Geriatrics SC048: Common Neurological Problems In Older People Flashcards
Balance of neurologic changes with aging
Innate regenerative capacity vs Stochastic aging of nervous system
- Young: regenerative > aging
- Elderly: aging > regenerative
Regenerative:
- Growth factors release
- Neurogenesis
- Axonal growth
- Dendritic growth
Aging:
- Molecular damage (e.g. lipid peroxidation, DNA mutations)
- Energy dysregulation (e.g. insulin resistance)
- Neurodegenerative (e.g. synapse loss)
- Glial / immune alteration (e.g. demyelination)
Neurological assessment in older adults
History:
- Both patient + collateral sources who know patient well
- Ensure accuracy of information since cognitive decline, lack of awareness / insight are common
- ***Premorbid status: baseline level of cognitive function, motor skills, level of independence
P/E:
- ***Age-appropriate
- “Normal” changes in neurologic examination with aging —> not pathological
1. Eyes
- smaller pupil size + reduced reactivity (esp. with cataract)
- presbyopia (decreased near vision)
- breakdown of smooth eye pursuits with saccadic intrusions
- reduced upgaze (but downgaze may be pathological) and convergence ability of eyes
- Ears
- ↓ hearing (high frequency)
- mild ↑ in muscle tone, ↓ in muscle bulk, subtle ↓ in muscle strength
- ↓ vibration sense in distal lower extremities
- ↓ ankle jerk reflexes
- presence of primitive reflexes
- senile gait: slight stooped, slower speed, reduced tandem gait ability —> not considered pathological
Modifications in neurological P/E in severe cognitive impairment patients:
- Visual field: Count fingers —> Detect hand movement / Blink to threat
- Eye movements: Track finger —> Track examiner’s face / patient’s own finger
- Strength: Resist movement of examiner —> Maintain limbs in antigravity position after release
- UMN screen: Pronator drift —> Look at symmetry during arm rolling
- Proprioception: Detect joint movements with eyes closed —> Only Romberg test
- LL coordination: Heel-shin test —> Toe to examiner’s finger
Common neurological problems in elderly
Acute neurological emergencies:
1. Delirium
2. Seizure
Chronic neurological conditions:
1. Dementia / Cognitive impairment
2. Gait and Balance disorders (Idiopathic Parkinson’s disease)
- Seizure
- Episodes of transient neurologic change due to hypersynchronous, hyperexcited neuronal activity
- Nearly 50% of new-onset seizures occur in individuals >65 yo
- Epilepsy: **Recurrent **unprovoked seizures
Causes:
1. Provoked / Acute symptomatic
- occur with identifiable immediate cause
- not expected to recur in absence of that particular cause / trigger (e.g. hypoglycaemia, electrolyte imbalance, alcohol withdrawal)
- Unprovoked
- without an identifiable immediate cause
***Causes of Provoked seizures in elderly
-
**Acute stroke (3-9%)
- Risk factors: lobar haemorrhage, large size of stroke, cortical involvement of ischaemic stroke, hyperglycaemia during stroke
- Ischaemic stroke: mostly within **48 hours of onset
- SAH: mostly within ***hours - Other intracranial problems
- Subdural haemorrhage
- Hypoxic-ischaemic brain injury post-cardiac arrest
- Hypertensive encephalopathy
- **Trauma (Underlying cause of 4-17% of provoked seizures)
- **CNS infection - Metabolic encephalopathy
- **Hypoglycaemia / Hyperglycaemia
- **Hyponatraemia
- **Uraemic encephalopathy
- **Hepatic encephalopathy - ***Drugs / Drug withdrawal (up to 10%)
- Alcohol
- BDZ / Barbiturate withdrawal
***Causes of Epilepsy (Recurrent unprovoked seizures) in elderly
- ***Post-stroke epilepsy
- ∵ Scar in brain (aka encephalopmalacia)
- Risk factors: haemorrhage, cortical involvement, large area of stroke - ***Neurodegenerative diseases / dementia
- Intracranial lesions
- **Tumours (e.g. Metastasis)
- **Vascular malformations (rare in elderly, usually present at younger age)
Clinical features of Seizure in elderly
Seizures in elderly are difficult to recognise:
- Often atypical clinical features + easily mistaken for other conditions
- Lack of aura / preceding warning
- Lack of motor features (e.g. no limb twitching)
- Comorbid dementia (cannot tell good history)
- Misdiagnosed as delirium
—> High level of suspicion needed
Typical features:
1. Limb twitching
Atypical features:
1. Confusion, behavioural change, unresponsiveness, fluctuating consciousness
2. Sudden falls with no recall / warning
3. Recurrent events occurring in various positions / circumstances
4. Arousal from sleep with confusion / disorientation
***Approach to Seizure in elderly
- History (most important): Detailed description of event by witness, medications, substances, past medical history
- Blood test
- CBC
- ***Electrolytes (Na, Ca, Mg, PO4)
- Muscle enzymes (↑ may suggest seizure)
- Toxicology (for OTC medications)
- Prolactin (∵ propagation of epileptic activity to hypothalamic-pituitary axis (from web)) - Imaging
- ***CT / MRI to rule out structural lesions (e.g. stroke, tumours) (esp. first onset) - ***CSF analysis
- CNS infection (e.g. chronic CNS infection may present with seizure without fever) - ***EEG
***Management of Seizure in elderly
Immediate:
1. Secure airway + stabilise vital signs
2. Check glucose
3. Anti-epileptic drug (AED) (for seizure abortion if prolonged)
Long-term:
1. Long term AED
- complex decision
- based on risk factors for seizure recurrence rather than age
- major risk factors for recurrent seizure:
—> remote symptomatic etiology (e.g. neuronal dysfunction, neurodegenerative disease)
—> first seizure arising from sleep
—> epileptiform discharge abnormality on EEG
—> structural abnormality on MRI brain (which is not reversible)
First unprovoked seizure:
- Long-term AED **only for documented potential **symptomatic cause of epilepsy (e.g. stroke, TBI, tumour)
—> based upon history, abnormal neurologic P/E, relevant abnormality on brain imaging (CT / MRI) +/- epileptiform discharges on EEG
> =2 well-documented **unprovoked seizure (i.e. **Epilepsy):
- AED should be started (even without features above)
Special points to note for elderly:
- Take into account their comorbidities, adverse effect profile, drug-drug interaction before starting AED
- Started at ***very low doses and titrated gradually (in contrast to younger patients) (∵ elderly sensitive to SE)
- Delirium
- Acute confusion
- Complex neuropsychiatric syndrome
- Disturbance of consciousness with reduced ability to focus, sustain, shift attention
- Acute onset + Fluctuating course
Symptoms:
- Wide range
- Non-specific
- 1/3-2/3 underdiagnosed in clinical practice
Clinical features:
1. ***Acute onset
- abruptly over hours / days
-
**Fluctuating course
- symptoms come and go / change in severity over 24 hour period
- characteristic **lucid intervals - ***Inattention
- difficulty focusing, sustaining, shifting attention
- difficulty maintaining conversation / following commands - ***Disorganised thinking
- disorganised / incoherent speech
- irrelevant conversation / unclear / illogical flow of ideas -
**Altered level of consciousness
- **clouding, reduced clarity of awareness of environment
- but can be ***hypervigilant
Other possible symptoms:
6. Cognitive deficits (e.g. poor memory, language impairment, disorientation)
7. Perceptual disturbance (e.g. illusions, hallucinations)
8. Psychomotor disturbance
- hyperactive (agitation, vigilance) / hypoactive (lethargy, decreased motor activity) / mixed
9. Altered sleep-wake cycle (e.g. daytime drowsiness, nighttime insomnia)
10. Emotional disturbances
***Causes of Delirium
Multifactorial
- Predisposing factors (Baseline vulnerability)
- >65
- Male
- ***Baseline cognitive impairment
- Visual / Hearing impairment
- Co-existing medical conditions
- Functional dependence
- Immobility
- Pain
- Constipation
- Sleep problem - Precipitating factors (Noxious insults)
- **Drugs (toxicity, anticholinergic, sedative, narcotic, anticonvulsant, withdrawal)
- **Infection
- Intercurrent illnesses (e.g. gouty arthritis pain, COPD, chronic lung / liver disease)
- **Neurological conditions (e.g. stroke)
- **AROU / Constipation
- **Metabolic conditions (e.g. electrolytes, glucose, acute adrenal insufficiency)
- Dehydration
- Surgery (stress from operation: ortho / cardiac)
- **Pain
- Environmental issues (e.g. stranger environment)
High Vulnerability —> Low Noxious insults enough to drive into delirium
Delirium vs Dementia vs Depression (3 “D”s in elderly)
Delirium:
1. Onset: **Acute
2. Course: **Fluctuating
3. Duration: Days - Weeks
4. Consciousness: Altered (Hypo / Hyper)
5. Attention: ***Impaired
6. Psychomotor change: Increased / Decreased (Hypo / Hyperactive)
7. Reversibility: Usually
Dementia:
1. Onset: Insidious
2. Course: Progressive
3. Duration: Months - Years
4. Consciousness: Clear
5. Attention: Normal (unless severe) (i.e. can follow conversation)
6. Psychomotor change: Often normal
7. Reversibility: Rarely
Depression:
1. Onset: Insidious
2. Course: Diurnal variation
3. Duration: Variable
4. Consciousness: Generally unimpaired
5. Attention: Unaffected
6. Psychomotor change: Psychomotor slowing
7. Reversibility: Control with medications
Approach to Delirium in elderly
- History taking from informant (most important)
- Baseline cognitive function
- Recent (past 2 weeks) changes in mental status: onset + course of symptoms
- Pain / discomfort (e.g. urinary retention, constipation, thirst)
- Medication (prescribed / ***OTC / herbal (esp. BDZ, Anticholinergics, Drug-drug interaction) —> most common reversible cause (22-39%)
- Alcohol - P/E
- Head to toe
- Vitals: temp, SaO2 (infection, COPD etc.), glucose
- Neurological: focal neurological changes (stroke), meningeal signs (CNS infection)
- Signs of occult infection (joints commonly missed, bedsores), dehydration, acute abdominal pain, DVT, other acute illness
- Assess for sensory impairments (visual / hearing can precipitate delirium)
- Palpable bladder - Diagnosis of Delirium: Confusion Assessment Method (CAM: screening tool)
A + B + C / D
- A: Acute onset + Fluctuating course
- B: Inattention
- C: Disorganised thinking
- D: Altered consciousness - Investigations
- Blood: CBC, Electrolytes (Na, Ca), Glucose, LRFT, TFT
- Drug concentration (e.g. digoxin, AED), NH3 concentration (chronic liver disease), Vit B12, Cortisol (adrenal insufficiency), ABG (hypercapnia: common cause of delirium)
- Urinalysis (occult UTI)
- ECG (acute MI)
- CXR / AXR (IO)
- CT / MRI brain (stroke, haemorrhage, tumours)
- EEG (seizure)
- LP as indicated
Management of Delirium
- Treat underlying cause
- Non-pharmacological (first strategy)
- Drug adjustment
- Address acute medical issues
- Reorientation strategies
- Maintain safe mobility
- Normalise sleep-wake cycle
Do:
- Provide environmental + personal orientation
- Ensure continuity of care
- Encourage mobility
- Reduce medication but ensure adequate analgesia
- Ensure hearing aids + spectacles are available and in good working order
- Avoid constipation / ROU
- Maintain good sleep pattern
- Maintain good fluid intake
- Involve relatives and carers
- Avoid complications (immobility, malnutrition, pressure sores, over sedation, falls, incontinence)
- Liaise with old age psychiatry service
Do NOT:
- Catheterise (if possible)
- Use restraint
- Sedate routinely
- Argue with patient
- Antipsychotic, Sedatives (for symptom control / confusion)
- start with low dose + titration until effect achieved
—> **Haloperidol 0.25-0.5mg PO/IM BD (Atypical antipsychotic: Quetiapine, Risperidone close in effectiveness)
- sedation of severely agitated patients in whom interruption of essential medical therapies (e.g. mechanical ventilation, dialysis catheter) / self-harm
- treating distressing / dangerous behavioural disturbances (e.g. in patients with extremely distressing psychotic symptoms e.g. delusion, hallucination)
- can prolong duration of delirium + associated cognitive impairments, worsen clinical outcome
—> **no evidence that improve prognosis (only improve symptom)
—> might switch patient from hyperactive to hypoactive
—> worsen cognitive impairment
—> complicate ongoing assessment of mental status (not sure if patient recovering)
—> impair patient’s ability to understand / cooperate with treatment
—> increase fall risk
—> impair rehabilitation progress
- Dementia / Cognitive impairment
DSM5:
1. Dementia (aka **Major neurocognitive disorders)
- Significant cognitive decline from previous level of performance in **>=1 cognitive area (memory, language, attention, executive function, perceptual-motor and social recognition)
* **AND
- Interference with independence in everyday activities
- Mild cognitive impairment (MCI) (aka **Mild neurocognitive disorder)
- Significant cognitive decline from previous level of performance in **>=1 cognitive area (memory, language, attention, executive function, perceptual-motor and social recognition)
* **WITHOUT
- Interference with independence in everyday activities
***MUST rule out active delirium before making diagnosis of dementia
Causes:
Primary:
1. **Alzheimer’s disease (most common)
2. **Vascular dementia (2nd common)
3. Mixed (AD + VD)
4. Frontotemporal dementia (uncommon)
5. Lewy body dementia (uncommon)
6. Parkinson’s disease dementia (uncommon)
Secondary:
1. Secondary causes of dementia (e.g. tumour, trauma, normal pressure hydrocephalus (NPH))
***Approach to Cognitive impairment
- History from reliable informants
- ***Temporal pattern
—> Indolent course
—> Progression over years
—> Unnoticed until a decompensating event / acute insult (e.g. Infection / surgery) that unmasks the decline
- Cognitive domains
—> Inattention (e.g. difficulty focus on task)
—> Executive function (e.g. difficulty multitasking)
—> ***Learning and memory (e.g. forget recent events (e.g. breakfast), repetitive questions)
—> Language (e.g. struggling to find words, difficulty comprehend words)
—> Perceptual-motor function (e.g. difficulty finding way back home, prosopagnosia (difficulty recognise face), performing learned tasks (e.g. using knifes))
—> Social cognition (e.g. changes in personality, behaviour, habits, beliefs)
- ***Objective cognitive assessments (grade severity)
- MMSE (total marks of 30)
- Montreal cognitive assessment (MOCA) (time-consuming, complex, more domains)
—> require sufficient level of alertness + attention for successful completion
—> hearing impairment / poor vision should be taken into account
—> MMSE: ceiling effect —> easy to do —> not sensitive in mild patients
—> MOCA more difficult —> more sensitive in mild patients
- Neuropsychiatric inventory
—> a questionnaire to grade behavioural and psychological symptoms of dementia
- Blood tests (for reversible causes)
- **TFT
- **Folate, Vit B12
- ***VDRL (neurosyphilis is treatable) - CT brain
- **NPH
- **Chronic subdural haematoma
- Old infarct (suggesting vascular dementia)
- AD: Medial temporal lobe, Hippocampal atrophy
Others:
5. MRI brain
6. EEG (esp. CJD)
7. CSF (if suspect chronic CNS infection)
8. **Functional imaging (FDG-PET, SPECT)
- AD: bilateral hypometabolism over temporal lobes
9. **Pathological imaging (Pittsburgh Compound B (C11-PIB))
- AD: amyloid plaque deposition —> prognostic (high loading —> poor prognosis)
***Dementia subtypes
- Vascular dementia
- History of stroke
- ***Stepwise deterioration - PD dementia
- Long standing history of PD (***>1 year of PD before dementia)
- ~ LB dementia - Lewy body dementia (LB)
- Cognitive impairment + Parkinsonian features all occur within ***1 year - Normal pressure hydrocephalus (NPH)
- Sequence: development of apraxic gait —> urinary incontinence (urge) —> dementia - Alcoholic dementia
- Drinking history - Traumatic brain injury
- History of chronic repetitive head injury (e.g. boxer) - Creutzfeldt-Jakob disease (CJD)
- ***Rapidly progressive dementia (over months / weeks)
- 90% die within 1 year
- No cure
- Very non-specific symptoms: Pyramidal / extrapyramidal symptoms, Visual / cerebellar disturbance, Myoclonus, Akinetic mutism - Neurosyphilis, HIV infection
- Sexual history
- VDRL
Diagnostic criteria for Major Neurocognitive Disorder (Dementia)
- Significant cognitive decline from a previous level of performance in ***>=1 domains (complex attention, executive function, learning and memory, language, perceptual-motor, social cognition) based on informants / cognitive tests
- Interfere with independent living
- Not better explained by other mental disorder (e.g. delirium, depression, schizophrenia)
Treatment of Alzheimer’s disease
- AChE inhibitor (Donepezil, Rivastigmine (oral / patch), Galantamine)
- Mild to moderate AD
- Cholinergic SE: anorexia, N+V, diarrhoea, bradycardia (CI in heart block) - NMDA receptor antagonist (Memantine)
- Moderate to severe AD
- Block excitotoxicity of glutamate on brain
- Mild SE: headache, dizziness, sedation, agitation, constipation
- Gait and Balance disorders
Senile gait:
- Gait with slight stooped, slower speed, reduced tandem ability
- Not consider pathological
Causes of Gait and Balance disorders:
1. Neurological causes
- **Parkinsonism
- **Cerebellar ataxia
- **Stroke (Pseudoparkinsonism)
- **Normal pressure hydrocephalus
- **Cervical myelopathy
- **Peripheral neuropathy (Sensory / Motor) (e.g. ***DM)
- Non-neurological causes
- Reduced vision / hearing
- Arthritis / Pain
- Deconditioning
- Obesity
- Dementia / Cognitive impairment
- **Dizziness from various causes (e.g. postural hypotension, **drug-induced)
- Footwear
Approach to Parkinsonism
Clinical features:
1. Tremor
2. Rigidity
3. Akinesia / Bradykinesia
4. Postural instability
Causes:
1. Idiopathic PD
- Pseudoparkinsonism: Stroke, Vascular etiology
- Extensive subcortical small vessel disease can manifest with ***symmetrical parkinsonism and gait disorder including hyperreflexia + increased tone
- Less response to Levodopa - Drug-induced (e.g. Anti-psychotic drugs esp. 1st gen)
- Extrapyramidal SE from antipsychotics initially started for BPSD - Atypical parkinsonian disorders (e.g. Parkinson plus syndrome)
- Secondary causes of PD
- Repeated head injury
- Encephalitis
***Idiopathic PD
2nd most common neurodegenerative disorder after AD
Possible presentations:
- ***Fall (common)
- Gait and balance problem, postural instability
- Slowness
- Tremor
- Hyposmia, REM sleep behaviour disorder (early features) (REMBD + Parkinsonism —> highly suggestive of IPD)
- Dysphagia (late)
- Dementia / Cognitive impairment (late)
- Other non-motor symptoms
Clinical features:
Motor
Craniofacial:
- Masked face
- Decreased eye blinking
- Speech disturbance
- Dysphagia (late)
- Sialorrhoea
Visual:
- Blurred vision
- Decreased saccadic movement of eyes (Hypometric saccades)
- Impaired vestibuloocular reflex
- Impaired upward gaze, convergence
- Lid apraxia
Musculoskeletal:
- Micrographia
- Dystonia
- Myoclonus
- Stooped posture
- Camptocormia (severe anterior flexion of thoracolumbar spine)
- Pisa syndrome (subacute axial dystonia with lateral flexion of trunk, head, neck)
Gait:
- Shuffling, short-stepped gait
- Freezing
- Festination
Non-motor symptoms:
- Cognitive impairment
- Psychosis
- Mood disorders
- Sleep disorders
- Fatigue
- Autonomic dysfunction (***late vs early in Parkinson plus syndrome) (urinary frequency / urgency, constipation, erectile dysfunction)
- Olfactory dysfunction (e.g. Hyposmia)
- Pain and sensory disturbance
- Seborrhoea
Mechanism of fall:
- Rigidity of lower extremity musculature
- Bradykinesia: Inability to correct sway trajectory due to slowness in initiating movement (esp. during turning) / freezing of gait
- Hypotensive drug effects (e.g. Levodopa, Dopamine agonist —> postural hypotension)
- Cognitive impairment
Diagnosis of IPD
Clinical diagnosis: UK PD Society Brain Bank Clinical Diagnostic Criteria
- Diagnosis of Parkinonian syndrome
- ***Bradykinesia + Rigidity / Resting tremor / Postural instability not caused by visual, vestibular, cerebellar, proprioceptive dysfunction - ***Exclusion criteria for PD
- Repeated stroke
- Repeated head injury
- Encephalitis
- Sustained remission
- Strictly unilateral
- Supranuclear gaze palsy, Cerebellar signs, Early severe autonomic involvement —> Parkinson plus syndrome - ***Supportive prospective positive criteria for PD
- Unilateral onset —> Bilateral later
- Resting tremor present
- Progressive
- Persistent asymmetry
- Excellent response to Levodopa
- Severe Levodopa-induced chorea
- Levodopa response for >=5 years
- Clinical course of >=10 years
Clinical subtypes of PD
- Tremor-predominant PD
- prominent resting tremor
- better response to Levodopa
- slower course of disease
- less neuropsychological impairment - Akinetic-rigid form PD
- postural instability, increased tone, hypokinesia more than tremor
- lesser response to Dopaminergic agents
- rapid course of disease
- more debilitating
However:
- PD progression highly variable among individuals
- Subtypes can change as disease progresses
Treatment of Parkinson’s disease
Pharmacological (for Motor symptoms)
- Very mild S/S of PD with no interference with QoL —> NOT necessarily need medications
- Levodopa
- for older patients with PD symptoms that affect daily life - Dopamine agonist
- avoid in 1st line
- less effective than Levodopa to improve motor function + QoL
- less well tolerated in elderly - Anticholinergic
- avoid in elderly esp. those with dementia
- reserved for younger patient in whom ***tremor is predominant
Treatment of PD dementia
Dementia:
- Symptomatic treatment only, no therapies have shown to modify course of disease / influence prognosis
- Many drugs may worsen cognitive function: Anticholinergics, Dopaminergic drugs for PD motor symptoms
Treatment:
1. AChE inhibitor
2. Memantine
Psychosis:
1. Reduce dose / Stop PD medications (but monitor motor functions)
2. Antipsychotics if inadequate response (e.g. ***Pimavanserin: licensed for PD psychosis)
Principles of Neuro-rehabilitation
WHO new definition of Impairment, Activity, Participation:
- Less negative connotation
- “Disability” changed to “Activity”
- “Handicap” changed to “Participation”
- Places more emphasis on individual’s abilities rather than disabilities
- More emphasis given to social context
- “Medical model” changed to “Social model” of disability
Basic principles of Neuro-rehabilitation:
1. Approaches that reduce disability
2. Approaches designed to acquire new skills + strategies —> adapt to disability + maximise activity
3. Approaches that help to alter the environment, both physical + social, so that a given disability carries with it minimal consequent handicap
Process of rehabilitation:
1. Work with disabled person + family
2. Give accurate information + advice about nature, natural history and prognosis of disability
3. Listen to needs + perceptions of disabled person and family
4. Work with other professional colleagues in a multidisciplinary team
5. Establish realistic rehabilitation goals which are both appropriate to that person’s disability + family, social and employment needs
