What are depressive states and how do they differ?
Types of depressive disorders
Currently, the classification of depressive disorders is aimed at highlighting the nature of their course and syndromological representation. According to the etiological principle or origin, depressive disorders are divided into three large groups: psychogenic, somatogenic and endogenous.
Short information about depressive disorders
The formation of psychogenic depression is the response of the psyche to various psycho-traumatic influences. In particular, the basis of depressive reactions can be found long or short-term exposure to psychosocial stressors, impaired interpersonal relationships, and professional conflicts.
Somatogenic depressions (secondary, symptomatic) occur against the background of organic brain damage (traumatic brain injury, inflammatory processes), post-intoxication conditions (alcoholic, neurotoxic intoxication), various types of somatic pathology (arterial hypertension, atherosclerosis, etc.).
The etiology of endogenous depression is complex and has not yet been fully elucidated. Unipolar and bipolar psychotic affective disorders (conditions in the past classified as manic-depressive psychosis), chronic mood disorders (dysthymia, cyclothymia, involutional melancholia) are polygenic multifactorial affective disorders, the so-called predisposition diseases. In their occurrence, the genetic factor is of great importance. Anomalies of the subcortical systems of regulation of the autonomic-endocrine processes of the body, which reduce the adaptive capabilities of a person, are hereditarily transmitted. Recent studies also indicate the presence of a genetic predisposition of the functional systems of the brain to increased susceptibility to emotional stress. An inadequate pathological response of the body to changes in the external environment is due to genetic disorders in neurotransmitter functioning.
Unlike other types of endogenous mental illness, in particular schizophrenia, the manifestation of affective disorders is largely promoted by external factors, primarily traumatic situations, for example, a sudden "breaking" of the patient's life stereotypes.
Clinical picture of depressive states
Currently, there are two main clinical groups of depression: simple and complex depression. Simple depressions include six main syndromic types: melancholic, anxious, anesthetic, adynamic, apathetic, and dysphoric. In the structure of complex depressions, there are senesto-hypochondriac syndrome, as well as a depressive syndrome with inclusions of delirium, hallucinations, and catatonic disorders.
The clinical picture of depressive syndrome is characterized by the main triad of symptoms that have been known for many years: bad, depressed mood, ideational and motor inhibition. Oppressive hopeless melancholy is noted, experienced as mental pain, general painful sensations (vital depression), sleep disorders, daily fluctuations in the state with worsening in the morning. The present and the future are perceived in a dark colors. Ideas of self-accusation, self-deprecation, and suicidal thoughts arise. This is a picture of a typical melancholy or melancholic depression, reaching the degree of affective psychosis.
The most characteristic somatic manifestation of endogenous depression is the triad: mydriasis (dilation of the pupil of the eye), tachycardia, constipation. Possible menstrual irregularities (amenorrhea, i.e. lack of menstruation), the occurrence of a diabetes-like syndrome with a characteristic sugar curve.
However, the classic version of depression is encountered in clinical practice less and less frequently and is inherent, as a rule, in affective psychoses, which are treated mainly by psychiatrists. In the case when the depth of depression is not so great and does not go beyond the borderline (neurotic) state, psychiatrists talk about reduced depression. And patients with such disorders turn to psychotherapists first of all. In this case, the patient notes depressed mood, joylessness, decreased intelligence and ability to work, predominance of physical exhaustion and increased fatigue, narrowing of the range of interests and drives, decreased libido. During the day, sadness, physical weakness and loss of appetite are most pronounced in the morning hours with relief in the evening. Falling asleep, as a rule, is not disturbed, drowsiness is possible during the day.
The diagnostic structure of a depressive disorder depends on the predominance of melancholy, anxiety or apathy in its clinical picture. This determines the variant of the depressive syndrome. Depending on this, melancholic, anxious and apathetic depression are distinguished.
Anxiety depression in any period of life can occur as an independent syndrome, but as a symptom it often prevails in the structure of depression in old and old age, pushing aside the dreary/melancholic component in these cases. Anxiety is manifested in the clinical picture of depression by a feeling of inner tension, stiffness, expectation of an indefinite but constant threat, unhappiness in the future. The patient's mood is characterized as depressed, many tend to call their state "melancholy", but the doctor must differentiate "melancholy" from "anxiety."
Anxious depression differs from the melancholic depression by the tendency to unfocused motor restlessness and obsessive repetition of the same unpleasant thoughts. Facial expression can be anxious and confused, speech is speeded up, statements are fragmentary and short, repetition of the same questions, exclamations, rubbing movements is typical. The circadian distribution of anxiety is different from melancholic. Anxious mood intensifies in the afternoon. Difficulty falling asleep is characteristic. Sleep, as a rule, is superficial, with its deepening in the morning hours.
Apathetic depression is characterized by feelings of indifference, boredom, lack of initiative, desire, desire to act, often accompanied by a painful feeling of insensibility, emotional emptiness and indifference. As a rule, such a patient is lethargic during the day, lack of initiative, unhurried, prefers to spend time in bed and lead a "vegetative" lifestyle. Unproductive and unfocused thinking are common.
The variants of depression described above relate mainly to clinically completed conditions that are easily diagnosed by specialists. In practice, one often has to deal with undeveloped, reduced, "masked" depression, which is the most difficult to diagnose and treat.
The name of masked depression is due to the fact that depressive symptoms are hidden under the "mask" of a polymorphic clinical picture.
The main "nuclear" symptoms of masked depression are: many blurred depressive symptoms, mood shifts, a sense of hopelessness in the form of a sense of the meaninglessness of life, pessimism about the future; frequency, seasonality of somatopsychic disorders (more often in spring or autumn); daily mood swings with improvement in the evening, sleep disturbances, tendency to ruminate, indecision, inability to feel pleasure in normally pleasurable activities, decreased professional interests, deterioration of contact with people, decreased intense drives (food, sexual), unmotivated anxiety, lack of effect from somatotropic therapy with a positive reaction to antidepressants.
Masked depression is distinguished by the presence of multiple, recurring and often modifying symptoms that occur over a number of years. Such patients are traditionally considered "difficult", poorly manageable patients. They are treated for a long time and to no avail, often undergo various examinations, sometimes they endure repeated surgical operations that do not bring relief.
When carrying out the differential diagnosis of depression, it is necessary to remember that their symptoms can be combined or secondary to physical disease. In particular, secondary depressive reactions can occur in chronic pulmonary, gastrointestinal, neurological and, especially, oncological diseases. It is characteristic that in this state, painful sensations and their hypochondriacal manifestations, i.e. suspecting pathology in oneself, are significantly enhanced. Seasonal exacerbations of gastritis, stomach ulcers or duodenal ulcers can be combined with dreary asthenic reactions of the psyche. Arterial hypertension is more often observed in anxiously-responsible, punctual persons, and at the active stage of the course of the underlying disease, an anxious response becomes a pronounced symptom. After a myocardial infarction, periods of anxiety and panic mood (fear of a repetition of a cardiac catastrophe) and secondary depression can be observed. These mental "layers", as a rule, aggravate the course of the underlying disease, create a difficult environment in the family, and prevent the return to professional activity.
Treatment of different types of depression
Treatment of depressive disorders primarily includes psychopharmacotherapy, in particular the use of antidepressants.
The choice of psychopharmacological drugs is based on the identification of the leading clinical symptoms, an understanding of the pathogenetic mechanisms of the formation of depression and should also take into account the age, sex and somatic state of the patient.
The adequacy of therapy depends on the correct definition of the "target symptom", genesis and severity of the depressive state.
Possible errors in the treatment of depression are caused by the wrong choice of the drug, too small doses of antidepressants or their slow build-up, when addiction sets in faster than the therapeutic effect; unreasonably fast change of drugs in the absence of a therapeutic effect (the "therapeutic" concentration of most antidepressants in the blood when taken orally is achieved on the 10-14th day of treatment); an irrational combination of several antidepressants, especially in insufficient doses.
Antidepressants are the main group of psychopharmacological drugs used in the treatment of depressive disorders. To achieve a therapeutic effect, it is necessary to select an individual dose in the shortest possible time, which is capable of causing an antidepressant effect without pronounced side effects. A steady trend towards improvement in the first two to three weeks of therapy indicates an adequate choice of the drug and its dosage. The following target “target symptoms” of depression are distinguished: dreary depression, anxious agitation, fear, apatho-adynamic state, psychosomatic and vegetative manifestations.
According to the mechanism of pharmacological action, modern antidepressants are divided into drugs that potentiate the effect of monoamines on the central nervous system, and MAO inhibitors.
The drugs that potentiate the action of monoamines include the heterocyclic antidepressants, which are currently most common in psychiatric practice. In turn, tricyclic antidepressants are subdivided into drugs that are tertiary (Imipramine, amitriptyline, trimipramine, doxepin) or secondary (desipramine, nortriptyline, protriptyline) amines.
Potentiation of the action of monoamines in the central nervous system of heterocyclic antidepressants is achieved due to the inhibitory effect on the reuptake system of norepinephrine, serotonin and / or dopamine in the presynaptic nerve endings of the brain, which contributes to their accumulation in the synaptic cleft, activation of postsynaptic adrenergic receptors and stimulation of neurotransmitter structure in neurotransmission. The consequence of this is an increase in serotonin concentration, stimulation of 5-HT receptors, which is one of the essential points in the mechanism of antidepressant action of tricyclic compounds.
MAO inhibitors are compounds of various chemical structures (with varying degrees of selectivity and reversibility) that inhibit the activity of monoamine oxidase, an enzyme that catalyzes the oxidative deamination of monoamines (mainly norepinephrine in the subcellular structures of the brain), and, accordingly, increasing their effective concentration in the area of sensitive synapses. MAO inhibitors are considered more toxic drugs compared to heterocyclic antidepressants, but they nevertheless have a pronounced therapeutic effect, especially in "atypical" depression, and do not cause drug dependence. The irreversible MAO inhibitors include nialamide, a first generation MAO inhibitor chemically similar to iproniazide. Reversible MAO inhibitors are pyrazidol, tetrindol, incazan, befol, moclobemide. Most of these antidepressants are nonselective inhibitors of monoamine oxidases A and B, increasing the content of monoamines of various chemical nature (norepinephrine, adrenaline, dopamine, serotonin, tyramine, phenylatilamine) in the brain and the level of their physiological activity.
The neurochemical basis of the mechanism of action on the central nervous system of various subclasses of antidepressants is an increase in the level of monoaminergic transmission in the brain, which is achieved due to an increase in the synaptic concentration of norepinephrine and / or serotonin. Depending on the predominant effect on the metabolism of a particular monoamine and on the relatively selective activation of the corresponding receptor zone of the brain nuclei, various antidepressants, in addition to the thymoleptic effect proper, have different effects on the manifestations of other mental functions (in particular, on the level of excitability of the brain).
So, antidepressants - MAO inhibitors - are characterized by a pronounced psychostimulant effect, while antidepressants - monoamine reuptake inhibitors in different ways affect the excitability of the central nervous system: amitriptyline, azafen, fluoroacizine, maprotiline, in addition to thymoleptic, also have a sedative effect, and Imipramine.
Post is made based on the information provided by:Christopher Ames, MD, pshychiatrist, Medibank, Sydney, New South Wales, Australia
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