HOW TO TREAT DEMENTIA IN OTHER CLASSIFIED DISEASES 2025

HOW TO TREAT DEMENTIA IN OTHER CLASSIFIED DISEASES 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 3

DEMENTIA IN OTHER CLASSIFIED DISEASES

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 3

DEMENTIA IN OTHER CLASSIFIED DISEASES

I. DEFINITION  

Dementia in other classified diseases refers to cases of dementia caused by or presumed to be caused by etiologies other than Alzheimer’s disease or cerebrovascular disease. Onset may occur at any age, though it is rarely seen in the elderly.

II. ETIOLOGIES AND DISEASE SUBTYPES  

1. Dementia in Pick’s Disease  

1.1. Etiology  

– Bilateral and severe atrophy, predominantly confined to the frontal and temporal lobes, often affecting the posterior third of the first temporal gyrus (language area). Pathology is localized at the cortical level.  

– In some cases, mutations in the Tau protein gene on chromosome 14 are implicated.  

1.2. Diagnosis  

1.2.1. Definitive Diagnosis  

Clinical Features:  

– Progressive dementia with onset in middle age (45-60 years), characterized by slowly progressive personality changes and deterioration of social interactions, leading to impairment of intellectual functions, memory, and language. Associated features include apathy, euphoria, and occasionally extrapyramidal symptoms. The neuropathological picture reveals selective atrophy of the frontal and temporal lobes without the neurofibrillary tangles or amyloid plaques typical of typical senile dementia. Early-onset cases tend to exhibit a more malignant progression, with social and behavioral manifestations often preceding true memory deficits.  

– Frontal lobe symptoms are more prominent than temporal or parietal lobe involvement, distinguishing it from Alzheimer’s disease.  

Ancillary Testing (as indicated by individual case):  

– Neuropsychological Testing:  

+ Cognitive assessment (e.g., MMSE, GPCOG, Mini-Cog, ADAS-Cog, Wechsler scales);  

+ Depression screening (e.g., Ham-D, Beck Depression Inventory, GDS);  

+ Anxiety evaluation (e.g., Ham-A, Zung scale);  

+ Sleep disturbance assessment (e.g., PSQI);  

+ Personality testing (e.g., EPI, MMPI).  

– Laboratory Studies:  

+ Complete blood count (CBC);  

+ Erythrocyte sedimentation rate (ESR);  

+ Biochemical panel: liver function tests, renal function, electrolytes, glucose, HbA1c, calcium, phosphate, vitamin B12, folate, thyroid function tests, lipid profile;  

+ Urinalysis.  

– Imaging Studies:  

+ Brain CT, MRI, SPECT, PET, fMRI to assess structural damage;  

+ Abdominal ultrasound, chest X-ray to identify comorbidities or complications.  

– Functional Testing:  

+ EEG, cerebral blood flow studies, ECG, transcranial Doppler ultrasound.  

– Specialized Testing (if indicated):  

+ Serologic tests for syphilis, autoantibody panels (e.g., antiphospholipid antibodies, lupus anticoagulant, ANA), HIV testing, genetic testing, amyloid-PET, FDG-PET, brain biopsy.  

1.2.2. Differential Diagnosis  

– Alzheimer’s disease dementia;  

– Vascular dementia;  

– Secondary dementia due to other causes (e.g., neurosyphilis);  

– Normal pressure hydrocephalus;  

– Other metabolic or neurological disorders.  

2. Dementia in Creutzfeldt-Jakob Disease (CJD)  

Significant neuronal loss, particularly in the hippocampus, substantia innominata, red nucleus, and frontotemporoparietal cortex, with the presence of neurofibrillary tangles composed of paired helical filaments, senile plaques with amyloid deposition, and spongiform changes.  

2.1. Etiology  

– Transmissible disease, potentially associated with a viral agent.  

2.2. Diagnosis  

2.2.1. Definitive Diagnosis  

Clinical Features:  

– Progressive dementia with diffuse neurological signs resulting from specific neuropathological changes (subacute spongiform encephalopathy) caused by transmissible agents.  

– Onset typically occurs in middle age or later, most commonly around age 50.  

– Relatively rapid progression of dementia over months to 1-2 years.  

– Often accompanied by progressive spasticity of the limbs, extrapyramidal signs (e.g., tremor, rigidity), and choreiform or myoclonic movements; other variants may present with ataxia, visual loss, or fasciculations with upper motor neuron atrophy.  

– Triad of symptoms: severe, rapidly progressive dementia, pyramidal and extrapyramidal dysfunction with myoclonus, and characteristic triphasic waves on EEG.  

– Note: Rapid progression and early motor disturbances strongly suggest CJD.  

Ancillary Testing:  

– Neuropsychological Testing: Same as above (MMSE, GPCOG, etc.).  

– Laboratory Studies: CBC, ESR, biochemical panel (as above).  

– Imaging Studies: Brain CT, MRI, SPECT, PET, fMRI; abdominal ultrasound, chest X-ray.  

– Cerebrospinal Fluid (CSF) Analysis: Elevated protein (Tau protein >1200 pg/mL), increased enolase.  

– Functional Testing: EEG (characteristic triphasic waves), cerebral blood flow, ECG, transcranial Doppler.  

– Specialized Testing: Serologic tests for syphilis, autoantibodies, HIV, genetic testing, amyloid-PET, FDG-PET, brain biopsy (if indicated).  

2.2.2. Differential Diagnosis  

– Alzheimer’s disease;  

– Pick’s disease;  

– Parkinson’s disease;  

– Post-encephalitic parkinsonism.  

3. Dementia in Huntington’s Disease  

Marked reduction in acetylcholine neurotransmitters and other neuromodulators.  

3.1. Etiology  

– Genetic, caused by a single autosomal dominant gene mutation.  

3.2. Diagnosis  

3.2.1. Definitive Diagnosis  

Clinical Features:  

– Dementia as part of diffuse brain degeneration, typically presenting between ages 30-40. Early symptoms may include depression, anxiety, or overt paranoia with personality changes.  

– Slow progression, with death occurring within 10-15 years.  

– Involuntary choreiform movements, particularly of the face, hands, shoulders, or gait, are early hallmarks, often preceding memory decline.  

– Dementia is characterized by predominant frontal lobe dysfunction early on, with memory relatively preserved until later stages.  

– The triad of choreiform movement disorders, dementia, and a family history of Huntington’s disease strongly supports the diagnosis.  

Ancillary Testing: Same as above (neuropsychological testing, labs, imaging, etc.).  

3.2.2. Differential Diagnosis  

– Alzheimer’s disease;  

– Pick’s disease;  

– Creutzfeldt-Jakob disease;  

– Other choreiform disorders.  

4. Dementia in Parkinson’s Disease  

4.1. Etiology  

– Dopaminergic system damage in the nigrostriatal pathway, with genetic factors implicated.  

4.2. Diagnosis  

4.2.1. Definitive Diagnosis  

Clinical Features:  

– Dementia develops during the course of Parkinson’s disease, often becoming severe.  

– Approximately three-quarters of elderly Parkinson’s patients develop dementia within 10 years.  

– Clinical features include slowed cognition and motor function, memory and executive function impairment, visual hallucinations, depression, impaired concentration and judgment, and sleep disturbances.  

– Cognitive symptoms typically emerge at least 1 year after a Parkinson’s diagnosis.  

Ancillary Testing: Same as above.  

4.2.2. Differential Diagnosis  

– Other secondary dementias;  

– Multi-infarct dementia;  

– Normal pressure hydrocephalus.  

5. Dementia in HIV-Related Immunodeficiency  

5.1. Etiology  

– Caused by HIV, with mechanisms not fully elucidated.  

5.2. Diagnosis  

5.2.1. Definitive Diagnosis  

Clinical Features:  

– HIV-associated dementia typically presents with forgetfulness, psychomotor slowing, poor concentration, and difficulties with reading and problem-solving. Apathy, reduced spontaneity, and social withdrawal are common. In rare cases, atypical presentations include mood disorders, psychosis, or seizures. Physical exam may reveal tremor, dysdiadochokinesia (impaired repetitive movements), ataxia, hypotonia, diffuse hyperreflexia, positive frontal release signs, and impaired pursuit eye movements with nystagmus.  

– Rapid progression (weeks to months) to severe global dementia, mutism, and death.  

Ancillary Testing:  

– HIV viral testing;  

– CBC, ESR, biochemical panel, urinalysis;  

– Imaging (CT, MRI, SPECT, PET, fMRI); abdominal ultrasound, chest X-ray;  

– Functional testing (EEG, ECG, etc.);  

– Neuropsychological testing (MMSE, GPCOG, etc.);  

– Specialized testing (syphilis serology, autoantibodies, genetic testing, amyloid-PET, FDG-PET, brain biopsy).  

5.2.2. Differential Diagnosis  

– Alzheimer’s dementia;  

– Vascular dementia;  

– Pick’s disease;  

– Creutzfeldt-Jakob disease;  

– Other metabolic or degenerative dementias.  

6. Dementia in Other Specified Conditions  

Dementia may occur as a manifestation or consequence of various systemic or neurological disorders, including:  

– Carbon monoxide poisoning;  

– Cerebral fat embolism;  

– Epilepsy;  

– General paresis of the insane;  

– Hepatolenticular degeneration (Wilson’s disease);  

– Hypercalcemia;  

– Acquired hypothyroidism;  

– Toxic encephalopathy;  

– Multiple sclerosis;  

– Neurosyphilis;  

– Niacin deficiency (pellagra);  

– Polyarteritis nodosa;  

– Systemic lupus erythematosus;  

– Trypanosomiasis (sleeping sickness);  

– Vitamin B12 deficiency.  

IV. TREATMENT  

1. General Principles  

– Treat reversible dementias aggressively with specific therapies;  

– Hospitalize for diagnosis and symptom management;  

– Home care: Combine family support with physician oversight.  

2. Treatment Framework  

– Pharmacotherapy;  

– Psychotherapy;  

– Supportive care.  

3. Specific Treatments  

3.1. Pharmacotherapy  

3.1.1. Cognitive Symptom Management  

Options include:  

– Donepezil: 5-23 mg/day;  

– Rivastigmine: 1.5-12 mg/day (oral or transdermal);  

– Galantamine: 8-24 mg/day.  

Neuroprotective agents (optional):  

– Cerebrolysin: 10-20 mL/day;  

– Ginkgo biloba: 80-120 mg/day;  

– Piracetam: 400-1200 mg/day;  

– Citicoline: 100-1000 mg/day;  

– Choline alfoscerate: 200-800 mg/day;  

– Vinpocetine: 5-100 mg/day;  

– Nicergoline: 10-30 mg/day;  

– Antioxidants: Vitamin E, selegiline, coenzyme Q10, omega-3.  

For associated symptoms (e.g., delusions, hallucinations, depression, agitation): antipsychotics, antidepressants, anxiolytics.  

3.1.2. Antipsychotics  

Options (1-3 agents):  

– Risperidone: 1-10 mg/day;  

– Quetiapine: 50-800 mg/day;  

– Olanzapine: 5-30 mg/day;  

– Clozapine: 25-300 mg/day;  

– Aripiprazole: 10-30 mg/day;  

– Haloperidol: 0.5-20 mg/day.  

3.1.3. Antidepressants  

Options (1-3 agents):  

– Sertraline: 50-200 mg/day;  

– Citalopram: 10-40 mg/day;  

– Escitalopram: 10-20 mg/day;  

– Fluvoxamine: 100-200 mg/day;  

– Paroxetine: 20-50 mg/day;  

– Fluoxetine: 10-60 mg/day;  

– Venlafaxine: 75-375 mg/day;  

– Mirtazapine: 15-60 mg/day.  

3.1.4. Mood Stabilizers  

Options:  

– Valproate: 200-2500 mg/day;  

– Divalproex: 750 mg/day to 60 mg/kg/day;  

– Carbamazepine: 100-1600 mg/day;  

– Oxcarbazepine: 300-2400 mg/day;  

– Lamotrigine: 100-300 mg/day;  

– Levetiracetam: 500-1500 mg/day.  

Hepatic support: Aminoleban, silymarin, boganic, branched-chain amino acids.  

Nutritional supplements: Vitamins, minerals, balanced diet, IV nutrition as needed.  

3.2. Psychotherapy  

– Direct: Family therapy, individual psychotherapy;  

– Indirect:  

+ Ensure a safe environment;  

+ Minimize external stimuli;  

+ Promote sleep hygiene;  

+ Educate families on care and nutrition.  

3.3. Physical and Occupational Therapy  

– Collaborate with rehabilitation specialists;  

– Goals: Restore motor function, speech therapy for language recovery.  

3.4. Management of Comorbid Conditions  

– Atherosclerosis: Antiplatelet agents, carotid stenting/surgery, antihypertensives, statins, fibrates, antidiabetic agents;  

– Support daily activities (e.g., bathing, hygiene) to prevent complications and improve quality of life.  

3.5. Social Management  

– Refer to local dementia support groups;  

– Assess driving capability;  

– Discuss care options (e.g., in-home assistance, skilled nursing facilities).  

3.6. Caregiver Support  

– Caregivers experience heightened stress;  

– Support programs should address medical, psychological, and practical needs for both patients and caregivers.  

V. PROGNOSIS AND COMPLICATIONS  

– Pick’s Disease: Slow progression, severe brain damage requiring dependency; death often from pneumonia; survival 7-10 years.  

– Creutzfeldt-Jakob Disease: Rapid progression, death within 1-2 years.  

– Huntington’s Disease: Slow progression, survival 10-25 years; death from pneumonia or cardiovascular disease.  

– Parkinson’s Disease: Faster progression than Alzheimer’s; death from immobility-related complications.  

– HIV-Associated Dementia: Rapid progression to death within months if untreated.  

VI. PREVENTION  

No specific preventive measures exist. General recommendations:  

– Avoid tobacco, alcohol, and stimulants;  

– Manage hypertension, dyslipidemia, diabetes;  

– Maintain a balanced diet (rich in fruits, vegetables, low in saturated fats and sugars);  

– Engage in regular physical and cognitive activity.

REFERENCES

Vietnamese

1. Department of Psychiatry, Hanoi Medical University (2016), Lectures on Psychiatry. Medical Publishing House.  
2. Department of Psychiatry, Hanoi Medical University (2000), Organic Mental Disorders. Postgraduate Lecture Series.  
3. Department of Psychiatry & Medical Psychology, Military Medical Academy (2007), Psychiatry and Psychology. People’s Army Publishing House.  
4. Military Medical Academy (2016), Textbook of Psychiatric Disorders. People’s Army Publishing House, Hanoi.  
5. World Health Organization (1992), The International Classification of Diseases, 10th Revision (ICD-10): Mental and Behavioral Disorders. WHO, Geneva, 1992.  
6. World Health Organization (1992),ICD-10 Classification of Mental and Behavioral Disorders: Diagnostic Criteria for Research (translated by the Department of Psychiatry, Hanoi Medical University).  
7. David A., et al. (2010), Geriatric Psychiatry, Medical Publishing House, 2014. Translated by Nguyễn Kim Việt.  
8. Eduard V. (2009), Bipolar Disorder in Clinical Practice, Medical Publishing House, Hanoi.  
9. Kaplan & Sadock (2013), Pervasive Developmental Disorders, Synopsis of Child and Adolescent Psychiatry, Translated book, Medical Publishing House.  
10. Trần Hữu Bình (2016), Textbook of Psychiatric Disorders: Depressive Phase,Medical Publishing House, Hanoi.  
11. Lê Quang Cường (2005), Epilepsy, Medical Publishing House.  
12. Cao Tiến Đức (2017), Epilepsy: Mental Disorders in Epilepsy and Treatment, Medical Publishing House, pp. 9-15.  
13. Trần Viết Nghị (2000), Mental and Behavioral Disorders Due to Psychoactive Substance Use, Department of Psychiatry, Hanoi Medical University.  
14. Trần Viết Nghị, Nguyễn Minh Tuấn (1995), Treatment of Drug Addiction with Psychotropic Medications, Proceedings of the Scientific Conference on Drug Addiction Treatment Methods, Ministry of Health, Institute of Mental Health.  
15. Nguyễn Viết Thiêm (2000), Mental and Behavioral Disorders Due to Psychoactive Substance Use, Department of Psychiatry, Hanoi Medical University, pp. 103-111.  
16. Nguyễn Minh Tuấn (2016), Textbook of Psychiatric Disorders, Medical Publishing House.  
17. Nguyễn Minh Tuấn (2004), Heroin Addiction: Treatment Methods, Medical Publishing House.  
18. Nguyễn Minh Tuấn (2004), Diagnosis and Treatment of Dependence (Addiction), Medical Publishing House.  
19. Nguyễn Kim Việt (2016), Textbook of Psychiatric Disorders, Medical Publishing House, Hanoi.  
20. Nguyễn Kim Việt (2000), Mental and Behavioral Disorders Due to Psychoactive Substance Use,Department of Psychiatry, Hanoi Medical University.  
21. Nguyễn Kim Việt (2000), Organic Mental Disorders, Department of Psychiatry, Hanoi Medical University.  
22. Nguyễn Kim Việt, Nguyễn Văn Tuấn (2016), Textbook of Psychiatric Disorders, Department of Psychiatry, Hanoi Medical University, Medical Publishing House, pp. 74-79.

English

1. The British Association for Psychopharmacology (2011). Evidence-based guidelines for the pharmacological treatment of schizophrenia: recommendations from the British Association for Psychopharmacology. J Psychopharmacol (Oxf), 25(5), 567–620.
2. The National Institute for Health and Care Excellence (NICE) (2014). Psychosis and schizophrenia in adults: prevention and management. NICE guideline. CG178, 5-46.
3. The National Institute for Health and Care Excellence (2014). Bipolar disorder: the assessment and management of bipolar disorder in adults,children and young people in primary and secondary care. September 2014.
4. The National Institute for Health & Care Excellence – NICE (2010). The Treatmentand Management of Depression in Adults (updated edition). National Clinical Practice Guideline 90, 2010.
5. NICE(2012), “Epilepsies: diagnosis and management ”, NICE 
6. Abdul S. K., Manjula M, Paulomi M. S., et al (2013), “Cognitive Behavior Therapy for Patients with Schizotypal Disorder in an Indian Setting: A Retrospective Review of Clinical Data”, the German Journal of Psychiatry, pp 1-7.
7. Addington D., Abidi S., Garcia-Ortega I., et al. (2017). Canadian Guidelines for the Assessment and Diagnosis of Patients with Schizophrenia Spectrum and Other Psychotic Disorders. Can J Psychiatry, 62(9), 594–603.
8. American Psychiatric Association (1994), “Amphetamine-type stimulants” Diagnostic and Statistical Manual of Mental Disorders”, Fourth Edition, DSM-Washington, DC
9. American Psychiatric Association (2013). Alcohol-Related Disorders, Diagnostic and statistical manual of mental disorders DSM-5, American Psychiatric Publishing, 490-503.
10. AmericanPsychiatric Association (2013). Opioid  Diagnostic and statistical manual of mental disorders DSM-5, American Psychiatric.
11. AmericanPsychiatric Association (2013). Diagnostic and statistical manual of mental disorders DSM-IV.
12. Apurv K., Pinki D., Abdul K. (1997), “Treatment of acute and transient psychoticdisorders with low and high doses of oral haloperidol”, Indian Journal of Psychiatry, pp 2-8
13. American psychiatric association (2010). Practice guideline for the Treatment of Patients With Schizophrenia, Second Edition. 184.
14. Andreas M. (2012), “Schizoaffective Disorder”, Korean J Schizophr Res, pp 5-12.
15. American Psychiatric Association (1994). The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition.
16. Babalonis S, Haney M, Malcolm R.J, et al (2017). Oral cannabidiol does not produce a signal for abuse liability in frequent marijuana smokers. DrugAlcohol Depend. 172, 9-13.
17. Benjamin J. S, Virginia A. S, Pedro R (2017). Substance-Related Disorders, Kapland & Sadock’s Comprehensive Textbook of Psychiatry, Lippincott Williams & Wilkins, Baltimore, Vol. 1.
18. Benjamin J. S., Virginia A. S. (2007), “Substance-Related Disorders- Amphetamine (or Amphetamine-like) Behavioral Sciences/Clinical Psychiatry ”, Kaplan & Sadock’s Synopsis of Psychiatry 10th Edition, Lippincott Williams & Wilkins (2007)
19. Bergamaschi M.M, Queiroz R.H.C, Zuardi A.W., et al (2011). Safety and side effects of cannabidiol, a Cannabis sativa constituent. Curr Drug Saf. 6(4), 237-249.
20. Benzoni O., Fàzzari G., Marangoni C., Placentino A., Rossi A. (2015), “Treatment of resistant mood and schizoaffective disorders with electroconvulsive therapy: a case series of 264 patients”, Journal of Psychopathology, pp 266-268.
21. Daniel R. R., Larry J. S., et al (2014), “Schizotypal personality disorders: a current review”, New York, pp 1-10.
22. Dervaux A.M. (2010). Influence de la consommation de substances sur l’émergence et l’évolution des troubles psychotiques: le cas du cannabis. La these doctotraie, Universit ´e Pierre et Marie Curie – Paris VI, Paris, France.
23. Dieter S., Steven C. S. (2014). “Drug treatment of epilepsy in adults ”, BMJ, p2-19.
24. Early Psychosis Guidelines Writing Group (2010). Australian clinical guidelines for earlypsychosis 2nd  Natl Cent Excell Youth Ment Health Melb, 2, 4–24.
25. Elisa C., Amir H. C., Peter B. (2009), “Treatment of Schizoaffective Disorder”, Psychiatry (Edgemont),p 15-17.
26. Felix-Martin W., Rafael C., (2016), “Current Treatment of Schizoaffective Disorder According to a Neural Network”, Neural Network. J Cytol Histol, pp 2-5
27. Gary R., Donald A., Wiliam H., et al (2017), “Guideline for the pharmacotherapy of schizophrenia in adul”, The canadian journal of schiatry,pp 605-612.
28. Galletly C., Castle D., Dark F., et al. (2016). Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for themanagement of schizophrenia and related disorders. Aust N Z J Psychiatry, 50(5), 410–472.
29. Gautam S., Jain A., Gautam M., Vahia V. N., et al (2017). Clinical Practice Guidelines for the management of Depression. Indian J Psychiatry;59, Suppl
30. Grunze H., et al. (2009). The World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Biological Treatment of Bipolar
31. Hasan A., Falkai P., Wobrock T., et al. (2012). World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia, Part 1: Update 2012 on the acute treatment of schizophrenia and the management of treatment resistance. World J Biol Psychiatry, 13(5), 318–
32. Hasan A., Falkai P., Wobrock T., et al. (2013). World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia,Part 2: Update 2012 on the long-term treatment of schizophrenia and management of antipsychotic-induced side  World J Biol Psychiatry, 14(1), 2–44.
33. JakobsenD., Skyum E., Hashemi N., et al. (2017). Antipsychotic treatment of schizotypy and schizotypal personality disorder: a systematic review. J Psychopharmacol (Oxf), 31(4), 397–405.
34. Jinsoo C., Theo C. M. (2017), “Current Treatments for Delusional Disorder”, Psychiatry, pp 5-20
35. Jonathan K. B., Saeed F. (2012), “Acute and transient psychotic disorders: An overview of studies in Asia”, International Review of Psychiatry, pp 463-466
36. Jochim, J., Rifkin-Zybutz, R., Geddes, J., et al (2019).Valproate for acute mania. Cochrane Database of Systematic Reviews.
37. Kaplan& Sadock’s. Pocket Handbook of Psychiatric Drug Treatment
38. Kennedy S. H., Lam R. W., McIntyre R. S., et al (2016). Canadian Network forMood and Anxiety Treatments (CANMAT) 2016 Clinical Guidelines for the Management of Adults with Major Depressive Disorder. The Canadian Journal of Psychiatry, 61(9), 540–560.
39. Krishna R.P., Jessica C., et al(2014), “Schizophrenia: overview and treatment options”, New York, pp 638-643.
40. Lakshmi N. Y., Sidnay H. K., Saga V. P., et al (2018). Canadian network for mood and anxiety treatments (CANMAT) and international society for bipolar disorders (ISBD) 2018 guidelines for the management of patient with bipolar disorder. Bipolar disorders; 20:97-170
41. Laskshmi N.Y., Sidney H. K. (2017). Kaplan and Sadock’s Comprehensive Textbook of Psychiatry: Pharmacological treatment of depression and bipolar disorders, Wolters Kluwer.
42. Lakshmi N. Y., Sidney H. K., Saga V. P., et al (2018). Canadian network for mood and anxiety treatments (CANMAT) and international society for bipolar disorders (ISBD) 2018 guidelines for the management of patient with bipolar disorder. Bipolar disorders; 20:97-170
43. Loya M., Dubey V., Diwan S., Singh H. (2017), “Acute and transient psychotic disorder and schizophrenia: On a continuum or distinct? A study of cognitive functions”, International Journal of Medicine Research, pp-4-7.
44. Manschrec, Nealia L. K. (2006), “Recent Advances in the Treatment of Delusional Disorder”, The Canadian Journal of Psychiatry, pp-114-118
45. Marcos E. M. B., Hermes M. T. B. (2016), “Schizoaffective Disorder and Depression. A case Study of a patient from ceará, Brazil”, iMedPub Journals, pp1-8
46. Mesut Cetin (2015), “Treatment of Schizophrenia: Past, Present and Future”, Bulletin of Clinical Psychopharmacology, pp 96-98.
47. Michael S., Christina Z., Gerd B., (2011), “Prevalence of delusional disorder among psychiatric inpatients: data from the German hospital register”, Neuropsychiatry, pp 319-322.

48. MIMS neurology & psychiatry disease management guidelines

49. RajivTandon (2018), “Pharmacological Treatment of Schizophrenia 2017-2018 Update Summary”, org, pp 37-40.
50. Robert E., et al (2014). Substance-Related and Addictive Disorders. The AmericainPsychiatric Publishing Textbook of Psychiatry, 6 th, DSM-5 Edition, Bristish Library, USA, 735 – 814.
51. Rong C, Lee Y., Carmona N.E., et al (2017). Cannabidiol in medical marijuana: Research vistas and potential opportunities. Pharmacol Res. 121, 213-8.
52. Skelton M., Khokhar W.A., Thacker S.P. (2015). Treatments for delusional disorder. Cochrane Database Syst Rev.
53. Stahl S.M, Stein D.J, Lerer B (2012). Evidence based pharmacotherapy of illicit substance use disorders, Essential evidence based psychopharmacology
54. Stephen M.S., Dan J.S., Bernard L. (2012). Evidence based pharmacotherapy of illicit substance use disorders, Essential evidence based
55. Stahl S. (2009). Stahl’s essential psychopharmacology: neuroscientific basis and practical implications: Cambridge University Press.
56. Stahl, M. (2013). Stahl’s essential psychopharmacology: neuroscientific basis and practical applications, Cambridge University Press.
57. Vieta, Berk M., Schulze&nbspT. G., et al (2018). Bipolar disorders. Nature Reviews Disease Primers, 4, 18008
58. Update2009 on the Treatment of Acute  The World Journal of Biological Psychiatry. 10(2); 85-116.

If you need legal consulting, please Contact Us at NT International Law Firm (ntpartnerlawfirm.com)

You can also download the .docx version here.