HOW TO TREAT SCHIZOPHRENIA 2025

HOW TO TREAT SCHIZOPHRENIA 2025

GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF COMMON MENTAL DISORDERS

(Enacted under Decision No. 2058/QĐ-BYT dated May 14, 2020, by the Minister of Health)

Article 13

SCHIZOPHRENIA

CHIEF EDITOR

Associate Professor, PhD Nguyễn Trường Sơn

CO-EDITOR

Associate Professor, PhD Lương Ngọc Khuê

PhD Nguyễn Doãn Phương

CONTRIBUTING AUTHORS

PhD Trần Thị Hà An

MSc Trịnh Thị Vân Anh

PhD Vũ Thy Cầm

MSc Trần Mạnh Cường

PhD Nguyễn Văn Dũng

PhD Vương Ánh Dương

PhD Lê Thị Thu Hà

MSc Trần Thị Thu Hà

MSc Phạm Công Huân

MSc Đoàn Thị Huệ

Specialist Doctor II Nguyễn Thị Minh Hương

MSc Vũ Thị Lan

1. Nguyễn Phương Linh

Specialist Doctor II Nguyễn Thị Phương Loan

MSc Bùi Văn Lợi

MSc Nguyễn Thị Phương Mai

PhD Trần Nguyễn Ngọc

MSc Bùi Nguyễn Hồng Bảo Ngọc

MSc Trương Lê Vân Ngọc

MSc Bùi Văn San

PhD Dương Minh Tâm

MSc Phạm Xuân Thắng

MSc Lê Thị Phương Thảo

MSc Lê Công Thiện

MSc Vương Đình Thủy

Associate Professor, PhD Nguyễn Văn Tuấn

Specialist Doctor II Ngô Văn Tuất

MSc Đặng Thanh Tùng

MSc Vũ Sơn Tùng

MSc Cao Thị Ánh Tuyết

MSc Nguyễn Thị Ái Vân

Specialist Doctor II Hồ Thu Yến

MSc Nguyễn Hoàng Yến

CONTRIBUTORS TO EVALUATION AND FEEDBACK

Associate Professor, PhD Nguyễn Thanh Bình

PhD Vũ Thy Cầm

PhD Nguyễn Hữu Chiến

Specialist Doctor II Võ Thành Đông

PhD Lê Thị Thu Hà

Specialist Doctor II Đỗ Huy Hùng

PhD Nguyễn Mạnh Hùng

MSc Nguyễn Trọng Khoa

Specialist Doctor II Ngô Hùng Lâm

Associate Professor, PhD Phạm Văn Mạnh

Specialist Doctor II Trần Ngọc Nhân

PhD Dương Minh Tâm

MSc Đặng Duy Thanh

PhD Vương Văn Tịnh

Specialist Doctor II Lâm Tứ Trung

PhD Lại Đức Trường

PhD Cao Văn Tuân

Associate Professor, PhD Nguyễn Văn Tuấn

SECRETARIAT TEAM

MSc Đặng Thanh Tùng

MSc Trương Lê Vân Ngọc

BA Đỗ Thị Thư

Article 13

SCHIZOPHRENIA

I. DEFINITION  

Schizophrenia is a severe, progressive psychotic disorder with a tendency toward chronicity. It causes individuals to gradually withdraw from external life into an internal world. Emotional expression becomes increasingly cold and distant, while the ability to work or study declines, accompanied by bizarre, incomprehensible thoughts and behaviors. Schizophrenia affects approximately 0.3-0.5% of the population and typically emerges between ages 18 and 40.

II. ETIOLOGY  

The precise cause and pathogenesis of schizophrenia remain unclear, classifying it as an endogenous disorder influenced by multiple factors: genetics, immunity, toxicity, etc. Current research focuses primarily on genetic abnormalities and disruptions in neurotransmitter systems.

III. DIAGNOSIS  

1. Definitive Diagnosis (ICD-10)  

Diagnosis requires at least one clear symptom from groups 1-4 or two from groups 5-9, persisting for most of a month or longer:  

1. Thought Echo, Theft, or Broadcasting:Hearing thoughts aloud, feeling thoughts stolen, or broadcasted.  
2. Delusions of Control or Passivity: Clear connection to body movements, limbs, specific thoughts, actions, sensations, or delusional perceptions.  
3. Hallucinatory Voices: Continuous commentary on behavior, discussions about the patient, or voices from specific body parts.  
4. Persistent, Culturally Inappropriate Delusions:Implausible beliefs (e.g., controlling weather, communicating with extraterrestrials).  
5. Persistent Hallucinations: Any type, with transient/incomplete delusions lacking emotional content or persistent overvalued ideas recurring daily for weeks/months.  
6. Thought Disruption: Interruption or insertion in speech, leading to incoherence, irrelevant speech, or neologisms.  
7. Catatonic Behavior: Agitation, posturing, waxy flexibility, negativism, mutism, or stupor.  
8. Negative Symptoms: Marked apathy, poverty of speech, blunted/incongruous emotional responses, social withdrawal, or reduced social/occupational performance (not due to depression or antipsychotics).  
9. Significant Behavioral Change:Loss of interest, aimlessness, idleness, self-absorption, and social isolation.  

– Schizophrenia is not diagnosed if extensive depressive/manic symptoms are present (unless psychotic symptoms precede mood disturbances), or if evident brain disease or drug intoxication is present.

2. Clinical Subtypes (ICD-10)  

– Paranoid Schizophrenia  

– Hebephrenic Schizophrenia  

– Catatonic Schizophrenia  

– Undifferentiated Schizophrenia  

– Post-Schizophrenic Depression  

– Residual Schizophrenia  

– Simple Schizophrenia  

3. Differential Diagnosis  

– Organic Psychosis: Similar symptoms but lacks full schizophrenia criteria; neurological and lab findings indicate a clear organic cause.  

– Substance-Induced Psychosis (Alcohol/Drugs): Emerges during or after use, characterized by vivid hallucinations (often auditory, multi-sensory), persecutory delusions, psychomotor disturbances (agitation/stupor), intense fear, and confusion. Symptoms typically subside partially within a month and fully within 6 months. Clinical/lab evidence confirms intoxication or substance use.

4. Ancillary Testing  

4.1. Basic Labs  

– Blood: Hematology, biochemistry, microbiology (HIV, HBV, HCV).  

– Urine: General analysis, drug screening, syphilis serology.  

4.2. Imaging/Functional Tests  

– Chest X-ray, abdominal ultrasound.  

– EEG, ECG, cerebral blood flow, transcranial Doppler.  

– CT/MRI brain (select cases).  

4.3. Psychological Assessments  

– PANSS (Positive and Negative Symptom Scale).  

– Personality: EPI, MMPI.  

– Others: BDI, Zung, HDRS, HARS, HAD, MMSE.

IV. TREATMENT  

1. Treatment Principles  

– Etiology is unclear; treatment focuses on symptom management, early detection, and intervention.  

– Pharmacotherapy is key, especially for positive symptoms; combine with psychotherapy, occupational therapy, and social reintegration, particularly for negative symptoms.  

– Prefer monotherapy; if response is poor, combine two antipsychotics, avoiding three or more to limit side effects.  

– Closely monitor drug use to detect and manage side effects promptly.  

– Educate families/communities to reduce stigma and foster collaboration with healthcare providers.  

– Identify and address relapse triggers promptly.  

– Maintain treatment post-first episode, with community monitoring to prevent recurrence.

2. Treatment Framework  

– Pharmacotherapy alongside psychotherapy and community rehabilitation.

3. Specific Treatments  

3.1. Pharmacotherapy  

– Antipsychotics: 1-3 agents (prefer monotherapy; switch or combine up to 3 if ineffective):  

  – Typical:  

    – Chlorpromazine (25 mg tabs/vials; 50-250 mg/24h).  

    – Levomepromazine (25 mg tabs; 25-250 mg/24h).  

    – Haloperidol (1.5-5 mg tabs, 5 mg vials; 5-30 mg/24h).  

    – Thioridazine (50 mg tabs; 100-300 mg/day).  

  – Atypical:  

    – Amisulpride (50-400 mg tabs; 200-800 mg/24h).  

    – Clozapine (25-100 mg tabs; 50-800 mg/24h).  

    – Risperidone (1-2 mg tabs; 1-12 mg/24h).  

    – Olanzapine (5-10 mg tabs; 5-60 mg/24h).  

    – Quetiapine (50-300 mg tabs; 600-800 mg/day).  

    – Aripiprazole (5-30 mg tabs; 10-30 mg/day).  

  – Doses may increase based on condition and response.  

– Long-Acting Injectables (LAIs): For non-compliant patients; test short-acting equivalents first:  

  – Haldol Decanoate (50 mg/ml IM; 25-50 mg every 4 weeks).  

  – Flupentixol Decanoate (20 mg/ml IM; 20-40 mg every 2-4 weeks).  

  – Fluphenazine Decanoate (25 mg/ml IM; 12.5-50 mg, max 100 mg/day, every 3-4 weeks).  

  – Aripiprazole (300-400 mg IM every 4 weeks).  

– Adjunctive Treatments:  

  – Anxiolytics: Benzodiazepines (diazepam, lorazepam, bromazepam, alprazolam), non-benzodiazepines (etifoxine, zopiclone).  

  – Beta-Blockers: Propranolol.  

  – Antidepressants: SSRIs, TCAs, SNRIs, NaSSAs.  

  – Mood Stabilizers: Valproate, divalproex, carbamazepine, oxcarbazepine.  

  – Neuroprotection: Piracetam, ginkgo biloba, vinpocetine, choline alfoscerate, nicergoline.  

  – Nutrition: Vitamins (B-group), minerals, IV feeding if needed.  

  – Hepatic support, cognitive enhancers.  

– Monitoring:  

  – Side Effects:  

    – Extrapyramidal symptoms (acute dystonia, akathisia, parkinsonism): Cholinesterase inhibitors (trihexyphenidyl, benztropine), beta-blockers, sedatives.  

    – Neuroleptic malignant syndrome: Early detection, ICU management.  

    – Metabolic disorders: Monitor BMI, blood tests every 3-6 months.  

    – Clozapine: White blood cell count every 3 months.  

    – Tardive dyskinesia: Muscle relaxants, sedatives, vitamin E, anticholinergics.

3.2. Electroconvulsive Therapy (ECT) and Transcranial Magnetic Stimulation (TMS)  

– ECT: Effective for catatonia, suicidal ideation/behavior, treatment-resistant delusions/hallucinations, or agitation.  

– TMS: Useful for persistent auditory hallucinations.

3.3. Psychotherapy  

– Individual, family, or group therapy; behavioral therapy is crucial for schizophrenia patients. Support groups aid patients and families.

3.4. Occupational and Rehabilitation Therapy  

– Start activities at the patient’s capability level to rebuild confidence, gradually increasing intensity without causing stress.  

– Tailor vocational rehabilitation to the patient’s socio-economic-cultural context.

3.5. Physical Therapy and Community Management  

– Ongoing monitoring and treatment in the community.

V. PROGNOSIS AND COMPLICATIONS  

– Age of Onset: Later onset correlates with milder course.  

– Subtype: Episodic with remission has better prognosis than continuous progression or worsening deficits.  

– Premorbid Personality: Good social adaptation pre-illness predicts better outcomes than introverted/isolated traits.  

– External Triggers: Presence of triggers improves prognosis compared to spontaneous onset.  

– Genetics: Less genetic loading improves prognosis.  

– Negative Symptoms: Fewer/absent negative symptoms predict better outcomes.

IV. PREVENTION  

– No absolute prevention due to unclear etiology.  

– Foster teamwork and adaptability in children to cope with life’s challenges.  

– Monitor individuals with a family history of schizophrenia (parents, siblings, close relatives) for early detection and intervention.  

– Educate patients/families about the illness, relapse triggers, and treatment adherence.  

– Post-discharge follow-up, sustained consolidation treatment, and proactive management of infections/physical illnesses to prevent relapse.

REFERENCES

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