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FRACP Shuyu > Neurology > Flashcards

Neurology Flashcards

1
Q

Femoral nerve:

  1. Nerve Roots
  2. Motor function
  3. Reflex 4) Sensory
  4. Clinical causes of neuropathy
A
  1. Lumbar plexus L2-4
  2. Knee extension, hip flexion
  3. Knee jerk
  4. Anterior thigh and medial lower leg (saphenous nerve)
  5. Diabetes, femoral nerve block, pelvic fractures, THR, childbirth, psoas abscess, posterior abdoinal neoplasms
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2
Q

Multiple sclerosis is a disease primarily of the …

A

Oligodendrocytes

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3
Q

MS involves the attack of the following proteins..

A

Myelin basic protein and myelin oligodendrocyte glycoprotein (MBP and MOG)

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4
Q

Function of oligodendrocytes

A

Creates the myelin sheath in the CNS (Schwann cells are the myelin sheath in the PNS)

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5
Q

HLA associated with MS

A

HLA-DR15 (only 2-3x fold increase risk)

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6
Q

Internuclear opthalmoplegia to right clinical finding

A

If R) sided INO - R) eye cannot adduct and horizontal nystagmus to the right

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7
Q

transverse myelitis clinical features

A

Rapid onset of weakness, sensory alterations and or bowel,bladder dysfunction

Usually sensory level is detected

Initially flaccid then spastic weakness

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8
Q

transverse myelitis on MRI - signal change in which sequence?

A

T2 hyperintense signal change

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9
Q

transverse myelitis on LP

A

Pleocytosis +/- OCB

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10
Q

causes of transverse myelitis

A

post-infectious (50%) neuroinflammatory conditions (inc MS) autoimmune conditions

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11
Q

diagnosis of MS + updates in 2017 criteria

A

demonstrate CNS demyelination with dissemination in space and time updates in 2017 criteria: - demonstrating oligoclonal bands (CSF specific)

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12
Q

typical MS lesions

A

Juxtacorticaol lesions Dawson’s fingers Pontine lesions Spinal cord lesions GAD-enhancing lesions

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13
Q

clinically isolated syndrom

A

Objective evidence for a single attack typical for MS related demyelination Isolated to a single attack in time (not necessarily space) Risk of progression to MS

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14
Q

radiologically isolated syndrome

A

Incidental brain or spinal cord MRI findings that are highly suggestive of MS in an asymptomatic patient - no hx/sx of MS

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15
Q

Treatment in MS (disease modifying treatment) principles

A

Escalation vs induction therapy (Starting with less effective medication and progressing to more potent DMT vs starting with a potent DMT at the beginning) Some risk factors (e.g. disease burden on MRI and lots of enhancing lesions)

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16
Q

Natalizumab (Tysabri)

A

300mg IV monthly infusion Monoclonal antibody that binds to alpha4 subunit of 2 integrin adhesion molecules. Tries to prevent the extravasation of inflammatory cells through the BBB into the CNS Risk - PML

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17
Q

PML vs MS relapse

A

PML worsens over weeks where as MS relapse worsens over days

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18
Q

Diagnosis of PML

A

MRI and JCV PCR in CSF

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19
Q

How often to monitor JCV

A

Serum JCV every 6 months

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20
Q

Biggest risk factor for PML on Tysabri

A

Duration (over 2 years) Previous exposure to other immunosuppressants

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21
Q

PML imaging

A

See Rosenfeld lecture Sharply demarcated border at grey-white junction

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22
Q

Ocrelizumab

A

IV 300mg infusion twice 2 weeks apart then 600mg 6 months Humanised monoclonal antibody against CD20 (B cell action) Approved for RRMS and PPMS Adverse effects: infections, PML (see Rosenfeld lecture)

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23
Q

Cladribine

A

Tablet taken over 2 years - no evidence for further courses Mechanism: synthetic deoxyadenosine analogue - reduction in peripheral T and B lymphocytes and resting cells as well Adverse effect: signficant lymphopenia

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24
Q

Alemtuzumab

A

Probably most effective Binds CD52 - expressed on loymphocytes, natural killer cells, monocytes and dendritic cells Safety concerns - unveils autoimmune diseases - ITP, Autoimmune thyroid disease, Goodpasture’s syndrome; pancreatitis Needs monitoring for autoimmune sequelae for 4 years post treatment

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25
Q

Malignancy screening for MS DMTs

A

Population screening

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26
Q

Fingolimod

A

0.5mg daily Binds sphingosine-I-phosphate receptor causing it to be internalised from cell surface. Lymphocyte retention Adverse effects: macula degen - requires OCTs 3 monthly

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27
Q

Interferon beta

A

Decreases T cell activity Many adverse effects

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28
Q

Glatiramer acetate

A

Shifts population of T cells from Th1 T cells to Th2 T cells Alters macrophage function

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29
Q

Tecfidera

A

Oral tablet Mechanism is unclear Reports of PML

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30
Q

Teriflunomide

A

Oral tablet - active metabolite of lefluomide Inhibits proliferation of actively proliferation cells through inhibition of DHODH Teratogenic

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31
Q

MS in pregnancy

A

Encourage conception when stable Relapse declines during pregnancy but increases post partum Control disease activity prior conception

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32
Q

What MS meds are not recommended during pregnancy

A

fingolimod and tysabri (natalizumab) - both have high risk of rebound Teriflunomide (VERY TERATOGENIC) - need chelation and drug elimination prior contraception and also alemtuzumab (high risk of autoimmune thyroiditis)

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33
Q

NMO spectrum disorder clinical features + mechanism

A

Inflammatory demyelinating disease of the CNS AQP4 Ab in 80% AQP4 is a water channel protein located in the spinal cord grey matter, periaqueductal and periventricular regions and astrocytic foot processes Clinical features: longer segment transverse myelitis; relapsing; OCB in 30%

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34
Q

NMOSD treatment

A

Steroids, PLEX Steroid sparing agent considered

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35
Q

Anti-MOG disease

A

Diagnosis via antibodies Rosenfeld lecture

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36
Q

Approved for PPMS

A

ocrelizumab

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37
Q

intracranial haemorrhage with blood along floor of the anterior cranial fossa - suspicious for?

A

anterior communicating artery aneurysm

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38
Q

intracranial haemorrhage with blood around the Sylvia fissure - suspicious for?

A

MCA aneurysm

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39
Q

Low CBV on CT perfusion

A

Irreversibly damaged dead tissue

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40
Q

Delayed TTP

A

Collateral territory

41
Q

Risk of stroke in the first week after TIA (untreated)

A

10%

42
Q

when to have delayed MRI for investigation of intracerebral haemorrhage

A

~8 weeks

43
Q

Antithrombotics for minor stroke/TIA

A

DAPT for 3-4 weeks as per CHANCE/POINT trials unless atrial fibrillation

44
Q

When to do PFO closure in strokes

A

otherwise cryptogenic stroke age <60

45
Q

When to do left atrial appendage closure for AF

A

contraindication to anticoagulation

46
Q

Blood pressure management in ischaemic stroke

A

Acute: - Gently lower <185/105 if thrombolysis - Otherwise only treat if >220/120 Longer term: - Aim SBP <140 mmHg

47
Q

Symptomatic carotid stenosis 70-99%

A

carotid endarterectomy between 2 days and 2 weeks if not alr severely disabled

48
Q

Symptomatic carotid stenosis 50-70%

A

carotid endarterectomy if low surgical morbidity and good life expectancy

49
Q

Symptomatic carotid occlusion/trickle flow

A

low risk of recurrent stroke - generally not suitable for surgery

50
Q

Rate of ololingual angiooedema post tPA

A

2% (5% if taking ACEI)

51
Q

Age limits for thrombectomy

A

Age shouldn’t affect thrombectomy (Goyal Lancet 2016)

52
Q

IV thrombolysis in parallel with endovascular thrombesctomy?

A

Yes if eligible

53
Q

What criteria for extended timing for endovascular thrombectomy (6-24hr)

A

<70ml core (and other generic thrombectomy criteria)

54
Q

Perimesencephalic haemorrhage

A

SAH not associated with aneurysm + midbrain blood

55
Q

Reversible vasoconstriction syndrome clinical features

A

Month-6 weeks of episodic thunderclap headaches. Most have good prognosis and a very small proportion can have cerebral ischaemia and have neurological sequalae Treatment is expert opinion. Usually CCB

56
Q

Causes of lobar haemorrhages

A

Amyloid (elderly) AVM Pretty much anything else aside from HTN

57
Q

Mechanism of trigeminal neuralgia

A

Microvascular compression

58
Q

Clinical features of trigeminal neuralgia

A

Electric sudden pain, recurrent, often triggered by sensory stimulus in other affected area ephaptic transmission of sensory/compression input Can rarely be seen in patient in MS

59
Q

Treatment for trigeminal neuralgia

A

carbamazepine

60
Q

Characteristic of migraine aura

A

Starts off as central visual disturbance, then spreads and expands. The edge has a shimmering quality and zim zag (fortification spectra). Persists for ~20min. Key features is that it migrates. Generally preceds headaches

61
Q

Cause of migraine aura

A

Neuronal dysfunction - spreading depression of Leao

62
Q

New migraine mAb

A

CGRP inhibitor (Erenumab)

63
Q

MOA for tripans

A

5HT1B and 5HT1D agonist Those things are thought to inhibit the release of CGRP

64
Q

What CN is affected in IIH

A

CN VI due to its long and vertical course and predisposition to be compressed by the increased pressure (lateral visual palsy)

65
Q

Ventricle size in IIH

A

Small unlike NPH

66
Q

Acute management of cluster headache

A

High flow oxygen at least 8L/min Triptan - sumitriptan by subcut injection

67
Q

Long term management of cluster headache

A

Verapamil - start at 160mg, uptitrate up to 720mg+ (need ECGs) Can use prednisolone (75mg) as transitional therapy GON block

68
Q

Where does surface electrode for median nerve go

A

APB abductor pollicis brevis

69
Q

What are DML and PML in NCS

A

Distal motor latency and proximal motor latency

70
Q

Are amplitudes of sensory conduction responses bigger or motor responses

A

Motor because you are getting the response from the whole muscle rather than over a nerve directly

71
Q

Can you do a direct calculation of velocity from motor latencies or sensory latencies

A

Sensory because there’s no NM junction

72
Q

Are sensory or motor nerves first affected by a peripheral neuropathy

A

sensory and distal before proximal sural nerve often used

73
Q

Nerve compression pathology

A

focal demyelination localised slowing

74
Q

NCS finding of guillian barre/conduction block

A

decreased amplitudes across different segments

75
Q

What does very very slow conduction velocities suggest

A

Inherited demyelinations - e.g. charcot marie tooth

76
Q

Critical illness myopathy - why does it produce low amplitude on NCS

A

low amplitude due to decrease in muscle mass

77
Q

Normal EMG findings

A

No response at rest Gradual recruitment of individual muscle fibres Interference pattern when multiple muscle units are recruited

78
Q

Findings of deinnervation and reinnervation of EMG

A

Deinnervation = fibrillation and reinnervation - larger amplitude fibrillation happens first

79
Q

Findings of myopathy is EMG

A

No fibrillation (not generally), no spontaneous activity. Activity is low amplitude and brief Often polyphasic because the the muscle fibre is damaged and there is re-innervation between the muscle fibres

80
Q

What myopathies do you see fibrillation

A

When there is a lot of degeneration going on ICU myopathy, duchenne in active phase, active myositis, necrotising myositis

81
Q

EMG for Myasthenia gravis

A

Fast repetitive stimulation to see decremental response (Lambert eaton is incremental response)

82
Q

Single muscle EMG in myasthenia

A

lack of activation of the second fibre (blocking) as the acetylcholine becomes insufficient to reach the action potential required to active adjacent muscle fibres Another sign is “jitter” because there is an exaggerated difference in the response of the second recruited muscle

83
Q

Fasciculations meaning

A

single motor unit firing by itself happens in chronic deinnervation

84
Q

myokymia

A

post radiotherapy common in limbs due to spontaneous firing of individual fibres

85
Q

demyelination

A

increased latency and dispersion (Due to different degrees of demyelination in different nerves)

86
Q

painful neuropathy

A

generally small fibre B6 toxicity proximal/small fibre amyloid paraneoplastic HIV assoc cryoglobuliaemia

87
Q

B6 toxicity

A

painful neuropathy

88
Q

where is demyelination more common in GBS

A

proximal demyelination lesions so f waves are important in GBS

89
Q

anti GQ1 positive GBS variant

A

ataxia bulbar ophthalmoplegia

90
Q

diver bomb EMG

A

myotonia

91
Q

what is spared in MND

A

diplopia and micturition as the theory is that only monosynaptic pathways are involved

92
Q

split hand syndrome

A

in MND APB and 1st interosseous and more affected preserved ulnar side and hypothena muscles are not affected must thought it’s because the first 4 fingers have a greater representation in the hand

93
Q

brachioradialus weakness

A

listen to recordinf

94
Q

C7 radioculopathy signs

A

slight weakness in wrist and ifnger extension (grade 2/3) weakness of elbow extension overlap with radiopalsy typically lose triceps jerk sensation middle or sometimes index finger too

95
Q

inflammatory brachial plexopathy

A

very painful, restless pain preceeds weakness selects out individual peripheral/adjacent nerves commonest cause of a winged scapula also called neuralgic amyopathy

96
Q

differentiating between L5 nerve root injury and peroneal nerve injury

A

hip abduction - significant L5 component ankle jerk is present in peroneal but absent in tibial but the exam ans is tibialis posterior

97
Q

most common cause for foot drop post hip replacement

A

stretch of sciatic nerve the sciatic nerve has already divided into the peroneal and tibial branches

98
Q
A

FRACP Shuyu (65 decks)

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