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Neurology Flashcards

1
Q

Causes of sensorimotor polyneuropathy?

A

(ABCDEs)

Alcohol
An underactive thyroid
A high urea

CIDP/GBS
Charcot-Marie-Tooth
Paraneoplastic (cancer)

Diabetes
Drugs (vincristine, cisplatin, nitrofurantoin, amiodarone)

Vasculitis (every vasculitis)

Sarcoidosis

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2
Q

Causes of a motor neuropathy?

A

Porphyria
Lead
Diptheria
CIDP/GBS
Dapsone

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3
Q

Causes of a sensory neuropathy?

A

Alcohol
An underactive thyroid
A high urea

CIDP/GBS
Charcot-Marie-Tooth
Paraneoplastic (cancer)

Diabetes
Drugs (isoniazid, metronidazole, hydralazine)

Vasculitis (every vasculitis)

Sarcoidosis

IN ADDITION:
Vitamin B12 deficiency
Amyloidosis
Infections (HIV, Lyme, leprosy)

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4
Q

Causes of an autonomic neuropathy?

A

GBS
Botulism
Porphyria
Paraneoplastic
Diabetes
Chagas
HIV
Amyloidosis

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5
Q

What does ‘small fibre neuropathy’ mean?

A

Subtype of peripheral neuropathies in wich there is impairment of small calibre sensory nerve fibres (myelinated A-delta fibres (cold, pain) and unmyelinated C fibres (warmth))

Vibration sense and proprioception preserved

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6
Q

What are the causes of demyelinating polyneuropathies?

A

CIPD
Multiple myeloma
Hereditary causes
Refsum’s disease
HIV

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7
Q

Drugs causing neuropathy?

A

Sensory: isoniazid, metronidazole, hydralazine

Motor: dapsone

Sensorimotor: vincristine, cisplatin, nitrofurantoin, amiodarone

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8
Q

Causes of mononeuritis multiplex?

A

Diabetes
Vasculitis (GPA, eGPA, MPA, PAN)
RA, SLE, Sjogren’s

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9
Q

How would you investigate a patient with peripheral neuropathy?

A

FBC, ESR, U+E, LFT, glucose, thyroid, B12 and folate, protein electrophoresis, autoimmune profile

Urine for glycosuria

Nerve conduction studies

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10
Q

Charcot Marie Tooth findings?*

A

Wasting of distal LL with preservation of thigh muscle (inverted champagne)

Pes cavus (imbalance between anterior and posterior tibialis)

Weakness of distal muscles

Glove and stocking sensory loss (mild)

High stepping gait (foot drop)

Palpable lateral popliteal nerve in 1A

N.B. Pain and temperature usually not affected in CMT as these fibres are not myelinated

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11
Q

Subtypes of CMT?*

A

Divided according to neurophysiological findings (axonal versus demyelinating) and inheritance pattern

Type 1A most common (autosomal dominant demyelinating)

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12
Q

How would you manage a CMT patient?

A

MDT (neurologists, orthopoedic surgeons, physiotherapists, OTs)

Patient education
Exercises
Walking aids
Orthotics for foot drop
OT
Analgesia for MSK/neuropathic pain
Orthopoedic surgery to correct deformities
Genetic counselling

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13
Q

Difference between stroke and TIA??*

A

Rapid onset focal neurological deficit due to a vascular lesion lasting >24 hours versus <24 hours (typically <30 minutes)

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14
Q

How would you investigate?*

A

FBC, CRP/ESR, HbA1c, lipids, renal function

ECG AF

CXR aspiration

CT head infarct or bleed, territory

MRI brain salvageable versus irreversibly infarcted brain tissue

24 hour Holter

Echo

Carotid doppler

Consider CT angiogram, MRA or MVA if suspecting dissection or VST, clotting screen if suspecting thrombophilia, vasculitis screen in young stroke

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15
Q

Management of stroke?*

A

Thrombolysis within 4.5 hours

Thrombectomy up to 24 hours of acute ischaemic stroke if CTA shows proximal occlusion

Aspirin 300mg for first two weeks

Referral to specialist stroke unit for MDT

DVT prophylaxis

Refer for carotid endarterectomy if anterior circulation stroke and >70% stenosis of ipsilateral internal carotid

Anticoagulation if AF (not in acute phase)

Address CV risk factors

DVLA advice

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16
Q

Bamford classification of stroke?*

A

TACS
Hemiplegia, Homonymous hemianopia, Higher cortical dysfunction (dysphasia, dyspraxia, neglect)

PACS
2/3 above

LACS
Pure hemi-motor or sensory loss

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17
Q

Lateral medullary syndrome?*

A

(PICA stroke)
Vertigo, vomiting, ipsilateral Horner’s, ipsilateral facial loss of pain and temperature, contralateral loss of pain and temperature sensation

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18
Q

Signs of MS?*

A

Wheelchair
Catheter if spinal plaques

INO, RAPD/optic atrophy/reduced VA

Sensory and UMN signs

DANISH

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19
Q

Diagnostic criteria for MS?

A

Requires dissemination in time and space
McDonald criteria allows MS to be diagnosed after a single attack using paraclinical tests

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20
Q

Subtypes of MS?*

A

RRMS 85%, can progress to secondary progressive with a median age of 15 years
PPMS 15%

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21
Q

Cause of MS?*

A

Incompletely understood
A third of disease risk is genetic
Another third reflects environmental risk (EBV, smoking, vitamin D deficiency)
The remaining third reflects interactions between genes and environment

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22
Q

Investigation of MS?*

A

Clinical diagnosis plus:
-CSF oligoclonal bands
-MRI lesions in brain or spinal cord (typical T2 hyperintense lesions in periventricular white matter)
-Visual evoked potentials delayed velocity but normal amplitude (optic neuritis)

Other features:
Fatigue depression cognitive
Autonomic (urinary, impotence, bowel problems)
Uthoff’s (heat-induced condution block of partially demyelinated fibres)
Lhermitte’s (neck flexion results in electric shock sensation, indicates dorsal column involvement or cervical cord)

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23
Q

Treatment of MS?*

A

MDT (specialist nurses, PT, OT, orthotics team, social worker, neuropsychologist)

Disease modifying drugs e.g. natalizumab, interferon-beta, glatiramer

Symptomatic drugs:
Methylprednisolone shortens relapses but doesn’t alter prognosis

Anti-spasmodics e.g. baclofen
Gabapentin, pregabalin, amitriptyline for neuropathic pain

Laxatives and intermittent catheterisation/oxybutynin

SSRIs for depression

Amantadine for fatigue

In pregnancy:
Reduced relapse rate during pregnancy but increased in post-partum period
Safe for foetus
2% risk of MS in children

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24
Q

Pathophysiology of MS?*

A

Idiopathic demyelinating disorder of the CNS characterised by demyelinating plaques separated in both space and time

Characterised as an autoimmune disease

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25
Q

What is an INO?*

A

Impairment of ipsilateral adduction
Normal abduction in contralateral eye with nystagmus
Results from medial longitudinal fasciculus

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26
Q

Signs of myotonic dystrophy?*

A

-Myopathic facies
-Bilateral ptosis
-Frontal balding
-Dysarthria

-Myotonia ‘grip my hand and let go’ or ‘screw eyes up then open’
-Wasting and weakness of distal muscles and areflexia
-Percussion myotonia

-Cataracts
-PPM scar
-Diabetes

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27
Q

Diagnosis of myotonic dystrophy?*

A

Clinical features
‘Dive-bomber’ potentials on EMG
Genetic testing

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28
Q

Management of myotonic dystrophy?*

A

MDT (PT/OT, orthotics)
No treatment for weakness
Mexiletine may help myotonia
Advise against GA
Manage diabetes, ocular and cardiac involvement
Genetic counselling

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29
Q

Differentials for myopathies? (180)

A

Hereditary:
Facio-scapulo-humeral
Limb girdle

Acquired:
Neuromyotonia
Paraneoplastic

MG

Mitochondital myopathies

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30
Q

Causes of ptosis?*

A

Bilateral: MD, MG, congenital

Unilateral: 3rd nerve palsy (pupil enlarged if surgical or compressive, normal if medical or ischaemic), Horner’s (pupil small)

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31
Q

Causes of CN 3 palsy? (180)

A

-PCA aneurysm
-Cavernous sinus thrombosis (usually with 4 and 6)
-SOL
-Raised ICP (false localising sign)
-Microvascular occlusion secondary to diabetes or HTN
-MG and thyroid eye disease can mimic

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32
Q

Genetics of myotonic dystrophy?*

A

Autosomal dominant

DM1 (more common) trinucleotide repeat on chromosome 19, presents in 20s-40s

DM2 tetranucleotide repeat on chromosome 3, presents later

Genetic anticipation seen in DM1

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33
Q

Clinic signs of cerebellar syndrome?*

A

DANISH

N.B. Cerebellar hemisphere lesions produce ipsilateral limb signs
Midline lesions cause truncal ataxia

In cerebellar nystagmus, fast phase direction changes with changing of gaze (not the case for vestibular lesions, where fast phase is always away from side of lesion)

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34
Q

Causes of cerebellar syndrome?*

A

Paraneoplastic
Alcohol (Wernicke’s subacute or degeneration chronic)
Sclerosis (MS)
Tumour
Recessive (Friedrich’s, ataxia telangiectasia) or dominant (spinocerebellar ataxia)
Iatrogenic (phenytoin toxicity)
Endocrine (hypothyroidism)
Stroke (cerebellar or brainstem vascular event)

STS = lesions of the ipsilateral cerebellar hemisphere

Remaining = lesions of the vermis or global cerebellar degeneration

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35
Q

Investigations for cerebellar syndrome (180)

A

FBC and MCV
B12 and folate
MRI brain

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36
Q

Spastic legs causes?*

A

-MS
-Spinal cord compression/myeloma/trauma
-MND (if no sensory signs)

Less commonly:
-Anterior spinal artery stroke (dorsal columns preserved)
-Neuromyelitis optica, SLE
-HSP
-B12 deficiency
-Friedrich’s (if also cerebellar signs and peripheral neuropathy)

37
Q

Myotomes and dermatomes?

A
38
Q

Syringomyelia clinical signs?*

A

-Weakness and wasting of small muscles of hand
-Loss of reflexes in upper limbs
-Loss of pain and temperature sensation cape-like (preserved of joint position and vibration sense)
-Signs may be asymmetrical

39
Q

Differentials for syringomyelia? (180)

A

Arnold-Chiari malformation
Tumour of central cord
Cervical spondylosis
Trauma

40
Q

Clinical signs MND?*

A

Combination of LMN and UMN with preserved sensation

41
Q

What is MND?*

A

Progressive disease of unknown aetiology
Axonal degeneration of U and LMN

Divided into 4 types:
-ALS (combined upper and lower)
-PLS (just UMN)
-Progressive spinal muscular atrophy (only LMN)
-Progressive bulbar palsy (LMN brainstem signs)

42
Q

Differentials for patient with pure motor involvement? (180)

A

Cervical myelopathy (UMN and LMN)
MG
Myopathies
Polymyositis/dermatomyositis
Spinal muscular atrophy
Lyme, HIV, syphilis

43
Q

How to investigate MND?*

A

-Clinical diagnosis
-EMG shows denervation (rules out NMJ or demyelination)
-MRI brain spinal cord to exclude lesions which may mimic

44
Q

Treatment of MND?*

A

-MDT (PT, OT, specialist nurses, dietician, SLT, palliative care)
-Supportive (PEG and NIPPV)
-Riluzole slows disease progression by 3 months but doesn’t improve function or QoL
-Baclofen (spasticity), anti-cholinergic (salivation)

45
Q

Signs of PD?*

A

-Hypomimia and reduced movements
-Coarse pill-rolling 2-5Kz tremor
-Bradykinesia
-Cogwheel rigidity
-Gait is shuffling and festinant, reduced arm swinging
-Speech hypophonic and monotonous

In addition do:
-L/S BP (MSA)
-Ataxia (MSA)
-Vertical eye movements (PSNP)
-Cognitive impairment (LBD, PSNP)
-Pulse and carotids (vascular Parkinsonism)
-Ask about medication history (secondary Parkinsonism)

46
Q

Causes of parkinsonism?*

A

-PD
-Parkinson’s plus (MSA, PSNP (both symmetrical), corticobasal degeneration (asymmetrical))
-Drug-induced (prochloperazine, metoclopramide, antipsychotics)
-Vascular (acute basal ganglia stroke or diffuse SVD)
-Lewy body dementia
-Wilson’s disease
-Post-encephalitis

47
Q

Pathology of PD?*

A

Degeneration of the dopaminergic neurones between substantia nigra and basal ganglia

48
Q

Investigations for PD? (180)

A

History (cognition, hallucinations, mood, sleep)

Clinical diagnosis
MRI brain (vascular changes)
DaT scan

49
Q

Treatment of PD?*

A

MDT (SN, PT, OT)

L-dopa with peripheral dopa-decarboxylase inhibitor e.g. co-beneldopa (nausea, later wearing off and peak-dose dyskinesias)

Dopamine agonists e.g. ropinirole sometimes used in younger patients (slightly less effective and higher risk of impulsivity)

More advance therapies (DBS, apomorphine infusions/rescue injections)

50
Q

How to deal with wearing off?*

A

-More frequent dosing
-MR preparations
-Drugs to reduce dopamine breakdown (COMT inhibitor and MAO inhibitor)

51
Q

Causes of tremor?*

A

Resting (Parkinsonism)

Action tremor:
Postural: BET, dystonic tremor, enhanced physiological
Kinetic: ipsilateral cerebellar lesion

52
Q

Sign’s of FA?*

A

-Bilateral cerebellar signs
-Combined UMN and LMN signs (leg wasting and absent reflexes due to peripheral neuropathy with upgoing plantars due to corticospinal tract degeneration)
-Posterior column signs (loss of joint vibration and proprioception)

Also:
-Kyphoscoliosis
-Optic atrophy
-High-arched palate
-SN deafness
-Murmur of HOCM
-Diabetes

53
Q

Tell me about FA?*

A

-Autosomal recessive
-Onset during teens
-Survival rarely exceeds 20 years from diagnosis
-Association between HOCM and dementia

54
Q

Oculomotor nerve palsy signs and cause?*

A

‘Down and out’ due to unopposed action of LR and SO; usually complete ptosis

Surgical causes often impinge on superficially located papillary fibres:
-PCA aneurysm
-Cavernous sinus thrombosis (4, 5, 6 may also be affected)
-Cerebral uncus herniation

Medical causes:
-Mononeuritis multiplex e.g. diabetes
-Midbrain infarction; Weber;s
-MS
-Migraine

55
Q

Horner’s pupil signs and causes?*

A

PEAS

Ptosis
Endopthalmos
Anhydrosis
Small pupil

Central causes:
Brain stem causes: MS, Wallenberg’s

Pre-ganglionic causes:
Neck: branchial plexus lesion, Pancoast’s tumour

Post-ganglionic:
Carotid artery dissection, cavernous sinus mass

56
Q

Holme’s Adie pupil signs and causes?*

A

Dilated pupil with poor response to light and sluggish response to accommodation

With absent or diminished ankle reflexes

Benign condition

57
Q

Argyll Robertson signs and cause?*

A

Small irregular pupil, which accommodate but doesn’t react to light

Atrophied and depigmented iris

Usually a manifestation of quaternary syphilis but can also be caused by DM

58
Q

Optic atrophy signs and causes?*

A

RAPD

-Glaucoma
-Retinitis pigmentosa
-Central retinal artery occlusion
-Frontal brain tumour (Foster-Kennedy)
-MS
-Friedrich’s ataxia
-Paget’s
-Tertiary syphilis

59
Q

Neurofibromatosis clinical signs?*

A

-2 or more cutaneous neurofibromas
-Cafe-au-lait 6 or more
-Axillary freckling
-Lisch nodules
-Hypertension
-Neuropathy with palpable nerves
-Optic glioma

60
Q

What do you know about neurofibromatosis?*

A

Autosomal dominant
Type 1 (chromosome 17) classical peripheral form
Type 2 (chromosome 22) bilateral acoustic neuromas and sensori-neural deafness

Associated with pheochromocytomas and RAS

Complications include epilepsy, sarcomatous change, scoliosis, mental retardation

61
Q

Tuberous sclerosis signs?*

A

-Angiofibromata
-Periungal fibromas
-Shagreen patch
-Ash leaf macules

Other associations:
-Cystic lung disease
-Polycystic kidneys or renal angiomyolipomata or RCC
-Retinal phakomas
-LD

62
Q

Tell me about TS?*

A

AD with variable penetrance
80% have epilepsy
Cognitive defects in 50%

Skull films: ‘railroad track’ calcification
CT head: tuberous masses
Echo and abdominal masses: hamartomas and renal cysts

63
Q

Myasthenia gravis signs?*

A

-Bilateral ptosis
-Complicated bilateral extra-ocular palsies
-Myasthenic snarl
-Nasal speech, poor swallow
-Proximal muscle weakness with fatiguability
-Sternotomy scars (thymectomy)
-FVC

N.B. Can either be generalised or ocular MG

64
Q

Differentials for fatigable weakness? (180)

A

MG
LEMS
Myopathies
Other causes of complex opthalmoplegia e.g. thyroid

65
Q

Associations with MG?*

A

DM
RA
Thyrotoxicosis
SLE
Thymomas

66
Q

Tests for MG?*

A

-Anti-AChR antibodies in 80%
-Anti-MuSK often positive if above negative
-EMG decrement with repetitive stimulation and ‘jitter’ is characteristic
-TFTs and ESR to rule out thyroid and inflammatory myopathy

-Also CT/MRI of the mediastinum (thymoma in 10%)
-TFTs (Grave’s in 5%)
-TPMT if likely to start IS

67
Q

Treatment of MG?*

A

-If purely ocular only need pyridostigmine
-Otherwise, need pyridostigmine plus IS (steroids titrate up +/- steroid sparing agent)
-If bulbar or severe limb weakness consider IVIg or PLEX
-Thymectomy
-Avoid medications e.g. aminoglycosides, quinolones, beta blockers

68
Q

LEMS?*

A

-Pelvic then pectoral weakness plus autonomic (dry mouth and sphincter) with ptosis later
-Diminished reflexes that become brisker after exercise
-70% paraneoplastic (SCC)

To investigate:
-VGCC antibodies and EMG (increment on repetitive stimulation)

Treatment:
-Treat cause (immunosuppress if no cancer)
-Potentiate synaptic transmission with 3,4-diaminopyridine for symptom control

69
Q

How to distinguish between UMN and LMN facial weakness?*

A

UMN weakness spares the forehead and eye closure
LMN involves the forehead and eye closure
Bell’s phenomenon: eyeball normally rolls up on attempted eye closure (visible if orbicularis oculi weakness)

70
Q

Bell’s palsy?*

A

-Rapid onset 1-2 days
-HSV-1 implicated
-Induced swelling and compression of the nerve within the facial canal causes demyelination and temporary conduction block
-Prednisolone within 72 hours onset plus aciclovir if severe
-Remember eye protection (artificial tears, tape eye closed at night)
-80% full recovery
-More common in pregnancy, and outcome may be worse

71
Q

Causes of bilateral LMN facial weakness?*

A

GBS (AIDP)
Rarer: sarcoidosis, MG, Lyme, syphilis

72
Q

Conductive versus SNHL? (180)

A

CHL:
Cerumen
Otitis externa/media
Chronic psoriasis
SCC
Eustachian tube dysfunction
Trauma to tympanic membrane
Otosclorosis

SNHL:
Maternal rubella or CMV
Childhood measles
Presbycusis
Ototoxic drugs
Meniere’s
NF2
SOL affecting CP angle
Demyelination

73
Q

Retinal pathology?*

A
74
Q

Chorea?

A

Acute:
-Stroke
-Hyperglycaemia

More chronic:
-Sydenham’s chorea (post-infective)
-SLE
-Huntington’s (trinucleotide repeat disorder, anticipation)

75
Q

Monocular blindness differentials? (180)

A

If absent red reflex:
-Corneal opacity e.g. trauma, corneal dystrophy
-Lens opacity

If vitreous opacity:
-Haemorrhage
-Inflammation
-Infection

If RAPD:
-Inflammatory demyelination
-CRAO
-Ischaemic optic neuropathy
-Retinal detachment
-Glaucoma
-SOL

76
Q

Investigations for monocular blindness? (180)

A

-Inflammatory markers (GCA)
-Imaging of the orbit
-VEP to evaluate optic nerve function

77
Q

Homonymous hemianopia differentials? (180)

A

Stroke
SOL

N.B. PITS

78
Q

Further investigation of HH? (180)

A

-CT/MRI head
-Blood tests including HbA1c and lipids
-Carotid doppler
-TTE and Holter

79
Q

Bitemporal hemianopia differentials? (180)

A

-Pituitary adenoma (galactorrhoea, acromegaly, Cushing’s)
-Craniopharyngioma

80
Q

CN6 differentials? (180)

A

-Microvascular occlusion (associated with DM, HTN)
-Raised ICP causing false localising sign
-6 (with 5, 7, 8) temporal bone
-6 (with 3, 4, opthalmic) cavernous sinus e.g. carotid aneurysm

81
Q

CN6 investigations? (180)

A

-Neuroimaging
-HbA1c
-Acetylcholine antibodies
-TFTs (thyroid eye disease and MG can mimic CN palsies)

82
Q

CN4 differentials? (180)

A

-Idiopathic
-Traumatic
-Microvascular occlusion (diabetes)
-Raised ICP causing false localising sign

83
Q

CN 5 7 8 differentials? (180)

A

Lesions affecting CP angle:
Usually an acoustic neuroma
Meningioma
Arachnoid cyst

84
Q

Bulbar palsy? (180)

A

MND
GBS
Syringobulbia
MG
Poliomyelitis

N.B. Due to diseases affecting nuclei of 9-12

Pseudobulbar is due to lesions affecting corticobulbar tracts

85
Q

Jugular foramen syndrome differentials? (180)

A

CN 9-11
Glomus jugulare tumour
Base of skull metastases
Lymphoma, TB, sarcoid

86
Q

Cervical myelopathy findings? (180)

A

Wasting of deltoids and biceps
Brisk triceps reflex and absent biceps and supinator
C5-C7 sensory loss
Pseudoathetosis

87
Q

Cervical myelopathy differentials? (180)

A

Cervical spondylosis
Tumour
Trauma

88
Q

Brachial neuritis findings? (180)

A

Pain
Peri-scapular wasting
Weakness (patchy involvement of muscles supplied by C5-C6)

89
Q

Present peripheral neuropathy, PD, CMT disease, abnormal gait, spastic paraparesis, cerebellar syndrome, myotonic dystrophy, MG, post-polio syndrome, acromegaly.

A

PACES (4 decks)

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