Dementia and Depression

Dementia is a clinical syndrome caused by a range of underlying diseases — it can be associated with conditions as diverse as Parkinson’s disease and multiple sclerosis, and is classified into four main types (or a mix of these):

• Alzheimer’s dementia — insidious, gradual cognitive decline, particularly affecting new memory formation.
• Vascular dementia — classically a “subcortical” picture with general slowing of mental processing; more variable in presentation than Alzheimer’s, with scattered changes across cognitive domains.
• Lewy body dementia — early visuospatial/attention impairment, often with fluctuating confusion, visual hallucinations, parkinsonism, and REM sleep behaviour disorder.
• Frontotemporal dementia — early executive/language impairment, usually presenting with behavioural, language, or personality change.

Diagnosis (DSM-5)

• Significant cognitive decline from a previous level, in one or more domains (complex attention, executive function, learning/memory, language, perceptual-motor, or social cognition) — based on concern from the patient, an informant, or the clinician, plus substantial impairment on standardised neuropsychological testing (or another quantified assessment where that’s unavailable).
• The deficits interfere with independence in everyday activities — at minimum, needing assistance with complex instrumental activities (paying bills, managing medications).
• Not occurring exclusively during delirium.
• Not better explained by another mental disorder (e.g. major depression, schizophrenia).

Depression can accelerate and mimic dementia onset in elderly patients — include a cognitive test (e.g. MMSE) as part of the mental health assessment.

Breaking the diagnosis: a dementia diagnosis brings loss of independence, adverse emotional reactions from the patient/family, and stigma (fear it’s a “death sentence”). Handle it with the same tact and care as any bad-news conversation — provide a clear plan for ongoing management and monitoring without overloading the patient with information. Involve a geriatrician early if there’s concern about rapid progression (more typical of vascular or Lewy body dementia).

Work-up

1. Cognitive function test — SMMSE, GPCog, clock drawing, or the modified KICA (for Aboriginal and Torres Strait Islander patients).
2. Pathology — FBC, U&E, calcium/magnesium/phosphate, glucose, TFTs, B12, folate, vitamin D (consider syphilis/HIV serology if risk factors present).
3. Imaging — CT brain, CXR, DEXA (falls/fracture risk).
4. Assess for depression — depression can mimic dementia, and a trial of antidepressants plus psychological support may reverse apparent cognitive decline if the depression responds. Citalopram is a reasonable SSRI choice — start at half dose and titrate as tolerated, monitoring serum sodium fortnightly (hyponatraemia is common). Avoid TCAs given their anticholinergic burden.
5. Medication review — check for drugs affecting brain function; deprescribe where possible before finalising a dementia diagnosis, doing so slowly.
6. Functional assessment — dementia can’t be diagnosed without functional interference, though distinguishing this from physical decline can be difficult. Refer to OT for functional assessment, or to a dementia assessment service (geriatrician + dementia nurse team) for a home-based review and access to government-funded supports.

Don’t miss uncorrected hearing loss — it can masquerade as a cognitive problem.

Depression in dementia

People with dementia of any type have a high incidence of major depression. The incidence of depression may be 30% in vascular dementia and in Alzheimer’s disease, and over 40% in the dementia associated with Parkinson’s and Huntington’s diseases. Sustained and disabling major depressive episodes are more common in people with dementia than in age-matched controls without dementia. The occurrence of a first major depressive episode in an older adult is itself a risk factor for developing dementia — diagnosis of the dementia will be difficult until the depressive episode has remitted or at least improved.

Clinical picture: mood is most commonly low but can be irritable, angry, or anxious, with disturbed sleep, appetite and energy. Overall cognitive ability may decline significantly due to the depression alone, and attributing cognitive impairment to the dementia or the depressive disorder may be difficult until an adequate trial of treatment for depression has occurred. Some signs of dementia may strongly resemble those of a major depression, such as social withdrawal, lack of interest in self or others, low initiative and poor motivation. Apathy is a particularly confounding sign for diagnosis, and specialist assessment may be needed.

Assessment: rating scales for depression validated in the elderly population may provide useful additional information in the assessment. The Cornell Scale for Depression in Dementia has particular validity in dementia. The 15-item Geriatric Depression Scale is useful when time is limited. Uncertainty of diagnosis should lead to consultation with a specialist psychogeriatrician or geriatrician.

Management should be enthusiastic, aiming to optimise quality of life, using both non-pharmacological and pharmacological strategies with a collaborative approach between the clinician, family, and carers. For non-pharmacological strategies: offer relief and support if daily personal care becomes too difficult during the depressive episode, maximise pleasant but not onerous social and physical activity within the person’s capability, and encourage positive thinking while discouraging negative thinking — the severity of cognitive impairment may preclude useful formal cognitive therapy, but CBT, interpersonal psychotherapy and counselling have been used with some benefit in mild dementia specifically.

For pharmacological strategies: selective serotonin reuptake inhibitors are the first-line pharmacotherapy for depression in dementia, although they are less likely to be effective in older people generally; mirtazapine has a role when initial insomnia is a dominant symptom. Tricyclic antidepressants can cause anticholinergic effects that may further impair cognitive function in people with dementia, so should be avoided. Titrate doses slowly, using the highest tolerated dose — it is not appropriate to continue an ineffective low dose. Trial an antidepressant for 4–6 weeks at the optimum dose before changing; if there is no benefit after six weeks, it should be slowly tapered and stopped. Check serum sodium before starting a medication, and then after a fortnight at least, because hyponatraemia is a common adverse effect of many antidepressants that usually develops within the first weeks of treatment.

Referral: management of a possible major depression in someone with dementia should not be delayed. Seek specialist advice from a psychiatrist, particularly one with expertise in treating older people, in cases of diagnostic uncertainty, or when the depressive disorder is complicated by psychosis, persistent self-harm ideas, or failure to respond to management. Electroconvulsive therapy is effective and safe in older people with dementia, for those who need hospital-level care.

Ongoing management

• Functional capacity — review regularly and put supports in place as decline progresses.
• Decision-making capacity and advance care planning — identify areas of difficulty early and use shared decision-making for complex choices. Discuss power of attorney and an end-of-life plan while the patient still has capacity, rather than leaving this burden to next-of-kin later.
• Physical comorbidities — dementia can impair the visual cortex, increasing falls risk; weight loss and poor oral health/dentition are common (not always due to poor diet/hygiene — malabsorption and intrinsic gum decline both contribute); seizures occur in up to 10% of patients. A Mediterranean diet, regular exercise, and social contact have growing evidence for slowing progression.

Behavioural and psychological symptoms of dementia (BPSD)

Most patients with dementia have some behavioural and psychological symptoms — about 90% display at least one problematic behaviour. While aggression and agitation are easily recognised, symptoms such as apathy may be overlooked, since few if any externalising behaviours result despite the distress experienced by the person with dementia. Before prescribing anything, it’s important to exclude other causes of altered behaviour, such as pain or infection — some symptoms may be artefacts of memory loss rather than psychosis; a “delusion” of theft, for example, is reported in around 22% of patients with dementia and may be better understood as an artefact of poor memory than as a truly psychotic symptom.

Drugs should only be used when behavioural interventions have failed — they are a treatment of last resort in most cases. The evidence for most structured non-drug therapies is both limited and inconsistent: a meta-analysis failed to support the routine use of reminiscence therapy, simulated presence therapy, validation therapy, acupuncture, aromatherapy or light therapy, though there’s limited evidence that music therapy, pet therapy and hand massage or touch therapy may reduce agitation. Simple techniques — distraction, redirection, reassurance and reorientation — form the core of practical behavioural interventions and require little beyond staff time; individualise the choice of intervention to the patient and the specific behaviour, paying attention to its triggers. Consider referral to local aged psychiatry services or the national Dementia Behaviour Management Advisory Service (DBMAS) if more structured behavioural support is needed.

If drug therapy is used, general principles for prescribing in older people apply: target the drug to the symptom (antipsychotics for hallucinations/delusions, an anxiolytic for agitation/anxiety, a hypnotic only for persistent insomnia); start low and go slow; use one drug at a time at the lowest effective dose (multiple psychotropics should prompt specialist review or a residential care medication management review); and review early and often for adverse effects, since older people have a greater likelihood of developing extrapyramidal effects that often emerge during treatment rather than at initiation. Within the PBS, only risperidone (among the atypical antipsychotics) is subsidised for psychotic symptoms and aggression, restricted to patients with Alzheimer’s dementia and limited to 12 weeks of approved treatment. Benzodiazepines are not a “safe” alternative to antipsychotics in this population — they carry their own additional risks from sedation and higher rates of falls, fractures and death.

Patients with dementia prescribed antipsychotic drugs have an increased risk of falls, hospitalisation and death, and should be regularly monitored for adverse effects — nursing home patients prescribed antipsychotics are 1.9–2.4 times as likely to have an adverse event requiring hospitalisation, or to die, within 90 days of starting treatment, and for patients whose treatment begins in the community the risk is elevated 3.2–3.8 times. Placebo response rates are very high for any drug prescribed for BPSD, partly reflecting that symptoms naturally wax and wane with disease progression and environmental factors — there should be no reluctance to trial deprescribing within 2–3 months of a behaviour settling, and stop the drug if the symptoms don’t return. Drugs are an augmentation to behaviour management, not a replacement for it: behavioural management strategies should continue regardless of whether pharmacotherapy is also started.

Medication

Acetylcholinesterase inhibitors (donepezil, rivastigmine, or galantamine — the NHMRC recommends any one of the three) are used for mild-to-severe Alzheimer’s disease, Parkinson’s dementia, Lewy body dementia, vascular dementia, or mixed dementia. Avoid in frontotemporal dementia — severe side effects, and may worsen BPSD in this subtype.

Initial PBS-subsidised prescribing (PBS-funded for Alzheimer’s disease only) requires specialist (geriatrician or psychiatrist) input, and continuation requires evidence of clinical improvement within the first 6 months. Monitor for: nausea, vomiting, diarrhoea, dizziness, increased urinary incontinence/frequency, falls, muscle cramps, weight loss, anorexia, headache, insomnia. Heart block is rare but serious — obtain a baseline ECG before starting, and check thyroid function; watch for a prescribing cascade if incontinence emerges.

Memantine (an NMDA-receptor antagonist) is an option for moderate-severe Alzheimer’s disease, and may also help moderate-severe vascular dementia — authority- prescribed, continued only with a clinically meaningful response.

Stopping either drug class should be gradual, with regular review (e.g. every 4 weeks) — abrupt withdrawal has been linked to worsening cognition in case reports.

Emerging therapy

Lecanemab (Leqembi), an anti-amyloid monoclonal antibody, showed positive phase 3 results in early Alzheimer’s disease (CLARITY AD trial) — around 27% slower cognitive/functional decline over 18 months versus placebo, the first disease-modifying (rather than purely symptomatic) Alzheimer’s therapy with positive trial data. TGA/PBS availability in Australia is not confirmed — check current status before relying on this as an available option; it does not replace the acetylcholinesterase-inhibitor/memantine approach above, which remains the current PBS-funded standard.