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Neuro Flashcards

1
Q

Symptoms of migraine

A

Headache: unilateral, throbbing, severe (impairs functioning), lasts 4-72h

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2
Q

Management of migraine

A

Acute: oral triptan + NSAID/paracetamol
Prophylaxis: topiramate/propranolol (if ≥2 attacks/month)

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3
Q

Symptoms of temporal arteritis

A

Headache
Jaw claudication
Tender scalp

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4
Q

Management of temporal arteritis

A

Oral prednisolone

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5
Q

Symptoms of tension headache

A

headache: bilateral, tight band

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6
Q

Management for tension headache

A

Aspirin
Paracetamol
NSAID

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7
Q

Symptoms of cluster headache

A

Intense pain around eye
Eye watering
Lasts 15m-2hrs

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8
Q

Management for cluster headache

A

Acute: 100% O2, SC triptan
Prophylaxis: verapamil

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9
Q

What defines medication overuse headache

A

≥15 days / month
Worsened with medication

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10
Q

Define TIA

A

a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

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11
Q

Investigations for TIA

A

Bedside: BP, ECG
Bloods: cholesterol, lipids, glucose, clotting
Imaging: Carotid US

+ Score systems:
ABCD2 (risk of stroke)
CHA2DS2VASc (risk of stroke in those with AF)
HASBLED: risk of bleeding events on anticoagulation (AF)

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12
Q

Management for TIA

A

300mg aspirin
First line: clopidogrel (75mg, PO, OD) + statin
Second line: aspirin + dipyridamole + statin
Consider carotid artery endarterectomy

<7 days since first TIA: <24h specialist review
>7 days since first TIA: <7 days specialist review
> 1 TIA/suspected cardioembolic source/severe carotid stenosis/on anticoagulation/bleeding disorder → ADMIT + investigate

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13
Q

When is aspirin not given in TIA

A

> 7 days since S/S
Bleeding disorder / on an anticoagulant
Takes regular low-dose aspirin
Aspirin CI

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14
Q

Indications for carotid artery endarterectomy

A

stenosis ≥50% [NASCET criteria], <2w of S/S

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15
Q

Define stroke

A

rapid onset neurological deficit of a vascular origin that does not completely resolve within 24 hours

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16
Q

Aetiology of stroke

A

80% ischaemic (thrombotic, embolic)
20% haemorrhagic (intracerebral haemorrhage, sub-arachnoid haemorrhage / SAH)

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17
Q

What is the Bamford classification of stroke

A

Total anterior circulation (TACS)
Partial anterior circulation (PACS)
Posterior circulation (POCS)
Lacunar anterior circulation (LACS)

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18
Q

What signs and symptoms suggest TACS

A

All three of:
Hemiparesis/Hemisensory deficit
Homonymous hemianopia
Higher cortical dysfunction (dysphasia, neglect, apraxia)

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19
Q

What signs and symptoms suggest PACS

A

2/3 of TACS

Hemiparesis/Hemisensory deficit
Homonymous hemianopia
Higher cortical dysfunction (dysphasia, neglect, apraxia)

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20
Q

What signs and symptoms suggest POCS

A

One of:
Cerebellar syndrome (ataxia, nystagmus, vertigo)
Brainstem stroke (Locked in)
Homonymous hemianopia
Cranial nerve palsy + contralateral motor/sensory deficit
Bilateral motor/sensory deficit

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21
Q

What signs and symptoms suggest LACS

A

One of:
Pure motor: post. limb of internal capsule
Pure sensory: post. thalamus (VPL)
Mixed sensorimotor: internal capsule
Dysarthria / clumsy hand
Ataxic hemiparesis: ant. limb of internal capsule

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22
Q

Investigations for stroke

A

Bedside: ECG, glucose
Bloods: FBC, U&Es, clotting, CRP, glucose, lipids
Imaging: Non-contrast CT, carotid doppler, MRI head (diffusion/perfusion weighted, MRA, FLAIR)

Scoring:
NIHSS (on admission): severity, guide treatment, predict outcomes (>21 = major)
Rosier (on admission): assess symptoms
CT ASPECT: assess early CT ischaemic changes

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23
Q

What would you see on CT for a stroke

A

Non-contrast CT ± perfusion CT ± CTA
Hyperdense (white) = acute clotted blood (haemorrhage, hyperdense artery sign)
Isodense = hyperacute active bleeding (rarely imaged; often swirling / mixed density)
Hypodense (dark) = ischaemic infarct, chronic clotted blood

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24
Q

How are stroke changes on CT classified according to time

A

Early hyperacute (0 to 6h): Hyperdense artery, loss of grey-white matter interface
Late hyperacute (6 to 24h): Hyperdense artery, loss of grey-white matter interface
Acute: (24h-1w): Hypodense (denser than CSF density), swelling
Subacute (1-3w): Normal density appearance (‘fogging’), reduced swelling
Chronic (>3w): ‘Encephalomalacia’ and CSF density achieved

Sub-acute infarcts : Poorly demarcated, Hypodense, Mass effect
Chronic infarct: Well demarcated, CSF density

25
What is the penumbra
area of hypoxic parenchyma that is still salvageable
26
management/Ix for SAH/haemorrhagic stroke
CT head → 12 hours later → LP (xanthochromia) Nimodipine (CCB), 21 days First line: coiling (IR) Second line: surgical clipping (requires craniotomy)
27
Management for ischaemic stroke
1. Aspirin (300mg), OD/PR 2w 2. AF? - Yes: Clopidogrel 75mg OD (Lifelong) --- Clopidogrel CI → aspirin + dipyrimadole - No: Apixaban (Xai)/warfarin 3. Statin <4.5 hours: thrombolysis (Alteplase) <4.5 hours with occluded proximal anterior circulation: thrombolysis + thrombectomy <6 hours: thrombectomy Supportive Fluid: Oral > IV (0.9% day 1, 5% dextrose day 2) Glycaemic control BP control: HTN emergency (encephalopathy/HF/MI/PET) → IV labetalol/nicardipine Cholesterol control: >3.5 → Statin (After 48h) SALT assessment: consider NG tube, nasal bridle tube, gastrostomy Disability assessment: Barthel index (functional status + improvement)
28
Define multiple sclerosis
Autoimmune demyelinating disorder of the CNS characterised by multiple plaques separate in time and space revised McDonald criteria, demonstration of lesions disseminated in time and space):
29
Aetiology of multiple sclerosis
Aetiology: genetic (HLA-DRB1), environmental, viral Pathophysiology: CD4-mediated destruction of oligodendrocytes → demyelination + eventual neuronal death
30
What is the classifications of multiple sclerosis
Relapsing-remitting (80%) - RRMS Primary progressive (10%) - PPMS Secondary progressive* - SPMS Progressive relapsing - PRMS RRMS may transform into SPMS
31
What are the symptoms and signs of multiple sclerosis
Tingling Eye / optic neuritis (CRAP = Central scotoma, RAPD, Acuity (↓ central vision, ↓colour vision), Pain on movement) Ataxia (and other cerebellar signs – DANISH) Motor (spastic paraparesis – i.e. shoulder paralysis) Lhermitte’s sign (neck flexion → electric shocks in trunk/limbs) Uhthoff’s sign (temporary worsening of MS symptoms with increased temperature – i.e. a hot bath, exercise) Internuclear Ophthalmoplegia (INO) – lesion in the medial longitudinal fasciculus (MLF) connecting CN6 to CN3 (and CN 4) which has S/S of weak adduction of ipsilateral eye and nystagmus of the contralateral eye
32
What investigations should be done for multiple sclerosis
Contrast MRI (gadolinium-enhanced, T2-weighted) LP (IgG oligoclonal bands) Blood antibodies: - Anti-MBP (myelin basic protein) - NMO-IgG (neuromyelitis optica) Evoked potentials NMO-IgG → Devic’s syndrome (S/S: MS + transverse myelitis + optic atrophy)
33
Differentials for multiple sclerosis
Stroke, tumour, CNS sarcoidosis, SLE, Devic’s syndrome (neuromyelitis optica / NMO)
34
Management for an acute attack of multiple sclerosis
Methylprednisolone (1g IV/PO, OD 3 days)
35
Management for chronic multiple sclerosis
DMARDs: - IFN-beta (reduces relapses by 30%) - Glatiramer Biologicals: - Natalizumab (anti-VLA-4 AB) (1st line RRMS (reduces relapses by 66%)) - Alemtuzumab (anti-CD52) (2nd line RRMS) + symptomatic Fatigue: modafinil Depression: SSRI (citalopram) Pain: amitryptyline, gabapentin Spasticity: 1st: baclofen + gabapentin; 2nd: dantrolene Urgency/frequency: oxybutynin, tolterodine ED: sildenafil Tremor: clonazepam
36
Prognosis for multiple sclerosis
Good signs: female, sensory signs, <25yo, long interval in relapses, few MRI lesions Bad: male, older, motor signs, short interval relapses, many MRI lesions, axonal loss
37
Define myasthenia gravis
an autoimmune disorder characterised by insufficient functioning nicotinic acetylcholine receptors
38
Aetiology of myasthenia gravis
Anti-ACh-R in are seen in 85-90% of cases Associations: thymoma (15%), thymic hyperplasia (50-70%), AI disease (PA, AI thyroid, RhA, SLE)
39
What are the symptoms and signs of myasthenia gravis
Muscle fatigability (progressively weaker during periods of activity and slowly improve after rest) Extraocular muscle weakness → diplopia, ptosis Proximal myopathy (face, neck, limb girdle) Dysphagia
40
What medications exacerbate myasthenia gravis
Penicillamine Beta blockers Phenytoin Quinidine, procainamide Lithium ABx e.g. gentamicin, macrolides, quinolones, tetracyclines
41
Investigations for myasthenia gravis
Single fibre EMG (≥92% sensitivity) Repetitive nerve stimulation (test fatiguability) Serial pulmonary function testing (test fatiguability) Antibodies: Anti-ACh-R AB (85-90%) Anti-muscle-specific-receptor TK AB (40%) Tensilon test (IV edrophonium bromide relieves muscle weakness temporarily)
42
Management for myasthenia gravis
1st line (symptomatic) = long-acting AChE inhibitors (pyridostigmine, neostigmine) 1st line (long-term control) = immunosuppression: - 1st: prednisolone - 2nd: azathioprine, cyclosporine, mycophenolate mofetil Surgical → thymectomy
43
What is a thymoma and what is it associated with
Most common tumour of ant. mediastinum (50-70yo) Associations: MG (30-40%), red cell aplasia, dermatomyositis, SLE, SIADH Death by compression of airway or cardiac tamponade
44
What is a myasthenic crisis and how is it managed
Characterised by FVC ≤1L, negative inspiratory force ≤20cmH2O, and need for ventilation S/S: reduced RR, background of MG - Accessory muscle usage (weak inspiratory muscles) - Weak cough (weak expiratory muscles) Ix: ABG (hypercapnia before hypoxia), FVC Mx: plasmapheresis, IVIG, intubation
45
What is lambert eaton syndrome and how does it present
LEMS is seen in association with SCLC (and breast and ovarian cancer) and is caused by an antibody directed against presynaptic voltage-gated calcium channel (VGCC) in the peripheral nervous system Repeated muscle contractions lead to increased muscle strength (seen in only 50% of patients) Limb-girdle weakness (affects lower limbs first) Hyporeflexia ANS symptoms (dry mouth, impotence, difficulty micturating) Eye signs are rarer (ophthalmoplegia and ptosis not commonly a feature)
46
What investigations should be done for lambert-eaton syndrome and how is it managed
EMG Incremental response to repetitive electrical stimulation Treat cancer Immunosuppression (prednisolone ± azathioprine)
47
Define motor neurone disease
motor neurone loss from cortex, brainstem, spinal cord and ant. horn cells of spinal cord
48
What are the types of motor neurone disease
Amyotrophic lateral sclerosis (ALS) - 50% - Corticospinal tracts - S/S: mixed UMN/LMN Primary lateral sclerosis - 30% - Loss of Betz cells in motor cortex - S/S UMN → spastic leg weakness + pseudobulbar palsy (CN5,7,9-12), no cognitive decline Progressive muscular atrophy - 10% - Anterior horn cell lesions - S/S: LMN → distal to proximal signs (best prognosis) Progressive bulbar palsy - 10% - CN 9-12 - S/S: bulbar palsy (worst prognosis)
49
What are the signs and symptoms of motor neuron disease
Neurological body exam: - Inspection (wasting & fasciculations – esp. tongue) - Tone (spastic) - Power (weak) - Reflexes (absent, extensor plantars) - Sensation (NORMAL) Cranial nerves: - Speech (bulbar = nasal; pseudobulbar = hot potato) - Jaw-jerk (bulbar = absent; pseudobulbar = brisk) - Eye movements (NORMAL; preserved until very late)
50
What is the difference between bulbar and pseudobulbar palsy
Bulbar palsy = LMN signs Cranial nerves 9, 10, 11, 12 Pseudobulbar palsy = UMN signs Cranial nerves 5, 7 Cranial nerves 9, 10, 11, 12
51
What investigations should be done for motor neuron disease
Diagnostic criteria: Revised El Escorial criteria): MRI brain / spinal cord: exclude structural causes EMG (fasciculations) LP: exclude inflammatory conditions
52
What are the differentials for mixed UMN and LMN signs
MAST (MND, Ataxia [Friedrich’s], SCDC, Taboparesis)
53
Management for motor neuron disease
MDT management = neurologist, physio, OT, dietician, GP, specialist nurse Riluzole (extends life by ~3 months) Supportive management: - Drooling: Amitriptyline - Dysphagia: NG/PEG - Respiratory failur: NIV - Pain: analgesic ladder - Spasticity: Baclofen, botulinum
54
Causes of UMN lesions
Cortex: Functional, abscess, CVA, tumour, demyelination Brainstem: abscess, CVA, tumour, demyelination Spinal: MS, cord compression, trauma, MND, syringomyelia, SCDC, anterior spinal artery occlusion Anterior horn cell: spinal muscular atrophy, polio, MND (ALS)
55
What are the signs of UMN lesions
Insepction: atrophied muscle, contracture Gait: - Unilateral → Circumducting gait - Bilateral → scissoring gait Neuro: - Weakness (Pyramidal pattern) - Hypertonia (Arm: flexors > extensors, leg: extensors > flexors) - Hyperreflexia - Clonus - Babinski's +ve, Hoffman's +ve Sensation should be intact - if there is a level → suggests cord lesion
56
What are the causes of bilateral UMN lesions (Spastic paraparesis)
MS Cord compression Cord trauma Cerebral palsy
57
What are the causes of unilateral UMN lesions
Hemicord: MS, cord compression Hemisphere: MS, stroke, SOL, cerebral palsy
58
What are the causes of a mixed UMN/LMN lesion
MND (ALS) Ataxia (Friedrich's) SCDC (B12 deficiency) Taboparesis
59
What investigations should be done for UMN lesions
MRI brain/spine

Y6 Revision (7 decks)

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