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Neuropathy Flashcards

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1
Q

F wave in NCS

What is it?

A

Give powerful nerve stimulation then see how long it takes to travel down the nerve

Most sensitive in GBS

Decreased persistence and increased latency

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2
Q

What is EMG?

A

Put needle in muscle to record muscle activity

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3
Q

Sensory neuropathy causes

A

Diabetes

B12/thiamine (inhale NO, blocks B12 metabolism) - if severe, can affect motor nerves and can be permanent

Renal failure

Amyloid

Sjogren’s (ganlionopathy)

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4
Q

Motor neuropathy cases

A

Rare
Demyelination

Acute motor axonal neuropathy (variation of GBS; motor weakness instead of sensory) - Japanese people

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5
Q

Painful neuropathy causes

A

Worse getting into bed at night

ETOH/nutritional

Diabetes/impaired glucose control - if you improve BSL, this can be reversed

B6 toxicity

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6
Q

GBS/AIDP

1) onset
2) Clinical features
3) Diagnosis
4) Rx
5) Prognosis
6) NCS
7) Pathogenesis

A

1) 4 weeks

2)
Ascending numbness + weakness from feet
Proximal + distal weakness (predominant feature)
Weakness is maximum by 2-4 weeks
Lose reflexes over time
+/- Radicular lumbar and neuropathic pain
+/- autonomic dysfunction

Antecedent infection (C jejuni, viruses, vaccines) 1-4 weeks before GBS

3) 
CSF (raised protein, no cells)
NCS 
- Takes time to become abnormal 
- Prolonged F wave latency 
- Prolonged distal latencies/reduced velocity (demyelination) 
Anti-GM1 (AMAN)
Anti-GM2 (CMV)
Anti-GD1a (AMAN)
Anti-GQ1 (Miller fisher)

FVC <1L = ICU

4)
IVIG or plasma exchange (both effective but plasmaX is more $$$)
No steroids!!!

5) 85% full recovery, 5% severe disability
6) clinical symptoms come first then nerve conduction studies. Clinical symptoms improve first before NCS improve.
7) B cell mediated –> segmental demyelination. Starts at nerve root because of weakest nerve blood barrier –> radiculopathy

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7
Q

GBS variants
Acute motor-sensory axonal neuropathy (AMAN)

MILLER FISHER

A

Acute motor-sensory axonal neuropathy (AMAN)

  • Japanese people
  • NCS shows motor block
  • C. jejuni
  • GM1 and GD1a

Miller Fisher

  • Ataxia, opthalmoplegia, areflexia
  • Anti-GQ1
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8
Q

AIDP vs CIDP

A

AIDP
Progresses over 4 weeks
Proximal weakness

CIDP
Progresses over >8 weeks (cut off is >4 weeks)
Proximal and distal weakness
Usually milder than AIDP

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9
Q

CIDP Dx

A

CSF: raised protein, no cells
NCS: demyelination/conduction block (similar to AIDP/GBS)

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10
Q

CIDP Rx

A

IVIG or plasmaX +/- steroids +/- steroid sparing agents

Ab positive disease/response to plasmaX: rituximab

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11
Q

What’s hereditary neuropathy with liability to pressure palsy (HNPP)?

A

Autosomal dominant

Transient and recurrent motor and sensory mononeuropathies, typically carpal tunnel, ulnar groove and fibular head

Mild mild pressure –> palsy can last hours-weeks

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12
Q

Amyloid neuropathy clinical features

A

Protein disposition

Small fiber painful neuropathy
Autonomic dysfunction e.g. orthostatic hypotension

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13
Q

Diabetic neuropathy clinical features

A

Length dependent die back
Small fibre loss leading to pain
Weakness is not a predominant feature till late

Others
- Autonomic neuropathy - resting tachycardia, orthostatic hypotension

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14
Q

Management diabetic neuropathy

A

BSL control
Gastric bypass
Foot care

Pain neuropathy

1) amitryptyline
2) duloxetine and venlafaxine
3) gabapentin and prgabalin

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15
Q

What’s a mononeuropathy? What’s a mononeuritis?

A

Individual peripheral nerve problem e.g. radial nerve palsy
Typically pressure related - e.g. CT syndrome

Mononeuritis is inflammation/infection of a single nerve

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16
Q

Carpal tunnel risk factors

A 
Female
Diabetes
Pregnancy
Hypothyroidism
Haemodialysis 
Steroid use 
RA
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17
Q

Infective cause of mononeuritis?

A

Leprosy
Consider in patients from low/middle income countries with skin lesions, cutaneous sensory loss, thickened nerves to palpation, or focal mononeuropathies

Before DM, leprosy was the #1 cause of neuropathy. Now its #2.

Responsive to abx

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18
Q

Autoimmune causes of mononeuritis?

A

Vasculitis

Sarcoid

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19
Q

Which CNs have parasympathetic activity?

A

TV channels!

CN 3 (SBS lol), 7, 9, 10

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20
Q

What does CN3 do?

A

Oculomotor nerve

Carries parasympathetic fibers –> constrict pupils
Moves eye down and out

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21
Q

Vasculitic neuropathies

1) Pathophysiology and causes
2) Presentation
3) Diagnosis

A

1)
- Infarct of nerve –> kills axon
- Causes a mononeuritis multiplex (multiple single inflamed nerves)
- Causes: PAN, RA, Sjogren’s

2) Hyperacute presentation
Both small fibers (pain) as well as larger motor and sensory fibers are affected

3) Nerve and muscle biopsy

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22
Q

Sarcoidosis neuropathy

1) Presentation
2) Most common nerve affected

A

1) Peripheral nerve involvement
- Polyradiculoneuropathy, peripheral neuropathy, mononeuropathy multiplex

2) CN7
When you get bilateral CN7 involvement, always think of sarcoid!

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23
Q

Typical features of peripheral neuropathy

A

Symmetrical
Progressively ascends up the lower limbs (stocking distribution)
Distal parts are not getting enough nutrients = “die back”, affects longest nerves first (legs)
Majority are axonal > demyelination

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24
Q

Infective peripheral neuropathy

1) Presentation
2) Cause

Study These Flashcards
A

1) Distal, symmetrical, sensory predominant, small sensory fibers (pain) in isolation +/- large sensory fibers
Usually no motor symptoms

2) HIV

25
Causes of peripheral polyneuropathy/polyneuritis
Multiple nerves are affected Polyneuritis 1) Infection - HIV 2) Paraneoplastic - anti Hu, anti CV2, paraproteinaemic (MGUS, Waldenstrom's, MM, POEMS, amyloidosis) Polyneuropathy 1) Extrinsic - tumour 2) Intrinsic - Genetic: Charcot Marie Tooth - Metabolic: Diabetes - Nutritional: B12, B1 - Drugs: chemo, RT, HAART, ETOH
26
What's Charcot Marie Tooth peripheral neuropathy?
Group of genetic neuropathies Peripheral neuropathy Symptom onset during infancy Long and slowly progressing Foot deformities (due to sensory loss in childhood) Gradual distal weakness, sensory loss, reflex loss, starts at feet.
27
Paraneoplastic peripheral neuropathy What kind of neuropathy? Which antibodies are implicated? Which cancers?
``` Anti Hu (small fiber) Anti CV2 ``` Can cause sensory, motor, small fiber neuropathy Many possible Cancers - Small cell lung cancer - Adenocarcinoma - Lymphoma - Thymoma - Ovarian cancer
28
Chemotherapy induced peripheral neuropathy | Which chemotherapy agents?
Very common Dose related Platinum based compounds e.g. cisplatin, carboplatin, oxaliplatin = Sensory neuropathy Taxanes (paclitaxel, docetaxel) and vinca alkaloids (vincrinstine, vinblastine) = length dependent sensorimotor peripheral neuropathy Bortezomib (protease inhibitor for MM) = sensory neuropathy
29
Which nutritional deficits/toxicity are related to peripheral neuropathy?
B12/thiamine deficiency = length dependent, motor predominant polyneuropathy B12 deficiency = subacute combined degeneration (dorsal column + corticospinal tract + peripheral neuropathy) B6 toxicity = sensory polyneuropathy affecting legs B1 deficiency Vitamin E, copper
30
Common cause of radiculitis
VZV/shingles Virus lives in dorsal root ganglia --> reactivated --> rash and neuropathic pain in dorsal root ganglion + dermatome
31
Sciatica radiculopathy 1) Most common sites of pathology 2) Presentation
1) L4-5, L5-S1 radiculopathy 2) Pain shooting down leg +/- back pain Can occur suddenly with physical activity or slowly Mild parasthesia in dermatome <50% have weakness (primarily a sensory problem) Reflex loss based on corresponding nerve root
32
What do you expect to see on NCS and EMG in radiculopathy?
NCS Nothing Cause its pre-ganglionic (nerve root problem), NCS will not show abnormality EMG Stick a needle into the muscle and you'll be able to seen abnormal changes - increased amplitude, polyphasia, decreased recruitment
33
Sciatica radiculopathy treatment
Analgesia - short term benefit only Steroid injection may relieve pain but doesn't reduce progression to surgery Physiotherapy! Surgery is indicated if it's not improving spontaneously Unclear if surgery improves weakness or does it just resolve with time General rule: if there's motor involvement of >4/12, refer to neurosurgery
34
What don't you want to give in GBS?
Steroids | Contraindicated
35
Dorsal root ganglinopathy Presentation Causes
Pure sensory loss including proprioceptive loss --> can get severe ataxia as they don't know where their hand is and they're trying to find their position B6 toxicity and deficiency Sjogrens, SLE Paraneoplastic - anti-Hu Infections - HIV, HTLV1, VZV, leprosy, EBV
36
What's a small fiber neuropathy? Causes?
Involvement of thinly myelinated and/or unmyelinated fibers Pain may be the only feature +/- autonomic involvement Diabetes/pre-diabetes ETOH
37
What kinda nerve fibers are the following? 1) Motor 2) Touch and dorsal column 3) Pain and temp 4) Pain 5) Autonomic
1) Large myelinated 2) Large myelinated 3) Small thinly myelinated 4) Small unmyelinated 5) Thin unmyelinated
38
Why do we do NCS? | What can and can't it test?
Where is the lesion? Is this myelin or axon? High sensitivity, poor specifcity - Tests only from skin to dorsal root ganglia (any lesion pre ganglion will NOT be picked up e.g. radiculopathy) - Tests from anterior horn cell to muscle including NMJ Can only test large myelinated fibers - motor, touch, dosal column. Cannot test small fibers e.g. neuropathic pain or autonomic fibers.
39
What's Wallerian degeneration?
Die back | Nerve dies from distal to proximal
40
What does NCS pick up?
1) Amplitude - Shows us HOW MANY axons are excited - The more people screaming, the louder the sound, the higher the amplitude - Small amplitude = axonal death 2) Distance Velocity = distance/time Increase in latency + decreased amplitude = demyelination
41
What happens to NCS in compression of the nerve?
Compression --> myelin affected first --> reduced velocity at a focal point --> later pushes on axon --> reduced amplitude usually affecting sensory first then motor
42
What's sensory nerve action potentials (SNAP) in NCS?
The sum of all the resultant action potentials Slowly dial up electricity to stimulate all the nerve fibers
43
Indication for reperfusion therapy in stroke
Good functional status TPA: no established infarct, NIHSS 2 or more, <4.5h from onset ECR: NIHSS 5 or more, <6h from onset or 6-24h from onset with favourable penumbra
44
Whats penumbra and core on CTP?
Mismatch between CBF (flow) and CBV (volume) Core is match between CBF and CBV
45
What's amaurosis fugax?
Transient blurring of unilateral eye Due to embolism in ipsilateral opthalmic artery or retinal branch from carotid artery Can evolve to stroke with contralateral hemiparesis
46
Reduced light reflex in the right eye and the right eye in an inferolateral abducted position Where is the problem?
CN3 palsy | Posterior communicating artery aneurysm
47
``` Acute Rt leg weakness and drowsiness CTB hyperdensity in the brainstem Most likely aetiology is A) Cavernous haemangioma B) Hypertensive haemorrhage C) Basilar artery rupture D) Lacunar E) Glioma ```
B) Hypertensive haemorrhage within the brainstem Due to small penetrator arteries Often they're subcortical and supply pons, midbrain, thalamus, putamen and caudate (rather than lobar that's seen in cerebral amyloid angiopathy) Not C) Basilar artery rupture would cause a SAH
48
AVM - where does it bleed?
Bleed in unusual location E.g. adjacent to dura, posterior fossa location No hypertension is a clue!
49
Complication of SAH
Hydrocephalus secondary to blood clots obstructing blood flow Vasospasm
50
59F sudden onset headache 10 hours prior, feels like struck on the head with a brick. She presented 2 weeks earlier with a similar headache. Pain is worse on bending over to pick up her bag. Non-contrast CTB normal What is the most useful diagnostic test for her?
Recurrent thunderclap headache = SAH 1st headache is the typical sentinel headache due to aneurysm leak - days to weeks prior to rupture. Worse on bending = raised ICP CTB done within 6 hours has good sensitivity. Beyond 6 hours the evidence is less clear. CTA will miss some aneurysms Answer: LP (xanthochromia) - can't be done too early within first 2- 4 hours (false negative) cause it takes time for blood to breakdown; can be done up to first few days
51
DDx thunderclap headache
``` SAH Cervical artery dissection CVST Pituitary apoplexy Reversible Cerebral Vasoconstriction Syndrome ```
52
Persistent vertigo | What features as part of HINT exam is most concerning for a stroke?
Negative head impulse test Direction change nystagmus Test of skew - vertical misalignment on cover/uncover PLUS - unidirectional hearing loss If all 3 present, best sensitivity than DWI MRI in the first 48h
53
Rx venous sinus thrombosis
IV heparin
54
``` Which one of the following features is least likely to be present in CJD? A) visual field defect B) cognitive decline C) myoclonus D) Cerebellar ataxia E) areflexia ```
Areflexia - this is a LMN sign hence unlikely to get in CJD
55
Which chromosome contains the gene for the Alzheimer amyloid precursor protein?
Chromosome 21 People with trisomy 21/Down's has premature dementia - Alzheimer type
56
Neurofibrillary tangles are seen in ?
Alzheimer's
57
Numbness and tingling in both hands involving the thumb especially at night. What is it?
Carpal tunnel Median nerve dysfunction at the wrist - sensory goes first followed by motor
58
How do we differentiate DLB and PD with dementia?
PD with dementia - PD occurs for at least 12 months first before dementia DLB - dementia first then PD
59
How to differentiate lumbar radiculopathy from peroneal neuropathy in foot drop?
Ankle inversion weakness = L5

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