The Neurology Block

Cases 64–69 · 8,642 words · Download this chapter as PDF

This block covers the neurological teaching of both internal medicine courses. The first course supplies cases 64 and 66; the second course supplies cases 67 and 69.

The localisation lecture is served by the system opener, which sets out the upper versus lower motor neurone distinction and the site-by-site table. Coma is Seminar 10 and dementia is a Part Two case; both are second-course seminars.

System Opener · The Neurological History and Examination

The history — tempo tells you the pathology

• Make the patient describe the symptom rather than name it. "Dizzy" may mean vertigo, presyncope, unsteadiness or anxiety, and these have entirely different differentials. "Numb" may mean loss of sensation or weakness. Ask what they actually felt and what they could not do.

• Obtain a witness account for any episode involving altered consciousness. Without it, blackouts cannot reliably be diagnosed — and the witness is frequently in the corridor and never asked.

• Record handedness, functional impact, occupation, and driving, which has legal consequences in stroke and epilepsy.

The examination — localise before you diagnose

First: upper or lower motor neurone?

A caution: in the first hours to days of an acute upper motor neurone lesion — an acute stroke, or spinal shock after cord injury — the limb may be flaccid with absent reflexes. The upper motor neurone signs develop later. Do not localise on tone alone in the acute setting.

Then: where along the neuraxis?

The sequence

• Higher function and speech — orientation, attention, and whether the problem is dysphasia (a language disorder — expressive, receptive or mixed), dysarthria (a motor speech disorder with intact language), or dysphonia.

• Cranial nerves, including fundoscopy and visual fields.

• Motor: inspection for wasting and fasciculation, tone, power graded on the Medical Research Council scale, reflexes, plantars, coordination.

• Sensory, tailored to the hypothesis rather than performed exhaustively — look for a level, a dermatome, or a glove-and-stocking pattern.

• Gait — the single most informative part of the neurological examination, and the one most often omitted because the patient is already on the bed.

Case 64 · Acute Ischaemic Stroke

1. Focused History — Four Things, Fast

• The time of onset, or the time the patient was last known to be well. This is the single most important fact in the entire encounter. If he woke with the deficit, the clock starts when he was last seen normal — although advanced imaging now allows selected patients outside the conventional window to be treated.

• Contraindications to thrombolysis: recent surgery or major trauma, active bleeding, previous intracranial haemorrhage, known aneurysm or vascular malformation, recent stroke, anticoagulant use and the time of the last dose, and any bleeding disorder.

• Was there a seizure at onset, or a preceding headache and vomiting? The first raises a postictal deficit; the second raises haemorrhage.

• Premorbid function, which shapes decisions about aggressive intervention — obtained from the family in a few sentences.

2. Physical Examination

• Airway, breathing, circulation, conscious level, and capillary glucose — in that order, and glucose within the first minute.

• A formal stroke severity score, which guides thrombectomy decisions and allows objective comparison later.

• Blood pressure in both arms, cardiac rhythm and murmurs, carotid bruits, peripheral pulses, temperature, and a search for a source of embolism including signs of endocarditis.

3. Localising the Stroke

4. Investigations

• Immediate non-contrast computed tomography of the head — its first purpose is to exclude haemorrhage. Early ischaemic signs include loss of grey–white differentiation, loss of the insular ribbon, sulcal effacement, and the hyperdense artery sign of thrombus within the vessel.

• Computed tomographic angiography to identify a large vessel occlusion, which determines eligibility for thrombectomy. Perfusion imaging selects patients for treatment in the extended time window.

• Glucose, complete blood count, coagulation screen, urea and electrolytes, and an electrocardiogram, which here shows atrial fibrillation and identifies the mechanism.

• Later, to determine aetiology and secondary prevention: prolonged cardiac monitoring for paroxysmal atrial fibrillation, carotid imaging, echocardiography, lipids and glycated haemoglobin. Magnetic resonance imaging with diffusion-weighted sequences where the diagnosis is uncertain or the stroke is posterior.

• In a young patient, extend the workup: arterial dissection, patent foramen ovale, thrombophilia, vasculitis, and infective endocarditis.

5. Management

Reperfusion

• Intravenous thrombolysis within 4.5 hours of onset in the absence of contraindications. Blood pressure must be below 185/110 mmHg before treatment and controlled afterwards.

• Mechanical thrombectomy for large vessel occlusion, conventionally within 6 hours and extending to 24 hours in patients selected by perfusion imaging. This patient has a middle cerebral artery occlusion and should be referred for thrombectomy at the same time as thrombolysis is being given.

• Do not delay transfer to a thrombectomy centre in order to complete a thrombolysis infusion. The two run in parallel.

The first 48 hours

• Stroke unit care — the intervention that benefits the largest number of patients, more than any drug.

• Aspirin 300 mg — immediately if not thrombolysed, or after 24 hours and a repeat scan if thrombolysed. Given rectally or by nasogastric tube if swallowing is unsafe.

• Maintain normoglycaemia and normothermia; oxygen only if hypoxic; intermittent pneumatic compression rather than routine early heparin for venous thromboembolism prophylaxis; early mobilisation and pressure care.

• Malignant middle cerebral artery syndrome — deteriorating consciousness with massive infarction in the first 48 hours. Decompressive hemicraniectomy improves survival in selected younger patients and must be discussed early, before the patient deteriorates beyond eligibility.

Secondary prevention and rehabilitation

• Anticoagulation for atrial fibrillation, with timing determined by infarct size — larger infarcts are anticoagulated later because of haemorrhagic transformation risk.

• Antiplatelet therapy where the mechanism is not cardioembolic; high-intensity statin; blood pressure control started after the acute phase; diabetes and smoking.

• Carotid endarterectomy within two weeks for symptomatic severe stenosis — the benefit falls sharply with delay.

• Multidisciplinary rehabilitation — physiotherapy, occupational therapy, speech and language therapy; nutrition; screening for post-stroke depression; driving advice; and, for an aphasic patient, deliberate attention to how consent and communication are managed.

6. Teaching Points and Viva Questions

• Check the glucose before anything else. Hypoglycaemia mimics everything.

• Time last known well, recorded to the minute, drives every subsequent decision.

• Do not treat the blood pressure in ischaemic stroke — the penumbra depends on it.

• Swallow screen before the first tablet or sip.

• Vertigo with ataxia and vascular risk factors is a posterior circulation stroke until proved otherwise, and the computed tomogram will not reassure you.

• Thrombolysis and thrombectomy referral happen together, not one after the other.

Questions you should be able to answer:

• Classify this stroke syndrome and name the vessel.

• His blood pressure is 196/104. What do you do, and why?

• He was found on the floor at 07:00 having gone to bed at 23:00. What time do you use, and what are his options?

• The nurse asks whether she can give his morning tablets. What is your answer?

• When would you start anticoagulation for his atrial fibrillation?

Case 65 · Seizures and Status Epilepticus

1. Managing Status Epilepticus

• Complications to anticipate: hypoxia and aspiration, rhabdomyolysis with acute kidney injury, hyperthermia, arrhythmia, lactic acidosis, fractures and dislocations, and neuronal injury from prolonged seizure activity.

2. Once She Has Stopped — the History

Get the witness account. A seizure diagnosis made without one is unreliable, and the witness is usually available in the department for only a short time.

• Before: what she was doing, any warning or aura, posture, and triggers such as sleep deprivation, alcohol, missed medication or flashing lights.

• During: focal onset or generalised from the start, head or eye deviation, duration, colour change, lateral tongue biting — which is relatively specific — incontinence, and injury.

• After: duration of confusion, focal weakness (Todd paresis), headache, muscle pain.

• In a known epileptic, find the precipitant: missed or stopped medication, a new interacting drug, infection, sleep deprivation, alcohol, or menstruation.

3. Investigations

• Glucose, sodium, calcium, magnesium, complete blood count, liver and renal function, creatine kinase, and drug levels where relevant. Toxicology and a pregnancy test. Blood cultures if febrile.

• A raised lactate is expected immediately after a generalised convulsion and clears within an hour or two. It is a useful confirmatory finding and is regularly misread as evidence of sepsis or shock.

• Computed tomography of the head for a first seizure with a focal deficit, persistent alteration of consciousness, head injury, fever, anticoagulation, immunosuppression or known malignancy.

• Lumbar puncture where meningitis or encephalitis is suspected, with imaging first where indicated.

• Electroencephalography supports the diagnosis and classifies the epilepsy syndrome, but a normal recording does not exclude epilepsy — most patients are normal between seizures. Magnetic resonance imaging is the structural investigation of choice in focal epilepsy.

4. Longer-Term Management

• Match the drug to the seizure type. Focal epilepsy: lamotrigine, levetiracetam, carbamazepine. Generalised epilepsy: valproate, lamotrigine, levetiracetam. Carbamazepine can worsen generalised epilepsies — classification matters.

• After a first unprovoked seizure, treatment is not automatic. It depends on the risk of recurrence — an abnormal electroencephalogram, a structural lesion, a focal or nocturnal seizure — and on the patient’s own priorities, including driving and occupation.

• Driving. The patient must be advised not to drive and to inform the licensing authority. Have the conversation and document it — it is a legal obligation as well as a clinical one.

• Safety advice: showers rather than baths, never swim alone, caution with heights, unguarded machinery and cooking, and a rescue medication plan taught to the family.

• Women: folic acid; interactions between enzyme-inducing drugs and hormonal contraception in both directions; and preconception counselling well before pregnancy.

• Discuss sudden unexpected death in epilepsy honestly. The risk is reduced by good seizure control and by adherence, which is itself a reason to have the conversation.

5. Teaching Points and Viva Questions

• Five minutes defines status epilepticus. Start treating at five, not at thirty.

• Under-dosing the benzodiazepine is the commonest reason status persists.

• Thiamine before glucose in anyone malnourished or alcohol-dependent.

• A raised lactate after a convulsion is expected, not alarming.

• A normal electroencephalogram does not exclude epilepsy.

• Ask why she stopped the tablets, and document the driving conversation.

Questions you should be able to answer:

• At what point did this become status epilepticus, and what is your first drug?

• She is still fitting after two doses of lorazepam. What next, and in what order?

• Her creatine kinase is 8400. What is the complication and how do you manage it?

• How would you distinguish this from a psychogenic non-epileptic attack?

• She asks when she can drive again, and whether she can take valproate. Answer both.

Case 66 · Acute Neuromuscular Weakness

1. Localise First

The absence of a sensory level and of sphincter disturbance, with global areflexia and a preceding diarrhoeal illness, places this in the peripheral nerves — Guillain–Barré syndrome. But if there had been any suspicion of a cord lesion, magnetic resonance imaging of the spine comes before anything else.

2. Focused History

• Antecedent illness — *Campylobacter* gastroenteritis is the classic trigger, along with cytomegalovirus, Epstein–Barr virus, *Mycoplasma*, and recent surgery or vaccination.

• Tempo — Guillain–Barré syndrome progresses over days to a maximum at up to four weeks. Weakness progressing over months is a different disease.

• Pain — severe back and limb pain is present in most patients, is often the first symptom, and is regularly under-treated because it is not expected.

• Bulbar and respiratory symptoms: difficulty swallowing, nasal speech, weak cough, breathlessness on lying flat.

• Autonomic symptoms: palpitations, fainting, constipation, urinary retention, sweating changes.

• If the pattern suggests myasthenia instead: fatigability worse towards the end of the day, ptosis, diplopia, and precipitating drugs — aminoglycosides, macrolides, quinolones, beta blockers and magnesium.

3. Physical Examination

• Pattern and grading of weakness; reflexes and plantars; a careful search for a sensory level; assessment of fatigability by sustained upgaze and repeated arm abduction where myasthenia is possible.

• Bulbar function — speech, swallow, cough strength — and neck flexion strength, which parallels diaphragmatic strength.

4. Investigations

• Serial forced vital capacity, as above, charted like an observation.

• Lumbar puncture: albuminocytological dissociation — a raised protein with a normal cell count. It is frequently normal in the first week, so an early normal result does not exclude the diagnosis. A raised cell count should prompt consideration of infection, including human immunodeficiency virus, and of malignant infiltration.

• Nerve conduction studies and electromyography — demyelinating features in Guillain–Barré syndrome; a decremental response on repetitive nerve stimulation in myasthenia gravis.

• Anti-ganglioside antibodies, including anti-GQ1b in the Miller Fisher variant of ophthalmoplegia, ataxia and areflexia; stool culture and serology for *Campylobacter*.

• If myasthenia is suspected: acetylcholine receptor and muscle-specific kinase antibodies, thyroid function, and computed tomography of the chest for thymoma.

• Exclude the mimics: potassium, magnesium, calcium and phosphate; creatine kinase; vitamin B12; human immunodeficiency virus; and consider botulism, tick paralysis, porphyria, vasculitic neuropathy, and heavy metal poisoning.

• Magnetic resonance imaging of the spine wherever a cord lesion is conceivable. Cord compression is the diagnosis you cannot afford to miss, and it is the one that most closely mimics an ascending paralysis.

5. Management

• Admit to a monitored bed with four-hourly vital capacity and continuous cardiac monitoring. Involve intensive care early, before deterioration.

• Immunotherapy: intravenous immunoglobulin or plasma exchange. They are of equivalent efficacy, and they are not combined. Intravenous immunoglobulin is more widely available and easier to give.

• Autonomic instability is a leading cause of death. Monitor the rhythm, avoid drugs that swing the blood pressure, be alert for bradyarrhythmias, ileus and urinary retention, and treat labile hypertension cautiously.

• Treat the pain properly — neuropathic agents together with simple analgesia. Patients are fully conscious throughout.

• Venous thromboembolism prophylaxis in every immobile patient; pressure area care; nutrition and swallow assessment; early physiotherapy.

• Psychological support. A patient who is progressively paralysed but entirely alert and aware is frightened, and communication becomes harder exactly as the fear increases. Explain what is happening and what will happen next, repeatedly.

• Myasthenic crisis: intravenous immunoglobulin or plasma exchange, treatment of the precipitant, withdrawal of the offending drug, and cautious corticosteroid introduction — steroids can transiently worsen weakness at the start of treatment.

• Prognosis: most patients with Guillain–Barré syndrome recover substantially, but recovery takes months, a significant minority require ventilation, and mortality is not negligible. Say this honestly to the family.

6. Teaching Points and Viva Questions

• Localise before you diagnose — and exclude cord compression first.

• The vital capacity is the observation. Saturations and gases reassure you right up until they do not.

• Areflexia with ascending symmetrical weakness after a diarrhoeal illness is Guillain–Barré syndrome until proved otherwise.

• A normal lumbar puncture in the first week excludes nothing.

• Steroids are ineffective in the acute syndrome, and immunoglobulin and plasma exchange are not combined.

• Autonomic instability, not weakness, is what kills these patients.

• Treat the pain, and keep talking to a patient who cannot answer.

Questions you should be able to answer:

• Which findings place the lesion in the peripheral nerves rather than the cord?

• His saturations are 98% on air. Does that reassure you? Justify your answer.

• The lumbar puncture on day 4 shows normal protein. What do you conclude?

• A colleague suggests high-dose methylprednisolone. How do you respond?

• His heart rate drops to 38 during suctioning. What is happening?

Case 67 · Peripheral Neuropathy

1. Four Questions That Classify Any Neuropathy

Neuropathy has an intimidating list of causes and a very manageable structure. Answer these four questions and the list becomes short.

2. The Causes

Around a quarter remain idiopathic after full investigation, and it is legitimate to say so once the treatable causes have been excluded — but only then.

3. Focused History

• Onset, progression and distribution; which fibre types are involved; the character of any pain.

• Function, which is what the patient actually cares about: falls, unnoticed injuries and burns, difficulty with buttons and keys, tripping, and unsteadiness in the dark.

• Autonomic symptoms: postural dizziness, early satiety and vomiting, altered bowel habit, bladder and sexual dysfunction, sweating changes.

• Alcohol quantified; diet, vegan practice and bariatric surgery; every drug including chemotherapy and over-the-counter vitamins; occupational and toxin exposure.

• Family history — and examine the parents’ and siblings’ feet if you can, because hereditary neuropathy is often undiagnosed in the family.

• Red flags demanding urgent investigation: rapid progression, prominent or asymmetrical motor involvement, autonomic failure, weight loss, or systemic features.

4. Examination

• Establish the pattern first, then map the sensory level and test vibration, joint position, pinprick and temperature separately.

• Reflexes; power tested with attention to a distal-to-proximal gradient; gait and Romberg test; pes cavus and clawing.

• Palpate for thickened nerves — the ulnar nerve at the elbow, the greater auricular in the neck, the common peroneal at the fibular neck. Thickened nerves mean leprosy or hereditary neuropathy, and take fifteen seconds to check.

• Inspect the feet and the footwear, as in Case 25 — this man has already ulcerated and burned himself.

• Postural blood pressure; and a search for the systemic causes above.

5. Investigations

• Second line, guided by suspicion: antinuclear and antineutrophil cytoplasmic antibodies, rheumatoid factor, coeliac serology, angiotensin-converting enzyme, copper and caeruloplasmin, vitamin E, heavy metals, anti-ganglioside antibodies, and genetic testing.

• Nerve conduction studies and electromyography to confirm, localise, and classify as axonal or demyelinating.

• Normal nerve conduction studies in a patient with burning feet do not exclude neuropathy — they suggest small fibre disease, which is confirmed by skin biopsy or quantitative sensory testing where available.

• Nerve biopsy occasionally — for suspected vasculitis, amyloidosis or leprosy. Imaging of the spine where a myelopathy or radiculopathy is possible.

6. Management

• Treat the cause. Glycaemic control slows progression; alcohol abstinence with thiamine replacement; B12 and thyroid replacement; withdrawal of the offending drug; treatment of the vasculitis, paraprotein or leprosy.

• Falls prevention, physiotherapy and occupational therapy, an ankle-foot orthosis for foot drop, and driving assessment.

• Autonomic management: compression stockings and fludrocortisone or midodrine for postural hypotension; prokinetics for gastroparesis.

• Do not accept a chronic progressive demyelinating neuropathy as untreatable. Chronic inflammatory demyelinating polyradiculoneuropathy responds to corticosteroids, immunoglobulin or plasma exchange — in contrast to Guillain–Barré syndrome, where steroids do not work (Case 66). It deserves referral rather than resignation.

• Genetic counselling in hereditary disease.

7. Teaching Points and Viva Questions

• Classify by fibres, distribution, tempo, and axonal versus demyelinating.

• The cheap first-line screen finds most of the treatable causes — and includes a paraprotein screen.

• Normal nerve conduction studies with burning feet means small fibre neuropathy, not a normal patient.

• Palpate for thickened nerves.

• Mononeuritis multiplex means vasculitis or diabetes.

• Promise 30 to 50 per cent pain relief, not abolition.

• Foot protection prevents amputation; chronic demyelinating neuropathy is treatable.

Questions you should be able to answer:

• Which four questions would you ask of any neuropathy, and what are the answers in this man?

• He has diabetes and drinks heavily. Why still send the full screen?

• A patient with burning feet has entirely normal nerve conduction studies. What do you conclude?

• What will you tell him about how much his pain will improve?

• A 45-year-old has a two-year progressive weakness with globally absent reflexes and demyelinating conduction studies. Why does this matter?

Case 68 · Myelopathy and Demyelinating Disease

1. Compressive Myelopathy — the Emergency

• Causes: metastatic malignancy — breast, lung, prostate, myeloma and lymphoma — which is the commonest cause in an adult; epidural abscess (fever, back pain, immunosuppression, diabetes, intravenous drug use, recent spinal instrumentation); epidural haematoma (anticoagulation or a recent procedure); disc prolapse and vertebral fracture; and tuberculous or brucellar spondylitis, which are important here and may present with a gibbus (Cases 41 and 43).

• Red flags: progressive leg weakness, a sensory level, urinary retention or new incontinence, saddle anaesthesia, band-like pain around the trunk, back pain worse at night or on straining, fever, or a known malignancy.

2. Non-Compressive Myelopathy

3. Multiple Sclerosis

• The diagnosis requires dissemination in space and in time — lesions in more than one site, occurring on more than one occasion. This patient has optic neuritis, a brainstem episode and now a myelitis, with characteristic imaging and oligoclonal bands.

• Phenotypes: relapsing–remitting, secondary progressive, primary progressive; and the clinically isolated syndrome.

• Typical presentations: optic neuritis — painful monocular visual loss with a relative afferent pupillary defect, recovering over weeks and leaving optic atrophy; transverse myelitis; brainstem syndromes with internuclear ophthalmoplegia, vertigo or diplopia; sensory disturbance; Lhermitte sign — an electric sensation down the spine on neck flexion; Uhthoff phenomenon — symptoms worse in heat; and the features patients rate as most disabling: fatigue, bladder dysfunction, spasticity and cognitive change.

Investigations

• Magnetic resonance imaging of the brain and the whole spine with contrast — periventricular, juxtacortical, infratentorial and cord lesions, with enhancement indicating active inflammation.

• Cerebrospinal fluid oligoclonal bands with a normal or mildly raised cell count; visual evoked potentials.

• Aquaporin-4 and MOG antibodies, and exclusion of the mimics: B12, human immunodeficiency virus, syphilis, antinuclear antibody, angiotensin-converting enzyme, thyroid function and the vasculitides.

Management

• Acute relapse: high-dose corticosteroid shortens the relapse but does not change the long-term course, and is used only where the relapse is disabling. Exclude infection first — urinary infection both mimics and precipitates relapse, and should be treated before any steroid is given.

• Disease-modifying therapy in relapsing disease, started early, because disability accrues early and is not recovered later. Agents range from interferons and glatiramer through dimethyl fumarate and teriflunomide to natalizumab, fingolimod, ocrelizumab, alemtuzumab and cladribine, selected by disease activity and risk. Screen before starting: JC virus serology, hepatitis B, tuberculosis, varicella status, and pregnancy planning.

• Pregnancy: the relapse rate falls during pregnancy and rises in the puerperium; plan drug changes in advance rather than reacting to a positive test.

• Multidisciplinary care with a specialist nurse, physiotherapy, occupational therapy and continence services; and an honest conversation about prognosis, which is far more variable than patients expect.

4. Teaching Points and Viva Questions

• A sensory level plus sphincter disturbance means imaging the whole spine today.

• Flaccid areflexic legs early do not exclude a cord lesion.

• The commonest compressive cause in an adult is metastatic malignancy — and here, think tuberculous and brucellar spondylitis too.

• Send aquaporin-4 antibodies: neuromyelitis optica is treated differently and some multiple sclerosis drugs worsen it.

• Steroids shorten a relapse but do not change the course — and treat the urinary infection first.

• Start disease-modifying therapy early; disability accrues early.

• Measure the post-void residual before treating the bladder.

Questions you should be able to answer:

• What does the sensory level at T10 tell you, and what is your first investigation?

• Her legs are flaccid with absent reflexes on day one. Does that exclude a cord lesion?

• Which two antibodies must you send, and why does the answer matter?

• She has a relapse and is dysuric. What do you do before prescribing methylprednisolone?

• Give four symptoms you would ask about that will not appear on her scan.

Case 69 · Parkinson Disease and the Extrapyramidal Disorders

1. The Causes

2. The Tremor Differential

3. Focused History

• Motor: slowness, micrographia, quiet voice, loss of dexterity, difficulty turning in bed, freezing in doorways, falls.

• The full drug history, and specifically the antiemetics — a course of metoclopramide or prochlorperazine is the commonest thing to find, and it is reversible.

• Family history; occupational and toxin exposure; and the impact on function, work, driving and — importantly — on the carer.

4. Examination

• Observe before you touch: facial expression, blink rate, posture, and tremor at rest with the hands in the lap.

• Demonstrate bradykinesia properly — finger tapping, hand opening and closing, and foot tapping, watching for decrement in amplitude and speed, which is what distinguishes bradykinesia from simple weakness or slowness.

• Rigidity, with and without contralateral activation to bring out cogwheeling.

• Gait: initiation, stride length, arm swing, turning, festination and freezing — plus the pull test for postural instability.

• Eye movements, especially vertical saccades and pursuit; postural blood pressure; cognitive screen; speech and swallowing; and Kayser–Fleischer rings in a younger patient.

5. Investigations

• The diagnosis is clinical. No test confirms Parkinson disease, and students expect one.

• Structural imaging where the picture is atypical, to exclude vascular disease, hydrocephalus or a structural lesion.

• Dopamine transporter imaging distinguishes degenerative parkinsonism from essential tremor and from drug-induced parkinsonism — but it does not distinguish Parkinson disease from the atypical degenerative syndromes, which is the distinction that usually matters clinically.

• Caeruloplasmin, copper and liver function in anyone under 50; thyroid function; vitamin B12.

• The levodopa response is itself diagnostic information — a clear and sustained response supports Parkinson disease, and a poor one argues for an atypical syndrome.

6. Management

• Refer to a specialist before starting treatment where possible, and do not start antiparkinsonian drugs simply to see what happens in an unclear case.

• Non-motor management, which is where most of the quality of life is: constipation, orthostatic hypotension, bladder symptoms, drooling, sleep disorder, depression — common and under-treated, pain, and cognitive impairment, for which rivastigmine is used in Parkinson disease dementia.

• Multidisciplinary care: a Parkinson specialist nurse, physiotherapy for gait and falls, occupational therapy, speech and language therapy for voice and swallow, and dietetics. Exercise has genuine evidence for slowing functional decline. Driving advice, carer support and advance care planning.

• Atypical syndromes are managed supportively, with particular attention to falls, swallowing and autonomic failure, and earlier involvement of palliative care.

7. Teaching Points and Viva Questions

• Parkinsonism is bradykinesia plus one. Then find the cause.

• Ask about every drug, and especially the antiemetics.

• Anosmia and dream enactment precede the tremor by years.

• Know the red flags that argue against Parkinson disease.

• The diagnosis is clinical, and dopamine transporter imaging does not separate the degenerative syndromes.

• Do not delay levodopa, and ask about impulse control at every visit.

• Never stop levodopa, never give metoclopramide, and give the doses on time.

Questions you should be able to answer:

• Which features here support idiopathic Parkinson disease rather than an atypical syndrome?

• What is the significance of his anosmia and his sleep behaviour?

• Give five red flags that would make you doubt the diagnosis.

• He is admitted with pneumonia and is nil by mouth. What must happen to his medication?

• His wife telephones to say he has gambled away their savings. What has happened?