потенциирование клозапина метадоном в терапии резистентной к лечению шизофрении без героиновой зависимости

We postulate a possible mechanism that might explain our patient's response. It is
possible that methadone could have acted synergically with clozapine at glutamate NMDA receptor(NMDAR) site. Clozapine and methadone are, respectively, agonist and antagonists at NMDAR site 4, 5. We think that the interaction of clozapine and methadone at NMDAR site might explain our patient's improvement, according to Shim and
colleagues' hypothesis [4]. They hypothesise that an ideal set-point of NMDAR stimulation is needed to achieve symptomatic remission. Our hypothesis is that methadone (an NMDAR antagonist)in association with clozapine (NMDAR agonist)

Methadone augmentation of clozapine in treatment-resistant schizophrenia without opiates addiction: a case report.

SeCA-депрессия

Тревога, сниженный фон настроения, (ауто)агрессивность часто взаимосвязаны, так же как и нозологические категории расстройств настроения и тревожных расстройств. Вследствие этого возникают сложности и в клинической практике, и в исследовательской работе. В клинике перед врачом встают вопросы: какие симптомы или расстройства надо лечить? Надо ли лечить все? В исследовательской работе - какие симптомы или расстройства коррелирует с полученными данными? Для решения этих проблем предложено два подхода: правила иерархического исключения и комбинированные диагнозы. Применение первого подхода является не вполне адекватным, так как ни одна проблема не может быть решена путем ее исключения. Второй подход, связанным с применением комбинированного диагноза, к примеру, атипичная депрессия, или смешанные тревожно-депрессивные расстройства, также не вполне правомочен. Предложенная нами недавно концепция “тревожно-агрессивной депрессии, провоцируемой стрессом, индуцируемой кортизолом и связанной с серотонином” (СеТА депрессии) определяет (пока гипотетически) подтип депрессии, при которой неконтролируемую чувства тревоги и агрессивность предшествуют и задают ритм снижению настроения. Повышенная ранимость, обусловленная невротическими особенностями личности, предрасполагает к возникновению СеТАдепрессии. В основе ее развития от психотравмирующих переживаний к психопатологии - сначала тревоги и агрессивности, а затем депрессии — лежит нарушение функции опальной связи между серотонинергической и гипоталамо-гипофизарно-адренокортикальной системами.

Депрессия, тревожные расстройства, агрессия: попытки распутать гордиев узел

Микседематозная кома вызванная комбинацией арипипразола и сертралина

Myxedema Coma Associated with Combination Aripiprazole and Sertraline Therapy
Chelsea O Church, PharmD BCPS

Associate Professor of Pharmacy Practice, College of Pharmacy, Southwestern Oklahoma State University, Weatherford, OK

Erin C Callen, PharmD BCPS

Associate Professor of Pharmacy Practice, College of Pharmacy, Southwestern Oklahoma State University

Reprints: Dr. Church, Department of Pharmacy Practice, Southwestern Oklahoma State University College of Pharmacy, Pasteur Medical Building, Pharmacy Education, 1111 North Lee, Ste. 241, Oklahoma City, OK 73103, fax 405/601-1201, chelsea.church@swosu.edu

OBJECTIVE: To describe a case of myxedema coma (MC) associated with combination aripiprazole and sertraline therapy.

CASE SUMMARY: A 41-year-old male presented to the emergency department with confusion, right-sided numbness and tingling, slurred speech, dizziness, and facial edema. His blood pressure was 160/113 mm Hg, with a pulse of 56 beats/min and temperature of 35.4 °C. Initial abnormal laboratory values included creatine kinase (CK) 439 U/L; serum creatinine 1.6 mg/dL; aspartate aminotransferase 85 U/L; and alanine aminotransferase 35 U/L. Repeat cardiac markers revealed an elevated CK level of 3573 U/L with a CK-MB of 24 ng/mL. Thyroid function tests showed thyroid-stimulating hormone 126.4 µIU/mL and free thyroxine 0.29 ng/dL. Home medications of unknown duration were sertraline 200 mg and aripiprazole 20 mg daily. He was admitted to the intensive care unit and initially treated with intravenous levothyroxine and dexamethasone. By hospital day 4, the patient was clinically stable and discharged to home.

DISCUSSION: Myxedema coma, the most significant form of hypothyroidism (HT), is a rare but potentially fatal condition. The known precipitating causes of MC were ruled out in this patient, which left his home medications as the likely cause. Cases of HT caused by certain atypical antipsychotics and antidepressants are found in the literature, but none was reported with aripiprazole therapy. There are also no reported cases of sertraline or aripiprazole inducing MC. Use of the Naranjo probability scale indicates that the combination of aripiprazole and sertraline was a probable inducer of MC in this patient.

CONCLUSIONS: Due to the widespread use of psychotropic medications, clinicians should be reminded of the rare, yet life-threatening, occurrence of MC when treating patients, especially with combination therapies such as sertraline and aripiprazole.

Myxedema Coma Associated with Combination Aripiprazole and Sertraline Therapy

Таблица взаимодействия веществ с P450

P450 Drug Interaction Table

Кататония - обзор

http://www.psyobsor.org/1998/35/3-4.html

mycobacterium vaccae и депрессия

Mycobacterium vaccae, a harmless bacteria normally found in dirt, has been found to stimulate the immune system of mice and boost the production of serotonin, a mood-regulating brain chemical.
The bacterium has already been successfully used in people as a vaccine against tuberculosis. It is also being tested as a treatment for cancer patients and in asthma sufferers, as a way to control the allergic reaction and help 'rebalance' the immune system.
Interest in the unusual antidepressant properties of M.vaccae arose by accident following an experimental treatment for human lung cancer led by cancer researcher Mary O'Brien at the Royal Marsden Hospital in London, England. Under that treatment, patients received heat-killed inoculations of the bacteria.
Following the tests, O'Brien's team observed not only fewer symptoms of cancer, but also improvements in their patients' vitality, emotional health and mental abilities.
Lowry and his colleagues speculated that the bacteria in these earlier experiments might have activated brain cells to release mood-lifting chemicals. To investigate the idea further, they injected heat-killed bacteria into a group of mice and found that they initiated an immune response, which activated serotonin-producing neurons in the brain.
Low levels of serotonin cause depression – an illness which afflicts around 1.3 million Australians. The most commonly prescribed antidepressant medications help treat depression by delaying the re-uptake of serotonin, thus raising levels in the brain.
According to Lowry, the strange effect of the bacteria may work by prompting the body's immune cells to release cytokines, chemicals known to activate sensory nerves that stimulate the brain. The findings are published in the journal Neuroscience.
Therapeutic Gardening against Clinical Depression

шизофреноподобный психоз вследствие дефицита цианокобаламина

Although cobalamin deficiency is widely known and usually presents with hematologic and neuropsychiatric manifestations, the psychiatric symptoms are not usually the predominant manifestation. We describe a young single male vegetarian who developed a cobalamin-induced psychotic episode without preceding neurologic manifestations and without any hematologic symptoms. He recovered after a short course of antipsychotics and oral cobalamin supplementation and remained asymptomatic and functionally independent at 1 year of follow-up.
Schizophrenia-like psychotic episode precipitated by cobalamin deficiency.

МРТ-предикторы шизофрении

Researchers at Columbia University led by Dr. Scott A. Small used MRI scanning to look at the brains of 18 normal adolescents, 18 youths who had schizophrenia, and 18 with preliminary symptoms. These symptoms included paranoid thinking, such as subjects believing someone was looking at them in a troubling way while knowing that’s not a realistic perception. In full schizophrenia, which affects about 1 percent of the population, people are so disconnected from reality that they believe paranoid thoughts are real.

The researchers scanned the high-risk subjects and then followed them for two years. When they looked back at the scans of those who went on to develop psychotic disorders like schizophrenia, they found 70 percent of them had shown unusually high activity in a particular part of the hippocampus, a key brain structure dealing with memory.

Is there any way to predict the onset of schizophrenia?

депрессия и остеопороз

Depression as Risk Factor for Bone Loss

военные неврозы 1917г.

видео
War Neuroses [electronic resource] : Netley Hospital,1917

Кататония в психиатрической классификации

Catatonia in Psychiatric Classification: A Home of Its Own

новые алгоритмы терапии депрессии при БАР

Algorithm for the treatment of bipolar I depression



Step 1: Treat bipolar I depression for 8 weeks with

* Quetiapine 600 mg daily
or
* Lithium 0.8 mEq/L daily (or another mood stabilizer) along with lamotrigine 50 - 200 mg daily

If there is no treatment response, move on to step 2



Step 2: For treatment-resistant bipolar I depression

* Use a combination of olanzapine 6 - 12 mg plus fluoxetine 25 - 50 mg (OFC) daily
or
* Increase dose to > 600 mg of quetiapine along with lamotrigine 50 - 200 mg daily

If there is no treatment response, move on to step 3



Step 3: Treat refractory bipolar I depression

* Adjust OFC dose
or switch to
* Lithium 0.8 mEq⁄L daily plus an SSRI 20 - 40 mg and bupropion 150 - 300 mg daily
or
* Increase dose to > 600 mg of quetiapine and 20 - 40 mg of an SSRI and 150 - 300 mg of bupropion daily
or
* Use novel therapies such as modafinil or pramipexole

If there is no treatment response, move on to step 4



Step 4: Treat intractable bipolar I depression, with

* Electroconvulsive therapy

If there is still no response, the patient may have involutional bipolar I disorder
Adapted from Pacchiarotti I et al. Acta Psychiatr Scand. 2009.1


Algorithm for the treatment of bipolar II depression



Step 1: Treatment of bipolar II depression for 8 weeks with

* Lithium 0.8 mEq/L daily (or another mood stabilizer) along with lamotrigine 50 - 200 mg daily
* Quetiapine 600 mg daily
or

If there is no treatment response, move on to step 2



Step 2: For treatment-resistant bipolar I depression, use

* Lithium 0.8 mEq⁄L daily along with an SSRI 20 - 40 mg and bupropion 150 - 300 mg daily
or
* Quetiapine 300 - 600 mg daily along with an SSRI 20 - 40 mg and bupropion 150 -300 mg daily

If there is no treatment response, move on to step 3



Step 3: Treat refractory bipolar I depression

* Adjust OFC dose or switch to
* Quetiapine 300 - 600 mg daily and a monoamine oxidase inhibitor (MAOI) such as tranylcypromine 20 - 100 mg daily
or

* Lithium 0.8 mEq⁄L daily and an MAOI such as tranylcypromine 20 - 100 mg daily
or
* Novel therapies such as modafinil or pramipexole

If there is no treatment response, move on to step 4



Step 4: Treat intractable bipolar I depression with

* Electroconvulsive therapy

If there is still no response, the patient may have involutional bipolar II disorder
Adapted from Pacchiarotti I et al. Acta Psychiatr Scand. 2009.1

New Algorithms for the Management of Treatment-Resistant Bipolar Depression

Транскраниальная магнитная стимуляция в терапии резиcтентной к лечению депрессии

Of the 15 patients who participated in the study, the mean HAM-D score decreased from 29 at baseline to 11 after the treatment period. In 86% of patients, the HAM-D score decreased by at least 50%, and 57% of all patients reached remission. Three patients experienced tolerable focal pain, and this disappeared during the treatment period. No patients experienced seizure or manic symptoms.

rTMS May Be Effective in Patients With Treatment-Resistant Bipolar Depression

Инициальные признаки манифестации и экзоцербации психоза

Schizophrenia: early warning signs

вигабатрин в терапии кокаиновой зависимости

OBJECTIVE: Cocaine dependence is associated with severe medical, psychiatric, and social morbidity, but no pharmacotherapy is approved for its treatment in the United States. The atypical antiepileptic vigabatrin ({gamma}-vinyl gamma-aminobutyric acid [GABA]) has shown promise in animal studies and open-label trials. The purpose of the present study was to assess the efficacy of vigabatrin for short-term cocaine abstinence in cocaine-dependent individuals. METHOD: Participants were treatment seeking parolees who were actively using cocaine and had a history of cocaine dependence. Subjects were randomly assigned to a fixed titration of vigabatrin (N=50) or placebo (N=53) in a 9-week double-blind trial and 4-week follow-up assessment. Cocaine use was determined by directly observed urine toxicology testing twice weekly. The primary endpoint was full abstinence for the last 3 weeks of the trial. RESULTS: Full end-of-trial abstinence was achieved in 14 vigabatrin-treated subjects (28.0%) versus four subjects in the placebo arm (7.5%). Twelve subjects in the vigabatrin group and two subjects in the placebo group maintained abstinence through the follow-up period. The retention rate was 62.0% in the vigabatrin arm versus 41.5% in the placebo arm. Among subjects who reported prestudy alcohol use, vigabatrin, relative to placebo, was associated with superior self-reported full end-of-trial abstinence from alcohol (43.5% versus 6.3%). There were no differences between the two groups in drug craving, depressed mood, anxiety, or Clinical Global Impression scores, and no group differences in adverse effects emerged. CONCLUSIONS: This first randomized, double-blind, placebo-controlled trial supports the safety and efficacy of short-term vigabatrin treatment of cocaine dependence.

Randomized, Double-Blind, Placebo-Controlled Trial of Vigabatrin for the Treatment of Cocaine Dependence in Mexican Parolees

Нелекарственная терапия при шизофрении

Treatments
Medication. All participants received Food and Drug Administration-approved antipsychotic medications for the treatment of schizophrenia, schizoaffective disorder, and schizophreniform disorder as indicated by a study psychiatrist. Medication changes were allowed, although every effort was made to stabilize participants on a tolerable and efficacious antipsychotic regimen before the initiation of psychosocial treatment. All participants were seen by a clinical nurse specialist at least biweekly to monitor medication side effects and efficacy. Most participants (>98%) were given second-generation antipsychotics throughout the study, and no significant differences emerged with regard to antipsychotic dosage, type, or clinician-estimated compliance between treatment groups. [A table detailing the between-group differences in baseline demographic, clinical, and medication characteristics is available as an online supplement to this article at ps.psychiatryonline.org.]

Cognitive enhancement therapy. CET is a comprehensive, developmental approach to the remediation of social and nonsocial cognitive deficits in schizophrenia. It seeks to facilitate the development of adult social-cognitive milestones (such as perspective taking and appraisal of one's social context) by shifting thinking from reliance on effortful, serial processing to a "gistful" and spontaneous abstraction of social themes. The treatment consists of approximately 60 hours of computer-assisted neurocognitive training in attention, memory, and problem solving and 45 social-cognitive group sessions that use experiential learning opportunities to foster the development of social wisdom and success in interpersonal interactions. A broad, theoretically driven array of social-cognitive abilities are targeted in the social-cognitive groups, which range from abstracting the "gist" or main point in social interactions to perspective taking, social context appraisal, and emotion management (39,43). Participants engage in the social-cognitive groups by responding to unrehearsed social exchanges, presenting homework, participating in cognitive exercises that focus on experiential learning, providing feedback to peers, and chairing homework sessions. CET typically begins with approximately three months of weekly one-hour neurocognitive training in attention, after which participants begin the weekly 1.5-hour social-cognitive groups. Neurocognitive training then proceeds concurrently with social-cognitive groups throughout the remaining course of treatment. A complete description of the treatment has been provided elsewhere (16).

Enriched supportive therapy. Enriched supportive therapy (EST) is an illness management and psychoeducation approach that draws on components of the basic and intermediate phases of the demonstrably effective personal therapy (44). In this approach, outpatients are seen on an individual basis to learn and practice stress management techniques designed to forestall late postdischarge relapse and enhance adjustment. The EST treatment is divided into two phases. Phase 1 focuses on basic psychoeducation about schizophrenia, the role of stress in the disorder, and ways to avoid or minimize stress. Phase 2 involves a personalized approach to the identification and management of life stressors that pose particular challenges to adequate social and role functioning. Participants move through the two phases of EST at their own pace, although each phase is typically provided for a year. By design, phase 1 was provided on a weekly basis, and phase 2 was provided on a biweekly basis. Although no attempt was made to match CET and EST approaches with regard to hours of treatment, EST served as the active control for this trial, in part to control for the potential effects on outcome of illness management and education interventions (45), which are provided in both CET and EST. All psychosocial interventions were administered by three master's-level psychiatric nurse specialists, and clinical supervision was provided by the two treatment developers.

Cognitive Enhancement Therapy for Early-Course Schizophrenia: Effects of a Two-Year Randomized Controlled Trial

Transcranial Magnetic Stimulation for Depression: Not so Effective, but FDA Approved