Peripheral Nerves Flashcards

1
Q

Shoulder Abduction

A

Axillary Nerve
C5

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2
Q

Elbow Flexion weakness

A

Musculocutaneous

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3
Q

Elbow Extension weakness

A

Radial

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4
Q

Wrist extension weakness

A

Radial

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5
Q

Wrist flexion weakness

A

Median

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6
Q

Finger extension weakness

A

Radial

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7
Q

Finger flexion weakness

A

Median/(Ulnar)

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8
Q

Axillary Nerve

A

Deltoid muscle
Shoulder abduction 20-90deg
Regimental patch

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9
Q

C5

A

Critical movement: Elbow flexors
Controls shoulder

Other:
Half of biceps and brachioradialis jerk
Also shoulder abduction

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10
Q

C6

A

Elbow joint
Wrist extensors

Also
Elbow flexion with C5
Part of bicps an brachioradialis jerk

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11
Q

C7

A

Wrist joint
Elbow extension

Triceps Jerk
Also related to wrist extension/flexion

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12
Q

C8

A

Finger flexion/extension
Key movement is flexion

Part of triceps jerk

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13
Q

T1

A

Finger abductors
Also involved in finger adduction

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14
Q

Radial Nerve

A

Extension of everything

Elbow weakness if injury above spiral groove

Brachioradialis, wrist and finger weakness: injury in spiral groove

finger abduction appears weak because hard to spread fingers if not straight!

Sensation:
Posterior aspect of arm
Posterior aspect of hand
Snuffbox
Location of lesion

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15
Q

What does it mean in the upper limb if extension and flexion are weak at the same joint?

A

Can’t be a peripheral nerve lesion

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16
Q

Sensation of medial aspect of forearm

A

From brachial plexus

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17
Q

Winging of Scapula

A

Proximal lesion

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18
Q

Musculocutaneous Nerve

A

Motor: Elbow Flexion
Sensory: Lateral forearm

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19
Q

Sensation loss involving forearm and hand

A

Radiculopathy

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20
Q

Median Nerve

A

Wrist flexion
Finger flexion
Lumbricals
Thumb Abduction

LOAF of hand (thenar eminence): lateral 2 lumbricals, opponens pollicis brevis, abductor pollicis brevis, flexor pollicis brevis

Weakness: wrist and finger flexion
Hand of benediction → unable to flex middle and index finger

Sensation: lateral 3.5 digits
Plus don’t forget palmar branch

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21
Q

Ulnar Nerve

A

Finger abduction
Finger adduction

For digit 4 + 5: Flexor digitorum profundus and lumbricals

Wasting of intrinsic muscles of hand except thenar
Weak finger abduction and adduction

Ulnar claw hand: hyperextension of MCPJ, flexion at PIPJ and DIPJ
(Higher the lesion, less the deformity - because FDP also weak and doesn’t try to overcome lumbrical weakness)

Froment’s sign: Adductor pollicis weakness, flexor pollicis longus activats instead

Sensory medial aspect 1.5 fingers

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22
Q

Biceps Jerk

A

C5/C6
Musculocutaneous

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23
Q

Brachioradialis Jerk

A

C5/C6
Radial

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24
Q

Triceps Jerk

A

C7/C8
Radial

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25
Q

Upper Trunk Brachial Plexus injury

A

Loss of C5 and C6
Loss of shoulder movement
Loss of elbow flexion

“waiter’s tip position”

Sensory: lateral aspect of arm and forearm (musculocutaneous)

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26
Q

Lower Trunk Brachial Plexus Injury

A

C8 - T1
Loss of everything in the hand
Loss of sensation along medial aspect of hand and forearm

Can get a Horner’s syndrome because the sympathetic pathways come from C8-T1 too.

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27
Q

Femoral Nerve

A

Hip Flexion
Knee Extension (Quads)

Sensation: medial aspect of thigh
Loss of knee jerk

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28
Q

Sciatic Nerve

A

Knee flexion
Plus distal movement
Flaccid foot drop

Loss of sensation below knee
Loss of ankle jerk and plantar response

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29
Q

Tibial Nerve

A

Posterior compartment

Plantarflexion
Ankle Inversion

Loss of ankle jerk
Sensory: most of sole of foot

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30
Q

Common Peroneal Nerve

A

Ankle eversion (Superficial peroneal)
Dorsiflexion - foot drop (Deep peroneal)

Sensory:
Superficial: lateral aspect leg, dorsum of foot
Deep: between 1st and 2nd toe

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31
Q

Inferior Gluteal Nerve

A

Gluteus Maximus - Hip extension

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32
Q

Obturator Nerve

A

Hip Adductors

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33
Q

L2

A

Hip Flexors

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34
Q

L3

A

Knee Extensors

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35
Q

L4

A

Ankle Dorsiflexion
Inversion

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36
Q

L5

A

Long toe extensors
Inversion/eversion

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37
Q

S1

A

Ankle plantar flexion
Eversion

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38
Q

Myotomes for lower limb

A

Count down joints
Then around joints

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39
Q

L3 versus Femoral lesion

A

L3 has addition to hip adduction weakness

Otherwise:
Knee extension weakness
Hip flexion weakness
Loss of Knee Jerk
Sensation similar - down onto knee

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40
Q

Knee Jerk

A

Femoral Nerve
L3 L4

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41
Q

Ankle Jerk

A

Tibial Nerve
S1 S2

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42
Q

Foot Drop

A

L4/L5: loss of inversion/eversion, but jerk present

Sciatic: everything gone

Common peroneal: eversion gone, but jerk and inversion present (because tibial does this)

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43
Q

Unmyelinated nerves

A

Small fibre nerves
Pain and autonomic signals

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44
Q

What does Nerve Conduction Studies test?

A

Large Myelinated fibres record best
Aids localisation

Can’t test small fibres or autonomic fibres

Motor: anterior horn cell to muscle (Includes NMJ)

Sensory: skin to dorsal root ganglia

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45
Q

NCS in sensory radiculopathy

A

Normal

46
Q

Amplitude loss on NCS

A

Axonal loss

47
Q

Conduction Velocity slowing on NCS

A

Demyelination

Initial finding in compression is sensory CV slowing

48
Q

Temporal dispersion on NCS

A

Marker of demyelination

49
Q

F wave on NCS

A

Signal goes wrong way up to anterior horn then bounces back, so can assess proximal segment of nerve

May be the only abnormality in early GBS

50
Q

Inflammatory Peripheral Neuropathy

A

Onset is subacute

Proximal and Distal: AIDP, CIDP

Asymmetric: Multifocal motor neuropathy, Mononeuritis multiplex

Constitutional symptoms

51
Q

Leprosy

A

Mycobacterium leprae
Consider: low/middle income countries with skin lesions, cutaneous sensory loss, thick nerves on palpation, focal mononeuropathies

Sparing of reflexes and dorsal columns

Responsive to antibiotics

52
Q

Focal, asymmetric axonal loss

A

Mononeuritis Multiplex

53
Q

Bilateral CN VII Palsy

A

Most commonly affected nerve in sarcoidosis

Parotid swelling can also cause this, part of Heerfordt Syndrome with uveitis, transverse myelitis

54
Q

Sarcoidosis

A

Small fibre neuropathy is most common presentation for nerve involvement

Bilateral CN VII is the key nerve involvement

55
Q

Hereditary Neuropathy with Liability to Pressure Palsy (HNPP)

A

Deletion of ch 17p11.2 containing PMP22 gene
AD inheritance

Predisposition to getting compressive neuropathies

56
Q

HIV Neuropathy

A

Distal, symmetric, sensory neuropathy affecting small sensory fibres or both

Posirtive and negative symptoms, most have pain

Usually no motor symptoms

Isoniazid exposure, advanced age increase risk

57
Q

Paraneoplastic Peripheral Neuropathy

A

Sensory, motor and small fibre
Axonal or demyelinating

Anti Hu, Anti CV2

58
Q

Charcot Marie Tooth Neuropathy

A

Genetic condition with peripheral neuropathy main manifestation.

Insidious onset, can develop during infancy, can develop foot deformities.

Lack of positive sensory symptoms despite clear sensory involvement.

Loss of reflexes

Loss of fine motor movement in hands is a late finding

AD inheritance Demyelinating (CMT1): motor predominant
AD inheritance Axonal (CMT2): sensory predominant

Also X linked and AR forms

59
Q

Diabetic Neuropathy

A

Broad spectrum of involvement, including small fibres and autonomic fibres. Even cranial nerves.

Distal symmetric sensorimotor peripheral neuropathy, sensory predominant. Positive and negative symptoms.

Positive and negative symptoms, including pain. Weakness unusual early.

60
Q

Diabetic Autonomic Neuropathy

A

Impacts morbidity and mortality
T1DM > T2DM
Increases with time
Resting tachycardia, exercise intolerance, postural hypotension, gastroparesis, dry skin

61
Q

Best agent for painful peripheral neuropathy

A

Amitriptyline has lowest NNT

Duloxetine, venlafaxine, gabapentin and pregabalin are other options.

62
Q

Drug related Peripheral Neuropathies

A
63
Q

Key Chemotherapy agents causing Peripheral Neuropathy

A

Aensorimotor axonal length dependent neuropathy in majority

Platinum based (platins): develop very quickly, within weeks. Due to binding to DNA inducing apoptosis.

Taxanes (Paclitaxel, docetaxel) and Vinca alkaloids (Vincristine, vinblastine). Due to disruption of microtubules.

Bortezomib (Proteasome inhibitor) That is frequently dose limiting

64
Q

Nutritional Causes of Peripheral Neuropathy

A

Vitamin B1
Vitamin B6
Vitamin B12 (subacute combined degeneration of dorsal column and spinocerebellar - UMN + proprioceptive loss)
Vitamin E
Copper
Thiamine deficiency

65
Q

Nerve Compression (Radiculopathy) IN Lumbar Spine

A

Disc Herniation: lower of the two involved Vertebrae = involved nerve
Foraminal stenosis: upper of the two involved vertebrae = involved nerve

66
Q

Radiculopathy Investigations

A

Sensory studies normal
Motor studies: normal or reduced amplitude
EMG: neurogenic changes in affected myotome muscle groups (increased amplitude, polyphasia, decreased recruitment)

67
Q

Sciatica Management

A

Remain active
Don’t give opioids or pregabalin
Steroids variable
Physiotherapy
33% resolve within 2 weeks, 90% in 3 months spontaneously
Surgery may be helpful if pain persists past 4 months, unclear if improves weakness

68
Q

Pathogenesis of Guillain-Barré Syndrome

A

AIDP
Mean age of onset 40, M > F

Humorally mediated disorder leading to TT lymphocyte infiltration and intense macrophage associated segmental demyelination in proximal nerve segments and nerve roots

Antibodies
Axonal subtype: GM1 GD1a
Miller Fisher: GQ1b

IgG and complement deposition

Molecular mimicry with campylobacter jejuni can play a role

Weakness predominant ascending pattern is most common but lots of others

69
Q

Miller Fisher Syndrome features

A

Viral prodrome 1-2 weeks prior

Ophthalmoplegia
Loss of reflexes
Ataxia

GQ1b antibodies

70
Q

Triggers for GBS

A

Prodromal illness in 4 weeks prior in 60-70% of cases

URTI and campylobacter jejuni most common

Surgery, malignancy (esp. Hodgkin Lymphoma), pregnancy, mycoplasma pneumoniae, CMV, EBV, HIV, VZV, HBV/HCV, Zika

Post immune checkpoint inhibitors

71
Q

Classic CSF finding in GBS

A

Albuminocytologic dissociation

So markedly raised protein in CSF with normal or slightly raised white cell count

May be delayed if taken early

72
Q

NCS in GBS

A

Prolonged F wave latency
Prolonged distal latencies/reduced velocity (motor before sensory)
Conduction block

Sural often preserved

Sensitivity is poor early in disease

73
Q

Management of GBS

A

PLEx or IVIg

PLEx:
- Removes autoantibodies, immune complexes, cytokines
- Needs to be given within 2-4 weeks
- Reduces time to walk unaided by 32-41 days and time on ventilator by 2 weeks

IVIg:
- Benefit seen within 2 weeks in those unable to walk unaided
- Repeat dosing at 4 weeks if slow improvement is not necessarily helpful

No benefit of both
Oral Steroids → worse outcome

74
Q

Infections with bad prognosis in GBS

A

Campylobacter jejuni
CMV

75
Q

CIDP

A

Chronic version of AIDP, nadir past 4 weeks, usually progressive >8 weeks.

Lower limb predominant, but similar pattern of proximal and distal weakness. Usually milder than AIDP

NCS and LP findings similar

Treat with steroids
- Pulse MP 3 days, then monthly 1 day ongoing
- Long term IVIg often required

76
Q

Nodopathy

A

Antibodies to the nodes and paranodal proteins.

Atypical disease

Specific antibodies

Rituximab for management

77
Q

Checkpoint Inhibitor Induced Neuropathy

A

Can present like AIDP, also as a cranial neuropathy

Mechanism not fully understood

CSF pleocytosis typical compared to AIDP/CIDP

Treat with steroids

78
Q

IgM Paraprotein Neuropathy

A

Older men
Sensory ataxia, mild weakness
Prolonged distal latency on NCS

50% have anti-MAG antibody

Rituximab

Can mimic CIDP - all with CIDP like presentation need paraproteins sent

79
Q

Amyloid Peripheral Neuropathy

A

Painful length dependent small fibre peripheral neuropathy with generalised autonomic failure

Orthostatic hypotension common

for ATTR, can use Inotersen (antisense oligonucleotide) and Patisiran (RNA interference agent)

80
Q

Multifocal Motor Neuropathy

A

Motor only components of peripheral nerves → asymmetric

Upper limb predominant
Decreased tendon reflexes in affected areas

Investigations:
- Serum anti-GM1 antibodies
- Motor conduction block

IVIg for management
steroids can worsen

81
Q

Pure sensory loss of upper limbs at same time as or before lower limbs

A

Think about dorsal root ganglionopathy

82
Q

HSV-2 Lumbosacral Radiculopathy

A

Radicular pain, paraesthesia, genital discomfort, lower extremity weakness.

If conus or caua equina involved, urinary retention can occur.

MRI: nerve root enlargement, T2 hyperintensity
CSF: lymphocytic pleocytosis, high protein

Aciclovir IV if immunocompromised
Otherwise Valacyclovir

83
Q

Parsonage-Turner Syndrome

A

Severe pain in shoulder
Vasculitis of brachial plexus

Followed by weakness and atrophy of muscles of shoulder

Mostly middle aged men

Axonal loss as vessels infarct

Recover well with steroids

84
Q

Lumbosacral Radiculoplexopathy

A

New name for diabetic amyotrophy

85
Q

NMJ Dysfunction

A
  • Weakness with no sensory symptoms
  • Fatiguability
  • Proximal symmetric weakness
  • Respiratory symptoms
  • Neck weakness
86
Q

Motor Unit

A

1 motor nerve fibre and all the muscle fibres it innervates

Number of muscle fibres innervated by a single motor nerve fibre varies.

87
Q

Spontaneous Activity

A

Abnormal

Denervated fibres express ACh receptors along their entire length, which leads to spontaneous firing due to background levels of ACh

Sign of active denervation

Fibrillation and positive spark waves

88
Q

Fibrillation potentials and positive sharp waves

A

Abnormal spontaneous firing of individual muscle fibres, sign of active denervation and inflammatory myopathies

89
Q

Fasciculations

A

Firing of part or all of a motor unit

Can be normal (Classic group is doctors and medical students)

Mostly abnormal however and occur when there are sick or dying axons
- MND
- CIDP
- Chronic nerve entrapments

90
Q

Neurogenic Morphology on EMG

A
  • Broad and polyphasic morphology as there muscle axons are messy
  • Also increased amplitude because more muscles fibres firing from the same muscle axon
  • Reduced recruitment with maximum contraction as fewer motor units
91
Q

Myopathic Morphology

A

Smaller amplitude as fewer fibres in each motor unit so smaller signal

Increased or early recruitment as need lots of motor units for same force

92
Q

Presynaptic NMJ Dysfunction

A
  • Lambert Eaton Myasthenic Syndrome (Voltage gated calcium channel disorder)
  • Botulism (vesicle problem)
93
Q

Postsynaptic NMJ Dysfunction

A

Myasthenia Gravis (Ab against ACh receptors)
Organophosphate poisoning (Acetylcholinesterase problem)

94
Q

Most common presentation of Myasthenia

A

Ocular symptoms: Ptosis, diplopia

Can mimic just about anything

Generalised weakness, fluctuating and fatiguable

Bulbar weakness, neck weakness, limb girdle, respiratory weakness.

Check accomodation

95
Q

Myasthenia Gravis Diagnosis

A
  • Ice test
  • Check for antibodies: AChR (85%), MuSK (6-10%)
  • Single nerve fibre (good for ocular) and repetitive nerve stimulation (10% decrement diagnostic - good for general)
  • Tensilon test (Edrophonium administration)
  • Hold eyes up, double vision occurs
96
Q

Ocular Myasthenia

A

15% of patients have isolated ocular myasthenia (although often the presenting symptom of generalised)

50% AChR Ab positive
66% will progress to generalised within 2 years
90% who don’t generalise within 2 years remain ocular

97
Q

MuSK Disease

A

IgG4 disease, non complement activating. Receptors not destroyed and thus respond quite well to Rituximab

Early onset, severe disease. Not related to thymoma

98
Q

Management of Myasthenia Gravis

A

Remove Thymoma if present (unless MuSK Ab)

Cholinesterase inhibitors: Pyridostigmine

Steroids: reduce risk of developing generalised MG, however can worsen before improving if give too much

AZA, MMF, Tac, MTX

IVIg, PLEx as rescue therapy

Evidence for Rituximab as a single dose for new onset AChR+ve disease

99
Q

Complement Inhibition and Myasthenia Gravis

A

Eculizumab, Ravulizumab, zilucoplan

Used for generalised AChR+ moderate severity disease who’ve already had some form of immunosuppression which they’ve failed.

Need meningococcal vaccine prior

Works rapidly

100
Q

Neonatal Fc Receptor Myasthenia Gravis

A

Neonatal Fc Receptor molecule recycles IgG, extending half life. Keeps IgG around, and thus maintains availability of IgGZ autoantibodies in IgG mediated disease

Efgartimod and Rozanolixizumab are human IgG1 Ab Fc-fragment, with higher affinity to the FcRn → outcompetes endogenous IgG → Pathogenic IgG degraded

Improves outcomes.

IVIg is essentially a blunt tool to overwhelm FcRn. More expensive.

101
Q

Benefits of Thymectomy in MG

A

Thymoma should be removed. Thymic hyperplasia should be removed if ACHr+ generalised disease.

Lower disease scores
Lower pred requirement
Fewer patients on AZA
Fewer admissions
Fewer immunosuppression side effects

102
Q

Myasthenic Crisis

A

Severe respiratory weakness due to fatigue

Treatment
- Intubate
- IVIg
- PLEx
- Supportive Care
- Immunosuppression

5% mortality

103
Q

Medications that can trigger Myasthenic Crisis

A

Aminoglycosides
Fluoroquinolones
Tetracyclines
Macrolides
Beta blockers
CCB (Verapamil)
Phenytoin
Lithium

104
Q

HLA-B8-DR3

A

NOn paraneoplastic Lambert Eaton

105
Q

Triad of:
- Proximal weakness that temporarily improves post exercise
- Autonomic Features: dry mouth, urinary retention, orthostatic hypotension
- Areflexia: post exercise facilitation

A

Lambert Eaton Myasthenic Syndrome

106
Q

Lambert Eaton Diagnosis

A

NCS: Attentuated CMAP without muscle mass loss, increases post exercise

EMG: abnormal

VGCC Ab positive in 90-100% of patients

Malignancy screen

107
Q

Lambert Eaton Treatment

A
  • Tumour resection if present
  • 3-4-diaminopyridine: blocks efflux of potassium ions, prolonging depolarisation (as disease is due to problems with calcium channels)
  • Immunosuppression, IVIg
108
Q

Mechanism of Botulinium Toxin

A

Blocks presynaptic Acetylcholine release

109
Q

Foodborne Botulism

A

2 day incubation
Starts in eyes and descends
Symmetric descending flaccid paralysis
Autonomic symptoms
Internal and external ophthalmoplegia (fixed pupils)
Reflexes and cognition preserved

110
Q

Management of Botulism

A
  • Avoid aminoglycosides
  • Remove unabsorbed toxin if appropriate, e.g. ileus
  • Equine trivalent (A, B, E) antitoxin: lowers mortality, shortens course of illness. Stabilises but doesn’t reverse disease

Recover over months, but some symptoms can persist for years.