Случай необычного снохождения

There's a party in my dream and everyone's invited:

Депрессии, витамин D и сердечно-сосудистые заболевания

Background Depression is associated with cardiovascular (CV) disease, and it has been hypothesized that vitamin (vit)D deficiency may be associated with depression and a contributing factor to excess CV events. Therefore, we evaluated whether there is an association between vitD and incident depression among a CV population.
Methods Patients (N = 7,358) ≥50 years of age, with a CV diagnosis (coronary artery disease, myocardial infarction, congestive heart failure, cerebrovascular accident, transient ischemic accident, atrial fibrillation, or peripheral vascular disease), no prior depression diagnosis, and a measured vitD level were studied. Vitamin D (ng/mL) was stratified into 4 categories: >50 (optimal [O] n = 367), 31 to 50 (normal [N] n = 2,264), 16 to 30 (low [L] n = 3,402), and ≥15 (very low [VL] n = 1,325). Depression was defined by International Classification of Diseases, Ninth Edition, codes: 296.2 to 296.36, 311. VitD categories were evaluated by Cox hazard regression with adjustment by standard CV risk factors.
Results Age averaged 73.1 ± 10.2 years, and 58.8% were female. When compared to O, VL, L, and N were associated with depression (adjusted: VL, hazard ratio [HR] 2.70 [1.35–5.40], P = .005; L, HR 2.15 [1.10–4.21], P = .03; N, HR 1.95 [0.99–3.87], P = .06). This association remained even after adjustment by parathyroid hormone levels. Parathyroid hormone was significantly associated with depression, however, became nonsignificant after adjustment by vitD. Winter (December-February) enhanced this association. Significant associations remained when stratifications were made by age (<65, ≥65), sex, and diabetes, although the associations among those age ≥65 and male sex were enhanced.
Conclusion Among a CV population ≥50 years with no history of depression, vitD levels were shown to be associated with incident depression after vitD draw. This study strengthens the hypothesis of the association between vitD and depression.

Association of Vitamin D Levels with Incident Depression among a General Cardiovascular Population

Психические расстройства при гипотиреозе и гипертиреозе

The symptoms and signs of hyperthyroidism resemble those of primary mental disorders. Overactivity of the adrenergic system caused by hyperthyroidism may explain the similarity between the clinical presentations of hyperthyroidism and mania or anxiety, as well as the precipitating role of hyperthyroidism in the development of mania or anxiety disorder. It may also explain the increased sense of well being often experienced in the early stages of hyperthyroidism.[20,21]

The relationship between hyperthyroidism and depression is less clear. Depression is usually linked to hypothyroidism, not to hyperthyroidism. However, prolonged hyperthyroidism might exhaust noradrenergic transmission and thus contribute to depression. Noradrenergic exhaustion might well occur in patients with hyperthyroidism who have bipolar disorder. In the initial phase of hyperthyroidism, thyroid hormone stimulation of the noradrenergic system may cause mania; later, when noradrenergic neurotransmission is exhausted, it may contribute to depression.[21]

Mental symptoms and disorders secondary to hyperthyroidism should be treated first by restoring euthyroidism. Most mental symptoms, including depression, usually resolve once euthyroidism has been regained. Treatment with beta-adrenergic antagonists alone may quickly relieve many symptoms, including mental symptoms, even if euthyroidism is not restored,[22] providing evidence that overactivity of the adrenergic system is largely responsible for mental symptoms in hyperthyroidism.

Thyroid deficits are frequently observed in bipolar patients, especially in women with the rapid cycling form of the disease.[24] Both subclinical hypothyroidism and subclinical hyperthyroidism increase the risk for Alzheimer's disease, especially in women.[25] However, most hypothyroid patients do not meet the criteria for a mental disorder.

A recent study evaluated brain glucose metabolism during T4 treatment of hypothyroidism. A reduction in depression and cognitive symptoms was associated with restoration of metabolic activity in brain areas that are integral to the regulation of mood and cognition.[26••]

In hypothyroidism, replacement therapy with T4 remains the treatment of choice and resolves most physical and psychological signs and symptoms in most patients. However, some patients do not feel entirely well despite doses of T4 that are usually adequate.[27] In T4-treated patients, it was found that reduced psychological well being is associated with occurrence of polymorphism in the D2 gene,[28••] as well as in the OATP1c1 gene.[29]

Thyroid hormone replacement with a combination of T4 and T3, in comparison with T4 monotherapy, improves mental functioning in some but not all hypothyroid patients,[30,31•] and most of the patients subjectively prefer combined treatment.[32] Two studies have evaluated whether D2 polymorphism is associated with changes in psychological well being after combined T4 and T3 treatment. One underpowered study[33] reported a trend toward improvement. In a second study[28••] involving a very large sample, D2 polymorphism was associated with improvement in psychological well being after T4 and T3 treatment.

Thyroid Disease and Mental Disorders: Cause and Effect or Only comorbidity?

Ранняя шизофрения: сравнение эффективности и переносимости антипсихотиков

OBJECTIVE: To examine the long-term safety and efficacy of three antipsychotics in early-onset schizophrenia spectrum disorders. METHOD: Patients (8 to 19 years old) who had improved during an 8-week, randomized, double-blind acute trial of olanzapine, risperidone, or molindone (plus benztropine) were eligible to continue on the same medication for up to 44 additional weeks under double-blind conditions. Adjunctive medications were allowed according to defined algorithms. Standardized symptom, safety, and functional assessments were conducted every 4 weeks. RESULTS: Of the 116 youths randomized in the acute trial, 54 entered maintenance treatment (molindone, n = 20; olanzapine, n = 13; risperidone, n = 21). Fourteen (26%) completed 44 weeks of treatment. Adverse effects (n = 15), inadequate efficacy (n = 14), or study nonadherence (n = 8) were the most common reasons for discontinuation. The three treatment arms did not significantly differ in symptom decrease or time to discontinuation. Akathisia was more common with molindone and elevated prolactin concentrations more common with risperidone. Although weight gain and metabolic adverse events had occurred more often with olanzapine and risperidone during the acute trial, no significant between-drug differences emerged in most of these parameters during maintenance treatment. CONCLUSIONS: Only 12% of youths with early-onset schizophrenia spectrum disorders continued on their originally randomized treatment at 52 weeks. No agent demonstrated superior efficacy, and all were associated with side effects, including weight gain. Improved treatments are needed for early-onset schizophrenia spectrum disorders.

Double-Blind Maintenance Safety and Effectiveness Findings From the Treatment of Early-Onset Schizophrenia Spectrum (TEOSS) Study.

Double-Blind Comparison of First- and Second-Generation Antipsychotics in Early-Onset Schizophrenia and Schizo-affective Disorder: Findings From the Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS) Study

ДСМ5: Синдром малой психотической симптоматики

Attenuated Psychotic Symptoms Syndrome

Идентификация группы риска развития биполярного аффективного расстройства

Bechdorf points out that while rate of development of bipolar disorder in the BAR group (22.7 percent) is more than 100 times that in the general population, “Prospective studies in bigger samples and with longer follow-up periods, better controlled antidepressant use and psychometric measures of conversions are warranted to provide further validity of these criteria.”

Identifying Youth at High Risk for Bipolar Disorder

Интраназальный инсулин и когнитивные функции

A small, randomized trial of 2 doses of intranasal insulin showed improvements in memory and functioning and improved CSF biomarker profiles among patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD) with treatment over placebo.

The SNIFF-120 trial was a 4-month, randomized, double-blind trial of placebo vs 2 doses of intranasal insulin: 20 or 40 IU daily. One hundred four patients with AD or amnestic MCI participated; patients with diabetes were excluded.

Intranasal Insulin Shows Benefit in Mild Cognitive Impairment and Alzheimer's Disease

Ведение пациентов с первым приступом психоза

ВЕДЕНИЕ ПАЦИЕНТОВ С ПЕРВЫМ ПРИСТУПОМ ПСИХОЗА

Ребоксетин+Оланзанин

Reboxetine Enhances the Olanzapine-Induced Antipsychotic-Like Effect, Cortical Dopamine Outflow and NMDA Receptor-Mediated Transmission

продром, длительность нелеченного психоза, первый психотический эпизод

Most patients presenting to health services with an 'at risk mental state' will not develop psychosis. In the original Yung and McGorry study, transition rates were 40% over 12 months, but more recent studies found rates more in the vicinity of 15-30%. This still represents a level of risk increased a thousand-fold over the general population...
These early trials raise the possibility of primary or at least secondary prevention of psychotic disorders, although many questions remain. There are ethical issues in treating a group of people of whom 80% will not in any case progress to psychosis in the short term. Also, the base-rates, specificity and sensitivity of these at risk mental states in predicting psychosis may still mean this approach is of limited value at a population level...
Recovery rates from the first episode are high, with 85% achieving remission over a mean time of 3 months. Individuals in the first episode are sensitive both to the therapeutic effects and the adverse effects of antipsychotic drugs. This means they are more likely to respond to lower doses than in later episodes, but also are more susceptible to motor side effects. Most expert opinion advocates second generation antipsychotics as first line treatment (e.g. initially 0.5-2 mg risperidone or 2.5-7.5 mg olanzapine per day). Benzodiazepines are often used as adjuncts for agitation or catatonic symptoms. Poor adherence with treatment is if anything more problematic than at later stages of illness, since placebo controlled trials show a greater benefit of antipsychotics in first episode treatment and first relapse prevention yet up to 50% of individuals will be non-adherent in the first year. Cognitive behaviour therapy in addition to drug treatment is indicated.

Early Detection of Schizophrenia: Post-Detection: Early Treatments in the First Episode

Роль L-метилфолата в терапии депрессивных расстройств

Folate is a water soluble B vitamin (B9), considered one of the 13 essential vitamins. The primary function of folate is the transfer of methyl and formyl groups, thus, it is essential for cell growth and reproduction, the breakdown and utilization of proteins, the formation of nucleic acids, red blood cell maturation, and a variety of CNS reactions. Dihydrofolate is the dietary form found in orange juice, spinach, asparagus, beans, liver, yeast, whole grain cereals, and eggs. Folic acid is the synthetic form of folate in over-the-counter vitamins and used to fortify the food supply (to help prevent neural tube defects, the FDA mandated folic acid fortification of flour in 1998). Folic acid is also the predominant form used in prescription strength prenatal vitamins. Both folic acid and dihydrofolate are not biologically active forms of folate, but are essentially pro-drugs, and must undergo enzymatic transformation to L-methylfolate in order to be used by cells, and unlike other forms of folate, L-methylfolate readily crosses the blood-brain barrier for use in the CNS.


Almost 85% of dietary folate and nearly all supplemental folic acid is absorbed into the venous system in the proximal small intestine. The enzymatic conversion begins in the intestinal wall—it is a three step process for dihydrofolate, and a four step process for folic acid (Slide 3). Folic acid is converted to dihydrofolate (DHF) by dihydrofolate reductase enzyme (DHFR), and DHF is then converted to tetrahydrofolate (THF). The conversion of THF to 5,10-methyleneTHF follows. Finally, the conversion of 5,10-methyleneTHF to L-methylfolate is achieved by the methyltetrahydrofolate reductase enzyme (MTHFR). This last step completes the four step transformation process by which the bioactive cofactor, L-methylfolate, is made available to the brain to be used in the synthesis of monoamine neurotransmitters associated with mood regulation (serotonin, norepinephrine, and dopamine).

There are five trials that examine folate therapy in depressive disorders. In a study59 with patients who had low or borderline low RBC folate, depressed patients on tricyclic antidepressants or MAOIs were augmented with methylfolate 15 mg (L-methylfolate 7.5 mg) experienced significantly greater clinical improvement and social improvement at 3 months (P<.02) and 6 months (P<.01) compared to patients treated with antidepressants alone. The methylfolate-augmented patients continued to improve for 6 months compared to patients augmented with placebo, and none experienced relapse. In a separate double-blind, controlled trial60 comparing methylfolate 50 mg/day to trazodone 100 mg/day, depressed patients experienced a significant decrease in HAM-D scores at 4 and 8 weeks in both groups, with response rates in the methylfolate group at 45%, and in the trazodone group (not statistically significant) at 29%.


An open label trial61 of methylfolate as monotherapy in elderly depressed subjects demonstrated an 81% response rate (>50% reduction in HAM-D) by 6 weeks of therapy. A second monotherapy study examined a depressed population of 36 chronic alcoholics. After a week of placebo wash-out, subjects received 4 weeks of 90 mg methylfolate therapy. This dosing (30 mg TID) significantly improved depressive symptoms based on the HAM-D scale with the majority reporting improved mood and less fatigue (P<.01).62 Alpert and colleagues63 conducted an open label trial augmenting selective serotonin reuptake inhibitor (SSRIs) with folinic acid in patients who had failed at least 4 weeks of SSRI therapy. The response to folinic acid was not robust (P<.01, n=22), but it was well tolerated overall.

The standard dose of L-methylfolate for the augmentation of antidepressants is one 7.5 mg tablet/day. No titration is necessary, and it is not associated with withdrawal symptoms at discontinuation. The maximum amount of L-methylfolate that can be absorbed in one dose is ~15 mg.67 If more than one 7.5 mg tablet/day is needed, it may be prudent to give in divided doses. All reported adverse events occur at placebo rates or lower, and overall it is an extremely well tolerated agent, allowing patients to continue L-methylfolate therapy as long as necessary to maintain remission. There are no known contraindications and no known drug interactions.

The Role of L-methylfolate in Depressive Disorders

STAR*D

The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial was a longitudinal, multi-center, 5-year study of common strategies for treating depression. To date, it is the United States’ largest National Institute of Mental Health funded study including over 4,000 patients. This four level trial compared traditional augmentation strategies with switching agents (Slide 2).30-34 Unlike most depression studies, in STAR*D the outcome measure was full remission.
In Level 1, the initial monotherapy phase, citalopram (mean dose of 41.8 mg) was effective at achieving remission for only ~30% of subjects. This finding has been accepted as an accurate reflection of clinical experience with any initial monotherapy. The remaining 70% were randomized to either receive bupropion or buspirone augmentation, or switched to one of three antidepressants as monotherapy—bupropion, venlafaxine, or sertraline. Augmentation resulted in a 30% response, while switching antidepressants resulted in ~20% of patients achieving remission. Level 3 included those non-remitters from Level 2 who were then randomized to either T3 or lithium augmentation, resulting in remission rates of 25% and 16% respectively. A Level 3 switch to nortriptyline (NTP) or mirtazapine (MTZ) was in general less successful than Level 3 augmentation, with 20% of NTP patients and 12% of MTZ patients remitting. Level 4 treatment options (monoamine oxidase inhibitors [MAOIs] or venlafaxine–mirtazapine-combination therapy) were provided to patients who had not responded satisfactorily to previous levels of the treatment protocol, and very few experienced full remission (14% and 7% respectively).12,35


An overall analysis of STAR*D results indicates that the chances of achieving and maintaining remission in patients with difficult-to-treat depression diminishes with every additional strategy needed. Those who fully remit early in the course of treatment have a better chance of remaining well than those who experience only symptomatic improvement. STAR*D does not tell us which treatment works better as a first or second adjunct, simply that the greatest chance of recovery appears to lie with the first two sequential treatments.

The Role of L-methylfolate in Depressive Disorders

Стимуляторы при БАР

Clinical studies of stimulant use in patients with bipolar disorder

Stimulant(s) studied	Study design	Patients studied	Clinical outcomes
Traditional stimulants
Adjunctive methylphenidate	Chart review, naturalistic	16 adults (5 with comorbid ADHD, 11 with bipolar depression)	Improvements in depression, overall functioning, and ability to concentrate; sleep disturbance, irritability/agitation reported
Adjunctive methylphenidate or racemic mixture of AMPH salts	Chart review of sedation and depressive symptoms	8 adults (BD II)	Improved clinical impression of bipolar illness; no manic switches, changes in cycling patterns, or substance abuse noted
Adjunctive methylphenidate	12-week open study, bipolar depression	12 adults (10 BD I, 2 BD II)	Significant clinical improvements in depressive symptoms; no change in manic symptoms; anxiety, agitation, and hypomania reported
Multiple stimulants	Chart review, history of stimulants and bipolar illness course	34 hospitalized adolescents	Prior stimulant treatment associated with earlier age of illness onset
Adjunctive mixed amphetamine salts	Randomized, placebo-controlled; comorbid BD and ADHD	30 children with ADHD symptoms stabilized on divalproex sodium	Decrease in ADHD symptoms with adjunctive amphetamine treatment but not with divalproex sodium alone; 1 case of mania
Novel stimulant
Adjunctive modafinil	Case series	Mixed sample of depressed adults (4 unipolar, 3 bipolar)	Significant improvement in depressive symptoms
Adjunctive modafinil	Randomized, double-blind, placebo-controlled	85 adults with bipolar depression	Treatment group showed greater response and remission of depressive symptoms compared with placebo group; no difference in development of manic symptoms
ADHD: attention-deficit/hyperactivity disorder; AMPH: amphetamine; BD: bipolar disorder; NOS: not otherwise specified

Adding a stimulant could improve residual symptoms, but it also might cause serious side effects, toxicities, and destabilization.

Stimulants for adult bipolar disorder?

Низкий уровень холестерина как фактор риска аффективных расстройств

In the early 1990s several studies suggested a link between low cholesterol (< 160 mg/dL) and unnatural deaths, including suicide.2-4 Follow-up studies confirmed associations between low cholesterol and suicide attempts, especially violent ones.5 These associations are compelling given the neurobiologic effects of cholesterol, such as a net reduction of serotonergic function (Box 1). Low cholesterol may predispose an individual to aggression, impulsivity, and violence (Table 1).6 Many studies have found that patients with mood disorders have lower cholesterol levels;7 however, other research suggests they are at increased risk of hyperlipidemia, typically hypertriglyceridemia rather than hypercholesterolemia.

The neurobiologic effects of low cholesterol—particularly those related to serotonergic hypofunction—are thought to be mediate impulsive, aggressive, and violent behaviors that may predispose an individual to suicide.a,b The CNS contains one-fourth of the body’s free cholesterol,c which is synthesized primarily in situ.

Cholesterol improves membrane stability, reduces permeability, and may influence serotonergic function. Cholesterol depletion may impair function of 5-HT1A and 5-HT7 receptorsd,e and serotonin transporter activity.f Reduced cholesterol after treatment with simvastatin—an HMG-CoA reductase inhibitor that readily crosses the blood-brain barrier—resulted in acute (1-month) increases in serotonin transporter activity followed by subacute (>2 months) decreases.g Lower cholesterol levels may further decrease expression of serotonin receptors and cause a net reduction in serotonergic activity.

In addition, cholesterol is necessary for synapse formation and myelin production. Cholesterol depletion may have more diffuse effects on neurotransmission, such as gamma-aminobutyric acid receptors,hN-methyl-D-aspartate receptors,i opioid signaling,j and excitatory amino acids transport.k

Impulsivity associated with low serotonergic function and low total cholesterol has been suggested as a potential pathway for suicide.l Low cholesterol is associated with self-report measures of impulsivity;m however, increased impulsivity associated with lipid-lowering therapy may be temporary,n which is similar to the time-limited changes in serotonin transporter activity.g Human and animal data have suggested that low cholesterol may be linked to violent behaviors, including suicide.o

Multiple randomized controlled trials have not shown increased depression and suicide with use of lipid-lowering agents in healthy populations

Closely monitor individuals with mood disorders for changes in behavior or mental status after starting a lipid-lowering agent

Cholesterol, mood, and vascular health: Untangling the relationship

К казуистике синдрома Кандинского-Клерамбо

приведённом клиническом наблюдении даже такой значительный органический дефект как глухонемота не трансформировал вербальную псевдогаллюцинацию в зрительную, а только «перенёс» её в систему другого анализатора. Для синдрома Кандинского–Клерамбо обязательны вербальные псевдогаллюцинации и поэтому наша больная испытывала их в виде уникальных «жесто-речевых ложно-зрительных псевдогаллюцинаций».

К КАЗУИСТИКЕ СИНДРОМА КАНДИНСКОГО–КЛЕРАМБО

Анти-NMDA-рецепторный энцефалит

Of 100 patients with anti-NMDA-receptor encephalitis, a disorder that associates with antibodies against the NR1 subunit of the receptor, many were initially seen by psychiatrists or admitted to psychiatric centres but subsequently developed seizures, decline of consciousness, and complex symptoms requiring multidisciplinary care. While poorly responsive or in a catatonic-like state, 93 patients developed hypoventilation, autonomic imbalance, or abnormal movements, all overlapping in 52 patients. 59% of patients had a tumour, most commonly ovarian teratoma. Despite the severity of the disorder, 75 patients recovered and 25 had severe deficits or died.
This disorder largely affects young people, and its diagnosis is facilitated by the characteristic clinical picture that develops in association with CSF pleocytosis. By contrast to the consistency of the clinical picture, MRI findings are less predictable; only 55% of patients had increased FLAIR or T2 signal in one or several brain regions, without significant correlation with patients’ symptoms (data not shown). Our study indicates that 41% of patients with anti-NMDA-receptor encephalitis do not have a clinically detectable tumour, and that men and children can also be affected. Therefore, although the presence of a tumour that expresses NMDA receptors likely contributes to breaking immune tolerance, other unknown immunological triggers seem to be involved. This paradigm is similar to the Lambert-Eaton myasthenic syndrome, an antibody-mediated disorder of the neuromuscular junction that can occur with or without tumour association.16 In Lambert-Eaton myasthenic syndrome the presence of a small-cell lung cancer confers a poor neurological prognosis; however, in anti-NMDA-receptor encephalitis, detection of teratoma is a good prognostic factor, probably because this tumour is curable.

Anti-NMDA-receptor encephalitis represents a new category of immune-mediated disorder that is often paraneoplastic, treatable, and can be diagnosed serologically. Future studies should clarify the best type and duration of immunotherapy, the role of prodromal events in triggering the immune response, and the molecular mechanisms involved in decreasing the number of NMDA receptors.

Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies

Patients who received cognitive enhancement therapy demonstrated significantly greater preservation of gray matter volume over 2 years in the left hippocampus, parahippocampal gyrus, and fusiform gyrus, and significantly greater gray matter increases in the left amygdala (all corrected P < .04) compared with those who received enriched supportive therapy. Less gray matter loss in the left parahippocampal and fusiform gyrus and greater gray matter increases in the left amygdala were significantly related to improved cognition and mediated the beneficial cognitive effects of cognitive enhancement therapy.

Neuroprotective Effects of Cognitive Enhancement Therapy Against Gray Matter Loss in Early Schizophrenia

Механизмы действия галлюциногенов

The Neuropharmacology of Hallucinogens

Ассоциация между симптомами депрессии и сезонной аллергией на пыльцу

Partam Manalai, M.D., of the Mood and Anxiety Program in the University of Maryland Psychiatry Department and colleagues identified an association between allergy related to seasonal pollen exposure and depressive mood symptoms during the peak pollen season.

Among the 100 recruited study participants with a prior diagnosis of either major depressive disorder or bipolar disorder, approximately half had positive allergen-specific immunoglobulin E (IgE) in blood samples, indicating an allergic reaction to airborne pollen. Their allergy symptoms were measured with the Allergy Symptom Severity Assessment (ASSA) scale, and their mood symptoms were assessed using the questionnaire Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorders Version (SIGH-SAD).

After controlling for various confounding factors with multiple regression analysis, the researchers found that the participants' score change in the typical depression portion of the SIGH-SAD was statistically associated with worse ASSA score (p=0.008), and the change in the atypical depression portion of the SIGH-SAD was associated with IgE positivity (p=0.033). “The relationship between … [the] allergen-specific IgE and changes in mood supports a biological … mediation of the association between allergy and depression,” the authors wrote.

psychiatryonline.org

Аспирин

If aspirin may be able to reduce schizophrenia symptoms, how might it do so? By correcting an imbalance in the production of pro-inflammatory and antiinflammatory cytokines by helper T cells, the researchers proposed. Other researchers have implicated such an imbalance in schizophrenia.

Aspirin Regimen May Help Counter Schizophrenia Symptoms

Лекарства снижающие уровень холестерина и депрессия

The scientists turned to the statin medication mevastatin to find out.

In lab tests using human serotonin receptors expressed in animal cells, they showed that long-term use of the drug caused significant changes in the structure and function of serotonin cell receptors.

Adding cholesterol to cells treated with mevastatin restored them to normal.

The results represent the first report describing the effect of long-term cholesterol depletion on this type of cell receptor and suggest that chronic, low cholesterol levels in the brain might trigger anxiety and depression, the scientists say.

Link Between Cholesterol Drug and Depression

Полиморфизм гена DRD2 и эффективность антипсихотической терапии

The DRD2 genetic variation is associated with clinical response to antipsychotic drug treatment. These data may provide proof-of-principle for pharmacogenetic studies in schizophrenia.

D2 Receptor Genetic Variation and Clinical Response to Antipsychotic Drug Treatment: A Meta-Analysis

Литий vs флуоксетин в профилактике депрессивных фаз при БАР

These findings suggest that long-term fluoxetine monotherapy may provide superior relapse-prevention benefit relative to lithium monotherapy after recovery from bipolar II major depressive episode without an increase in hypomanic mood conversion episodes.

Efficacy and Safety of Long-Term Fluoxetine Versus Lithium Monotherapy of Bipolar II Disorder: A Randomized, Double-Blind, Placebo-Substitution Study

Прегабалин: злоупотребление, зависимость, синдром отмены

Pregabalin is a GABA-analog that selectively binds to the alpha2 delta subunit of voltage-gated calcium channels. It inhibits the release of excitatory neurotransmitters and increases neuronal GABA levels. Like some other compounds that modulate GABA-ergic neurotransmission, pregabalin might have a potential for abuse. Our patient had a history of drug addiction, which may be important in the reward effect of pregabalin. We therefore recommend being especially cautious when using pregabalin to treat patients with a history of drug or alcohol dependence.

Pregabalin Abuse, Dependence, and Withdrawal: A Case Report

Pittenger C, Desan PH: Gabapentin abuse, and delirium tremens upon gabapentin withdrawal. J Clin Psychiatry 2007

Vicctorio-Vigneau C, Guerlais M, Jolliet P: Abuse, dependency and withdrawal with gabapentin: a first case report