Akarachkova E.S., Vershinina S.V.

For many years in Russia and the CIS countries the term “vegetative dystonia syndrome” has been actively used to designate a number of patients; (SVD), by which most practitioners understand psychogenically caused multisystem autonomic disorders. It is the psychovegetative syndrome that is defined as the most common variant of SVD, behind which there are anxiety, depression, and adaptation disorders. In such cases, we are talking about somatized forms of psychopathology, when patients consider themselves to be somatically ill and turn to doctors of therapeutic specialties. According to the results of a survey of 206 neurologists and therapists in Russia, 97% of respondents use the diagnosis of “SVD” in their practice, of which 64% use it constantly and often. In more than 70% of cases, SVD is included in the main diagnosis under the heading of somatic nosology G90.9 - disorder of the autonomic nervous system, unspecified or G90.8 - other disorders of the autonomic nervous system.

At the same time, epidemiological studies demonstrate the high prevalence of depressive disorders among primary care patients, but they are often ignored by general practitioners. According to the Russian epidemiological program COMPASS (2004), the prevalence of depressive disorders in general medical practice ranges from 24 to 64%. The researchers emphasize that the identified high prevalence of depressive spectrum disorders (45.9%) and depressive conditions (23.8%) among patients of the general medical network requires widespread implementation of screening procedures for affective (depressive) disorders in the work of institutions of the general medical health care network. However, according to another large-scale Russian study, SAIL, conducted two years later, the diagnosis of depressive conditions in general medical practice is actually not carried out, which is associated not only with the existing system of organizing care, when there are no clear diagnostic criteria for indicating manifestations of non-somatic origin (and this leads to subsequent difficulties in explaining symptoms), but also with the impossibility of applying psychiatric diagnoses by general practitioners.

According to RAMS academician, prof. A.B. Smulevich, an important contribution is made by the underestimation by practicing physicians of the role of psychotraumatic situations, which, as was demonstrated in the SAIL study, occurred in 86.5% of patients during the year preceding the study.

It was also found that the diagnosis of depressive conditions is difficult due to the clinical features of depression, a significant part of which is of a so-called “masked” nature. In the majority of the examined patients, depression corresponds to a mild degree of severity, which is characterized by the erasure of the key diagnostic manifestations of hypothymia (melancholy, depression, etc.). At the same time, they are widely represented by various psycho-vegetative (somato-vegetative) symptoms, which are considered within the framework of common mental and somatic pathologies. These symptoms occurred in all patients in the studied sample. And some of them are increased fatigue, headaches, irritability, lethargy, loss of strength, decreased ability to work, deterioration of memory and attention, insomnia, dizziness, heart pain, back pain, palpitations, neck pain, sweating, joint pain, shortness of breath, pain in the legs, drowsiness, lack of air, abdominal pain, heart failure - noted in more than half of the patients. The researchers suggested that these symptoms were considered by general practitioners only as a manifestation of physical illness and were not associated with depression. It is the somatization of mental disorders in the clinic of internal medicine that makes a significant contribution to underdiagnosis, when, behind a multitude of somatic and vegetative complaints, it is difficult for a general practitioner to identify psychopathology, which is often subclinically expressed and does not fully satisfy the diagnostic criteria for a mental disorder, but leads to a significant decrease in the quality of life, professional and social activity and is widespread in the population. According to Russian and foreign researchers, about 50% of individuals in society have either threshold or subthreshold disorders.

According to foreign studies, up to 29% of patients in general somatic clinics have subthreshold manifestations of depression in the form of somatic symptoms that are difficult to explain by existing somatic diseases, and their identification is contested by numerous cross-sectional and syndromic diagnoses, which contributes to a negative iatrogenic effect in the form of a possible increase or exacerbation of somatovegetative complaints . In clinical practice, there are frequent situations when doctors react negatively to symptoms that they cannot explain from the perspective of organic pathology. The patient undergoes intensive examination. And if the results do not confirm the presence of a physical disease, doctors tend to underestimate the severity of symptoms (such as pain or disability). For their part, patients may perceive intensive medical diagnostics as persistent and sometimes even hostile towards them. In such cases, patients' expectations of medical advice may differ from those of the doctor. Along with this, somatized patients actively use medical terminology to describe their symptoms. They may be deeply convinced of their physical (somatic) origin, and also that the doctor is mistakenly assessing their sensory symptoms. It should be noted that the diagnostic label is very important for the patient and can either suit (if the diagnosis is perceived as confirmation of the reality of the problem), or offend the patient (if a “psychological” term is used). Given that it is very difficult for a general practitioner without experience to find differences, most researchers are of the opinion that psychiatric diagnoses should be made by mental health professionals. However, in practice, most of these patients are referred to those who have very limited psychiatric experience. As a result, the seriousness of the pathology is underestimated, which can lead to detrimental consequences in the form of a high risk of developing iatrogenic harm.

Thus, clinically significant depression is the most common psychiatric condition observed in the population in 20% of women and 10% of men. Among patients with chronic diseases, this percentage is much higher - from 15 to 60%. More than 40% of patients suffer from clinically significant depressive disorders, most of which can be classified as major depressive disorder (in ICD-10 this condition is classified as recurrent depressive disorder - F33). However, in the primary health care network there is still a contrast between the high comorbidity of depression and the burden of disease, on the one hand, and insufficient diagnosis and treatment of depression, on the other. Moreover, often “bodily” (somatic) symptoms of depression are associated with concomitant anxiety, which, in turn, further increases somatic and emotional distress and contributes to diagnostic difficulties. To date, sufficient evidence has been accumulated that anxiety disorders usually precede depression, increasing the risk of its development by approximately 3 times. It is known that in the first three decades of life there is a high risk of developing anxiety disorders, which, as a rule, are primary and lead to the development of secondary depression.

Anxiety disorders and depression are associated with a wide range of psycho-social disorders in the form of a negative impact on treatment, career, work productivity, partner and interpersonal interactions, quality of life, and suicidal behavior. It has been found that about 10% of depressive disorders can be prevented through successful early intervention for social phobia. If all anxiety disorders among 12–24 year olds were successfully treated, 43% of all depressive episodes in early adulthood could be prevented.

Despite the impossibility of general practitioners using psychiatric diagnoses, somatovegetative manifestations of depression in a large number of patients can be identified at the syndromic level in the form of psychovegetative syndrome. Such syndromic diagnosis includes:

1. Active identification of multisystem autonomic disorders.

2. Exclusion of somatic diseases based on the patient’s complaints.

3. Identification of the connection between the dynamics of the psychogenic situation and the appearance or worsening of vegetative symptoms.

4. Clarification of the nature of the course of autonomic disorders.

Active identification of mental symptoms accompanying autonomic dysfunction, such as reduced (sad) mood, anxiety or guilt, irritability, sensitivity and tearfulness, feelings of hopelessness, decreased interests, impaired concentration, as well as deterioration in the perception of new information, changes in appetite, feeling of constant fatigue , sleep disturbance.

It is important for the doctor to identify psychopathology and assess its severity. In the classical sense, depression is a mental disorder characterized by depressed mood (hypotymia) with a negative, pessimistic assessment of oneself, one’s situation in the present, past and future. Along with depression (in typical cases in the form of vital melancholy), depression includes ideational and motor inhibition with a decrease in motivation for activity or anxious arousal (up to agitation). Mental hyperalgesia (mental pain) characteristic of depressed patients is associated with feelings of guilt, decreased self-esteem, suicidal tendencies, and a painful physical feeling is associated with “somatic” symptoms (sleep disorders; a sharp decrease in appetite up to depressive anorexia with a decrease in body weight of 5% or more from the initial one for a month; decreased libido, menstrual irregularities up to amenorrhea; headaches; decreased salivation; dryness of the tongue and other mucous membranes and skin and other somatovegetative dysfunctions). Depressed mood persists throughout the entire depressive episode and is little subject to fluctuations depending on changes in the patient’s life circumstances. A typical sign of depression is also an altered circadian rhythm: improvement or (less often) worsening of well-being in the evening. The identification of depression is facilitated by clear diagnostic criteria. The main symptoms of depression according to ICD-10 include:

A decrease in mood, obvious in comparison with the patient’s normal norm, prevails almost every day and most of the day and lasts for at least 2 weeks, regardless of the situation;

A distinct decrease in interest or enjoyment in activities usually associated with positive emotions;

Decreased energy and increased fatigue.

Additional symptoms include:

Reduced ability to concentrate and pay attention;

Decreased self-esteem and feelings of self-doubt;

Ideas of guilt and self-deprecation;

Gloomy and pessimistic vision of the future;

Disturbed sleep;

Impaired appetite;

Excitement or inhibition of movements or speech;

Ideas or actions regarding self-harm or suicide;

Decreased sexual desire.

For a reliable diagnosis, the presence of any 2 main and 2 additional symptoms is sufficient. It is important that information about the presence of the listed criteria can be obtained primarily from answers to questions posed not in terms of the presence of specific symptoms (do you experience melancholy, depression, anxiety or indifference), but related to changes in general well-being, mood, lifestyle (not whether the joy of life has disappeared, whether tears are close, whether a pessimistic assessment of events has long prevailed) . Manifestations of ideomotor agitation or retardation, suicidal ideas or attempts, as well as decreased sexual desire indicate the presence of severe depression in the patient, which requires immediate assistance from a psychiatrist.

The success of treatment for depressive disorders depends on correct diagnosis and selection of adequate therapeutic tactics. The current standards of treatment for patients with SVD, and in particular, with a diagnosis defined by ICD-10 code G90.8 or G90.9, along with symptomatic drugs (ganglionic blockers, angioprotectors, vasoactive drugs) recommend the use of sedatives and tranquilizers , antidepressants, minor neuroleptics. It should be noted that most symptomatic drugs are ineffective. Patients require prescription of psychotropic medications. Explaining to the patient the essence of the disease allows one to argue for the need to prescribe psychotropic therapy.

The first choice drugs for the treatment of depressive, anxiety and mixed anxiety-depressive disorders are currently antidepressants from the group of selective serotonin reuptake inhibitors (SSRIs), because Predominantly, the deficiency of this neurotransmitter realizes psychovegetative manifestations of psychopathology. The advantages of SSRIs include a small number of side effects, the possibility of long-term therapy and a wide therapeutic spectrum with fairly high safety. However, despite all their positive aspects, SSRIs also have a number of disadvantages. Side effects of SSRIs include increased anxiety, nausea, headaches, dizziness during the first few weeks of treatment, and frequent lack of effectiveness. In older adults, SSRIs may cause unwanted interactions. SSRIs should not be prescribed to patients taking NSAIDs because the risk of gastrointestinal bleeding increases, as well as for patients taking warfarin, heparin, because SSRIs enhance the antithrombotic effect, which poses a risk of bleeding.

Dual-acting antidepressants and tricyclic antidepressants are the most effective drugs. In neurological practice, these drugs, in particular selective serotonin and norepinephrine reuptake inhibitors (SNRIs), have shown high effectiveness in patients suffering from chronic pain syndromes of various localizations. However, as efficacy increases, the tolerability and safety profile may deteriorate. Along with a wide range of positive effects, these drugs have a wide range of contraindications and side effects, as well as the need for dose titration, which limits their use in the general somatic network.

In this regard, the domestic original drug Azafen (pipofezin), including its new retardated form - Azafen-MB, which was created specifically for use in therapeutic practice and has been widely used since 1969, is of particular interest. The drug is a worthy competitor to modern antidepressants: being a representative of TCAs, it has a fairly pronounced antidepressant and sedative (anxiolytic) effect, relieving both mental and somatic symptoms of anxiety. At the same time, Azafen does not cause pronounced sedation, relaxation and drowsiness during the daytime. At the same time, it has practically no M-anticholinergic activity and does not affect the activity of monoamine oxidase, does not have a cardiotoxic effect, which makes it well tolerated and the possibility of widespread use in outpatient settings, in somatic patients, as well as in the elderly. Taking the drug in the evening promotes better sleep. Azafen is well tolerated, which allows its use in elderly patients, including those with somatic pathologies, and long-term courses as relief and maintenance therapy. Treatment can be carried out both in a hospital and on an outpatient basis. The creation of a new form of the drug, Azafen-MB, seems promising not only in terms of ease of use, but also in obtaining new indicators of effectiveness and safety. Plain Azafen at a dose of 75–100 mg/day has proven itself to be an effective drug for mild depression, and at a dose of 100–150 mg/day for moderate depression. Azafen-MB at a dose of 150–300 mg/day is effective for moderate depression, and at a dose of 300–400 mg/day it significantly reduces symptoms in severe depression. Our own experience of using Azafen at a dose of 100 mg/day, divided into 2 doses, shows that the psychotropic effect of Azafen is associated with a combination of thymoanaleptic, activating and tranquilizing properties. According to our data, the antidepressant effect of Azafen is not accompanied by a negative effect on attention, speed and accuracy of task completion, as well as on the state of the cardiovascular system. It is important to note that in patients with initial tachyarrhythmia, the heart rhythm normalized during treatment. Subjective improvement in patients' condition began on average from the 12th day of therapy. In our practice, side effects occurred in 7% of patients, which manifested themselves in general weakness, drowsiness, and dizziness. The severity of these phenomena was weak. However, it was not possible to establish a clear connection with taking the drug, because These patients initially complained of general weakness, dizziness and drowsiness during the day due to night sleep disturbances.

Thus, Azafen is effective for depressive conditions of various origins, has a beneficial effect on patients with borderline neurotic conditions, especially with anxiety-depressive (reduces feelings of anxiety, internal tension, eases stiffness of movements) and asthenic disorders, with neurogenic anorexia, menopausal syndrome, with masked depression, manifested by algic phenomena (cephalgia), sleep disorders. The drug has been noted to have the ability to normalize sleep with the absence of subsequent drowsiness. Azafen can be used as a corrector for the prevention and relief of extrapyramidal disorders that occur with long-term use of antipsychotics.

Given the difficulties in managing patients during the initial period of treatment with antidepressants, the use of a “benzodiazepine bridge” is recommended. The optimal drugs in this situation are GABA-ergic, serotonin-, noradrenergic, or drugs with multiple actions. Among GABAergic drugs, benzodiazepines are the most suitable. However, in terms of tolerability and safety profile, this group is not a first-line drug of choice. Much more often, high-potency benzodiazepines such as alprazolam, clonazepam, and lorazepam are used in the treatment of patients with pathological anxiety. They are characterized by a rapid onset of action, they do not cause an exacerbation of anxiety in the initial stages of therapy (unlike selective serotonin reuptake inhibitors). But these drugs are not without the disadvantages characteristic of all benzodiazepines: the development of sedation, potentiation of the effect of alcohol (which is often taken by these patients), lead to the formation of dependence and withdrawal syndrome, and also have an insufficient effect on symptoms comorbid with anxiety. This makes it possible to use benzodiazepines only in short courses (in the first 2–3 weeks of the initial period of antidepressant therapy).

General practitioners often face difficulties in determining the duration of prescribed therapy. This is due to insufficient information about the optimal duration of treatment and the lack of standards for its duration. It is important to remember that short courses (1–3 months) often lead to subsequent exacerbation. For a practicing physician, the following treatment regimen can be recommended:

– after 2 weeks from the start of using a full therapeutic dose of an antidepressant, one can judge the initial effectiveness and side effects of treatment. During this period, it is possible to use a “benzodiazepine bridge”;

– with good and moderate tolerability, as well as if there are signs of positive dynamics in the patient’s condition, it is necessary to continue therapy for up to 12 weeks;

– after 12 weeks, the question of continuing therapy for the next 6–12 months or searching for alternative methods should be decided;

– management of patients with resistant conditions by general practitioners is undesirable. In these situations, the help of a psychiatrist or psychotherapist is necessary. In this regard, there are no clear recommendations. In the absence of specialized assistance and the existing need, it is recommended to switch to antidepressants with a different mechanism of action.

Cancellation of the drug can occur abruptly (the so-called “break” of treatment) or gradually (graduated withdrawal), or by switching to “mild” anxiolytics. It is important to note that the choice of drug withdrawal tactics depends primarily on the patient’s psychological mood. If the patient is afraid of stopping a long-term medication, stopping the drug itself may cause a worsening of the condition. In this regard, the most suitable methods would be gradual withdrawal or transfer of the patient to mild, including herbal, remedies.

As non-drug interventions and when stopping antidepressants, various methods of psychotherapy can be used, in particular, cognitive-behavioral and rational psychotherapy, as well as relaxation techniques: autogenic training, breathing-relaxation training, progressive muscle relaxation, relaxation techniques using biofeedback.

Thus, the high representation of patients with depression in general somatic practice necessitates the need to promptly identify these disorders and determine their severity. In his practical work, a doctor can syndromatically identify identified psychopathology in the form of psychovegetative disorders against the background of vegetative dystonia syndrome, followed by the prescription of adequate psychotropic therapy, and also refer patients for consultation with psychiatrists.

Literature

1. Autonomic disorders: clinical picture, treatment, diagnosis./ed. A.M. Veina. – M.: 1998. – 752 p.

2. Krasnov V.N., Dovzhenko T.V., Bobrov A.E., Veltschev D.Yu., Shishkov S.N., Antipova O.S., Yaltseva N.V., Bannikov G.S., Kholmogorova A.B., Garanyan N.G., Kovalevskaya O.B. “Improving methods for early diagnosis of mental disorders (based on interaction with primary care specialists) / Ed. V.N. Krasnova.–M.: ID MEDPRACTIKA–M, 2008. 136 p.

3. Fink P., Rosendal M., Olesen F. Classificatin of somatization and functional somatic symptoms in primary care. // Aust N Z J Psychiatry. 2005 Sep;39(9):772–81

4. Oganov R.G., Olbinskaya L.I., Smulevich A.B., Drobizhev M.Yu., Shalnova S.A., Pogosova G.V. Depression and depressive spectrum disorders in general medical practice. Results of the COMPASS program // Cardiology, 2004, No. 9, pp. 1–8

5. Smulevich A.B., Dubnitskaya E.B., Drobizhev M.Yu., Burlakov A.V., Makukh E.A., Gorbushin A.G. Depression and the possibilities of their treatment in general medical practice (preliminary results of the SAIL program) // Consilium of Medicum. – 2007. – Volume 2. – No. 2. – Mental disorders in general medicine. – pp. 23–25

6. Stein MB, Kirk P, Prabhu V, Grott M, Terepa M. Mixed anxiety–depression in a primary–care clinic.//J Affect Disord. 1995 May 17;34(2):79–84

7. Katon W, Hollifield M, Chapman T et al. Infrequent panic attacks: psychiatric comorbidity, personal characteristics and functional disability. J Psych Research 1995; 29:121–131

8. Broadhead W, Blazer D, George L, Tse C. Depression, disability days and days lost from work in a prospective epidemiological survey. JAMA 1990; 264:2524–8

9. Vorobyova O.V. Clinical features of depression in general medical practice (based on the results of the COMPASS program). Consilium Medicum 2004; 6:2:84-87

10. Sansone RA, Hendricks CM, Gaither GA, Reddington A. Prevalence of anxiety symptoms among a sample of outpatients in an internal medicine clinic. Depression and Anxiety 2004;19 (133–136

11. Page LA, Wessely S// J R Soc Med 2003; 96: 223–227 Medically unexplained symptoms: exacerbating factors in the doctor–patient encounter

12. van Dulmen AM, Fennis JF, Mokkink HG, van der Velden HG, Bleijenberg G. J Psychosom Res 1994;38:581 –90 Doctors’ perception of patients’ cognitions and complaints in irritable bowel syndrome at an out–patient clinic

13. Peters S, Stanley I, Rose M, Salmon P. Patients with medically unexplained symptoms: sources of patients’ authority and implications for demands on medical care // Soc Sci Med 1998; 46:559 –565

14. Stone J, Wojcik W, Durrance D, Carson A, Lewis S, MacKenzie L, Warlow CP, Sharpe M What should we say to patients with symptoms unexplained by disease? The “number needed to offend.”//BMJ 2002; 325:1449–1450

15. Chambers J, Bass C, Mayou R Heart 1999; 82: 656–657 Noncardiac chest pain

16. Arolt V, Rothermundt M. Depressive disorders with somatic illnesses//Nervenarzt. 2003 Nov;74(11):1033–52; quiz 1053–4

17. Sayar K, Kirmayer LJ, Taillefer SS. Predictors of somatic symptoms in depressive disorder // Gen Hosp Psychiatry. 2003 Mar–Apr;25(2):108–14

18. Wittchen H–U, Carter RM, Pfister H, Montgomery SA, Kessler RC. Disabilities and quality of life in pure and comorbid generalized anxiety and major depression in a national survey. //Int Clin Psychopharmacol 2000;15:319–28

19. Kessler RC, Stang P, Wittchen H–U, Stein MB, Walters EE. Lifetime comorbidities between social phobia and mood disorders in the US National Comorbidity Survey. Psychol Med 1999;29:555–67

20. Goodwin R, Olfson M. Treatment of panic attack and risk of major depressive disorder in the community. Am J Psychiatry 2001;158:1146–8

21. Mosolov S.N. Anxiety and depressive disorders: comorbidity and therapy. Artinfo Publishing, Moscow 2007

22. Zigmond A.S., Snaith R.P. The Hospital Anxiety and Depression scale/|| Acta Psychitr. Scand. 1983 – Vol.67 – P.361–370 Adapted by Drobizhev M.Yu., 1993

23. Appendix No. 1 to the ORDER OF THE HEALTH COMMITTEE OF THE MOSCOW GOVERNMENT DATED 03/22/2000 N 110 “ON MOSCOW CITY STANDARDS OF ADVISORY AND DIAGNOSTIC CARE FOR THE ADULT POPULATION

24. Akarachkova E.S., Vorobyova O.V., Filatova E.G., Artemenko A.R., Toropina G.G., Kurenkov A.L. Pathogenetic aspects of the treatment of chronic headaches. //Journal of Neurology and Psychiatry. Korsakova, 2007, Issue 2, Practical neurology (supplement to the journal), p. 8–12

25. Akarachkova E.S., Drobizhev M.Yu., Vorobyova O.V., Makukh E.A. Nonspecific pain and depression in neurology//Journal of Neurology and Psychiatry named after. Korsakova, 2008 No. 12, pp. 4–10

26. Solovyova A.D., Akarachkova E.S., Toropina G.G., Nedostup A.V. Pathogenetic aspects of the treatment of chronic cardialgia.//Journal of Neurology and Psychiatry named after. S.S. Korsakova 2007; Vol. 107, No. 11:41–44

27. Damulin I.V. Features of depression in neurological diseases // Farmateka 2005; 17:25–34

28. Mashkovsky M.D. “Medicines. In two parts. Part 1 – 12th ed., revised. and additional – M.: Medicine, 1993. – 736 p.

29. Morozov P.V. Antidepressants in the practice of a clinic therapist // District therapist No. 5 / 2009 Consilium-medicum

30. Akarachkova E.S., Shvarkov S.B., Shirshova E.V. Experience of outpatient use of the antidepressant Azafen in neurological patients.//Special issue Man and Medicine Pharmateka No. 7(142), 2007, pp. 74–78

31. Tyuvina N.A., Prokhorova S.V., Kruk Ya.V. The effectiveness of Azafen in the treatment of mild to moderate depressive episodes // Consilium–Medicum 2005; 4(7): 198–200

32. Shinaev N.N., Akzhigitov R.G. Return of azafen to clinical practice // Journal of Neurology and Psychiatry named after. S.S. Korsakova 2001; 10(101): 55–56

Autonomic depression is a type of mental disorder, the main symptoms of which are disorders of the autonomic nervous system. This condition requires mandatory supervision by the attending physician. The symptoms of this type of depression are quite varied. The disease can occur in people of different ages, genders, social status, and professions. If you have symptoms of pathology, you should promptly seek help from a specialist.

Clinical picture

Autonomic depression is characterized by a wide range of different symptoms. This psychosomatic disease provokes multiple manifestations of physical ailments. With typical depression, the patient's mood decreases, he becomes apathetic, and a pessimistic outlook on life prevails. Emotions, if they arise, are negative. The patient loses interest in what is happening around him, his self-esteem decreases significantly, and suicidal thoughts may arise.

Autonomic depression is characterized by a predominance of autonomic disorders. The patient experiences many unpleasant or painful sensations that are not associated with any physical pathologies.

Physical manifestations of a depressive disorder can include not only pain of various types, but also dizziness, nausea, digestive system upset, excessive sweating, loss of appetite, and shortness of breath. The patient constantly feels weak, gets tired quickly, and even minor loads require serious effort from him. At the same time, sleep disturbances occur, the patient develops insomnia, and is haunted by nightmares. There is a decrease in libido, a change in body weight, both in the direction of increase and decrease (usually weight loss develops).

Other symptoms of autonomic disorder may also be observed. The most striking manifestations of the pathology are panic attacks and vegetative crisis. These are paroxysmal autonomic disorders. Also, autonomic disorders can manifest themselves in the form of permanent disorders.

Diagnosis

Only a specialist can make a reliable diagnosis. If depression is larvalized (occurs in a latent form), then its symptoms resemble many different diseases. After a comprehensive examination of the patient, the diagnosis can be established. It is also important to find out the reason that led to the development of the disease. There can be many causes of depression.

Treatment of pathology

Treatment of vegetative depression is carried out comprehensively. Therapy of psychovegetative disorders is carried out with the help of drugs such as antidepressants, tranquilizers, and antipsychotics. Vegetotropic agents are also used. Depending on the indications, other drugs may be used.

In addition to drug treatment, the patient may be recommended psychotherapy, which, together with medications, will speed up the healing process. Additionally, various physiotherapeutic procedures can be used to improve the general condition of the body. Yoga, swimming, breathing exercises, reflexology, and breathing exercises will be useful. Massage combined with aromatherapy and regular physical activity will also improve the patient’s condition. Proper nutrition also plays a significant role.

Catad_tema Autonomic dysfunction syndrome (AVDS) - articles

Autonomic dysfunction associated with anxiety disorders

"Clinical effectiveness" »»

Doctor of Medical Sciences, Prof. O.V. Vorobyova, V.V. Rusaya
First Moscow State Medical University named after. THEM. Sechenov

Most often, autonomic dysfunction accompanies psychogenic diseases (psycho-physiological reactions to stress, adaptation disorders, psychosomatic diseases, post-traumatic stress disorder, anxiety-depressive disorders), but can also accompany organic diseases of the nervous system, somatic diseases, physiological hormonal changes, etc. Vegetative dystonia cannot be considered as a nosological diagnosis. It is acceptable to use this term when formulating a syndromic diagnosis, at the stage of clarifying the category of psychopathological syndrome associated with autonomic disorders.

How to diagnose autonomic dystonia syndrome?

The majority of patients (over 70%) with psychogenically caused autonomic dysfunction present exclusively somatic complaints. Approximately a third of patients, along with massive somatic complaints, actively report symptoms of mental ill-being (feelings of anxiety, depression, irritability, tearfulness). Typically, patients tend to interpret these symptoms as secondary to a “severe” somatic illness (reaction to the disease). Since autonomic dysfunction often mimics organ pathology, it is necessary to conduct a thorough somatic examination of the patient. This is a necessary stage in the negative diagnosis of vegetative dystonia. At the same time, when examining this category of patients, it is advisable to avoid uninformative, numerous studies, since both the ongoing studies and the inevitable instrumental findings can support the patient’s catastrophic ideas about his disease.

Autonomic disorders in this category of patients have multisystem manifestations. However, a particular patient can strongly focus the doctor’s attention on the most significant complaints, for example in the cardiovascular system, while ignoring symptoms from other systems. Therefore, a practicing physician needs knowledge of typical symptoms to identify autonomic dysfunction in various systems. The most recognizable symptoms are those associated with activation of the sympathetic division of the autonomic nervous system. Autonomic dysfunction is most often observed in the cardiovascular system: tachycardia, extrasystole, chest discomfort, cardialgia, arterial hyper- and hypotension, distal acrocyanosis, heat and cold waves. Disorders in the respiratory system can be represented by individual symptoms (difficulty breathing, “lump” in the throat) or reach a syndromic level. The core of the clinical manifestations of hyperventilation syndrome are various respiratory disorders (a feeling of lack of air, shortness of breath, a feeling of suffocation, a feeling of loss of automatic breathing, a feeling of a lump in the throat, dry mouth, aerophagia, etc.) and/or hyperventilation equivalents (sighs, coughing, yawning) . Respiratory disorders are involved in the formation of other pathological symptoms. For example, a patient may be diagnosed with muscular-tonic and motor disorders (painful muscle tension, muscle spasms, convulsive muscular-tonic phenomena); paresthesia of the extremities (feelings of numbness, tingling, “crawling”, itching, burning) and/or nasolabial triangle; phenomena of altered consciousness (presyncope, feeling of “emptiness” in the head, dizziness, blurred vision, “fog”, “mesh”, hearing loss, tinnitus). To a lesser extent, doctors focus on gastrointestinal autonomic disorders (nausea, vomiting, belching, flatulence, rumbling, constipation, diarrhea, abdominal pain). However, disorders of the gastrointestinal tract quite often worry patients with autonomic dysfunction. Our own data indicate that gastrointestinal distress occurs in 70% of patients suffering from panic disorder. Recent epidemiological studies have shown that more than 40% of patients with panic disorder have gastrointestinal symptoms that meet the criteria for a diagnosis of irritable bowel syndrome.

Table 1. Specific symptoms of anxiety

Type of disorder	Diagnostic criteria
Generalized anxiety disorder	Uncontrollable anxiety, formed regardless of from a specific life event
Adjustment disorders	Excessive painful reaction to something in life event
Phobias	Anxiety associated with certain situations (situational anxiety that occurs in response to the presentation of a known stimulus), accompanied by an avoidance reaction
Obsessive-compulsive disorder	Obsessive (obsessive) and forced (compulsive) components: intrusive, repetitive thoughts that the patient is unable to suppress, and repeated stereotypical actions performed in response to an obsession
Panic disorder	Recurrent panic attacks (vegetative crises)

It is important to assess the development of autonomic symptoms over time. As a rule, the appearance or worsening of the intensity of patient complaints is associated with a conflict situation or a stressful event. In the future, the intensity of vegetative symptoms remains dependent on the dynamics of the current psychogenic situation. The presence of a temporary connection between somatic symptoms and psychogenic ones is an important diagnostic marker of autonomic dystonia. It is natural for autonomic dysfunction to replace one symptom with another. “Mobility” of symptoms is one of the most characteristic features of vegetative dystonia. At the same time, the appearance of a new “incomprehensible” symptom for the patient is additional stress for him and can lead to worsening of the disease.

Autonomic symptoms are associated with sleep disturbances (difficulty falling asleep, light shallow sleep, night awakenings), asthenic symptom complex, irritability in relation to habitual life events, and neuroendocrine disorders. Identification of the characteristic syndromic environment of autonomic complaints helps in diagnosing psychovegetative syndrome.

How to make a nosological diagnosis?

Mental disorders obligately accompany autonomic dysfunction. However, the type of mental disorder and its severity vary widely among patients. Mental symptoms are often hidden behind a “façade” of massive autonomic dysfunction and are ignored by the patient and those around him. The ability of a doctor to see in a patient, in addition to autonomic dysfunction, psychopathological symptoms is decisive for the correct diagnosis of the disease and adequate treatment. Most often, autonomic dysfunction is associated with emotional and affective disorders: anxiety, depression, mixed anxiety-depressive disorder, phobias, hysteria, hypochondriasis. The leader among psychopathological syndromes associated with autonomic dysfunction is anxiety. In industrialized countries, recent decades have seen a rapid increase in the number of alarming diseases. Along with the increase in incidence, the direct and indirect costs associated with these diseases are steadily increasing.

All anxious pathological conditions are characterized by both general and specific anxiety symptoms. Autonomic symptoms are nonspecific and are observed with any type of anxiety. Specific symptoms of anxiety, relating to the type of its formation and course, determine the specific type of anxiety disorder (Table 1). Because anxiety disorders differ from each other primarily in the factors that cause anxiety and in the evolution of symptoms over time, situational factors and the cognitive content of anxiety must be accurately assessed by the clinician.

Most often, patients suffering from generalized anxiety disorder (GAD), panic disorder (PD), and adjustment disorder come to the attention of a neurologist.

GAD usually occurs before the age of 40 (the most typical onset is between adolescence and the third decade of life), and runs chronically for years with pronounced fluctuations in symptoms. The main manifestation of the disease is excessive anxiety or restlessness, observed almost daily, difficult to control voluntarily and not limited to specific circumstances and situations, in combination with the following symptoms:

• nervousness, anxiety, feeling on edge, on the verge of a breakdown;
• fatigue;
• impaired concentration, “disconnection”;
• irritability;
• muscle tension;
• sleep disturbances, most often difficulty falling asleep and maintaining sleep.

In addition, nonspecific symptoms of anxiety can be presented unlimitedly: vegetative (dizziness, tachycardia, epigastric discomfort, dry mouth, sweating, etc.); gloomy forebodings (worries about the future, premonitions of the “end”, difficulty concentrating); motor tension (motor restlessness, fussiness, inability to relax, tension headaches, chills). The content of anxious fears usually concerns the topic of one’s own health and the health of loved ones. At the same time, patients strive to establish special rules of behavior for themselves and their families in order to reduce the risks of health problems to a minimum. Any deviations from the usual life pattern cause increased anxiety. Increased attention to one's health gradually forms a hypochondriacal lifestyle.

GAD is a chronic anxiety disorder with a high likelihood of symptoms returning in the future. According to epidemiological studies, in 40% of patients, anxiety symptoms persist for more than five years. Previously, GAD was considered by most experts to be a mild disorder that reaches clinical significance only in the case of comorbidity with depression. But increasing evidence of impaired social and professional adaptation of patients with GAD makes us take this disease more seriously.

PR is an extremely common disease prone to chronicity that manifests itself at a young, socially active age. The prevalence of birth defects, according to epidemiological studies, is 1.9-3.6%. The main manifestation of PR is repeated paroxysms of anxiety (panic attacks). A panic attack (PA) is an inexplicable, painful attack of fear or anxiety for the patient in combination with various vegetative (somatic) symptoms.

Diagnosis of PA is based on certain clinical criteria. PA is characterized by paroxysmal fear (often accompanied by a feeling of imminent death) or anxiety and/or a feeling of internal tension and is accompanied by additional (panic-associated) symptoms:

• pulsation, palpitations, rapid pulse;
• sweating;
• chills, tremors, feeling of internal trembling;
• feeling of lack of air, shortness of breath;
• difficulty breathing, suffocation;
• pain or discomfort in the left side of the chest;
• nausea or abdominal discomfort;
• feeling dizzy, unsteady, lightheaded, or lightheaded;
• feeling of derealization, depersonalization;
• fear of going crazy or committing an uncontrollable act;
• fear of death;
• numbness or tingling sensation (paresthesia) in the limbs;
• sensation of waves of heat or cold passing through the body.

PR has a special stereotype of the formation and development of symptoms. The first attacks leave an indelible mark on the patient’s memory, which leads to the appearance of the syndrome of “expectation” of an attack, which in turn reinforces the repetition of attacks. Repeating attacks in similar situations (in transport, being in a crowd, etc.) contributes to the formation of restrictive behavior, i.e. avoidance of places and situations that are potentially dangerous for the development of PA.

The comorbidity of PD with psychopathological syndromes tends to increase as the duration of the disease increases. The leading position in comorbidity with PD is occupied by agoraphobia, depression, and generalized anxiety. Many researchers have proven that when PR and GAD are combined, both diseases manifest themselves in a more severe form, mutually aggravate the prognosis and reduce the likelihood of remission.

Some individuals with extremely low stress tolerance may develop a painful condition in response to a stressful event that is not beyond the scope of normal or everyday mental stress. Stressful events that are more or less obvious to the patient cause painful symptoms that disrupt the patient’s usual functioning (professional activity, social functions). These disease states have been called adjustment disorder - a reaction to overt psychosocial stress that appears within three months of the onset of stress. The maladaptive nature of the reaction is indicated by symptoms that go beyond the norm and expected reactions to stress, and disturbances in professional activities, normal social life, or in relationships with other persons. The disorder is not a reaction to extreme stress or an exacerbation of a pre-existing mental illness. The maladjustment reaction lasts no more than 6 months. If symptoms persist for more than 6 months, the diagnosis of adjustment disorder is reconsidered.

The clinical manifestations of adaptive disorder are extremely variable. However, it is usually possible to distinguish psychopathological symptoms and associated autonomic disorders. It is vegetative symptoms that force the patient to seek help from a doctor. Most often, maladjustment is characterized by an anxious mood, a feeling of inability to cope with the situation, and even a decrease in the ability to function in everyday life. Anxiety is manifested by a diffuse, extremely unpleasant, often vague feeling of fear of something, a feeling of threat, a feeling of tension, increased irritability, and tearfulness. At the same time, anxiety in this category of patients can manifest itself as specific fears, primarily concerns about their own health. Patients are afraid of the possible development of stroke, heart attack, cancer and other serious diseases. This category of patients is characterized by frequent visits to the doctor, numerous repeated instrumental studies, and careful study of the medical literature.

The consequence of painful symptoms is social maladjustment. Patients begin to cope poorly with their usual professional activities, they are haunted by failures at work, as a result of which they prefer to avoid professional responsibility and refuse the opportunity for career growth. A third of patients completely stop their professional activities.

How to treat autonomic dystonia?

Despite the obligatory presence of autonomic dysfunction and the often disguised nature of emotional disturbances in anxiety disorders, the basic method of treating anxiety is psychopharmacological treatment. Medications successfully used to treat anxiety act on various neurotransmitters, particularly serotonin, norepinephrine, and GABA.

Which drug should I choose?

The range of anti-anxiety drugs is extremely wide: tranquilizers (benzodiazepine and non-benzodiazepine), antihistamines, α-2-delta ligands (pregabalin), minor antipsychotics, sedative herbal preparations and, finally, antidepressants. Antidepressants have been successfully used to treat paroxysmal anxiety (panic attacks) since the 1960s. But already in the 90s it became clear that, regardless of the type of chronic anxiety, antidepressants effectively relieve it. Currently, selective serotonin reuptake inhibitors (SSRIs) are recognized by most researchers and practitioners as the drugs of choice for the treatment of chronic anxiety disorders. This position is based on the undoubted anti-anxiety effectiveness and good tolerability of SSRI drugs. In addition, with prolonged use they do not lose their effectiveness. For most people, the side effects of SSRIs are mild, usually appearing during the first week of treatment and then disappearing. Sometimes side effects can be mitigated by adjusting the dose or timing of the medication. Regular use of SSRIs provides the best treatment results. Typically, anxiety symptoms are relieved after one or two weeks from the start of taking the medication, after which the anti-anxiety effect of the drug increases in a graduated manner.

Benzodiazepine tranquilizers are mainly used to relieve acute symptoms of anxiety and should not be used for more than 4 weeks due to the risk of developing a dependence syndrome. Data on the consumption of benzodiazepines (BZs) indicate that they remain the most commonly prescribed psychotropic drugs. The fairly rapid achievement of an anti-anxiety, primarily sedative effect, and the absence of obvious adverse effects on the functional systems of the body justify the well-known expectations of doctors and patients, at least at the beginning of treatment. The psychotropic properties of anxiolytics are realized through the GABAergic neurotransmitter system. Due to the morphological homogeneity of GABAergic neurons in different parts of the central nervous system, tranquilizers can affect a significant part of the functional formations of the brain, which in turn determines the wide range of their effects, including unfavorable ones. Therefore, the use of BZ is accompanied by a number of problems associated with the peculiarities of their pharmacological action. The main ones include: hypersedation, muscle relaxation, “behavioral toxicity,” “paradoxical reactions” (increased agitation); mental and physical dependence.

The combination of SSRIs with BZ or minor antipsychotics is widely used in the treatment of anxiety. It is especially justified to prescribe minor antipsychotics to patients at the beginning of SSRI therapy, which makes it possible to level out SSRI-induced anxiety that occurs in some patients during the initial period of therapy. In addition, while taking additional therapy (BZ or minor antipsychotics), the patient calms down, more easily agrees with the need to wait for the development of the anti-anxiety effect of SSRIs, and better complies with the therapeutic regimen (compliance improves).

What to do if the response to treatment is insufficient?

If therapy is not sufficiently effective within three months, alternative treatment should be considered. It is possible to switch to broader-spectrum antidepressants (dual-acting antidepressants or tricyclic antidepressants) or to include an additional drug in the treatment regimen (for example, minor antipsychotics). Combination treatment with SSRIs and minor antipsychotics has the following advantages:

• influence on a wide range of emotional and somatic symptoms, especially pain;
• faster onset of antidepressant effect;
• higher likelihood of remission.

The presence of individual somatic (vegetative) symptoms may also be an indication for combination treatment. Our own studies have shown that patients with BD who have symptoms of gastrointestinal distress respond worse to antidepressant therapy than patients who do not have such symptoms. Antidepressant therapy was effective only in 37.5% of patients complaining of gastrointestinal vegetative disorders, versus 75% of patients in the group of patients without complaints of gastrointestinal tract. Therefore, in some cases, medications that target specific anxiety symptoms may be helpful. For example, beta blockers reduce tremor and stop tachycardia, drugs with anticholinergic effects reduce sweating, and minor antipsychotics affect gastrointestinal distress.

Among the minor antipsychotics, alimemazine (Teraligen) is most often used to treat anxiety disorders. Clinicians have accumulated significant experience in treating patients with autonomic dysfunction with Teraligen. The mechanism of action of alimemazine is multifaceted and includes both central and peripheral components (Table 2).

table 2. Mechanisms of action of Teraligen

Mechanism of action	Effect
Central
Blockade of D2 receptors of the mesolimbic and mesocortical system	Antipsychotic
Blockade of 5 HT-2 A-serotonin receptors	Antidepressant, synchronization of biological rhythms
Blockade of D2 receptors in the emetic trigger zone and cough center of the brain stem	Antiemetic and antitussive
Blockade of α-adrenergic receptors of the reticular formation	Sedative
Blockade of H1 receptors in the central nervous system	Sedative, hypotensive
Peripheral
Blockade of peripheral α-adrenergic receptors	Hypotensive
Blockade of peripheral H1 receptors	Antipruritic and antiallergic
Blockade of acetylcholine receptors	Antispasmodic

Based on many years of experience in using alimemazine (Teraligen), we can formulate a list of target symptoms for prescribing the drug for the management of anxiety disorders:

• sleep disturbances (difficulty falling asleep) is the dominant symptom;
• excessive nervousness, excitability;
• the need to enhance the effects of basic (antidepressive) therapy;
• complaints of senestopathic sensations;
• gastrointestinal distress, in particular nausea, as well as pain, itching in the structure of complaints. It is recommended to start taking Teraligen with minimal doses (one tablet at night) and gradually increase the dose to 3 tablets per day.

How long does it take to treat anxiety disorders?

There are no clear recommendations for the duration of treatment for anxiety syndromes. However, most studies have proven the benefits of long courses of therapy. It is believed that after the reduction of all symptoms, at least four weeks of drug remission must pass, after which an attempt is made to discontinue the drug. Stopping the medication too early can lead to an exacerbation of the disease. Residual symptoms (most often symptoms of autonomic dysfunction) indicate incomplete remission and should be considered as a basis for prolonging treatment and switching to alternative therapy. On average, the duration of treatment is 2-6 months.

List of used literature

1. Autonomic disorders (clinic, diagnosis, treatment) / ed. A.M. Veina. M.: Medical Information Agency, 1998. P. 752.
2. Lydiard R.B. Increased Prevalence of Functional Gastrointestinal Disorders in Panic Disorder: Clinical and Theoretical Implications // CNS Spectr. 2005. Vol. 10. No. 11. R. 899-908.
3. Lademann J., Mertesacker H., Gebhardt B.. Psychische Erkrankungen im Focus der Gesundheitsreporte der Krankenkassen // Psychotherapeutenjournal. 2006. No. 5. R. 123-129.
4. Andlin-SobockiP., JonssonB., WittchenH.U., Olesen J. Cost of disorders of the brain in Europe // Eur. J. Neurol. 2005. No. 12. Suppl 1. R. 1-27.
5. Blazer D.G., Hughes D., George L.K. et al. Generalized anxiety disorder. Psychiatric Disorders in America: The Epidemiologic Catchment Area Study / eds. Robins L.N., Regier D.A. NY: The Free Press, 1991. pp. 180-203.
6. Perkonigg A., Wittshen H.U. Epidemiologie von Angststorungen // Angst-und Panikerkrankung / Kaster S., Muller H.J. (eds). Jena: Gustav Fischer Ver-lag, 1995. P. 137-56.

According to experts, at least 30% of all therapists’ patients are people with various depressive disorders. It is worth noting that in the field of neuroscience such a climber may be higher. It is necessary to take into account that patients who actively complain of low mood, depression, despondency, lack of interest in life, usually do not go to a therapist or neurologist, but turn to a psychiatrist in a clinic or to a neuropsychiatric dispensary. When visiting a general practitioner, patients complain primarily of somatovegetative disorders.

It is in such cases that doctors try unsuccessfully to understand the diagnosis and treatment of various long-term cardialgia, hypertension, shortness of breath, constant nausea, sweating, as well as sudden ones, which are also known as vegetative paroxysms. As a rule, in the future, with active and targeted questioning in these patients, it is possible to identify sleep disturbances, appetite, changes in body weight, decreased libido, constant weakness, fatigue, decreased interest in the environment and other symptoms indicating the presence of depressive disorders. Subclinical manifestations of depression in such patients also determined the corresponding terminology: hidden, masked, atypical, alexithymic depression. It is known that autonomic disorders of central origin or psychovegetative syndromes can manifest themselves in the form of both paroxysmal and permanent disorders.

Paroxysmal autonomic disorders

Autonomic crisis, or represents the most striking and dramatic paroxysmal manifestation of psycho-vegetative syndrome.

Diagnostic criteria for panic attack

The term panic attack is now recognized throughout the world thanks to the classification of diseases proposed by the American Psychiatric Association in 1980 in the reference manual DSM-III. According to the official definition, they are the main manifestation of so-called panic disorders. Subsequently, this classification was refined and currently, in its latest version (DSM-IV) and in the International Classification of Diseases (ICD-10), the following criteria for diagnosing panic disorders have been adopted.

Recurrence of attacks in which intense fear or discomfort combined 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, suffocation;
• pain or discomfort in the left side of the chest;
• nausea or abdominal discomfort;
• dizziness, unsteadiness;
• weakness, lightheadedness, faintness;
• numbness or tingling sensation ();
• waves of heat and cold;
• sensation;
• fear of death;
• fear of going crazy or committing an uncontrollable act.

The occurrence of a panic attack is not caused by the direct physiological effect of any substances, for example, drug dependence or taking drugs, or somatic diseases, for example, thyrotoxicosis.

In most cases, panic attacks do not occur as a result of other anxiety disorders, such as social and simple phobias, obsessive-phobic disorder, post-traumatic stress disorder.

According to recent statistics, between 1.5 and 4% of the adult population suffer from panic disorder at some point in their lives. Among those seeking primary medical care, patients with c make up to 6%. The disease most often debuts at the age of 20 - 30 years and develops extremely rarely before 15 and after 65 years. Women are affected two to three times more often than men.

Main clinical manifestations

The criteria needed to diagnose panic attacks can be summarized as follows:

• - paroxysmalness;
• - polysystem vegetative symptoms;
• - emotional and affective disorders.

It is obvious that the main manifestations of panic attacks are vegetative and emotional disorders. Already from the list of symptoms presented above, it is clear that vegetative symptoms affect various systems of the body: 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), pronounced tachycardia, often an increase in extrasystoles, and there may be an increase in temperature to a subfebrial or febrile level. All these symptoms, arising suddenly and without cause,” contribute to the emergence and persistence of another group of symptoms—emotional and affective disorders.

The range of the latter is unusually wide. Thus, a feeling of unreasonable fear, reaching the level 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 panic attack is subsequently transformed into specific fears - fear of myocardial infarction, stroke, loss of consciousness, falling, insanity. In some patients, the intensity of fear even in the first attacks may be minimal, but nevertheless, upon careful questioning, patients report a feeling of internal tension, anxiety, and restlessness.

In neurological and therapeutic practice, the emotional manifestations of an attack can differ significantly from the typical situation. So, during an attack, the patient may not experience fear or anxiety; It is no coincidence that such panic attacks are called “panic without panic” or “uninsured panic attacks.” Some patients experience a feeling of irritation during an attack, sometimes reaching a degree, in some cases - a feeling of melancholy, depression, hopelessness, and report causeless crying at the time of the attack. It is the emotional and affective symptoms that give the attack such an unpleasant and even repulsive character.

In a large category of patients with diagnosed panic disorders, the structure of the attack is not limited to the vegetative-emotional symptoms described above, and then the doctor can detect another type of disorder, which we conventionally call atypical. They can be represented by local or diffuse pain (headaches, abdominal pain, spinal pain), muscle tension, vomiting, senestopathic sensations and/or psychogenic neurological symptoms.

In the interictal period, patients, as a rule, develop secondary psychovegetative syndromes, the structure of which is largely determined by the nature of the paroxysm. In patients with panic attacks, soon after the onset of paroxysms, the so-called agoraphobic syndrome develops. literally means fear of open spaces, but in the case of panic patients, fear refers to any situation that is potentially threatening for the development of an attack. Such situations may be being 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.

Agoraphobia determines appropriate behavior that allows one to avoid unpleasant sensations: patients stop using transport, are not left alone at home, do not move far from home, and ultimately become almost completely socially maladapted.

The fears of patients with panic attacks may relate to a specific disease, which, according to the patient, is associated with the symptoms that worry him: for example, fear of a heart attack or stroke. Obsessive fears force the patient to constantly measure his pulse, check his 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 hypochondriacal syndrome.

As secondary syndromes, depressive disorders often develop, manifested by a decrease in social activity, interest in the outside world, increased fatigue, constant weakness, loss of appetite, sleep disturbances, and sexual motivation. Patients with demonstrative seizures, as a rule, exhibit hysterical personality disorders with clinical manifestations of hysteria in the somatic or neurological sphere.

Permanent autonomic disorders

Permanent autonomic disorders mean subjective and objectively recorded disorders of autonomic functions that are permanent or occur sporadically and are not combined with autonomic paroxysms or panic attacks. These disorders may manifest predominantly in one system or have a distinct multisystem nature. Permanent autonomic disorders can be manifested by the following syndromes:

• in the cardiovascular system: cardiac rhythmic, 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, a feeling of suffocation, difficulty breathing;
• in the gastrointestinal system: dyspeptic disorders, nausea, vomiting, dry mouth, belching, abdominal pain, dyskinetic phenomena, constipation, diarrhea;
• in the thermoregulatory and sweating systems: non-infectious subfebrile condition, periodic “chills”, diffuse or local hyperhidrosis;
• in vascular regulation: distal acrocyanosis and hypothermia, Raynaud's phenomenon, vascular cephalgia, lipotimic conditions, heat and cold waves;
• in the vestibular system: non-systemic dizziness, feelings of instability.

Autonomic disorders and depression

When examining a patient suffering from panic disorder, the doctor should be alert to possible endogenous depression, since the risk of suicidal actions requires immediate intervention by a psychiatrist.
According to modern criteria, depression is characterized by low mood, decreased or lack of interest or pleasure, combined with decreased or increased appetite, weight loss or gain, insomnia or hypersomnia, psychomotor retardation or agitation, feelings of fatigue or loss of energy, feelings of worthlessness, and inadequate feelings. guilt, decreased ability to think or concentrate, and recurrent thoughts of death or suicide.

For the clinician, an important question is about the nature of depression: is it primary or secondary? To resolve this issue, two diagnostic criteria are important: the time factor and the severity of depressive symptoms. Scientists propose using both criteria and establishing which of the disorders occurs without the other in the patient’s history. If episodes of depression appeared before panic disorder, and panic attacks appear only during depression, then panic disorder is secondary to depression. If depression appears only in the presence of panic disorders and, as a rule, at a certain stage of their development, then, most likely, we are talking about primary panic disorder and secondary depression.

It was shown that patients with depression with panic attacks had a longer course, were often of the endogenous, agitated type and had a worse prognosis; their depression was more severe.
It is believed that secondary depression often occurs in panic disorders. The following picture of the dynamics of panic disorder is considered typical: panic attacks, hypochondria, secondary depression. In one study of 60 people, 70% were found to be depressed, and in 57% of cases it occurred after the first panic attack. According to some data, secondary depressive overgrowth is observed in 70 - 90% of cases with long-term existence of panic disorder.

Since with primary depression, especially its severe forms, the risk of suicide is high, and the use of psychotherapy is also difficult, a differential diagnosis of panic disorder and depression with panic attacks is necessary. If primary depression is suspected, it is necessary to focus on weight loss, severe disturbances in concentration and sleep disorders, and severe motivational disorders. Secondary depression has a milder course and usually regresses when panic disorder is relieved.

Currently, the pathogenetic connection between panic disorder and depression is being actively discussed, the reason for which is the frequent combination of panic disorder and depression and the obvious effectiveness of antidepressant drugs in both cases. However, a number of facts refute the assumption of a single disease: these are, first of all, different effects when exposed to biological markers. Thus, sleep deprivation improves the condition of patients with major depression and worsens it with panic disorder; the dexamethasone test is positive in the first case and negative in the second; the administration of lactic acid naturally causes panic disorder in patients or in patients with depression combined with panic disorder, but not in patients suffering only from major depression. Thus, it can be assumed that the presence of depression is a factor contributing to the manifestation of panic disorder, although the mechanisms of this interaction remain 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 hysterodepressive disorders dominate. According to researchers, hysterical depression is one of the most common psychogenic reactions, accompanied by pronounced somatovegetative and hysterical neurological symptoms. Most often, such manifestations of the disease are observed during menopause.

Therapy of psychovegetative disorders

• Currently, the following groups of drugs are used in the treatment of vegetative syndromes, both paroxysmal and permanent:
• (HELL);
• (typical and atypical benzodiazepines - ABD);
• small (MN);
• vegetotropic agents.

It has already been proven through many controlled (double-blind, placebo-controlled) studies that the basic drugs in the treatment of autonomic disorders are those used as monotherapy or in combination with other drugs.

It should be emphasized that antidepressant therapy is indicated not only when autonomic disorders are a manifestation of depression, including masked depression, 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 , panic disorder with), in cases of mixed anxiety-depressive and hysterical-depressive (combination of somatoform and depressive) disorders. This situation reflects modern trends in psychopharmacotherapy, where antidepressants occupy the leading place, and tranquilizers (mainly typical benzodiazepines) are given the role of symptomatic, auxiliary, corrective therapy. The exception is the combination with antipsychotics (alprazolam and clonazepam), which in some cases can also be used as basic pharmacotherapy. Neuroleptics are used as additional drugs when combination therapy is necessary. Vegetotropic drugs (adrenoblockers, vestibulolytics), as a rule, are introduced into treatment as symptomatic therapy or to correct the side effects of antidepressants.

It should be noted that it is advisable to combine the use of any psychotropic drugs with vegetotropic therapy, especially if the drug used in addition has mechanisms of cellular neurotropic effects, or neurometabolic cerebroprotection. In particular, the prescription of vinpocetine (Cavinton) allows, due to these effects, to significantly improve treatment results.

Pharmacotherapy of patients with paroxysmal and permanent psychovegetative disorders involves several therapeutic strategies: relief of panic attacks; prevention of recurrence of paroxysms; relief of permanent psychovegetative syndromes.

How to stop panic attacks?

Tranquilizers of the benzodiazepine group (Relanium, Tazepam, Phenazepam, Xanax) are the most effective means for relieving panic attacks. However, with this symptomatic method of treatment, the dose of the drug has to be increased over time, and irregular use of benzodiazepines and the associated rebound phenomenon can contribute to an increase in panic attacks, progression and chronicity of the disease.

How to prevent the recurrence of panic attacks

Numerous double-blind, placebo-controlled studies have convincingly shown that the most effective in preventing the development of panic attacks are two groups of drugs: antidepressants and a combination of antidepressants with tranquilizers and antipsychotics.

Today, the range of antidepressants effective against PR has expanded significantly and includes at least 5 groups of drugs: tricyclic antidepressants - (melipramine), (tryptisol, nortriptyline), clomipramine (, gidifen); four-cyclic antidepressants - (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), (Zoloft), paroxetine (Paxil), (Cipramil).

The last antidepressant from this group, citalopram, is of considerable interest. The high selectivity of the drug and low potential for interactions, a favorable side effect profile, coupled with high efficiency, make it possible to consider cipramil as the drug of choice for many depressive conditions, in particular, in general somatic and gerontological practice. The presence of citalopram, along with thymoleptic, also has a distinct anxiolytic effect, indicates the possibility of using citalopram for anxiety disorders and, in particular, for panic attacks.

The most probable theory is considered to be one that links the anti-panic effectiveness of antidepressants 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 antidepressants, especially tricyclics, in the first ten days of treatment, an exacerbation of symptoms may be observed: anxiety, restlessness, agitation, and sometimes an increase in the number of panic attacks. Adverse reactions to tricyclic antidepressants are largely associated with anticholinergic effects and can manifest as severe tachycardia, extrasystole, dry mouth, dizziness, tremor, constipation, and weight gain. The above-described symptoms may lead in the first stages to forced refusal of treatment, especially since the clinical effect, as a rule, occurs two to three weeks after the start of therapy. Significantly fewer adverse reactions are observed when using drugs from the group of selective serotonin reuptake inhibitors. Their better tolerability, the possibility of a single daily dose and the painlessness of quick withdrawal at the end of treatment have made these drugs leaders in the treatment of PR.

Atypical benzodiazepines include clonazepam (Antelepsin, Rivotril) and alprazolam (Xanax, Cassadane). Benzodiazepines, typical and atypical, have been found to enhance the effects of GABA, or g-aminobutyric acid, which is the main inhibitory neurotransmitter in the central nervous system. A significant advantage of this group of drugs is the speed of onset of the clinical effect, which is three to four days. There is evidence that in large doses, from 6 to 8 mg, alprazolam has an antidepressant effect.

The choice of drug will depend on the clinical picture of the disease and the characteristics of the drug. If PA has recently appeared and there is no agoraphobic syndrome, then it is advisable to start combined therapy with antidepressants and or antipsychotics. If panic attacks are combined with agoraphobia or other secondary syndromes, for example, depression, phobia syndrome, hypochondria, then it is advisable to use antidepressants. First of all, it is recommended to use antidepressants with minimal side effects. In some cases, the combined use of antidepressants and tranquilizers with antipsychotics is required, which ensures an early onset of clinical effect and also helps to stop panic attacks before the onset of antidepressants.

How to treat permanent psychovegetative disorders?

First of all, it is necessary to take into account the nature of the emotional psychopathological syndrome itself. Obviously, in the case of depressive disorders, the most common treatment method is the use of antidepressants, and quite often they are the only treatment available. The main group of antidepressants can be called selective serotonin reuptake inhibitors. When a depressive disorder is combined with other mental illnesses, combination therapy can be prescribed: antidepressants and tranquilizers or antipsychotics (melleril (sonapax), teralen, neuleptil, eglonil, chlorprothixene, etaprazine).

Psychovegetative syndromes are currently successfully treated with a combination of individual selection of drugs, the prescription of small doses, cognitive behavioral therapy and social adaptation.

Various disorders of the autonomic nervous system occur: sweating, fluctuations in blood pressure, palpitations, dry mouth, weakness, hand tremors, intestinal disturbances, etc. The patient is often cold, he cannot warm up, the tips of his fingers are frozen (maybe this is where the symptoms appear). patients with depression desire to stand for a long time under a hot shower or take a warm bath).

Depression is accompanied by circadian rhythm disturbances. This results in increased severity at certain times of the day. Previously, it was believed that the manifestations of depression usually intensify in the first half of the day (80% of patients with depression), but recently it has been believed that circadian rhythm disturbances in depression depend on the individual biological characteristics of the sick person.

Typically, when a person is depressed. Sexual desire decreases, erection is impaired, and the feeling of orgasm is dulled. In women, the menstrual cycle is disrupted, sometimes menstruation stops completely.

During depression, the digestive system suffers. Appetite decreases or disappears altogether. However, in rare cases it even intensifies - usually in relation to certain products. It is no coincidence that it is often accompanied by symptoms of depression (a person “eats melancholy”) and is treated. During depression, many people note that “food has lost its taste,” it becomes like “grass.” The resulting weakness prevents you from going to stores for groceries, choosing them, cooking and eating, and thinking about food even makes you feel nauseous.

A common symptom of depression, especially in old age, is persistent constipation, bloating, and abdominal pain. A person noticeably loses weight or less often; on the contrary, when he starts eating heavily, he gains weight.

Changes in appetite in people who suffer from physical diseases in addition to depression - peptic ulcers, hypertension, diabetes - can complicate the course of the latter.

A frequent “response to depression” from the cardiovascular system.

Sometimes breathing problems also arise: a person feels a lack of air, incomplete inhalation. Breathing may be slow.

Frequent companions of depression are: headaches (a feeling of heaviness in the head), in the neck, lower back, joints, and others, often occurring in places of former wounds, traces of surgery. At the same time, the perception of pain itself can be changed: it seems stronger, has a special character, becomes unbearable and persistent due to a decrease in the threshold of pain sensitivity. Note that chronic pain syndrome can also be successfully treated with antidepressants.