Neurology Flashcards

Question

How are subarachnoid haemorrhages assessed initially?

Answer 1

Investigation: Non-contrast CT head first-line – hyperdense blood in basal cisterns, sulci, ventricular system If CT head done within 6 hours of symptom onset and is normal, consider alternative diagnosis If CT head done more than 6 hours after symptom onset and is normal – do an LP at least 12 hours after symptom onset LP – xanthochromia, normal/raised opening pressure If CT shows evidence of SAH immediate referral to neurosurgery Further investigation: CT angiogram to identify vascular lesion +/- digital subtraction angiogram (catheter angiogram)

Answer 2

Supportive: Bed rest Analgesia VTE prophylaxis Discontinuation of anti-thrombotics (reversal or anticoagulation if present) Antiepileptics for seizures Nimodipine – prevent vasospasm Aneurysms are at risk of rebleeding, intervention within 24 hours – interventional radiology coiling (minority get craniotomy and clipping)

Answer 3

Re-bleeding – 10%, most commonly within first 12 hours, should repeat CT if suspected Hydrocephalus – can treat with temporary drain or permanent ventriculoperitoneal shunt Vasospasm Hyponatraemia – SIADH Seizures

Answer 4

Infection – immunocompromised, fever, photophobia, neck stiffness Vomiting Thunderclap headache New-onset neurological deficit/cognitive dysfunction Change in personality Impaired consciousness Recent (within 3 months) head trauma Worse with cough, Valsalva Changes with posture Visual disturbance Substantial change in characteristics of headache Wakes from sleep Pregnancy – pre-eclampsia Papilloedema on fundoscopy

Answer 5

Recurrent Mild ache across forehead, band-like Come on and resolve gradually No other symptoms, don’t interfere with ADLs Associated triggers – stress, alcohol, skipping meals, dehydration Management: Simple analgesia – aspirin, paracetamol, NSAID Acupuncture Amitriptyline for prophylaxis (not recommended by NICE)

Answer 6

Unilateral, excruciating/stabbing/burning pain Ipsilateral to pain – conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, ptosis/miosis Last 15 minutes – 3 hours, 1-2x per day for 4-12 weeks (clusters) MRI with contrast for investigation Neurology referral Acute management – 100% oxygen, SC triptan Prophylaxis – verapamil (?prednisolone)

Answer 7

Severe, unilateral, throbbing headache Associated with nausea, photophobia and phonophobia Can last up to 72 hours Classically have aura before migraine – visual, 5-60 minutes of hemianopic disturbance or spreading scintillating scotoma Can have hemiplegic migraines – exclude stroke Triggers – stress, alcohol, lack of food or dehydration, food (cheese, chocolate), menstruation, bright lights

Answer 8

Acute treatment: 1st line – oral triptan + NSAID/paracetamol (in 12-17 year olds consider nasal triptan) If not effective or tolerated give non-oral metoclopramide or prochlorperazine + non-oral NSAID or triptan Prophylaxis: Given if migraines are having significant impact on QOL and daily function e.g., frequent (more than once per week) or are prolonged and severe despite acute treatment One of – propranolol, topiramate (avoid in women of childbearing age), amitriptyline Other options – acupuncture, riboflavin, candesartan, Erenumab (MAB against calcitonin gene-related peptide) Predictable menstrual migraines – frovatriptan or zolmitripan as ‘mini-prophylaxis’

Answer 9

5-HT1 agonists Available as oral, nasal, SC Adverse effects – tingling, heat, chest/throat tightness Contraindications – history of or significant risk factors for ischaemic heart disease or cerebrovascular disease

Answer 10

Present for 15 days or more per month (more than every other day) Medications which can trigger – triptans, opioids, paracetamol Management – abruptly withdraw simple analgesics, withdraw opioids gradually Headaches may initially worsen, withdrawal symptoms e.g., vomiting, hypotension, tachycardia, restless, sleep disturbance, anxiety

Answer 11

Compression of trigeminal nerve roots – usually idiopathic, can be tumour/vascular cause Unilateral, brief electric shock-like pain, abrupt onset and termination Limited to one or more division of trigeminal nerve Commonly triggered by light touch, cold, caffeine, citrus fruits or spontaneous Management – carbamazepine first-line

Answer 12

Risk factors Obesity Female sex Pregnancy Drugs – COCP, steroids, tetracyclines, retinoids/vitamin A, lithium Presentation – headache, blurred vision, papilloedema, enlarged blind spot, CN VI Management Weight loss Diuretics – acetazolamide Topiramate LP for temporary reduction in ICP Surgery – ventriculoperitoneal shunt, optic nerve sheath decompression to prevent damage

Answer 13

Thunderclap – reaches maximal intensity within 1-5 minutes of onset Associated focal neurological deficit Associated systemic features – fever, weight loss, night sweats Age >50

Answer 14

History – patient and witnesses Circumstances, prodromal symptoms, appearance during event, duration, recovery after event Previous TLoC, PMHx, DHx, FHx Lying and standing BP ECG Cardiovascular or neurological signs Referral for neurological assessment if seizure suspected and cardiovascular assessment if cardiovascular cause suspected

Answer 15

Syncope – vasovagal, cardiovascular, orthostatic Seizures Head injury Psychogenic – psychogenic pseudosyncope, psychogenic non-epileptic seizures Rare causes – vertebrobasilar TIA, SAH, cyanotic breath holding spell, subclavian steal syndrome

Answer 16

Relapsing-remitting (most common) – episodes of exacerbations of symptoms followed by recovery and periods of stability Secondary progressive – gradual accumulation of disability unrelated to relapses, which become less frequent or stop 2/3 with relapsing-remitting progress to secondary progressive Primary progressive – steady progression and worsening from onset, without remission

Answer 17

Onset or new symptoms or worsening of pre-existing symptoms Attributable to demyelinating disease Lasting more than 24 hours After stable period of at least a month

Answer 18

Largely unknown, risk factors: Genetics Vitamin D deficiency Smoking EBV Female Immune-mediated inflammation in response to environmental triggers in genetically predisposed T-cells attack oligodendrocytes, damaging axons May initially have some re-myelination of axons, eventually irreversible loss of function of affected nerves

Answer 19

Typical presentation 20-50 Presenting features: Optic neuritis Unthoff’s phenomenon – worsening of symptoms with increase in body temperature (e.g. taking hot bath) Internuclear opthalmoplegia – ipsilesional adduction deficit and contralateral abducting saccade/nystagmus on gaze to contralateral side Sensory – paraesthesias, numbness, trigeminal neuralgia, Lhermitte’s syndrome Spastic weakness Ataxia Tremor Urinary incontinence Sexual dysfunction Diagnosis: Requires evidence of two or more relapses Clinical evidence of two or more lesions or evidence of one lesion and reasonable historical evidence of previous relapse MRI evidence of two lesions (e.g., Dawson fingers) If not enough evidence – CSF for oligoclonal bands

Answer 20

Lesion involving medial longitudinal fasciculus in paramedian area of midbrain and pons – controls horizontal eye movements via CN III, IV and VI Features – impaired adduction in ipsilateral eye, horizontal nystagmus of abducting eye on contralateral side

Answer 21

Acute relapse: High dose steroids (e.g., oral or IV methylprednisolone) for 5 days, shortens length of relapse but does not alter degree of recovery Disease modifying drugs: Typically if 2 relapses in past 2 years and able to walk 100m (if relapsing-remitting) or 10m (in secondary progressive) Options e.g. Natalizumab (alpha-4 beta-1 integrin antagonist) Ocrelizumab (anti-CD20) Fingolimod Beta-interferon Management of complications: Fatigue – amantadine, CBT Spasticity – baclofen, gabapentin, physiotherapy Bladder dysfunction – US, self-catheterisation (if significant residual volume), anticholinergics (if no significant residual volume)

Answer 22

Loss of dopaminergic neurones in the substantia nigra of the basal ganglion Clinical features: Classic triad is bradykinesia, tremor, and rigidity Asymmetrical Bradykinesia/hypokinesia – short, shuffling steps, reduced arm swinging, difficulty initiating movement Tremor – resting, 3-5 Hz, improved with voluntary movement, typically ‘pill-rolling’ Rigidity – lead pipe, cogwheel Reduced dexterity Mask-like face Stooped posture Festinating gait Anosmia Psychiatric features – depression, dementia, psychosis, sleep disturbance Autonomic dysfunction – postural hypotension, constipation, excessive salivation or sweating, urinary dysfunction, sexual dysfunction

Answer 23

Drug-induced: Rapid onset, bilateral Rigidity and rest tremor uncommon

Answer 24

Clinical diagnosis If unclear – single photo emission computerised tomography (SPECT)

Answer 25

First-line: If motor symptoms are affecting quality of life – levodopa If motor symptoms are not affecting quality of life – dopamine agonist, levodopa or monoamine oxidase B inhibitor If continuing to have symptoms with levodopa add dopamine agonist, MAO-B inhibitor or catechol-O-methyl transferase (COMT) inhibitor as an adjunct Levodopa nearly always given with decarboxylase inhibitor (e.g., carbidopa) – prevents peripheral metabolism of levodopa to dopamine outside brain to reduce side effects

Answer 26

Dry mouth Anorexia Palpitations Postural hypotension Psychosis Difficult to achieve steady dose – end-of-dose wearing off, on-off phenomenon, dyskinesias at peak dose (dystonia, chorea, athetosis) Important to take consistently

Answer 27

Examples – bromocriptine, ropinirole, cabergoline Ergot-derived (bromocriptine, cabergoline) – associated with pulmonary, retroperitoneal and cardiac fibrosis, perform baseline tests and monitor closely Impulse control disorders Excessive daytime somnolence – may not be able to drive Hallucinations – higher risk than levodopa in older patients Nasal congestion Postural hypotension

Answer 28

Selegiline Inhibits breakdown of dopamine by monoamine oxidase B

Answer 29

Entacapone, tolcapone COMT is involved in breakdown of dopamine – inhibit breakdown Used in conjunction with levodopa in patients with established Parkinson’s disease

Answer 30

Parkinson’s disease Drug induced – antipsychotics, antiemetics (metoclopramide) Progressive supranuclear palsy – unsteadiness, dysphagia, gaze palsies Multiple system atrophy – unsteadiness, falls, autonomic dysfunction Wilson’s disease Lewy body dementia Essential tremor – increases on action, improved at rest, improved with alcohol, bilateral, not confined to hands

Answer 31

Missing doses can cause akinesia (freezing) and can precipitate neuroleptic malignant syndrome

Answer 32

Predominantly motor loss: Guillain-Barre syndrome Poryphria Lead poisoning Hereditary sensorimotor neuropathies – Charcot-Marie-Tooth Diphtheria Predominantly sensory loss: Diabetes Uraemia Leprosy Alcoholism Vitamin B12 deficiency Amyloidosis

Answer 33

Ascending tracts: Anterior spinothalamic tract – touch and pressure Lateral spinothalamic tract – pain and temperature Spinocerebellar tracts – proprioception Descending tracts: Pyramidal tracts – voluntary control of muscles Extrapyramidal tracts – involuntary and automatic control of muscles (tone, balance, posture)

Answer 34

Most common – injury/compression More rarely toxic/metabolic – tend to be mononeuritis multiplex, multiple single nerves affected sequentially Diabetes Drugs Vasculitis Infection – HIV/Lyme

Answer 35

Radial nerve – ‘Saturday night palsy’ Presentation – wrist/finger drop, usually painless Sensory loss in radial nerve distribution (proximal half of thumb, 1st, 2nd and lateral half of 3rd finger)

Answer 36

Common peroneal nerve

Answer 37

Bloods – Glucose, FBC, U&Es, LFTs, TFTs, B12, folate, protein electrophoresis LP – not routine in length dependent neuropathy Nerve conduction studies

Answer 38

Acute rapidly progressive flaccid paralysis Weak proximally and distally Prominent pain/sensory symptoms +/- respiratory, bulbar, autonomic involvement Areflexic Post-infective - classically campylobacter jejuni Diagnosis – clinical + raised protein in CSF (normal WCC), nerve conduction studies Treatment – IV Igs or plasma exchange

Answer 39

Antibodies to acetylcholine receptors Muscle fatigability – weaker during activity, improve with rest Extraocular muscle weakness – diplopia Proximal muscle weakness – face, neck, limb girdle Ptosis – exacerbated by repeated blinking Dysphagia Associations: Thymoma – 15% Autoimmune disorders – pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE

Answer 40

Diagnosis: Single fibre electromyography CT thorax to exclude thymoma CK normal Antibodies to acetylcholine receptors Tensilon test – IV edrophonium reduces muscle weakness temporarily (not done anymore) Management: Long-acting acetylcholinesterase inhibitors – pyridostigmine first-line Longer term often need immunosuppression with prednisolone, azathioprine, cyclosporine etc. Thymectomy Management of myasthenic crisis: Plasmapheresis IV Igs

Answer 41

Penicillamine Quinidine Beta-blockers Lithium Phenytoin Antibiotics – gentamicin, macrolides, quinolones, tetracyclines