How Do I Stop A Panic Attack?

A panic attack is a sudden panic experience. Symptoms are often manifestations of the patient's self. In some cases, the patient suddenly feels panic, out of control, madness, collapse, as if death is coming, panic, and calling for help. At the same time, it is accompanied by severe autonomic dysfunction, its onset is rapid, and its termination is fast. Its performance will last for several minutes or dozens of minutes of acute symptoms, and the onset is self-limiting.

This disease is one of the most active fields in modern research, and can be summarized in the following aspects:

1. The typical manifestation of a panic attack is that the patient is performing daily activities, such as reading a book, eating,

Panic disorder

When walking, meeting, or doing housework, I suddenly felt palpitations, as if my heart was about to jump out of my mouth; chest tightness, chest pain, and pressure on my chest; or difficulty breathing, blocked throat, as if breathless and about to suffocate. At the same time there is a strong sense of fear, as if about to die, or about to lose reason. This tension makes the patient intolerable. So screamed and called for help. Some appear hyper-ventiladtion, dizziness, non-realism, sweating, facial flushing or paleness, gait instability, tremor, numbness of hands and feet, gastrointestinal discomfort and other symptoms of autonomic nerve excitement, as well as exercise disturbed. The onset of the attack is short, usually 5-20 minutes, and rarely more than an hour. Symptoms can resolve on their own or end with yawning, urination, or falling asleep.

2. Anticipation of anxiety Most patients are worried about recurrence during the intermittent period after recurrent panic attacks, so they are uneasy, and some symptoms of autonomic nervous activity may appear.

3. In the case of panic attacks, for help and avoidance behavior, patients cannot bear it due to their strong sense of fear, and often ask for urgent help immediately. In the intermittent period of the attack, 60% of patients are prone to avoid some activities because they are worried that they will not be helped when they develop the disease, such as unwilling to go out alone, unwilling to go to crowded places, unwilling to travel by car, etc., or when going out To accompany others; that is, secondary phobia.

Clinical manifestation

Panic disorder refers to repetitive, and sometimes unexpected, onsets of anxiety or panic attacks that are sudden and extremely distressing, lasting a few minutes or more. Some episodes of panic disorder are not limited to occurring in a specific and predictable situation. After a panic attack, you will continue to worry about another attack.

A typical manifestation of a panic attack is that the patient is performing daily activities, such as reading a book, eating, walking, and having a meeting.

Panic disorder

Suddenly shortness of breath, dizziness or mild headache, syncope, tremor or tremor, unrealism, dry mouth, difficulty concentrating or speaking, blurred vision, chest tightness, chest pain, chest pain or dyspnea, blocked throat However, suffocation is about to suffocate, heart palpitations, heart beating, as if the heart is about to jump out of the mouth; hand numbness, suffocation, sweating, hot flashes, or chills, eager to escape the nauseous muscle tension, fear of losing control or going crazy. At the same time, a strong sense of fear appeared, as if dying or losing his mind. This tension makes the patient intolerable. Therefore, some people exclaimed for help, such as hyperventilation, dizziness, non-realism, sweating, facial flushing, or pale gait instability, tremor, numbness, gastrointestinal discomfort, and other symptoms of autonomic nervous excitement, as well as motor disturbance. Patients are generally struggling to escape a special function situation in anticipation of a panic stop, or to seek help in the event of a collapse, heart attack, or madness. This kind of attack is sudden, the consciousness is clear during the attack, it lasts for a short time, usually 5-20 minutes (the peak is reached within 10 minutes), and rarely exceeds 1 hour, it can relieve itself; or yawn, urinate and fall asleep to end the mental state of the attack is normal. After the attack, the patient consciously behaves as usual, and can recall the episodes of the attack but can suddenly re-emerge soon, and the person can frequently attack more than 3 times a month. 2. Anticipated Anxiety Most patients have an intermittent period after recurrent panic attacks and often worry about recurrence. Therefore, nervousness can also cause some symptoms of hyperactive autonomic nervous activity, which is called anticipatory anxiety that can last for more than 1 month. Should be distinguished from generalized anxiety.

Help and avoidance behaviors Because of a strong sense of fear during panic attacks, patients ca nt stand it. They often ask for urgent help immediately. During the intermission, 60% of patients are afraid to get help during the onset, so they actively avoid some activities. Going out alone is not willing to go to crowded places where people are crowded, not willing to travel by car, etc., or to be accompanied by others when going out; that is, secondary square phobia panic attacks sometimes (not always) lead to square fear avoidance in certain situations , Feeling evasive or embarrassing in this situation, or feeling unable to get help from others immediately. Therefore, there are two types of occasional panic attacks (ie, the frequency of panic attacks is not enough to make a diagnosis of panic disorder), which can be divided into two types: panic disorder with square phobia and panic disorder without square phobia. It can also appear in other mental disorders. Especially in other anxiety disorders.

complication

Panic disorder cases are often accompanied by depressive symptoms, and the increased suicidal tendency of such patients requires clinical attention.

The disease often has no obvious inducement. Sudden onset of a variety of autonomic symptoms, especially palpitations, tightness of breath, dizziness, sweating, etc. are the most prominent; the symptoms develop rapidly to a peak in a short period of time with strong fear; the duration is short, and it will relieve itself intermittently. In addition to the expected anxiety and fear of recurrence, there may be no symptoms of discomfort. Intervals often repeated may be short or long. Frequent attacks and expected anxiety can easily be misdiagnosed as generalized anxiety disorder. Many cases of secondary phobia DSM-IV classify the disease as: panic disorder with plague horror and panic disorder without plague horror. Subtypes with major depression Those should be diagnosed separately.

The diagnosis of panic attacks according to the diagnostic criteria of ICD-10 is based on at least 3 attacks within 1 month, and each interval does not exceed 2h. The interval between the two episodes, which obviously affects daily activities, has no obvious symptoms except fear of recurrence. And has the following characteristics:

There is no real danger in the context of radon.

Is not limited to known or predictable situations (see Specific Phobia or Social Phobia).

Almost no symptoms of anxiety during panic attacks (although often worrying about the next panic attack).

is not the result of physical fatigue, physical illness (such as hyperthyroidism), or substance abuse.

The purpose is to control panic attacks as soon as possible to prevent recurrence and cause plague in the square.

When dealing with the first panic attack, early treatment should explain to the patient that the physical symptoms caused by anxiety appear to be terrible, but they are actually harmless, and explain that the patient's "worry about losing self-control or dying" thought is a cognitive disorder caused by anxiety Puts anxiety into a vicious circle and prevents the further development of panic disorder. Patients should be informed about the importance of avoidance behaviors. Avoiding places where panic disorder can lead to square fear

The following drugs can be used for drug treatment:

Tricyclic antidepressants: Some antidepressants have anti-panic effects when used in large doses. Therefore, it is often used as a first-line drug, and the daily dose of imipramine is 50 ~ 300mg. It can be started from a small dose of 10mg or 25mg, and gradually increased the daily dose of at least 150mg or more for most patients to take effect. Clomipramine (clomipramine) (25-200mg / d) can also be used. For those who cannot tolerate the cholinergic side effects, dexipramine (normetazine) can be used instead. In elderly people prone to hypotension, nortriptyline amitriptyline can be used to reduce panic attacks. Similar to benzodiazepines, and rarely cause dependence and withdrawal. However, the drug has slower onset and more adverse reactions, and the initial effects of amitriptyline on panic disorder are increased levels of arousal, including anxiety, insomnia, and sympathetic nerve excitement. Therefore, the drug needs to be started from a small dose. About 2/3 of patients who are effective for benzodiazepines or amitriptyline relapse after 6 weeks of discontinuation and need further treatment.

Serotonin recovery inhibitors: can be used as first-line drugs, especially those who cannot tolerate tricyclic side effects; patients with compulsive symptoms or social phobia can be the first choice. Commonly used drugs are: paroxetine (20-60 mg / d), fluoxetine (5-20 mg / d), sertraline (50-150 mg / d), and fluvoxamine (150 mg / d) in the morning with SSRI (such as New antidepressants such as fluoxetine, paroxetine, fluvoxamine, SNRI (venlafaxine and its slow-release agents), and NaSSA (mirtazapine) can also control the symptoms of panic attacks, with the same effect as amitripty I'm pretty. The drug does not have the anticholinergic and cardiovascular adverse effects of amitriptyline, but its specific adverse reactions can make some patients intolerable and discontinue the medication.

(3) Monoamine oxidase inhibitors: suitable for those who cannot tolerate other antidepressants; patients with atypical depression or social phobia can be used as the first choice of commonly used drugs: phenelzine (15-60 to 90mg / d) and transphenyl ring Propylamine (tranylcypromine, 10-80mg / d), take in the morning.

High-efficiency benzodiazepines: suitable for those who cannot tolerate various antidepressants; anxiety or horror avoidance is expected to be outstanding, and cases requiring rapid results are preferred. Commonly used drugs are: alprazolam and clonazepam. The latter drugs have a longer duration of action and less withdrawal reactions. Benzodiazepines must be used in large doses for several months while controlling panic attacks, but they can cause dependence and withdrawal reactions. The conventional drug is alprazolam, which has a higher potency than diazepam and a weaker sedative effect at the therapeutic dose. It usually takes 6mg / d to control the panic attack (equivalent to 60mg diazepam). Withdrawal needs to be slow in 2 to 3 weeks, usually over 6 weeks.

Other drugs: venlafaxine (50-75mg / d) and nefazodone (200-600mg / d) can be used in patients with poor efficacy of other drugs.

Because the disease is prone to recurrence, various treatment periods should not be shorter than half a year; some patients need to maintain medication for 3 to 5 years to fully relieve it.

Psychotherapy Drug therapy is often used to control panic attacks after psychological attacks in order to eliminate the expected anxiety and horror avoidance.

Supportive psychotherapy: Explain the nature of the disease to the patient to reduce the patient's mental burden. Encourage the patient to adhere to the treatment plan. Organize similar patients to participate in group treatment and help each other to achieve better results.

Cognitive Behavior Therapy: Cognitive therapy is a professional treatment performed by a clinical psychologist or psychiatrist. The short-term effects of cognitive therapy are comparable to those of drug therapy and have a lower recurrence rate. However, this treatment needs to be performed by a specialist, and it is more time-consuming. Generally, drug treatment should be performed before cognitive therapy.

The following methods can be selected: Patients with chronic hyperventilation during seizures and acute hyperventilation during spontaneous or induced panic attacks can cause hypocapnia and alkalosis and reduce cerebral blood flow and cause dizziness. Symptoms such as ambiguity and disintegration. Use anti-panic drugs to control panic attacks, or through breathing behavior training, teach patients to adjust the breathing frequency not to over-ventilate, which can significantly reduce panic attacks

Exposure therapy: Let the patient expose to the physical sensations during panic attacks through meditation to eliminate the patient's fear of various autonomic nerve reactions. For patients who have evasive acts of terror or secondary terror, on-site exposure should be adopted so that the patient can gradually adapt to the situation of fear.

Relaxation training: You can contract and relax the muscles of the head and face, upper thorax, and lower limbs in order from top to bottom in order to reduce anxiety. It can also allow patients to learn health Qigong, relax the whole body muscles, regulate breathing, and obey Dantian to eliminate distractions.

Cognitive Reconstruction: Give a reasonable explanation to the physical sensation and emotional experience of the patient at the time of the illness, so that the patient realizes that such sensations and experiences are benign and will not cause serious damage to health.

Panic Attack Overview

Panic disorder is a type of recurrent severe anxiety. There are many hypotheses explaining its etiology mechanism. The hypotheses of neurobiochemistry include the classical neurotransmitter GABA, 5-HT, DA and Ach and other abnormal functional hypotheses, and the neuropeptide CCK and DA imbalance hypothesis. Genetic factors may also play a role in the occurrence of panic disorders, because in the investigation of the ethnic family of the stove, it was found that the incidence of this disease among close relatives of patients with anxiety disorders is 15%, which is three times that of ordinary residents [1 ]; The survey of twins found that the monosexual twins had the same disease rate of 50% and the anxiety quality was 65%, while the twins twins had the same disease rate only 4% and the anxiety quality was only 13% [1]; these Studies have shown that panic disorder has a clear genetic predisposition, and its cause is at least partially genetic.

With the development of molecular genetics technology, many studies have been conducted on the etiology of panic disorder at the genetic level.

GABAA Panic attack GABAA receptor gene

GABA receptors are divided into two subtypes, GABAA and GABAB. The GABAA subtype receptor forms a complex with the chloride value and stability receptors. The complex is a tetramer composed of , , , and subunits, and is gated by the chloride value. The subunit has a stable binding point; the subunit has a GABA binding point; the subunit cannot bind to benzodiazepines or GABA, but it is when the oligomeric receptor and benzodiazepine have high affinity Necessary; there is no binding site on the delta subunit and its function is unclear. The peptide chains of the , , , and subunits all cross the cell membrane 4 times [2, 3].

The GABAA receptor-chlorine channel-stable receptor complex plays an important role in anxiety resistance; GABAA receptors are coupled to chloride channels and gate the chloride channels. GABAA receptor agonists (such as GABA) can activate GABAA receptors Body, open the chloride channel, increase the extracellular CI-influx and increase the chloride conductance, cause hyperpolarization of the post-synaptic membrane, produce an inhibitory effect on neurons, and thus produce an anxiolytic effect; benzodiazepine anxiolytic drugs ( (Such as diazepam, etc.) acting on diazepam receptors can up-regulate GABAA receptors, which in turn increases the affinity of GABAA receptors for GABA and increases the binding to GABA, thereby increasing the frequency of GABAA receptors opening chloride channels and enhancing GABA. The post-synaptic inhibitory effect of anthrax shows an anxiolytic effect; barbiturates directly act on the chloride channel, which prolongs the opening time of the chloride channel, and also has an anxiolytic effect. In short, GABAA receptor agonists, stability receptor agonists, and barbiturates have anxiolytic effects because they act on GABAA receptors, stability receptors, and chloride channels, respectively. In contrast, diazepam binding inhibitor (DBI) is an endogenous stable binding inhibitor, which can down-regulate GABAA receptors, reduce the binding of GABAA to ligands, and cause anxiety; -carbolin and stable stabilizers Body binding, weakening the effect of GABA, can also cause anxiety; Azadirachtin can close chlorine channels, antagonize the effect of GABA, can cause convulsions. Therefore, the GABAA receptor-chlorine channel-stable receptor complex plays a very important role in the occurrence and treatment of anxiety [2].

The subunits of the GABAA receptor-chlorine channel-stable receptor complex have great polymorphisms. There are 13 variants of the human GAGAA receptor complex subunits, of which there are 7 variants of the subunit (1 7) ), There are 3 variants of subunit (1 3), 2 variants of subunit (1 2), and no variants have been found in the subunit [3]. There is a hypothesis that the susceptibility to panic disorder and the responsiveness to drug treatment are related to the different GAGAA receptor complex subunit variants, and because each subunit variant is encoded by a unique gene and its corresponding mRNA Therefore, the hypothesis further suggests that the susceptibility to panic disorder and the responsiveness to drug treatment are related to GAGAA receptor complex gene polymorphisms and mRNA levels. Tanay (1996) [4] found that chronic administration of anti-frightening drugs imipramine, phenelzine, and metazolam to rats can change the mRNA levels of 1, 2, and 2 subunits in the brainstem GABAA receptor complex. In addition, the expression of subunits of specific GABAA receptor complexes is changed, and the changes in the expression of these genes are different from those caused by non-anti-panic anxiolytic drugs (buspirone), which strongly supports the above hypothesis. . Crowe (1997) [5] further tested the genes (1 5, 1, 3, 2) encoding the 8 subunit variants of the GABAA receptor complex. In 104 strictly defined panic disorder patients, 134 generalized Patients with panic disorder or sub-syndrome panic disorder were linked between the above genes, but the results showed that there was a linkage, which does not support the above hypothesis. It is believed that panic disorder is not caused by any of the eight GABAA receptor complex subunit genes tested. Gene mutation.

5-HT1D Panic attack 5-HT1D receptor gene

The anti-anxiety effect of the drug also involves other transmitter systems, such as the NE system, especially the central blue spot, which is the expected dangerous arousal center; the DA system may be related to emotional behavior and anxiety performance; the 5-HT system is particularly in the dorsal nucleus , Inhibit the adaptive behavior of anxiety. The above-mentioned transmitter systems work together at different levels in the brain [6].

The increase in plasma corticosteroids can accelerate the T-HT renewal rate and excessive 5-HT functional activity, which may be related to the occurrence of anxiety [7]; 5-HT can also promote the secretion of ACTH, thereby regulating and Affects anxiety and emotional response [1]. Anxiolytics benzodiazepines can reduce 5-HT activity, inhibit the renewal rate of 5-HT in the brain, and slow down the rate of 5-HT consumption, which may be related to its anxiolytic effect [1-7]; anxiolytics Buspirone can reduce the vitality of 5-HT energy neurons, and its anxiolytic effect is also related to this [8]. In short, the 5-HT system is closely related to the occurrence and treatment of anxiety disorders, and the 5-HT receptor gene has therefore become one of the candidate genes for panic disorder.

5-HT is divided into 14 training subtypes, in which 5-HT1D receptor can be further subdivided into 5-HT1D receptor gene at the 1080th base of C and T can be converted to form a 080 polymorphism [9 ]; The 276th base of the gene encoding the 5HT1D receptor can undergo A and C conversion to form the A276G polymorphism [9]; these two polymorphisms are static polymorphisms and do not directly change the encoded amino acid structure However, they may indirectly affect the expression level of 5-HT1D receptors, which in turn affects the susceptibility to panic disorder. Therefore, Ohara (1996) [9] studied a group of panic disorder patients and normal controls, and sequenced their 5-HT1D and receptor genes, but found that the above two polymorphisms were not significant between the two groups. The differences do not support the argument that 5-HT1D receptor genes affect panic disorder susceptibility.

D4 Panic attack D4 receptor gene

Dopamine D4 receptors are mainly distributed in the frontal cortex. Because the genes encoding D4 receptors are highly polymorphic, these polymorphisms may affect the function of D4 receptors, making this gene one of the candidate genes for evaluating panic disorder. . Ten polymorphisms were found in the D4 receptor gene, including three static polymorphisms and seven dynamic polymorphisms. The first 31 base C on the 11th codon upstream of the start codon of the D4 receptor gene can be converted to T, thereby forming a polymorphism C-31T, the allele A1 (that is, the first 31 base is C) The frequency is 0.93 and the frequency of A2 is 0.07 [10]; the 31st base G in the 11th codon downstream of the start codon of the D4 receptor gene can be converted to C, so that the encoded 11th amino acid Gly on the D4 receptor Substitution with the amino acid Arg to form the polymorphism Gly11Arg, the frequency of the allele A1 (that is, the 31st base G) is 0.99, and the frequency of A2 is 0.11 [10]; the D4 receptor gene is 21bp above the 36th to 42th codons The long base sequence can be deleted, the polymorphic allele A1 has no 21bp deletion, and the allele A1 has 21bp deletion [10]. Cichon (1995) [10] studied 148 normal Germans, 256 schizophrenics, 99 patients with emotional disorders and a group of panic disorders, and found that the polymorphisms C-31T, Gly11Arg of all patients were not significantly different from those of normal people The difference is that no 21bp deletion was found in patients with schizophrenia, affective disorders and normal people, but this rare mutation was found in one panic disorder patient, which may mean that the deletion mutation is involved in the occurrence of panic disorder. But it can also be an opportunistic false positive result.

CHRNA4 Panic attack CHRNA4 gene

The central neurotransmitter NE responds to the hypothalamic-pituitary-adrenal response induced by stress, and acetylcholine (Ach) can promote ACTH secretion, which can then regulate and affect the emotional response to anxiety [1]; another study found that anxiety Cholinesterase activity is significantly lower in patients with dysfunction, which suggests that anxiety is related to lower cholinesterase activity [1]. In short, the Ach energy system is closely related to the occurrence of anxiety.

Ach receptors are divided into N and M subtypes. N-type Ach receptors (nicotinic acetylcholine receptor (CHRN)) are widely distributed in the central nervous system, and are found in the hippocampus, amygdala, and striatum of the cerebral cortex and limbic system. distributed. The CHRN receptor is composed of four subgenes, and the subunits are named , , , and . Each subunit is a transmembrane glycoprotein with a molecular weight of about 55kD. They form the CHRN receptor according to the ratio of 2. The total molecular weight is about 275kD; the five subunits are arranged in a pentagonal shape, and together form the wall of the ion channel of the CHRN receptor. They are generally asymmetric dumbbell-shaped. On the glutamic acid residues at positions 192 and 193 of the subunit, they have the ability to recognize and bind Ach; when the Ach ion (mainly Na +) enters the cell through the ion channel, the post-synaptic membrane undergoes a potential change, Produce physiological effects [3].

The subunits that make up the CHRN receptor have multiple variants [3], of which the alpha subunit has 6 variants (2 to 7) and the beta subunit has 3 variants (2 to 4), and these variants can be changed For the function of the CHRN receptor, each variant is uniquely encoded, in which the gene encoding the 4 subunit (CHRNA4 gene) is located at the 20q13.3 locus [11]. Previous studies have found that anxiety disorder is associated with low-voltage EEG (LVEEG), and about 1/3 of VLEEG cases are linked to the locus 20q13.3 [1], so there is a hypothesis that the susceptibility to panic disorder may also be related to the CHRNA4 receptor. In order to explore the relationship between the two, Steinlein (1997) [11] tested the allele frequencies of three different CHRA4 gene polymorphisms in a group of panic disorder patients and normal people, and found no significant difference. The study does not support the association between the CHRNA4 gene and panic disorder.

CCKB Panic attack CCKB gene

Cholecystokinin (CCK) is a neuropeptide, which is mainly synthesized in cells. Its precursor is composed of 130 amino acids. After translation, it can produce active peptide fragments such as CCK39, CCK33, CCK8, and CCK4 [ 12]. Low doses of CCK4 can induce panic attacks in patients with panic disorder, so CCK may be involved in the occurrence of panic disorder.

CCK receptors are divided into two subtypes, namely CCKA and CCKB receptors. CCKA receptors are distributed in the periphery, while CCKB receptors are distributed in the cerebral cortex and striatum. Therefore, genes encoding CCKB receptors are candidate genes for panic disorder . Kato (1996) [13] screened mutations in the CCKB gene of probands in 22 panic disorder families using the SSCP method and found two polymorphisms: introns between exons 4 and 5 in 10 patients A polymorphism was found on 2491C A, and a missense mutation (1550G A, Val125 Ile) was found on the extracellular loop of exon 2 of a proband; in 34 other unrelated panic disorders This missense mutation was detected in patients and 112 normal controls, and it was found in 8.8% (3/34) of patients and 4.4% (5/112) of normal people. However, the differences between these mutations in patients and normal people were not significant, so it is believed that these mutations have no pathophysiological significance in panic disorders. ^[1]

Panic attack epilogue

Many molecular genetic studies on panic disorder have been carried out, mainly focusing on the relationship between panic disorder and GABAA, 5-HT1D, D4, CHRNA4 receptor genes and CCKB genes. Except that a 21 bp deletion mutation in the D4 receptor gene may be involved in the occurrence of panic disorder in these studies, the rest of the studies were negative. However, this does not make us lose confidence in finding susceptible genes for panic disorder, because there are still inadequacies in previous studies: The investigation of the subtypes and polymorphic types of candidate genes is incomplete: for example, the GABAA receptor Of the 13 subunit genes, only 8 have been investigated, and 5 have not yet been investigated. Of the 14 subtypes of 5-HT receptor genes, only 1 has been investigated, and 13 have not been investigated. 10 types of D4 receptor genes have been investigated. Only 3 polymorphisms were investigated, and 7 were not investigated; only 1 of the 11 subunit genes of CHRN receptor was investigated, and 10 were not investigated. Small sample size: Panic disorder may be a genetic heterogeneous disease that is caused by the superposition of the small genetic effects of multiple genes. Therefore, to investigate the relationship between each gene and panic disorder, a large sample is often required. Only in the previous study, the sample size was not large, it is difficult to rule out the possibility of false negative results, and the only study that found positive results may also be because the sample size is too small, it is difficult to rule out false positive results caused by chance. Therefore, the molecular genetics research on panic disorder is equivalent to further expanding the sample size and conducting in-depth and comprehensive research. [1]