affective mood disorder
Introduction
Introduction to affective mood disorder Also known as affective disorder (mooddisorders) and mood disorder (mooddisorders), formerly known as affective psychosis (affectivepsychoses). It is a group of mental disorders with significant and sustained high or low emotional as the main clinical features, often accompanied by corresponding thinking and behavioral changes. The performance of emotional disorders has great variation, and lighter ones can be negative for some kind. The reaction of sexual life events can be a serious recurrent or even chronic disabling disorder. In severe cases, there may be hallucinations, delusions and other psychotic symptoms. Often recurrent, most can be relieved, a few residual symptoms or turn chronic. The first onset of such mental disorders is between 16 and 30 years old. Clinically, it can be divided into four types: depressive episode, manic episode, bipolar disorder and persistent mood disorder. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: dementia
Cause
Causes of affective mood disorder
(1) Causes of the disease
As early as the Hippocrates era, the two terms of mania and depression, Kahlbaum (1882) first proposed that mania and depression are two stages of the same disease, not two independent diseases, 1896, Cray Yulin clearly classified the two as a disease classification unit, which was named Manic Depressive Psychosis. This name has been used until now. For a long time, people have made many explorations on the causes of mood disorders (emotional psychosis): Hippocrates According to the four kinds of body fluid theory, depression is excessive secretion of black bile; Kretchmer proposed temperament-body-disease-related theory, which is considered to be more common in some good communication, cheerful, active, wide-ranging, easy to be too happy or too Melancholy people are also more common in short-skinned people, and this temperament and body shape form the basis of this disease; Pavlov believes that mania is more common in people with strong and unbalanced nerve types, because such people The inhibition process is weak, and the excitatory process is dominant. Under certain adverse body conditions, manic depressive psychosis may occur.
With the advancement of science and technology, people have deepened and scientific understanding of the causes of mood disorders, especially in the past 20 years, scientists around the world have focused on biological factors (including genetic factors, quality factors, physical factors, physiology, pathology, biochemistry, etc.). Aspects and psychosocial factors have done a lot of research on the etiology of mood disorders, and accumulated a lot of valuable information, specifically in the pathogenesis.
(two) pathogenesis
1. Biochemistry:
(1) Biogenic amines: The relationship between biogenic amines and affective disorders is one of the most studied and well-understood areas to date. Many studies have reported abnormalities in biogenic amines or biogenic amine pathways and structural abnormalities in patients with affective disorders. Norepinephrine (NE) and serotonin (5-HT) are considered to be the most relevant. Table 2 lists changes in neurotransmitters and their metabolites in patients with depression.
In addition, in vivo tests, almost all antidepressants and effective physical therapy (such as electroconvulsive therapy) reduce post-synaptic adrenergic and 5-HT2 receptor sensitivity in long-term applications, as listed in Table 3. The results of this research, the changes brought about by this long-term treatment and the onset time of antidepressants are exactly the same.
1 The monoamine theory of affective disorder: Biochemical research on affective disorders begins with the emergence of antidepressants, the first two types of antidepressants, monoamine oxidase inhibitors (MAOI) and tricyclic antidepressants (TCAs). During the clearance of monoamines at the synaptic site, MAOI inhibits monoamine (NE, 5-HT, DA, and adrenaline) oxidases; while TCA blocks another major pathway for monoamines, reuptake, Schildkraut JJ ( 1965), Bunney WE & DavisJM (1965) first proposed the catecholamine theory of the onset of affective disorder, stating that "the occurrence of certain depression is related to the absolute or relative lack of catecholamines, especially NE in important brain regions, while mania is associated with "More about catecholamines", Van Praag HM et al (1970) found that cerebrospinal fluid 5-HIAA levels are low in patients with depression, so Coppen A et al (1972) suggested that 5-HT dysfunction is associated with depression and suicidal behavior, Prange A et al. According to the research on NE and 5-HT system, the theory of combining these two kinds of transmitter systems is proposed. It is believed that the low level of 5-HT system provides the basis for the affective disorder caused by the change of NE function, and the 5-HT function is low. On the basis, NE dysfunction, depression, and NE hyperthyroidism is manifested manic.
2 studies on monoamine neurotransmitters: changes in the level of catecholamine metabolites in cerebrospinal fluid of patients with affective disorders may provide direct evidence for this theory, but studies to date have found that changes in the content of NE metabolite MHPG in CSF in patients with depression There is no regularity, and the results of the CSF content of 5-HT metabolite 5-HIAA are consistent. This phenomenon is particularly prominent in patients with obvious suicidal tendency, because peripheral body fluids include blood, monoamine metabolites in urine. The source is not limited to the central nervous system.
3 Discussion on the function of NE receptors: The relationship between down-regulation of -receptor function and clinical antidepressant effect is the most consistent and most recognized discovery in the mechanism of action of antidepressants. The relationship exists in almost all antidepressant treatments, and has obvious temporal consistency with the production of clinical antidepressant effects. Other data show that presynaptic 2-receptors negatively regulate the release of NE, so Blocking 2-receptors can enhance the function of the NE system. Since presynaptic 2-receptors are also present in 5-HT neurons, drugs that block presynaptic 2-receptors actually act simultaneously. NE and 5-HT two neurotransmitter systems.
4 Discussion on the function of 5-HT receptor: the relationship between 5-HT system and the occurrence of affective disorder: depletion of 5-HT with reserpine can promote depression; cerebrospinal fluid in patients with depression who have suicidal tendency 5- The content of HIAA decreased, and the uptake function of platelets to 5-HT also decreased. Selective 5-HT reuptake inhibitors (SSRIs) mainly acted on 5-HT reuptake, and some new antidepressants mainly related to different subtypes. -HT receptor binding, such as nefazodone is a 5-HT2 receptor antagonist, and ipsapirone is a 5-HT1A receptor agonist. Long-term treatment with these drugs leads to post-synaptic membrane 5-HT2 Decreased number of receptors and decreased 5-HT reuptake function may be more directly related to antidepressant effects.
Researchers have attempted to use biomarkers to classify depression into NE and 5-HT types, and believe that it can be used primarily for the norepinephrine (NE) system (eg, maprotiline, nortriptyline, and armor Treatment with imipramine, etc. or 5-HT systems (such as SSRIs) to improve efficacy, but recent studies have found a close interaction between central NE and 5-HT system, mainly acting on a nerve The drug of the transmitter system can secondaryly affect the function of another or even multiple transmitter systems due to this interaction, such as the regulation of the 5-HT system by the 2-receptor described above. Therefore, the biological characteristics are adopted. It is still too early to classify depression.
5 Dopamine (DA) theory: Biochemical studies on depression mainly focus on NE and 5-HT neurotransmitter systems, but some studies also believe that DA plays an important role in the pathogenesis of affective disorders. Some studies have found that reducing DA Levels of drugs such as reserpine or diseases such as Parkinson's disease can cause depression, while drugs that improve DA function, such as L-dopa, bromocriptine, tyrosine, amphetamine, and bupropion, can alleviate depressive symptoms. Therefore, some people have recently proposed the theory that depression is associated with DA. One thinks that patients with depression have DA function disorder in the midbrain system, and another that patients with depression may have low function of dopamine D1 receptor.
(2) Amino acids, peptides: -aminobutyric acid (GABA) and neuroactive peptides such as vasopressin and endogenous opioids, also play a role in the pathogenesis of affective disorders, on GABA receptors The hypothesis of the relationship with the onset of affective disorder is mainly from the application of anti-epileptic drugs effective in the treatment of mania or bipolar disorder, such as sodium valproate, carbamazepine, studies have shown that cerebrospinal fluid and plasma in patients with depression GABA content decreased, while tricyclic antidepressants, MAOI, SSRIS and ECT all increased the number of GABA receptors. The main excitatory amino acids in the central glutamate system and GABA function have a mutual restriction. The receptor for glutamate can There are two major categories, one is coupled with ion channels, which may be related to the pathogenesis of epilepsy, and the other is coupled with G protein, which is metabolic glutamate receptor (mGluR), metabotropic glutamate The body is divided into five subtypes, of which mGluR2 may be associated with the onset of depression, and the mGluR2 receptor antagonist may become a promising new class of antidepressant drugs.
(3) Second messenger system: Rolipram is a selective inhibitor of phosphodiesterase, which shows antidepressant effects in clinical trials. It is believed that the function of cAMP second messenger system is related to the onset of affective disorder, depression. The patient has a low cAMP function. When the phosphodiesterase is inhibited, the cAMP inactivation process is blocked, which enhances its function and thus acts as an antidepressant.
The second messenger coupled with the G protein has a phosphoinositide (IP) system in addition to cAMP. The receptor binds to the excitatory ligand to activate the excitatory G protein (Gi), and Gi activates the phosphatidylinositol-specific phospholipid. Enzyme C (PLC), which acts on phosphatidylinositol diphosphate (PIP2) inside the phospholipid bilayer of the cell membrane to produce diglyceride (DAG) and inositol triphosphate (IP3), which is stored in the inner woven net. Ca2, while Ca2 interacts with DAG to activate protein kinase C (PKC), which activates many cytoplasmic proteases, which in turn triggers a variety of biological processes, including gene transcription processes. IP3 requires inositol monophosphatase after function is completed. Hydrolyzed, re-released free inositol, and then synthesized with DAG as IP to complete the whole cycle, while Li ion is an inhibitor of inositol monophosphatase, and the therapeutic concentration of Li blocks the phosphoric acid by inhibiting inositol monophosphatase. The inositol cycle leads to a change in the IP second messenger function, which in turn achieves the purpose of treating manic episodes. Therefore, some scholars speculate that the onset of affective disorder may be related to the abnormal function of IP second messenger.
2. Neuroendocrine: The hypothalamus is the central nervous system of neuroendocrine function, and the hypothalamus itself is regulated by different neurotransmitter systems, such as monoamine neurotransmitters. Therefore, neuroendocrine dysfunction occurs in patients with affective disorders. May mainly reflect the abnormal function of the monoamine neurotransmitter system, just like traditional antipsychotic drugs, can block the function of nodule-funnel dopamine, resulting in elevated levels of prolactin in patients, in theory, some sort of Specific neuroendocrine function changes may be the cause of affective disorder and are more likely to be a manifestation of basal brain dysfunction.
(1) Hypothalamic-pituitary-adrenal (HPA) axis:
1 cortisone concentration:
A. The regulation process of cortisone secretion is as follows:
a. Paraventricular nucleus neurons secrete corticotropin releasing hormone (CRH).
b. CRH is transported through the pituitary portal system to the posterior pituitary, stimulating the release of adrenocorticotropic hormone (ACTH) in the posterior pituitary.
c. ACTH reaches the adrenal gland through the systemic circulation, stimulating the release of glucocorticoid cortisone from the adrenal cortex.
d. Cortisone acts on the cortisone receptor of the hippocampus by a rapid regulation mechanism (sensitive to the rate of increase in cortisone concentration), reducing the release of ACTH.
e. Cortisone also acts on the pituitary and adrenal receptors through a slow-regulation mechanism (sensitive to cortisone steady-state concentrations) to reduce ACTH release and block its excitatory effects.
B. Hypothalamic-pituitary-adrenal axis dysfunction that can be found in patients with depression includes:
a. Hypercortisone, the rhythm of diurnal secretion changes, that is, does not appear in the bottom of the night half of the normal person.
b. Dexamethasone deinhibition occurs in approximately half of patients with depression.
c. Increased adrenal volume.
d. Increased secretion of glucocorticoids caused by ACTH.
e. Increased CRH levels in cerebrospinal fluid.
f. ACTH secretion of exogenous CRH response is slow, in general, the more severe the degree of depression, the older the HPA axis abnormality is more obvious.
Recent studies have found that patients with depression have elevated levels of ACTH, abnormal 24-hour secretion rhythms, and increased pituitary volume. Young et al (1997) used metyrapone to block adrenal secretion of cortisone, and studied exogenous CRH on ACTH. The effect of secretion, the authors found that despite the slow response of ACTH secretion caused by CRH stimulation in depressed patients, the response can be restored when a drug that blocks the secretion of cortisone is given, indicating that the ACTH secretion is slow in depressed patients. It is due to an increase in the level of cortisone.
Raadsher et al (1995) found that the number of neurons containing CRH and the mRNA level of CRH in the paraventricular nucleus of the hypothalamus increased in these patients, suggesting that the pituitary-adrenal function abnormalities and depression in patients with depression The secretion of CRH in the thalamus is related, and the slow response of ACTH secretion may be due to long-term CRH hyperfunction, which leads to down-regulation of pituitary CRH receptor function. At the same time, the increase of cortisone concentration also negatively regulates the secretion of ACTH.
Recent studies have found that CRH not only acts as an endocrine hormone to affect the release of ACTH in the posterior pituitary, but also as a neurotransmitter in the biological effects of different brain regions, and more importantly, the CRH receptor in the hypothalamus, ie The neural pathways that regulate ACTH release are different from the regulatory mechanisms of CRH receptors in other brain regions. Therefore, in addition to promoting the release of ACTH, CRH integrates hormones, behaviors, and autonomic nerves associated with stress, anxiety, and depression. The functioning process plays an important role.
In patients with depression, there are also changes in peripheral corticosteroid receptor function. There are two types of corticosteroid receptors. Type I receptors, also known as mineralocorticoid receptors, have high affinity for cortisone in blood. Related to the maintenance of circadian rhythm, type II receptor, also known as glucocorticoid receptor, has low affinity for cortisone, and is associated with negative feedback regulation caused by elevated cortisone levels, and also with dexamethasone. The role of corticosteroid receptor function changes during depressive episodes, weakening the role of glucocorticoids, thus cutting off the negative feedback regulation function of the HPA axis, resulting in a persistent and active function of the HPA axis, changes in receptor function It can also explain why patients with depression do not have signs of physical signs seen in patients with adrenal hyperfunction.
Although the study on the number of direct glucocorticoid receptors has not been consistently concluded, the results of studies on receptor function have consistently found that the glucocorticoid receptor function on cells in depressed patients is lower than that of normal people. The inhibitory effect of corticosteroids on the effector organs is lower than that of normal subjects. This difference is more prominent in subjects with positive dexamethasone suppression test. In the study, patients should take dexamethasone or the cells in vitro. Incubation with dexamethasone or cortisone, after the addition of mitogens, lymphocyte proliferation from patients with depression is not inhibited like normal cells, and natural killer cell activity is not inhibited. This phenomenon is improving in depression. After disappearing, Holsboer and Barden (1996) found that treatment of animals with several antidepressants or ECTs can enhance the negative feedback regulation of glucocorticoids, reducing the basal value of glucocorticoids and the post-stress increase. To increase the glucocorticoid receptor binding rate and mRNA content in important brain regions, it is more meaningful that this change is also in the drug 2 ~ It appeared 3 weeks later, consistent with the appearance of antidepressant effects. In vitro tests also found that antidepressants can increase the number of glucocorticoid receptors or enhance their function.
The function of CRH outside the hypothalamus is different from that of hypothalamic CRH. The regulation of CRH in cerebrospinal fluid may mainly reflect the functional status of CRH system outside the hypothalamus. A decrease in CRH receptors in the frontal cortex was found, suggesting that there may be an increase in presynaptic release of CRH and a downregulation of postsynaptic receptor function outside the hypothalamus. Injection of CRH into the brain or specific brain regions may result in the appearance of Anxiety-like behavior, which can be counteracted by CRH receptor antagonists, suggests that increased CRH in the brain may be the basis for depression, anxiety, and even depression, and anxiety.
2 Dexamethasone inhibition test (DST): Dexamethasone is a synthetic cortisone analogue with a much higher potency than cortisone. Oral dexamethasone can inhibit the secretion of cortisone. It was found that about 50% of patients with depression had unsuppressed secretion of cortisone after oral administration of dexamethasone, ie, the dexamethasone suppression test was positive. In the standard test, blood was taken at 11 pm to determine the concentration of cortisone and let the patient Oral dexamethasone 1mg, blood was taken at 16 o'clock (after 17h) and 23 o'clock (after 24h) on the second day to determine the concentration of cortisone. If the concentration of cortisone is higher than 5g%, it is DST positive, and DST has been used in the past. As an auxiliary diagnostic indicator of depression, Zhou Dongfeng et al reported that the positive rate of DST in bipolar disorder was 52%, and the positive rate of menopausal depression was 67%.
Although the normal DST positive rate is lower in normal people, DST also has a higher positive rate in other mentally ill patients, which makes the value of DST as a diagnostic index decline. Recent studies suggest that DST has certainty in evaluating patients' recurrence and guiding the maintenance of therapeutic drugs. The value of depression, if the depression state improved after treatment, and DST turned negative, the possibility of recurrence is small; conversely, if the depression is improved but DST continues to be positive, the probability of recurrence is greater, requiring long-term maintenance medication.
Since dexamethasone only acts on the cortisone receptor of the pituitary, it cannot be used to evaluate changes in the function of cortisone receptors in other sites. Therefore, in recent studies, cortisone was used instead of dexamethasone for this inhibition test. It has been found that there is a defect in the fast negative feedback regulation pathway of cortisone in patients with depression.
(2) Hypothalamic-pituitary-thyroid (HPT) axis: The functional features of the HPT axis are similar to those of the HPA axis. Thyroid stimulating hormone releasing hormone (TRH) secreted by the hypothalamus reaches the posterior pituitary gland via the pituitary portal system, stimulating thyroid stimulating TSH secretes TSH, which reaches the thyroid gland through the systemic circulation, leading to the release of thyroxine (T4) and 3,5,3-triiodothyronine (T3), which can also be transformed outside the thyroid gland. It is T3, and the release of TRH and TSH by T4 and T3 forms a negative feedback regulation to achieve physiological balance.
The relationship between thyroid function and mood is recognized early in the clinic. Hyperthyroidism is associated with a series of emotional symptoms such as anxiety, depression, agitation, fatigue, emotional instability, etc., while the clinical manifestations of hypothyroidism are not Less aspects can be confused with depression, such as motor lag, fatigue, sexual dysfunction, depression and suicidal tendencies. The excessive sleep and weight gain associated with hypothyroidism may cause doctors to misdiagnose it as atypical depression. disease.
If the effective treatment of the primary disease of the thyroid is not carried out, the anti-depressant alone is not effective in treating the emotional symptoms associated with it. On the other hand, the combination of tricyclic antidepressants and T3 is often used to treat refractory depression. Get better results.
In patients with depression, the circadian rhythm of thyroxine secretion may disappear or flatten, and the serum concentrations of TSH and T3 may also decrease, while the stimulatory effect of TRH on TSH secretion also disappears or decreases, that is, the TRH stimulation test is positive, and exogenous TRH cannot be promoted. The secretion of TSH may be due to the long-term existence of TRH hyperfunction in patients with depression, which leads to the down-regulation of TRH receptor function. It is found that there is an increase in the content of TRH in cerebrospinal fluid in patients with depression, and recent studies have also found that direct cerebrospinal fluid Injection of TRH produces an antidepressant effect (Marangell et al., 1997) because it reverses the physiological effects of downregulation of TRH receptor function.
The TRH excitatory test is one of the methods used to assist in the clinical diagnosis of depression by first measuring the basal levels of T3, T4 and TSH, and injecting 300-500 g of TRH intravenously at 9 am, 30, 60 after injection and Serum TSH levels were determined by blood sampling at 90 min. If the difference between the maximum value after administration and the baseline value before injection was less than 6 U/ml, it was positive for TRH stimulation test, and the positive rate of TRH test for depression patients was about 40%, but it was The positive DST test did not overlap completely. Combining these two tests, Chen Guang et al found that the positive rate in patients with depression reached 70%.
Recently, studies have found that 10% of patients with depression have anti-thyroid antibodies in their serum, which is most common in patients with bipolar I. In fact, the functional changes of these HPT axes seen in depression are not unique to depression. It can be seen in patients who are mad, alcohol dependent, etc. Therefore, its clinical significance needs to be further explored.
(3) Changes in other hormone secretion: the secretion of growth hormone (GH) has a circadian rhythm, which peaks during slow eye movement sleep, and the peak of flattening in patients with depression becomes flat. The GH secretion caused by clonidine is increased in patients with depression. It also became dull.
Depression can also be accompanied by changes in other hormone secretion rhythms, such as decreased secretion of melatonin, administration of tryptophan does not promote the secretion of prolactin, decreased secretion of urotropin and luteinizing hormone, and testosterone in men. The level drops.
3. Neuroimmunology: In recent decades, studies have found that the human immune system and the central nervous system have a two-way regulation, and the endocrine system plays a role in the bridge, due to endocrine, nervous system activities and even immune factors. Many, therefore, in understanding their relationship with affective disorders need to pay attention to the following two points: First, there is a close mutual adjustment between immune function and endocrine function, so mental disorders or life events affecting endocrine function may be immune function This has to be taken into account when treating somatic diseases, especially infections, and affective disorders associated with tumors. Furthermore, due to immune function, there is a reverse regulation of the functions of the nervous and endocrine systems, so immunomodulation such as cytokines and The immunological process may affect the function of the nervous system and the endocrine system, and thus play an important role in the pathophysiology of mental disorders. In general, the immune function changes accompanying the affective disorder may be fruit, which may affect the physiological function of the patient. May also be caused by Forming a barrier or delayed.
The effects of stress events on the immune system begin at the earliest. The impact of stress events on the immune system can be excitatory or inhibitory, depending on the duration of the event, and is found in studies of changes in immune function of bereaved people. The degree of depression in bereavement is closely related to changes in immune function. Early studies on depression found that the cellular immune response decreased, but the results of the subsequent studies were different, but severely depressed, older, male patients with immune function changes More prominent.
Emotional disorders and stress events can affect immune function, and changes in immune function may also be the cause of affective disorders. The initial evidence comes from behavioral symptoms, including depression, in various elevated levels of cytokines. Known as the sickness behavior, it is caused by the application of proinflammatory cytokines, including interleukin (IL) 2 and 3, tumor necrosis factor, interferon-/, etc. Debilitation, fatigue, fatigue, lack of pleasure, snooze, anorexia, social isolation, hyperalgesia, and inattention, and elevated levels of serum inflammatory cytokines, including IL-6, are also found in major depression. Fast-reacting proteins (such as haptoglobin, C-reactive protein, 1-acid glycoprotein), this rapid reaction process may lead to a decrease in L-tryptophan content, resulting in a decrease in 5-HT levels in the brain. In addition, IL-l The effect of glucocorticoids on effector tissue can be blocked by directly inhibiting the expression of glucocorticoid receptors and their function, thereby causing hyperactivity of the HPA axis by impairing its negative feedback regulation function.
4. Sleep and electroencephalogram abnormalities: difficulty falling asleep, waking up early, waking up when sleeping or oversleeping is a common symptom of depression, while when manic is often, sleep requirements are often reduced, therefore, affective disorder and sleep and sleep EEG The relationship of change has long been valued by researchers. The main findings are: delayed sleep, rapid eye movement (REM) sleep latency (time from sleep to REM sleep), first REM sleep duration, delta wave sleep Abnormalities, etc., EEG study found that patients with depression have prolonged P300 and N400 latency, and full sleep deprivation or REM sleep therapy has short-term good effect on depression, which also indicates that sleep rhythm changes are important in the pathogenesis of affective disorder.
Because anti-epileptic drugs are effective in treating bipolar disorder, people realize that there is a close relationship between electrophysiological activity and emotional activity. There is an "ignition" theory that repeatedly applying subthreshold stimulation to neurons will eventually lead to action potentials. Therefore, patients with affective disorders may have repeated "ignition" status of the temporal lobe cortex, leading to instability of neural activity, which may be related to bipolar disorder, while antiepileptic drugs such as sodium valproate and carbamazepine are due to This repeated subthreshold electrical stimulation is blocked to stabilize the mood.
5. Brain imaging research: There is no consistent and reproducible conclusive research on brain imaging studies of affective disorders. The existing research has the following findings:
1 part of the biphasic type I patient, especially male, has ventricular enlargement;
The ventricle enlargement of patients with severe depression is not as significant as that of bipolar I patients, but the ventricular enlargement of patients with depression with psychotic symptoms is more obvious;
3 magnetic resonance imaging (MRI) study also found that patients with major depression have a shortened caudate nucleus and atrophy of the frontal lobe;
4 patients with depression have abnormal T1 relaxation time in hippocampus;
5 patients with bipolar phase I were found to have deep white matter damage;
6 using single photon emission imaging (SPECT) or positron emission tomography (PET), blood loss in the cerebral cortex of some patients with depression, especially in the frontal cortex;
7 Magnetic resonance spectroscopy (MRS) technique was used to detect abnormalities in cell membrane phospholipid metabolism in patients with bipolar phase I, which coincided with the second messenger theory of bipolar disorder and the site of action of Li ions, and was also found in animal experiments. The effect of Li ions on phospholipid metabolism.
6. Genetics research: Genetic research to date has affirmed that genetic factors play an important role in the pathogenesis of affective disorders, but the mode of action of genetic influences is very complex, and only one factor of genetics is used to explain affective disorders. The occurrence of this is not feasible. Psychosocial factors play an important role not only in the pathogenesis of affective disorders, but also in certain patients, which may directly lead to the occurrence of obstacles. On the other hand, genetic factors have a greater impact on bipolar disorder than depression. Be strong.
(1) Family survey: The results of family surveys of affective disorder are relatively consistent. The incidence of bipolar disorder in first-degree relatives of probands with bipolar disorder is 8 to 18 times higher than that of normal relatives, and depressive disorder The incidence rate is 2 to 10 times higher than that of the first-degree relatives of the first-degree relatives of the depressive proband. The incidence of bipolar disorder is 1.5 to 2.5 times higher than that of the first-degree relatives of the normal person, and the incidence of depression is 2 to 3 times higher than that of the first-degree relatives. The gap is narrowed by the alienation of the blood relationship between the respondent and the proband. The heritability of bipolar disorder is also high. At least one of the parents of 50% of patients with bipolar disorder has an affective disorder, if one of the parents has If you have a bipolar disorder, your child's chance of developing an affective disorder is 25%. If both parents have a bipolar disorder, the chance of their child's affective disorder increases to 50% to 75%.
(2) Twins survey: The main findings of the twin survey are that the twin-child twins ask for a bipolar disorder with a prevalence rate of 33% to 90%, and the major depressive disorder rate is about 50%, while the twins are between twins. The incidence of bipolar disorder is 5% to 25%, and the rate of major depressive disorder is 10% to 25%. Although the rates of different diseases reported in each individual study are different, almost double eggs are found in each study. The co-morbidity rate of twins is significantly higher than that of fraternal twins.
(3) Foster child survey: Some researchers believe that parents with emotional disorders or families with such patients will have adverse environmental impacts on their children, which in turn leads to an increase in the incidence of mental disorders, that is, simply Family or twin surveys are not sufficient to fully confirm the role of genetic factors, while the foster child study is conducted by parents of biological children with emotional disorders who are fostered to other normal families after birth, because the child is born. Shortly after being fostered elsewhere, the environmental impact of blood relatives on children's growth and development can be basically ruled out. Such surveys also show that the affective disorder has a clear genetic predisposition, and Mendelwicz & Rainer (1977) investigated 29 cases of bipolar disorder fosters. Parents found that 31% of their blood relatives had affective disorder, while only 12% of their foster parents had affective disorder. The incidence of affective disorder in blood relatives of foster probands and the incidence of blood relatives of other bipolar disorder probands (26 %) is close to, significantly higher than the blood relatives of the normal fostering child (2% to 9%), other research results are similar, all found sick Parents children are still more likely to have a higher rate of affective disorder even if they are raised in a normal environment, and the incidence of affective disorder in the foster childrens foster children elsewhere is close to that of unfostered children, indicating that environmental factors are among them. The role played is not as direct and important as genetic factors.
(4) Gene linkage research: Using the latest restriction enzyme fragment length polymorphism (RFLP) technology, many researchers have conducted many useful exploratory studies on specific genes or gene markers and affective disorders, which have been reported. Genetic markers associated with affective disorders, especially bipolar disorder, include chromosomes 5, 11 and X. If considered together with biochemical changes in affective disorders, the dopamine D2 receptor gene can be found on chromosome 5, tyrosine The acid hydroxylase (the rate-limiting enzyme of the catecholamine synthesis pathway) gene is located on chromosome 11, and some of these studies are isolated single reports, some of which were repeated by later studies, and some were not successfully replicated in later studies. So far, no research results can be repeatedly verified. The reason may be related to the fact that a certain gene may be associated with a family's emotional disorder, but not necessarily universally. Egeland et al. (1987) on the Amish family biphasic The genetic linkage study of barriers is well represented, although the researchers successfully mapped the relevant genes to the short arm of chromosome 11. However, the results were not successfully repeated in subsequent studies. The results of the linkage study between the X chromosome and the bipolar disorder are similar. The X chromosome contains the color blind gene and the glucose-6-phosphate hydrolase gene. The disease is an X-linked hereditary disease. Studies have found that biphasic disorders are linked to these two genes, while others have denied this result. Perhaps this chain exists in some (perhaps not most). In any case, patients need to be cautious in interpreting the results of gene-linked studies.
7. Psychosocial factors: It is obvious that the use of a single genetic factor can not satisfactorily explain the etiology of affective disorder, especially depression. Even if genetic factors play an important role in its pathogenesis, the induction of environmental factors and even the pathogenic effect can not be ignored. Genetic factors may lead to a susceptibility to the development of affective disorders, such as the instability of certain neurotransmitter systems or other physiological functions, and those with such predisposing qualities are provoked by certain environmental factors. The susceptibility is not the existence of all or nothing, but a transitional state. People who are more susceptible may become ill under the influence of lighter environmental factors; while those who are less susceptible are still affected by more significant environmental factors. It may be ill, of course, the susceptibility is not necessarily derived from heredity. The impact of early life experiences such as childhood bereavement experience cannot be ignored. The safer assumption is that genetic factors have a greater impact on bipolar disorder, while environmental factors The role of depression is more important.
(1) Life events and environmental stress events: Traumatic life events are closely related to the incidence of mood disorders. There are often stressful life events before the onset of affective disorder. Some people report that there are major life events in the last 6 months, depression. The risk of seizures can be increased by 6 times, the suicide risk rate is increased by 7 times, the severity of life events is related to the onset time, and there are major negative life events such as accidental disasters, relative loss, large economic losses, and depressive episodes within 1 year. The risk is higher than the normal population. Chronic psychosocial stimuli such as unemployment and chronic diseases can also lead to depressive episodes. According to Western countries, the prevalence of low-level and high-level major depression is about 2 times higher than that of bipolar disorder. There are many high-level people, but it should be pointed out that not all people who suffer major events are sick or suffering from mood disorders.
The occurrence of this disease needs to be comprehensively considered from the comprehensive effects of genetic factors such as genetics, physiology, biochemistry, etc. One explanation is that the stressful life events that occur before the first episode will produce persistence in the patient's physiological activities. Change, this persistent change may change the functional status of some neurotransmitter systems and intracellular messenger systems, as well as organizational changes such as loss of neurons and reduction of synapse, thus placing the patient in a In a high-risk state, subsequent episodes may not require obvious stress events or may occur. There are different explanations for the status of stress events in the occurrence of depression. Some people think that it is etiological and directly leads to depression; Others believe that this kind of event only triggers a potential state and makes it premature. It is easier to understand the role of life events by using the above-mentioned susceptibility-environmental factor transition state theory.
(2) Psychological theory: There are many psychological theories about the occurrence of affective disorders, involving classical psychoanalytic theory, psychoanalytic-oriented psychodynamic theory, learning theory, cognitive theory, etc. Psychoanalytic theory emphasizes childhood experiences on adulthood disorders. The impact of depression as an attack on intimate people and a childhood depression experience that has not been rid of, and other psychoanalysts believe that depression is a contradiction between self and superego, or internal conflict .
Learning theory uses acquired helplessness to explain the occurrence of depression. In animal experiments, it is found that the animal is placed in a situation of repeated shocks that cannot escape. The animal will try hard to get rid of it at the beginning. After a while, it will Abandoning the effort altogether, so it understands that this situation cannot be undone, it is in a state of helplessness, and people with depression have the same helpless experience if the doctor gives the patient a state of self The sense of control and domination, the state of depression will improve, so the use of behavioral rewards and positive intensification methods for the treatment of depression is effective.
Cognitive theory believes that there are some cognitive misunderstandings in patients with depression, such as negative distortion experience of life experience, negative self-evaluation, pessimism and helplessness. The purpose of cognitive therapy is to identify these negative cognitive misunderstandings. Behavioral work methods to correct the patient's thinking.
Prevention
Affective mood disorder prevention
Psychologists believe that learning to maintain the best mentality is like a living fish, free to swim in the ocean of society, family and life. Then, how to maintain your best mentality in a complex social environment How to use various scientific and feasible methods to self-regulate psychological factors, promote psychological balance, achieve mental health, prevent general psychological problems, and psychological barriers can be achieved through self-psychological health care. Self-mental health care includes the following aspects:
1. Establishing a correct outlook on life and world view The determination of the outlook on life and the world view is the fundamental condition for preventing psychological abnormalities. It is an important guarantee for the mental health of adolescents. The correct outlook on life and world outlook enables young people to correctly understand the relationship between the outside world and individuals. The role and ability to coordinate and handle various relationships, to ensure the appropriateness of psychological reactions, to prevent anomalies, if a person's needs, ideas, ideals, behaviors violate social norms, naturally will hit the wall, suffer setbacks, endless in endless In troubles and pains, it leads to psychological unhealthy, visible, correct outlook on life and world view is the ideological basis and psychological basis for ensuring personal mental health.
2. Understanding the self, accepting the self can not correctly understand the self is often one of the important reasons for the formation of psychological barriers, to maintain mental health, not only to understand their strengths, interests, abilities, personality, better understand their own shortcomings and defects, and
3.
Complication
Complications dementia
Symptom
Asperge...
1.(depressive episode)33
(1)31
(hopelessness)(helplessness)(worthlessness)
(anhedonia)
3
(2)()()
(mood-congruent);(mood-incongruent)
;;10%15%
(psychomotor retardationpsychomotor agitation)
(3)
()
70%;
2.(manic episode)
(1)(),
(2)
(3)
(4)
(5)ICD-10
()
2
3.
;;2h;;;;15%;
Examine
There is currently no specific laboratory test for this disease. When other conditions, such as infection, occur, laboratory tests show positive results from other conditions.
Diagnosis
Diagnostic points
()(ICD-10DSM-CCMD-2-R)ICD-10
1.ICD-10
(1)
2
(F30)
(2)
12
(3)
()
()
(4)3(F32.0)24(F32.1)26DSM-
2h
()
(5%)
4
3(F32.2)(F32.3)2
2.
(1)
122
(2)
(F33.0)
(F33.1)
(F33.2)
(F33.3)
(F33.4)
3.ICD-10
(1)(F30.0)()
4
3
A.
B.
C.
D.
E.
F.
G.()
()
(2)(F30.1)
1()
3(4)
A.
B.()
C.
D.
E.
F.
G.
H.
I.
[(hyperacusis)]
(3)(F30.2)
C
-
()
F30.20(/);F30.21()
4.(F31);11
F31.0
F31.1
F31.2
F31.20
F31.21
F31.3
F31.30
F31.31
F31.4
F31.5
F31.6
()
2
1
F31.7
1()
1()
5.()(F34)ICD-10DSM-CCMD-()ICD-10
(1)(F34.1)()
2
2(F33.0)
A.
B.
C.
D.
E.
F.
G.
H.
I.
J.
K.
(20)(30501)
(2)(F34.0)()
2
2();
3
A.
B.
C.
D.
E.
F.
G.
H.
3
A.
B.
C.
D.
E.
F.
G.
H.
(20)(30501)
6.1ICD-103CCMD-3
(2)()()2
ICD-10()
ICD-10()ICD-10
Differential diagnosis
()()
1.()
(1)
(2)
(3)
2.
(1)
;
;
;
423
(2)50%75%
(3)
(4)()()
ICD-10A.
a.();
b.;
B.
a.;
b.;
c.;
d.;
e.;
f.
A23
ICD-10DSM--A.;B.;C.ICD-10
(1)()312(6)
1
(1)CCMD-2RCCMD-3CCMD-3;;CCMD-3
A.;();
B.
C.182
D.();()
