Geriatric psychiatry

• Geriatric psychiatry is the assessment, treatment and prevention of mental disorder in later life, where the same patient usually carries several medical illnesses, takes many medicines, and is shaped by bereavement, role loss and isolation.
• Late-onset depression is common, often hides behind somatic complaints, appetite and sleep change, and frequently brings cognitive symptoms that look like dementia. The two conditions overlap in both directions.
• Psychosis that begins after about 40–60 years is, in roughly 60% of cases, secondary to a medical, neurological, medication or substance cause until proven otherwise.
• Medication harm is predictable in older adults: anticholinergic, sedative and psychotropic load raise the risk of delirium, falls, fractures and cognitive decline. The AGS Beers criteria give a structured way to question every prescription. ^[4]
• For severe depression, especially with melancholic or psychotic features, severe suicide risk or catatonia, electroconvulsive therapy is the fastest and most effective treatment in older adults.
• Loneliness and social isolation are not merely psychosocial niceties: about a fifth to a third of older people are lonely or isolated, and loneliness doubles the risk of depression and is linked to cognitive decline, dementia and earlier death. ^[7]

By the end of this page you should be able to:

1. Define late-onset depression and explain why it so often presents with cognitive symptoms.
2. Separate a late-onset psychosis from psychosis secondary to dementia, delirium, medication or systemic illness.
3. Take a geriatric medication history that specifically looks for anticholinergic burden, psychotropic stacking, renal dosing and Beers-inappropriate prescribing.
4. Choose and monitor drug treatment for an older adult with depression, including lithium augmentation and antipsychotic augmentation.
5. Outline the indications, pre-treatment work-up, and side-effect profile of ECT in older people.
6. Assess and manage loneliness as a clinical risk factor, not just a social problem.

Geriatric psychiatry is not a single disease. It is the branch of psychiatry concerned with mental disorder in later life, where biology, psychology and social circumstance carry equal weight. For teaching purposes this page groups the conditions that dominate clinical practice into five classes.

Late-life depression. Depression may recur from younger life (early-onset depression) or appear for the first time in later life (late-onset, or late-life, depression). The most useful dividing line in the literature used here is onset past 60 to 65 years. ^[8] Early-onset and late-onset depression differ in presentation: early-onset illness tends to carry more crying, frank sadness, suicidal ideation and family history, whereas late-onset illness more often shows fearfulness, poor appetite, weariness, somatic complaints, reduced crying and thoughts of death rather than outright suicide intent. ^[8] Depression can also be secondary to a medical condition or substance use, and in older adults it often coexists with cognitive impairment.

Late-onset psychosis. The international consensus definitions classify schizophrenia spectrum illness by age of onset: early onset before 40 years, late onset at 40–60 years, and very-late-onset schizophrenia-like psychosis after 60 years. ^[5] Primary affective psychosis (psychotic depression, bipolar disorder with psychosis) becomes more common in later life; delusional disorder tends to begin in mid to late life. ^[5]

Psychosis secondary to another condition. In older adults this is the majority picture: neurocognitive disorders, delirium, prescribed medicines, toxins, infection and systemic illness. About 60% of psychosis in late life is secondary, and roughly 60% of all late-life psychosis arises this way. ^[5]

Neurocognitive disorders with behavioural and psychological symptoms. Depression, anxiety, agitation, hallucinations and delusions occur in a large minority of people with dementia and are often the reason families seek help.

Iatrogenic and substance-related disorder. Benzodiazepines, Z-drugs, anticholinergics, dopaminergic drugs and withdrawal states are common culprits. Alcohol use may be under-recognised in older men.

A geriatric assessment is therefore defined by its breadth: the presenting complaint is almost never the whole story.

Community studies and service data point in the same direction: depression is common in older adults and concentrates where disability and institutionalisation are high. The prevalence of major depression in people over 65 years is reported at about 5.5%, with the highest rates in nursing and other residential settings. ^[6] By comparison, major depressive disorder in the general population has been estimated at 8.3%. ^[8]

Psychotic illness is less common but far from rare in this age group:

• Schizophrenia prevalence in older adults is roughly 0.1–0.5%, against a lifetime prevalence of about 1%; the lower figure reflects excess mortality. ^[5]
• About 75% to 80% of schizophrenia cases begin early in life, with 20–25% beginning in late or very late life. ^[5]
• The 12-month prevalence of schizoaffective disorder in adults 60 and over is about 0.14%, and of delusional disorder about 0.03%. ^[5]
• The 1-year prevalence of bipolar disorder in older adults is about 0.1%, far below that in younger adults. ^[5]
• Psychotic depression increases with age: delusions occur in up to 45% of older patients admitted to hospital for depression. ^{[5] [8]}
• Psychosis is a core feature of several neurocognitive disorders. Roughly 40% of people with major neurocognitive disorder have psychotic symptoms; visual hallucinations occur in about 78% of people with dementia with Lewy bodies. ^[5]

Loneliness is its own epidemic. Studies suggest that 20–34% of older people in China, India, the United States and the regions of Europe and Latin America are lonely, with higher rates in institutions. ^[7] Up to 1 in 3 older adults are socially isolated. ^[7] Older adults who report loneliness or social isolation carry excess risks of depression, anxiety, cognitive decline, dementia, cardiovascular disease, stroke and earlier mortality. ^[7]

The most important shift in thinking is that late-life depression is often a brain disease as well as a psychological one.

• Vascular burden. The vascular depression hypothesis proposes that cerebrovascular disease predisposes to depression in some older adults, particularly through disruption of prefrontal and limbic connections. Patients often show psychomotor slowing, less guilt and poorer insight. ^[8] Silent cerebral infarction has been observed in about 93.7% of people with late-onset depression versus about 65.9% of those with early-onset depression, and white matter abnormality odds are over 4 times higher in late-onset illness. ^[8]
• Neurodegeneration. Depression can be both a risk factor for and a prodrome of dementia. Each depressive episode has been associated with an increased rate of dementia, by roughly 13–14% in large cohorts. ^[8]
• Medical and sensory illness. Stroke, chronic pain, visual and hearing impairment, frailty and disability are repeatedly implicated. Major depression occurs in about 19.3% of hospitalised and 23.3% of out-patient stroke survivors, against 8.3% in the general population. ^[8]
• Psychosocial factors. Bereavement, retirement, relocation, caregiver strain, financial strain and loneliness. People who are lonely are twice as likely to become depressed. ^[7]
• Iatrogenic factors. Drugs with central or anticholinergic effects, beta-blockers, corticosteroids, interferon and withdrawal from alcohol or benzodiazepines all feature. Interactions matter more than any single drug.

Risk factors include cognitive decline, poor physical health, sensory impairment (especially hearing loss), female sex, lower socioeconomic status, immigrant background, brain structural abnormalities, and premorbid paranoid or schizoid personality traits. ^[5] Older adults are particularly at risk of secondary psychosis because of higher medical comorbidity, polypharmacy and sensitivity to drug effects. ^[5]

Polypharmacy is not just a pill count; it is the use of medicines in ways that exceed benefit or create interactions. Risk rises with multimorbidity, multiple prescribers, care transitions, impaired renal or hepatic function and cognitive impairment. The Beers list exists because a very large fraction of drug-related harm in older adults is preventable.

Depression in older adults is now understood as a biologically heterogeneous syndrome.

1. Cerebrovascular injury disrupts fronto-subcortical circuits and produces the classic "vascular depression" phenotype: slowed processing speed, executive dysfunction and psychomotor retardation. Slowed processing speed most fully mediates the effect of age, depression severity and vascular risk on other cognitive domains. ^[8]
2. Hippocampal injury. Chronic stress hypersecretes glucocorticoids, is toxic to hippocampal neurons and reduces neurogenesis; structural MRI studies show smaller hippocampal volumes in depression, and these volumes correlate with delayed recall. ^[8]
3. Amyloid, inflammation and neurotrophic factors. Increased beta-amyloid deposition, chronic inflammation and reduced brain-derived neurotrophic factor provide further links to neurodegeneration. ^[8]
4. Reversibility is only partial. "Pseudodementia" describes cognitive impairment that mimics dementia but arises from depression. In a three-year study, irreversible dementia developed in about 43% of depressed elders with reversible dementia (pseudodementia) versus 12% of those with depression alone, a 4.69-fold higher risk. ^[8] Cognitive deficits in memory, verbal learning, motor speed, executive function and processing speed are consistently found and often persist even after mood recovers. ^[8]

Ageing alters dopaminergic, serotonergic and glutamatergic neurotransmission (reduced dopamine and serotonin binding, fewer serotonin and dopamine receptors) and produces white matter changes. Late-onset schizophrenia is more common in women and is associated with a weaker family history, better early psychosocial functioning and greater proximity of psychosocial stressors to onset than early-onset disease. ^[5] Very-late-onset schizophrenia-like psychosis is linked to sensory impairment, cognitive decline, social isolation and structural brain changes rather than to classic schizophrenia genes. ^[5]

Loneliness and social isolation act through chronic stress, sleep and activity changes, reduced access to care, poorer self-management of physical illness and reduced cognitive and social stimulation. They are not a consequence only of depression: depression can follow isolation, and isolation can follow depression.

Ageing reduces renal and hepatic clearance and increases tissue sensitivity. Anticholinergic drugs impair cognition and delirium; combined central nervous system depressants add up: three or more concurrent CNS-active drug classes are associated with more falls and fractures. ^[4] The Beers criteria translate these pharmacokinetic realities into an actionable list.

Few older adults say "I am depressed." They more often complain of fatigue, pain, poor sleep, appetite loss, constipation, memory worry, apathy or irritability. The bedside clues that separate a geriatric from a younger presentation are: ^[8]

Suicide risk is always present in late-life depression even when thoughts of death are vague rather than explicitly suicidal. Risk rises after bereavement, serious illness, pain and social isolation, and is highest in older men.

Cognitive overlap. A person with late-life depression may complain loudly of forgetfulness, answer "I don't know," give up early, and perform better on testing than they report. The decline is often abrupt and variable. A person with dementia tends to lose insight, confabulate, fail consistently, and have a stable low score. The two frequently coexist, and depression is both a risk factor for and a prodrome of dementia, so reassessment over time matters more than a single bedside impression. ^[8]

Key presenting features:

• Schizophrenia that begins after 40–60 years more often has persecutory delusions and auditory hallucinations, fewer negative symptoms, and better premorbid social function than early-onset disease. ^[5]
• Very late onset (after 60) often has a female predominance, visual as well as auditory hallucinations, partition or persecutory delusions, cognitive impairment at onset, and a weak family history. ^[5]
• Delusional disorder is often persecutory, tends to begin around middle age, and can preserve general functioning while destroying social trust. ^[5]
• Psychotic depression in an older adult: low mood, guilt, somatic preoccupation, hypochondriacal or nihilistic delusions, and often a marked suicide risk. ^[5]
• Psychosis in dementia more often involves visual hallucinations, misidentification, simple persecutory delusions and loss of insight; complex first-rank symptoms are rare. ^[5]
• Delirium produces visual hallucinations and rapidly fluctuating attention, usually from an acute medical cause. ^[5]

Take a history from the person and from someone who knows them well, because insight is commonly impaired. Cover onset, course, function, sleep, appetite, pain, sensory loss, falls, alcohol and every medicine including over-the-counter and herbal products. Perform a full mental state examination and a focused physical and neurological examination. Ask directly about suicidal and homicidal thoughts, self-neglect, finances, driving and capacity. ^{[1] [5]}

Order the basic set before calling a syndrome chronic or untreatable: full blood count, renal and liver function, electrolytes and calcium, glucose, thyroid function, vitamin B12 and folate, and HIV or syphilis testing where history or geography suggests it. ^[2] Review all medicines, including over-the-counter and anticholinergic products, before diagnosing an irreversible condition. ^[2]

NICE NG97 lists validated brief cognitive instruments such as the 10-point cognitive screener, 6-item cognitive impairment test, 6-item screener, Memory Impairment Screen, Mini-Cog and Test Your Memory. ^[2] Use them as aids, not as diagnoses, and interpret by age and education. Informant instruments (IQCODE, FAQ, AD8) help when insight is limited. Where the picture is unclear, neuropsychological testing is the gold standard for mild or atypical impairment. ^[2]

Structural brain imaging (CT or MRI) is indicated in new-onset cognitive decline after 60, first-episode psychosis, focal neurological signs, sudden onset, or poor recovery. ^{[2] [5]} Cardiovascular risk assessment (lipids, HbA1c, blood pressure) belongs in every depression plan, both for vascular risk and because depression itself worsens cardiovascular outcomes. ECG is needed before lithium or antipsychotic augmentation in anyone with cardiac risk. ^[1]

Major depressive episode is diagnosed on standard psychiatric criteria, summarised here in clinical terms rather than verbatim: a persistently low or empty mood or marked loss of interest/pleasure, together with vegetative and cognitive symptoms, producing functional impairment, not better explained by another disorder or a substance. ^[8] Late-life presentations are valid but less "typical", so a lower threshold for diagnosis is appropriate when somatic or cognitive complaints dominate.

The severity tools cited from the guidelines are:

• PHQ-9. NICE NG222 uses a score of 16 as a pragmatic separator: under 16 is "less severe" (subthreshold and mild), 16 or more is "more severe" (moderate and severe). ^[1]
• Acquired cognitive impairment. NICE NG222 advises clinicians to be alert to acquired cognitive impairment when assessing depression and to consult a specialist when developing the treatment plan. ^[1]

For dementia subtypes, NICE NG97 supports the use of validated criteria (for example NIA criteria for Alzheimer disease, NINDS-AIREN for vascular dementia, McKeith criteria for dementia with Lewy bodies). ^[2]

The first questions are always about safety: suicidal intent, self-neglect, dehydration, starvation, medication toxicity, and danger to others. NICE NG222 requires that clinicians ask directly about suicidal ideation and intent, and arrange help appropriate to the level of risk, particularly in the early weeks of treatment. ^[1] If there is considerable immediate risk, refer urgently to specialist mental health services. ^[1] Rapid assessment for delirium is essential when a confused older adult becomes psychiatrically ill, because delirium is reversible and its treatment is medical.

Catatonia, severe malnutrition, severe mania and psychotic depression with suicide risk warrant same-day specialist management; ECT may be the treatment of choice (see below).

Person-centred, relationship-based care is the foundation. NICE NG222 recommends continuity where possible, joint decision making about treatment, and attending to the person's strengths, relationships, lifestyle, losses and isolation. ^[1] NICE NG97 adds psychoeducation and skills training for dementia carers from diagnosis, tailored to carer needs and preferences. ^[2]

For geriatric depression, the American Psychological Association guideline recommends four evidence-based options: ^[3]

• Group cognitive-behavioural therapy (typically 7–15 weekly sessions), targeting current problems. ^[3]
• Interpersonal psychotherapy (16–20 weekly sessions), with grief, role transition, role dispute and interpersonal deficit as the problem areas most relevant to older adults. If medication is used, the panel recommends combining interpersonal psychotherapy with a second-generation antidepressant. ^[3]
• Group life-review/reminiscence therapy (typically 4–12 weekly sessions), built on life stories and transitions. ^[3]
• Second-generation antidepressants (SSRIs, SNRIs or NDRIs) combined with psychosocial treatment where drug treatment is indicated.

Physical activity, meaningful engagement, sensory aids (glasses, hearing aids), sleep hygiene, regular meals and social contact are all active treatments, not accompaniments. ^{[1] [2]}

For dementia, first-line management of distress is psychosocial and environmental: reduce noise and clutter, maintain routine, simplify tasks, treat pain, correct sensory loss, and support carers. ^[2]

Loneliness should be asked about directly, assessed with a brief, standard instrument where available, and written into the care plan. The WHO advocacy brief lists interventions with promise: ^[7]

• individual-level: social skills training, peer support and group activity, "befriending" services, and cognitive behavioural therapy;
• community-level: better transport, access to public and green space, and digital inclusion;
• society-level: reducing marginalisation and improving social cohesion.

In practice: restore sensory function; schedule regular contact; link to community groups, libraries, faith organisations and age-friendly services; use assistive technology; involve the primary care team and (where available) a social prescriber; and support carers, who are themselves at risk. Interventions work best face-to-face, sustained, and tailored to the person's mobility and cognition.

Antidepressants have the best evidence base in older adults. The APA recommends second-generation agents (SSRIs, SNRIs, NDRIs) because of reduced side-effect burden and safety in overdose. ^[3] The commonly prescribed geriatric dose ranges listed in that guideline are: bupropion 150–450 mg daily, duloxetine 20–120 mg daily, escitalopram 10–20 mg daily, paroxetine 20–40 mg daily, sertraline 100–200 mg daily, and venlafaxine 150–300 mg daily. ^[3] These are typical ranges, not prescriptions: start low, increase slowly, and individualise by comorbidity and interaction.

NICE NG222 adds the geriatric prescribing rules: ^[1]

• take into account physical health, comorbidities and other medicines;
• monitor carefully for side effects;
• be alert to increased risk of falls and fractures;
• be alert to hyponatraemia, especially with diuretics.

Tricyclics are largely obsolete in geriatric psychiatry. NICE advises against starting TCAs, except lofepramine, in people at significant suicide risk because of toxicity in overdose. ^[1] The AGS Beers criteria list antidepressants with strong anticholinergic activity (amitriptyline, clomipramine, doxepin over 6 mg daily, imipramine, nortriptyline, paroxetine and others) as drugs to avoid in older adults. ^[4] If a TCA is truly needed, nortriptyline is reserved for when SSRIs or SNRIs have failed or are not tolerated. ^[3]

For hyponatraemia risk, SSRIs, SNRIs, TCAs and mirtazapine are on the AGS Beers "use with caution" list and require sodium monitoring when starting or changing dose. ^[4] SSRIs, SNRIs and TCAs also appear on the Beers "avoid unless safer alternatives unavailable" list where there is a history of falls or fractures. ^[4]

Lithium augmentation. NICE NG222 recommends shared-care lithium management with renal, thyroid and calcium monitoring before treatment and at least 6-monthly (more often with renal impairment), serum lithium measured 12 hours post-dose after each change until stable. ^[1] Therapeutic levels for augmentation are usually at or above 0.4 mmol/L, with 0.4–0.6 mmol/L considered for people aged 65 or over. ^[1] Review dose carefully in the context of dehydration, infection, ACE inhibitors, angiotensin receptor blockers, diuretics and NSAIDs, which raise lithium levels. ^[1] ECG should be considered where cardiovascular risk exists. ^[1]

Antipsychotic augmentation in depression. Oral antipsychotic augmentation is sometimes used for treatment-resistant depression. NICE NG222 requires baseline pulse and blood pressure, weight, nutritional status, diet, physical activity, fasting glucose/HbA1c and lipids, then monitoring as set out in the summaries of product characteristics, with ECG in people with cardiovascular disease or QT risk, periodic assessment of whether to continue, and gradual withdrawal over at least 4 weeks. ^[1] AGS Beers notes that antipsychotics are only appropriate exceptions (for example adjunctive treatment of major depressive disorder) and otherwise should be avoided for behavioural problems of dementia or delirium unless non-pharmacological options have failed or there is substantial risk of harm. ^[4]

For people living with dementia. NICE NG97 is deliberately conservative. For mild to moderate dementia with mild to moderate depression or anxiety, consider psychological treatments, and do not routinely offer antidepressants unless indicated for a pre-existing severe mental health problem. ^[2] Treat pain, sensory loss and reversible contributors first. ^[2]

The first step is to search for and treat the secondary cause: discontinue offending drugs, treat delirium or infection, correct metabolic abnormalities, and image when indicated. Where an antipsychotic is needed, age-adjusted dosing is fundamental.

• Start at half the adult starting dose and titrate slowly, which reduces adverse effects. ^[5]
• Expert-consensus dosing listed by Tampi et al.: risperidone 1.25–3.5 mg/day as a first-line agent; quetiapine 100–300 mg/day; olanzapine 7.5–15 mg/day; aripiprazole 15–30 mg/day; amisulpride 50 mg/day as the minimally effective (and, over age 75, maximally tolerated) dose for psychosis accompanying Alzheimer disease. ^{[5] [8]}
• In dementia with Lewy bodies, antipsychotics can worsen parkinsonism and (rarely) provoke neuroleptic malignant syndrome; clozapine and quetiapine have some support, pimavanserin for Parkinson disease psychosis, and benzodiazepines can help REM sleep behaviour disorder. ^{[5] [2]}
• AGS Beers advises avoiding antipsychotics except for FDA-approved indications, with periodic deprescribing and lowest effective dose; the FDA black-box warning and increased risks of cerebrovascular events, metabolic effects and pneumonia in older adults must be discussed with the patient and family. ^{[4] [5]}
• NICE NG97 restricts antipsychotics in dementia to those at risk of harm or with severe distress, at the lowest effective dose and for the shortest time, review at least every 6 weeks, and discontinuation if there is no clear ongoing benefit. Risperidone and haloperidol are noted as licensed only under specific conditions. ^[2]

Drugs for dementia itself (cholinesterase inhibitors, memantine) and the choice of antipsychotic for behavioural symptoms are covered in the MedGrasp dementia topic.

The AGS Beers criteria are the standard frame, but they are a tool to start a conversation, not a rulebook. Key points from the 2023 edition: ^[4]

• applied to adults 65 years or older, in all ambulatory, acute and institutional settings, except hospice and end-of-life care;
• organised into five categories: potentially inappropriate medications; disease- or syndrome-specific interactions; drugs to be used with caution; drug–drug interactions; and dosages adjusted for renal function;
• designed in the United States but usable internationally, with awareness that indications and alternatives differ by country.

Practical psychotropic applications: ^[4]

• Avoid anticholinergic drugs for behaviour. First-generation antihistamines, antimuscarinics (except for incontinence), tertiary tricyclic antidepressants, many antiparkinsonian agents and Z-drugs are avoidable in older adults.
• Avoid benzodiazepines and Z-drugs in older adults (increased delirium, falls, fractures, cognitive impairment, motor vehicle crashes), reserving them for specific indications (seizures, withdrawal, REM sleep behaviour disorder, severe anxiety, periprocedural sedation).
• Use CNS-active drugs cautiously: avoid three or more concurrent CNS-active drug classes because of falls and fracture risk; avoid anticholinergic stacking.
• Use antidepressants cautiously where hyponatraemia, falls or fracture history already exist.
• Adjust doses by renal function (for example, avoid duloxetine if creatinine clearance under 30; reduce gabapentin and pregabalin below 60). ^[4]

NICE NG97 supports minimising medicines associated with high anticholinergic burden and reviewing medicines at every dementia care contact, using a validated tool where available. ^[2] NICE NG222 links to medicines adherence, medicines optimisation, multimorbidity and shared decision making as general practice. ^{[1] [4]}

Electroconvulsive therapy is the most effective and rapid treatment for several severe psychiatric syndromes in later life, and older adults as a group show a better response to ECT than younger adults. ^[6] About a third of ECT recipients are 65 or older, and 15.6% of older adults with affective disorders receive ECT versus 3.4% of those under 65. ^{[6] [3]}

Indications with the best evidence:

• severe depression, particularly melancholic or psychotic depression (delusions are more prevalent in late-onset depression), and where pharmacotherapy has failed; ^[6]
• high suicide risk requiring a rapid response; ^{[5] [6]}
• catatonia, which can be life-threatening in older adults; ^[6]
• severe mania; ^[6]
• medication intolerance or severe medical comorbidity where drugs pose more risk; ^[6]
• major depression superimposed on dementia, and (as a last resort) severe agitation or aggression in dementia when other measures fail; ^[6]
• selected neuropsychiatric conditions such as parkinsonism or post-stroke depression. ^[6]

Pre-treatment evaluation. ECT requires informed consent, a multidisciplinary team (psychiatrist and anaesthetist as a minimum), evaluation of medical and dental status, psychiatric history, current medicines, and routine laboratory tests (full blood count, basic metabolic panel and ECG). ^[6] Brain imaging is obtained for sudden onset of symptoms, focal neurological findings, significant cognitive impairment, or medication resistance. ^[6] Baseline cognitive and memory assessment is recommended, because older adults often have pre-existing impairment. ^{[6] [3]}

Technique (teaching summary). A brief-pulse stimulus is standard (pulse width 0.5–2.0 ms); ultrabrief pulse (under 0.5 ms) is more efficient in inducing seizure and is associated with fewer cognitive side effects. ^[6] The commonly used anaesthetic agents and doses in that source's table are methohexital 0.75–1.0 mg/kg, thiopental 2.0–4.0 mg/kg, propofol 1.0–1.5 mg/kg, etomidate 0.15–0.3 mg/kg and ketamine 1.5–2.0 mg/kg; succinylcholine 0.5–1.25 mg/kg and mivacurium 0.2 mg/kg are muscle relaxants. ^[6] Electrode placement matters: bilateral placement has a higher seizure threshold and more cognitive side effects; right unilateral placement has a lower threshold and (with adequate dosing, up to 6 times seizure threshold) equivalent antidepressant efficacy; high-dose right-unilateral (6 times seizure threshold) is as effective as high-dose bilateral (2.5 times seizure threshold). ^[6] Seizure threshold is higher with bilateral placement, in men and in older adults. ^[6]

Side effects. Postictal confusion and memory problems, usually transient over days to months; headache; aches; dental and anaesthetic risks. Older age itself is not a mortality risk factor for ECT, but older adults carry more cardiac comorbidity, so specialist evaluation is needed. ^[6] In dementia, ECT can improve cognition in some patients when depression is successfully treated, but others develop transient cognitive worsening; bilateral ECT in particular can worsen confusion. ^[6]

After ECT. Continuation treatment matters: nortriptyline plus lithium, or venlafaxine plus lithium, lowers relapse, and continuation ECT is an option when medications cannot be tolerated. In one 24-week trial, relapse rates were 39% on nortriptyline–lithium, 60% on placebo and 84% on nortriptyline alone. ^[6] Older adults with severe, psychotic depression are best referred to an ECT service early rather than after multiple failed drug trials.

• Specialist old-age psychiatry or geriatric medicine for first-onset psychosis after 40, complex differential diagnosis, severe depression, catatonia, mania, psychotic depression, suspected dementia, capacity and safeguarding concerns, and treatment-resistant illness.
• Geriatric medicine for frail patients, complex polypharmacy, falls, delirium and multimorbidity.
• Neuropsychology for atypical, mild or ambiguous cognitive impairment.
• Memory service for dementia subtype, care coordination and carer support.
• Early referral for ECT when criteria are met, because delays worsen outcomes in severe depression.

• Medical harm from psychotropics. Falls, fractures, hyponatraemia, delirium, stroke warned against on antipsychotics, metabolic syndrome, QT prolongation, and worsening of dementia. ^{[2] [4] [5]}
• Cognitive decline. Some deficits after depression (processing speed, executive function) do not fully resolve. ^[8] Pseudodementia carries an increased risk of later dementia. ^[8]
• Treatment-resistant and recurrent depression increases dementia risk cumulatively. ^[8]
• ECT-related cognitive effects, usually transient; persistent deficits are not the norm but must be monitored. ^[6]
• Loneliness-related excess mortality, cardiovascular disease, stroke, dementia and suicide. ^[7]
• Carer burden and breakdown, particularly in dementia. ^[2]

Late-life depression is usually treatable, and older adults respond at least as well as younger ones to adequate treatment; ECT adds speed and reliability for severe illness. ^[6] However, relapse is common without maintenance, cognition may not fully recover, and each episode increases long-term dementia risk. ^[8] Psychotic disorders beginning in late life have a relatively favourable premorbid picture (better early psychosocial function) but higher tardive dyskinesia risk, higher mortality and frequent medical comorbidity. ^[5] VLOS in particular is associated with progressive cognitive decline. ^[5] Where depression and isolation coexist, outcomes are worse; where isolation is reduced, mood and functioning improve.

• Brain health is vascular health. Midlife control of blood pressure, diabetes, lipids, smoking and obesity reduces late-life depression, cognitive decline and dementia. ^[8] Hearing correction and physical activity matter. ^[8]
• Ask, don't wait. Primary care should screen for depression with a validated scale (PHQ-9 or equivalent) in high-risk older adults and ask directly about loneliness; early treatment improves both mood and cognition. ^{[1] [7]}
• Review medicines. Reduce anticholinergic and psychotropic burden proactively, especially after falls or confusion. ^{[2] [4]}
• Dementia. The guidelines used here do not support routine population screening of asymptomatic individuals for dementia; assessment is triggered by concern from the patient, family or clinician, or by functional, medication or safety errors. ^[2]

• Nursing and residential care residents have the highest depression prevalence and the most polypharmacy. Staff training, access to psychosocial interventions, regular medication review and carer support are core clinical tasks. ^{[2] [6]}
• People with dementia need psychosocial interventions first and cautious, indicated use of antidepressants and antipsychotics. ^[2]
• Lewy body and Parkinson disease require caution with antipsychotics and with dopaminergic interactions. ^{[5] [2]}
• Renal impairment requires dose reductions for many psychotropics (duloxetine, gabapentin, pregabalin, tramadol) per Beers. ^[4]
• Sensory impairment masquerades as both cognitive and mood disorder; correct it before treating the psychiatric syndrome. ^[2]
• Carers of people with dementia have increased risk of depression and their support is a treatment intervention. ^[2]

• A careful history, physical examination, review of all medicines and a bedside cognitive test remain the most powerful tools; laboratory and imaging can be targeted rather than blanket.
• Treat reversible contributors (pain, infection, constipation, dehydration, anaemia, thyroid disease, sensory loss) before concluding that a cognitive or mood syndrome is irreversible.
• Minimise medicines with high anticholinergic burden; where newer antidepressants are unavailable, weigh the risks of TCAs carefully; avoid benzodiazepine overuse.
• Psychological and social interventions (engagement, activity, befriending, carer education) can be delivered by trained non-specialists.
• Ask routinely about loneliness and mobilise family, community and faith networks.
• If ECT is unavailable locally, refer early for severe, suicidal or psychotic depression.
• Keep the prescription simpler, monitor closely, and plan follow-up that a busy service can actually deliver.

The following MedGrasp topics cover the closely linked areas named in this page: Dementia: the neurocognitive disorders; Major depressive disorder; Persistent depressive disorder and adjustment disorder; Electroconvulsive therapy and neuromodulation; Neuropsychiatric symptoms in dementia; Vascular, frontotemporal and Lewy body dementia; Alzheimer disease and the dementias: approach; Psychiatric history and mental state examination. (Plain text only.) ^[8]