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FRACP Shuyu > Neurology Master > Flashcards

Neurology Master Flashcards

1
Q

Femoral nerve:

  1. Nerve Roots
  2. Motor function
  3. Reflex
  4. Sensory
  5. 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

Obturator nerve:

  1. Nerve Roots
  2. Motor function
  3. Reflex
  4. Sensory
  5. Clinical causes of neuropathy
A
  1. L 2-4
  2. Thigh adductors
  3. N/A
  4. Skin of medial thigh
  5. Damage during surgery involving the pelvis/abdomen; obturator nerve block
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3
Q

Sciatic nerve:

  1. Nerve Roots
  2. Motor function
  3. Sensory
  4. Reflexes
  5. Clinical causes of neuropathy
A
  1. L4 - S3
  2. Thigh extensors then divides into tibial and common fibular nerve
  3. No direct sensory functions but indirectly innervates skin of lateral leg, heel and both dorsal and plantar aspects of the foot
  4. Ankle
  5. Piriformis syndrome
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4
Q

Tibial Nerve:

  1. Nerve Roots
  2. Motor function
  3. Sensory
  4. Clinical causes of neuropathy
A
  1. L4 - S3
  2. Posterior compartment of the leg and majority of intrinsic foot muscles
    1. Unlocking knee
    2. Flexes toes and plantar flexes ankle
    3. Foot inversion
    4. Some knee flexion
  3. Posterolateral side of leg, lateral side of the foot and sole of the foot
  4. Tarsal tunnel syndrome due to OA, RA< trauma
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5
Q

Common peroneal nerve:

  1. Nerve Roots
  2. Motor function
  3. Sensory
  4. Clinical causes of neuropathy
A
  1. L4 - S2
  2. Lateral and anterior compartments of the leg
    1. Foot eversion
    2. Dorsiflexsion of the foot
    3. Toe extension
  3. Upper lateral and lower posterolateral leg. Also supplies (via branches) cutaneous innervation to the skin of the anterolateral leg, and the dorsum of the foot
  4. Fracture of the fibula/tight cast
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6
Q

Multiple sclerosis is a disease primarily affecting which cells?

A

Oligodendrocytes

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7
Q

MS involves the attack of the following proteins..

A

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

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8
Q

Internuclear opthalmoplegia to right clinical finding

A

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

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9
Q

transverse myelitis on MRI - signal change in which sequence?

A

T2 hyperintense signal change

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10
Q

what criteria (dissemination in space or time) can oligoclonal bands substitute for the diagnosis of MS?

A

dissemination in time

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11
Q

Typical MS lesions (5)

A
  1. Juxtacorticaol lesions
  2. Dawson’s fingers
  3. Pontine lesions
  4. Spinal cord lesions
  5. GAD-enhancing lesions
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12
Q

Natalizumab (Tysabri)

  1. Route
  2. MOA
  3. AE
A
  1. IV monthly
  2. 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
  3. PML
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13
Q

Alemtuzumab

  1. Route
  2. MOA
  3. AE
A
  1. IV daily for 5 days then in another 12 months
  2. Recombinant humanised monoclonal antibody that binds to CD52 antigen (present on the surface of most B and T lymphocytes)
  3. Infusion reactions, autoimmune disorders, infections, lymphopenia
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14
Q

Dimethyl fumarate

  1. Route
  2. MOA
  3. AE
A
  1. Oral
  2. Unknown
  3. Nausea, vomiting, diarrhoea, lymphopenia
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15
Q

Fingolimod

  1. Route
  2. MOA
  3. AE
A
  1. PO daily
  2. Sphingosine 1‑phosphate receptor modulator; reduces lymphocyte infiltration of the CNS by preventing lymphocytes leaving lymph nodes, thus reducing inflammation and demyelination
  3. Bradycardia, first degree AV block, infection, leukopenia, macula oedema, PRES, PML
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16
Q

Interferon beta

  1. Route
  2. MOA
  3. AE
A
  1. Subcut
  2. Antagonism of gamma interferon, reduction of cytokine release and augmentation of suppressor T cell function
  3. Rash, myalgia, headache, abdominal pain
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17
Q

Ocrelizumab

  1. Route
  2. MOA
  3. AE
A
  1. IV
  2. Recombinant humanised monoclonal antibody that selectively depletes CD20-positive B lymphocytes
  3. Infusion reactions (34% in clinical trials), infection, neutropenia

Approved for PBS for primary progressive MS

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18
Q

Teriflunomide

  1. Route
  2. MOA
  3. AE
A
  1. PO
  2. Inhibits pyrimidine synthesis in leucocytes by inhibiting activity of dihydro-orotate dehydrogenase (DHODH)
  3. Teratogenic and immunosuppressive
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19
Q

Cladrabine

  1. Route
  2. MOA
  3. AE
A
  1. PO
  2. Synthetic deoxyadenosine analogue - reduction in peripheral T and B lymphocytes and resting cells as well
  3. Significant lymphopenia
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20
Q

PML imaging findings

A

One or more hyperintense lesions on T2-weighted or FLAIR sequences with a sharp border at the grey-white junction and less distinct borders toward the white matter

  • Large >3cm lesions
  • Contrast enhancement in 41% with early PML
  • U-fibers (subcortical)
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21
Q

MS disease activity in pregnancy

A

Encourage conception when stable

Relapse declines during pregnancy but increases post partum

Control disease activity prior conception

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22
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

alemtuzumab (high risk of autoimmune thyroiditis)

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23
Q

Anti-MOG disease clinical features

A
  • Clinical features
    • Initial episode – optic neuritis, ADEM, transverse myelitis
    • Relapse – optic neuritis
  • Course
    • Monophasic or relapsing
  • OCB in <15% • MOG Ab in serum
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24
Q

anti-MOG MRI findings

A
  • ADEM like fluffy white matter, deep grey matter, brainstem
  • Optic nerve enhancement
  • Multiple spinal lesions; can be long or short segment
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25
Q

What DMARD is approved for primary progressive MS?

A

Ocrelizumab

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26
Q

Intracranial haemorrhage with blood around the Sylvia fissure - aneurysm location?

A

MCA aneurysm

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27
Q

Intracranial haemorrhage with blood along floor of the anterior cranial fossa - aneurysm location?

A

ACA aneurysm

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28
Q

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

A

10%

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29
Q

When are PFO closure in strokes indicated?

A

Otherwise cryptogenic stroke age <60

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30
Q

When to do left atrial appendage closure for AF

A

contraindication to anticoagulation

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31
Q

Blood pressure management in acute ischaemic stroke

A
  • Gently lower <185/105 if thrombolysis
  • Otherwise only treat if >220/120

Longer term: aim SBP <140 mmHg

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32
Q

Management of symptomatic cartoid stenosis:

  1. 70-99%
  2. 50-69%
  3. Occlusion/trickle
A
  1. Carotid endarterectomy between 2 days and 2 weeks if not alr severely disabled
  2. Carotid endarterectomy if low surgical morbidity and good life expectancy
  3. Low risk of recurrent stroke - generally not suitable for surgery
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33
Q

Rate of orolingual angiooedema post tPA

A

2% (5% if taking ACEI)

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34
Q

IV thrombolysis in parallel with endovascular thrombesctomy?

A

Yes if eligible

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35
Q

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

A

<70ml core (and other generic thrombectomy criteria)

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36
Q

Subarachnoid haemorrhage centred anteriorly to the pons and midbrain - diagnosis and investigations

A

Likely perimesencephalic subarachnoid hemorrhage

CTA only, does not need DSA if normal CTA as 95% of cases are non-aneurysmal

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37
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
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38
Q

Treatment of reversible vasoconstriction syndrome

A

Calcium channel blockers but mainly exert opinion

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39
Q

Mechanism of trigeminal neuralgia

A

Microvascular compression

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40
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

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41
Q

Treatment for trigeminal neuralgia

A

Carbamazepine

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42
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
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43
Q

Pathogenesis of migraine aura

A

Neuronal dysfunction - spreading depression of Leao

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44
Q

New monoclonal antibody available for migraines

A

CGRP inhibitor (Erenumab)

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45
Q

MOA for tripans

A
  • 5HT1B and 5HT1D agonist
  • Those things are thought to inhibit the release of CGRP
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46
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)

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47
Q

Ventricle size in IIH

A

Small unlike NPH

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48
Q

Pathophysiology of the trigeminal autonomic cephalagias

A

Incompletely understood..

Abnormality in the hypothalamus leading to hypothalamic activation with secondary activation of the trigeminal autonomic reflex, probably via a trigeminal-hypothalamic pathway

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49
Q

Which trigeminal autonomic cephalagias have a strong indomethacin effect?

A

Paroxysmal hemicrania and hemicrania continua

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50
Q

Acute management of cluster headache

A

High flow oxygen at least 8L/min

Triptan - sumitriptan by subcut injection

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51
Q

Long-term management of cluster headaches

A
  • Verapamil - start at 160mg, uptitrate up to 720mg+ (need ECGs)
  • Can use prednisolone (75mg) as transitional therapy
  • GON block
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52
Q

Where does surface electrode for median nerve go?

A

APB (abductor pollicis brevis)

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53
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

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54
Q

What is the pathology of nerve compression and what is the finding on NCS?

A

Focal demyelination localised slowing

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55
Q

NCS finding of guillian barre/conduction block

A

segmental nerve demyelination - decreased amplitudes across different segments

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56
Q

What does very very slow conduction velocities suggest?

A

Inherited demyelinations - e.g. charcot marie tooth

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57
Q

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

A

low amplitude due to decrease in muscle mass

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58
Q

Normal EMG findings

A
  • No response at rest
  • Gradual recruitment of individual muscle fibres
  • Interference pattern when multiple muscle units are recruited
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59
Q

Findings of deinnervation and reinnervation of EMG

A
  • Deinnervation = fibrillation
  • Reinnervation - larger amplitude

fibrillation happens first

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60
Q

EMG findings in myopathy

A
  • No fibrillation (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

The exception to fibrillation is conditions with a lot of degeneration (ICU myopathy, duchenne in active phase, active myositis, necrotising myositis)

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61
Q

EMG findings in myasthenia gravis

A

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

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62
Q

What is the pathology that causes fasciculations

A

single motor unit firing by itself happens in chronic deinnervation

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63
Q

What is myokymia and what is the pathology?

A

involuntary, spontaneous, localized quivering of a few muscles, or bundles within a muscle, but which are insufficient to move a joint

Commonly eyelid twitching

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

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64
Q

Findings of demyelination on NCS

A

Increased latency and dispersion - due to different degrees of demyelination in different nerves

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65
Q

Causes of a painful neuropathy

A

Generally small fibre

B6 toxicity proximal

small fibre amyloid paraneoplastic

HIV assoc cryoglobuliaemia

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66
Q

Where does demyelination most commonly occur in GBS (which part of a nerve)

A

Proximally so f waves are important in GBS

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67
Q

anti GQ1 positive GBS variant clinical syndrome

A

Miller Fischer variant - ataxia bulbar ophthalmoplegia

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68
Q

dive bomber EMG

A

myotonia

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69
Q

What is spared in MND

A

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

70
Q

What is the split hand syndrome and what condition is it found in?

A

Found in ALS

The thenar muscles 1st dorsal interosseous are more affected than the hypothenar. This is despite those muscles being innervated by the same spinal segments and ulnar nerve. The mechanism is thought to do with the portion of corticol representation of the first four digits.

71
Q

C5 radiculopathy vs axillary neuropathy

A

C5 has more functions:

Motor

  • Elbow flexion: biceps (C5, C6), brachioradialis (with the forearm in mid-pronation) (C5, C6)
  • Forearm supination: biceps (C5, C6)

Sensory

  • Lateral shoulder and upper arm, extending to lateral aspect of the elbow

Reflexes

  • Biceps
  • Brachioradialis
72
Q

C7 radiculopathy vs radial neuropathy

A

C7 has:

  • Forearm pronation (median nerve)

Radial neuropathy has:

  • Elbow extension (C5, 6)
  • Brachioradialis reflex

Sensory is dependent on the height of the radial neuropathy lesion.

Both do: elbow extension, wrist extension, write flexion, finger extension, thenar muscles; triceps reflex

73
Q

C8 radiculopathy vs ulnar neuropathy

A

C8:

  • LOAF muscles
    • Lateral 2 lumbricals
    • Opponens pollicis
    • Abductor pollicis brevis
    • Flexor pollicis brevis
  • Tricpes jerk
74
Q

Pathophysiology of neuralgic amytrophy

A

Inflammatory disorder of the brachial plexus

(Often amendable to steroids even though that would worsen the diabetes)

75
Q

Clinical presentation of neuralgic amyopathy

A
  • Severe pain shoulder girdle or lateral arm
  • Patchy weakness in the upper middle brachial plexus
  • Often involving winging of the scapula
  • Denervation on EMG
76
Q

L5 radiculopathy vs common peroneal neuropathy

A

L5:

  • Hip abduction
  • Foot inversion (but actually tibialis anterior does have a minor action) - but this is the exam answer!
77
Q

What anti-epileptic to avoid in mitochondrial epilepsy?

A

Valproate - will worsen epilepsy

78
Q

Are on EEG electrodes labelled?

A

right is even
left is odd
central is z

79
Q

Normal EEG findings

A
  • Posterior-dominant rhythm - 8.5 to 12 Hz alpha rhythm, maximal in the posterior part of the head
  • Attenuation with eye opening (alpha rhythm becomes lower voltage with eye opening and augments with eye closing)
80
Q

What sleep stage does sleep spindles and K-complexes appear?

A

Stage 2 sleep

81
Q

What is the Juvenile Myoclonic Epilepsy finding on EEG?

A

4Hz spike and wave

82
Q

When are triphasic waves seen on EEG?

A

hepatic encephalopathy
but also present in other forms of encephalopathy

83
Q

What are PLEDs in EEG?

A

Period lateralised epileptiform discharges

High of seizures

Often seen in HSV

84
Q

What are GPEDs in EEG?

A

Generalised periodic epileptiform discharges

Indicates a bad state of the brain e.g. severe hypoxic brain injury/other bad insults

85
Q

What anti-epileptics are P450 enzyme inducers? (6)

A

Phenytoin

Phenobarbitone

Primidone

Carbamazepine

Oxcarbazepine

Topiramate

86
Q

What anti-epileptic is a P450 inhibitor

A

Valproate

87
Q

What is the definition of drug-resistant epilepsy?

A

Uncontrolled seizures after failing 2 drugs at appropriate doses

88
Q

What is the effect of carbamazepine on bones?

A

Increases bone loss by increasing metabolism of vitamin D

89
Q

Perampanel

  1. MOA
  2. Metabolism
  3. AE
A
  1. Non-competitive AMPA-glutamate receptor antagonist
  2. Metabolised by liver
  3. Weight gain, falls, headache, fatigue
90
Q

Lacosamide

  1. MOA
  2. Metabolism
  3. AE
A
  1. Slow sodium channel blockers
  2. Renal excretion (requires supplementation after dialysis)
  3. Prolong PR, ataxia, vertigo, nausea

Good for focal status

91
Q

Clobazam

  1. MOA
  2. Metabolism
  3. AE
A
  1. Benzodiazepine that is different structually, a better antiepileptic and less sedating
  2. N/A
  3. Sedation, constipation, SJS/TENS

Used for drug-resistant focal epilepsy, sleep or clustering epilepsy

92
Q

Brivaracetam

  1. MOA
  2. Metabolism
  3. AE
A
  1. Binds to SV2A - inhibits release of neurotransmitters. Less AMPA activity compared with levetiracetam (hence less neuropsychiatric activity)
  2. Metabolism by the liver
  3. Similar to levetiracetam but less neuropsychiatric
93
Q

What part of cannabis is used for the treatment of epilepsy?

A

Cannabidoil (CBD)

THC part exacerbates seizures

94
Q

Carbamazepine:

  1. Indications
  2. Adverse effects
  3. MOA
A
  1. Good for focal seizures (PBS approved for first line therapy)
  2. Enzyme inducer, hypersensitivity in certain populations; drowsiness, dizziness, ataxia, decreased bone mineral density
  3. Voltage-ated sodium channel blocker
95
Q

Phenytoin:

  1. MOA
  2. AE
A
  1. Voltage-gated sodium channel
  2. Visual changes, gingival hyperplasia, decreased bone mineral density, cerebellar atrophy
96
Q

Valproate

  1. MOA
  2. AE
A
  1. Acts on sodium channels and has some calcium channel and some GABA synapse action
  2. Tremor, hepatotoxicity, weight gain, alopecia, PCOS, teratogenesis

Good for primary generalised epilepsies

97
Q

Topiramate

  1. MOA
  2. AE
A
  1. Dirty drug, some effects on sodium channels, Ca2+, GABA, GABA synape, glutamate receptors and is a weak carbonic anhydrase inhibitor
  2. Cognitive impairement, angle closure glaucoma
98
Q

risk of epilepsy to offsprings (generally)

A

5-8%

99
Q

targeted therapy for epilepsy in tuberous sclerosis

A

mTOR inhibitor therapy - everolimus

100
Q

HLA associated with carbamazepine in SJS

A

HLA-B*15:02

101
Q

What AEDs are bad for pregnancy

A

Valproate > phenobarbitol > topiramate > clonazepam > carbamazepine

102
Q

What AEDS need drug level monitoring inpregnancy?

A
  1. Lamotrigine
  2. Levetiracetam

Both have increasing clearance in pregnancy and usually require increase in levels

103
Q

What medication levels can be reduced by co-medication with OCP?

A

Lamotrigine (OCP remainds effective)

104
Q

WHat AEDs can reduce the efficacy of the OCP?

A

Carbamazepine, phenytoin, henobarcitol, oxcarbazepine, topiramate, felbamate, perampanel

105
Q

Unilateral spatial neglect and dressing apraxia stroke lesion

A

Non-dominant parietal lobe (MCA)

106
Q

Presentation of Brown-Sequard syndrome

A

Loss of ipsilateral motor/spastic hemoplegia

Loss of ipsilateral one sided fine touch and vibratory sensation loss

Opposite side pain and temperature (spinothalamic decussates straight away when entering the spinal cord)

107
Q

Genetic defect in Fredreich’s ataxia

A

Increased GAA repeats leading to the silencing of the frataxin gene.

Autosomal recessive.

Most common cause of hereditary ataxia

108
Q

Friedreich’s ataxia presentation

A

Limb and gait ataxia with cardiomyopathy

109
Q

Clinical presentation of subacute degeneration of the cord

A

Deficiency in vitamin B12 (cobalamin) leads to degeneration of the dorsal and lateral white matter of the spinal cord, producing a slowly progressive weakness, sensory ataxia, and paresthesias, and ultimately spasticity, paraplegia, and incontinence.

110
Q

What is the funciton of rubrospinal tract?

A

Skilled control of the distal musculature

111
Q

Features that indicates a poorer prognosis in Bell’s palsy?

A
  1. Severe complete paralysis
  2. Older age
  3. Hyeracusis (sensitivity to particular sounds)
  4. Altered taste
  5. EMG evidence of axonal degeneration
112
Q

Acalculia and finger agnosia lesion site

A

Dominant hemisphere parietal lobe

113
Q

Homonymous quadrantanopias - superior and inferior lesion location

A

Superior homonymous quandrantopias - temporal lobe

Inferior homonymous quadrantopias - parietal lobe

(PITS)

114
Q

Are EMGs or NCS more useful in motor neuron disease?

A

EMG because it is normally partial deinnervation with normal conduction

115
Q

Mechanism of action of Riluzole?

A

Sodium channel blocker that inhibits glutamate release.

Used in ALS

116
Q

What motor neuron disease has only upper motor neuron signs?

A

Primary lateral sclerosis

117
Q

Vigabatrin

  1. MOA
  2. AE
A
  1. Inhibits the breakdown of GABA
  2. Drowsiness, neuropsychiatric symptoms, weight gain, visual changes
118
Q

What aneurysm can cause a CN III palsy?

A

Posterior communicating artery aneurysm

119
Q

What is the most common symptom of excess levodopa?

A

Nausea and vomiting

120
Q

MOA and uses of entacapone

A

MOA: Inhibits catechol-O‑methyltransferase (COMT), mainly in peripheral tissues; increases the amount of levodopa available to the brain and prolongs the clinical response to levodopa

Used in conjunction with levodopa to reduces weaning off effects

121
Q

What dopamine antagonist (for nausea and vomiting) is most suitable for Parkinsons patients?

A

Domperidone - does not cross the CNS

122
Q

Pramipexole MOA

A

Dopamine agonist

123
Q

What antibiotic would reduce the therapeutic effect of sodium valproate?

A

Carbapenems

124
Q

Braak staging in Parkinson’s

A

The most common progression of abnormal proteins

Medulla -> midbrain -> cortex

Explains anosmia/REM sleep disturbance -> Parkinsonism -> Neuropsychiatric and cognitive

125
Q

Biggest risk factor for dementia in Parkinson’s disease

A

Age

126
Q

What is the best test to predictor cognitive disability in Parkinson’s disease

A

Intersecting pentagons - to detect visuospatial impairement

127
Q

MAO-B inhibitors

  1. Examples
  2. Side effects
A
  1. Rasagiline, selegeline
  2. Insomnia, low chance of serotinin syndrome (e.g. with SSRIs)
128
Q

Dopamine agonists

  1. Examples
  2. Side effects
A
  1. Pramipexole, rotigotine patches, apomorphine
  2. Impulse control disorder (20%), sleepiness, psychosis
129
Q

Major risk factors for onset of motor fluctuations in Parkinson’s disease

A

Age and disease duration (not levadopa exposure)

130
Q

1st line for depression in Parkinson’s

A

Dopamine agonist before SSRI/TCA

131
Q

How many cervical vertebrae and how many cervical roots?

Do cervical roots emerge above or below the vertebrae?

A

7 vertebrae and 8 roots

Cervical roots emerge above

132
Q

Does Lumbar/Thoracic nerve roots emerge above or below the vertebrae?

A

Below

133
Q

What syndrome does a L4/5 disc usual cause?

A

L5 because the L4 root exits very laterally.

However, if the disc protrusion was very lateral it could cause a L4 syndrome

134
Q

Where are the spinal tracts controlling the distal limbs movements and the axial proximal limb movements?

A

Distal: lateral corticospinal and rubrospinal tract (dorsal/lateral spinal cord)

Axial/proximal: vestibulospinal, ventral reticulospinal and tectopinal (ventral/lateral spinal cort)

135
Q

Distribution of weakness with extinsic cord compression compared with instrinsic?

A

Extrinsic affects sacral > lumbar > thoracic

Intrinsic is the opposite

136
Q

What is the most common cause of a syringomyelia?

A

Chiari malformation

137
Q

Presentation of Syringomyelia

A

the central cord lesion involved generslly the cervial/thoracic part and targets the decussating fibres of spinothalamic tract or entire cervical spinal cord

hence, there is disassociatve sensory loss (of only the pain and temperature fibres without vibration/proprioception most commonly in a cape like distribution.

138
Q

Subacute combined degeneration of the cord presentation

A

Normally dorsal columns affected but severe cases can involve the corticospinal tract

Cuased by B12, copper, vit E def; NO intoxication

139
Q

Most common cancer primary presenting with spinal metastases (not known to have cancer at the time of presentation)

A

Lung

140
Q

Most common symptom of spinal metastases

A

Leg weakness - 82%

Axial pain - 72%

141
Q

Most common sign of spinal metastases

A

Spinal tenderness (74%)

Sensory level (72%)

142
Q

UMN or LMN or both:

  1. Amyotrophic lateral sclerosis
  2. Primary lateral sclerosis
  3. Progressive muscular atrophy
A
  1. Both
  2. UMN
  3. LMN
143
Q

Best and worst types for prognosis of motor neuro disease

A

Best - primary lateral sclerosis

Worst - bulbar onset ALS

144
Q

Is axonopathy or demyelination more common?

A

Axonopathy (75%)

145
Q

Axonopathy vs demyelination

  1. Sensory vs motor
  2. Distal vs proximal
A

Axonopathy is sensory > motor; distal > proximal

Demyelination is motor > sensory; proximal > distal

146
Q

Treatment of CIDP

A
  1. Pred
  2. IVIG
  3. PLEX
  4. +/- azathioprine, cyclosporin, mycophenolate, ritux, cyclophosphamide
147
Q

How does multifocal motor neuropathy present?

A

Young adults with slowly progressive asymmetric distal weakness, wasting, fasciculations

Not UMN signs

148
Q

What antibody is associated with multifocal motor neuropathy

A

Anti-GM1 Ab in 60-80%

149
Q

What chemotherapy causes cold-induced parasthesias

A

oxalipatin induced neurotoxocity

150
Q

What chemotherapy agent can cause painful sensory axonal neuropathy

A

Bortezomib (proteasome inhibition)

151
Q

What are oligoclonal bands?

A

Evidence of CNS Ig synthesis

Present in half of MS cases at diagnosis

B-cell “oligo-clones”

152
Q

PML treatment options

A
  • Stop immunosuppressant
  • PLEX (but risk of IRIS and cerebral oedema)
  • Serotonin receptor blockers (e.g. mirtazepine)
153
Q

What chromosome is the amyloid precursor protein gene on?

A

Chromosome 21

154
Q

What are autosomal dominant genes for Alzhiemer’s dementia?

A

PSEN1, PSEN2, APP

155
Q

What is effective for prevention of Alzhiemer’s Disease?

A

Home based exercise +/- mediterranean diet

Hypertension

?Souvenaid (presented at conference)

Negative trials for oestrogens, statins, NSAIDs, gingko biloba, Vit E, omega-3 (fish oil)

156
Q

MOA of memantine

A

Non-competitive NMDA antagonist

157
Q

What pathology is the semantic variant of primary progressive aphasia associated with?

A

TDP-43+ inclusion

158
Q

What pathology is the non-fluent variant of primary progressive aphasia associated with?

A

Tau, amyloid deposits

159
Q

What is seen on the MRIs of semantic variants of frontal temporal dementia?

A

Left temporal lobe atrophy

160
Q

Findings on SPECT/PET for Lewy Body Dementia

A

Low dopamine transporter uptake in basal ganglia

161
Q

What is the clinical features of Gertsmann syndrome and what part of the brain is affected?

A

Angular gyrus in the posterior parietal lobe

Loss of ability to:

  1. Express thoughts in writing (agraphia, dysgraphia)
  2. Perform simple arithmetic problems (acalculia)
  3. Recognize or indicate one’s own or another’s fingers (finger agnosia)
  4. Distinguish between the right and left sides of one’s body
162
Q

What myopathies give a “distal arm/proximal leg weakness”

A

Inclusion body myositis, myotonic dystrophy

163
Q

What is the inheritance and the genetic defect in myotonic dystrophy 1?

A

Autosomal dominant with anticipation

Triplet repeat disorder in DMPK gene

164
Q

Myotonic dystrophy type 1 genetics

A

Myotonia

Weakness distal >proximal

Frontal balding

Cataracts

Intellectual impairement

Respiratory/swallowing difficulties

Cardiac conduction defects

165
Q

What is the difference in presentation between lipid storage myopathies and glycogen storage myopathies?

A

Lipid storage myopathies are precipitated by prolonged moderate exercise

Glycogen storage myopathies are precipitated by brief high intensity exercise

166
Q

MOA of pyridostigmine

A

Inhibits cholinesterases

167
Q

What antibody is associated with inclusion body myositis?

A

Anti-NT5c1A

168
Q

What antibody is associated with statin-associated autoimmuno myopathy?

A

Anti-HMGCR

169
Q

What antibody is associated with high cancer risk in dermatomyositis?

A

Anti-p155

170
Q

New drug for spinal muscular atrophy and MOA

A

Nusinersen

MOA:

  • Antisense oligonucleotide binds to mRNA in intro 7 and reduces deletion of exon 7 and increases n ormal SMN protein

Note also that gene therapy has shown great benefit in phase II trials

FRACP Shuyu (65 decks)

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