Schizophrenia occurs in young adults, with a point-in-time prevalence of about 1 to 11 per 1,000, with great variation from place to place. Clinical manifestations include disorders of perception, thinking, emotion, behavior, and other aspects, as well as uncoordinated mental activities. Patients are generally conscious and their intelligence is basically normal, but some patients may develop cognitive impairment during the course of the disease. The course of the disease is prolonged and progresses slowly, and may gradually worsen or deteriorate if not actively treated, with the possibility of developing into decline. Some patients may remain cured or largely cured. The disease has had a number of names, such as France Morel (1856) named early-onset dementia (dementia praecox); Germany Kahlbaum (1868) described cases of catatonia; Hecker (1870) reported cases of youthful dementia (hebephrenia); Germany Krapelin (1896) unified the above nomenclature into early-onset dementia (dementia paranoides), which was the first classification of mental illness. In 1911, through careful clinical observation, E. Bleuler pointed out that the disease was a split personality due to pathological thought processes and did not always end in decline, introducing the term “schizophrenia” into psychiatry for the first time, and it has been used ever since. The age of onset of schizophrenia tends to be in the 15-45 age group. According to information published by the World Health Organization (WHO) in 1992, the point-in-time prevalence of the disease was 1‰ to 11‰; the estimated lifetime prevalence of schizophrenia worldwide is approximately 3.8‰ to 8.4‰. The results of a 12-region epidemiological survey of mental illness in China in 1982 showed that the lifetime prevalence of schizophrenia was 5.69 ‰. 12-year follow-up conducted in 1994 showed an increase to 6.55 ‰, with urban prevalence higher than rural prevalence, 7.11 ‰ for the former and 4.26 ‰ for the latter. 1978 results of the National Sample Survey of Disabled Persons showed that the disability rate of schizophrenia was 1.67%. There was no significant difference in prevalence between men and women. Schizophrenia, although similarly documented in ancient texts but not clearly separated from other mental illnesses, may be equivalent to what Chinese medicine calls “epilepsy”, “madness”, or “nymphomania” in Chinese medical literature. It may be equivalent to what is known as “epilepsy” or “madness” in Chinese medicine, or “nymphomania”, “wind in the heart”, “wind evil”, or “dullness” in Chinese medical literature. The name of epilepsy is derived from the Nei Jing. The Ling Shu. Epilepsy” is the earliest special chapter on epilepsy. (a) Genetic factors Genetic factors play an important role in the development of schizophrenia. Family surveys have found that the risk rate of homozygosity among first-degree relatives of patients is about 4% to 14%, which is 10 times higher than that of the general population. If both parents have schizophrenia, the risk rate can be as high as 40%. In the second-degree relatives of patients, the risk rate is three times higher than that of the general population. The closer the blood relationship, the higher the prevalence. Twin studies have found that monozygotic twins (MZ) have four to six times the rate of homozygosity than dizygotic twins (DZ). The role of genetic factors in the pathogenesis of schizophrenia is similarly supported by studies of foster children, which found that children born to schizophrenic mothers and children born to normal mothers who grew up in the same living environment as foster children still had a higher prevalence rate in adulthood than children born to normal mothers, suggesting that genetic factors have a greater influence than environmental and other factors. Modern research on genetic factors has focused on finding chromosomal and genetic abnormalities in families with a high prevalence of schizophrenia. The most frequently reported of these are the long arm of chromosomes 5, 11, 21 and 8 and the short arm of chromosome 19 and the X chromosome. In recent years, the association of chromosomes 6, 13 and 22 with schizophrenia has also attracted attention. The “single gene theory” and the “accumulative effect theory of multiple causative genes” are hypotheses regarding the mode of inheritance. Molecular genetic research methods have focused on linkage analysis and candidate gene studies, but there are no accepted findings to date. (2) Neurobiochemical pathological hypothesis (1) Dopamine (DA) hyperfunction hypothesis DA receptor agonists such as amphetamine can increase the level of DA in the brain synaptic gap, leading to delusional schizophrenia-like psychotic disorder in normal people, and also aggravating the psychotic symptoms of schizophrenic patients; almost all antipsychotic drugs are blockers of D2 receptors. Postmortem autopsies of schizophrenic patients have revealed increased levels of brain tissue DA and its metabolite homovanillic acid (HVA) in some patients, and higher D2 receptor density than in normal controls. This hypothesis is based on the belief that the dopamine pathway in the brain is abnormal. In the last 20 years, this hypothesis has evolved again, suggesting that D1 receptors may be associated with negative symptoms, and some scholars have even begun to investigate the use of D1 receptor agonists to treat negative symptoms. Although the dopamine hypothesis of schizophrenia has dominated biochemical studies of schizophrenia, it has also been questioned by a number of contrary data, which suggest that the pathogenesis of schizophrenia is complex. 2. Abnormal pentazocine (5-HT) function hypothesis An indole complex lysergic acid diethylamide (LSD) is an anti-5-HT metabolite that can cause transient schizophrenia-like symptoms in healthy individuals; second-generation antipsychotic drugs such as clozapine, risperidone, and olanzapine have strong antagonistic effects on 5-HT2A receptors in addition to central D2 receptors, and can effectively improve both positive and negative symptoms in schizophrenic patients, and second-generation antipsychotics have a high affinity for 5-HT2A receptors, while 5-HT neuronal transmission can also modulate DA agonism and release. The above studies indirectly suggest that 5-HT plays an important role in the pathophysiological mechanisms of schizophrenia. 3. Amino acid neurotransmitter hypothesis The reduced function of central glutamate may be one of the pathologies of schizophrenia. Radioligand binding and magnetic resonance spectroscopy techniques have revealed significant changes in the binding of glutamate receptor subtypes in certain regions of the brain in schizophrenic patients; glutamate receptor antagonists, such as phencyclidine (PCP), can cause a range of schizophrenia-like positive and negative symptoms and cognitive impairment, while glycine can increase the function of glutamate receptors and can reduce schizophrenia when combined with antipsychotic drugs Patients with negative symptoms and positive symptoms, etc. 4. Other hypotheses Some people have proposed the acetylcholine (Ach) hypothesis, on the grounds that acetylcholine has anti-DAergic effects in the brain. Several studies have found that plasma monoamine oxidase (MAO) activity is lower in schizophrenia patients than in normal subjects. Studies on neuropeptides mainly involve studies on endorphins, thyrotropin-releasing hormone, adrenocorticotropic hormone, adrenocorticotropin-releasing hormone, cholecystokinin, growth inhibitory hormone, and neuropeptide Y. However, the mechanism of action is not clear. (iii) Neuropathological and neurodevelopmental theories 1. Neuropathological hypothesis A large number of studies have found that some schizophrenic patients have shrunken brain volume and enlarged ventricles, and the application of CT, MRI, SPEC and PET techniques since the 1970s has confirmed that brain tissue atrophy in schizophrenic patients exists in the frontal lobe, temporal lobe – limbic system and caudate nucleus; enlarged ventricles, especially the lateral and third ventricles are obvious; cerebral blood flow Decreased cerebral perfusion was evident in the frontal and temporal lobes. These changes are present in the early stages of psychiatric disorders, even before the start of treatment, suggesting that the etiology may be due to abnormalities in the development of the nervous system. 2, neurodevelopmental hypothesis Neurodevelopmental defects in schizophrenia are related to viral infection during maternal pregnancy affecting fetal neurodevelopment and structural disorders of nerve cells in the cerebral cortex; maternal pregnancy and perinatal comorbidities may increase susceptibility to schizophrenia. If the genetic factors are similar, whether or not to suffer from schizophrenia, these environmental factors have a great influence. (iv) Other biological factors Schizophrenia mostly develops during sexual maturity around puberty, and some women have a high incidence of acute onset after childbirth and relapse during menopause, indicating the role of endocrine in the pathogenesis. The presence of thyroid, gonadal, adrenocortical, and pituitary dysfunction in some patients has been suspected by some scholars as the cause of the disease, but none of these studies have been conclusive. It has been found that a significant proportion of schizophrenia has abnormal immune function involving components such as NK cells, lymphocyte subsets, lymphocyte conversion function, lymphokines, human leukocyte antigens, autoantibodies, anti-brain antibodies, immunoglobulins, and complement. These abnormalities have been linked to family history, disturbances in endostasis, neuroendocrine, and neurotransmitter changes, and in-depth studies are beneficial to further understanding of the pathogenesis.