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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
Malignancy screening for MS DMTs
Population screening
26
Fingolimod
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
27
Interferon beta
Decreases T cell activity Many adverse effects
28
Glatiramer acetate
Shifts population of T cells from Th1 T cells to Th2 T cells Alters macrophage function
29
Tecfidera
Oral tablet Mechanism is unclear Reports of PML
30
Teriflunomide
Oral tablet - active metabolite of lefluomide Inhibits proliferation of actively proliferation cells through inhibition of DHODH Teratogenic
31
MS in pregnancy
Encourage conception when stable Relapse declines during pregnancy but increases post partum Control disease activity prior conception
32
What MS meds are not recommended during pregnancy
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)
33
NMO spectrum disorder clinical features + mechanism
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%
34
NMOSD treatment
Steroids, PLEX Steroid sparing agent considered
35
Anti-MOG disease
Diagnosis via antibodies Rosenfeld lecture
36
Approved for PPMS
ocrelizumab
37
intracranial haemorrhage with blood along floor of the anterior cranial fossa - suspicious for?
anterior communicating artery aneurysm
38
intracranial haemorrhage with blood around the Sylvia fissure - suspicious for?
MCA aneurysm
39
Low CBV on CT perfusion
Irreversibly damaged dead tissue
40
Delayed TTP
Collateral territory
41
Risk of stroke in the first week after TIA (untreated)
10%
42
when to have delayed MRI for investigation of intracerebral haemorrhage
~8 weeks
43
Antithrombotics for minor stroke/TIA
DAPT for 3-4 weeks as per CHANCE/POINT trials unless atrial fibrillation
44
When to do PFO closure in strokes
otherwise cryptogenic stroke age \<60
45
When to do left atrial appendage closure for AF
contraindication to anticoagulation
46
Blood pressure management in ischaemic stroke
Acute: - Gently lower \<185/105 if thrombolysis - Otherwise only treat if \>220/120 Longer term: - Aim SBP \<140 mmHg
47
Symptomatic carotid stenosis 70-99%
carotid endarterectomy between 2 days and 2 weeks if not alr severely disabled
48
Symptomatic carotid stenosis 50-70%
carotid endarterectomy if low surgical morbidity and good life expectancy
49
Symptomatic carotid occlusion/trickle flow
low risk of recurrent stroke - generally not suitable for surgery
50
Rate of ololingual angiooedema post tPA
2% (5% if taking ACEI)
51
Age limits for thrombectomy
Age shouldn't affect thrombectomy (Goyal Lancet 2016)
52
IV thrombolysis in parallel with endovascular thrombesctomy?
Yes if eligible
53
What criteria for extended timing for endovascular thrombectomy (6-24hr)
\<70ml core (and other generic thrombectomy criteria)
54
Perimesencephalic haemorrhage
SAH not associated with aneurysm + midbrain blood
55
Reversible vasoconstriction syndrome clinical features
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
Causes of lobar haemorrhages
Amyloid (elderly) AVM Pretty much anything else aside from HTN
57
Mechanism of trigeminal neuralgia
Microvascular compression
58
Clinical features of trigeminal neuralgia
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
Treatment for trigeminal neuralgia
carbamazepine
60
Characteristic of migraine aura
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
Cause of migraine aura
Neuronal dysfunction - spreading depression of Leao
62
New migraine mAb
CGRP inhibitor (Erenumab)
63
MOA for tripans
5HT1B and 5HT1D agonist Those things are thought to inhibit the release of CGRP
64
What CN is affected in IIH
CN VI due to its long and vertical course and predisposition to be compressed by the increased pressure (lateral visual palsy)
65
Ventricle size in IIH
Small unlike NPH
66
Acute management of cluster headache
High flow oxygen at least 8L/min Triptan - sumitriptan by subcut injection
67
Long term management of cluster headache
Verapamil - start at 160mg, uptitrate up to 720mg+ (need ECGs) Can use prednisolone (75mg) as transitional therapy GON block
68
Where does surface electrode for median nerve go
APB abductor pollicis brevis
69
What are DML and PML in NCS
Distal motor latency and proximal motor latency
70
Are amplitudes of sensory conduction responses bigger or motor responses
Motor because you are getting the response from the whole muscle rather than over a nerve directly
71
Can you do a direct calculation of velocity from motor latencies or sensory latencies
Sensory because there's no NM junction
72
Are sensory or motor nerves first affected by a peripheral neuropathy
sensory and distal before proximal sural nerve often used
73
Nerve compression pathology
focal demyelination localised slowing
74
NCS finding of guillian barre/conduction block
decreased amplitudes across different segments
75
What does very very slow conduction velocities suggest
Inherited demyelinations - e.g. charcot marie tooth
76
Critical illness myopathy - why does it produce low amplitude on NCS
low amplitude due to decrease in muscle mass
77
Normal EMG findings
No response at rest Gradual recruitment of individual muscle fibres Interference pattern when multiple muscle units are recruited
78
Findings of deinnervation and reinnervation of EMG
Deinnervation = fibrillation and reinnervation - larger amplitude fibrillation happens first
79
Findings of myopathy is EMG
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
What myopathies do you see fibrillation
When there is a lot of degeneration going on ICU myopathy, duchenne in active phase, active myositis, necrotising myositis
81
EMG for Myasthenia gravis
Fast repetitive stimulation to see decremental response (Lambert eaton is incremental response)
82
Single muscle EMG in myasthenia
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
Fasciculations meaning
single motor unit firing by itself happens in chronic deinnervation
84
myokymia
post radiotherapy common in limbs due to spontaneous firing of individual fibres
85
demyelination
increased latency and dispersion (Due to different degrees of demyelination in different nerves)
86
painful neuropathy
generally small fibre B6 toxicity proximal/small fibre amyloid paraneoplastic HIV assoc cryoglobuliaemia
87
B6 toxicity
painful neuropathy
88
where is demyelination more common in GBS
proximal demyelination lesions so f waves are important in GBS
89
anti GQ1 positive GBS variant
ataxia bulbar ophthalmoplegia
90
diver bomb EMG
myotonia
91
what is spared in MND
diplopia and micturition as the theory is that only monosynaptic pathways are involved
92
split hand syndrome
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
brachioradialus weakness
listen to recordinf
94
C7 radioculopathy signs
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
inflammatory brachial plexopathy
very painful, restless pain preceeds weakness selects out individual peripheral/adjacent nerves commonest cause of a winged scapula also called neuralgic amyopathy
96
differentiating between L5 nerve root injury and peroneal nerve injury
hip abduction - significant L5 component ankle jerk is present in peroneal but absent in tibial but the exam ans is tibialis posterior
97
most common cause for foot drop post hip replacement
stretch of sciatic nerve the sciatic nerve has already divided into the peroneal and tibial branches
98

FRACP Shuyu (65 decks)

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