RFP Indian Journal of Medical Psychiatry

Background: Mental health disorders represent a major public-health challenge in India, affecting functioning, quality of life, families and health systems. Despite important policy developments, access to evidence-based care remains uneven. Objective: This narrative review synthesizes epidemiological evidence on mental morbidity in India, examines major determinants and vulnerable groups, describes treatment gaps and health-system barriers, and discusses emerging community, primary-care and digital strategies. Methods: Published epidemiological studies, systematic reviews, national survey findings and policy-related evidence were reviewed with emphasis on Indian data and recent syntheses. Results: The National Mental Health Survey reported a weighted lifetime prevalence of any mental morbidity of 13.67% and current prevalence of 10.56%, with an overall treatment gap of 84.5%. A later meta-analysis of 79 Indian studies estimated pooled prevalence of depression at 12.4%, alcohol-use disorder at 21.5%, and anxiety disorders at 11.6%. Evidence indicates substantial heterogeneity by age, setting and measurement approach. Stigma, low mental-health literacy, workforce shortages, affordability, geographical inequity and fragmented referral pathways continue to limit care. Digital initiatives, task-sharing, community-based services and primary-care integration offer opportunities to reduce these gaps. Conclusion: India requires sustained epidemiological surveillance, stronger community and primary-care mental-health services, expansion of the specialist and non-specialist workforce, suicide-prevention systems, and equitable digital mental-health access. Mental health promotion should be integrated across the life course and linked to social determinants of health.

Depression is among the leading causes of disability worldwide and contributes substantially to the burden of common mental disorders in India, where the treatment gap for mental illness exceeds eighty per cent. Given the acute shortage of psychiatrists and clinical psychologists, task-shifted models that place nurses and trained lay counsellors at the centre of depression care have attracted growing attention. This narrative review synthesises evidence on nurse-led interventions for depression, drawing on collaborative care trials, telephone-based case management studies, and community counsellor-delivered psychological treatments conducted in high-income and low-resource settings, including India. Nurse-delivered collaborative care, in which a nurse care manager coordinates screening, psychoeducation, medication monitoring, and stepped referral under psychiatrist supervision, has been shown in large randomised trials to substantially improve recovery rates compared with usual care and to produce benefits that persist over one to two years. Telephone-delivered case management does not diminish these benefits and extends reach to patients unable to attend frequent clinic visits. In India, lay-counsellor and nurse-delivered brief psychological treatments, and stepped-care programmes such as MANAS, have produced clinically meaningful reductions in depressive symptoms among primary care attenders. Behavioural activation, a core component of several of these programmes, is amenable to delivery by trained nurses with brief instruction and supervision. Barriers to scale-up include limited pre-service training in mental health nursing, absence of defined career pathways for psychiatric nurses, supervision gaps, and stigma. Strengthening the psychiatric nursing workforce through structured training, supervision, and integration into stepped-care pathways is essential to closing India’s depression treatment gap.

Newton was not the first of the age of reason. He was the last of the magicians, the last of the Babylonians and Sumerians, the last great mind that looked out on the visible and intellectual world with the same eyes as those who began to build our intellectual inheritance rather less than 10000 years ago.” - John Maynard Keyes, Address to the Royal Society Club (1942), as quoted in A Dictionary of Scientific Quotations (1977) by Alan L. MacKay, p.140 The Age of Reason [Enlightenment] began in the late 17th-18th centuries as a direct, rational extension of the Scientific Revolution [roughly 1543–1687]. It started when methods like empirical observation and deductive reasoning, pioneered by eminent philosophers and people of science like Francis Bacon, Galileo, and Isaac Newton, were applied to society, politics, and religion, challenging traditional authority. At the core of this intellectual shift was the application of the cause-and-effect chain [or causal reasoning] to everything from physics to social structures, asserting that the universe operates according to natural laws rather than arbitrary miracles. However, the brain’s cause-and-effect reasoning often fails. Synchronicity is a concept introduced by Swiss psychologist Carl Jung that challenges the linear view of cause-and-effect [causality]. Synchronicity is a phenomenon in which people interpret two separate but seemingly unrelated experiences as being meaningfully intertwined. Generalizations are deductions about the nature of things, derived from examples and instances. That is an inductive step, and the process steps back from reality into a model of reality. Science attempts to coerce the relationships among various experiences into this model of reality. Synchronicity may lie in the liminal space between psychiatry and spirituality where joy can be found as coming from knowing, feeling, or doing that which matters most. People need to trust other kinds of knowledge, not only that of science, to stay in touch with reality. Poetry might matter more than physics, intuitions more than theories.

Early-onset neurocognitive disorders may initially present predominantly with psychiatric symptoms and can therefore be mistaken for primary psychotic disorders. A 42-year-old man with no previous psychiatric illness or history of substance use presented with an abrupt onset of recurrent formed visual hallucinations, consisting of seeing a snake emerging from a hole in the wall and subsequently moving along the walls of his house. He developed persecutory beliefs that someone had deliberately placed the snake to harm him, accompanied by hypervigilance, severe sleep disturbance, irritability, aggression toward family members, social withdrawal, and reduced appetite. Three days before admission, he wandered away from home and was subsequently found in a dishevelled and perplexed state, unable to recall where he had been. Schizophrenia was initially considered. However, mental status examination demonstrated impaired attention, recent and remote memory, abstract thinking, insight, and judgement. His Mini-Mental State Examination score was 12/30. Routine investigations, including hepatic, renal, thyroid and vitamin B12 assessments, were within normal limits. Magnetic resonance imaging of the brain demonstrated bilateral periventricular and deep white-matter hyperintensities consistent with chronic ischemic changes, together with cerebral volume loss and frontal-predominant atrophy. Following neurological assessment, the diagnosis was revised to earlyonset major neurocognitive disorder with psychotic symptoms, with a possible vascular contribution. The case illustrates how early-onset neurocognitive disorders may present to psychiatric services with prominent symptoms of psychosis. Marked cognitive impairment, disorientation, and structural abnormalities on neuroimaging should prompt consideration of an underlying neurological disorder rather than assuming a primary schizophrenia-spectrum illness.

A 35-year-old man with bipolar affective disorder presented during a manic episode and was treated with intramuscular haloperidol 20 mg/day and promethazine 100 mg/day in divided doses, along with lithium 800 mg/day. On the fourth day of treatment, he developed high-grade fever, generalized rigidity, tremors, mutism, echolalia, altered consciousness, and marked autonomic instability, including tachycardia and labile blood pressure. Serum creatine phosphokinase was 2800 U/L, with leukocytosis and elevated CK-MB; troponin I was normal. A diagnosis of Neuroleptic malignant syndrome (NMS) was made, and all psychotropic medications were discontinued. He was treated with intravenous fluids, external cooling, and bromocriptine 15 mg/day. The fever, rigidity, and autonomic abnormalities improved over approximately 72 hours. However, after resolution of the acute NMS manifestations, severe agitation, aggression, and insomnia persisted. Lorazepam and nitrazepam provided inadequate behavioural control, while electroconvulsive therapy was considered unsuitable because of ongoing autonomic instability. Clozapine was initiated at 25 mg/day with close clinical and laboratory monitoring. Within 48 hours, marked reduction in agitation was observed, followed by improved cooperation and sleep. By the fifth day, behavioural stabilization was evident, without recurrence of fever, rigidity, autonomic instability, or clinically significant CPK elevation. This case illustrates the therapeutic challenge of persistent manic agitation following NMS. Clozapine may be considered in carefully selected patients when conventional antipsychotic treatment is considered unsuitable and other interventions are ineffective or temporarily contraindicated. However, clozapine itself can cause NMS Its use following NMS should therefore involve complete clinical resolution of the acute syndrome, conservative dosing, and close monitoring.