Tremor
Red Flags — features requiring urgent investigation or referral
| Red flag | Likely cause | Action |
|---|---|---|
| Acute-onset or very rapid onset tremor (days to weeks) with focal neurology | Structural brain lesion: stroke (thalamic or midbrain), space-occupying lesion, abscess, haemorrhage. Holmes tremor (rubral tremor): low-frequency rest + postural + intention tremor following midbrain lesion. Acute encephalitis. Any tremor with sudden onset and associated neurological deficit requires urgent brain imaging. | Urgent CT or MRI brain; neurological assessment; 999 if stroke suspected (FAST positive) |
| Tremor in patient under 55 years | Wilson's disease: copper accumulation; autosomal recessive; treatable if caught early; untreatable if missed too long. Also: juvenile Parkinson's (rare); drug-induced (any age); dystonic tremor; FXTAS (fragile X tremor/ataxia syndrome — males over 50; also affects younger men with premutation). Wilson's disease missed in young patients with tremor represents a significant diagnostic failure. | Wilson's screen: serum ceruloplasmin; serum copper; 24h urinary copper; slit-lamp exam for KF rings; LFTs; urgent neurology and hepatology |
| Worsening tremor in a patient on lithium | Worsening tremor is one of the earliest signs of lithium toxicity. Lithium therapeutic range 0.6-1.0 mmol/L (maintenance); toxicity at >1.5 mmol/L. Toxicity signs: coarse tremor; nausea/vomiting; diarrhoea; ataxia; confusion; seizures; coma. Precipitants: dehydration (vomiting, diarrhoea); NSAIDs (reduce lithium excretion); ACE inhibitors; thiazide diuretics; new low-sodium diet. | URGENT lithium level; renal function; ECG; withhold lithium; IV rehydration; nephrology if level >2.0 mmol/L (consider dialysis) |
| Tremor with early falls, vertical gaze palsy, or prominent autonomic failure | Atypical parkinsonism: Progressive Supranuclear Palsy (PSP) — early falls (backwards), vertical gaze palsy, square wave jerks, axial rigidity; Multiple System Atrophy (MSA) — cerebellar signs + parkinsonism + prominent autonomic failure; Corticobasal Degeneration (CBD) — alien limb phenomenon, asymmetric rigidity, apraxia. These conditions are clinically distinct from idiopathic PD and respond poorly or not at all to levodopa. | Urgent neurology referral; MRI brain; these conditions require specialist diagnosis; do not start levodopa without specialist confirmation |
| Tremor with psychiatric symptoms, liver disease, or Kayser-Fleischer rings (young patient) | Wilson's disease: neuropsychiatric symptoms (behavioural change, psychosis, mood disorder) + liver disease (hepatitis, cirrhosis) + movement disorder. KF rings: golden-brown deposits at corneal periphery (Descemet membrane); visible on slit-lamp; present in 95% of neurological Wilson's. If seen by GP on naked eye examination (rare to see without slit-lamp) → urgent ophthalmology + hepatology + neurology. | Urgent hepatology + neurology + genetics; Wilson's screen; treatable — outcome depends on early treatment |
| Parkinson's features NOT responding to levodopa trial | Atypical parkinsonism (MSA, PSP, CBD, DLB) typically does not respond meaningfully to levodopa, or the response is brief and minimal. If a patient on levodopa shows no improvement after 12 weeks at adequate dose, or has features suggesting atypical parkinsonism (early falls, cerebellar signs, prominent autonomic dysfunction, early dementia): re-refer to movement disorder specialist for diagnostic review. | Re-refer to movement disorder neurologist; MRI brain (characteristic atrophy patterns in MSA and PSP); DAT-SPECT; reconsider diagnosis |
Safeguarding Considerations — Parkinson's Disease and Advanced Tremor
🚗 Driving Safety
- Parkinson's disease: must notify DVLA; Group 2 (HGV/PSV) refused on diagnosis; Group 1 (car): continue if safe with annual medical review; driving cessation when symptoms impair safe driving
- Essential tremor: if tremor affects driving ability, patient must stop and notify DVLA; assess at each review
- GP legal duty: document driving advice given; if patient with unsafe tremor refuses DVLA notification and continues driving, GP may need to notify DVLA
- Dopamine agonists: somnolence and sudden sleep attacks (especially in car); warn patients to stop driving if episodes occur
💊 Impulse Control Disorders (Dopamine Agonists)
- Dopamine agonists (pramipexole, ropinirole, rotigotine): impulse control disorders in up to 17% — pathological gambling, hypersexuality, compulsive eating, compulsive buying
- Warn PATIENT AND CARER before prescribing; carer often notices before patient admits
- Document counselling at every dopamine agonist prescription review
- ICD may constitute a safeguarding concern if significant financial harm or relationship damage
- Stop or reduce dopamine agonist if ICD develops; switch to alternative PD medication
🏠 Carer Burden in Progressive Disease
- Progressive neurological conditions (PD) impose enormous carer burden; carers are at high risk of depression, anxiety, and burnout
- Carer wellbeing screen at every PD review: PHQ-9 for carer; carer's assessment (social services); respite services
- Parkinson's UK: carer support resources; helpline 0808 800 0303
- Power of attorney: discuss early (lasting power of attorney for health and welfare; property and financial affairs) while patient has capacity
🧠 Cognitive Impairment in PD
- Parkinson's dementia develops in up to 80% of PD patients by 20 years; mild cognitive impairment common earlier
- Medication complexity in PD: multiple medications with narrow therapeutic windows; dose timing critical (never withhold levodopa in hospital — causes acute immobility and aspiration risk); cognitive impairment worsens adherence
- Capacity assessment: if cognitive decline → lasting power of attorney; advance care planning; DNACPR discussion while capacity present
- Wandering risk (Parkinson's dementia): alert relatives; GPS tracker; falls risk assessment
🧠 Fear of Parkinson's
Parkinson's disease carries a powerful cultural fear — loss of control, progressive deterioration, loss of independence. Margaret's anxiety about this diagnosis is real and significant. The most therapeutic element of this consultation may be explaining, after examination, that the features are NOT those of Parkinson's — and why. The clinical examination is not just diagnostic; it is therapeutic when the findings are used to directly address the patient's central fear.
"I want to explain why I am examining the way I am. There are very specific features I am looking for to tell the difference between essential tremor and Parkinson's. You can watch me check for them, and I'll tell you what I find."👫 Derek's Role
Derek is present and has already contributed key clinical information — he has confirmed that Margaret does not shake in the armchair at rest. His observations about sleep (REM behaviour disorder), driving, and functional change are clinically essential. His wellbeing — as a potential carer, as a worried partner — also matters. If PD is confirmed, Derek will become central to the care plan. Acknowledging him explicitly as a clinical partner respects both him and Margaret.
"Derek — you've already been really helpful. I want to ask you a few things too: have you noticed any changes in her sleep? Does she ever kick or shout in her sleep? And has the shaking been getting worse, do you think?"🍷 Alcohol Response — a delicate conversation
Margaret's tremor improves with wine. This is diagnostically useful (ET characteristic) but also requires a sensitive conversation: the GP should not imply that alcohol as a coping strategy for tremor is appropriate (MOH-equivalent risk exists; alcohol dependence risk). The message: "the alcohol response helps us understand what type of tremor this is — but we shouldn't be using alcohol as treatment; there are much better options." This distinguishes diagnostic utility from therapeutic endorsement.
"The fact that the wine helps is actually very useful information — it tells me something specific about the type of tremor this is. But I don't want you to feel you need to drink more to manage it; I can give you a much more reliable option than that."🚗 Driving Identity
For many patients in Margaret's generation, driving represents independence, autonomy, and identity. The DVLA discussion must be handled with care — it is a legal discussion but it is also a conversation about vulnerability. The approach: "I need to talk to you about driving, not to take it away from you, but because there are rules I need to make sure you know about." If the tremor is not affecting driving: advise her to self-monitor and notify if it does. If affecting driving: DVLA notification is required and should be supported, not avoided.
"I want to ask about driving. For now, if the tremor isn't affecting your ability to drive safely, you don't need to stop. But if you ever feel it is affecting your control of the car, you'd need to let the DVLA know. And I need to document that I've told you this."- Not asking rest vs action — the single most diagnostically important question in tremor
- Not reviewing medications (especially metoclopramide/prochlorperazine) — most common preventable cause of tremor in GP
- Reassuring "probably not Parkinson's" without examination — premature; examination is required before this statement can be made
- Not addressing the DVLA question in a patient who drives
Same Day / 999
Act before completing history- Acute-onset tremor + focal neurology (FAST positive)Stroke or TIA; 999; brain imaging urgently; do not delay
- Lithium toxicity — worsening tremor + confusion/ataxiaUrgent lithium level + renal function; withhold lithium; IV hydration; nephrology if level >2.0
- Wilson's disease features (under 55)Urgent hepatology + neurology + genetics; treatable — time-critical
- Tremor + severe autonomic failure (orthostatic collapse)Same-day assessment; MSA consideration; IV fluids
Neurology / Movement Disorder Clinic
Before any dopaminergic treatment- Suspected Parkinson's disease — NICE NG71Refer to movement disorder specialist or geriatrician with PD expertise BEFORE starting any dopaminergic treatment; GP does not diagnose or treat PD
- Atypical parkinsonism features (early falls, cerebellar signs, rapid progression)Urgent neurology; MRI brain; DaTscan; do not start levodopa empirically
- Drug-induced parkinsonism not resolving 4 months after drug cessationNeurology referral; DaTscan to distinguish from idiopathic PD (normal DaTscan = drug-induced)
Primary Care
Most tremor in GP- Essential tremor — MargaretTFTs; medication review; propranolol if functionally significant; occupational therapy; DVLA discussion; review 6-8 weeks
- Drug-induced (metoclopramide/prochlorperazine)Stop the drug; review in 3-4 months; refer if persists
- Enhanced physiological tremor (anxiety, caffeine, thyroid)Treat the cause; TFTs; lifestyle; propranolol if needed
- Starting levodopa empirically in suspected PD without specialist referral — this directly contradicts NICE NG71 and is a serious clinical error
- Not testing bradykinesia — this is the mandatory Parkinson's examination; without it, the GP cannot say "no Parkinson's" with clinical authority
- Not explaining the examination findings to the patient — a missed opportunity to directly address the Parkinson's fear with evidence
- Ordering DaTscan from GP — this is a specialist investigation; not appropriate to order in primary care
- Not ordering TFTs — mandatory in all new tremor presentations
"Based on the examination — and I want to explain what I found — this looks very much like a condition called essential tremor, not Parkinson's disease. Essential tremor is the most common type of tremor; it affects about 1 in 20 people over 65. The key thing I checked was whether your movements were slowing down — because that slowing of movements is the most important feature of Parkinson's. I also checked whether there was a tremor when your hand was just resting in your lap. Neither of those was present. The tremor you have appears when your hand is in action — holding something, reaching — and that pattern, along with your family history and the improvement with wine, is characteristic of essential tremor rather than Parkinson's. Essential tremor is not Parkinson's disease. It does not lead to Parkinson's disease. It is a separate, distinct neurological condition. It tends to progress slowly over years, and most people manage it well — with medication if needed, and with adjustments to daily activities."
"How do you know it's not Parkinson's?"
"The most important feature of Parkinson's — more important than the tremor itself — is a slowing of movements. I tested for this specifically by asking you to do those alternating movements with your hands. Your movements were smooth, not slowed, and didn't get smaller and smaller with repetition. That is the key finding that makes Parkinson's unlikely. Parkinson's also causes a tremor specifically at rest — when the hand is just lying there doing nothing. Yours happens when you're using your hand, which is the opposite pattern. These are the two most discriminating examinations, and both were reassuring."
"Could it turn into Parkinson's later?"
"Essential tremor is a separate condition from Parkinson's. Having essential tremor does not mean you will develop Parkinson's. The lifetime risk of Parkinson's is not significantly higher in people with essential tremor. What essential tremor does is gradually — usually very slowly — progress over years. Some people find it barely changes over a decade; others find it gradually becomes more noticeable. It is very manageable."
Idiopathic PD
REST tremor (pill-rolling, 4-6 Hz, suppressed with use); BRADYKINESIA (mandatory); RIGIDITY (lead-pipe or cogwheel); asymmetric onset; anosmia; REM sleep disorder. Refer before treatment.
Drug-induced parkinsonism
Symmetrical parkinsonism; metoclopramide/prochlorperazine; stop drug; review 3-4 months; DaTscan normal. Most common and most missed differential.
Cerebellar tremor
INTENTION (worsens at target); dysdiadochokinesia; ataxia; nystagmus. MRI brain urgently — MS; alcohol; SOL.
Wilson's disease (<55)
Wing-beating tremor; psychiatric symptoms; liver disease; KF rings. Treatable — do not miss.
Atypical parkinsonism
PSP (early falls, vertical gaze palsy); MSA (autonomic + cerebellar); CBD (alien limb). Levodopa-resistant.
- Telling patient "it's not Parkinson's" without explaining the clinical basis — generic reassurance; does not address the fear; does not demonstrate clinical reasoning
- Starting propranolol before checking for asthma — propranolol is absolutely contraindicated in asthma; must ask before prescribing
Name the fear and address it with examination evidence
Margaret's central concern is Parkinson's disease. The GP who says "don't worry, it's probably not Parkinson's" without examination has provided comfort without clinical authority. The GP who says "I specifically tested for the features of Parkinson's and here is what I found — and what I did not find" provides therapeutic reassurance grounded in clinical reasoning.
"I want to address what I know has been worrying you. I checked specifically for the features that distinguish Parkinson's from essential tremor. The slowing of movements that is the hallmark of Parkinson's was not present. The rest tremor was not present. Those are the two things that matter most — and both were reassuring."Explain essential tremor as a manageable condition
Essential tremor can feel like a frightening diagnosis if the patient does not understand that it is NOT Parkinson's, does NOT progress to Parkinson's, and is highly manageable with medication and lifestyle adjustments. The prognosis conversation for ET should be honest (slowly progressive) and hopeful (very manageable; most patients find propranolol significantly helpful).
"Essential tremor is a separate condition from Parkinson's. It doesn't become Parkinson's. It tends to progress slowly — for most people, very slowly. The medication I am going to suggest — propranolol — works well for most people with essential tremor. Many people notice a significant improvement."Involve Derek — and address the alcohol conversation
Derek has been a key witness and deserves to be part of the outcome of this consultation. Also: Margaret's wine habit — which she mentioned improves the tremor — deserves a gentle, non-judgmental conversation. The goal: validate the observation (diagnostically useful); affirm that alcohol is not the right treatment (propranolol is more reliable and safer); avoid creating the impression that alcohol consumption is being encouraged.
"Derek — I wanted to tell you both the findings together. And on the wine: the improvement Margaret notices is genuinely useful information — it tells us something about the tremor mechanism. But I would recommend propranolol rather than relying on the wine; it works better and is much more reliable without the other effects of alcohol."Caffeine is a central nervous system stimulant that enhances physiological tremor and can exacerbate ET by increasing sympathetic nervous system activation. Strong coffee, tea, energy drinks, and cola are all significant sources. Many patients are unaware of the tremor-caffeine link. Reducing caffeine intake is simple, free, and effective for a subset of tremor patients. Gradual reduction (not abrupt cessation — caffeine withdrawal headache) over 1-2 weeks.
Switch to decaffeinated versions; reduce by 1 cup per day per week; note any improvement in diary. Caffeine reduction alone rarely resolves ET but can reduce background amplitude and improve response to medication.
Fatigue and psychological stress significantly worsen ET amplitude. Sleep deprivation increases sympathetic tone, lowers tremor threshold, and directly exacerbates any tremor type. Stressful social situations (eating at a restaurant; holding a teacup at a formal event) often trigger the most distressing episodes. Anticipatory anxiety about tremor creates a self-fulfilling cycle: worry about shaking → increased sympathetic activation → worse shaking → more anxiety.
Consistent sleep-wake times; relaxation techniques (mindfulness; progressive muscle relaxation); CBT if anxiety around tremor is prominent; beta-blocker (propranolol) also treats the somatic anxiety component. Addressing the cognitive component of "people are staring at my hands" with CBT or psychoeducation.
OT referral: essential for patients with functionally significant ET. Weighted utensils (cutlery, cups with lids) reduce tremor visible displacement by providing kinetic damping. Two-handed technique for cups. Writing aids (pen weights, guide frames). Ergonomic computer mouse (reduces fine motor requirement). Voice-to-text software for work or correspondence. Wide-grip pen or pencil for writing. These strategies are highly effective and should be offered before or alongside medication.
Acknowledging the tremor to family and close friends reduces the anxiety of concealment; most people are far more understanding than ET patients fear. Focusing on the task (look at the cup, not the hand) reduces attentional tremor amplification.
Alcohol improves ET in approximately 60% of patients — this is diagnostically useful and genuine. However: alcohol is not a treatment strategy because the effective dose approaches intoxication; rebound tremor worsens after the alcohol metabolises; and tolerance develops with regular use, requiring increasing amounts for the same effect. Some ET patients do develop alcohol use disorder partly driven by the symptom relief. The propranolol conversation must offer something more reliable and safer.
If the patient is already using alcohol to manage tremor: acknowledge this without judgment; offer propranolol as a more reliable and safer alternative; AUDIT score if alcohol use is significant; brief intervention if needed.
Essential tremor: DVLA notification required if tremor affects the ability to drive safely. If tremor is not currently affecting driving: no notification required, but patient should self-monitor and report to DVLA if it does. PD diagnosis: must notify DVLA. Group 2 (HGV/PSV): refused on PD diagnosis. GP must ask about driving at every tremor review and document the advice given. If in doubt about safety to drive: DVLA medical form completed; patient may choose an independent DVLA assessment (driving centre test).
Propranolol: does not impair driving ability at standard doses; some patients experience mild fatigue initially. Primidone: sedating (especially at initiation) — advise not to drive until stable dose established and no sedation.
Deep brain stimulation (VIM — ventral intermediate nucleus of the thalamus) is highly effective for severe, medically refractory essential tremor (failed adequate trials of propranolol + primidone). Focused ultrasound thalamotomy (FUS): NICE-approved non-invasive alternative to DBS for unilateral essential tremor; performed under MRI guidance; immediate tremor reduction; available at specialist centres. GP role: refer to neurology after two failed medication trials in patients with significant functional impairment from ET.
DBS also highly effective for advanced PD with motor fluctuations and dyskinesias; bilateral STN (subthalamic nucleus) stimulation; patient selection and programming by movement disorder specialist; GP role in ongoing monitoring and medication management.
- Before prescribing: ask about asthma and COPD — ABSOLUTELY CONTRAINDICATED
- Start 40mg BD; titrate every 2 weeks to 80-120mg BD (maximum 320mg/day); modified-release (propranolol LA 80mg) available for once-daily dosing — better for compliance
- Mechanism: beta-1 and beta-2 adrenoceptor blockade reduces physiological and essential tremor amplitude; peripheral (not central) effect for ET
- Response: 40-70% of patients achieve clinically meaningful improvement; assess at 6-8 weeks at therapeutic dose; titrate to maximum tolerated if partial response
- Do not stop abruptly (rebound hypertension; cardiac risk if IHD); taper over 2 weeks if stopping
- Start at very low dose: 12.5mg nocte initially (quarter of a 50mg tablet) — idiosyncratic first-dose acute sickness reaction in up to 25% if started higher
- Titrate slowly: 12.5mg, then 25mg, 50mg, 125mg, 250mg nocte — over several weeks; target 250-500mg/day in divided doses
- Mechanism: metabolised to phenobarbitone and phenylethylmalonamide; GABA enhancement; works independently of beta-adrenergic pathway — useful if propranolol fails or is contraindicated
- Side effects: sedation (common, especially at initiation — counsel on driving); nausea; ataxia; cognitive effects at higher doses
- Can be combined with propranolol if partial response to either alone (additive effect through different mechanisms)
- Levodopa/carbidopa (Sinemet/Madopar): most effective PD treatment; specialist initiates; GP continues; NEVER withhold in hospital (causes acute immobility, rigidity, aspiration risk, and hyperpyrexia); motor fluctuations and dyskinesias develop after years (wearing-off, on-off, peak-dose dyskinesias)
- Dopamine agonists (pramipexole, ropinirole, rotigotine patch): specialist initiates; preferred in younger patients (delay levodopa-related dyskinesias); IMPULSE CONTROL DISORDER warning mandatory at every review
- MAO-B inhibitors (rasagiline, selegiline): modest benefit; specialist initiates; selegiline: amphetamine metabolites
- GP ongoing role: medication timing (strict); monitor motor fluctuations; manage non-motor symptoms (autonomic, mood, cognition); falls prevention; carer support
- STOP metoclopramide, prochlorperazine, or other dopamine-blocking drug — this is the primary intervention; no anti-parkinsonian drug needed
- Review alternative: metoclopramide → domperidone (much lower CNS penetration; lower parkinsonism risk) or ondansetron; prochlorperazine → betahistine (for Meniere's) or antihistamine (promethazine)
- Timeline: tremor and parkinsonism typically begin to improve within weeks of drug cessation; full resolution may take 3-4 months (dopamine receptor resensitisation takes time)
- If NOT resolved at 4 months: DaTscan (specialist); persistent drug-induced parkinsonism vs co-existing idiopathic PD unmasked by the drug — these are different clinical entities; DaTscan differentiates
- If drug cannot be stopped (essential antipsychotic): liaise with psychiatrist; switch to quetiapine (least D2 affinity) or clozapine (specialist)
- Autonomic dysfunction: orthostatic hypotension (fludrocortisone; midodrine; review antihypertensives — reduce if BP-lowering causing falls); urinary urgency (oxybutynin — caution cognitive side effects; mirabegron); constipation (macrogol; high-fibre diet)
- Mood: depression common (SSRIs — sertraline preferred in PD; avoid tricyclics — anticholinergic cognitive effects; falls risk); anxiety (SSRI; CBT); avoid antidopaminergics for nausea (use domperidone)
- Cognitive impairment: mild cognitive impairment common; dementia in 80% by 20 years; rivastigmine (acetylcholinesterase inhibitor) — modest benefit for Parkinson's dementia; memantine (limited evidence); refer memory clinic
- Falls prevention: physiotherapy (gait training; balance); occupational therapy (home hazard assessment); hip protectors; medication review (sedating drugs; postural hypotension)
- Sleep: REM sleep behaviour disorder (clonazepam or melatonin); insomnia; excessive daytime somnolence (from dopamine agonists — reduce dose)
Select tremor scenario — personalised treatment recommendation
"This tablet works on the mechanism that makes the tremor worse — the adrenaline-type pathway. Most people with essential tremor notice an improvement, usually within the first few weeks. The most common side effect is feeling slightly tired or having cold hands initially — this often settles. Please don't stop it suddenly — come and see me first if you want to stop and we'll taper it gradually. And one important thing: if you have any problems with your breathing, chest tightness or wheeze, stop and contact us."
Propranolol: ABSOLUTELY CONTRAINDICATED in asthma/COPD — ask specifically before prescribing. ET first-line; also lithium tremor add-on. Takes 6-8 weeks for full assessment. Do not stop abruptly. Situational ET: 40mg single dose 45 min before event. Cerebellar tremor: does NOT respond to propranolol. Drug-induced parkinsonism: propranolol NOT indicated — stop the causative drug instead.
"I'm starting you on a very small dose — much smaller than the standard dose — because this particular tablet can cause a strong reaction if you start at full dose: nausea, dizziness, and feeling very unsteady. Starting at the tiny dose avoids this completely. Take it at bedtime. Please don't drive the first few times you take it until you know how it affects your sleep and the next morning. I'll increase it very gradually over the coming weeks."
Primidone: ET second-line. Critical dosing: start at 12.5mg (quarter tablet) — acute first-dose sickness reaction at higher initiation doses (25% of patients); starts as 12.5mg regardless. Titrate slowly over weeks. Enzyme inducer: check warfarin, OCP, anticonvulsant interactions. Sedation: no driving until stable. Teratogenic: pregnancy counselling. FBC + folate on long-term treatment.
"I want to give you a card to carry in your wallet. If you are ever admitted to hospital, show this card immediately. It tells the hospital that your Parkinson's medication must be given at exactly the times written on it — not at the general medication round. If doses are missed or delayed, your symptoms can worsen very quickly and very severely. Please make sure the hospital sees this card and that your family knows to advocate for you on this."
Levodopa: SPECIALIST INITIATES — never start in GP surgery. NEVER withhold in hospital — document on patient's hospital admission card. Timing is critical — patient-specific schedule; not hospital round times. Nausea: use domperidone (NOT metoclopramide — causes parkinsonism). Motor fluctuations develop after years — specialist manages. Impulse control disorders: more common with dopamine agonists but possible with levodopa too. GP role: continue prescription, manage non-motor symptoms, falls prevention, DVLA, carer support.
"Before you start this medication, I need to tell you about an important potential side effect. Some people taking this type of medicine develop compulsive behaviours — things like excessive gambling, changes in sexual behaviour, compulsive eating, or compulsive shopping. This doesn't happen to most people, but I need you — and your family — to be aware of it. If you or anyone close to you notices any changes in behaviour that feel compulsive or out of character, please tell us immediately. It's important that your family knows about this too."
Dopamine agonists: ICD warning is the most important safety counselling in PD prescribing. Must warn PATIENT AND CARER before prescribing. Screen at EVERY review — document. Sudden sleep attacks: stop driving if episodes occur; DVLA. ICD confirmed: reduce/stop dopamine agonist; switch to levodopa; specialist. Specialist initiates — GP continues and monitors. Preferred in younger PD patients to delay levodopa-related dyskinesias.
"The shaking and the slowness you have noticed — the most likely cause is the metoclopramide tablet you have been taking. That type of tablet can block the dopamine pathways in the brain, which is exactly what causes Parkinson's symptoms. The good news is that it is usually reversible: once we stop the tablet, the symptoms should gradually improve over the next few months. I do not want to give you a Parkinson's medication — because if the metoclopramide is the cause, those medications would not be appropriate and could cause side effects. I want to check you again in 3-4 months."
Drug-induced parkinsonism: STOP THE DRUG — do NOT start levodopa or dopamine agonist. Most common cause: metoclopramide; prochlorperazine/Stemetil; all antipsychotics. Resolution in 3-4 months if drug-induced. If persists: DaTscan (specialist); may be co-existing idiopathic PD unmasked by the drug. DaTscan: normal = drug-induced; abnormal = co-existing PD. Alternative for nausea: ondansetron (not metoclopramide). Alternative for dizziness: betahistine (not prochlorperazine).
"This tablet helps with the tremor by working on a different pathway in the brain. The main thing to watch for is whether it affects your memory or your thinking — if you notice that your concentration or memory is getting worse, that can be a side effect and we'd need to reduce it. Also: dry mouth and some constipation are common. Please don't stop it suddenly — come to see me first."
Trihexyphenidyl: AVOID over 70 (delirium, cognitive impairment, falls). Use only in tremor-predominant PD in younger patients (<70). Specialist initiates. Never for drug-induced parkinsonism. Significant anticholinergic burden: accumulates with other anticholinergic drugs. Cognitive monitoring at every review. Gradual withdrawal — do not stop abruptly. Alternative for tremor when trihexyphenidyl not appropriate: optimise levodopa; add MAO-B inhibitor; specialist review for DBS consideration.
Occupational Identity (Retirement)
Margaret is a retired teacher who derived significant identity from her professional role. Retirement, combined with a visible tremor, can compound feelings of diminished capability. The social situations most distressing for ET patients often mirror professional contexts: holding a teacup at a meeting; writing legibly; dining at a restaurant. OT strategies and propranolol allow re-engagement with these situations.
"The medication I am going to try — propranolol — has a very practical effect. Many people with essential tremor find they can do things again that the tremor was making difficult. The dinner table is typically one of the most distressing places — because you're aware of people watching. For a lot of people on propranolol, that problem largely resolves."Carer Relationship in PD
If PD is confirmed, Derek's role will shift from partner to carer over time. The implications — emotional, financial, physical — are significant for both. Carer assessment; lasting power of attorney discussion; advance care planning; Parkinson's UK support for carers. In the current consultation with Margaret (ET, not PD): Derek remains a clinical witness and supportive partner. Acknowledge his contribution and include him in the outcome communication.
"Derek — I want to tell you both together. The examination is reassuring: this is consistent with essential tremor, not Parkinson's. I know you have both been worried about that. The plan from here is..."Cognitive Anxiety in Parkinson's
Parkinson's disease carries a well-founded fear of dementia — and rightly so (80% of PD patients develop Parkinson's dementia by 20 years). Cognitive screening (MMSE/MoCA) at every PD review; early discussion of lasting power of attorney while capacity is present; advance care planning; memory clinic referral if mild cognitive impairment confirmed. For ET patients: no increased dementia risk — reassurance appropriate.
"Essential tremor does not increase the risk of dementia. That is one of the important differences from Parkinson's — essential tremor is a movement condition, not a progressive neurological degenerative disease in the same sense. Your thinking and memory are not at increased risk from this condition."Independence and Driving
Driving represents independence, particularly for the over-70s. The DVLA discussion — especially in a progressive condition like PD — can feel like a threat to autonomy. The approach: frame it as transparency and support, not removal. The GP's role is to inform, advise, and document — not to decide unilaterally to stop someone driving. The DVLA assessment process provides both medical evidence and due process for patients who contest a driving restriction.
"I need to ask about driving — not to take it away, but because there are rules I need to make sure you know. For the moment, if the tremor isn't affecting your driving, there is no immediate action needed. What I do need to document is that I've talked to you about this. If it ever does start to affect your control of the car, you'd need to let the DVLA know."Today — Examination + TFTs + Management Plan
Examination: rest tremor absent; bradykinesia absent; rigidity absent; action tremor bilateral — confirms ET pattern clinically. TFTs: requested today. Medication review: no dopamine-blocking drugs identified. Propranolol 40mg BD prescribed (asthma excluded first). DVLA advice: documented. ET diagnosis explained with clinical basis — Parkinson's fear addressed. OT referral discussed. Headache diary not relevant — tremor diary recommended instead. 6-8 week review.
6–8 Weeks — Propranolol Response
Tremor diary review: frequency and severity improvement? Functional assessment: still unable to hold teacup/write? BP and HR on propranolol. TFT result: confirmed normal (expected). Titrate propranolol if partial response: increase to 80mg BD. DVLA: still driving safely? If inadequate response at 160mg BD: consider adding primidone; neurology referral if diagnosis uncertain or two agents failed.
Annual Review — ET and PD Monitoring
ET: tremor diary; functional impact; medication dose; driving; side effects; DVLA status. If PD (separate pathway): UPDRS/functional review; motor fluctuations; non-motor symptoms (PHQ-9; cognitive screen MoCA; autonomic); DVLA Group 1 annual review; carer wellbeing; falls; medication timing; bone density. If drug-induced parkinsonism at 3-4 months: reassess resolution; DaTscan if persisting.
If Two Medication Trials Fail — Neurology
If both propranolol (adequate dose and duration) and primidone (adequate dose and duration) have failed in ET: neurology referral. Neurologist may offer: DaTscan (if diagnostic uncertainty); alternative medications (gabapentin, topiramate, clonazepam); consideration of deep brain stimulation (VIM) or MR-guided focused ultrasound thalamotomy (FUS) for severe refractory ET. FUS: NICE-approved; non-invasive; unilateral; immediate tremor reduction; available at specialist centres.
Tremor monitoring essentials
Essential tremor: tremor diary (frequency; severity; functional impact); propranolol dose (titrate to response; HR and BP); primidone (FBC and folate long-term; no driving until stable); DVLA annually if any driving concern. Parkinson's disease (GP continued prescribing): motor fluctuations diary; medication timing adherence; non-motor symptoms (PHQ-9; MoCA; autonomic); falls risk; DVLA annual review Group 1; Group 2 refused; levodopa — never withhold in hospital (patient letter and medical alert card). Dopamine agonists: ICD screen at EVERY prescription review — "any changes in gambling, sexual behaviour, eating habits, compulsive activities?"; document result; sudden sleep attacks (DVLA; driving cessation). Drug-induced parkinsonism: review at 3-4 months post drug cessation; if persisting: neurology + DaTscan. Lithium tremor: annual lithium level; renal function; electrolytes; thyroid; FBC; worsening tremor = urgent level. Benzhexol (if prescribed): MMSE/MoCA every 6 months; anticholinergic burden calculation; urinary symptoms; intraocular pressure.
⚠ Three essential safety-net conversations in tremor management
Documentation requirements at every tremor consultation
- Not testing bradykinesia — cannot say "not Parkinson's" without this examination; the mandatory criterion for PD
- Prescribing propranolol without asking about asthma — absolutely contraindicated in asthma/COPD
- Starting levodopa without specialist referral — directly contradicts NICE NG71; serious clinical error
- Not documenting DVLA discussion in a patient who drives
- Not reviewing medications (metoclopramide/prochlorperazine) — most common preventable cause of tremor
- Rest vs action distinction made; documentation
- Bradykinesia tested and result stated to patient
- Medication review (metoclopramide, prochlorperazine)
- TFTs ordered; Wilson's screen if under 55
- ET diagnosed with examination evidence; Parkinson's addressed with clinical reasoning
- Propranolol: asthma excluded; started; 6-8 week review
- NICE NG71: no levodopa without specialist confirmation
- DVLA documented
- Parkinson's fear addressed with examination evidence (not generic reassurance)
- ICE all three; Derek involved as clinical partner
- Alcohol response acknowledged diplomatically (diagnostically useful; not treatment)
- Propranolol offered as superior alternative to alcohol
- Closing question to both Margaret and Derek
Who you are
Margaret Cooper, 72, retired secondary school English teacher. Married to Derek, 74, a retired engineer who attends with you. You are otherwise well and active. You first noticed the shakiness about 2 years ago when holding a teacup — Derek mentioned it. It is bilateral, both hands, worse when you are doing something (reaching, holding, writing) and completely absent when you are just sitting in the armchair doing nothing. Derek has confirmed this several times. Your mother had exactly the same shaking from her 60s onwards and managed well into old age. You find that a glass of wine in the evening — usually 1-2 glasses — definitely improves it noticeably. You are on amlodipine 5mg for hypertension and atorvastatin 20mg. No respiratory problems, no asthma. You drive — the tremor has not affected your driving. You are worried this is the beginning of Parkinson's disease.
Hidden details (reveal only if asked)
Anosmia (PD non-motor screen): if asked "any change in your sense of smell?" — "now that you mention it, I have noticed food doesn't smell quite the same as it used to. I hadn't thought much of it." This is a deliberate detail to reward thorough non-motor screening, but the overall clinical picture still points to ET (absent rest tremor, no bradykinesia, family history, alcohol-responsive).
Sleep (REM sleep behaviour disorder): if Derek is asked — "she does occasionally call out in her sleep. I thought she was just dreaming." This is a mild/non-specific finding — reward for asking the question but not diagnostic for PD in context.
Driving detail: if asked specifically — "I do still drive. The shaking is there when I'm holding the wheel but it hasn't made me feel unsafe. Should I have told someone?" — responds well to a clear, non-threatening DVLA explanation.
Examination findings (for role-play)
- Observation at rest: NO tremor when hands resting in lap (Derek confirms)
- Bradykinesia: ABSENT — alternating hand movements smooth, no decrement, no amplitude reduction
- Rigidity: ABSENT — passive wrist rotation normal
- Action tremor: PRESENT bilaterally when holding arms outstretched or reaching; 6-8 Hz; bilateral; no intention worsening on finger-nose test
- Gait: normal; no arm swing loss; no festination
- Cognitive state: entirely normal; conversational; no word-finding difficulty
Reactions at key moments
- When bradykinesia is tested and explained: "So what does it mean that the movements didn't slow down?" — responds very well to the specific explanation; "So that's how you know it's not Parkinson's?" — "Exactly — that is the key finding."
- On the ET diagnosis: Initially relieved but wants confirmation: "Are you certain? My neighbour had similar shaking and it turned out to be Parkinson's." — responds well to: "Essential tremor and Parkinson's tremor are different conditions and they can look similar, but the examination tells them apart. Your examination is not consistent with Parkinson's."
- On alcohol: "I wasn't sure whether I should mention the wine — I didn't want you to think I was drinking too much." — responds very well to the diplomatic framing that it is diagnostically useful but propranolol is the better treatment.
- Derek's contribution: Derek is keen to be helpful. If the GP addresses him: "She really doesn't shake when she's just sitting — it's only when she's doing something. And the wine definitely helps — I've noticed that too." Derek should be acknowledged and involved in the closing summary.
- Challenge line: "How do you know it's not Parkinson's? My neighbour had something similar and it turned out to be Parkinson's." — requires clinical evidence from the examination (no bradykinesia; no rest tremor), not just reassurance.
Resolution: Margaret and Derek accept the consultation as satisfactory if: (1) the GP tested bradykinesia and explained the finding; (2) the rest tremor was specifically assessed and found absent; (3) the ET diagnosis was given with the clinical reasoning — not just "it's probably not Parkinson's"; (4) ET is explained as distinct from and not leading to PD; (5) propranolol offered (asthma checked first); (6) TFTs arranged; (7) DVLA advice given; (8) both Margaret and Derek included in the closing summary; (9) the alcohol response acknowledged without judgment. Margaret disengages if the Parkinson's fear is dismissed generically without examination evidence; if propranolol is prescribed without checking for asthma; or if Derek is ignored.
- Acute-onset + focal neurology → 999 stroke pathway
- Lithium toxicity (worsening tremor + confusion) → urgent level; withhold lithium
- Wilson's disease features (under 55) → urgent hepatology/neurology
- Suspected PD → refer BEFORE treatment (NICE NG71)
- Metoclopramide/prochlorperazine identified → STOP the drug
- Review in 3-4 months → DaTscan if not resolved
- DO NOT start levodopa; receptor blockade not degeneration
- Essential tremor: TFTs; propranolol (asthma excluded); OT; DVLA
- Enhanced physiological: treat cause (thyroid; caffeine; drug)
- Review 6-8 weeks; refer if two agents fail