Panic disorder

Introduction to panic disorder Panicdisorder, referred to as panic disorder, is characterized by repeated episodes of autonomic symptoms such as palpitations, sweating, and tremors, accompanied by a strong sense of sudden death or loss of control, fear of panic attacks that produce unfortunate consequences. An acute anxiety disorder. Sometimes unpredictable anxiety or panic attacks, sudden onset, extremely painful, lasting for a few minutes or more, in panic disorder, seizures are not limited to occur in specific predictable situations, and continue to worry after panic attacks Attack again. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: depression

Cause of panic disorder

(1) Causes of the disease

This disease is one of the most active areas of modern research, and it is summarized as follows:

Genetic factors (35%):

Crowe et al (1983), Harris et al (1983), Crow et al (1983) found that the risk of the disease in the first-degree relatives of the first-time relatives of the panic disorder was 24.7%, 20% and 17.3%, respectively; The risk of first-degree relatives was divided into: 2.3%, 4.8%, and 1.8%; this shows that the disease has family aggregation, and Torgersen (1983) reports a twin study with MZ with a disease rate five times that of DZ. Rate; but the same rate of MZ is only 31%, suggesting that non-genetic factors play an important role in the occurrence of this disease.

Physiological factors (25%):

EEG study data showed that the rhythm of patients with anxiety disorder was less than that of non-anxiety patients, and activity was mostly in the higher frequency range; suggesting that anxiety patients are often in a state of high alertness, Hon-Saric et al (1991) have 18 cases Patients with frequent panic attacks performed a series of physiological tests and compared with the control group without anxiety symptoms. It was found that in the basic state, patients with panic disorder had more electrical activity in the forehead, higher systolic blood pressure, faster heartbeat, and psychological In patients with stress, the increase in heart rate and systolic blood pressure were also more pronounced than in the control group; however, the skin resistance response of the control group varied greatly. The results of this study suggest that the vascular alertness of patients with frequent panic attacks is increased. The flexibility of skin resistance is reduced.

Psychological factors (18%):

According to psychoanalytic theory, neurosis anxiety is a response to unrecognized risk. This risk is not recognized by patients because of the neurological defense mechanism. Sometimes this risk is only symbolic. Neurosis anxiety can be Inspired by the re-emergence of past childhood, juvenile or unresolved conflicts in adulthood, Pan (1924) emphasizes that birth injury is the source of anxiety. Klein (1948) believes that anxiety stems from death instinct and is one of hostility and attack. Kind of reaction.

Behaviorism theory believes that anxiety is a conditional reflex that is feared by certain environmental stimuli. Take animal experiments as an example: if an animal presses a pedal to cause an electric shock, pressing the pedal will become a conditional stimulus before the electric shock. A conditional reflex that causes an animal to produce anxiety. This conditional reflex causes the experimental animal to avoid touching the pedal and avoid electric shock. The success of avoiding the unconditional stimulation of the electric shock strengthens the animal's avoidance behavior and thus reduces the anxiety level. This animal model It can be explained that the anxiety episode is a conditional response to a terrible situation obtained through learning.

1. Biochemistry: Various studies have been carried out, which are described as follows:

(1) Lactate: Cohen White (1950) first reported that patients with "nerve circulatory weakness" like anxiety had elevated serum lactate levels during moderate exercise compared with normal controls, Pitts and McClure (1967) The increase of serum lactate content may be related to anxiety attack, so 14 patients with anxiety and 16 normal people were intravenously instilled with 0.5 mol of sodium lactate 10 ml/kg under double-blind conditions, and the instillation was completed within 20 min. It was found that 13 patients with panic disorder experienced panic attacks during the instillation, while only 2 of the normal control group showed similar symptoms. The mechanism of this phenomenon is not fully understood. Possible explanations are: causing metabolic alkali Poisoning, hypocalcemia, abnormal aerobic metabolism, hyperactivity of -adrenergic, excessive release of peripheral catecholamines, increased sensitivity of central chemoreceptors, etc. There is also an explanation that lactic acid is metabolized to carbonic acid in the body and then hydrolyzed to CO2. And water; CO2 passes through the blood-brain barrier, which changes the redox state of the ventral medulla of the brain stem, or causes the release of noradrenergic neurons in the nucleus Addition, positron emission tomography and regional cerebral blood flow studies have shown that after intravenous infusion of lactate, in patients with lactic acid sensitivity, the blood flow and oxygen metabolism rate in the right hippocampal area is increased, reflecting this Increased activity at the site (Reiman et al., 1986).

(2) CO2: Gorman et al. (1984) inhaled 5% CO2 mixed gas in patients with anxiety disorders, like lactate, which can also cause panic attacks in patients. On the other hand, the chemistry of brain stems in such patients The susceptor may be overly sensitive to CO2, which may increase the impulse release of the nucleus.

(3) Neurotransmitters: Modern neurobiological studies on anxiety focus on noradrenergic, dopaminergic, serotoninergic and gamma-aminobutyric acid, four adrenergic systems, adrenergic systems, especially The blue spot nucleus plays a vigilant role and can cause a dangerous alertness. The dopaminergic system of the midbrain cortex is associated with emotional behavior and emotional expression. The serotoninergic system, especially the dorsal nucleus, can inhibit the anxiety-specific adaptability. Behavior; central serotonin activity has an important role in maintaining alertness and controlling anxiety, and gamma-aminobutyric acid is the major inhibitory neurotransmitter. These four neurotransmitter systems interact with each other at different parts of the brain and at different levels. The interaction of this complex intercellular signal, with the aid of the second messenger, cAMP and Ca2, is integrated at the subcellular level, causing different changes in the brain and various parts of the body, forming various clinical manifestations of anxiety.

The blue spot contains more than 50% of the noradrenergic neurons in the central nervous system. The nerve fibers are projected into the hippocampus, amygdala, marginal and frontal cortex. Animal experiments have found that electrical stimulation of blue spots can cause obvious fear. And anxiety response; at the same time, increased release of blue-spotted nerve impulses and accelerated acceleration of central norepinephrine, in humans, drugs that promote increased release of blue spots, such as yohimbine, can stimulate anxiety while reducing blue Spot-released drugs, such as clonidine, propranolol (propranolol), benzodiazepines, morphine, endorphin, tricyclic antidepressants, etc., have an anxiolytic effect, indicating blue spots And the noradrenergic system has an important influence on the onset of anxiety. In recent years, the use of serotonin recovery inhibitors to treat panic disorder has achieved good results, indicating that the serotoninergic system plays a role in panic disorder.

(4) Receptors: The symptoms of palpitations, tremors, and hyperhidrosis in patients with panic attacks are signs of a large amount of excitability of -adrenergic receptors. Some clinical observations have found that -adrenergic receptor blockers, Such as propranolol, has the effect of reducing panic attacks and anxiety; but these drugs can not prevent spontaneous and sodium lactate-induced panic attacks, therefore, the role of -adrenergic receptors in the pathogenesis of anxiety, pending Further studies have clarified that Mohler and Okada (1977), Squires and Braestrup (1977) have found benzodiazepine receptors in the mammalian brain, this receptor and the inhibitory neurotransmitter gamma aminobutyric acid (GABA). Adjacent to the receptor, GABA has two receptors: the GABAA receptor is coupled to the chloride ion (Cl-) channel, and the GABAA receptor interacts with GABA to promote the opening of the Cl-channel associated with it, and the GABAB receptor is associated with calcium ions. (Ca2), and possibly cAMP coupling, to help regulate the release of other neurotransmitters, benzodiazepines and their receptors can promote GABA function, significantly slow down nerve conduction; and block benzodiazepines with drugs Zhuo receptor, can make experimental animals produce Acute anxious symptoms, therefore, it is speculated that patients with anxiety are likely to produce a substance that interferes with benzodiazepine receptor function, leading to anxiety symptoms.

2. Neuroanatomy: German et al. (1989) provide a neuroanatomical hypothesis of panic disorder based on Klein's phenomenological model. Klein summarizes three characteristics of panic disorder:

(1) Acute panic attacks: Patients have significant autonomic symptoms due to panic attacks, and such episodes can be triggered by drugs acting on the brainstem, such as sodium lactate, CO2, and yohimbine. Therefore, German and others believe that the brain Dry, especially blue spots, are closely related to acute panic attacks.

(2) Expected anxiety: The marginal leaves are the center of basic emotions such as human anger, alertness and fear. Animal experiments have observed that the irritating lesions of the marginal structure can cause fear and startle response, and Penciled observes the same phenomenon in humans. Destructive lesions in this area reduce anxiety, and the marginal zone of the human brain is rich in benzodiazepine receptors. Intravenous injection of benzodiazepines is effective in reducing expected anxiety, but it is not effective in controlling panic attacks. These evidences suggest that expected anxiety may be associated with functional impairment of the marginal lobe.

(3) Terror avoidance: This is a learned behavior, which is related to the cognition and consciousness activities of the cerebral cortex. The nerve fibers from the frontal cortex to the brainstem can associate with the learned and origin of the prefrontal cortex. Knowing activities, passing to the brainstem, stimulating the brain nucleus of the brain stem, causing panic attacks, some anti-panic attacks are effective in controlling panic attacks and expected anxiety, but the effect of horror avoidance is often inferior to cognitive behavioral therapy.

(two) pathogenesis

1. Neurobiological Hypothesis German and other scholars have proposed a neurobiological hypothesis about panic attacks in recent years, and tried to explain why both drug therapy and cognitive-behavioral psychotherapy are effective treatments. Currently, animals are considered to be conditional fears. The stimuli response and the patient's panic attack response show striking similarities between physiological and behavioral consequences, that is, in animals, these responses are transmitted by the "fear network" in the brain, which is centered on the amygdala. The interactions between the hypothalamus and the medial frontal cortex, from the amygdala to the hypothalamus and brainstem, explain many of the apparent signs of conditional fear response, and similar neural networks exist in patients with panic attacks. One of the evidences is that genetic factors and stressful life events are associated with the development of panic disorder, especially in early childhood, where antidepressants (especially drugs that affect the 5-HT system) can project from the amygdala to the hypothalamus and brainstem. Network desensitization, effective psychosocial treatment can also reduce fear and cognitive misinterpretation associated with the anterior frontal cortex and hypothalamus. The study is correct imaging will help to verify these hypotheses.

Animal experiments have elucidated the brainstem pathway and related neurotransmitters that obtain conditional fear, that is, the sensory input of conditional stimulation through the anterior thalamus to the lateral nucleus of the amygdala, and then to the central nucleus of the amygdala, the amygdala The central nuclear nucleus is an information distribution center that dominates the autonomous and behavioral responses. The output of the central amygdala nucleus has many destinations: the parabrachial nucleus can speed up the respiratory rate; the lateral hypothalamic nucleus can activate the sympathetic nervous system. And cause spontaneous arousal and sympathetic discharge; blue spot, can lead to increased release of norepinephrine and increased fear of blood pressure, heart rate and behavior; and hypothalamic paraventricular nucleus, can cause an increase in the release of adrenocortical hormone In addition, there is an important interrelationship between the amygdala and the sensory thalamus, the anterior frontal cortex, the insula, and the primary somatosensory cortex. Patients with panic attacks may have a neurocognitive deficit in these cortical treatment pathways. It can lead to misinterpretation of sensory information, via excitatory input misleading to the amygdala, The fear network is inappropriately activated, with associated behavior and autonomic and neuroendocrine activation manifestations, for example, increased heart rate and respiration during panic attacks, although patients with panic disorder are more likely than normal volunteers or other mentally ill patients It is more anxious, intimidating, and breathing faster for inhaled CO2, but the physiologically most sensitive physiological indicator for inhaling CO2per minute ventilation changes/end CO2 tidal concentration tends to be the opposite, although some scholars have found panic disorder. Evidence of high sensitivity to CO2, but another group also found that they were in the normal range of this measurement. Only in the case of expected panic attacks, the level of cortisol in patients with panic disorder increased. In summary, there is evidence Some panic attacks are accompanied by autonomous and neuroendocrine activation.

The mechanism of action of selective 5-HT reuptake inhibitor (SSRI) drugs in panic disorder is currently thought to be related to the 5-transport of 5-HT, norepinephrine:

The projection of 15-HT neurons to the blue spot is generally inhibited. For example, the greater the activity of the 5-HT neurons in the nucleus raphe, the smaller the blue-spotted norepinephrine neurons. Coplan believes that after 12 weeks of treatment with fluoxetine, panic The level of 3-methoxy-4hydroxyphenethyl glycol, the major metabolite of norepinephrine in the plasma of patients with dysfunction, is reduced, suggesting that SSRI has a secondary reduction in norepinephrine activity by increasing the activity of 5-HT in the brain. Efficacy, which will lead to many cardiovascular symptoms associated with panic attacks, including elevated tachycardia and diastolic blood pressure.

2 The projection of the nucleus to the gray matter area around the water pipe can modify the defense/escape behavior. Viana and colleagues found that stimulating the dorsal nucleus can dramatically increase the acute release of 5-HT in the dorsal region of the gray matter around the water tube, which will result in The elimination of activity in the gray matter area around the water pipe supports the original assumptions of Deakin and Graeff that the projection from the 5-HT on the dorsal side of the nucleus has a modified defense and escape response by inhibiting the gray matter around the water pipe.

3 long-term use of SSRI treatment can reduce the level of corticotropin-releasing factor (CRF) release from the hypothalamus. CRF can trigger a cascade of events, which leads to cortisol producing its adrenal cortical products, which is also a central nervous system. Neurotransmitters, in many cases of preclinical models, have an increased fear effect. When applied directly to the brain, CRF also increases the firing rate of blue spots. CRF antagonists reduce the physiological and stimulating effects caused by CRF. Behavioral consequences, in fact, CRF antagonists have been used as anti-anxiety drugs in animal and human trials.

2. Genetic Hypothesis There are a large number of studies suggesting that the characteristic genetic locus of rodents on chromosomes is related to increased formation of passionate and fearful conditions. For example, Flint found three loci on mouse chromosomes 1, 12 and 15. In connection with the reduction in activity in the novel environment and the increase in stools, they concluded that these sites are associated with elevated passionateness and speculated that there are persuasive reasons for people to expect apathetic genetic basis in other species. The middle is similar and it may be based on the psychological characteristics of human anxiety susceptibility.

Numerous studies have shown that if first-degree relatives suffer from panic disorder, the chance of a pandemic disorder is higher than the basic prevalence in the population. At least three studies have examined the incidence of twins with panic disorder. The coincidence rate of disease has found that MZ has a higher prevalence rate than DZ. There is a special indication that panic attacks have a higher prevalence rate than the syndrome itself. However, there is no coincidence rate of MZ panic disorder. Close to 50% (range 14% to 31%), which means that if the gene is related to causing panic disorder, it is not the whole problem.

3. The environmental hypothesis of panic disorder suggests that early rupture of parental attachment is associated with the formation of panic disorder, such as the use of data from epidemiological studies, and Tweed reports the possibility of diagnosing claustrophobia with panic disorder. Adults who died before their mothers were almost seven times as likely as adults without early family deaths. Adults who were separated or separated from their parents before the age of 10 were almost four times as likely as adults without early parental separation. Stein found parents with panic disorder more than healthy controls. The group reported more childhood and physical abuse events, and the breakdown of emotional attachment relationships between children and dependents may be a risk factor for panic disorder, a view that is clinically observed to be perceived by the parents of panic disorder, threatening or actual The phenomenon of abnormal sensitivity is consistent. In fact, the likelihood of panic attacks in patients with panic fears is greatly reduced when there are trusted companions around them. One study showed that the presence of peers during CO2 inhalation reduced the likelihood of panic attacks.

There is evidence that traumatic or negative life events in childhood and adulthood are associated with the development of panic disorder, and that patients with panic disorder are more sensitive to traumatic effects than accessible individuals, especially those involving separation and attachment rupture. Consistent with this model, recent traumatic stress can play a role in triggering panic attacks in several forms, including increased autonomous autonomic activity or preventing proper interpretation and/or prevention of fear network signals. Appropriate feedback on the cortex that limits anxiety and panic response, therefore, the interaction between life event stress and genetic susceptibility is the underlying cause of adult panic disorder.

Panic disorder prevention

Due to the late development of psychiatry in the whole medicine, and because of the complexity of the basic theory of the profession, there are quite a few common causes and pathogenesis of common mental illnesses have not yet been elucidated, coupled with the influence of old ideas, the cause of mental illness is long The period is considered to be mysterious and neglected, thus hindering the development of psychiatric prevention. In fact, prevention of mental illness is not only an important issue in medical science, but also the development of social culture and social welfare. An important job of the cause.

At present, although the causes of many mental illnesses are not detailed, over the years, medical personnel have continuously observed the external connections and superficial phenomena of many mental illnesses in their work practices, and have formed some simple concepts. Try to prevent the occurrence of this kind of disease and improve people's mental health level, such as: 1 cultivating the whole body, including the development of brain function, and supporting it to be in a healthy state, so that the body is strong and full of spirit; Healthy development and strengthening exercise to adapt to the social environment, unity, and so on, these are effective measures to prevent mental illness.

Panic complications Complications depression

Cases of panic disorder are often accompanied by depressive symptoms. These patients have increased suicidal tendencies and need to be taken clinically.

Panic symptoms Symptoms Symptoms Syncope is not real, shortness of breath, chest tightness, forced phobia, useless feelings

1. Panic attacks : The typical performance is that patients are doing daily activities, such as reading a book, eating, walking, meeting or doing housework, suddenly feel shortness of breath, dizziness or mild headache, syncope, tremor or tremor, unrealistic, mouth Dry, difficult to concentrate on thinking or speaking, blurred vision, chest tightness, chest pain, chest tightness or pain or difficulty breathing, throat blockage, seems to be suffocating, suffocating, heart palpitations, heart beat, as if the heart wants to jump from the mouth Come out; hand numbness, foot numbness, suffocation, sweating, hot flashes or chills, eager to escape, nausea, muscle tension, fear of death, loss of control or madness, and a strong sense of fear, as if to die, or about to lose Reason, this tension makes the patient unbearable, thus screaming, calling for help, some hyperventilation, dizziness, non-photorealism, sweating, facial flushing or paleness, gait instability, tremors, numbness of hands and feet , gastrointestinal discomfort and other symptoms of autonomic over-excitability, as well as motor anxiety, patients in panic attacks generally try to escape some special function The situation stops with expectation of horror, or seeks help to prevent collapse, heart attack or madness. This kind of seizure is sudden, and the consciousness is clear when it occurs. It lasts for a short time, usually 5 to 20 minutes (peak within 10 minutes), rarely more than 1 hour. Self-relieving; or yawning, urinating, falling asleep and ending the episode, normal mental state during the interictal period, after the episode, the patient feels as usual, can recall the episode, but soon can be re-emergent, the patient can have frequent episodes, 1 More than 3 times a month.

2. Expected anxiety: Most patients in the intermittent period after recurrent panic attacks, often worried about recurrence, and thus nervous, there may be some symptoms of autonomic hyperactivity, called expectant anxiety, lasting more than 1 month Should pay attention to the identification of generalized anxiety.

3. Helping and avoiding behavior : When a panic attack occurs, the patient is unbearable because of the strong fear, and often asks for emergency help. In the intermittent period of the attack, 60% of the patients are evasive because they are worried about the disease. Some activities, such as not wanting to go out alone, do not want to go to crowded places, do not want to travel by car, or go out with others when you go out; that is, secondary to phobia, panic attacks sometimes (not always) will lead to It is difficult to avoid escaping in some situations, and it is difficult or embarrassing to avoid it in this situation, or feel that you can't get help from others immediately. Therefore, it can be divided into panic disorder with square phobia and panic disorder without square. Two types of phobias, occasional panic attacks (ie, the frequency of panic attacks is not sufficient to make a diagnosis of panic disorder) can also occur in other mental disorders, especially in other anxiety disorders.

The disease often has no obvious cause of sudden onset, and there are many autonomic symptoms, especially palpitations, tightness, dizziness, sweating, etc.; in a short period of time, the symptoms develop sharply, with strong fear; the duration is short. It will relieve itself. In addition to the expected anxiety in the intermittent period, there is no symptom of discomfort, often repeated attacks, intermittent periods can be long or short, frequent attacks, plus expected anxiety, easy to be misdiagnosed as a wide range of anxiety disorders, many Cases secondary to square phobia, DSM-IV distinguishes the disease as: panic disorder with square horror and panic disorder without square horror subtypes, combined with severe depression should be diagnosed separately.

Panic disorder check

At present, there is no specific laboratory test index for this disease.

As a group of comprehensive symptoms, panic attacks can be seen in a variety of mental and physical diseases. Only after the elimination of such diseases can the diagnosis of panic disorder be diagnosed. In addition to extensive anxiety disorders and depressive disorders, mental illnesses that need to be identified should also be noted. Identification with schizophrenia, personality disintegration disorders, somatoform disorders, medical diseases need to be identified: hyperthyroidism, hyperparathyroidism, arrhythmia, coronary insufficiency, pheochromocytoma, hypoglycemia, true Dizziness, drug withdrawal and alcohol withdrawal symptoms, especially confusing mitral valve prolapse, mitral valve prolapse is also sudden palpitations, chest pain, and tightness, fatigue, and even syncope, but no dizziness, out Sweat, tremors, facial fever or chills, as well as disintegration of personality, sudden death or loss of control, can be identified by echocardiography, but studies have reported that the two may be ill; and that panic disorder can lead to biceps Prolapse of the valve, if the panic disorder is controlled, mitral valve prolapse may disappear (German et al., 1981).

In patients with anxiety disorders, the alpha rhythm of EEG is decreased, and activity is mostly in the higher frequency range; it indicates that patients with anxiety are often in a state of high alertness.

Diagnosis of panic disorder

Diagnostic criteria

According to the diagnostic criteria of ICD-10, the diagnosis of panic attacks is based on at least 3 episodes within 1 month, each time not exceeding 2 hours. The episodes obviously affect daily activities, and the intermittent episodes of the two episodes are not afraid of recurrence. Obvious symptoms and have the following characteristics:

1. There is no real danger in the situation of the attack.

2. Not limited to known or predictable situations (see specific phobias or social phobias).

3. There is almost no anxiety in the intermittent phase of panic attacks (although often worried about the next panic attack).

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

For more detailed information, please refer to ICD-10, CCMD-III or DSM-IV.

Differential diagnosis

In the diagnosis of this disease, the first routine medical assessment to exclude the symptoms of anxiety caused by physical illness (such as heart disease, hyperthyroidism), usually patients with panic disorder have been treated by the physician, basically excluded the organic The possibility of disease, Table 1 briefly lists the identification of panic attacks and heart attacks.

Panic attacks can occur in other phobias, such as social phobias (when speaking to a group of people) or specific phobias (such as when you see a spider), in which panic attacks can be predicted, only in specific In the case of stimuli or situations, the diagnosis of panic disorder cannot be made in this case, and only an unpredictable panic attack can make a diagnosis of panic disorder.

Repeated panic attacks can also occur during the course of depressive disorder, and fear of recurrence. In some patients, depression can be secondary to panic disorder (ie, the experience of panic disorder makes the patient depressed), remember that panic attacks are relative For a short time, the patient who described himself as "all day frightened" was in a state of clinical anxiety rather than a panic attack.

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