Neurological aging reflects a balance between innate regenerative capacity (adaptive processes) and stochastic nervous system aging. ^[1]

The lecture presents this as a see-saw model:

The see-saw is a conceptual model, not a bedside diagnostic test: resilience and repair oppose accumulated molecular, metabolic and inflammatory injury. It helps explain increasing vulnerability with age, but a new focal, asymmetric or function-limiting deficit should not be dismissed as aging.

A thorough history must be obtained from both the patient AND collateral sources who know the patient well. ^[1]

This is fundamental in geriatric medicine and is a concept you'll see tested repeatedly. Why both sources?

• Cognitive decline → the patient may not accurately report symptoms (anosognosia = lack of insight into own deficits)
• Lack of awareness → many elderly patients minimize symptoms or attribute them to "just getting old"
• Premorbid status → you must know the patient's baseline level of cognitive function, motor skills, and independence. Without this, you cannot determine if there has been a true decline

Understanding what is normal aging vs. pathology is critical. If you don't know the normal changes, you'll over-diagnose pathology.

"Normal" changes in the neurologic examination with aging ^[1]:

Modifications in neurological examination for patients with more severe cognitive impairment ^[1]:

Why this matters: In clinical practice and OSCEs, you will encounter patients who cannot follow standard neurological examination instructions. You need to adapt. The examiners may test whether you know alternative methods.

Seizures are episodes of transient neurologic change due to hypersynchronous, hyperexcited neuronal activity. ^[1]

Nearly one-half of new-onset seizures occur in individuals over the age of 65 years. ^[1]

This is a critical fact. The elderly are actually the most common age group for new-onset seizures — not children as many students assume. Why?

• Accumulated brain pathology (strokes, tumours, neurodegeneration)
• Metabolic derangements are more common
• Polypharmacy increases drug-related seizure risk

Provoked seizures (acute symptomatic seizures): occur with an identifiable proximate cause and are not expected to recur in the absence of that particular cause or trigger. ^[1]

Unprovoked seizures: occur without an identifiable immediate cause. ^[1]

The slide shorthand is “recurrent unprovoked seizures.” ^[1] The current ILAE operational definition is broader: epilepsy is present after two unprovoked (or reflex) seizures more than 24 hours apart, after one such seizure when the estimated 10-year recurrence risk is at least 60%, or when an epilepsy syndrome is diagnosed ^[23].

Why this distinction matters enormously:

• Provoked (acute symptomatic) seizure → treat the cause; long-term antiseizure medicine is not automatic
• Unprovoked seizure → assess recurrence risk and whether the person meets the operational definition of epilepsy

Acute stroke (3-9%): ^[1]

• Risk factors: lobar hemorrhage, large size of stroke, cortical involvement of ischemic stroke, hyperglycemia
• Ischemic stroke: mostly within 48 hours of onset
• Subarachnoid hemorrhage: mostly within hours

Other intracranial: subdural hematoma, hypoxic-ischemic brain injury, hypertensive encephalopathy, acute head trauma, active intracranial infection. Trauma is the underlying cause of 4–17% of acute symptomatic seizures. ^[1]

Metabolic encephalopathy: hypoglycemia, hyperglycemia, hyponatremia, uremic and hepatic encephalopathy. ^[1]

Drugs and drug withdrawal: up to 10% — alcohol, benzodiazepine or barbiturate withdrawal. ^[1]

Post-stroke epilepsy (risk factors: hemorrhage, cortical involvement, large area of stroke) ^[1] Neurodegenerative diseases / dementia ^[1] Intracranial lesions — brain tumors, vascular malformations ^[1]

Post-stroke epilepsy is the single most common cause of epilepsy in the elderly. The mechanism: a stroke scar creates a focus of abnormal electrical activity (epileptogenic focus). Cortical involvement and larger strokes mean more scar tissue near excitable cortical neurons.

Seizures in older adults are difficult to recognize ^[1]:

• Lack of aura or preceding warning
• Lack of motor features
• Comorbid dementia
• Misdiagnose as delirium

Features that suggest seizure in older adults ^[1]:

• Confusion, behavioral change, unresponsiveness
• Sudden falls with no recall or warning
• Recurrent events occurring in various positions or circumstances
• Arousal from sleep with confusion or disorientation

History (Most important): Detailed description of the event by witness, medications and substances, past medical history. Recurrent events. ^[1]

Investigations ^[1]:

• Blood tests: blood counts, electrolytes, muscle enzymes, (toxicology)
• Neuroimaging: CT/MRI to rule out structural lesions
• CSF analysis: when suspicious of CNS infection
• Electroencephalography (EEG)

Why muscle enzymes? CK may rise after a generalised tonic–clonic seizure because of sustained muscle contraction, but it is delayed and non-specific; a normal result does not exclude seizure and an elevated result does not prove one.

Why EEG? Can show epileptiform discharges (interictal spikes) that support the diagnosis. Also essential to detect NCSE.

Emergency management: secure airway and stabilizing other vital signs ^[1] Check blood glucose ^[1] Anti-epileptic drug (AED) for abortion of seizure if prolonged ^[1] Long term AED ^[1]

The acute management follows standard ABCDE protocol. Glucose check is critical because hypoglycaemia is reversible. If a convulsive seizure lasts 5 minutes or longer, treat it as status epilepticus: follow the local emergency protocol, give a benzodiazepine first, and use an appropriate second-line intravenous antiseizure medicine if it persists. Do not delay treatment while awaiting tests.

A complex decision. Based on risk factors for seizure recurrence rather than age. ^[1]

Major risk factors for recurrent seizure: remote symptomatic etiology, first seizure arising from sleep, epileptiform abnormality on EEG, and structural abnormality on MRI of brain. ^[1]

The lecture proposes treatment after a first unprovoked seizure when examination, imaging or EEG identifies a high-risk substrate. ^[1]

Two or more well-documented unprovoked seizures: Antiseizure drug therapy should be started. ^[1]

NICE therefore does not make “first versus second seizure” an absolute treatment rule: it recommends starting an antiseizure medicine once epilepsy is confirmed and considering one after a first unprovoked seizure when a neurological deficit, unequivocal epileptic EEG, structural imaging abnormality or an unacceptable recurrence risk is present ^[24]. Diagnosis and the decision to treat remain related but distinct.

Taking into account their comorbidities, adverse effect profile, and drug-drug interactions. ^[1] Started at very low doses and titrated gradually, in contrast to younger patients. ^[1]

Why "start low, go slow"?

• Reduced hepatic and renal clearance → drugs accumulate faster
• Altered protein binding → more free drug
• Increased CNS sensitivity → more side effects at lower doses
• Polypharmacy → enzyme inducers (carbamazepine, phenytoin) interact with warfarin, statins, etc.
• Enzyme-inducing AEDs can reduce bone density (already at risk for osteoporosis)

For common focal-onset epilepsy, lamotrigine and levetiracetam are often suitable first-line options because they have fewer interactions, but treatment must match seizure type ^[24]. Phenytoin's narrow therapeutic window and enzyme induction, and carbamazepine's interactions/hyponatraemia risk, often make them less attractive in frail or highly medicated older adults; neither is an absolute prohibition.

Delirium = acute confusion. A complex neuropsychiatric syndrome. A disturbance of consciousness with reduced ability to focus, sustain, or shift attention. Acute onset and fluctuating course. ^[1]

The key conceptual framework: delirium is a global brain failure. Just as the heart can fail, the brain can acutely fail. It is NOT a primary psychiatric disorder; it is a medical emergency that indicates underlying illness.

1/3 to 2/3 of delirium goes unrecognised. ^[1]

Why so under-recognised?

• Hypoactive delirium (quiet, withdrawn, drowsy) is far more common than hyperactive (agitated) but looks like depression or "just being tired"
• Fluctuating course: patient may be lucid when the doctor visits
• Comorbid dementia masks new changes

Symptom Domains of Delirium

Symptoms of delirium are wide-ranging and nonspecific ^[1]:

Hypoactive delirium is the most commonly missed subtype because patients appear quiet and withdrawn rather than agitated.

Delirium = Predisposing factors (baseline vulnerability) + Precipitating factors (noxious insults) ^[1]

This is a key exam concept. A highly vulnerable patient (e.g., 90-year-old with dementia) can develop delirium from a minor insult (e.g., constipation, UTI). A robust patient (e.g., fit 70-year-old) requires a major insult (e.g., sepsis, major surgery) to become delirious.

Comparison Table ^[1]:

This table is an orientation aid, not a rule-out test. Delirium can persist for weeks or longer; advanced dementia or dementia with Lewy bodies may impair and fluctuate in attention; depression may coexist with either condition and is not defined by medication response. When uncertain between delirium and dementia, manage the delirium first ^[25].

Find out and treat the underlying cause(s). ^[1]

Non-pharmacological approaches should be the first strategy. ^[1]

The lecture warns that antipsychotics and sedatives can worsen cognition, mobility and clinical outcomes. ^[1] They do not treat the underlying cause and should not be used routinely.

Non-pharmacological management (British Geriatrics Society Do's and Don'ts) ^[1]:

Do:

• Reorientation: clocks, calendars, familiar objects from home
• Ensure sensory aids: glasses, hearing aids in good working order
• Adequate lighting (avoid shadows)
• Minimize environmental disruption (same nurses, same bed — ensure continuity of care)
• Early, safe mobilization and active range-of-motion work matched to clinical status
• Promote sleep-wake cycle: discourage daytime napping, encourage bright light exposure during the day, provide uninterrupted sleep period at night with low-level lighting
• Use non-pharmacological approaches for sleep and anxiety (music, massage, relaxation techniques)
• Ensure adequate hydration, nutrition
• Reduce medication burden but ensure adequate analgesia; avoid reflexive or open-ended as-required psychoactive prescribing
• Pain management
• Involve relatives and carers
• Liaise with old age psychiatry service
• Avoid complications: immobility, malnutrition, pressure sores, over-sedation, falls, incontinence

Do NOT:

• Catheterise without a clear indication
• Use physical restraints or unnecessary tethers; individualise observation and falls-safety measures
• Sedate routinely
• Argue with the patient

Pharmacological management — ONLY in specific situations:

Antipsychotics and sedatives were occasionally used ^[1]:

• For sedation in severely agitated patients in whom interruption of essential medical therapies (e.g. mechanical ventilation, dialysis catheters) or self-harm
• For treating distressing or dangerous behavioural disturbances

Potential drawbacks ^[1]:

• Might switch patient from hyperactive to hypoactive form
• Worsen cognitive impairment
• Complicate ongoing assessment of mental status
• Impair patient's ability to understand or cooperate with treatment
• Increase fall risk

The slide gives scheduled haloperidol 0.25–0.5 mg twice daily, but this should not be copied as a routine prescription. Current NICE/MHRA advice is to consider short-term haloperidol (usually 1 week or less) only when the person is distressed or poses a risk and verbal/non-verbal de-escalation is ineffective or inappropriate. Check contraindications, obtain a baseline ECG and correct electrolyte disturbance where feasible, then use the lowest clinically appropriate dose for the shortest time with frequent review and monitoring for QT-related and extrapyramidal toxicity ^[25][26]. Haloperidol is contraindicated in Parkinson's disease and dementia with Lewy bodies; do not automatically substitute another antipsychotic—seek specialist advice and follow local guidance.

Dementia (Major Neurocognitive Disorder) ^[1]: (a) Significant cognitive decline from a previous level of performance in ≥1 cognitive area(s) (memory, language, attention, executive function, perceptual-motor, social cognition) AND (b) Interference with independence in everyday activities.

Mild Cognitive Impairment (MCI) or Minor Neurocognitive Disorder ^[1]: (a) + no impairment in independence in everyday activities.

Not in the context of active delirium. ^[1]

The key discriminator between MCI and dementia is functional impairment. If a patient forgets things but still manages their finances, cooking, and medication independently → MCI. If they can no longer manage → dementia.

From supporting notes ^[4]:

• MCI: 1-2 SD below average (3rd–16th percentiles)
• Dementia: ≥2 SD below average (≤3rd percentile)
• Dementia severity: Mild = instrumental ADL affected; Moderate = basic ADL affected; Severe = fully dependent

Subtypes of Dementia ^[1]:

PDD versus dementia with Lewy bodies: both are Lewy-body disorders with overlapping cognitive, psychiatric and motor features. The conventional clinical distinction is timing: call it PDD when dementia develops in established PD; call it DLB when dementia precedes or occurs within about 1 year of parkinsonism. The consensus group explicitly describes this 1-year cut-off as useful but arbitrary ^[33].

AD-specific medications ^[1]:

Why cholinesterase inhibitors? The cholinergic hypothesis of AD: degeneration affecting basal forebrain cholinergic pathways reduces cortical acetylcholine. Acetylcholinesterase inhibition increases synaptic acetylcholine. This is symptomatic, not disease-modifying treatment; benefit and tolerability should be reviewed rather than promised for a fixed duration.

Why an NMDA antagonist? Memantine modulates pathological NMDA-receptor signalling while preserving physiological transmission. Under NICE guidance, use memantine alone for moderate AD when an AChE inhibitor is contraindicated/not tolerated, or for severe AD; add it to an existing AChE inhibitor in moderate disease when appropriate and offer the combination in severe disease ^[27].

Side effect logic:

• Cholinesterase inhibitors increase ACh everywhere → GI effects (nausea, vomiting, diarrhoea via muscarinic stimulation), bradycardia (vagal tone ↑)
• Check for pre-existing bradycardia or heart block before starting

Novel medications on the 2023 slide ^[1]:

• Aducanumab (FDA accelerated approval in 2021)
• Lecanemab (then described only as a positive phase III trial)

Current-status correction (jurisdiction matters): this slide is now outdated. Biogen discontinued aducanumab development and commercialisation in 2024 ^[30]. The US FDA converted lecanemab to traditional approval in July 2023 and approved donanemab in July 2024; both were studied for early symptomatic AD (MCI or mild dementia) with confirmed amyloid pathology, not established moderate/severe dementia ^[28][29]. Approval, funding and availability differ by jurisdiction.

These anti-amyloid antibodies produce a modest slowing of decline, not restoration of lost cognition. They require specialist selection, confirmation of amyloid pathology, counselling and MRI-based safety monitoring. Class harms include infusion reactions and amyloid-related imaging abnormalities (ARIA)—oedema/effusions and micro- or macrohaemorrhage; serious or fatal haemorrhage can occur. APOE ε4 status and antithrombotic/haemorrhage risk are important to the individual risk discussion ^[28][29].

Senile gait: gait with slight stoop, slower speed, and reduced tandem ability ^[1]

Gait and balance disorders in elderly — Multifactorial ^[1]:

• Neurological: Parkinsonism, cerebellar ataxia, peripheral neuropathy (sensory/motor), stroke (pseudoparkinsonism), cervical myelopathy, normal pressure hydrocephalus
• Non-neurological: Reduced vision, pain (e.g. arthritis), deconditioning/physical inactivity, obesity, cognitive impairment, dizziness (postural hypotension), drug-induced, footwear

The key clinical message: gait disorders in the elderly are almost always multifactorial. A patient may have mild parkinsonism, peripheral neuropathy, and osteoarthritis all contributing. Treatment requires addressing each factor.

Muscle rigidity, bradykinesia, tremor, postural instability ^[1]

Causes ^[1]:

• Idiopathic Parkinson disease
• Pseudoparkinsonism: vascular aetiology
• Drug-induced
• Atypical parkinsonian disorders

Parkinsonism is a clinical syndrome, not aetiology. Parkinson's disease is one cause; vascular, drug-induced and atypical neurodegenerative syndromes can resemble it. Suspected PD should be referred promptly and untreated to a clinician with diagnostic expertise, because the diagnosis is clinical and should be reviewed if atypical features emerge ^[31].

Vascular type: extensive subcortical small vessel disease can manifest with symmetrical parkinsonism and gait disorder including hyperreflexia and increased tone ^[1]

Drug-induced: extrapyramidal side effects from antipsychotics initially started for BPSD ^[1]

Consider starting levodopa for older patients with symptoms of PD that affect daily life. ^[1]

Dopamine agonists: in general less effective than levodopa, less well tolerated in older adults. ^[1]

Very mild signs and symptoms do not necessarily need medications, if no interference with quality of life. ^[1]

Anticholinergic drugs: avoid use in older patients esp. those with dementia. Should be reserved for younger patients in whom tremor is the predominant problem. ^[1]

Why levodopa is often favoured in an older patient: it is the most effective motor treatment, whereas dopamine agonists more often cause hallucinations, impulse-control disorders, excessive sleepiness and orthostatic hypotension. Age alone is not the prescribing rule: current guidance offers levodopa when early motor symptoms affect quality of life, and an individualised choice among levodopa, a dopamine agonist or an MAO-B inhibitor when they do not ^[31]. Discuss adverse effects with the person and carers, and obtain specialist advice before modifying therapy for wearing-off or dyskinesia.

Why avoid anticholinergics? They worsen cognitive impairment and can precipitate delirium in the elderly. Anticholinergic burden is a major concern in geriatric prescribing.

Dementia in PD ^[1]:

• Symptomatic treatment only. No disease-modifying therapies.
• Cholinesterase inhibitors (e.g. Rivastigmine, Donepezil), Memantine
• Drugs that may WORSEN cognitive function: Anticholinergic drugs and dopaminergic drugs for motor symptoms

Psychosis in PD ^[1]:

• Reduce dose or even stop PD meds (monitor motor functions)
• Start antipsychotics if inadequate response (e.g. Pimavanserin)

Current practice is more precise ^[31]:

• Offer a cholinesterase inhibitor for mild–moderate PDD and consider one in severe PDD; consider memantine only if a cholinesterase inhibitor is contraindicated or not tolerated.
• For hallucinations/delusions, first look for delirium, infection, medicine toxicity and other triggers. Do not treat well-tolerated symptoms automatically.
• If a PD medicine is a likely trigger, reduce it only after weighing withdrawal and motor deterioration and seeking PD-specialist advice—abruptly stopping dopaminergic therapy can be dangerous.
• If medication is required, NICE advises considering low-dose quetiapine only when there is no cognitive impairment and offering monitored clozapine when standard treatment fails. Pimavanserin has US approval, but access/approval varies and it is not a universal default.

This section records the historical ICIDH terminology shown in the slides. “Handicap” is no longer the preferred classification term, and contemporary practice uses respectful person-centred language rather than “the disabled person.”

Impairment: Any loss or abnormality of psychological, physiological or anatomical structure or function ^[1]

Disability: Any restriction or lack of activity resulting from an impairment to perform an activity in the manner or range considered normal for people of the same age, sex, and culture ^[1]

Handicap: A disadvantage for a given individual resulting from impairment or disability that limits or prevents the fulfilment of a role that would otherwise be normal for that individual ^[1]

Lecture-era linear model: Impairment (body level) → Disability (person level) → Handicap (society level). Use this only to interpret the historical slide; use the interactive ICF model below for current practice.

Example:

• Impairment = right hemiparesis (body structure/function affected)
• Disability = cannot walk independently, cannot write
• Handicap = cannot work as a factory manager, cannot drive

The slides show a 1998 development-stage formulation. The ICF was formally endorsed by the World Health Assembly in 2001 and remains WHO's framework for describing functioning and disability ^[32]. It is not merely a word-for-word renaming of the old linear sequence.

The new classification ^[1]:

• Has less negative connotations
• Places more emphasis on the individual's abilities rather than disabilities
• More emphasis on social context
• Medical model → Social model of disability

The final arrow is the slide's simplification. ICF is better understood as a biopsychosocial framework integrating body, activity, participation and context, rather than replacing a medical model with a purely social one.

Functioning is an interaction between the health condition and contextual factors. Avoid assuming that a body impairment maps inevitably to one activity or participation outcome: environmental modification and support can change both.

Three approaches ^[1]:

1. Approaches that reduce disability (more precisely: treat or reduce the impairment where possible)
2. Approaches designed to acquire new skills and strategies, which will maximise activity (compensatory strategies)
3. Approaches that alter the physical and social environment to reduce barriers and enable participation

Key principles ^[1]:

• Work with the person and, with consent, their family/support network
• Give accurate information and advice about the health condition, likely course and prognosis
• Listen to the person's needs and perceptions and, with consent, those of family/supports
• Work with other professional colleagues in an interdisciplinary fashion (team)
• Establish realistic rehabilitation goals which are both appropriate to that person's disability and their family, social and employment needs

67/M, manager of a factory, right hand dominant, drives to work, married with 2 sons, active social life. Admitted for left thalamic/basal ganglia hemorrhage. Right spastic hemiparesis power ~3/5. Right limb neuropathic pain. ^[1]

Application of ICF framework ^[1]:

• Impairments: right spastic hemiparesis and central neuropathic pain → targeted drug/non-drug treatment
• Activity limitations: walking, toileting/bathing and writing → task practice, a quadripod and, where appropriate, wheelchair skills
• Participation restrictions: work, driving and social/family roles → graded return-to-work planning and formal driving assessment
• Environmental facilitators: home rails/adaptation, accessible mobility, family training and employer adjustments
• Person-centred goals: agree specific, meaningful and reviewable goals, such as safe daytime independence in selected ADLs and return to a feasible work role