By Sean DadswellJune 2011

AimsDiscuss physiology associated to PNEDiscuss general signs and symptoms of PNEIdentify:

Case StudyClinical presentation PathophysiologyDifferential diagnosisDiagnostic technique/tests Treatment of some of the more common PNE’s

Neural PhysiologyNee & Butler 2005, Prinz et al 2005

Basic structure as shownNeurons have a cell body

which contains nucleus, cytoplasm, mitochondria and other organelles.

Dendrites which collect information and transport it to the cell body

Axon which transport information away from the cell body

Synapse which transfers info to other cells

How long is a neuron?How fast do they repair?

WHY?

Axoplasmic flowProcess by which nerve

cells transport proteins, lipids and other materials essential for the maintenance and repair of the cell from the cell body along the axon.

Also means of removing molecules responsible for axon degradation

Molecules are transported down microtubules by specific proteins and enzymes

The speed of this transport is from 0.1mm-400mm day

Axons can be 10000 times longer than the cell body

Cell Transport (Prinz et al, 2005)

Nerve injuryNerve injury secondary to compression or traction depends

on intensity and duration.

Seddon has classified nerve injuries into 3 categories:First, neuropraxia, is a transient episode of motor paralysis

with little or no sensory or autonomic dysfunction. No disruption of the nerve or its sheath occurs. With removal of the compressing force, recovery should be complete.

Second, axonotmesis, is a more severe nerve injury with disruption of the axon but with maintenance of the Schwann sheath. Motor, sensory, and autonomic paralysis results. Recovery can occur if the compressing force is removed in a timely fashion and if the axon regenerates.

Third, neurotmesis is the most serious injury. The nerve and its sheath are disrupted. Although recovery may occur, it is never complete, secondary to loss of nerve continuity.

Mechanical or chemical irritation

Compromised intraneural circulation

Reduced axoplasmic flow

Hypoxia and altered microvascular permeability

Subperineurial oedema

Intraneural fibrosis

Neural Injury Cascade

How does this lead to pain?Endoneurial oedema

increases sensitivity of nocioceptors in the nervi nervorum (nerves that innervate the neural sheath of larger nerves)

Intraneural fibrosis reduces extensibility of the nerves increasing mechanical stimulation of nervi nervorum

Reduced axoplasmic flow =>Reduced myelin thickness

Formation of Abnormal Impulse Generating Sites (AIGS)As nerve injury leads

to altered gene expression and increases number of ion channels along axon (as ion channels can only form on unmyelinated parts of axon)

Ion channels increase sensitivity of neurons

AIGS sensitive to adrenaline and noradrenaline so neuropathic pain often sensitive to stress

Afferent axons (ie those travelling from spinal cord outwards) can cause the release of pro-inflammatory chemicals into their target tissue (neurogenic inflammation) so can have a detrimental impact on the tissue it supplies

Central sensitisation and altered descending pathway inhibition

Other symptomsPositive Symptoms

(abnormal level of excitability of the nervous system)Pain (often deep)ParasthesiaDysesthesia

Hyperalgesia Allodynia

Spasm

Negative symptoms (reduced impulse conduction of neural tissue)Hypoestesia/

anesthesiaweakness

Carpal Tunnel Syndrome (Shapiro & Preston 2009)

Most common entrapment neuropathy

Median nerve compression by the transverse carpal lig

More women than menOften bilat but almost

without exception more prominent in the dominant hand

Paresthesia usually in median nerve distribution

(thenar eminance spared as supplied by palmar cutaneous sensory branch which comes off proximal to the carpal tunnel

Advanced cases may have thenar muscle weakness/wasting effecting thumb opposition and ab

Median nerve sensory distribution

Median nerve

Flexor tendonsTransver

se carpal ligament

Causes of CTS

Often idiopathicRepeated stress to

connective tissueRepetitive hand useIndividuals with small

carpal tunnelSystemic disorders (RA,

hypothyroidism, DM, sarcoid, amyloidosis

Mass in wrist (ganglion cyst, neurofibroma, arteriovenous malformation)

Pregnancy

Persistent wrist flex ie during sleep

Thenar eminence wasting

CTS contPhalan’s good specific

(75-93%) and moderate sensitive (64-75%) for CTS

Tinel’s similar spec & sens (tetro et al, 1995 Bolland et al, 2008)

Carpal compression test more spec less sensitive

NCS and EMG can help confirm diagnosis and discount others (however can be normal in 25% of cases)

Differential diagnosis:C6-7 radiculopathyBracial plexopathyProximal median

neuropathyThese can be identified

by pain in the neck, reduced reflexes, weakness outside median nerve distribution, sensory loss in the thenar eminence.

Treatments for CTSRemove causative

factorsSplints (night)NSAIDsInjection (beware >3

may => tendon rupture) may be particularly helpful during pregnancy or other reversible condition i.e. Hypothyroidism

Surgical decompression (open safer than closed but longer recovery)

Wrist stretchesWrist mobsMedian nerve mobs

www.emglaboratory.com

Ulnar Neuropathy at the Elbow (Robertson & Saratsiotis 2005)Second most common

PNE in upper limbCaused by compression

of ulnar nerve in the ulnar groove or cubital tunnel

Results from repeated trauma,OA following #, ganglion/tumours/fibrous tissue

Manifests as progressive loss of grip and pinch strength and interosseus muscle function

ClumsinessWasting of thenar and

hypothenar eminence

Thenar and hypothenar eminence wasting in the left hand

Interosseous muscle wasting

Ulnar neuropathy contMay be minimal sensory

loss reported but may be evident 4th and 5th finger on Ax

Elbow pain common spreading to wrist

Ulnar nerve may be palpable and tender

Paresthesia provoked by tinel’s, ulnar nerve compression or elbow flexion

Making a fist may result in 4th and 5th finger not flexing (FDP innervated by UN)

Thumb ab and opposition are spared

Ulnar neuropathy contSeveral classic hand

postures may be presentBenediction posture Wartenberg’s signFroment’s sign

Differential diagnosisC8-T1 radiculopathyBrachial plexopathyUNE forearm or wrist

There may be weakness in muscles not innervated by the ulnar nerve or loss of sensation extending up the forearm

AxAll previously

mentioned findingsNCSEMG

Treatment for UNEConservative treatment ie

avoid aggrevating factors Jt protectionElbow splintSurgical options

Transportation Decompression cubital

tunnel Medial epicondylectomy

Many will recover spontaneously but surgery very effective (Padua et al 2002)

90% of pt’s with mild symptoms will recover with conservative Rx (Robertson & Saratsiotis 2005)

Ulnar nerve transportation

Ulnar nerve compression at the wrist

Similar manifestation with weakness of the hand intrinsics and thenar and hypothenar eminences

Exacerbated by activities such as riding bike or manual labour that repetitively compresses ulnar side of the wrist and Guyon’s canal

#, trauma, ganglion cysts, ulnar artery thombus

May require MRI or CT for diagnosis as well as EMG and NCS

Conservative treatment usually successful but may require decompression if mass present

Radial Neuropathy at the Spiral Groove (Shapiro & Preston 2009)Saturday night palsyPresents with complete wrist

and finger dropNumbness in the lat dorsum

of the handAlso weak supination and

elbow flexElbow ext normalFinger abd should be

unaffected (must be tested in neutral)

Triceps reflex normalBrachioradialis reflex

reduced or absent

Radial nerve entrapment cause.Radial nerve lies in

juxtaposed to spiral groove making it liable to compression

Prolonged compression leads to demylination

Can result from # humerus, vasculitis or stenuous muscle effort

Differential diagnosisRadial nerve compression

other sites i.e. Axilla

Posterior interosseous neuropathy (PIN)

Posterior cord radial plexus lesion

Unusual C7 radiculopathy

Central lesion

Will result in reduced elbow ext and numbness ext post forearm and upper arm

Radial dev during wrist extNo loss of reflexes

Weak lat dorsi and deltoid and weak all

Weak C7 innervated muscles including pronation and wrist flex

UMN S&S

Diagnosis and TreatmentEMG and NCS

should be done to define location of entrapment

High resolution US thought to be accurate (Lo et al, 2008; Bianchi, 2008)

Treatment usually conservative

Protection (proper crutch use)

Wrist splintRecovery depends on

demylination (several weeks) or axonal damage (several months to > 1 year)

Surgery for ongoing symptoms

Suprascapular NeuropathyAldridge et al, 2001

Presents insidious onset wasting over infra and suraspinatus

Inability to lat rot / abduct (Pt may be unaware)

Pain post sh and on palpCommon in weight liftersNerve trapped in

suprascapular notch beneath transverse scapular lig

Less common entrapment at spiroglenoid notch

Causes Suprascap nerve entrapmentCertain activities

which i.e. throwing, dancing, lifting

Ganglions, sarcoma, carcinoma

Surgical positioningDirect trauma

Differential diagnosis DiagnosisC5-6 radiculopathy

Neck painReduced biceps and

brachiorad reflexWeakness other C5-6

innervated musclesSensory changes

Brachial plexopathyAs above no neck pain

Rotator cuff tearMOIMay be difficult to

differentiate

EMG and NCSUS to differentiate rot

cuff injury

TreatmentConservative i.e stop

offending activitySurgery especially if

mass identifiedConservative and

surgical treatment equally effective usually

Peroneal Neuropathy at the Fibular HeadUsually involves both

deep and superficial peroneal nerves

Therefore weakness in ankle df and eversion

Sensory loss over dorsum of the foot and lat calf

May be pain and Tinel’s over fib neck

Ankle inversion spared as innervated by Tib nerve.

Causes

Habitual leg crossingRepetitive stretch from squattingThin pt’s Ganglions etcAssociated to ankle inversion injury including

# fibTraction to nerveProlonged immobilisation (especially sedated

pt’s)

Differential Diagnosis DiagnosisSciatic neuropathyL5 radiculopathy

Both identifiable by sensory changes lat knee and/or under/lat foot

Weak inversionReduce reflexes

CRPS

EMG and NCSMRI’s in slowly

progressing to check for masses

Treatment (Shapiro&Preston 2009; Williams&Robinson 2009)Can be injectedAFOStretches to prevent

contracturesGait rehabProprioceptive workEliminate offending

activities ie leg crossingSurgery rarely needed

except where extensive nerve damage or mass present

Meralgia Paresthetica (Williams and Trizl, 1991; Grossman et al, 2001)Classic presentation of

lateral femoral cutaneous neuropathy is burning and numbness lat thigh with no reduction in reflexes or motor power

Lat fem cutaneous nerve purely sensory

From L2-3 passes under inguinal lig

My also be hypersensitiveSymptoms may be

exacerbated by walking/standing and relieved by hip flex

Positive tenderness or Tinel’s at Inguinal lig

Causes Differential DiagnosisIdiopathicObesity Tight underwear,

wearing tool beltDMAbdominal aortic

aneurysm TumoursPregnancyPost surgeryRarely caused by

trauma

Femoral neuropathyLumbar plexopathyLumbar radiculopathy

Usually numbess less well defined

Reduce reflexWeaknessDiagnosis usually

clinical as EMG not good for these pt’s. MRI if mass suspected

TreatmentUsually time limitedReduce causitive

factor (tight clothes)Lose weightHave babyLocal steroid injNSAID’sProlonged symptoms

may require anaesthetic creams/patches

Tricyclic, anticonvulsants, anti depressants

Surgery decompression or transection

Conservative treatment successful in 91% cases

Surgical treatment successful in 95% cases

Tarsal Tunnel Syndrome and Plantar Heel/Foot pain (Alishami et al, 2008) Compression of the tibial

nerve branches under the flexor retinaculum

Pain medial ankle, burning, numbness, tingling under foot

More common women than men

Worst with weight bearingPossible wasting of intrinsics

in footTinel’s positive in tarsal

tunnelReduced light touch on soles

of foot

CausesIrritation to medial or

lateral plantar nerve or medial calcaneal nerve

IdiopathicAnkle sprain/#RA/Degenerative jt

diseaseDMHypothyroidismVV => compressionGanglionRepetitive jogging/wt

bearing

PresentationAlways pain abductor

hallucisPain after rest

particularly morningPain may radiate

distally with palp of nerve (should not in plantar fascitis)

Pain may easy with walking

Reduce d sensation over medial sole

Differential DiagnosisPlantar Fascitis

DF with eversion then SLR

Tinel’s not +ve in pfEMG/NCSHigh resolution US

Fat pad atrophyMore pain over fat

padVisible loss of fat

pad

Proximal nerve lesionCheck LspTibial nerve

entrapment in popliteal fossa

TreatmentGood evidence very

limitedRestNSAID’sSteroid InjectionsHeel padsOrthosesStretching exercises

for PF and calfAND techniques

Surgery to decompress is a last option and should only be considered if conservative treatment has failed for 6-12 months

Interdigital neuropathyMorton’s Neuroma (Cochranes review, 2011; Williams & Robinson, 2009))Compression of the

Plantar digital nerves in the space between the metatarsal heads

Usually 3rd space followed by 2nd and rarely 1st or 4th space

Can give pain which is debilitating as mobility severely limited

Pain often relieved by removing tight footwear

May be accompanied by numbness of toes adjacent to pain

Cause Differential DiagnosisMost likely etiology

is repetitive compression of common plantar digital nerve between MT heads and the transverse metatarsal lig.

TTSCan be very difficult

to differentiatePlantar fascitisTMT OA

Both of these will have no neurological S&S

Also compression of the MT heads should not be exquisitely painful

Diagnosis TreatmentEMG/NCS may help

exclude other peripheral nerve or Nerve root problems

MRI may be of more benefit but can often pick up none clinically relevant lesions

US good for predicting size of neuroma (92% Sens 100% Spec)

No good evidenceConservative

treatment helps 50%InsolesStop offending

activitiesSteroid injAlcohol inj x4Physio (not specified)

Surgery neurectomy/neurolysis (variable outcomes)

SummaryLots of nerve root entrapmentsLocation of entrapment very important in

symptomsDifferentiation relies on multiple symptomsConsider could neuropathy be adding to

symptoms/preventing/slowing recovery

Questions?

THE END