Vegetative Disorders and Depression
At a general practitioner appointment, patients with depressive syndromes make up more than 30%. This figure is probably even higher for neurological practice. It should be borne in mind that patients who are actively complaining of a decreased mood, depression, depression, lack of interest in life, usually do not go to a therapist or a neurologist, but turn to a psychiatrist in a clinic or in a neuropsychiatric clinic. At an appointment with an internist, patients complain primarily about somatovegetative disorders. It is known how difficult the diagnosis and treatment of persistent cardialgia, prolonged and “inexplicable” hyperthermia, constant shortness of breath, persistent sensation of nausea, debilitating sweating, dizziness, dramatic and frightening patients with vegetative paroxysms or, in modern terminology, “panic attacks” (PA) and .d. As a rule, with active and targeted questioning in these patients, it is possible to identify sleep disturbances, appetite, weight loss, decreased libido, constant weakness, fatigue, decreased interest in the environment and other symptoms that indicate the presence of depressive disorders. Subclinical manifestations of depression in such patients also led to the corresponding terminology: “hidden”, “masked”, “larvated”, “atypical”, “alexithymic”, “depression without depression”.
It is known that autonomic disorders of central genesis or psycho-vegetative syndromes can manifest themselves in the form of both paroxysmal and permanent disorders [1].
Paroxysmal autonomic disorders
Vegetative crisis (VK), or PA, is the most striking and dramatic paroxysmal manifestation of the psycho-vegetative syndrome.
Terminology
The name “vegetative crisis”, traditional for domestic medicine, emphasizes that vegetative symptoms are of primary importance in an attack. In foreign medicine, especially in English, the leading role in autonomic paroxysm is given to emotional-affective disorders (fear, anxiety), which accordingly is reflected in the terms used – “anxiety attacks”, “panic attacks”.
Diagnostic criteria
The term Panic Attack has gained worldwide recognition today due to the classification of diseases proposed by the American Psychiatric Association in 1980 (DSM-III). According to the latter, PAs are the main manifestation of Panic Disorders (PR). Subsequently, this classification was refined and is currently in its latest version – DSM-IV – and in the International Classification of Diseases – ICD-10 [2, 3] – the following criteria for the diagnosis of PR are adopted.
A. Recurrence of seizures in which intense fear or discomfort in combination with four or more of the following symptoms develop suddenly and reach their peak within 10 minutes:
– pulsations, palpitations, rapid pulse;
– sweating;
– chills, tremors;
– feeling of lack of air, shortness of breath;
– difficulty breathing, choking;
– pain or discomfort in the left half of the chest;
– nausea or abdominal discomfort;
– dizziness, instability;
– weakness, lightheadedness, fainting state;
– a feeling of numbness or tingling (paresthesia);
– waves of heat and cold;
– a feeling of derealization, depersonalization;
– fear of death;
– fear of losing your mind or committing an uncontrolled act.
B. The occurrence of PA is not due to the direct physiological effect of any substances (for example, drug dependence or taking drugs) or somatic diseases (for example, thyrotoxicosis).
B. In most cases, PA does not occur as a result of other anxiety disorders, such as Phobias – Social and Simple, Obsessive-Phobic Disorders, and Post-Traumatic Stress Disorders.
ICD-10 PR includes rubrics of “anxiety” and “phobic” disorders, which in turn are included in the class of “Neurotic, stress-related and somatoform disorders”.
Epidemiology
According to statistics, from 1.5 to 4% of the adult population suffer from PR during certain periods of their lives. Among those seeking primary care, patients with PA make up 6%. The disease makes its debut most often at the age of 20-30 years and is extremely rare before 15 and after 65 years. Women suffer 2–3 times more often than men [4].
The main clinical manifestations
The criteria necessary for the diagnosis of PA can be summarized as follows:
– paroxysmality;
– polysystemic autonomic symptoms;
– emotional and affective disorders.
Obviously, the main manifestations of PA are autonomic and emotional disorders. Already from the above list of symptoms, it is evident that autonomic symptoms affect various body systems: these are respiratory, cardiac, vascular reactions (central and peripheral), changes in thermoregulation, sweating, gastrointestinal and vestibular functions. An objective examination, as a rule, reveals a rise in blood pressure (sometimes to high values and more often during the first attacks), severe tachycardia, often an increase in extrasystoles, and there may be a rise in temperature to a subfebrile or febrile level. All these symptoms, arising suddenly and “without reason,” contribute to the appearance and fixation of another group of symptoms – emotional-affective disorders. The range of the latter is unusually wide. So, a sense of causeless fear, reaching the point of panic, usually occurs during the first attack, and then in a less pronounced form is repeated in subsequent attacks. Sometimes the panic of the first PA subsequently transforms into specific fears – fear of myocardial infarction, stroke, loss of consciousness, fall, madness, etc. In some patients, the intensity of fear (even in the first attacks) may be minimal, but nevertheless, with careful questioning, patients report a feeling of internal tension, anxiety, anxiety, a feeling that “something will explode inside.” In neurological and therapeutic practice, the emotional manifestations of an attack can differ significantly from a typical situation. So, in an attack, the patient may not experience fear, anxiety; it is no coincidence that such PAs are called “panic without panic” or “non-insurance PAs” [5]. Some patients experience a feeling of irritation in the attack, sometimes reaching a degree of aggression, in some cases – a feeling of melancholy, depression, hopelessness, report a “causeless” cry at the time of the attack. It is the emotional-affective symptoms that give the attack such an unpleasant and even repulsive character.
In a large category of PR patients, the structure of the attack is not limited to the autonomic-emotional symptoms described above, and then the doctor can detect another type of disorder, which we arbitrarily called “atypical”. They can be represented by local or diffuse pains (headaches, pains in the abdomen, in the spine, etc.), muscle tension, vomiting, senestopathic sensations (sensation of heat, “frostbite”, “stirring”, “transfusion” of something , “Voids”) and (or) psychogenic (hysterical) neurological symptoms (sensation of “coma in the throat”, weakness in the arm or leg, impaired speech or voice, consciousness, etc.) [6].
In the interictal period, patients usually develop secondary psycho-vegetative syndromes, the structure of which is largely determined by the nature of paroxysm. In patients with PA, the so-called agoraphobic syndrome develops soon after the onset of paroxysms. “Agoraphobia” literally means “fear of open spaces,” but in the case of panic patients, fear applies to any situation that is potentially “threatened” for the development of an attack. Such situations may be staying in a crowd, in a store, on the subway or any other form of transport, moving away from home for some distance or staying at home alone, etc. Agoraphobia determines the appropriate behavior that avoids discomfort: patients stop using transport, do not stay alone at home, do not move far from home and ultimately become almost completely socially disabled.
The fears of patients with PA can relate to a certain disease with which, according to the patient, his symptoms are associated with him: for example, fear of a heart attack, stroke, etc. Obsessive fears force the patient to constantly measure the pulse, check blood pressure, do repeated electrocardiograms and even study the relevant medical literature. In such cases, we are talking about the development of obsessive fears or hypochondriac syndrome.
As secondary syndromes, depressive disorders often develop, manifested by a decrease in social activity, interest in the outside world, increased fatigue, constant weakness, decreased appetite, sleep disturbances, and sexual motivations. In patients with demonstrative seizures, as a rule, hysterical personality disorders with clinical manifestations of hysteria in the somatic or neurological sphere are revealed.
Permanent vegetative disorders
By permanent autonomic disorders are meant subjective and objectively recorded violations of autonomic functions that are permanent or occur sporadically and are not combined with autonomic paroxysms (panic attacks). These disorders can occur predominantly in one system or have a distinct polysystemic character. Permanent autonomic disorders can be manifested by the following syndromes:
– in the cardiovascular system – cardiorhythmic, cardialgic, cardiosenestopathic, as well as arterial hyper- and hypotension or amphotonia;
– in the respiratory system – hyperventilation disorders: a feeling of lack of air, shortness of breath, feeling of suffocation, shortness of breath, etc .;
– in the gastrointestinal system – dyspeptic disorders, nausea, vomiting, dry mouth, belching, abdominal pains, dyskinetic phenomena, constipation, diarrhea;
– in thermoregulatory and sweating systems – non-infectious subfebrile condition, periodic “chills”, diffuse or local hyperhidrosis, etc .;
– in vascular regulation – by distal acrocyanosis and hypothermia, Raynaud’s phenomenon, vascular cephalalgia, lipothymic states, waves of heat and cold;
– in the vestibular system – unsystematic dizziness, sensations of instability.
Vegetative Disorders and Depression
There is an extensive literature on the relationship of depression and anxiety. This problem is also relevant for PR, since a combination of PR and depression is possible.
When examining a patient suffering from PR, the doctor should be wary of possible endogenous depression, since the risk of suicidal actions requires immediate intervention by a psychiatrist.
According to modern criteria, depression is characterized by a decrease in mood, a decrease or lack of interest or pleasure, combined with a decrease in appetite or an increase in body weight, a decrease or increase in body weight, insomnia or hypersomnia, psychomotor inhibition or agitation, a feeling of fatigue or loss of energy, a sense of worthlessness, inadequate feeling guilt, diminished ability to think or concentrate, and repeated thoughts of death or suicide.
For the clinician, the question of the nature of depression is important – is it primary or secondary? To resolve this issue, two diagnostic criteria are important: the time factor and the severity of depressive symptoms. R. Jacob et al. [7] suggest using both criteria and establish which of the disorders occurs without the other in the patient’s history. If episodes of depression appeared before PR, and PA only appeared during the period of depression, then PR are secondary to depression. If depression appears only in the presence of PR and, as a rule, at a certain stage of their development, then, most likely, we are talking about primary PR and secondary depression.
It was shown that patients with depression with PA had a longer course, often had an endogenous, agitated type and had a worse prognosis, i.e. their depression was more severe.
It is believed that secondary depression is often found in PR. The following pattern of PR dynamics is considered typical: panic attacks – agoraphobia – hypochondria – secondary depression. In a study by A. Breier [4] of 60 patients with AF with PR, depression was detected in 70%, and in 57% of cases it occurred after the first PA. According to some reports, secondary depressive fouling is observed in 70 – 90% of cases with prolonged existence of PR [8].
Since in primary depression, especially its severe (acute) forms, the risk of suicide is high, and the use of psychotherapy is difficult, differential diagnosis of PR and depression with PA is necessary. If you suspect a primary depression, it is necessary to focus on weight loss, severe impaired concentration of attention and sleep disorders, gross motivational disorders. Secondary depressions have a milder course and usually regress with relief of PR.
Currently, the pathogenetic relationship between PR and depression is being actively discussed, the reason for this is the frequent combination of PR and depression and the obvious effectiveness in both cases of antidepressant drugs. However, a number of facts refute the assumption of a single disease: these are primarily various effects when exposed to biological markers. So, sleep deprivation improves the condition of patients with major depression and worsens with PR; the dexamethasone test is positive in the first case and negative in the second, the administration of lactic acid naturally causes PA in patients with PR or in patients with depression in combination with PR, but not in patients suffering only major depression. Thus, discussing the combination of PR with major depression, it can be assumed that the presence of depression is a factor contributing to the manifestation of PR, although the mechanisms of this interaction are still unclear.
Permanent autonomic disorders also occur in the structure of various affective and emotional-psychopathological syndromes. In most cases, we are talking about depressive disorders (masked, somatized and other variants) or mixed syndromes, among which anxiety-depressive, depressive-hypochondriacal and hysterodressive disorders dominate. According to A.B. Smulevich et al. [9], hysterical depression is one of the most common psychogenic reactions, accompanied by severe somatovegetative and hysterical neurological symptoms. Most often, such manifestations of the disease are observed in the menopause.
Therapy for psycho-vegetative disorders
Currently, in the treatment of vegetative syndromes of both paroxysmal and permanent nature, the following groups of drugs are used:
– antidepressants (BP);
– tranquilizers (typical and atypical benzodiazepines – ABD);
– small antipsychotics (MN);
– vegetotropic drugs.
It has already been proved with the help of many controlled (double-blind, placebo-controlled) studies that the basic drugs in the treatment of autonomic disorders are blood pressure, which are used as monotherapy or in combination with other drugs [10]. It should be emphasized that blood pressure therapy is indicated not only when autonomic disorders are a manifestation of depression, including masked, but also when autonomic disorders (permanent and paroxysmal) occur within the framework of anxiety and anxiety-phobic disorders, even if obvious depression is not detected (for example , PR with agoraphobia), in cases of mixed anxiety-depressive and hysterically depressive (a combination of somatoform and depressive) disorders. This situation reflects current trends in psychopharmacotherapy, where blood pressure takes the leading place, and tranquilizers (mainly typical benzodiazepines) are given the role of symptomatic, supportive, corrective therapy. The exception is ADB (alprazolam and clonazepam), which in some cases can also be used as basic pharmacotherapy. Antipsychotics are used as additional drugs if combination therapy is needed. Vegetotropic drugs (adrenergic blockers, vestibulolytics, etc.) are usually administered as symptomatic therapy or to correct the side effects of blood pressure.
It should be noted that the use of any psychotropic drugs should be combined with vegetotropic therapy, especially if the applied drug in addition has mechanisms of cellular neurotropic effects (neurometabolic cerebroprotection). In particular, the appointment of vinpocetine (cavinton) allows, due to these effects, significantly improve treatment results.
Pharmacotherapy of patients with paroxysmal and permanent psycho-vegetative disorders involves several therapeutic strategies: relief of attacks (PA); prevention of recurrence of paroxysms; relief of permanent psycho-vegetative syndromes.
PA stopping
The tranquilizers of the benzodiazepine group (relanium, tazepam, phenazepam, xanax, etc.) are the most effective means for stopping PA. However, with this symptomatic method of treatment, the dose of the drug has to be increased over time, and the irregular intake of benzodiazepines and the associated recoil phenomenon can contribute to increased PA, progression and chronicity of the disease.
PA re-occurrence prevention
Numerous double-blind, placebo-controlled studies have convincingly shown that two groups of drugs — AD and ABD — are most effective in preventing PA. [10-12]
Today, the range of ADs effective against PR has expanded significantly and includes at least 5 groups of drugs: tricyclic antidepressants – imipramine (melipramine), amitriptyline (tryptisol, nortriptyline), clomipramine (anafranil, gidifen); four-cyclic antidepressants – mianserin (miansan, lerivon); monoamine oxidase inhibitors – moclobemide (aurorix); antidepressants with an insufficiently known mechanism of action – tianeptine (coaxil, stablon); selective serotonin reuptake inhibitors (SSRIs) – fluoxetine, fluvoxamine (avoxin), sertraline (zoloft), paroxetine (paxil), citalopram (cipramil).
Significant interest is the last antidepressant from this group – citalopram. High selectivity of the drug and low potential for interactions, a favorable profile of side effects, coupled with high efficiency, allow cipramil to be considered as the drug of choice for many depressive conditions, in particular, in general somatic and gerontological practice. The presence of citalopram, along with timoleptic, also has a clear anxiolytic effect indicates the possibility of using citalopram for anxiety disorders and, in particular, for panic attacks. Currently, two Russian clinics have already begun studying the effectiveness of citalopram in panic disorders.
The most likely theory is that which links the anti-panic effectiveness of blood pressure with a predominant effect on the serotonergic systems of the brain. A positive effect can be achieved by using small daily doses of drugs. However, when using blood pressure, especially tricyclic, in the first decade of treatment, exacerbation of symptoms can be observed – anxiety, anxiety, agitation, and sometimes an increase in PA. Adverse reactions to tricyclic blood pressure are largely associated with anticholinergic effects and can be manifested by severe tachycardia, extrasystole, dry mouth, dizziness, tremor, constipation, weight gain. The above symptoms can lead to forced refusal of treatment at the first stages, especially since the clinical effect usually occurs 2 to 3 weeks after the start of therapy. Significantly fewer adverse reactions are observed when using drugs of the SSRI group. Their best tolerance, the possibility of a single daily intake and the painlessness of rapid withdrawal at the end of treatment made these drugs leaders in the treatment of PR.
Atypical benzodiazepines include clonazepam (antelepsin, rivotril) and alprazolam (xanax, cassadan). It has been shown that benzodiazepines (both typical and atypical) enhance the action of GABA (g-aminobutyric acid), which is the main inhibitory mediator in the central nervous system. A significant advantage of this group of drugs is the rapid appearance of the clinical effect (3 – 4 days). There is evidence that in high doses (6-8 mg) alprazolam has an antidepressant effect.
The choice of drug is determined mainly by the clinical picture of the disease and the characteristics of the drug. If PA appeared recently and there is no agoraphobic syndrome, then it is advisable to start therapy with ABD. If PA are combined with agoraphobia or other secondary syndromes (depression, phobic syndrome, hypochondria), then the use of blood pressure is necessary. First of all, it is recommended to use blood pressure with minimal side effects. In some cases, the combined use of AD and ABD is required, since ABD, firstly, provides an early clinical effect (almost as early as in the 1st week of treatment), and secondly, helps to stop PA before the onset of AD.
Treatment of permanent psycho-vegetative disorders
When choosing tactics for the treatment of permanent psycho-vegetative disorders, they proceed primarily from the nature of the emotional-psychopathological syndrome. In the case of depressive disorders, the main, and often the only, drugs are blood pressure. SSRIs are currently preferred. When depression is combined with other syndromes, combined therapy is used – a combination of blood pressure with tranquilizers (ABD) or small antipsychotics: meleryl (sonapax), teralen, neuleptyl, eglonil, chlorprotixen, etaperazine.
An individual selection of pharmacological preparations, the use of small doses, and, if necessary, a combination with cognitive-behavioral psychotherapy and social adaptation allow us today to successfully cope with such widespread and socially maladaptive suffering as psycho-vegetative syndromes.