Агрессивность может быть связана со снижением функции дофаминергической системы

The neurobiology of aggression is not well understood, but scientists are aware of a relationship between the neurotransmitter serotonin and certain aggressive behaviors. The objective of this study was to explore whether higher levels of another brain chemical called dopamine, involved in pleasure and reward, increased aggressive response in its subjects. To scientists' surprise, it was not as they first theorized.

"The results of this study were astonishingly opposite of what was previously hypothesized," says Ingo Vernaleken, M.D., lead author of the study and research scientist for the department of psychiatry at RWTH Aachen University in Aachen, Germany. "Subjects with more functional dopaminergic reward-systems were not more aggressive in competitive situations and could concentrate even more on the game. Subjects with lower dopaminergic capacity were more likely to be distracted by the cheating behavior."

Molecular Imaging Finds Link Between Low Dopamine Levels and Aggression

Неотложные состояния при аффективных расстройствах

Pharmacological treatments for bipolar disorder can cause or compound patients' behavioral disturbances. Treatment with antipsychotics can increase the risk of agitation or aggression by causing akathisia, which can be associated with severe exacerbation of symptoms or even suicide attempts. The risk of akathisia is reduced but not eliminated by the use of atypical antipsychotics. Antidepressant agents can cause activation or mood destabilization, and some of these agents have been reported to cause akathisia.

Principles of treatment

A treatment strategy for impulsivity or aggression requires knowledge about possible interacting causes of the behavioral disturbance, its course, and its context. This information is helpful in formulating initial treatment and is even more helpful in developing a long-term strategy that will, if successful, reduce the patient's need for future emergency care.

Factors that influence treatment of pathological impulsivity and aggression include:

* Degree of premeditation versus degree of impulsiveness.
* Role of nonpsychiatric conditions (drug toxicity, drug withdrawal, delirium, dementia, infection, metabolic abnormality).
* Relationship to a DSM-IV Axis I psychiatric disorder.
* Relationship to a personality disorder.
* Course (acute/fluctuating versus chronic).
* Presence of prominent overstimulation.
* Environmental context (legal, relationship, and/or economic problems or changes).
* Personal context (personality characteristics, conflicts).

Candidate mechanisms of treatment for impulsive aggression or agitation include:

* Enhancing an inhibitory system, such as serotonin or GABA.
* Inhibiting an activating system, such as dopamine.
* Stabilizing fluctuations in inhibitory and/or excitatory systems.
* Protecting against overstimulation or normalizing arousal.

Psychiatric Emergencies in Bipolar and Related Disorders

Самоповреждения, эмоции, brain imaging

Why Self-Harm Feels Good in the Brain

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

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

Низкий уровень гликогена может объяснить, почему некоторые люди всегда очередь агрессивны и склонны к насилию, когда напиваются. К такому выводу пришли финские исследователи.
Найден виновник агрессии алкоголиков