Schizophrenia
I. Overview.
Basic features of schizophrenia: basic personality changes; splitting of thinking, emotions, and behavior; and incompatibility of mental activity with the environment.
1857 French Morel- called: early-onset dementia
1874 Kalbaum, Germany – called catatonia
1871 Hecker- called youthful dementia
1896 Kraepelin, Germany – considered that the above mentioned diseases are actually different types of the same disease, called: early-onset dementia
E. Bleulre, Switzerland, 1911 – believed that the central problem was split personality, called schizophrenia
Second, the etiology and mechanism
Etiology: 1. Genetic factors
2, personality traits
3.Environmental and psychosocial factors
4. organic problems
5.Biochemical abnormalities
Dopamine (DA) hyperfunction theory, around the 1970s, some basic research found that schizophrenia patients with hyperfunction of DA in the brain
1, anti-schizophrenia drugs have anti-dopamine effect;
2, amphetamine (pro-DA release), which can cause schizophrenia-like symptoms;
3, DA iterations in the brain.
(1) substantia nigra-striatal pathway
(2) Midbrain-limbic pathway
(3) Midbrain-cortical pathway
(4) Mesencephalon: nodal-funnel; subthalamic-septum; subthalamic-spinal cord
D1- nigrostriatal, nucleus ambiguus, limbic itinerary
D2-similar to D1, striatum, pituitary gland predominant
D3-olfactory node, hypothalamus, nucleus ambiguus, septum, substantia nigra, ventral tegmental area; pituitary gland without stage D3
D4-frontal, limbic
D5-frontal lobe, limbic system
DA-self receptors are located in the substantia nigra, ventral tegmental area of DA neurons, and presynaptic membranes of nerve insertions
Improvement of the dopamine hyperfunction theory
1. Frontal dopamine insufficiency; DA neural activity in the prefrontal lobe can inhibit DA neural activity in the subsurface of the dermatome; frontal dopamine insufficiency is mainly characterized by emotional indifference and lack of volition;
2. In those with positive symptoms, the DA hyperactivity area in the brain is mainly in the subcortical nuclei.
Clinical manifestations
1. General changes
2. Perceptual disorders: delusion, hallucination, perceptual syndrome
3. Thought disorders: altered coherence of speech, logical disorders, delusions
4. Emotional disorders: indifference, inversion, vulnerability, childishness, high, low
5. Behavior disorders: bizarre, nervousness and rigidity, repetition, injury, destruction
6. Self-awareness: deficiency
7, intellectual disorders: normal at first, then gradually decline.
IV. Diagnosis
1. Characteristic symptoms: verbal hallucinations
Commentary hallucinations
Scattered thoughts, rupture
Thought interruption
Logical inversion
Pathological symbolic thinking
Sense of insight
Sense of being controlled
Delusions of victimization
Passive experience
Primary delusions
Emotional indifference
Emotional inversion
Bizarre behavior
Nervousness and rigidity
2. Decreased social function, partial or total loss of self-awareness
3. Duration of illness more than 1 month
4. Exclusion diagnosis: organic brain disorder, affective mental disorder, psychoactive substance-induced mental disorder, stress disorder.
V. Treatment.
1.Traditional medications.
Chlorpromazine
Fenazaquin
Haloperidol
2. Non-traditional drugs
Risperidone
Olanzapine
Aripiprazole
Quetiapine
Clozapine
Ziprasidone