Peripheral Nerves, Myotomes, Dermatomes Flashcards
Axillary Nerve
Motor: Deltoid (shoulder abduction 20-90 deg)
Sensory: Regimental patch
Radial Nerve
Motor: Elbow, wrist, finger extension
Sensory:
- Posterior cutaneous nerve of arm - dorsal arm
- Low lesions - only anatomical snuffbox
Musculocutaneous Nerve
Motor: Elbow flexion
Sensory: Lateral Forearm
Median Nerve
Motor:
- Wrist flexion, finger flexion (apart from ulnar doing medial 2 FDP)
- 1/2LOAF: lateral 2 lumbricals, Oponens pollicis brevis, abductor pollicis brevis, flexor pollicis longus
Sensory:
- lateral 3.5 digits palmar surface
Median nerve lesions:
Lesion at the wrist:
- Loss of abductor pollicis brevis (thumb abduction, pen touch test)
Lesion at the elbow:
- Loss of flexon digitorum superficialis
- HAND OF BENEDICT, unable to flex lateral 3 fingers.
Ulnar Nerve
Motor: Finger abduction and adduction (PADs and DABs), flexor digitorum profundus digit 4 and 5.
Sensory: medial 1.5 digits
Ulnar nerve lesion
Wasting of intrinsic hand muscles apart from 1/2 LOAF (median).
Ulnar claw due to paralysis of lumbricals
- with ulnar paradox (distal lesion results in worsening of ulnar claw as the FDP is still active)
Froments sign:
- failure of adductor pollicis due to ulnar nerve palsy, requires flexion by flexor pollicis longus to compensate
How to differentiate between a L5 radiculopathy and common peroneal lesion ?
The differentiator is FOOT INVERSION.
L5 - weakness if dorsiflexion, inversion and eversion.
Peroneal - weakness in dorsiflexion and eversion, but preserved inversion by tibialis posterior innervated by tibial nerve.
How to differentiate between a femoral nerve lesion and L3-L4 lesion?
The difference is ADDUCTION.
Femoral nerve lesion will have preserve adduction with is performed by obturator nerve.
L3-4 lesion will have weak adduction.
NCS Patterns
Compound Muscle Action Potential (CMAP)
- reduced amplitude could be due to axonal damage, NMJ dysfunction, myopathy.
Sensory Nerve Action Potential (SNAP)
Reduced amplitude - axonal loss
Reduced velocity/increased latency, temporal dispersion - demyelination
EMG Patterns
Looks at spontaneous activity, MUPs and recruitment.
Neurogenic - increase spontaneous activity, large/prolonged/polyphasic MUP, reduced recruitment.
Myopathic - maybe increased spontaneous activity, small/short MUPs, increased/early recruitment.
Differential Diagnosis of Multiple mononeuropathy
Mononeuritis:
Infection: Leprosy
Inflammatory: Vasculitis (PAN, RA, Cryoglobulinaemia), Sarcoidosis
Mono-Neuropathy:
Extrinsic
- Trauma
- Compression
Intrinsic:
- Vascular
- Genetic
- Diabetes
DDx for Peripheral Neuropathy
Neuritis:
- Infection - HIB
- Paraneoplastic - Anti-Hu, Anti-CV2, Paraproteinaemia
Neuropathy:
- Extrinsic - infiltrative
- Intrinsic: Genetic (CMT), Metabolic (Diabetes), Nutritional (B12/B1), Drugs or Toxins (chemo, RTx, HAART, ETOH)
HIV neuropathy
Distal, symmetrical, sensory predominant neuropathy.
Usually small fibre predominant.
Paraprotein associated neuropathy
IgM most common
Distal Large Fibre Sensory Predominant
50% of IgM MGUS have anti-MAG Ab
Can mimic CIDP
AL amyloidosis associated neuropathy
painful, length dependent peripheral neuropathy with prominant autonomic failure
Charcot Marie Tooth Disease
Group of genetic peripheral neuropathies. Caused by genetic defect is important proteins within the neuron.
CMT1 - demyelinating, motor, autosomal dominant
CMT2 - Axonal, sensory, autosomal dominant
X linked CMTX
Autosomal recessive CMT4 (Rare)
Suspicion for genetic neuropathy if:
- early onset
- long and slowly progressive
- foot deformities
- lack of positive symptoms with clear sensory involvement.
Prevalence 1:2500
Management of diabetic neuropathy
1 - Amitriptyline (NNT 3.5 for reduction in pain)
2 - Duloxetine and venlafaxine
3 - Gabapentin and Pregabalin
Chemotherapy induced neuropathy
Platinum based (cisplatin, carboplatin, oxaliplatin)
Taxanes (paclitaxel, docetaxel)
Vinca alkaloids (Vincristine, vinblastine)
Bortezomib (proteasome inhibitor)
AIDP vs CIDP
AIDP nadir <4 weeks
- IVIG = PLEX
- NO STEROIDS, worse outcomes
CIDP nadir > 4 weeks
- Steroids used
- IVIg, PLEX, Steroid sparing agents, Rituximab in Ab positive disease
Antibodies in AIDP
GM1 GD1a in Axonal Subtype
GQ1b in Miller Fisher Syndrome
Pathophysiology of AIDP
Infection (C Jejuni) –> molecular mimicry –> auto Ab production by B cells –> IgG and complement depoition on Schwann cells –> Myelin stripping affecting predominantly the NERVE ROOTS and PROXIMAL NERVE (Blood nerve barrier lacking)
Presentation AIDP
Prodrome within 4 weeks prior - URTI/Diarrhoea
Acroparesthesia followed 7-10 days later by symmetric ascending weakness (legs, arms, face)
Severe radicular lumbar and neuropathic pain in 2/3 cases.
Nadir 2-4 weeks.
30% need ventilation.
Investigations in AIDP
Bloods:
- LFT and CK may be elevated
- Serology for C jejuni, HIV, CMV, EBV
- GQ1b Ab
CSF:
- Albuminocytologic dissociation
PFTs:
- Measure FVC, if <1L need to go to ICU
NCS in AIDP
Prolonged F wave latency
Prolonged distal latency / reduced velocity (motor before sensory)
Temporal Dispersion or Conduction block at 2 weeks
Tx of AIDP:
PLEX = IVIG for efficacy
- usually IVIG is used as is easier to deliver.
- Give within 2-4 weeks of onset
NO role for steroids, worse outcome.
Multifocal Motor Neuropathy
Immune mediated condition affecting only motor neurons. Asymmetric.
Serum Anti-GM1 Ab
NCS showing demyelination with conduction block.
Dorsal Root Ganglionopathy
THink of when pure sensory neuropathy with hands and feet onset at same time.
Think:
- Sjogrens
- Paraneiplastic
- B6 toxicity
HINTS Exam
Head Impulse - Abnormal in peripheral cause, normal in stroke.
Nystagmus:
- Unidirectional horizontal nystagmus, Follows Alexanders Law (nystagmus increased with gaze towards the fast phase - away from lesion) - peripheral.
- Vertical, bidirectional - central
Test of Skew - Abnormal in Central cause.
