Summary for All LMN UL and Cranial nerve

LMN  General approach:

summary 1. Proximal weakness, no sensory loss: AHC, muscle, NMJ
a) AHC (polio, SMA): severe wasting, asymmetry, STATIC course not progressive
b) NMJ E.g. MG: fatiguability, ocular and bulbar involvement, with NO wasting
c) Muscle: symmetric
2. Proximal weakness, sensory loss: root (C5-6), plexus + GBS/CIDP
3. Distal weakness, no sensory loss: AHC, pure motor polyradiculopathy, distal myopathy
a) AHC (AMLS): severe wasting, tongue fasciculations, bulbar involvement, mixed UMN and
LMN
b) Pure motor polyradiculopathy (MMN): not much wasting. Nerve pattern – MCPJ much
weaker than IPJ
4. Distal weakness, sensory loss: root/plexus, peripheral neuropathy, mononeuritis
multiplex
a) C7-8 radiculopathy / plexopathy: segmental weakness! Both MCPJ and IPJ are innervated
by C7-8, but MCPJ is supplied by radial nerve while IPJ are supplied by ulnar and median
nerve. Hence if BOTH MCPJ and IPJ are weak, this suggests C7/8 issue rather than a nerve
problem!
b) Peripheral neuropathy: see below
c) Mononeuritis multiplex: see below

 Mononeuritis multiplex:
1. Skin is the key – usually has rash or thickening!
2. Painful, patchy (not glove and stocking) numbness
3. Usually sequential/progressive, with acute or subacute history!
4. Causes = WARDS PLC: Wegener’s, AIDS/amyloid, RA, DM, Sarcoid/SLE, PAN, Leprosy,
Cancer

 Diffuse polyneuropathy:
1. Congenital: CMT, light chain/familial amyloidosis
- CMT: deformity extremely severe (pes cavus, clawed toes), young, thickened nerves. NCS:
uniform smooth changes in genetic diseases rather than patchy. CMTX: disproportionate
wasting of thenar eminence.
- amyloidosis: restrictive CMP, acquired form has light chain w edema
2. Metabolic/endocrine: alcohol, DM, B12 def, hypothyroid
3. Neoplastic/paraneoplastic: anti-Hu Ab +ve - pure sensory neuropathy in elderly!
4. Inflammatory: Sjogren's, GBS/CIDP, HIV
- consider especially if rapidly progressive!
- CIDP-POEMS (HIV): polyneuropathy, organomegaly, endocrinopathy (hypothyroid and
hypocortisolism), M-protein (light chain paraproteinaemia), skin changes. Classic
appearance: hyperpigmented, hypertrichosis, cachexic wasted face due to lipodystrophy,
clubbing, lyphadenopathy, ascites and edema. +/- autonomic sx - pupils sluggish, postural
giddiness, post prandial fullness, nocturnal diarrhoea, urinary urgency and incomplete
micturtion, excessive sweating
5. Drugs/toxins
6. Infection: lyme, diphtheria, leprosy

MND  Features of MND in general

approach 1. Fasciculation or tremor
2. Patterns: UMN, LMN prox or LMN distal
3. Prominent wasting.
- Diffuse: bilat wasting with bulbar involvement. Non diffuse: localized wasting
4. Mixed LMN and UMN signs
5. No ocular, sensory or cerebellar involvement

 Classification:
1. Diffuse: bulbar involvement
a) Spinobulbar muscular atrophy (SMA): sex-linked version involving trinucleotide repeat
mutation in androgen receptor gene is known as Kennedy’s disease. Has diffuse proximal
weakness and gynaecomastia!
b) AMLS
2. Non diffuse: localized wasting
a) Hirayama disease / monomyelic amtroptrophy: localized/focal wasting of one upper
limb!! Common in young oriental men, particularly in Sg
b) Polio: asymmetric wasting, patchy involvement of UL and LL but STATIC course!

 Mgt of ALS:
1. Riluzole 50mg BD
2. Aggressive ST and PT
3. Monitor noctural hypoventilation, early NIV
4. Dysphagia: PEG
5. Screen for depression, SSRI
6. End of life discussion.
UMN See LL notes – divided by sensory!
Summary How to tell UMN: through COMBINATION of tone, reflex, power, sensory
Soft sign: big toe dorsiflex MORE than rest of ankle

 Co-existing pathology E.g. UMN + cerebellar

1. 2 common disease: C myelo + DM peripheral neuropathy
2. Multisite disease: MS, SCD, MSA
3. Occurring at border-zone btw CNS and PNS: myeloradiculitis, syringomyelia
Cranial  Approach to localize any CN palsy:
nerve 1. Cranial nerve clubs: 2, 3, V1, 6
approach 2. Brainstem signs (long tract): pronator drift, cerebellar
Summary 3. Systemic E.g. GBS: reflexes (areflexia), sensation (peripheral neuropathy)
4. Meninges/base of skull: epistaxis, lymphadenopathy, RT/surgical marks

 Uniocular visual loss:

1. Correctable by pinhole/glasses: refraction error, as in myopia/cataract
2. Not correctable + RAPD:
a) Optic neuropathy
b) Massive retinal problem: CRAO, CRVO, complete RD. If no evidence of this, expect pallor
(optic atrophy)

 Features of optic neuropathy / RAPD:

 1. Uniocular visual loss, not correctable by pinhole/glasses, with RAPD!
2. Does not cause asymmetric pupils in normal light, only when shine torch
3. Part of pathophysio of RAPD involves difference in visual acuity btw the R and L eye.
Therefore if both eyes are equally blind, RAPD should not occur!

 Causes of optic neuropathy: uniocular visual loss, uncorrectable, with RAPD

1. Inflammatory/infectious*: NMO (more common in Asian), MS, Anti-MOG Ab +ve (less
common form of NMO), sarcoidosis/SLE/GPA
2. Neoplastic/paraneoplastic*: optic glioma, meningioma
3. Metabolic-endocrine: B12 deficiency, thyroid eye disease
4. Vascular-degenerative (hyperacute): AION, PION, arteritic AION in temporal arteritis
5. Drugs: trauma, radiation, methanol, ethambutol
6. Congenital: Leber’s optic atrophy, Friederich’s ataxia

 Binocular visual loss:

1. Diplopia: vision improves when one eye is closed!
a) Muscle: thyroid eye disease, CPEO
b) NMJ: MG
c) Cranial nerve (EOM deficit): CN3, 4, 6. See approach to CN to localize!!
d) Brainstem: INO, skew deviation. Subcortical and cortical pathology do not cause diplopia,
only brainstem!
2. Vision does NOT improve with one eye closed -> do VF!!
a) VF defect: approach to homonymous or bitemporal hemianopia
b) If both fields affected, refractive or retinal issue
Etiology  How to give ddx for etiology:
1. Patient demographic: young or old
2. Disease characteristic: duration (acute, subacute, chronic, genetic), progressive (unlikely
to be metabolic)
3. Treatable diseases
4. Common diseases

 6 common etiologies for ALL!

From very chronic to acute! CD MINI V + Human!
1. Congenital: young, very chronic
2. Degenerative: old, chronic
3. Metabolic-endocrine – do NOT say this as first ddx as it is too common! Also static and
not progressive!
4. Inflammatory: young to middle age, subacute, progressive, relapsing-remitting course
5. Neoplastic/paraneoplastic: old, subacute
6. Infective: subacute to acute, constitutional symptoms
7. Vascular: old, hyperacute
8. Human activity E.g. meds, radiation, trauma

 Common tested etiology for CD MINI VH:

1. Congenital
2. Metabolic-endocrine: alcohol, B12, Cushings, DM, hyper/hypothyroid (do NOT mention
this as first ddx!)
3. Inflammatory:
a) NMO (more common in Asian), MS, ADEM
 b) SLE, Sjogrens
c) GCA/Takayasu, Wegener’s granulomatosis
4. Infectious:
a) Bacteria: mycoplasma, TB, lyme, syphilis,
b) Virus: zoster
c) Fungal
d) Parasite: cysticercosis
5. Neoplastic: dermatomyositis, SOL (leukemia, lymphoma, intracranial SOL E.g.
meningioma)
6. Vascular: aneurysm, infarct, C-C fistula!
7. Human:
a) Toxins, drugs
b) Radiation, trauma
Invx  Summary statement for all: XX is ultimately a clinical diagnosis, but I would like to
confirm the diagnosis and look for underlying etiology with radiological, serological,
electrophysiological tests.

 Tests:
1. Radiology:
a) I would like to exclude a structural lesion by performing a dedicated MRI of the spine /
brain/ orbit
b) CXR: E.g. cervical rib, mediastinal mass, lung mass
2. Electrophysiological:
a) EMG: differentiate nerve, muscle and AHC cause
- Muscle: fibrillations, positive sharp waves
- Electrical myotonia: repetitive firing of muscle action potentions following a stimulus, with
discharge classically decreasing in amplitude and frequency with time
- Nerve, Axonal (AA!): decreased Amplitude
- Nerve, demyelinating: decreased velocity and prolonged latency
b) NCS:
3. Serological:
a) FBC RP TFT B12 folate electrolytes VDRL caeruloplasmin
b) Specific antibodies: MG (AChR Ab, MSK), MMN (Anti GM1 ganglioside), NMO (aquaporin
4) +/- genetic testing!
c) CK, aldolase
4. I would also perform tests looking for complications of disease, including:
a) ECG for LVH / arrhythmias from conduction blocks / prolonged QTc, TTE for
cardiomyopathy
b) CXR for cardiomegaly and aspiration pneumonia
c) Endocrine tests for DM (fasting glucose), hypogonadism (testosterone, FSH/LH),
hypothyroidism (TFT)
d) PSG for OSA / nocturnal hypoventilation
Mgt  Standard mgt for ALL:
1. Education and counselling: genetic counselling +/- end of life discussion, fertility planning
2. Multidisciplinary approach, with aggressive physiotherapy (AFO, back brace, walking aid)
and speech therapy
3. Manage complications:
a) Immobility: pneumonia, pressure sore, DVT
b) Dysphagia: NGT, early PEG
 c) Screen for conduction blocks, dilated CMP
d) PSG for OSA / nocturnal hypoventilation, followed by early initiation of NIV
e) Screen for depression
f) Screen for vit D deficiency, osteoporosis
g) Additional for myotonia dystrophica: DM, thyroid/hypogonad, cataract, ANA
4. Medications to slow disease progression / symptoms:
a) ALS: ropinirole 50mg BD
b) Spasticity: baclofen
c) Neuropathic pain: gabapentin, TCA
d) Cramps: quinidine, phenytoin
e) Myotonia: Mexiletine or flecainide

 Mgt of SE of immunosuppressants (common question!):

1. Infection: screen Hep B/C/pTB, vaccines
2. Bone density: vit D and osteoporosis
3. PUD
4. Control CV RF: DM, HTN
- diet: low salt, low fat, low sugar
5. Cataract, IOP
6. Replace K
Wasted / Claw hands (Distal weakness of UL!!)
Claw,  Pathophysio of claw hand: weakness of intrinsic muscles causing hyper-extension of the
wasted MCPJ and flexion of the IPJ
hands
approach  Ddx:
- Approach to distal weakness + cord, RA!
- Claw hand = include partial claw. Usually does not include distal myopathy
- Wasted hand = same approach as claw hand + distal myopathy!
1. Partial claw: ulnar nerve
2. Distal, NO sensory loss:
a) AHC: MND, SMA, polio*
b) Pure motor polyradiculopathy: MMN*
c) Distal myopathy: myotonia dystrophica*, inclusion body myositis
3. Distal, with sensory loss:
a) Root/plexus: C8/T1 radiculopathy E.g. Pancoast, lower brachial plexopathy (cervical rib)
b) Peripheral neuropathy: combined median and ulnar nerve, CMT, leprosy*
c) Mononeuritis multiplex
3. Cord: C myelopathy/spondylosis, syringomyelia
4. Disuse atrophy from RA/CTD, Volkmann’s ischemic contracture
Steps 1. Screen open/close fist at start
2. UL neuro exam – rmb to differentiate power of MCPJ and IPJ to determine whether this
is a segmental or nerve pattern of weakness!
3. Specific ulnar nerve exam if suspect ulnar nerve lesion, test thumb APB (point towards
nose) for median nerve
4. Specific tests: myotonia and ptosis if suspect myotonia dystrohica, look for thickened
nerves (leprosy)

Invx 1. Radiological: MRI of spine to rule out structural lesion or cervical myelopathy
+/- CXR for Pancoast tumour, cervical rib
 2. Serological:
a) Fasting blood glucose and HBA1c
b) Anti GM1 ganglioside antibodies for MMN (rare)
c) Autoimmune screen if suspect disuse atrophy from MCTD
3. Electrophysiological:
a) Nerve conduction study
b) EMG if suspect myotonic dystrophica, muscles biopsy if inclusion body myositis
Proximal weakness / myopathies
Exam 1. Inspect: look for ptosis, fasciculation, hearing aid (FSHD 75% or mitochondrial), rash,
endocrine/metabolic (alcohol, thyroid, cushings)
2. UL Neuro: symmetric weakness with not much wasting, reflexes can help differentiate
3. Ocular: EOM (ptosis), fatiguability (look up and to the side for 20s, lift one eyelid)
4. Bulbar: stick out tongue. Look for wasting and fasciculations
5. Facial weakness / CN7
- FSHD – lower facial weakness worse than upper facial weakness
6. Neck flexion – forehead against hand
7. Specific tests depending on suspicion:
a) FSHD: stretch out arms to look for “curious scapula” and stick-like humerus
b) Myotonia tests:
- Grip myotonia: ask pt to open and close fist. Fingers will take time to open
- Percussion myotonia: lightly percuss thenar eminence. Thumb will go inwards
c) MG:
- Fatiguability: look up and to the side to elicit, raise one eyelid
- Offer icepack test (improve with ice)
- Cogan’s eye twitch: ask pt to look down at object, then look straight at you at their eye
level. For pts with MG, the eyelid will twitch up and down a few times.
8. Offer: gait/gower’s sign (squat to stand), swallowing assessment, NIF/FVC (</=15ml/kg)
Present 1. This pt has proximal myopathy
2. Bilat UL weakness more prominent proximally, in a LMN pattern
a) Weakness of neck flexion
b) Normal tone
c) Reflexes: normal (MG), decreased (myotonia dystrophica, LEMS), areflexic (MF)
d) Sensation is intact
3. This is seen in association with (5 possibilities):
a) MG: fatiguability, ocular, bulbar involvement
b) Myotonia dystrophica:
- Face: bilat ptosis, frontotemporal balding, temporalis wasting, hollow cheeks
- Grip and percussion myotonia
c) Dermatomyositis: rash
d) Muscular dystrophy: pseudohypertrophy/kyphoscoliosis, FSHD signs
e) Endocrine: alcohol, thyroid, Cushings
Ddx  Ddx for SYMMETRICAL proximal weakness (2): muscle, NMJ!
1. Muscle = see causes of myopathy
2. NMJ: MG, LEMS
AHC has prominent wasting and fasciculations so not included in ddx!

 Causes of myopathy:
1. Congenital (from most common tested to least): FSHD, myotonia dystrophica, Beckers,
 LGMD
2. Endocrine-metabolic:
a) Endocrine: alcohol, hyper/hypothyroid, Cushings, vit D deficiency
b) Metabolic: glycogen storage disease (McArdles), mitochondrial myopathy
3. Neoplastic/paraneoplastic: dermatomyositis
4. Inflammatory/infectious:
a) Dermatomyositis/polymyositis
b) Inclusion body myositis – prominent finger flexor weakness
c) Necrotizing autoimmune myopathy (NAM) – subset of polymyositis that is SRP /
HMGCR+ve. Presents like LGMD but no CTD or famhx. Always offer this as ddx as it is
treatable by IVIG!!
5. Human: statin, fibrate, hypoK, colchicine
Congenital  FSHD (AD, most common):
causes 1. Lower face weaker than upper face
2. Arms outstretched:
a) Winging of scapula from back
b) “Curious scapula” from front – scapula “looks over” the shoulder like a lump –
pathognomonic!
c) Prominent axillary folds due to weakness of pectoralis
3. Stick-like humerus
4. Disproportionate biceps weakness
5. Beevor sign: umbilicus moves upward when pt tries to do crunch/situp

 Myotonia dystrophica (trinucleotide repeat):

1. Face (5): bilat ptosis, frontotemporal / male pattern balding, wasting of the
temporalis/masseter/SCM, weakness of facial muscles with hollow cheeks
+/- bilat cataracts: early onset, iridescent, posterior subcapsular
2. UL: distal weakness particularly affecting finger flexors and elbow extensors, with normal
tone, decreased reflexes, intact sensation
- can also cause proximal weakness
3. Myotonia: grip, percussion, difficulty opening eyes after forceful closure
4. LL: bilat footdrop/AFO
5. Complications = offer:
a) CVS: MVP, ICD due to heartblock/malignant tachyarrthyhmias, CCF
b) PHTN, aspiration pneumonia
c) Thyroid exam for hypothyroid, examine testes for hypogonadism
d) Cataract
 Ddx for myotonia dystrophica:
1. Causes of myotonia (4): myotonia congenita (Thomsen’s/Beckers), paramyotonia
congenita, hypoK periodic paralysis, drugs (clofibrate)
2. Causes of distal weakness (4): CMT, distal SMA, inclusion body myositis,
oculopharyngodistal myopathy

 Becker’s (X-linked recessive):

1. Well adult male (onset 5-25 years old)
- Duchenne NOT tested as most have died by adulthood (onset 3-6 years old)!
2. Calf muscle pseudohypertrophy
3. Kyphoscoliosis
4. Gower’s sign, waddling gait
 5. Complications (4): arrhythmias due to fibrosis of LV wall, dilated CMP (displaced apex
beat, functional MR), PHTN, respi failure

 LGMD (AR):
1. Heterogeneous group of disorders involving weakness of shoulder and pelvis, sparing the
face and heart
2. NO calf hypertrophy
3. Bilat UL resembling calf heads on a trophy – diagnostic for Miyoshi myopathy / LGMD
2B/dysferlinopathy!
Invx 1. Clinical diagnosis
2. Serological looking for underlying etiology:
a) CK, aldolase
b) Autoimmune (extractible nuclear antigen ENA including Anti-Jo1, anti-MI2, ANA, RF),
endocrine (TFT, fasting glucose, electrolytes especially K)
c) AChR and anti-MUSK for MG, anti P/Q voltage gated calcium channels for LEMS
3. Electrophysiological i.e. EMG:
a) Muscular dystrophy: abnormal spontaneous activity (fibrillation and positive sharp
waves)
b) Myotonia dystrophica: electrical myotonia
c) MG: see MG section!
4. Genetic testing! Most useful test for myotonia dystrophica is in fact DNA testing of
leukocytes!!
Mgt 1. Genetic counselling:
a) FSHD: AD in 80%
b) Myotonia dystrophica: AD (50%) from trinucleotide CTG repeat and has anticipation
hence worse in subsequent generations!
c) DMD/Becker’s: X-linked recessive, boys
d) LGMD: AR
2. Multidisciplinary: PTOT for rehab and AFO, ST (NG, PEG)
3. Mgt of symptoms: melixatide / flecainide for myotonia
4. Mgt of complications:
a) Heart block, CMP – annual ECG, TTE, KIV ICD
b) PSG for OSA KIV nocturnal NIV
c) Screen for vit D deficiency, osteoporosis
d) Screen for depression
*Additional for Myotonia dystrophica:
a) DM, hypogonad
b) Cataract
c) Avoid depolarizing anaesthetic agents during surgery for myotonia
5. Flu, pneumococcal vaccine
MG
Present 1. This pt has myasthenia gravis, as evidenced by:
a) Symmetric proximal muscle weakness in a lower motor neuron pattern, with weakness
of neck flexion
b) Reflexes are preserved (reduced in LEMS, arreflexic in MF) and sensation is intact
c) There is fatiguability with ptosis after exertion
d) Ocular: complex opthalmoplegia with binocular diplopia
e) Bulbar involvement (3): slurred/nasal speech, weakness of palatal elevation, NGT/PEG
suggestive of swallowing dysfunction
 2. Treatment complications:
a) Midline sternotomy scar suggestive of previous thymomectomy
b) Cushingoid appearance suggestive of chronic steroid therapy
c) Central line suggestive of recent hospitalization
3. In terms of associated features:
a) Signs of other autoimmune diseases: Graves/Hashimoto thyroiditis, DM, RA
(penicillamine induced), SLE
b) Cachexia/LN - suggests Lambert Eaton
4. In summary, this pt has evidence of myasthenia gravis with ocular, bulbar and limb
involvement

 Main ddx:
1. Lambert Eaton: cachexia/cervical LN, decreased reflexes
2. Miller Fisher: arreflexia, patchy sensory loss
3. Botulism
4. Mitochondrial myopathy (hearing aid)
Definition  Definition:
1. Chronic autoimmune disorder of the post synaptic membrane at the neuromuscular
junction in skeletal muscles
2. Age: female 20-30 years old, male >50 years old
3. 3 clinical presentations: ocular, oropharyngeal (bulbar), generalized

 MG Foundation of America grading of severity:

1. Grade 1: ocular only
2. Grade 2: muscles other than ocular
a) 2A: limb and axial
b) 2B: respiratory and bulbar muscles
3. Grade 3: moderate weakness, grade 4 severe weakness, grade 5 require intubation

 MUSK Ab +ve MG variant:

1. Not much ocular sx
2. Prominent weakness of neck flexion, bulbar sx (trident pattern of tongue with 3 lines due
to wasting)
3. Profound facial weakness – unable to close eyes completely!
Invx "MG is a clinical diagnosis supported by serological and electrophysiological tests"
1. Serological tests:
a) Nicotinic acetylcholine receptor Ab: positive in 50% ocular, 85% generalized
b) Muscle specific kinase Ab: 70% of those with acetylcholine receptor -ve
c) Anti P/Q voltage gated calcium channel Ab for LEMS
+/- Tensilon test: improvement in weakness after giving edrophonium
2. Electrophysiology:
a) Repetitive nerve stimulation (place electrode over end plate region of muscle): >10%
decline in compound muscle action potential (CMAP) amplitude between the 1st and 4th
potential in a train of 10 stimulations
- LEMS: doubling of CMAP post exercise!
b) Single fibre electromyography: evidence of neuromuscular blockade with abnormally-
increased jitter. More sensitive and specific than RNS but less readily available/more
technically difficult
3. Imaging:
 a) CT thorax: 15% thymoma, 75% thymic hyperplasia
b) CXR: anterior mediastinal mass, aspiration pneumonia, small cell lung Ca
4. NIF/FVC to screen for respi muscle weakness
5. FBC, RP, LFT prior to starting immunosuppressive therapy
Mgt  Stable disease mgt:
1. Immunosuppression: steroids (watch for paradoxical worsening) +
azathioprine/cyclophosphamide
2. Anti-cholinesterase pyridostigmine
3. Thymomectomy

 Emergency:
1. Secure airway with intubation and mechanical ventilation
2. Withdraw anti-cholinesterase meds
3. Plasma exchange or IVIG

 Myasthenic crisis: exacerbation requiring mechanical ventilation

1. Definition:
a) FVC 15ml/kg or less (normal >/=60ml/kg)
b) NIF 20cmH2O or less (normal >/=70cmH2O)
2. Ppt:
a) Non-compliance to meds
b) Infection
c) Stress: pregnancy, post-partum, surgery
d) Meds: aminoglycosides, procainamide, phenytoin

 Cholinergic crisis
1. Definition: weakness due to over-treatment with anti-cholinesterase
2. Presents as flaccid paralysis with cholinergic manifestations – diarrhoea, salivation,
miosis
Median nerve
Steps in 1. Look:
O/E a) Wasting of forearm muscle and thenar eminence
c) Make a fist  Benediction sign (suggest elbow lesion), clawed hands
2. Feel:
a) Numbness over palmar aspect of lateral 3.5 digits (thumb to 4th finger)
- test split finger sign of 4th finger!
b) Sensation of thenar part of palm. Numbness = lesion proximal to wrist (palmar
cutaneous branch) i.e. not CTS!
3. Move:
a) "OK": AIN - opponens pollicis
b) "Good" / "push up against my thumb": abductor pollicis brevis (APB)
c) "Push in against my thumb": flexor pollicis
d) Cross fingers for ulnar intrinsics
e) Test if can bend DIPJ of 1st to 3rd fingers (isolate at PIPJ) -> FDP, high lesion
4. Special tests:
a) Phalens: elicit pain when wrist held in flexion for 60s + can do compression test
(Durkans) at same time!
b) Tinels: tapping above wrist crease (in which median nerve is entrapped) causes electric
shooting sensation down radial 3.5 fingers within 30s
 5. Overall, the level of the lesion is at___ and the likely etiology is__
Present 1. This pt has a median nerve palsy, with:
a) Wasting of the thenar eminence
b) Weakness of thumb abduction, flexion and opposition
c) Sensory loss over palmar aspect of first 3.5 fingers
d) Tinel's and Phallens are positive
2. Level of lesion (3):
a) High lesion: Benediction sign, inability to flex DIPJ of medial 3.5 fingers (FDP)
b) Low/CTS: sparing of thenar sensation!
c) AIN: when only lesion is cannot do OK sign!
3. Associated findings/etiology:
a) Endocrine: acromegaly, hypothyroid/myxoedema
b) Joint deformities: RA, gout
c) Trauma/surgery: scars from supracondylar humeral fracture
d) DM/ANCA-associated vasculitis: mononeuritis multiplex!!
e) Infiltrative: amyloidosis, renal failure, sarcoidosis
f) Infection: Lyme, HSV
Ddx 1. C7 radiculopathy: C7 elbow extension, C6 wrist extension, no splitting of sensation of 4th
finger
Anatomy  Supply of median nerve:
1. Motor:
a) Anterior forearm compt, superficial: pronator teres, FCR, flexor digitorum superficialis
(PIPJ flexion), palmaris longus
b) Anterior forearm compt, deep: FPL, pronator quadratus, medial half of FDP (DIPJ flexion)
c) Hand: lateral 2 lumbricals (MCPJ), opponens pollicis, APB, FPB i.e. supplies thumb
opposition, flexion and abduction!
2. Sensory:
a) Palmar aspect of lateral 3.5 fingers
b) Palmar sensation - supplied by palmary cutaneous branch proximal to the wrist crease/
not in carpal tunnel

 Course of the median nerve

1. Origin: arise from medial and lateral cord of brachial plexus
2. Arm: enters arm closely related to brachial artery - does not have branches above elbow
3. Cubital fossa: most medial structure (MBTR)
4. Forearm:
a) Passes through 2 heads of pronator teres
b) Supplies all flexors in the forearm except the FCU and ulnar half of the FDP. The AIN
supplies 3 muscles: FPL, FDP, pronator quadratus
c) Supplies hand muscles: LOAF - lateral 2 lumbricals, opponens pollicis, abductor pollicis
brevis, flexor pollicis brevis (deep head supplied by ulnar nerve). The APB is the only muscle
exclusively supplied by the median nerve!
d) Palmar cutaneous branch of the median nerve is given off at wrist before flexor
retinaculum, provides sensory supply to the thenar eminence, and hence is not affected in
low median nerve lesions.
Invx, mgt  Invx:
1. Nerve conduction study to confirm diagnosis and assess severity
- would also consider an EMG of thenar eminence/APB. Recent denervation is suggested by
fibrillation potentials, vs electrically silent
 2. Imaging - XR of hand/forearm
3. Bloods looking for causes of secondary CTS:
a) Endocrine: fasting glucose, HbA1c, TFT, IGF1-R
b) Renal panel
c) Autoimmune panel: ANA, RF/anti-CCP, ANCA, ENA (extractible nuclear antigens)
d) If suspect Lyme, screen for Borrelia

 Mgt:
1. Education and counselling: job modification
2. Supportive: OT, wrist splint
3. Symptoms: NSAIDs, intra-articular steroids
4. Surgery: carpal tunne release - operative division of anterior carpal ligament. Indication:
muscle wasting indicating severe nerve compression, failed conservative treatment
5. Treat underlying cause

 Prognosis:
1. Neuropraxia: no disruption to sheath or axon. Complete recovery, rapid within weeks
2. Axonotmesis: disruption of axon but intact Schwann sheath. Complete recovery but
slower 1mm/day
3. Neuronotmesis: incomplete recovery
Radial nerve palsy
Steps in 1. Look:
O/E a) Wrist drop (ECR, ECU), finger drop
b) Scars: axilla, arm, elbow, forearm
c) Wasting of the posterior compartment of the forearm
2. Feel: anatomical snuffbox or first dorsal webspace
3. Move:
a) Elbow extension (triceps)
b) Elbow flexion with forearm held between supination and pronation (brachioradialis)
c) Forearm supination (supinator)
d) Wrist extension (ECR, ECU)
e) Finger extension at MCPJ (hold out wrist first then ask pt to straighten finger)
f) Sparing of Thumb abduction / flexion (median), adduction (ulnar)!
4. Special test:
a) Reflexes: triceps jerk is reduced ONLY in lesions at the axilla!
b) Tinels along course of radial nerve
Present 1. This pt has a radial nerve palsy, with:
a) Weakness of elbow extension  axillary lesion
b) Weakness of elbow flexion and forearm supination  spiral groove of humerus
c) Weakness of wrist and MCPJ extension  proximal forearm/PIN
d) Completely intact motor  wrist/radial neck lesion
2. There is Sensory loss over the 1st dorsal webspace
- no sensory loss = PIN in prox forearm!
3. Triceps reflex is preserved.
- triceps reflex lost = axillary lesion!
Ddx 1. C7 radiculopathy:
a) shoulder adduction and wrist flexion also gone!!
b) Additional loss of sensation over palmar aspect of medial finger!
2. Plexopathy
Anatomy  Supply of radial nerve:
1. Motor:
a) Triceps, brachioradialis, extensor carpi radialis longus (ECRL), anconeus
b) Deep branch: ECRB, supinator
c) PIN supply: all wrist extensors except the ECRL/ECRB (ECU), all finger extensors (extensor
digitorum of the MCPJ, extensor indicis, extensor digiti minimi, extensor pollicis brevis and
longus) + abductor pollicis longus (APL), supinator
2. Sensory:
a) Anatomical snuffbox - dorsal aspect of radial 3.5 finges
b) Posterior cutaneous, inferior lateral cutaneous -> posterior aspect of forearm and distal
arm

 Course of the radial nerve:

1. Radial nerve arises from the posterior cord of the brachial plexus (C5-T1).
2. It travels through the triangular interval of the axilla, and then continues in the spiral
groove between the lateral and medial heads of the triceps
3. At the lower 1/3 of the arm, it pierces the intermuscular septum to enter the anterior
compartment of the arm
4. At the elbow, it passes anterior to the lateral epicondyle to enter the forearm, where it
divides into the superficial and deep branch
a) The superficial branch descends under the brachioradialis and mainly supplies sensation
of the dorsal radial 3.5 fingers.
b) The deep branch pierces the supinator muscle, after which it is known as the PIN. It
supplies all extensors of the forearm, the abductor pollicis longus and the supinator. The
ECRL and ECRB are given off before PIN arises.
Causes and  Causes of radial nerve palsy
localization 1. Axilla: crutch palsy, humeral head #
2. Spiral groove of humerus: mid-shaft humerus fracture, Sat Night palsy
3. Elbow/prox forearm (PIN): : neck of radius #, elbow dislocation, tight cast, rheumtoid
nodules
4. Wrist: distal radius fracture, tight watch/jewelry/handcuff
5. Mononeuritis multiplex

 Localizing radial nerve lesion:

1. Axilla: all motor affected till elbow extension! Triceps reflex reduced.
2. Spiral groove of humerus:
a) If upper 1/3 humerus: same as axilla i.e. all motor and sensory gone
b) If middle 1/3 humerus: triceps/elbow extension normal!
c) If lower 1/3: triceps and brachioradialis normal!
3. Proximal forearm/elbow (PIN): normal elbow extension and flexion, supination (ECRL
given off before PIN). Only has wrist and finger drop. Sensation is NORMAL as PIN is pure
motor branch!
4. Wrist: all motor normal! Sensory loss over anatomical snuffbox still present!

Ulnar nerve
Steps 1. Look:
a) Wasting of hypothenar eminance
b) Ulnar claw:
 - results from unopposed extension of the MCPJ due to paralysis of the medial two
lumbricals, and flexion of the DIPJ (medial half of FDP)
- Ulnar paradox: lesion at wrist cause more deformed claw. Because proximal lesions
paralyse medial half of FDP, reducing the flexion deformity
2. Feel:
a) Palmar medial 1.5 (4th and 5th)
b) Dorsal medial 1.5: numbness indicates lesion prox to wrist!
c) Test 4th finger split. Numbness over the radial half of 4th finger implies a C8 lesion rather
than ulnar!
3. Move:
a) FCU: wrist flexion in ulnar direction
b) FDP medial 1.5: flex DIPJ of 4th and 5th finger
- lesion is distal if preserved!
c) PAD = Palmar interossei, ADduction: clip paper btw fingers
d) DAB = Dorsal interossei, ABduction: spread fingers
e) Thumb adduction / Froments sign: ask pt to hold piece of paper between extended
thumb and index, then try to pull out paper. +ve if pt has to flex or abduct the thmb to
maintain grip on paper!
4. Provocation tests:
a) Flex elbow 1 min
b) Tinels: tap along course of ulnar nerve from medial 1.5 fingers to medial epicondyle!
Anatomy  Supply:
1. Motor:
a) Forearm: FCU, medial half of FDP (DIPJ)
b) Small muscles of the hand: digiti minimi (little finger), interosseous muscles, adductor
pollicis, medial two lumbricals
2. Sensory: palmar and dorsal aspects of medial 1.5 fingers
Ddx  Ddx:
1. C8/T1 palsy
2. Cervical syringomyelia

 Causes of ulnar nerve lesions

1. Elbow: elbow fracture, arthritis, compression from prolonged leaning on flexed elbow or
during surgical procedure, cubital tunnel syndrome
2. Wrist: hook of harnate fracture, laceration, repetitive strain injury (due to propulsion of
wheelchair), wrist ganglia
3. General mononeuritis: leprosy, vasculitis, hereditary neuropathy, acromegaly
Invx, Mgt  Invx: NCS, XR of wrist/elbow tro underlying fracture
 Mgt: splinting, avoid exacerbating activities, surgery