestibular afferents are distributed widely to areas of the diencephalon and cortex, including areas believed to be involved in the regulation of mood. In accordance with these observations, imaging studies have shown widespread though largely contralateral hemispheric activation following the procedure.

Vestibular stimulation in mania: acase report

Психозы гиперчувствительности, психозы "отдачи", поздние психозы

* Антиаритмические препараты могут провоцировать аритмии, антибиотики могут способствовоать развитию новых видов инфекций, а антипсихотические препараты могут вызывать психоз.
* Как мы можем отличить поздний психоз от шизофрении?
* Не является ли иногда резистентная шизофрения на самом деле поздним психозом?
* Снижает ли применение некоторых новых антипсихотиков вероятность развития позднего психоза?

АНТИПСИХОТИЧЕСКИЙ ПСИХОЗ

Биология депрессии

The Biology of Depression: Guiding Treatment Selection

Скополамин и депрессия

An intravenous infusion of scopolamine induced significant depression improvement in three to five days. The effect persisted for at least two weeks after three doses.

The hunt for a fast-acting antidepressant moved a step forward with a report of the efficacy of scopolamine, a drug commonly used to treat vertigo, in a clinical trial.

A muscarinic cholinergic receptor antagonist, scopolamine is commonly available in a type of transdermal patch indicated for treating motion sickness. The patch delivers up to one milligram of scopolamine over three days.

Vertigo Drug Shows Promise as Depression Treatment

Эквиваленты доз флуфеназина таблетированного и пролонга

Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. Fluphenazine decanoate injection may be given intramuscularly or subcutaneously. A dry syringe and needle of at least 21 gauge should be used. Use of a wet needle or syringe may cause the solution to become cloudy.
To begin therapy with fluphenazine decanoate the following regimens are suggested:
For most patients, a dose of 12.5 to 25 mg (0.5 to 1 mL) may be given to initiate therapy. The onset of action generally appears between 24 and 72 hours after injection and the effects of the drug on psychotic symptoms becomes significant within 48 to 96 hours. Subsequent injections and the dosage interval are determined in accordance with the patient’s response. When administered as maintenance therapy, a single injection may be effective in controlling schizophrenic symptoms up to four weeks or longer. The response to a single dose has been found to last as long as six weeks in a few patients on maintenance therapy.
It may be advisable that patients who have no history of taking phenothiazines should be treated initially with a shorter-acting form of fluphenazine before administering the decanoate to determine the patient’s response to fluphenazine and to establish appropriate dosage. For psychotic patients who have been stabilized on a fixed daily dosage of fluphenazine hydrochloride tablets, fluphenazine hydrochloride elixir, or fluphenazine hydrochloride oral solution, conversion of therapy from these short-acting oral forms to the long-acting injectable fluphenazine decanoate may be indicated.
Appropriate dosage of fluphenazine decanoate injection should be individualized for each patient and responses carefully monitored. No precise formula can be given to convert to use of fluphenazine decanoate; however, a controlled multicentered
study1, in patients receiving oral doses from 5 to 60 mg fluphenazine hydrochloride daily, showed that 20 mg fluphenazine hydrochloride daily was equivalent to 25 mg (1 mL) fluphenazine decanoate every three weeks. This represents an approximate conversion ratio of 0.5 mL (12.5 mg) of decanoate every three weeks for every 10 mg of fluphenazine hydrochloride daily.
Once conversion to fluphenazine decanoate is made, careful clinical monitoring of the patient and appropriate dosage adjustment should be made at the time of each injection.
Severely agitated patients may be treated initially with a rapid-acting phenothiazine compound such as fluphenazine hydrochloride injection (see package insert accompanying that product for complete information). When acute symptoms have subsided, 25 mg (1 mL) of fluphenazine decanoate may be administered; subsequent dosage is adjusted as necessary.
“Poor risk” patients (those with known hypersensitivity to phenothiazines, or with disorders that predispose to undue reactions): Therapy may be initiated cautiously with oral or parenteral fluphenazine hydrochloride (see package inserts accompanying these products for complete information). When the pharmacologic effects and an appropriate dosage are apparent, an equivalent dose of fluphenazine decanoate may be administered. Subsequent dosage adjustments are made in accordance with the response of the patient.
The optimal amount of the drug and the frequency of administration must be determined for each patient, since dosage requirements have been found to vary with clinical circumstances as well as with individual response to the drug.
Dosage should not exceed 100 mg. If doses greater than 50 mg are deemed necessary, the next dose and succeeding
doses should be increased cautiously in increments of 12.5 mg.

FLUPHENAZINE DECANOATE INJECTION, USP

Лечение шизофрении пролонгированными формами флуфеназина, галоперидола и рисперидона

Treatment of Schizophrenia With Long-Acting Fluphenazine, Haloperidol,
or Risperidone

Селективность антипсихотиков in vitro и ex vivo

In a recent human [11C]-(+)-PHNO positron emission tomography study, olanzapine, clozapine, and risperidone occupied D2 receptors in striatum (STR), but, despite their similar in vitro D2 and D3 affinities, failed to occupy D3 receptors in globus pallidus. This study had two aims: (1) to characterize the regional D2/D3 pharmacology of in vitro and ex vivo [3H]-(+)-PHNO binding sites in rat brain and (2) to compare, using [3H]-(+)-PHNO autoradiography, the ex vivo and in vitro pharmacology of olanzapine, clozapine, risperidone, and haloperidol. Using the D3-selective drug SB277011, we found that ex vivo and in vitro [3H]-(+)-PHNO binding in STR is exclusively due to D2, whereas that in cerebellar lobes 9 and 10 is exclusively due to D3. Surprisingly, the D3 contribution to [3H]-(+)-PHNO binding in the islands of Calleja, ventral pallidum, substantia nigra, and nucleus accumbens was greater ex vivo than in vitro. Ex vivo, systemically administered olanzapine, risperidone, and haloperidol, at doses occupying ~80% D2, did not occupy D3 receptors. Clozapine, which also occupied ~80% of D2 receptors ex vivo, occupied a smaller percentage of D3 receptors than predicted by its in vitro pharmacology. Across brain regions, ex vivo occupancy by antipsychotics was inversely related to the D3 contribution to [3H]-(+)-PHNO binding. In contrast, in vitro occupancy was similar across brain regions, independent of the regional D3 contribution. These data indicate that at clinically relevant doses, olanzapine, clozapine, risperidone, and haloperidol are D2-selective ex vivo. This unforeseen finding suggests that their clinical effects cannot be attributed to D3 receptor blockade.

The Antipsychotics Olanzapine, Risperidone, Clozapine, and Haloperidol Are D2-Selective Ex Vivo but Not In Vitro

Обзор побочных эффектов антипсихотиков и нормотимиков

Adverse Effects of Antipsychotics and Mood Stabilizers

К определению бреда. К вопросу о двойственности его понятия: и «развитие личности», и «процесс»?

Мы прервём изложение истории болезни на этом месте и подведём краткие итоги. Нет сомнения, что наш пациент страдает параноидной шизофренией с вербальными псевдогаллюцинациями, вычурными сенестопатиями, при которой навязчивые расстройства, имевшие место в дебюте заболевания, постепенно перерастали в начальные проявления синдрома Кандинского-Клерамбо. Что же такое есть утверждение пациента о наличии у него шизофрении, при том, что она действительно имеет место быть? Да, может показаться при поверхностном взгляде, что мы имеем дело с неординарной личностью, склонной к рефлексии, с грамотным начитанным молодым человеком, блестяще распознавшим диагностировавшим у себя самого психическое заболевание. Был грех, так мы и думали при первом знакомстве с Иваном. Проведя «работу над ошибками», мы осознали, что это далеко не так. Конечно же, дело не в том, верно или нет больной диагностирует у себя ту или иную форму заболевания. Вся динамика состояния, смена одних психопатологических феноменов другими, личностная оценка своего состояния и суждения о прогнозе своего заболевания, постоянные обвинения врачей и медицины в терапевтической несостоятельности и упорное доказывание наличия у себя того, что давно и всем очевидно (психического заболевания – шизофрении), свидетельствует вовсе не о критике, а о формировании ипохондрического бреда, при котором на фоне многолетнего развития многочисленных расстройств восприятия, появления отдельных симптомов синдрома Кандинского-Клерамбо возникает бредовая интерпретация своего состояния, оформленная в психиатрический диагноз, полностью совпадающий с реальностью.

Что такое «расстройство критики»?