manic depression
Introduction
Introduction to Manic Depression Manic depression, also known as affective disorder (affectivedisorders), is a mental illness with emotional morbidity as the main symptom. Manic depression manifests as recurrent episodes of either mania or depression (single phase), or alternating episodes (biphasic). The cause may be related to the imbalance of monoamines in the brain, but 5-HT deficiency is the common biochemical basis. On this basis, the NA function is hyperactive, the patient's mood is high during the attack, the association is agile, and the activity increases. Insufficient NA function is depression, which is characterized by depression, reduced speech, mental and motor retardation, self-blame and sin, and even attempted suicide. The vast majority of patients require hospitalization, and severe cases require mandatory hospitalization. Isolation of the patient from others, making it quiet, ensuring food intake, and paying attention to water and electrolyte balance. The use of the antipsychotic drugs chlorpromazine, haloperidol, and clozapine helps to quickly control excitement. Lithium salt has a good therapeutic effect on manic episodes and can prevent recurrence, each time 1 ~ 2g, 2 to 3 times a day for 4 weeks, should not be combined with haloperidol. basic knowledge The proportion of illness: 0.0005% Susceptible people: no specific population Mode of infection: non-infectious Complications: mental illness
Cause
Manic depression
Genetic factors (25%):
Genetic factors play an important role in the occurrence of this disease, and the evidence is:
(1) The first-degree relatives (parents, siblings, hands and children) of patients with affective disorder have a lifetime of 12% to 15%, which is much higher than the general population (1% to 2%).
(2) The incidence rate of monozygotic twins (MZ) was 67% (46 pairs), and that of twin twins (DZ) was 14% (276 pairs). Another 12 pairs of .MZ raised their respective rates of up to 65%. The study of the host also proved that the influence of genetic factors was significantly higher than the environmental impact. However, as far as the current data are concerned, affective disorders are related to heredity, but there is not enough evidence to show that it is a hereditary disease.
Psychosocial factors (25%):
Major negative life events, that is, unpleasant, loss of loss and frustrating life events, are not only related to neuropathic depression and psychogenic depression, but also can be endogenous emotional manic depression disorders. Causes or causes of the disease. For example, Paykel pointed out that in the past six months, there were significant life events, the risk of depression increased by 6 times, and the risk of suicide increased by 7 times. Moreover, the severity of life events is related to the onset time, and the probability of developing depression is higher than usual in a year that is subject to a serious threat to personal safe living.
There is not enough evidence to believe that the innate quality of affective disorder is influenced or altered by a particular encounter or experience in childhood. It seems that this causal relationship is still difficult to determine. As for the relationship between childhood and the relationship between parents and the onset of this disease, it is difficult to be sure.
Neurobiochemical factors (20%):
(1) Monoamine neurotransmitters: studies of monoamine neurotransmitters for affective disorders, mainly around norepinephrine (NE) and 5-HT.
1NE: There are many reports that the urinary NE metabolite MHPG excretion in patients with bipolar depression is reduced in depression and increased in mania. The amount of urinary MHPG in patients who had been relieved by antidepressant treatment increased. The urinary MHPG excretion varies greatly among patients with unipolar depression, and those who are significantly lower may be part of a bipolar disorder, although there has been no manic episode so far.
25-HT: Depression 5-HT dysfunction is reported in the cerebrospinal fluid (CSF) 5 HT metabolite 5 HI depression AA level is reported more. The level of 5-HT in CSF was negatively correlated with suicide, suicide attempt and aggression. In recent years, seasonal depression has attracted people's attention. The onset of winter depression is accompanied by a decrease in 5-HT and 5-HTAA in CSF. Receptor studies found that antidepressants are closely related to the 5-HT2 receptor. Long-term use of antidepressants can reduce the number of post-synaptic 5-HT2:receptors. At the same time, it was also found that the density of platelet 5-HT uptake in patients with depression decreased.
Affective disorder factors (20%):
(1) Endocrine causes: due to certain endocrine diseases, symptoms such as Cushing, Edison, and hyperthyroidism may occur, and patients with depression may have certain endocrine abnormalities, premenstrual and menopausal. Depression after childbirth may be associated with endocrine changes. Therefore, some people have proposed the endocrine cause of affective disorder. But a lot of research can't confirm this hypothesis. Other physical diseases can only be used as a cause or cause of the disease.
(2) Abnormal water and electrolytes: It has been reported that both manic or depression have increased intracellular sodium. Some people say that sodium, potassium and ATPase in red blood cells change. However, these findings do not clarify the cause of the disease.
(3) Electrophysiological studies: Although abnormal findings, such as depression, sleep EEG can reduce total sleep, arousal times, eye movement sleep (REM) latency shortened, non-REM sleep first phase increased and third and fourth phase reduction Wait, but not as a cause.
4) Cerebral blood flow study: The results are quite inconsistent, and the number of cases in PET research is too small, and there is no positive result.
(5) Changes in biological rhythm: Studies have shown that many physiological functions of affective disorders (such as body temperature, sleep and cortisol and other endocrine) have biological circadian rhythm changes, but its significance remains to be explored.
Pathogenesis
Biochemistry
(1) Biogenic amines: The relationship between biogenic amines and affective disorders is one of the most well-understood areas of research to date. Many studies have reported abnormalities in the presence of biogenic amines or biogenic amines in patients with affective disorders. The hormone (NE) and serotonin (5-HT) are considered to be the most relevant. Table 2 lists the changes in neurotransmitters and their metabolites in patients with depression.
In addition, almost all antidepressants and effective physical therapy (such as electroconvulsive therapy) in the in vivo test reduce post-synaptic adrenergic and 5-HT2 receptor sensitivity in long-term use. Table 3 lists the results of this research. The changes brought about by this long-term treatment coincide with the onset time of antidepressants.
(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. The hypothesis about the relationship between GABA receptors and the onset of affective disorder is mainly derived from the application of anti-epileptic drugs effective in the treatment of mania or bipolar disorder such as sodium valproate and carbamazepine studies showing cerebrospinal fluid in patients with depression and The plasma GABA content decreased. Tricyclic antidepressants, MAOISSRIS, and ECT all increase the number of GABA receptors. The main excitatory amino acids in the central glutamate system have a mutual restriction on GABA function. The receptors of glutamate can be coupled into ion channels in two major categories, which may be related to the onset of epilepsy. Coupling with G protein is a metabolic glutamate receptor (mGluR). Metabotropic glutamate receptors are divided into five subtypes. Among them, mGluR2 may be associated with the onset of depression and mGluR2 receptor antagonist may become a promising new class of antidepressant drugs.
(3) Second messenger system: Rolipram is a selective inhibitor of phosphodiesterase and has been shown to have antidepressant effects in clinical trials. According to this, the function of cAMP second messenger system is related to the onset of affective disorder. Depressive patients have a low level of 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 to the G protein, in addition to cAMP, also has a phosphoinositide (IP) system receptor that binds to the excitatory ligand to activate the excitatory G protein (Gi) Gi to activate the phosphatidylinositol-specific phospholipase C. (PLC) The latter acts on phosphatidylinositol diphosphate (PIP2) on the inner side of the phospholipid layer of the cell membrane to form diglyceride (DAG) and inositol triphosphate (IP3). IP3 releases Ca2+ stored in the inner web. While Ca2+ interacts with DAG, activation of protein kinase C (PKC) PKC activates many cytoplasmic proteases, which in turn trigger various biological processes including gene transcription. After the function is completed, IP3 needs to be hydrolyzed by inositol monophosphatase to release free inositol, and then synthesized with DAG as IP to complete the whole cycle. Li+ ions are inhibitors of inositol monophosphatase. The therapeutic concentration of Li+ inhibits the inositol monophosphatase and blocks the phosphoinositide cycle leading to a change in the IP second messenger function, thereby achieving the goal of treating manic episodes. Therefore, some scholars speculate that the incidence of affective disorder may be related to the abnormal function of IP second messenger.
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 in patients with affective disorders may mainly reflect the abnormal function of monoamine neurotransmitter system. Just like traditional antipsychotic drugs, it can block the function of nodule-funnel dopamine, resulting in elevated levels of prolactin in patients. In theory, a certain neuroendocrine function change may be the cause of the affective disorder and more likely to be a manifestation of the underlying brain dysfunction.
(1) Hypothalamic-pituitary-adrenal (HPA) axis:
1 cortisone concentration:
A. The regulation process of cortisone secretion is as follows:
B. Hypothalamic-pituitary-adrenal axis dysfunction that can be found in patients with depression includes:
(2) Hypothalamic-pituitary-thyroid (HPT) axis: The functional characteristics 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 endocrine cells containing thyroid stimulating hormone (TSH) to release TSHTSH to the thyroid gland to cause thyroxine (T4) and 3,5, Release of 3-triiodothyronine (T3) T4 can also be converted to T3 in addition to the thyroid and T4 and T3 form a negative feedback regulation of TRH and TSH release to achieve physiological balance.
(3) Changes in other hormone secretion: The secretion of growth hormone (GH) has a circadian rhythm that reaches a peak during slow eye movement sleep. This peak becomes flat in patients with depression. The increase in GH secretion caused by clonidine has also become dull in patients with depression.
Depression can also be accompanied by changes in other hormone secretion rhythms such as decreased secretion of melatonin. Administration of tryptophan does not promote prolactin secretion, urinary tropoelastin and luteinizing hormone secretion decrease, and testosterone levels in men. Decline.
Neuroimmunology
Recent decades of research have found that the human immune system and the central nervous system have a two-way regulation and play a role in the endocrine system. Because of the many factors affecting the activity of the endocrine nervous system and even the immune function, we need to pay attention to the following two points when understanding their relationship with affective disorders: First, there is a close mutual adjustment between immune function and endocrine function, thus affecting the spirit of endocrine function. Obstacle or life events can have an impact on immune function. This must be fully considered when treating physical illnesses, especially those associated with tumors. Furthermore, because immune function has a reverse regulation of the function of the neuroendocrine system, immunomodulation such as cytokines and immunological processes may affect the functions of the nervous system and endocrine system, and thus play an important role in the pathophysiology of mental disorders. . In summary, changes in immune function accompanying affective disorders may be both fruit and affect the patient's physiological function, or may be caused by the formation or delay of affective disorder.
The impact of stress events on the immune system begins earliest. The effects of stress events on the immune system can be excitatory or inhibitory depending on the duration of the event. In the study of immune function changes of bereaved people, it was found that the degree of depression of bereaved people 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 severe depression, older men The patient's immune function changes are more prominent.
Emotional disorders and stress events can affect immune function, and changes in immune function can also be the cause of affective disorders. The initial evidence comes from behavioral symptoms that appear in various elevated levels of cytokines, including depression. These manifestations are called sickness behaviors. They are caused by the application of proinflammatory cytokines, including leukocyte mediators. (IL) 2 and 3 tumor necrosis factor, interferon-/ and the like. Symptoms include debilitating fatigue, loss of burnout, snooze, anorexia, social isolation hyperalgesia, and lack of concentration. Elevated levels of serum inflammatory cytokines have also been found in major depression, including IL-6 and fast response proteins (eg, haptoglobin, C-reactive protein alpha 1-acid glycoprotein). This rapid response process may result in a decrease in the L-tryptophan content resulting in a decrease in 5-HT levels in the brain. In addition, IL-1 can block the action of glucocorticoids on effector tissues by directly inhibiting the expression of glucocorticoid receptors and their functions, thereby causing hyperactivity of the HPA axis by impairing its negative feedback regulation function.
Sleep and brain
It is a common symptom of depression to have difficulty in falling asleep with physiological abnormalities, waking up when sleeping, or being oversleeping when waking up early. In the case of mania, sleep requirements are often reduced. Therefore, the relationship between affective disorder and sleep and sleep EEG changes has long been valued by researchers. The main findings are: sleep-prone rapid eye movement (REM) sleep latency (from sleep to REM sleep) shortens the first REM sleep The time course prolongs the delta wave sleep abnormality and the like. EEG study found that P300 and N400 latency in patients with depression extended full sleep deprivation or REM sleep therapy has a 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 are aware that there is a close relationship between electrophysiological activity and emotional activity. There is an "ignition" theory that repeatedly applying subthreshold stimulation to a neuron ultimately leads to an action potential. 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. Antiepileptic drugs such as sodium valproate and carbamazepine are blocked. This repeated subthreshold electrical stimulation plays a role in emotional stabilization.
Brain imaging
Research on brain imaging studies of affective disorders has no consistent and repeatable conclusive research results. The existing research has the following findings: 1 part of the biphasic type I patients, especially males, have ventricular enlargement. The ventricle enlargement in patients with severe depression is not as pronounced as that in patients with depression who have significant psychotic symptoms in bipolar I patients. 3 Magnetic Resonance Imaging (MRI) studies also found that the caudate nucleus of patients with major depression decreased the amount of frontal atrophy. 4 The hippocampal T1 relaxation time was abnormal in patients with depression. 5 bipolar I patients found deep white matter damage. 6 Single-photon emission imaging (SPECT) or positron emission tomography (PET) is used, and blood flow in the cerebral cortex, especially in the frontal cortex, is reduced in some patients with depression. 7 Using magnetic resonance spectroscopy (MRS) technology, it was found that the abnormality of cell membrane phospholipid metabolism in patients with biphasic type I was consistent with the second messenger theory of the onset of bipolar disorder and the action site of Li+ ions. The effect of Li+ ions on phospholipid metabolism was also found in animal experiments.
Genetic research
Genetic studies to date have affirmed that genetic factors play an important role in the pathogenesis of affective disorders, but the mode of action of genetic influences is very complicated. Only one factor of genetics is used to explain the occurrence of affective disorders is a psychological society that does not work. Factors not only play an important role in the pathogenesis of affective disorders, but some patients may play a decisive role, leading directly to the occurrence of obstacles. On the other hand, genetic factors have a stronger effect on bipolar disorder than depression.
Psychological society
Factors using a single genetic factor can not explain satisfactorily to affect the emotional disorder, especially the cause of depression. Even if genetic factors play an important role in its pathogenesis, the induction of environmental factors, and even the pathogenic role can not be ignored. It is generally believed that genetic factors may lead to a susceptibility to a susceptibility to a certain neurotransmitter system or other physiological function in the development of affective disorders. However, people with such susceptibility qualities are not all or nothing under the trigger of certain environmental factors, but present a transitional state. People who are more susceptible may become ill under the influence of lighter environmental factors. People with lesser susceptibility may still be affected by more significant environmental factors. Of course, the quality of susceptibility does not necessarily come entirely 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, and environmental factors are more important for the development of depression.
Prevention
Manic depression prevention
1. Establish 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. A correct outlook on life and a world outlook enables young people to correctly understand the relationship between the outside world and individuals, and give full play to their roles and abilities to coordinate and handle various situations. Relationships ensure that the psychological response is moderately preventive. If a person's needs and ideal behaviors violate social norms, they will naturally suffer from setbacks and fall into endless troubles and pains, leading to psychological unhealthy visibility. The correct outlook on life and worldview is The ideological foundation and psychological basis for ensuring personal mental health.
2. Understand yourself and accept yourself
Failure to know yourself correctly is often one of the important reasons for the formation of psychological barriers. To maintain mental health, you must not only understand your strengths and abilities, but also understand your deficiencies and shortcomings and face them. If you don't understand yourself and don't accept it, then you don't feel uncomfortable. When you are not at birth, you are cynical and arrogant, or you are overly inferior and anxious, leading to psychological imbalance. Therefore, young people should have self-knowledge on the basis of fully understanding themselves, not only high self-estimation or self-deception, so that they can reduce their psychological conflicts and maintain mental health.
3. Recognize reality and face up to adversity
In real life, objective reality and not subject to human subjective will, as long as individuals are required to fully understand and understand reality, adapt and transform reality, this requires young people to face reality and unify their individual desires and demands with the real society. stand up. Of course, young people have the right to "self-design", but this design must not deviate from the real track or "self-design" can only be a fantasy. In addition, young people have to face the adversity is also inevitable, such as the hard work of learning, the hard work of the cadres, the failure of the exam, the professional restrictions, the hardships of the hard-working classmates in the employment, and so on. In this regard, young people should take the courage to cultivate their own psychological quality that is not chaotic and coping with it. To form this kind of good quality, we must love life, love learning and work, learn to look at problems comprehensively and objectively, not care, not short-sighted. The long-term is not good, the high-dealing, the need to have difficulties and frustrations at any time, and the ability to adjust the self-social relationship.
4. Establish good interpersonal relationships
Good interpersonal relationship is not only a condition of mental health, but also a good performance of mental health. The establishment of interpersonal relationship is not based on welcoming and charming, but on the character of honesty, strictness, and willingness to help others. Therefore, young people should exercise their good qualities in social interactions, and be confident that they will be self-respecting and self-help. Properly handling interpersonal relationships means dealing with the opposite sex of parents, teachers, classmates and friends. Especially the relationship between friends is the most important to deal with interpersonal relationships with a "good size." Good size refers to the ability to learn and imitate others. This will not only create a harmonious atmosphere with the people around them, but also help to cultivate and stabilize the best mentality, and it is easy to handle the surrounding things.
5. Work and rest combines scientific brain
Certain learning pressures can stimulate interest in learning and improve learning efficiency, which is beneficial to mental health. Therefore, we advocate diligence in using the brain. However, excessive use of the brain will destroy the nerve activity of the brain, leading to mental fatigue, mental decline, mental dysfunction, insomnia and exhaustion. Psychological fatigue not only fails to complete the task but also seriously hinders the healthy development of the mind. Therefore, it is necessary not only to diligently use the brain but also to use the brain scientifically to achieve the combination of work and rest. The so-called scientific brain refers to letting the various nerve cells of the brain rotate in order to balance the excitement and inhibition process of the brain. First, we must learn to scientifically arrange the day of study, work and life, and the learning time is controlled. Within 10 hours; the second is to rest well to ensure adequate sleep; the third is to strengthen physical exercise and actively participate in extracurricular activities to broaden the scope of interest. In this way, the learning life is tight and lively, so as to better improve the learning efficiency and maintain physical and mental health.
6. Maintain a healthy mood and master the ways to overcome bad moods.
Emotion is an important factor affecting physical and mental health. Therefore, to maintain physical and mental health, it is necessary to maintain a healthy mood, learn to be the master of emotions, and not to be a slave to emotions. And the power of reason to suppress the impulse of emotions, to be good at suppressing personal emotions, to promptly guide the pressure of the negative emotions that have been formed to relieve the spirit. Everyone's emotions will not be static, good or bad, when the waves fluctuate, and when the calm is like a mirror. Therefore, we must learn to control emotions, especially in the shortest possible time to eliminate bad emotions in the bud, so that they will not expand, spread, or even cause disasters. First, we must pay attention to the use of "sense adjustment." Psychology believes that people lose their temper and fight, often because of the emotional breakthrough of the door to reason. Therefore, everything should be thought twice. Otherwise, it is easy for the other party to understand that the leakage has formed a sudden contradiction, resulting in a loss of rational balance between the haste. In the event of encountering the "top cow", you must first be good at pressing the "fire", to show your generosity and noble personality. Secondly, the "retreat" that is good at "retreating" and "retreating" as "advance" is a positive psychological factor to eliminate "warfire."
Complication
Manic depression complications Complications
Severe mental illness, usually without complications.
Symptom
Manic Depressive Symptoms Common Symptoms Melancholy Anxiety Insomnia Appetite Depressed Illness Suicidal Suicidal Behavior Crying Screaming Pleasure Lack of Helplessness
Clinical manifestation
1 Depressed state : Depressed mood is a characteristic symptom of depressive disorder. The emotional tone is low and dark. It can range from mild mood, upset, distressed, sad, pessimistic and desperate. On this background, anxiety and agitation can occur. The patient's expression is tense, uneasiness, uneasiness, inability to lose interest, can not experience fun; energy loss; low self-evaluation; mental retardation; suicidal concept and behavior; patient's mood has a heavy rhythm change, is Depression is a typical symptom of endogenous depression, physical or biological symptoms such as dry mouth, constipation, indigestion, and decreased gastrointestinal function.
2 Manic state: The mood is high, and the performance is relaxed, happy, enthusiastic, optimistic, elated, playful, and self-satisfied; thinking and running, the association process is obviously accelerated, the concept is followed, the voice is loud, the volume is too much, the mouth is overwhelming, the feeling of self-feeling Good, over-evaluating yourself; mental sports excitement, manifested in a wide range of patients' interests, likes to lively scenes, more communication, work is often anticlimactic, and the spirit is extremely strong.
Examine
Manic depression check
1, serum corticosteroids to determine abnormal secretion of corticosteroids, showing increased secretion, normal secretion of circadian rhythm, dexamethasone can not inhibit this secretion. Determination of luteinizing hormone levels in patients with menopausal depression. Determination of serum thyroid stimulating hormone levels to patients with thyroid stimulating hormone release hormone, thyroid stimulating hormone secretion decreased. Cerebrospinal fluid 5 - HT, 5 - HIAA detection of depression 5 - HT function is manifested in the cerebrospinal fluid (CSF) 5- HT metabolite 5 - HIAA level is reduced. The level of 5-HT in CSF was negatively correlated with suicide, suicide attempt and aggression. The onset of winter depression is accompanied by a decrease in 5-HT and 5-HIAA in CSF.
2, mental and psychological examination, is a functional disease, but need to rule out emotional changes caused by brain organic diseases.
Diagnosis
Manicure depression diagnosis
diagnosis
The diagnostic criteria for affective disorders can be divided into the diagnostic criteria for depression and manic episodes, as well as the classification criteria for various types of affective disorders. Although countries have considerable differences in the classification of affective disorders, the main diagnostic criteria for the diagnosis of depressive manic episodes There is little difference between classification systems (such as ICD-10, DSM-IV, and CCMD-2-R). In the common classification system, the definition of depressive episodes needs to first investigate whether there is a manic episode in the medical history. Inclusion in bipolar disorder or inclusion in depressive episodes. ICD-10 is now taken as an example.
1. Depressive episodes In ICD-10, depressive episodes do not include depression in bipolar disorder. Therefore, depressive episodes only include first episodes of depression or recurrent depression.
2. Recurrent depressive disorder Recurrent depressive disorder uses the same diagnostic criteria as depressive episodes.
(1) General criteria for recurrent depressive disorder:
(2) subtypes of recurrent depressive disorder: according to the current state of attack can be further divided into:
3. Diagnostic criteria for manic episodes The criteria for manic episodes and hypomanic episodes are separately described in ICD-10.
(1) Gentle mania (F30.0): Symptomatic criteria can also be divided into core symptoms (ie, increased or irritating) and additional symptoms.
(2) Manic, without psychotic symptoms (F30.1).
(3) Manic, with psychotic symptoms (F30.2):
4. Bipolar disorder (F31) is defined as a diagnosis of a phased or mixed phase episode followed by a biphasic disorder followed by a two-phase disorder: this episode meets the criteria for a certain episode above; At least one other episode of affective disorder, such as this type of depressive episode, has been preceded by at least one episode of hypomania, mania, or mixed affective disorder.
5. Persistent mood (affective) disorder (F34) In view of ICD-10DSM-IV and the forthcoming CCMD-III, persistent mood disorders, namely depressive neurosis (mood bad mood) and circulatory affective disorder are included in the mood disorder chapter. The ICD-10 diagnostic criteria for the two disorders are listed here for reference.
6. Relevant discussion Classification of mood disorders Because a considerable number of patients have only one episode, they are distinguished from biphasic and repeated episodes. At the same time, the severity is related to treatment and care, so ICD-10 is divided into mild moderate and severe grades. According to the actual needs of China, CCMD-3 only divides two grades of mild and severe.
Bipolar disorder is characterized by repeated (at least 2) episodes of mood and activity levels, sometimes manifested by high moods, increased energy and activity (mania or madness) and sometimes low mood And reduced activity (depression and mild depression). The interictal period usually resolves or is substantially relieved. However, it should be noted that depressive mood accompanied by hyperactivity and verbal urges for several days to weeks and manic state and exaggeration are accompanied by agitation, energy and initiative, and rare symptoms of depression and madness or paralysis. Madness can also be quickly converted or even different every day. If the two sets of symptoms are prominent most of the time in the current episode of the disease and the episode lasts for at least 2 weeks, a diagnosis of mixed bipolar disorder should be made.
Differential diagnosis
The diagnosis of affective disorder should be based primarily on the analysis of symptomology (cross section) and disease duration (longitudinal). Previous mania or depressive episodes have important reference significance for the diagnosis of this episode and are the basis for further classification, and should be collected. The following is a brief description of the differential diagnosis of manic and depressive episodes.
Differential diagnosis of manic (light mania) attacks
(1) Schizophrenia:
Patients often have excitement, sometimes confused with manic episodes. The excitement of youthful excitement is called "inconsistency". It refers to the excitement of the patient. The symptoms of schizophrenia are incompatible with the environment. The emotions and thinking of oneself are not coordinated. The tone of the emotion is not high and it is stupid and silly. It can't make others resonate and the family history of affective disorder. The pleasant and high-incidence of acute onset emotions is more common in manic episodes.
(2) Physical illness: Different from depressive episodes, manic episodes have stronger characteristics and are not common among other mental disorders. However, manic episodes may be accompanied by certain physical illnesses, especially brain diseases.
This kind of manic episode caused by physical illness is generally not manifested as a typical emotional upswing. There is no "happy" clinical feature, but the experience of emotional instability, anxiety and tension is mainly related to the primary disease. The mania of brain organic diseases is dominated by the euphoric experience, which does not have the distinctiveness and appeal, and patients do not actively participate in the environment. Detailed physical and laboratory tests can be identified.
(3) Drugs: Certain drugs (Table 5) can lead to manic-like performance.
This episode has a close relationship with medication. Patients are often accompanied by varying degrees of consciousness disorder and are generally not difficult to identify.
Differential diagnosis of depressive episodes
(1) Physical illness: Many physical illnesses may be associated with or cause depressive disorders.
At this time, the relationship between depression and physical condition can be: 1 physical illness is the direct cause of depression, that is, as a biological cause of depression, such as emotional changes caused by endocrine diseases; 2 physical illness is the occurrence of depressive disorder The incentive is that physical illness exists as a psychological factor of affective disorder; 3 physical illness and depressive disorder are accompanied by no direct causal relationship. Even in this case, the two states still have a mutually reinforcing effect; 4 depressive disorder is the body The immediate cause of the situation, such as physical symptoms associated with depression. The diagnosis of physical illness at this time may be a misdiagnosis. The differential diagnosis is actually to distinguish these situations one by one. This distinction is obviously not possible in all patients but there are still some principles for reference.
Since these patients are mainly diagnosed in general hospitals for safety reasons, doctors will first consider the exclusion of obvious physical illnesses. Complete medical history, detailed physical and neurological examinations, supplemented by routine blood and urine tests can provide important evidence. Care should be taken to minimize special examinations. This may aggravate the patient's psychological burden, leading to further depression and anxiety. Except or establish the fourth case. However, even if the diagnosis of physical illness is established, it cannot be considered that the patient's depression is completely due to physical illness and is not actively interfered because there are still cases 2 and 3. Even the first case may be treated with antidepressant. There is a certain effect, so active intervention is still necessary.
(2) Nervous system diseases: Depression secondary to brain organic diseases is common in cerebral arteriosclerosis, brain degenerative diseases, brain tumors, epilepsy and other brain organic diseases. Symptoms of organic diseases can be found through medical history and examination. Laboratory tests and special tests for signs can also provide evidence. The most common neurological disease that causes depression is Parkinson's disease. The incidence of depressive symptoms in patients with Parkinson's disease is 50% to 75%. The symptoms of depression are not related to the degree of disability caused by physical illness, the age or duration of the patient, but are related to the results of neuropsychological assessment. Such patients with antidepressant drugs or electroconvulsive therapy for effective temporal lobe epilepsy can also be associated with depressive episodes, especially when the epilepsy lesion is located in the right brain.
(3) Dementia: Depression, especially in the elderly, may be accompanied by obvious cognitive changes, similar to dementia called pseudo-dementia, when the incidence is more urgent than the slowness of Alzheimer's disease Onset, clinical manifestations have certain requirements for treatment and self-knowledge sometimes self-blame, clinical symptoms may have morning and night light day and night changes in the psychological test when depressed patients are more reluctant to answer questions and demented patients will do Possiblely fabricated. Antidepressant treatment can alleviate depression and improve cognitive function in a short period of time.
(4) Other mental disorders: Many mental disorders can be accompanied by depressive symptoms, which should be considered in differential diagnosis. These include other affective disorders (bipolar disorder, dysthymia, circulatory affective disorder, etc.), and other mental disorders (substance dependence, psychotic disorders, eating disorders, adaptation disorders, somatoform disorders, anxiety disorders, neurasthenia, etc.) Other affective disorders should be classified according to their respective diagnostic criteria according to the status quo, medical history and duration of the disease.
