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Y6 Revision > Neuro > Flashcards

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
Q

What is the penumbra

A

area of hypoxic parenchyma that is still salvageable

26
Q

management/Ix for SAH/haemorrhagic stroke

A

CT head → 12 hours later → LP (xanthochromia)

Nimodipine (CCB), 21 days
First line: coiling (IR)
Second line: surgical clipping (requires craniotomy)

27
Q

Management for ischaemic stroke

A
  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
Q

Define multiple sclerosis

A

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
Q

Aetiology of multiple sclerosis

A

Aetiology: genetic (HLA-DRB1), environmental, viral
Pathophysiology: CD4-mediated destruction of oligodendrocytes → demyelination + eventual neuronal death

30
Q

What is the classifications of multiple sclerosis

A

Relapsing-remitting (80%) - RRMS
Primary progressive (10%) - PPMS
Secondary progressive* - SPMS
Progressive relapsing - PRMS

RRMS may transform into SPMS

31
Q

What are the symptoms and signs of multiple sclerosis

A

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
Q

What investigations should be done for multiple sclerosis

A

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
Q

Differentials for multiple sclerosis

A

Stroke, tumour, CNS sarcoidosis, SLE, Devic’s syndrome (neuromyelitis optica / NMO)

34
Q

Management for an acute attack of multiple sclerosis

A

Methylprednisolone (1g IV/PO, OD 3 days)

35
Q

Management for chronic multiple sclerosis

A

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
Q

Prognosis for multiple sclerosis

A

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
Q

Define myasthenia gravis

A

an autoimmune disorder characterised by insufficient functioning nicotinic acetylcholine receptors

38
Q

Aetiology of myasthenia gravis

A

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
Q

What are the symptoms and signs of myasthenia gravis

A

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
Q

What medications exacerbate myasthenia gravis

A

Penicillamine
Beta blockers
Phenytoin
Quinidine, procainamide
Lithium
ABx e.g. gentamicin, macrolides, quinolones, tetracyclines

41
Q

Investigations for myasthenia gravis

A

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
Q

Management for myasthenia gravis

A

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
Q

What is a thymoma and what is it associated with

A

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
Q

What is a myasthenic crisis and how is it managed

A

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
Q

What is lambert eaton syndrome and how does it present

A

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
Q

What investigations should be done for lambert-eaton syndrome and how is it managed

A

EMG
Incremental response to repetitive electrical stimulation

Treat cancer
Immunosuppression (prednisolone ± azathioprine)

47
Q

Define motor neurone disease

A

motor neurone loss from cortex, brainstem, spinal cord and ant. horn cells of spinal cord

48
Q

What are the types of motor neurone disease

A

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
Q

What are the signs and symptoms of motor neuron disease

A

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
Q

What is the difference between bulbar and pseudobulbar palsy

A

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
Q

What investigations should be done for motor neuron disease

A

Diagnostic criteria: Revised El Escorial criteria):
MRI brain / spinal cord: exclude structural causes
EMG (fasciculations)
LP: exclude inflammatory conditions

52
Q

What are the differentials for mixed UMN and LMN signs

A

MAST (MND, Ataxia [Friedrich’s], SCDC, Taboparesis)

53
Q

Management for motor neuron disease

A

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
Q

Causes of UMN lesions

A

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
Q

What are the signs of UMN lesions

A

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
Q

What are the causes of bilateral UMN lesions (Spastic paraparesis)

A

MS
Cord compression
Cord trauma
Cerebral palsy

57
Q

What are the causes of unilateral UMN lesions

A

Hemicord: MS, cord compression
Hemisphere: MS, stroke, SOL, cerebral palsy

58
Q

What are the causes of a mixed UMN/LMN lesion

A

MND (ALS)
Ataxia (Friedrich’s)
SCDC (B12 deficiency)
Taboparesis

59
Q

What investigations should be done for UMN lesions

A

MRI brain/spine

Y6 Revision (7 decks)

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