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General neurology Flashcards

1
Q

What % of those with ALS have FTD?

A

13%

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2
Q

What is the major genetic cause shared by ALS and FTD?

A

C9orf72

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3
Q

TDP-43 is found in which diseases?

A

FTD and ALS

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4
Q

What is Onuf’s nucleus responsible for?

A

Sphincter control

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5
Q

How do triptans work (in migraine)?

A

Activators of 5-HT receptors, 1B/1D/1F

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6
Q

What options are available for migraine prophylaxis?

A

Amitriptyline, nortriptyline, pizotifen, candesartan, propranolol, sodium valproate, topiramate, verapamil

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7
Q

Which nerves pass through the jugular foramen?

A

IX, X, XI

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8
Q

What passes through the cavernous sinus?

A

CN III, IV, V1, V2, VI

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9
Q

What causes autonomic dysreflexia?

A

Spinal cord injuries above T6.

  • HTN and bradycardia
  • Below T6 allows splanchnic innervation and therefore dilatation to bring down BP
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10
Q

What are the common side effects of phenytoin?

A

Gingival hyperplasia, hirsutism, rash, folic acid depletion, osteoporosis, cerebellar signs

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11
Q

What is the prognosis at diagnosis?

A

3-5 years

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12
Q

What does reinnervation look like on EMG?

A

High amplitude CMAPs

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13
Q

How is conduction block defined on Nerve Conduction Studies?

A

A reduction in CMAP area/amplitude of at least 20% compared with distal CMAP area/amplitude.
The duration of the proximal CMAP should not increase by >20% (see temporal dispersion)

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14
Q

Which antibody is multifocal motor neuropathy associated with?

A

anti-GM1

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15
Q

How is primary lateral sclerosis distinguishable?

A

Affects upper motor neurons only

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16
Q

How is progressive muscular atrophy distinguishable?

A

Affects lower motor neurons only

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17
Q

What are the 2 most commonly found mutations in ALS?

A

C9orf72 and SOD1

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18
Q

How is EPHA4 implicated in prognosis in ALS?

A

Lower EPHA4 = longer survival

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19
Q

Which exposure is the strongest risk factor for ALS?

A

Military service.

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20
Q

How does riluzole work in ALS?

A

Suppresses excessive motor neuronal firing

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21
Q

How does edaravone work in ALS?

A

Suppresses oxidative stress

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22
Q

What is the treatment for cluster headaches?

A

Acute: 100% O2, triptan
- Severe refractory => indomethacin or dihydroergotamine
Bridging: prednisone or occipital nerve block with methylpred
Prophylactic: Verapamil

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23
Q

What is the genetic mutation responsible for Wilson’s disease?

A

ATP7B mutation on chromosome 13 (autosomal recessive)

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24
Q

Which mutation is associated with the highest risk of multiple sclerosis?

A

HLA DRB1*1501

Other risk = *0801

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25
Q

What is first line treatment in primary progressive MS and what is its mechanism of action?

A

Ocrelizumab - fully humanised anti-CD20 that suppresses B cell

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26
Q

What does downbeating nystagmus represent?

A

Lesion in the foramen magnum

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27
Q

What does upbeating nystagmus represent?

A

Lesion in the midbrain or floor of the fourth ventricle

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28
Q

How do you distinguish between myositis and myopathy on EMG?

A

Spontaneous firing in myositis, but not myopathy

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29
Q

What are the causes of predominantly sensory neuropathy?

A 
Diabetes
B12 deficiency
Uraemia
HIV
Malignancy
Sjogren's
Hereditary sensory and autonomic neuropathy
Amyloid
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30
Q

What are the causes of predominantly motor neuropathy?

A 
AIDP
Acute motor axonal neuropathy
Hereditary motor and sensory neuropathy
Lead
Porphyria
Multifocal motor neuropathy
Diphtheria
Diabetic
Amyloid
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31
Q

Painful neuropathy

A 
EtOH
Diabetes
Cryoglobulinaemia
HIV
Paraneoplastic
GBS
B6 toxicity
Amyloid
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32
Q

Which antibodies may be positive in GBS?

A

GM1, GM2 and GD1

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33
Q

What is the triad found in Miller-Fisher and what is the antibody associated with it?

A

Ataxia, ophthalmoplegia and areflexia

Anti-GQ1

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34
Q

What does CSF show in GBS and CIDP?

A

Albuminocytologic dissociation - high protein / low cells

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35
Q

What is the treatment for GBS?

A

IVIG or plasma exchange

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36
Q

What are the treatment options for CIDP?

A

Steroids
IVIG or plasma exchange
Steroid-sparing agents: AZA or MMF (faster action)

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37
Q

In which variant of CIDP is asymmetry classic?

A

MADSAM

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38
Q

What is POEMS? Which serum level is diagnostic?

A 
Polyneuropathy
Organomegaly
Endocrinopathy
Monoclonal protein
Skin changes

VEGF level is doagnostic

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39
Q

What pedal changes would be seen in Charcot-Marie-Tooth disease?

A

Pes cavus

Hammer toes

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40
Q

What is the mutation responsible for hereditary sensitivity to pressure palsies (HSPP)?

A

PMP22

- Prolonged distal motor latencies

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41
Q

What does nerve biopsy show in Charcot-Marie-Tooth disease?

A

Onion bulbs

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42
Q

Where is a biopsy taken form for diagnosis of amyloidosis? What does it show?

A

Fat pad

Apple-green birefringence on congo red stain

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43
Q

What are the treatment options for diabetic neuropathy?

A

1 Amitriptyline,

2 duloxetine or pregabalin or gabapentin

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44
Q

What are the features of Morvan Syndrome and which antibody is implicated?

A

Features:

  • Fasciculations
  • Paraesthesia
  • Thymoma
  • Encephalophathy
  • Neuromyotonia

Antibody:
- Caspr-2 => directed at Voltage-gated K channels

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45
Q

Which antibodies are implicated in 60% of cases of stiff person syndrome?

A

Anti-GAD

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46
Q

What antibodies are associated with myasthenia gravis?

A 
ACh receptor Ab 
- 80-90% sensitive
MuSK Ab 
- positive in 40% of AChR-negative patients. 
- more severe weakness, not affecting eyes or limbs
- not associated with thymic disease.
LRP4 Ab 
- mild-moderate disease
- not associated with thymic disease.
Anti-striated muscle Ab 
- positive in 90% of thymomas
Ryanodine receptor Ab 
- positive in 70% of thymomas with MG
- marker for severe disease
Titin Ab (in addition to ACh R Ab) 
- thymoma and late-onset MG
Agrin Ab
- poor sensitivity but specific for MG
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47
Q

What should be specifically checked for on examination in myasthenia gravis?

A
  • Sustained upward gaze - weakness of eyelid elevators and oculomotor muscles
  • Peek sign - eyelids separate after 30sec of closing, and sclera is visible.
  • Dysarthria - palate weakness
  • Dysphonia on counting - bulbar weakness
  • Smiling causes snarling expression
  • Neck flexion weakness
  • Flap 1 arm then test muscle strength together - asymmetrical due to fatigue of one arm
  • Improvement of ptosis with ice cube application
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48
Q

What does EMG show in myaesthenia gravis?

A

Repetitive stimulation shows progressive decrease in amplitude of action potentials
Needle examination - motor unit potential variation and, sometimes, fibrillation potentials and myopathic changes
Single-fibre EMG - increased jitter (variable interpotential interval). 80% sensitive.

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49
Q

What other investigations should be performed in myaesthenia gravis?

A

Thymoma search - CXR, chest CT or MRI

Respiratory function tests - weakness in muscles of respiration

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50
Q

What is myasthenic crisis and how is it treated?

A

Crisis involves respiratory weakness causing respiratory failure. Often caused by an infection.

Treatment: Antibacterial
IVIG or plasma exchange

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51
Q

What is first line treatment for myaesthenia gravis?

A

Acetylcholinesterases - pyridostigmine

K supplements and K-sparing diuretics may improve symptoms but are rarely used

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52
Q

What if acetylcholinesterase inhibitors fail in myaesthenia gravis?

A

Steroids - may worsen symptoms and therefore should be monitored closely during initiation.
Immunosuppressants next line - azathioprine may be used as steroid-sparing agent, however should never be used as monotherapy.
Rituximab in desperate cases

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53
Q

What % of myasthenia gravis have isolated ocular signs?

A

15%

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54
Q

Which antibodies are implicated in isolated ocular myasthenia gravis?

A

Acetylcholine and LRP4 (not MuSK)

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55
Q

What autoimmune diseases are often associated with myasthenia gravis?

A 
Thyroiditis (most commonly)
SLE and RA
Polymyositis
NMO
ALS
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56
Q

Kv1.4, ryanodine and titin antibodies in myasthenia gravis are associated with which coexisting cardiac condition?

A

Myocarditis

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57
Q

What is the most effective cholinesterase inhibitor used in myasthenia gravis?
Which subpopulation is it less effective in?

A

Pyridostigmine

Less effective in MuSK positive patients

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58
Q

What is second line Rx for myasthenia gravis?

Third? Fourth?

A

2nd - Prednisone + AZA
3rd - Mycophenolate (mild) or rituximab (moderate)
4th - Methotrexate, cyclosporin, tacrolimus

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59
Q

How is myasthenic crisis treated?

A

IVIG or plasmapheresis

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60
Q

Which myasthenia patients should have a thymectomy?

A

Recommended in:

  • Those with thymomas
  • Early-onset myasthenia gravis
  • Generalised myasthenia gravis and ACh receptor Abs. 70% of these show improvement after thymectomy.
  • Seronegative MG with generalised disease and biomarkers similar to early-onset MG

Not recommended in:

  • MuSK or LRP4 Ab positive
  • Ocular MG
  • Seronegative MG
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61
Q

Which medications may precipitate a myasthenic crisis?

A 
Aminoglycosides
Tetracyclines
Fluoroquinolones
Macrolides
Muscle relaxants
Beta blockers
Calcium channel blockers
Botox
Iodine
Penicillamine
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62
Q

What side effects are associated with pyridostigmine?

A

Abdominal cramps, diarrhoea

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63
Q

Which features of Lambert-Eaton Myasthenic Syndrome distinguish it from myasthenia gravis?

A
  • No ophthalmoparesis, facial weakness or bulbar involvement
  • Poor response to cholinesterase inhibitors
  • Autonomic symptoms
  • Reduced deep tendon reflexes
  • Increase in size of CMAP on repetitive nerve stimulation
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64
Q

Anti-Hu antibodies are associated most strongly with which cancer?
What paraneoplastic syndromes are they associated with?

A
  • Lung cancer (mostly small cell)
  • Encephalomyelitis, limbic encephalitis, brain stem encephalitis, cerebellar degeneration, multi-segmental myelitis, sensory neuronopathy, sensorimotor neuronopathy, autonomic neuronopathy
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65
Q

Anti-Yo antibodies are associated with which cancers?

Which paraneoplastic syndrome are they associated with?

A
  • Ovarian and breast

- Subacute cerebellar degeneration

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66
Q

Anti-CRMP5 antibodies are associated with which cancers?

A
  • Small cell lung cancer, thymoma
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67
Q

Anti-Ma2 antibodies are associated with which cancers?

A
  • Testicular cancer
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68
Q

Anti-Ri antibodies are associated with which cancers? Which syndrome is most associated with it?

A
  • Breast, ovarian, SCLC

- Associated with opsoclonus-myoclonus syndrome

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69
Q

Anti-amphiphysin antibodies are associated with which cancers?
Which paraneoplastic syndrome are they associated with?

A
  • Breast, SCLC

- Limbic encephalitis, stiff person syndrome

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70
Q

Lhermitte’s sign is suggestive of a lesion in which part of the nervous system?

A

Dorsal columns of C-spine or caudal medulla

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71
Q

Which antibodies in neuromyelitis optica are associated moreso with optic neuritis than myelitis?

A

MOG antibodies

- Also found in ADEM

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72
Q

What is the order of progression in multiple sclerosis medications?

A
  1. Glatiramer acetate, beta-interferon
  2. Daclizumab, teriflunomide
  3. Fingolimod, dimethyl fumarate
  4. Natalizumab, alemtuzumab
  5. Autologous HSCT
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73
Q

What is the mechanism of action of fingolimod?

A
  • S1P receptor agonist. Causes

- Prevention of lymphocytes from migrating out of lymph nodes

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74
Q

What side effects are associated with alemtuzumab?

A

Autoimmune thyroid disease
Immune thrombotic thrombocytopenia
Membranous GN and anti-GBM disease

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75
Q

What does CADASIL stand for and what is the mutation responsible for it?

A

CADASIL = Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leucoencephalopathy

Notch 3 mutation - chromosome 19q12

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76
Q

Which 2 areas of the brain are classically involved in CADASIL?

A

Anterior temporal lobes

External capsule

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77
Q

What is the mechanism of action of glatiramer?

A
  • Competition with myelin antigens for binding to T cells

- Induction of Th2 suppressor cells that downregulate inflammation

78
Q

What is the mechanism of action of alemtuzumab?

A

CD52 mAb - stimulates antigen dependent cell-mediated cytotoxicity

79
Q

What side effects of dimethyl fumarate should be monitored for?

A

Lymphopenia

LFT derangement

80
Q

What side effects are associated with fingolimod?

A

Herpes infections
Macular oedema
Bradycardia

81
Q

What are the 3 main clinical presentations associated with neuromyelitis optica? What are 3 less common presentations?

A

Most common:

  • Optic neuritis
  • Longitudinally extensive transverse myelitis
  • Area postrema syndrome (nausea/vomiting/hiccups)

Less common:

  • Other brainstem lesion
  • Narcolepsy or diencephalic syndrome with MRI lesion
  • Symptomatic cerebral syndrome with MRI lesion
82
Q

What is the treatment for neuromyelitis optica?

A

Plasma exchange

83
Q

What does dimethyl fumarate act on to down-regulate inflammation?

84
Q

How does teriflunomide act?

A

Inhibition of DHODH, which is necessary for pyimidine synthesis in prolferating lymphocytes.

85
Q

What are the risk factors for Sudden Unexplained Death in EPilepsy (SUDEP)?

A 
Multiple antiepileptics
Nocturnal seizures
Long duration of therapy
Early onset epilepsy
Male
86
Q

What is the approximate incidence of SUDEP in epileptic adults?

87
Q

What is the most common genetic generalised epilepsy?

What are the typical features of it?

A

Juvenile myoclonic epilepsy

  • Typical absence seizures, usually precede myoclonic jerks by 1-9 years
  • Myoclonic jerks on wakening
  • Generalised tonic clonic seizures develop months to years after myoclonic jerks
  • Very sensitive to EtOH and sleep deprivation
  • Autosomal dominant
88
Q

What is first line treatment for juvenile myoclonic epilepsy?

A

Sodium valproate

89
Q

What is the most commonly affected area in temporal lobe epilepsy?

A

Mesial temporal lobe (hippocampus) - 65%

90
Q

During which period of sleep do sleep-related hypermotor epileptic seizures usually occur?

91
Q

What is the classic finding in GLUT1 deficiency and how is it treated?

A

Low CSF glucose

Treat with ketogenic diet

92
Q

What is the classic finding in GLUT 2 deficiency?

A

Paroxysmal exercise-induced dystonia

93
Q

Which 2 HLA genes are associated with Stevens Johnson Syndrome?

A

HLA-B*1502: Taiwan

HLA-A*3101: Europeans and Japanese

94
Q

Which form of epilepsy is anti-GAD antibody associated with?

A

Temporal lobe epilepsy

95
Q

What does levetiracetam bind to?

A

Presynaptic SVA2

96
Q

Where do gabapentin and pregabalin act on?

A

Post-synaptic calcium channels

97
Q

What are the 2 sites of action of lacosamide?

A

CRMP-2 pathway (pre-synaptic)

Na channel inactivation (pre-synaptic)

98
Q

What is the primary site of lamotrigine?

A

Na channels

99
Q

Which antiepileptic is 1st line in absence seizures?

A

Ethosuxamide

100
Q

What % of patients become seizure-free after their first antiepileptic agent?

101
Q

What happens in coadministration of COCP and lamotrigine?

A

Lamotrigine metabolism increased by COCP - dose must be increased

102
Q

What is the main teratogenic risk involved with sodium valproate and carbamazepine?

A

Spina bifida

103
Q

What side effects are associated with sodium valproate?

A 
Weight gain
Drowsiness
Alopecia
Liver dysfunction
Tremor
PCOS
104
Q

What side effects are associated with carbamazepine?

A

SIADH
Drowsiness
OP

105
Q

What side effects are associated with phenytoin?

A 
Gum hypertrophy
Coarsening of facial features
Hirsutism
OP
Cerebellar atrophy
106
Q

What side effects are associated with topiramate?

A

Weight loss
Renal calculi
Word-finding difficulties
Suicidality

107
Q

What is the most effective treatment in mesial temporal lobe epilepsy?

A

Temporal lobectomy

108
Q

What are the first line antidepressants for epileptics?

A

Citalopram and sertraline

109
Q

What are the 2 main genetic forms of Parkinson’s Disease?

A

Parkin, DJ-1 (recessive) also PINK1

Lrrk2, SNCA (Dominant)

110
Q

Name the 3 main synucleinopathies?

A

Parkinson’s Disease
Lewy Body Dementia
Multiple System Atrophy

111
Q

What is the main part of the brain affected in Parkinson’s Disease?

A

Substantia nigra pars compacta

112
Q

Which receptors do pramiprexole and ropinirole act on?

113
Q

Which receptor does rotigotine act on?

Which population are they useful in?

A

D2

Useful in dysphagia

114
Q

What are the ergot-derived dopamine agonists and which receptors do they act on?

A

Cabergoline, pergolide

D1/2

115
Q

What are the MAO-B inhibitors used in Parkinson’s Disease?

A

Rasagiline and selegiline

- Reserved for late disease

116
Q

What is the mechanism of action of apomorphine?

A

D2 receptor agonist

117
Q

What is amantadine used for?

A

Dyskinesias in Parkinson’s Disease

118
Q

Which part of the brain is deep brain stimulation targeted at?

A

Subthalamic nucleus

Globus pallidus internus

119
Q

Which antipsychotic has evidence supporting treatment of psychosis in Parkinson’s Disease?

A

Clozapine

Trial reduction in anti-PD meds first

120
Q

What is the first line treatment for depression in Parkinson’s Disease?

A

Nortriptyline

121
Q

What are the approved treatments for dementia in Parkinson’s Disease?

A

Rivastigmine

Donepezil may be useful for hallucinations and cognitive impairment

122
Q

What are the treatment options for REM sleep behaviour disorder?

A

Clonazepam

Amitriptyline

123
Q

How do Parkinsonian tremor and essential tremor differ from each other?

A

PD - Rest tremor, 5Hz, asymmetrical

Essential tremor - Postural tremor, 10Hz, symmetrical

124
Q

What is the putaminal slit sign specific for?

A

MSA Parkinsonian type

125
Q

What is the classic pontine finding in multiple system atrophy - cerebellar type?

A

Hot cross bun type

126
Q

How does midodrine act?

A

apha-1 agonism

127
Q

What is the mechanism of action of mirabegron?

A

Beta3 agonism

128
Q

What is a side effect of levodopa in MSA?

A

Exacerbation of orthostatic hypotension

129
Q

What is the first eye movement to be affected in Progressive Supranuclear Palsy?

A

Downward gaze

130
Q

What is the MRI brain classic finding in PSP?

A

Hummingbird sign - midbrain atrophy

131
Q

What are the treatment options in PSP?

A

Levodopa and amantadine

132
Q

Which Parkinsonian condition demonstrates myoclonus and limb apraxia?

A

Corticobasal degeneration

133
Q

Which of the Parkinsonian syndromes has the worst median survival from diagnosis?

A

Corticobasal degeneration

134
Q

What can be used to treat dystonias in corticobasal degeneration?

A

Botox if painful

135
Q

What is the genetic mutation responsible for Huntington’s disease?
When does it become symptomatic?

A

CAG triplet repeat disorder of the huntingtin gene on chromosome 4.
Symptomatic at >37 repeats

136
Q

Which neurons are affected in Huntingtin’s Disease?

A

GABAergic neurons

137
Q

Which part of the brain may show atrophy in Huntington’s Disease?

138
Q

What is the treatment for tardive dyskinesia?

A

Tetrabenazine, benztropine

139
Q

Which brain structure is damaged in hemibalism?

A

Subthalamic nucleus

140
Q

How does Brown-Sequard syndrome present and what is it caused by?

A
  • Ipsilateral paralysis
  • Ipsilateral vibration, proprioception and light touch discrimination
  • Contralateral pain and temperature

Caused by cord hemisection.

141
Q

What is the genetic mutation responsible for Wilson’s Disease? What is its mode of inheritance?

A

ATP7B

Autosomal recessive

142
Q

How is Wilson’s Disease diagnosed?

A

Low caeruloplasmin
High urinary copper
Kayser-Fleischer rings
High copper levels on liver biopsy

143
Q

What are the treatment options in Wilson’s Disease?

A

Penicillamine
Trientene if intolerant of penicillamine
Levodopa

144
Q

What is the genetic mutation responsible for Fragile X-associated tremor/ataxia syndrome (FXTAS)? What is the mode of inheritance?

A

CGG triplet repeat 55-200 in FMR1 gene

X-linked dominant

145
Q

What is the classic MRI sign found in FXTAS?

A

Middle cerebellar peduncle sign

146
Q

Name 3 dopamine receptor agonists approved for restless legs syndrome

A

Pramipexole, ropinirole, rotigotine

147
Q

Name 5 causes of restless legs syndrome

A 
Iron deficiency
ESRF
Pregnancy
Drug induced - metoclopramide
Multiple sclerosis
Neuropathy
148
Q

What ar the windows for IV thrombolysis and IA thrombectomy?

A

thrombolysis - 4.5 hours

thrombectomy - 6 hours

149
Q

What is the mechanism of action of idaracizumab?

A

Monoclonal antibody that competitively inhibits dabigatran (competes with FIIa)

150
Q

In cervical artery dissection, is anticoagulation or antiplatelet therapy more effective?

A

No difference

151
Q

What is the prefered class of antihypertensives in ischaemic stroke?

A
  • Calcium channel blockers

- Beta blockers may increase risk of ischaemic stroke, however are indicated in concurrent ischaemic heart disease

152
Q

When should patients be mobilised after an ischaemic stroke?

A

After 24 hours

153
Q

What is the mechanism of action of evolocumab?

A
  • PCSK9 inhibitor - increases hepatocyte LDL receptors available to degrade LDL
  • PCSK9 degrades LDL receptors
154
Q

How does amyloid angiopathy present and in which population?

A

Lobar, juxta-cortical haemorrhages in the elderly

155
Q

Where do hypertensive intracerebral haemorrhages tend to present?

A

Putamen, thalamus, pons

156
Q

Which levels of the Modified Rankin Scale qualify for thrombolysis?

157
Q

Which medication should be used for DVT prophylaxis post-ischaemic stroke?

A

Enoxaparin (more effective than heparin in this population)

158
Q

Which patiets with an ischaemic stroke would benefit from hemicraniectomy?

A

Large ischaemic MCA stroke and age<60

159
Q

When should a NOAC be commenced post-stroke in non-valvular AF?

A

small stroke - day 3
moderate stroke - day 6
large stroke - day 12

160
Q

When is TIA or stroke recurrence highest?

A

3 weeks to 3 months

161
Q

What consitutes valvular atrial fibrillation

A

AF with the absence of mitral stenosis or mechanical heart valve

162
Q

Which patients should have carotid endarterectomies and within what time frame?

A
  • Treat SYMPTOMATIC carotid artery stenosis 70-99%.

- Carotid endarterectomy within 2 weeks of event

163
Q

When should patent foramen ovale be closed?

A
  1. PFO + atrial septal aneurysm + large shunt

2. Young patient with ambolic ischaemic stroke and no other cause identified for stroke

164
Q

How does the OCP affect stroke risk?

A

Elevated risk with oestrogen but not progesterone

165
Q

What are the 4 clinical features associated with Creutzfeldt-Jakob Disease?

A

Myoclonus
Visual or cerebellar disturbance
Pyramidal/extrapyramidal disturbance
Akinetic mutism

166
Q

Which tumour are NMDA receptor antibodies associated with?

167
Q

What should be tested for in hypokalaemic periodic paralysis?

A

Thyrotoxicosis

168
Q

Alexia without agraphia is specific for which arterial territory?

A

Dominant PCA

169
Q

What are the 4 types of Creutzfeldt-Jakob Disease?

A

Sporadic - most common (85%)
Iatrogenic - from dural grafts, etc
Variant - from bovine spongiform encephalopathy
Familial

170
Q

What is the classic MRI finding in CJD?

A

FLAIR and DWI: Cortical ribboning and basal ganglia hyperintensity

171
Q

What is necessary to diagnose CJD?

A
  • Brain biopsy showing PrPsc

- PRNP gene testing must be performed to exclude familial CJD

172
Q

What might CSF show in CJD?

A
  • Pleocytosis (lymphocytes)
  • Elevated protein
  • 14-3-3 protein
173
Q

Which muscles are affected in a deep peroneal nerve palsy? Which sensory distribution?

A

Muscles:

  • Tibialis anterior: ankle dorsiflexion, foot eversion
  • Extensor hallucis: big toe extension
  • Extensor digitorum longus: lateral 4 toes extension
  • Extensor digitorum brevis: big toe and medial 3 toes extension

Sensory: first dorsal webspace

174
Q

How can an L5 nerve palsy be distinguished from common peroneal nerve palsy?

A

L5: Foot inversion and hip abduction affected, unlike peroneal nerve

175
Q

How might CSF help distinguish between multiple sclerosis and neuromyelitis optica?

A

MS: oligoclonal bands
NMO: NO oligoclonal bands

176
Q

What is the treatment for neuromyelitis optica?

A

Rituximab and MMF

177
Q

A lesion in which vascular territory is responsible for the syndrome of alexia without agraphia?

A

Dominant PCA

178
Q

What is the mechanism of action of pimavanserin and what is it used for?

A

Inverse agonist of 5-HT2A receptor.

Used for psychosis in Parkinson’s Disease.

179
Q

What are the first and second line treatments for trigeminal neuralgia?

A
  1. Carbamazepine

2. Oxcarbazepine

180
Q

What are the first and second line treatments for greater occipital neuralgia?

A
  1. Occipital nerve block

2. Gabapentin or pregabalin

181
Q

Which nerves are most likely to be affected by a cerebellopontine angle tumour?

A

V, VII, VIII

182
Q

Which muscle flexes the distal interphalangeal joints in the fingers?

A

Flexor digitorum profundus

183
Q

What is the mechanism of action of benztropine in Parkinson’s Disease?

A

Atypical competitive inhibitor of dopamine reuptake

184
Q

How can central retinal artery occlusion and central retinal vein occlusion be differentiated on fundoscopy?

A

CRAO

  • Grossly swollen and pale retina
  • Prominent fovea (cherry red spot)

CVRO
- Disc is massively swollen with splotches of haemorrhage and cotton wool spots

185
Q

How does an ophthalmic artery occlusion differ on fundoscopy from central retinal artery occlusion?

A

Ophthalmic artery occlusion

- No cherry red spot and vision is reduced to light perception only.

186
Q

What are the tauopathies?

A 
Alzheimer’s disease
Frontotemporal dementia
PSP
Corticobasal degeneration
Dementia pugilistica / chronic traumatic encephalopathy
187
Q

What are the synucleinopathies?

A

Parkinson’s Disease
Dementia with Lewy Bodies
Multiple system atrophy

188
Q

Huntington’s Disease and spinocerebellar ataxia are examples of what type of neurodegenerative diseases?

A

Polyglutamine diseases

189
Q

CSF neurofilament light proteins (cNFL) elevation distinguishes between which diseases?

A

Elevated in fronto-temporal dementia and HIV dementia

Elevated in idiopathic Parkinson’s Disease vs Parkinson’s Plus syndromes

190
Q

What is the classic MRI finding in MSA?

A

Slit-like void sign: hypointense putamen with hyperintense rim on T2

Neurology (3 decks)

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