Definitions

• Mild Neurocognitive Disorder (Mild NCD / MCI): Modest cognitive decline from a previous level of performance in one or more cognitive domains, not interfering with independence in everyday activities (may require greater effort or compensatory strategies).
• Major Neurocognitive Disorder (Major NCD / Dementia): Significant cognitive decline in one or more domains that interferes with independence and daily activities.

Causes and aetiologies

NCDs have multiple causes — neurodegenerative, vascular, metabolic, infectious, toxic, traumatic and psychiatric. Identifying the cause guides prognosis and management.

• Alzheimer’s disease: Progressive episodic memory impairment with medial temporal lobe atrophy — commonest cause of major NCD.
• Vascular cognitive impairment: Stroke-related or small vessel disease causing stepwise or mixed decline.
• Lewy body disease & Parkinson’s disease dementia: Early visuospatial deficits, fluctuating cognition and visual hallucinations.
• Frontotemporal lobar degeneration (FTLD): Early behavioural change, disinhibition, language variants.
• Traumatic brain injury (TBI): Single severe or repetitive mild injuries.
• Medical & metabolic causes: thyroid dysfunction, vitamin deficiencies (B12, thiamine), hepatic/renal failure.
• Infectious causes: HIV-associated NCD, chronic meningitis, neurosyphilis, post-encephalitic syndromes.
• Autoimmune & inflammatory: autoimmune encephalitis, CNS vasculitis.
• Normal-pressure hydrocephalus (NPH): gait disturbance, urinary incontinence, and cognitive impairment — potentially reversible.
• Medication/toxin-induced: anticholinergics, sedatives, alcohol-related brain damage (Korsakoff), heavy metals.

Symptoms — cognitive, behavioural and functional

• Cognitive domains: memory, executive function, attention, language, visuospatial skills and social cognition.
• Behavioural and psychiatric: depression, apathy, agitation, psychosis, disinhibition (varies by aetiology).
• Functional impact: difficulty with complex tasks (finances, medications), driving, work performance and eventually basic ADLs in major NCD.
• Onset and course: insidious progressive (neurodegenerative) vs stepwise (vascular) vs acute/subacute (infectious, metabolic, autoimmune).

Assessment — practical priorities

1. Establish baseline and timeline: onset, progression, fluctuation.
2. Collateral history from family/caregivers for functional changes and behavioural symptoms.
3. Screening cognitive tests: MoCA, MMSE, ACE-III — choose tools validated locally when possible.
4. Domain-focused neuropsychological testing for detailed profiling and differential diagnosis.
5. Medication review for iatrogenic contributors (anticholinergics, benzodiazepines, opioids, antipsychotics).
6. Assess for delirium (acute fluctuating attention/awareness) and treat medical causes urgently.
7. Evaluate capacity-related issues: driving, financial decisions, consent to medical care.

Investigations — essential and targeted

• Baseline blood tests: CBC, electrolytes, glucose, renal and liver function, TFTs, B12, folate, vitamin D, inflammatory markers.
• Infectious screen: HIV, syphilis serology when indicated.
• Neuroimaging: MRI brain preferred for structural changes (atrophy patterns, vascular lesions); CT for acute or urgent evaluation.
• EEG: when seizures, non-convulsive status, or rapidly progressive decline suspected.
• CSF analysis & biomarkers: amyloid/tau markers, autoimmune antibody panels when clinically suggested.
• Functional imaging: FDG-PET or DaTscan for differentiating Parkinsonian syndromes and Lewy body disease when necessary.

Treatment principles

Management aims to treat reversible causes, slow decline where possible, manage behavioural symptoms and support function and caregivers.

Address reversible causes

• Correct metabolic disturbances, treat infections, replete vitamins, and remove offending medications.
• Consider neurosurgical options for NPH, tumour resection when indicated.

Pharmacological strategies

• Alzheimer’s disease: cholinesterase inhibitors (donepezil, rivastigmine) and memantine for moderate–severe cases.
• Lewy body dementia: rivastigmine recommended; antipsychotics used cautiously due to sensitivity.
• Vascular cognitive impairment: manage vascular risk factors (BP, lipids, diabetes, smoking cessation).
• Symptom-targeted medications: SSRIs for depression/anxiety, antipsychotics for severe psychosis (lowest effective dose, monitor side effects), stimulants or dopaminergic agents in select cases for apathy (specialist input recommended).

Non-pharmacological & rehabilitative care

• Cognitive rehabilitation and training tailored to deficits.
• Occupational therapy for ADL support, home safety and adaptive strategies.
• Speech & language therapy for language and swallowing problems.
• Exercise programs and physiotherapy to maintain mobility and reduce fall risk.

Caregiver & psychosocial support

• Psychoeducation about disease trajectory and realistic expectations.
• Support groups, respite services and social care planning.
• Legal and financial planning: advance directives, power of attorney, guardianship where needed.

Key takeaways

• Differentiate delirium and treat reversible medical causes early.
• Use targeted investigations to identify aetiology; MRI and blood tests are core.
• Treatment combines cause-specific medical care, symptomatic pharmacology, rehabilitation and caregiver support.
• Regular follow-up to monitor progression, safety and capacity-related decisions is essential.