Panic disorder

Panic disorder, or episodic paroxysmal anxiety, is a mental disorder characterized by the spontaneous occurrence of panic attacks from several times a year to several times a day and the anticipation of their occurrence. A characteristic feature of the disorder is

attacks of severe anxiety (panic), which are not limited to a specific situation or circumstances and are therefore unpredictable

Other names for this disease are "episodic paroxysmal anxiety," "cardioneurosis," "VVD (vegetative vascular dystonia) with a crisis course," "NCD (neurocirculatory dystonia).

In panic attacks there may be palpitations, chest pain, shortness of breath, muscle cramps, dizziness, nausea. Sometimes, there can be a feeling of unreality of events (derealization) and detachment from one's own body (depersonalization - the feeling of being out of the body and observing what is happening from outside). Symptoms during an attack are uncontrollable, greatly demoralizing, and cause a feeling of powerlessness and despair. The person's desire to consciously control their condition during a panic attack makes the symptoms even more intense. Often the anticipation of a possible attack is more excruciating than the attack itself. The person fears in advance that he or she will not be able to cope with the panic attack or will not be able to get help. For this reason, many patients begin to avoid situations in which an attack may occur (for example, staying alone or leaving the house).

Clinical picture and diagnostic criteria

People suffering from panic disorder tend to have a series of intense episodes of extreme (and usually unexplained) anxiety - panic attacks. Panic attacks usually last about 10 minutes, but can also be brief, about 1-5 minutes, or prolonged, up to 30 minutes, with feelings of anxiety lasting for up to 1 hour. Panic attacks may vary in the set of symptoms or may be uniform (i.e., tachycardia, sweating, dizziness, shortness of breath, tremors, experiencing uncontrollable fear, etc.). Some patients experience these conditions on a regular basis, sometimes daily or weekly. The external symptoms of a panic attack often lead to negative social consequences (e.g., embarrassment, social censure, social isolation). Nevertheless, patients who are aware of their illness can often have intense panic attacks with very few external manifestations of the condition.

A special scale is used to determine the severity of panic disorder; it also exists in the form of a self-assessment questionnaire as a test for panic attacks.

• Repeated, unpredictable attacks (not limited to a certain situation) of expressed anxiety (panic).
• Accompanying anxiety are vegetative pain symptoms, derealization and depersonalization.
• Secondary fears of death and insanity.
• Secondary avoidance of a situation in which a panic attack first occurred.
• Secondary fears of loneliness, crowded places, repeated panic attacks.
• Panic disorder is the primary diagnosis in the absence of any phobia as a primary disorder(otherwise, a panic attack is considered a sign of a pronounced phobia).
• A reliable diagnosis of panic disorder requires that several severe attacks of anxiety have occurred over a period of at least one month and meet the following requirements:
  1. Panic disorder occurs in circumstances unrelated to an objective threat(anticipatory attack anxiety is possible).
  2. Panic disorder is not limited to a known, predictable situation.
  3. Presence of anxiety-free periods between attacks.

1. Recurrent panic attacks.
2. At least one seizure has occurred within 1 month (or more) with the following additional symptoms:
   • Persistent concern about seizures.
   • Concern about the consequences of an attack (e.g., fear of loss of self-control, myocardial infarction, fear of going insane).
   • Significant changes in behavior related to attacks.

• The presence (or absence) of agoraphobia.
• The symptomatology is not a consequence of direct physiological effects of the substance (e.g., drug abuse, medication) or of any disease (e.g., arterial hypertension, hyperthyroidism, pheochromocytoma, etc.).
• The symptomatology cannot be explained by the presence of another mental or behavioral disorder, such as somatoform autonomic cardiovascular dysfunction, hypochondria, social phobia, other phobias, obsessive-compulsive disorder, post-traumatic stress disorder, or separation anxiety disorder.

According to the DSM-IV-TR diagnostic and statistical manual, panic attacks are not treated as a separate disorder, but are coded as part of the diagnosis of other anxiety disorders.

Panic disorder must be distinguished from a number of somatic diseases and conditions, which include cardiovascular disorders, chronic obstructive pulmonary disease, some endocrine and metabolic disorders (Cushing's disease, electrolyte metabolism disorders, hyperthyroidism, hyperglycemia, parathyroid gland diseases), epilepsy, especially temporal peptic ulcer, pheochromocytoma, pulmonary embolism, CNS tumors, bronchial asthma, the effects of certain drugs and narcotics, conditions after severe burns and extensive surgery.

In addition, panic disorder must be distinguished from other mental disorders accompanied by panic attacks: e.g., established phobic disorder (F40.x), post-traumatic stress disorder, obsessive-compulsive disorder, somatoform disorders (F4x.x) and other similar disorders. Panic attacks may be secondary to depressive disorders of the anxiety spectrum, especially in men, and if criteria for a depressive disorder are identified, then panic disorder should not be established as the primary diagnosis.

Panic disorder usually begins at a young age, less often in childhood and adulthood. Studies have shown that about 1.7% of adults in the United States have had symptoms of panic disorder (women are 2-3 times more likely to have it). The disease has a fluctuating course; about half of patients generally recover, the rest lead relatively normal lives, despite the persistence of symptoms and the presence of relapses.

Inadequate and untimely treatment measures contribute to a prolonged course of panic disorder. Anxiety disorders, including panic disorder, are diagnosed in only 50% of patients with obvious symptoms. Fewer than 50% of patients receive any treatment and less than 30% receive adequate therapy.

Despite the obligatory presence of autonomic dysfunction in an attack and the often implicit nature of emotional disturbances, psychotherapy and psychopharmacology are the main treatments for panic disorder.

Antidepressants of SSRI group are used - long term, not less than 6 months; and tranquilizers (alprazolam, clonazepam) for a short course - up to 14 days.

For some time, highly active benzodiazepines such as alprazolam and clonazepam were considered the drugs of first choice in the treatment of panic disorder. But their lack of efficacy for symptoms of depression, which is often combined with panic attacks, and their severe side effects have reduced their popularity. The first-line drugs of choice were SSRIs.

In patients with a history of manic states, benzodiazepines are preferred because, unlike antidepressants, they do not provoke mania.

The use of so-called vegetotropic drugs (anapriline, pyrroxan, beloid, bellaspon) in combination with vascular and metabolic therapy (cinnarizin, cavinton, trental, nootropil, piracetam, cerebrolysin) is ineffective, which undermines faith in the possibility of cure and promotes the chronicity of the disease.

Not all classes of psychotropic drugs are equally effective for panic disorder. With the right approach, panic disorder can be treated well. An individualized treatment plan for each patient is necessary and should be developed by the patient with his or her physician.

Psychotherapeutic aid (assistance from a psychotherapist or psychologist) for panic disorder can help to recognize a psychological problem, see ways to resolve it, and work through a psychological conflict.

Cognitive-behavioral psychotherapy has been shown to be effective in the treatment of panic disorder (including cognitive-behavioral psychotherapy delivered over the Internet). According to a meta-analysis, cognitive-behavioral psychotherapy had a higher rate of effect size in the treatment of panic attacks compared to pharmacological treatment and combined treatment (i.e., psychopharmacotherapy combined with psychotherapy). Fewer patients interrupted treatment when using cognitive-behavioral psychotherapy compared to pharmacological and combination treatment. There is evidence of greater counter-cycling activity with cognitive-behavioral psychotherapy for panic disorder compared with pharmacotherapy. Cognitive-behavioral psychotherapy also contributes to the successful discontinuation of benzodiazepines in patients with panic disorder and helps them maintain the therapeutic effect without resorting to medication.

In particular, within the framework of cognitive-behavioral psychotherapy, the "thought stop" technique can be used to eliminate disturbing thoughts causing a panic attack. Techniques such as symptom replication in the laboratory may also be used. The technique of symptom replication in the laboratory consists in reproducing some of the physiological components of a panic attack - sweating, rapid heartbeat, etc. - using various techniques (Clark lung hyperventilation, use of caffeine or rapid climbing of stairs). The patient's interpretations of these physical sensations and emotional reactions are then identified. If the therapist correctly interprets the patient's resulting sensations, he/she draws the patient's attention to the connection between the interpretation and his/her emotional state ("You explain the palpitations by running up and down the stairs, not by a heart attack, and you are absolutely calm.) The therapist also suggests that the patient look for an alternative explanation for the palpitations in everyday life instead of believing that the palpitations are a definite sign of a heart attack, and to rely on laboratory experience to do so.

Within the limits of cognitive-behavioral psychotherapy, the patient can also be taught relaxation skills and Clark's controlled breathing techniques during therapy sessions, after which the patient is recommended to use these skills in between sessions during episodes of intense anxiety.

Psychoanalysis is also used in the treatment of panic disorder. From the point of view of psychoanalysts, the main cause of panic disorder is considered to be displaced psychological conflicts that do not find an outlet, cannot be realized and resolved by the person due to various reasons.

Theories about the origin of the disease

1. Serotonin theory - data on the role of serotonin in the pathogenesis of panic disorders have been obtained in pharmacological studies. Studies of neuroendocrine reactions in response to the administration of serotonergic drugs have revealed certain changes in patients with panic disorders (changes in cortisol secretion in response to the administration of fenfluramine and metachlorophenylpiperazine). It is possible that patients with panic disorder have altered serotonin-associated platelet protein content. There have also been studies on the association of panic disorder with the production of serotonin antibodies. The interaction of serotoninergic and other neurotransmitter systems is important. The relationship between the serotonergic and noradrenergic systems helps to explain the autonomic dysregulation in panic disorder. SSRIs may also reduce panic disorder symptoms indirectly, through effects on the noradrenergic system. For example, fluoxetine can normalize the MHPG response to clonidine administration in patients with panic disorder.
2. Respiratory theories - attribute the onset of panic disorder to a malfunction in respiratory regulation and the occurrence of an "emergency" response. Panic attack is provoked by excessive breathing through activation of a presumed "choking center.
   • The neuroanatomical model suggests that panic attack is associated with hyperactivation of stem structures, which is manifested by altered respiratory function, dysfunction of serotonergic and noradrenergic structures. The rest of the manifestations this model associates with disturbances in the functioning of other parts of the brain - limbic structures - anticipation anxiety, disturbances in the prefrontal cortex - restrictive behavior.
3. Genetic hypotheses - The attempt to identify the genetic loci responsible for the development of panic disorder remains without success to this day. Panic disorder often occurs in close relatives, which may suggest a role for heredity. Comorbidity with diseases such as bipolar affective disorder and alcoholism has also been established.
4. Autonomic theories are based on the study of cardiac indicators of interaction between parasympathetic and sympathetic systems and responses to noradrenergic drugs (studies with clonidine). In adult patients a flattening of the growth hormone secretion curve in response to clonidine administration was found, indicating a decrease in hypothalamic α2-adrenoreceptor sensitivity, and an increase in blood pressure and MHPG levels was also observed. When panic disorder is successfully treated, there is a restoration of the normal response in the form of a decrease in MHPG in response to clonidine administration.
   • Locus ceruleus model - with administration of yohimbine and α2-adrenoreceptor agonists stimulating locus ceruleus an increase in anxiety is observed.
5. Conditioned reflex theory - it is hypothesized that any anxiety response results from the interaction of the amygdala with the stem structures, basal ganglia, hypothalamus, and cortical pathways. Internal stimuli are regarded as conditioned stimuli capable of triggering a panic attack. Panic attack results from the activation of nerve pathways that provide the conditioned-reflex phobic response in response to normal fluctuations in physiological functions. This theory is also supported by the fact that a conditioned reflex can be developed based on the respiratory and physiological response to carbon dioxide inhalation.
6. Cognitive theories - a number of cognitive factors are hypothesized to influence the development of panic attacks. Patients with panic disorder have increased anxiety sensitivity and a decreased threshold for perceiving signals from internal organs. Such individuals report a greater number of symptoms when anxiety is provoked by physical exertion.