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Aisha > Dunedin-Neurology > Flashcards

Dunedin-Neurology Flashcards

1
Q

How to diagnose Parkinson’s disease?

A

2 of the 3 features:

Bradykinesia + resting tremor OR rigidity

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2
Q

What are some motor symptoms in parkinsons that are not levodopa responsiveness?

A

voice change
freezing
gait ignition failure

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3
Q

What are the key prodomal features of parkinsons?

A

*RBD (REM sleep behaviour disorder) –> movements of body or limbs associated with dreaming with at least one of the following
- potentially harmful sleep behaviour
- dreams that appear to be acted out
- sleep behaviour that disrupts sleep continuity

*hyposmia
*anxiety
* constipation

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4
Q

What are some mutations related to Parkinsons disease?

A

GBA (glucocerebrosidase)
LRRK2

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5
Q

Describe the order of pathological changes in PD

A

starts in the medulla, and the olfactory bulb, then spreads upwards to substantial nigra, then finally into the cortex

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6
Q

Where is levodopa absorbed? What is the half life.

A

absorption in duodenum and jejunum. it competes with amino acids for gut absorption

therefore relies on gastric emptying.

half life 1.5 hours

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7
Q

What can cause increased plasma concentration/dose of levodopa?

A

advanced age
low body weight

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8
Q

What are some S/E of levodopa?

A

nausea
orthostatic hypotension
hallucinations
sleepiness and sleep attacks
confusion
motor fluctuations and dyskinesia
contributes to impulse control disorders

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9
Q

What are some medications for the treatment of PD?

A
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10
Q

What is the MOA of dopamine agonist in parkinsons disease?

A

directly stimulate the post-synaptic dopamine receptors

longer half life than levodopa

but less potent and greater S/E than levodopa

e.g. apomorphine, pramipexole, ropinirole, rotigotine, piribedil

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11
Q

What are S/E of dopamine agonist?

A

*nausea
*orthostatic hypotension
*confusion and *hallucinations
*sleepiness/sleep attacks
*peripheral oedema, ankle swelling, facial oedema
*skin irritation/rash (rotigotine)

*impulse control disorders

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12
Q

How to manage impulse control disorders when using dopamine agonists?

A

reduce or change dopamine agonist

this is associated with things like pathological gambling, hypersexuality, compulsive (binge) eating, compulsive shopping

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13
Q

What is punding?

A

often due to taking too much dopamine
often associated with marked dyskinesias and off-state dysphoria and with over-use of levodopa

mx: reduce levodopa

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14
Q

What is the MOA of MOA inhibitors such as rasagiline

A

prevents apoptotic cell death
irreversible inhibitor

MAO-type b- 80% of all MAOs in the brain

half life is 40 days

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15
Q

What is “wearing off” in parkinsons disease using Levodopa and how to treat?

A

Dose starts to wear off
treat:
* add entacapone or rasagiline
*decrease dose intervals
* increase levodopa dose size
* add dopamine agonist

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16
Q

Describe levodopa-induced dyskinesia

A

Peak dose: 30-60 min after levodopa, mainly chorea, entire body or upper half, person not aware
Treat: reduce levodopa dose size, add amantadine, add dopamine agonist and reduce levodopa, stop entacapone

End of dose: 3-4 hours post levodopa, or early morning, dystonia, often foot/leg, often painful
Treat: add entacapone or selegiline, decrease dose interval, increase levodopa dose size, add amantadine, add dopamine agonist

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17
Q

What are COMT inhibitors and difference between them and S/E

A

prolong action of levodopa

entacapone and tolcapone

tolcapone more likely to cause liver problem however it can cross blood brain barrier

S/E: insomnia, lived reticular, confusion, leg oedema, blurred vision

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18
Q

What is treatment of RBD (rapid eye movement sleep disorder)?

A

1) clonazepam
2) melatonin
3) small case series suggest: Pramipexole, donepezil, cannabinoids

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19
Q

How to treat dementia in parkinsons disease

A

Cholinesterase inhibitor:
- rivastigmine ,donezpezil

memantine

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20
Q

How to treat psychosis in Parkinson’s?

A

Benign hallucinations –> don’t treat

Paranoid psychosis –> quetiapine, reduce PD drugs, cholinesterase inhibitors (donepezil) if dementia/confusion, clozapine if ongoing psychosis

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21
Q

What are some advanced therapies for Parkinsons disease?

A

*apomorphine subcutaneous infusions
* DuoDopa Gel via PEG-J placement
*pallidotomy
* deep brain stimulation

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22
Q

What is the selection of patients for deep brain stimulation in Parkinson’s disease

A

1) typical PD and levodopa-responsiveness
2) medically healthy
3) No dementia
4) no psychosis or severe hallucinations
5) <70 years

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23
Q

What is the difference between MSA-C and MSA-P?

A

Automonic dysfunction + motor features (parkinsonsism or ataxia)

MSA-C: multiple system atrophy, the cerebellar predominant form (nystagmus, dysarthria, ataxia)

MSA-P: the parkinsons predominant form (symmetric rigidity, little tremor, poor postural reflexes)
- erectile failure, urinary incontinence, postural hypotension

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24
Q

What do you see in the brain for Multiple system atrophy?

A

alpha synucleiopathy

hot cross bun sign: atrophy of pons and cerebellum
MCP atrophy

putaminal rim sign

increased diffusion putamen

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25
Q

Is Progressive Supranuclear palsy a tauopathy?

A

Yes
neurofibrillary tangles (made up of tau) in brain stem, flame-shaped NFTs, coiled bodies, neuronal loss and gloss

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26
Q

What are the types of PSP?

A

1) Richardson’s syndrome: classic features of PSP early onset falls, slow vertical saccades, supra nuclear vertical gaze palsy, postural instability, frontal dementia, axial rigidity

2) PSP-parkinsons: asymmetric onset, tremor, response to levodopa, better prognosis

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27
Q

What is the radiological sign of PSP?

A

hummingbird or ‘kind penguin’ sign ie mid brain atrophy

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28
Q

Is Corticobasal syndrome a tauopathy?

A

yes

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29
Q

What is a common presentation of corticobasal syndrome?

A

rigid jerking arm

apraxia, frontal lobe dementia
+/- supra nuclear gaze palsy but not as severe as PSP

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30
Q

What are core features of dementia with Lewy bodies?

A

dementia has to start before or within a year of motor symptoms

core features (need 2)
a) fluctuating cognition
b) recurrent visual hallucinations
c) parkinsonsim

Suggestive
a) REM sleep behaviour disorder
b) severe neuroleptic sensitivity

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31
Q

What chromosome is the Huntingtin gene on?

A

Chromosome 4
CAG repeat (>40 repeats for sure, 36-39 increased risk, 6-25 unaffected)

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32
Q

What are the main features of Huntingtons disease?

A

1) involuntary movements (chorea, dystpnoa and Parkinsonism)

2) Behavioural disorders

3) cognitive impairment and dementia

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33
Q

Age of onset is based on size of CAG repeat expansion. True or false?

A

True

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34
Q

Treatment of Huntington?

A

symptomatic:
atypical antipsychotics
- tetrabenazine
- risperidone, olanzpine
- aripriprazole

antidepressants

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35
Q

What is the diagnostic criteria for restless legs syndrome?

A

1) an irresistible urge to move the legs, usually but not always accompanied by uncomfortable and unpleasant sensations in the legs

2) Worse during rest or inactivity

3) symptoms partially or totally relieved by movement

4) worse in evening or night

5) no other conditions (myalgia, venous stasis, leg oedema, arthritis, leg cramps, positional discomfort, habitual foot tapping)

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36
Q

Describe anti-LGL1 encephalitis

A

a type of limbic encephalitis

faciobrachial dystonic seizures

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37
Q

How to treat NMDA receptor antibody-mediated encephalitis?

A

corticosteroids
IVIG
plasma exchange
rituximab
cyclophosphamide

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38
Q

What are common features of limbic encephalitis?

A

memory impairment

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39
Q

Describe common types of limbic encephalitis

A

LGL1 (most common)- hyponatraemia, faciobracial seizures

GABABR and AMPAR

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40
Q

What is the MRI finding in limbic encephalitis

A

Mesial temporal lobe hyperintensty

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41
Q

What are the characteristics of DPPX antibodies encephalitis?

A

onset subacute to chronic
weight loss and GI symptoms
cognitive dysfunction
CNS hyper excitability (hypereflexia, myoclonus)
ataxia
eye movement disorder

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42
Q

What is Lhermitte’s and Uhthoff’s symptoms?

A

Lhermittes: transient sensation of an electric shock that extends down the spine and extremities upon flexion and/or movement of the neck.

Uhthoff: transient worsening of neurological function lasting less than 24 hours that can occur in multiple sclerosis patients due to increases in core body temperature

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43
Q

What are the types of multiple sclerosis?

A
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44
Q

What is the best imaging for MS?

A

MRI
GAD enhancement shows up “active lesions”

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45
Q

What is the characteristic appearance of MS on neuroimaging?

A

– periventricular, corpus callosum, centrum semiovale
– radiating out from corpus callosum = Dawson’s fingers
– brainstem, cerebellum
– hyperintense on T2 & Proton Density (PD) sequences
– hypointense on T1 (black holes) = axonal damage

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46
Q

What does ring-like enhancement suggest in MS lesions?

A

peripheral inflammation & complete central demyelination ( = reactivation at periphery of a chronic lesion).

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47
Q

What are things we can use in the diagnose of MS?

A

*MRI
*Evoked potential (EPs)
*Central motor conduction time (CMCT)
*Lumbar puncture - CSF- oligoclonal bands +ve in CSF but NOT In serum. Increased CSF IgG synthesis

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48
Q

What are some Multiple Sclerosis mimics?

A

*NMOSD & MOGAD
*Inflammatory disease (SLE, Sjogrens, PAN, Behcets etc)
*Infectious disease
*Granulmonatous disease
* diseases of myelin
*CADASIL

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49
Q

What is true about pregnancy in MS?

A

relapse rate reduced during pregnancy, especially in 3rd trimester

increase in relapse rate in 6 months after delivery

breastfeeding decreases early relapse rate

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50
Q

What are poor prognostic factors of MS?

A

Male
>40 years

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51
Q

What are MRI features that suggest poor prognosis of MS?

A

*high T2 lesion load
*>2 GAD enchanting lesions
*>T1 hypointense lesions
*early atrophy
* infratentorial as opposed to supratentorial lesions

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52
Q

Describe the treatment of MS

A

Acute: methylpred. Avoid pred in optic neuronitis

Continuous
- low efficacy: IFN, GA (glatiramer acetate), teriflunomide
- medium efficacy: S1PR (sphingosine-1-phosphate receptor eg ozanimod, pronesimod), DMF (dimethyl fumarate)
- high efficacy: Natalizumab (akpha-4-integrin blocker), B cell therapies (ocrelizumab, ofatumumab)
- alemtuzumab anti-cd52 is used but less often

Pulse
- medium efficacy: cladribine
- high efficacy: alemtuzumab, HSCT

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53
Q

What are side effects of alemtuzumab (CD52)

A

Profound depletion of T cells (for >1 year), profound depletion of B cells

autoimmune thyroid disaese

Immune mediated conditions including hepatitis and haemophagocytic lymphohistiocytosis, bleeding in lungs, MI, stroke, arterial dissection and severe neutropaenia

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54
Q

What is the MOA of fingolimod?

A

Decreases ability of lymphocytes to enter CNS by preventing the
egress of lymphocytes from lymphatic tissues.

Down regulates four sphingosine-1-phosphate receptor subtypes

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55
Q

What is the MOA of teriflunomide?

A

Inhibits pyrimidine synthesis (dihydroorotate dehydrogenase inhibitor)

a metabolite of leflunamide

S/E: HTN, LFT and RBS abnormal, alopecia and diarrhoea

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56
Q

Is stem cell transplant an option for MS?

A

Possibly

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57
Q

What antibodies occur in neuromyelitis optica spectrum disorder (NMOSD)

A

aquaporin 4 abs

in high conc in foot processes of astrocytes along endothelial lining of blood brain barrier

pathology: complement mediated destruction of astrocytes with secondary demyelination

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58
Q

What are spinal cord MRI abnormalities noted in NMOSD?

A

longitudinally extensive (>3 segments) spinal cord MRI abnormalities

(LETM= longitudinally extensive transverse myelitis)

often have optic nerve disease

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59
Q

What is the CSF like in NMOSD?

A

significant pleocytosis

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60
Q

What is the pathophysiology of NMOSD?

A

complement mediated destruction of astrocytes with secondary demyelination

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61
Q

What antibody is involved in Myelin Oligodendrocyte Glycoprotein Associated Disease (MOGAD)?

A

anti-MOG

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62
Q

What are some symptoms of MOGAD?

A

Optic neuritis and transverse myelitis

63
Q

What is the pathophysiology of MOGAD?

A

Oligodendrocyte directed pathology = Oligodendrocytopathy

64
Q

What are the greatest risk factors for ischaemic stroke? Haemorrhagic stroke?

A

Ischaemic:
1) Age
2) Hypertension
3) Atrial fibrillation

Haemorrhagic
1) HTN
2) cerebral amyloid antipathy

65
Q

Describe the cerebral circulation

A
66
Q

What is Gerstman syndrome?

A

location: inferior parietal lobule of dominant hemisphere

Dysgraphia/agragraphia
dyscalculia/acalculia
finger agnosia
left-right disorientation
+/- aphasia
+/- apraxia

67
Q

What is lateral medullary syndrome?

A

AKA Wallenberg syndrome AKA PICA syndrome AKA vertebral artery syndrome

Location: lateral medulla
Vessels: vertebral artery, PICA, superior middle and inferior medullary artery

Symptoms:
*contralateral trunk/limb numbness (pain/temp)
*ipsilateral facial numbness
*skew deviation/room tilk
* dysphagia/hoarseness/gag
*horners syndrome
*Limb ataxia
*Palatal myoclonus
* vertigo/nystagmus

68
Q

What is the top of basilar syndrome?

A

AKA Ponto-mesencephalic stroke

symptoms:
*Ptosis
*dilated pupils
*ocular motor deficits
*somnolence, hallucinations, dreamlike behaviour
*motor function otherwise preserved

69
Q

What is Anton syndrome?

A

stroke syndrome
bilateral occipital lesions, cortical blindness

70
Q

What is Benedikt syndrome?

A

Midbrain stroke, posterior cerebral artery or penetrating branches of basilar artery, CN III palsy, ataxia/choreoathetosis

71
Q

What is Balint syndrome?

A

B/L parietal/occipital junction lesions: e.g. watershed

simultagnosia
oculomotor apraxia
optic ataxia

72
Q

What is anterior spinal artery syndrome?

A

loss of power distally (usually up to thoracic) +/- loss of temp/pain

posterior column unaffected

73
Q

What is the BP target in ICH?

A

SBP 140

74
Q

Where is surgical intervention relevant in ICH?

A

posterior fossa

75
Q

What is the work-up for subarachnoid haemorrhage?

A

*Head CT with CTA
*lumbar punture for xanthrochromia
*MRI with SWI

76
Q

What is the treatment of subarachnoid haemorrhage?

A

*Lower BP <140
*clip/coil aneurysm to fix the underlying problem
*oral nimodipine to prevent vasospasm

77
Q

Describe the timing of IV thrombolysis and ECR for stroke

A

IV thrombolysis: <4.5 hours (or 9 if small core)

Endovascular thrombectomy: <6-7 hours (or 24 hours if small core and mismatch volume >15ml)

extended window possible using advanced imaging

78
Q

What vessels can we access with ECR?

A

ICA and M1
M2
ACA and PCA
Basilar

79
Q

What are contraindications for tPA

A
  • known hx of ICH
  • prior stroke or serious head injury within 3 months
  • sustained BP >185/110
    -dabigatran within 48 hours
  • heparin within the last 48 hours
  • major surgery within past 14 days
80
Q

Describe herniation syndromes

A
81
Q

What is is most significant risk factor for stroke?

A

hypertension

82
Q

What is the LDL target in stroke?

A

<1.8

83
Q

When do you do a Carotid endarterectomy?

A

if symptomatic AND
ipsilateral 70-99% stenosis

some evidence for 50-69% stenosis

84
Q

What anti-seizure medication work on inhibitory synapses vs excitatory synapses?

A

Excitatory synapse:
- Phenytoin, carbamezapine, valproid acid, lamotrigine, topiramate, oxcarbezine
- levetiracetam
- topiramate
- felbamate
- gabapentin/pregabalin

Inhibitory synapse:
- benzodiazepine
-topiramate
- barbiturates
- vigabatrin

85
Q

What is the MOA of levetiracetam?

A

synaptic vesicle protein 2A, inhibition Ca current

95% really excreted

S/E- irritability, mood swings

86
Q

What is the MOA of Perampanel (Fycompa)

A

glutaminergic AMPA antagonist
adjunctive for focal seizures

87
Q

What is the role of vagus nerve stimulation?

A

role in medically refractory epilepsy

88
Q

Describe HLA related to carbimazole

A

HLA B1502 –> CBZ induced SJS
HLA A 3101 –> CBZ induced rash

89
Q

Which anti-eleptics are teratogenic?

A

phenobarbitone
valproate

90
Q

What is an adverse reaction with using lamotrigine and valproate together?

A

Rash

91
Q

What is the adverse effects with OCP and lamotrigine?

A

reduced Seizure control

92
Q

What is the adverse effect carbamazepine to warfarin?

A

reduced INR

93
Q

What are some antibodies involved in autoimmune epilepsy

A
94
Q

What are common causes of multiple mononeuropathies?

A

Diabetes
vasculitis
leprosy
sarcoidosis
demyelinating neuropathies
heredity liability to pressure palsies
neurofibromatosis
entrapment/compressive neuropathies
multifocal mononeuropathy with conduction block (MMNCB)

95
Q

Describe large vs small nerve fibres

A

Small fibres: pain and temp
larger fibres: motor & JPS, vibration

96
Q

What are some causes of pure sensory neuropathy?

A

diabets
b12 deficiency
HIV
amyloidosis
Sjogrens syndrome
sarcoid
paraneoplastic
pyridoxine (vit B6) intoxication
hereditary causes

97
Q

What part of the neuron is involved in axonal pathology vs demyelination?

A

axon= axonal pathology
Schwann cell= demyelination

98
Q

What infection is related to GBS?

A

campylobacter jejuni

99
Q

What is the management of demyelinating neuropathies?

A

plasmapharesis
IVIG
Steroids (not for GBS)
immunosuppression

100
Q

What is pet cavus

A
101
Q

What is “stork leg”

A

long standing problem

102
Q

What are the subtypes of hereditary neuropathy

A
  • HMSN 1 - Demyelinating
  • HMSN 2 - Axonal
  • CMT1X - x-linked
  • CMT4 – autosomal recessive types
103
Q

What does the CSF show in paraneoplastic sensory neuropathy?

A

increased protein
pleocytosis (<100 cell/dl), lymphocytes
OCBs positive, IgG ratio abnormal

104
Q

Describe GBS/AIDP

A
  • progressive limb and cranial nerve weakness over days
  • relative symmetry of weakness
  • sensory loss, dysesthesia, pain
  • loss or decreased deep tendon reflex
  • dysautonomia- HR, BP lability
  • resp and bulbar impairment
  • previous acute illness (diarrhoea- c jejuni)
  • monophonic illness
105
Q

What are the investigations for GCS/AIDP and what does it show?

A

NCS- demyelination, prolonged F waves, prolonged distal motor latencies, slowing NCVs. NCS may be relatively normal in the beginning.

CSF- raised protein, acellular or <10wbc

106
Q

What are some GBS/AIDP variants?

A

Acute motor axonal neuropathy (AMAN)
- associated with ganglioside GM1 antibodies

Miller Fisher syndrome (MFS)
- ophthalmoplegia, ataxia, areflexia, Gq1b abs

107
Q

Treatment of GBS/AIDP?

A

IVIG, plasma exchange (can get autonomic instability)

NOT steroids

108
Q

What are the characteristics of CIDP?

A

relapsing ongoing symptoms (proximal and distal weakness, decreased to loss DRTs, autonomic features, variable sensory features, rarely papilloedema)

CSF: raised protein, <10 wbc

109
Q

What is the treatment of CIDP?

A

steroids, IVIG, rarely PLEX in early severe cases, mycophenolate, azathioprine

110
Q

What antibodies are associated wth multifocal motor neuropathy?

A

possible GM1 antibodies

111
Q

What antibodies are associated with DADS (distal acquired demyelinating sensory Ny)

A

anti-MAG antibiotics

might mention paraprotein

112
Q

Which antibodies are associated with paranodopathies?

A

Neurofascin NF155, contactin 1

113
Q

What is POEMS? And treatment

A

polyneuropathy, organomagaly, endocrinopathy, IgM paraprotein, skin changes

often have sclerotic bone lesions and elevated VEGF levels

management: lenalidomide, bortezomib, melphalan

114
Q

What are the antibodies related to myasthenia gravis? HLA association

A

AChR (80%), MuSK antibodies (20%)
LPR4 (generalised or ocular)
Agrin (Gen>ocular)
Collagen XIII (Gen)
HLA DR14- DQ5 association

115
Q

What conditions is myasthenia gravis associated with?

A

Hyperthyroidism, SLE, Scleroderma, RhA

116
Q

What is the typical phenotype for MuSK Mg?

A

severe facial and bulbar weakness with atrophy of affected muscles.

Limb muscles often less affected

tend to be milder

117
Q

What is Simpsons test?

A

a test in ocular MG , drooping of one upper lid when looking up

118
Q

Describe the treatment of MG

A

*Acetylcholinesterase inhibitors (pyridostigmine)
* steroids (prednisone)
* steroid sparing agents: azathioprine, mycophenolate mofetil

Efgartigimod
Rozanolixizumab
ravuluzimab
zilucuoplan
eculuzimab
rituximab

119
Q

How to treat myasthenia crisis?

A

ICU
treat infection if present
increase prednisone
plasma exchange or IVIG
thromboprophylaxis

120
Q

What is the main paraneoplastic cause of Lambert eaton myasthenia gravis?

A

SCLC

121
Q

What is the pathophysiology behind Lambert eaton myasthenia gravis?

A

IgG antibodies against voltage-gated calcium channels

122
Q

What is the clinical presentation of Lambert eaton myasthenia gravis?

A

Mainly proximal disease
worse in lower limbs
not usually fatiguable
distal symmetrical sensory neuropathy
autonomic neuropathy (dry mouth/eyes and impotence)
reflexes depression, but potentiate as does power

bulbar weakness and diplopia less common

123
Q

What is the treatment of Lambert eaton myasthenia syndrome?

A

potassium channel blocker (3-4 diaminopyridine)

immunosuppression
successful treatment of cancer

124
Q

What are some clinical tests for MG?

A

Ice Pack test
- put on ptosis, painful, however improved neuromuscular transmission at lower temperatures
- sensitivity 80%

Tensilon test
- short acting acetylcholine esterase inhibitor
- target muscle, inject, reassess at 1 minute
- can get false positive like MND
- can cause Brady

125
Q

Discuss brachial plexus

A
126
Q

What is brachial neuritis?

A

AKA neuralgic amyotrophy/Parsonage Turner syndrome/inflammatory brachial plexopathy

can be seen post infection/vaccination

clinical presentation: severe shoulder pain at onset, followed by weakness and wasting often around shoulder girdle. sensory loss often outer upper arm.

winging of scapula.

127
Q

What is neurogenic thoracic outlet syndrome?

A

a cause of brachial plexus injury
fibrous band over lower trunk brachial plexus
insidious onset pain and sensory loss/paraestheisae
positional
“punched out”

128
Q

What nerve does shoulder dislocation affect?

A

suprascapular nerve affecting infraspinatus and supraspinatus

axillary nerve: deltoid, teres minor
sensory loss deltoid

brachial plexus injury

129
Q

Describe Ulnar vs C8 root problem

A

Motor:
- Ulnar: all muscles except LOAF
- C8 root: all muscles including LOAF (responsible for flexion)

LOAF:
lateral two lumbricals.
opponens pollicis.
abductor pollicis brevis.
flexor pollicis brevis.

Sensory: more sensory loss with C8

129
Q

Describe the sensory distribution of the hand

A
130
Q

What is a common antibody in paraneoplastic neuropathy?

A

Anti-Hu

131
Q

What is the treatment for trigeminal neuralgia?

A

Carbamezapine , Gabapentin, lamotrigine, surgical decompression

132
Q

What is Foster Kennedy Syndrome?

A
  • Olfactory groove meningioma
  • Ipsilateral anosmia, ipsilateral visual loss and optic atrophy
  • Contralateral papilledema
133
Q

What is neuralgia paraesthetica?

A
  • Pain/dysesthesia affecting anterolateral thigh due to compression of lateral femoral cutaneous nerve (inguinal ligament
134
Q

Describe features of femoral neuropathy

A
  • Hip flexion and knee extension weakness
  • Absent patellar reflex
  • Sensory loss anterior thigh and medial lower leg
135
Q

Describe ankle movements, nerves involved and muscles involved.

A

Ankle movements
- Dorsiflexion: tibialis anterior, deep branch of peroneal (L4,L5)
- Eversion: peroneus longus, superficial branch of peroneal (L5,S1)
- Inversion: Tibialis posterior, tibial nerve (L4,L5)
- Plantarflexion: gastrocnemius and soleus, tibial nerve (S1, S2)

Peroneal nerve: up and out
Tibial nerve: Down and in

136
Q

What drug induced neuropathy does ethambutol cause?

A

optic neuritis

137
Q

What drug-induced neuropathy does nitrous oxide cause?

A

B12 deficiency
o Subacute combined degeneration of spinal cord
o Increase homocysteine and MMA

138
Q

What drug-induced neuropathy does anti-TNFalpha cause?

A

CNS +/- PNS demyelination

139
Q

What is onion bulb histology?

A

Seen in Charcot-Marie Tooth syndrome, also seen in CIDP

140
Q

Describe the neuronal antibodies

A
141
Q

What are F wave and H reflexes?

A

o F wave: a late motor response elicited by the backfiring of motor neurons after supramaximal electrical stimulation of a peripheral nerve

o H reflexes: involves both sensory and motor nerves. It is elicited by stimulating a sensory nerve (e.g., tibial nerve), which triggers a reflex response in the corresponding motor nerve.

142
Q

Describe the timing of motor vs sensory loss after injury

A
  • Motor > sensory
  • Motor by day 3, sensory by day 5
143
Q

Describe NCS: normal conduction values, latency, amplitudes

A

Conduction velocity
o UL 50-60ms
o LL 40-50ms
Latency
o <4ms
Amplitudes
o Sensory >6uV
o Motor >4 uV

144
Q

Describe changes in neuropathy vs myopathy

A
145
Q

Describe antibodies associated with classic paraneoplastic syndromes (neruology) and their treatment

A

Hu
CRMP5
Ma2
amphiphysin

treatment: anti-T cell –> rituximab, cyclophosphamide

146
Q

Distinguishing between types of limbic encephalitis

A

GABAAR- refractory status epilepticus

CASPR2- peripheral-nerve hyperexcitability, neuropathic pain

DPPX- hyperekplexia, myoclonus

147
Q

What can you use is tuberous sclerosis that are high risk for seizures?

A

mTOR- everolimus and sirolimus

148
Q

Causes of motor only neuropathy?

A

motor neuron disease
poliomyelitis
lead
botulinism
drugs (vincristine, dapsone, amiodarone)

149
Q

What is the role of neurofascin antibodies?

A

For paranodopathies (form of CIPD), especially if patient resistant to usual CIPD treatments (steroids and or IVIG)

150
Q

What are genes associated with migraines?

A

KCNK18 and CSNK1D genes

151
Q

What is the treatment of a migraine?

A

Acute: anti-emetic (IV prochlorperazine), triptan

Status migrainous –> SC sumatriptan or IV ketoralac or IV chlorpormzine

Prophylaxis
- Insomnia –> TCA, pregabalin, gabapentin, propranolol, candesartan, topiramate

152
Q

Compare the different headaches syndromes

A

Aisha (47 decks)

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