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]

Epilepsy is defined as a condition of recurrent unprovoked seizures. ^[1]

Why this distinction matters enormously:

• Provoked seizure → treat the cause, usually NO long-term AED
• Unprovoked seizure → epilepsy risk, may need long-term AED

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 rises after generalized tonic-clonic seizures due to sustained muscle contraction. An elevated CK supports that a convulsion occurred (useful when the event was unwitnessed).

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 a reversible cause. If the seizure is prolonged ( > 5 minutes), it becomes status epilepticus and requires IV benzodiazepines (lorazepam or diazepam) followed by phenytoin/levetiracetam if refractory.

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]

First unprovoked seizure: AED only for documented potential symptomatic cause of epilepsy (e.g. stroke, traumatic brain injury, brain tumor) based upon history, an abnormal neurologic examination, a relevant abnormality on brain imaging (CT or MRI) +/- epileptiform discharges on EEG. ^[1]

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

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)

Preferred AEDs in elderly: Lamotrigine, Levetiracetam (fewer interactions, better tolerated). Avoid phenytoin (narrow therapeutic window, enzyme inducer, osteoporosis risk) and carbamazepine (hyponatraemia, enzyme inducer) if possible ^[2].

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

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]:

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

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

Antipsychotics and sedatives can prolong the duration of delirium and associated cognitive impairments, and worsen clinical outcomes. ^[1]

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

• Reorientation: clocks, calendars, familiar objects from home
• Ensure sensory aids: glasses, hearing aids
• Adequate lighting (avoid shadows)
• Minimize environmental disruption (same nurses, same bed)
• Early mobilization
• Promote sleep-wake cycle (no unnecessary night-time obs)
• Ensure adequate hydration, nutrition
• Pain management
• Remove unnecessary catheters and lines
• Avoid restraints

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

If absolutely needed: low-dose haloperidol (0.5-1mg) is traditionally first-line. In patients with Parkinson's disease or Lewy body dementia, use quetiapine instead (haloperidol worsens parkinsonism via D2 blockade) ^[2][3].

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]:

AD-specific medications ^[1]:

Why cholinesterase inhibitors? The cholinergic hypothesis of AD: the nucleus basalis of Meynert (a major source of cholinergic neurons) degenerates early in AD → reduced acetylcholine in the cortex → cognitive decline. By inhibiting acetylcholinesterase, you increase available ACh at the synapse. This is symptomatic treatment — it does NOT halt disease progression but can stabilize/slow decline for 6-12 months.

Why NMDA antagonist? In moderate-severe AD, excessive glutamate (excitotoxicity) damages neurons via NMDA receptor over-activation. Memantine is a partial NMDA antagonist that reduces excitotoxic damage while allowing normal glutamate signalling. Used for moderate-severe stages where cholinesterase inhibitors are less effective alone.

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 for Alzheimer's disease ^[1]:

• Aducanumab (FDA approved June 2021)
• Lecanemab (Positive phase III trial)

These are anti-amyloid monoclonal antibodies that target amyloid-beta plaques. They represent a shift from symptomatic to disease-modifying therapy. Major side effect: ARIA (amyloid-related imaging abnormalities — brain oedema and microhaemorrhages). They are controversial due to modest clinical benefit versus significant cost and risk.

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 the clinical syndrome. Parkinson's disease is one specific cause (idiopathic, due to loss of dopaminergic neurons in the substantia nigra pars compacta).

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 first in the elderly (not dopamine agonists)?

• Dopamine agonists (pramipexole, ropinirole) cause more side effects in the elderly: hallucinations, impulse control disorders (pathological gambling, hypersexuality), excessive daytime somnolence, orthostatic hypotension
• In younger patients, dopamine agonists are often started first to delay levodopa-associated motor complications (wearing off, dyskinesias), but elderly patients have less time to develop these complications and are more vulnerable to agonist side effects
• Levodopa is the most effective drug and is better tolerated in the elderly

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)

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]

Think of it as levels: Impairment (body level) → Disability (person level) → Handicap (society level).

Example:

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

New terminology ^[1]:

• Impairment → still "Impairment"
• Disability → now "Activity"
• Handicap → now "Contextual factors / Participation"

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

Three approaches ^[1]:

1. Approaches that reduce disability (now called "reduce impairment" — treat the underlying condition)
2. Approaches designed to acquire new skills and strategies, which will maximise activity (compensatory strategies)
3. Approaches that help to alter the environment, both physical and social, so that a given disability carries with it minimal consequent handicap (environmental modification)

Key principles ^[1]:

• Work with the disabled person and their family
• Give accurate information and advice about the nature of the disability, natural history, prognosis
• Listen to the needs and perceptions of the disabled person and their family
• 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]:

• Disability (impairment level): reduce disability through drug and non-drug treatments for limb spasticity and neuropathic pain
• Activity: learn new skills — walks with external support with quadripod indoors/outdoors +/- wheelchair
• Participation: approach employer to change nature of work or reduce hours (no longer writing well with right hand); installation of rails at home for toileting/bathing; carer training to wife; occupational assessment of driving
• Setting up a realistic goal: to perform most basic ADL independently at home as wife also working in daytime. To return to work if possible.

1. An 80-year-old man with known dementia is brought to A&E with acute confusion, visual hallucinations, and fluctuating consciousness over 24 hours. Which of the following is the MOST IMPORTANT initial management step? A. Start haloperidol B. Start donepezil C. Investigate and treat the underlying cause D. Restrain the patient for safety → Answer: C. Delirium management = find and treat the cause. Non-pharmacological approaches first. Haloperidol only if severe agitation threatening safety.

2. Which of the following is the MOST common reversible cause of delirium in the elderly? A. Urinary tract infection B. Medications C. Dehydration D. Constipation → Answer: B. Medications account for 22-39% of delirium causes.

3. A 75-year-old woman with Parkinson's disease dementia develops visual hallucinations. Which antipsychotic is MOST appropriate? A. Haloperidol B. Risperidone C. Quetiapine D. Olanzapine → Answer: C. Quetiapine has lowest D2 affinity and is safest in PD. Haloperidol and risperidone will catastrophically worsen parkinsonism.

4. A 72-year-old man presents with a first unprovoked seizure. MRI brain shows an old left MCA territory infarct. EEG shows left temporal epileptiform discharges. Should you start an anti-epileptic drug? Justify your answer. (3 marks) → Yes. First unprovoked seizure with a documented potential symptomatic cause (old stroke on MRI) + epileptiform discharges on EEG → high risk of recurrence → start AED. Start at low dose and titrate gradually given age.

5. List four features of the CAM (Confusion Assessment Method) and state which are required for a diagnosis of delirium. (4 marks) → (a) Acute onset and fluctuating course, (b) Inattention, (c) Disorganized thinking, (d) Altered consciousness. Requires (a) + (b) + either (c) or (d).

6. Compare and contrast the tremor-predominant and postural instability gait difficulty (PIGD) subtypes of Parkinson's disease. (4 marks) → Tremor-predominant: rest tremor dominant, better levodopa response, slower disease course, less cognitive impairment. PIGD/akinetic-rigid: gait and balance difficulty dominant, lesser levodopa response, more rapid and debilitating course.

7. A 67-year-old right-handed factory manager presents with right spastic hemiparesis after a left thalamic haemorrhage. Using the WHO ICF framework, outline a rehabilitation plan. (6 marks) → Impairment: Right hemiparesis, neuropathic pain → treat spasticity and pain. Activity: Learn to walk with quadripod, compensatory strategies for right hand function. Participation: Employer negotiation for modified work, home modifications (grab rails), carer training for wife, driving assessment. Goal: Independent basic ADL at home, return to modified work if possible.