Peripheral Nerve Lesions



Classification

Neurotmesis

Complete division of a nerve
Means "nerve cutting" but also applied to a nerve which has been severely scarred that it cannot regenerate spontaneously
Majority have some evidence of return by 4 months if regeneration is possible

Axonotmesis

Incomplete division of a nerve
Incomplete in that only the axons are divided, the endoneural tubes are undamaged and spontaneous recovery is likely
70% likelihood of return but high velocity injuries® take longer

Neurapraxia

Refers to physiological interruption of a nerve
The only lesion is degeneration of the myelin sheaths and larger motor fibres are mainly affected, the smaller sensory fibres less so but subjective tingling is common

May be a mixed injury with rapid recovery of fibres affected by Neurapraxia and much slower recovery of axons with Wallerian degeneration

 

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Anatomy

Cell body in the ventral horn (motor) or dorsal root ganglion
Blood supply is from numerous small branches of adjacent arteries (vasanervorum)

 

Epineurium

Longitudinally arranged areolar collagen and elastin that both separates fascicles and holds them together
Separates the nerve from the surrounding structures and comprises 30 - 75% of the nerve
Provides primary protection against compression and permits lengthening of the nerve without strain

Perineurium

Most important physiologically
Distinctive sheath of fibrous tissue containing elastin and collagen providing a thin but distinctive sheath for fascicles
Establishes the blood nerve barrier and maintains an intra fascicular pressure which promotes a proximal to distal flow of axoplasm
Assists in protecting the nerve from stretch
Can mobilise neural stumps 8 - 10cm without disrupting inter fascicular blood supply

Endoneurium

Delicate connective tissue within fascicles that surrounds axons and forms a tube encompassing Schwann cells, myelin and axon

Myelin Sheath

Immediately surrounds the axon and is broken into segments longitudinally and is composed of lipoprotein in a laminated configuration
Formed from compacted layers of schwann cell plasma membranes
Nodes of Ranvier are small gaps that interrupt the sheath at regular intervals

Schwann Cell

Each cell establishes a relationship with only one axon® formation of the myelin sheath

 

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Electrodiagnosis

Nerve stimulation

-nerve is stimulated by a short duration current and contraction of muscles supplied by that nerve is seen or felt by the examiner
-in neuropraxia- normal conduction is seen below lerve lesion
-in more severe lesions- can take up to 5 says for degeneration to develop distal to lesion
therefore get normal conduction in this time

 

Electromyography

- a fine needle is inserted into the muscle and electrical activity at rest is measured
-Normal muscle is electrically silent at rest
-Embryonic muscle fibres fibrillate until they are innervated (~6th wk foetus)

Denervation


if muscle fibres lose innervation -fibres evert to their embryonal state of spontaneously contracting- fibrillation starts ~ 18-21 days after denervation
-Detection of fibrillation potentials in 3 or more areas is absolute evidence of denervation
-If reinnervation occurs fibrillation reduces; and voluntary effort®motor unit action potentials smaller in amplitude than normal ( due to small no of fibres contracting)

The motor unit

comprises 1 anterior horn cell +axon and the muscle fibres it innervates
- eg 1st dorsal interosseous- ~340 fibres/unit
- the smallest effort is associated with the firing of one motor unit; as effort �®increased frequency and number of units firing- eventually obliterating the horizontal trace on the screen = interference pattern

Partial denervation

- denervated muscle fibres may be reinnervated from an adjacent intact nerve- this motor unit now has more fibres than normal, therefore amplitude +duration of activity greater than normal = giant motor units . Are typical of chronic denervation

Myopathy

muscle fibres are damaged -each motor unit has reduced no of fibres.
therefore motor unit potentials shorter duration and lower amplitude- but as no denervation there is no reduction in numbers of motor units
Thus get a full pattern of small potentials with normal motor and sensory nerve conduction

 

Conduction Studies

Normal velocity ~ 50m/s in motor nerves, slightly faster in sensory nerves
If myelin is abnormal® slowed conduction
If myelin is lost then conduction occurs along the axis cylinder at ~ 10m/s
Compression of a nerve®derangement of myelin®slowing of conduction across the compressed segment- but as long as compression is not severe enough to cause actual Wallerian degeneration, conduction remains normal above and below the compressed segment.

Motor conduction

measuring the latencies to electrical stimulation at various levels of the nerve with a needle electrode in themuscle or with a surface electrode
-eg Ulnar nerve- electrodes in ADM + nerve stimulated at the wrist,below elbow, above elbow and in the axilla. At each site latency is measured , distance between stimulating and recording electrodes noted and condudtion velocities calculated

Sensory conduction

ring electrodes placed on digits, stimulated, and resultant sensory potential recorded proximally (amplitude measured and conduction velocity calculated) = orthodromic technique
- can use antidromic technique also (get larger amplitude potentials )Conduction studies (cont)

Late responses

1. F wave

- evaluates the entire length of the motor nerve up to the ant horn cell
-is obtained by supramax. stimulation of the motor nerve distally®all axons depolarised and transmit the nerve action potential orthodromically to produce a standard M-wave. In addition the nerve action potential is conducted antidromically to the ant horn cells- a subset of these cells are activated and nerve action potential returns to the muscle- recorded as a small F-wave after the M-wave.

 

2. H-reflex


-Obtained by stimulation of a sensory nerve, activating muscle spindle afferent fibres- the SNAP travels proximally to synapse on the ant horn cell which transmits a potential to the muscle, which depolarises, generating a potential called the H-reflex

 

Somatosensory Evoked Potentials

- can be recorded by averaging up to 500 responses after submaximal stimulation of a peripheral nerve- averaging techniques used as SNAPamplitudes are only a few microvolts and thus a single SNAP may not be distinguishable from background. recording electrodes may be placed over any proximal portion of the nerve- eg brachial plexus, scalp

 

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Clinically

Anaesthetic skin feels smooth, cool and dry
Patient able to map out areas of altered sensation
Muscle tone and power is diminished and muscle bulk is diminished
Earliest sign of recovery is Tinel's sign by tapping the nerve along its course, starting distally where the patient feels pain or tingling in the distribution of the nerve indicates how far recovery has progressed
Deafferentation pain more common following avulsion or limb amputation with 5 - 10% having true phantom pain and 90% have pain at some stage

X-Rays

Bones may decalcify

 

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Investigations

EMG® evaluation of function of the lower motor neurones starting at the anterior horn cell and proceeding distally to the muscle and conduction velocity can be calculated using the difference in the latency of two different stimulation sites (stimulation of the nerve is usually done through skin electrodes)
Needle electrode study of a muscle® normally there is no spontaneous activity when a muscle is completely relaxed. Fasciculation potentials are due to spontaneous discharge of a single motor unit and are non specific
Fibrillation (spontaneous asynchronous firing of muscle fibres) indicates denervation of a muscle and evident at 2 - 3 weeks following injury
Motor conduction velocities in the newborn are approximately 50% of the lower limit of normal in the adult and they reach the adult value by about 3 years. Over 60 years there is a mild slowing in conduction velocity
Normal conduction velocity depends on the calibre of the nerve with small fibres® ~ 12m/s and larger fibres® 50 - 70m/s
Nerve conduction velocities tend to be inversely proportional to the length of the nerve
Sensory nerve conduction studies evaluate the sensory nerves as far as the dorsal root ganglia and by convention the sensory distal latency is measured to the negative peak
Measurement of distance is the major source of error in determining nerve conduction velocity
Evaluation of deep nerves may require the use of needles to improve the quality of the measured potential

 

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Pathology

Traumatic injury to the nerve may sever the nerve or cause axonal destruction without loss of integrity of the myelin sheath or connective tissue
Pressure on the nerve may cause disruption of the integrity of the myelin sheath without destroying the axon® conduction block
Blood clot occupies the space between the cut ends of a nerve, this organises and schwann cells from each stump grow into the defect
Distally the axons degenerate and are removed by phagocytosis
Proximally degeneration extends for about 1cm
Within a few days the cut axons proliferate and streams of axoplasm grow towards the gap which if obstructed® formation of a neuroma otherwise they enter the schwann tubes (not necessarily the right ones)
Wallerian degeneration:
Essentially a distal phenomenon with loss of conduction of the distal segment within 72 hours and subsequent degeneration of axons and myelin sheaths
Endoneural tubes shrink to 40 - 50% of original size within 4 - 6 months
Proximal degeneration for several mm's to cm's depending on the magnitude of the injury
The advancing axon is followed by advancing myelination and eventually joins the end organ which enlarges if in the mean time it hasn't become degenerate
Experimentally axons grow at a speed of 4mm per day but there is delay in starting regeneration, in crossing the gap and in connecting with the end organ
In practice the speed of recovery is about 1 - 1.5mm per day

 

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Treatment

Wait with expectation
Operation indicated;
  1. The nerve is known to be divided because the lesion was seen at the time of debridement
  2. The nerve is likely to be divided because of the nature of the injury eg a knife wound
  3. The nerve is presumed divided because recovery of the most proximally innervated muscle is not evident in the expected time or there is a palpable neuroma evident (EMG helpful in this regard)
  4. Occasionally indicated for diagnosis
Choice of nerve repair
Epineural® sutures through the epineural sheath application in pure motor or pure sensory nerves, digital, radial and median nerves, sharply or evenly severed nerves
Group fascicular® connection of matching groups or bundles of fascicles by placement of sutures in epi-fascicular epineurium application in larger nerves and partially severed or unevenly transected or avulsed nerves
Fascicular® connection of isolated fasciculi by placement of sutures in the perineurium application in neuroma in continuity in small nerves, partially severed nerve when only a few fascicles are severed
While awaiting recovery® physio to maintain movement. Splint to prevent deformity
Direct repair should be performed as soon as this can be done safely (ie not in the presence of a contaminated wound)
Early repair of cleanly divided nerves produces the best results
Nerve grafting indicated if gap 3 - 7cm or if cannot repair nerve without tension
Nerves which can be used as grafts are the lateral cutaneous nerve of the thigh, the saphenous nerve, the sural nerve, and the medial cutaneous nerve of the forearm
If ulnar + median nerves irreparable can use segment of the ulnar nerve to bridge the median nerve
If the graft nerve diameter is small and the use of several strips may be needed (cable graft) and grafts should be 15% too long to avoid tension
Post operative care® motion block splints to prevent tension in repair (less time in the splint required if graft used and no tension)
Tendon transfer® restore function

 

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Prognosis

Neurapraxia always recovers fully, axonotmesis usually recovers well, neurotmesis has the worse prognosis
80 - 90% of nerve injuries associated with closed fractures recover spontaneously
The higher the lesion the worse the prognosis
The prognosis is better in children than in adults and purely motor or purely sensory nerves recover better than mixed nerves
Beyond a critical resection length grafting is not successful (?15cm)
After a few months recovery following suture becomes progressively less likely with delay of repair® loss of 1% of neural function for each week of delay beyond the third week
With the passage of time the prospect of recovery is reduced because the activity of the sprouting axons diminishes after 7 - 12 days and the schwann tubes become narrow, motor end plates degenerate and muscles atrophy, the brain also forgets how to use the muscle
In the upper limb radial nerve repairs have a better prognosis than the median and the ulna nerve has the poorest prognosis and in the lower limb tibial nerve have a more favourable prognosis than the peroneal nerve

 

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Brachial Plexus

Anatomy

Branches from the roots

  1. Dorsal scapular nerve (C5)® rhomboids and levator scapulae and runs down deep to levator scapulae
  2. Nerve to subclavius (C5,6)® subclavius passing over the trunks of the plexus in front of the subclavian vein and may contain accessory phrenic fibres
  3. Long thoracic nerve (C5,6,7)® serratus anterior and runs posterior to the brachial plexus

Branches of the upper trunk

Suprascapular nerve (C5,6)® supplies supraspinatus and infraspinatus

Branches of the Lateral cord

  1. Lateral pectoral nerve (C6)® supplies upper fibres of pec major
  2. Musculocutaneous nerve (C5,6,7)® supplies coraco-brachialis, biceps and brachialis and then becomes cutaneous as the lateral cutaneous nerve of the forearm
  3. Lateral head of median nerve (C6,7)

Branches of the Medial cord

  1. Medial pectoral nerve (C7,8)® pierces pec minor and supplies it then supplies the sternocostal fibres of pec major
  2. Medial cutaneous nerve of the arm (T1)® runs with the axillary vein
  3. Medial cutaneous nerve of the forearm (C8, T1)® runs between axillary artery and vein and pierces fascia with the basilic vein
  4. Ulnar nerve (C7,8 & T1)® supplies the ulnar forearm flexors and most of the intrinsic muscles of the hand, runs behind the brachial artery and slopes backwards to pierce the medial intermuscular septum
  5. Medial head of median nerve (C8 & T1)® crosses the axillary artery to joint the lateral head and supplies most of the flexor muscles of the forearm, the three thenar muscles and two lumbricals

Branches of the posterior cord

  1. Upper subscapular nerve (C6,7)® passes straight back into upper part of subscapularis
  2. Thoraco dorsal nerve (C6,7,8)® inclines forwards and enters the deep surface of latisimus dorsi just behind the anterior border
  3. Lower subscapular nerve (C6,7)® supplies the lower part of subscapularis and teres major
  4. Axillary nerve (C5) passes backwards through the quadrilateral space in contact with the neck of the humerus and supplies deltoid and teres minor
  5. Radial nerve (C5,6,7,8 & T1)® is the nerve to the extensor compartment of the arm and leaves the axilla through the triangular space below teres major
    Intraneural anatomy of the plexus is such that fascicles containing mixed motor and sensory fibres are more common than either pure motor or pure sensory

 

Incidence

Usually young males (15 - 30 years)
Motorcyclists at particular risk
Obstetric injury 0.35 - 0.87 / 1000 births (Erb's most common)

Classification of BP injuries

Closed

  1. Supraclavicular
    ® preganglionic
    ® postganglionic
  2. Infraclavicular
  3. Mixed

Open

eg sharp laceration or gunshot and blast injuries

Post anaesthetic palsies

(general or regional)

Radiation injury

Obstetric injury

Sunderland has classified the extent of damage into five degrees
  1. Conduction block without morphologic changes (Neurapraxia)
  2. Loss of continuity of axons with other structures intact (axonotmesis)
  3. Loss of continuity of axons and endoneural structures with intact perineurium (axonotmesis)
  4. Continuity preserved by connective tissue only (neurotmesis)
  5. Complete loss of continuity (neurotmesis)

Clinically

Birth injury associated with breech presentation and forceps delivery
May be a Horner's syndrome (enophthalmos, miosis, ptosis and anhydrosis) if T1 root avulsed
Presence of Tinel's sign on tapping over the brachial plexus above the clavicle implies a post ganglionic or distal rupture rather than a root avulsion
C5,6 lesion® paralysis of deltoid and lateral rotators of the humerus and elbow flexors, wrist extensors may or may not be paralysed as well
C5,6,7 lesion® as above with loss of active wrist and elbow extension and finger extension
If serratus anterior is weak or paralysed suggests root avulsion
If serratus anterior intact and supraspinatus and infraspinatus weak or paralysed suggests infra ganglionic lesion
If these muscles are intact and deltoid paralysed suggests lesion may be located distal to the brachial plexus
C7,8 & T1 lesion more common in obstetric injuries® loss of active finger flexion and extension as well as all intrinsic function of the hand
Whole plexus injury® "Flail anaesthetic limb"
There is a high incidence of severe pain following brachial plexus injuries with between 10 and 20% of trunkal brachial plexus injuries and 40% of all total avulsions being affected
Pain may be burning, crushing or electric shock and this may be influenced by weather, intercurrent infection, emotional stress and distraction
Pain may be due to de-afferentation, neuroma or spontaneous abnormal epileptic activity

Investigations

Plain X-Rays


associated cervical rib or clavicular fracture

CT myelogram

should be delayed between 1 week and 1 month to reduce the chance of clots® incomplete picture, root avulsion® pseudo-meningocele

MRI

may be superior in identifying BP lesions with increased resolution of scans obviating the need for invasive investigations

EMG


after 3 weeks if muscle denervation® fibrillation and as posterior cervical musculature innervated by posterior primary rami of roots contributing to the BP® denervation of these muscles indicates root avulsions
EMG may also be useful to assess re-innervation of peripheral muscles

Nerve conduction velocity

absence of motor conduction and presence of the sensory conduction indicates root avulsion as the sensory pathway via the dorsal root ganglion remains intact (sensory conduction in an anaesthetic limb is a bad prognostic sign)
Somato-sensory evoked potentials useful intra operatively to identify parts of the plexus with central connection for re-anastomosis with distal parts of the plexus

Axon reflex testing

not used much, involves histamine on surface of skin in distribution of peripheral nerve under evaluation® scratch skin® vasodilatation, wheel formation and flare in normal individuals but if the injury is distal to the ganglion there is vasodilatation and wheel but no flare

 

Treatment

Locally

Low velocity injury® good prognosis for recovery
High velocity injury® early diagnosis and treatment
Early surgical exploration® easier dissection and shorter grafts are needed but difficulty in differentiating damaged from recoverable tissue
Associated vascular injury requires exploration and repair ?® plexus repair at the same time (availability of expertise)
Open injuries® immediate exploration +/- repair
Exploration as early as 2 weeks or wait until 3 - 6 months as between one month and six weeks fresh scar tissue makes dissection difficult
Priority for restoration of function are;
Elbow flexion (C5,6)
Wrist extension (C6,7)
Finger flexion (C7,8)
Shoulder abduction (C5)
Direct repair is rarely possible except perhaps in stab wounds
Most traction injuries® extensive longitudinal damage to the nerves such that nerve grafts will be required (from sural nerves, the medial cutaneous nerve of the forearm, the superficial radial and the ipsilateral ulna nerve if there is avulsion of the T1 and C8 roots)

Neurotization

(transfer of nerves) eg intercostals or accessory nerve to innervate proximal muscles also useful

Arthrodesis

of various joints (shoulder and wrist) may free up active muscles that can be used for transfers to other groups

Multiple muscle transfers


have been described eg;
Steindler flexorplasty® move common flexor origin proximally 6 - 7cm
Clark pectoralis major transfer® transfer costal (lower 1/3) fibres of pectoralis major to the biceps tendon to restore flexion of the elbow
Latisimus dorsi transfer may be used to restore elbow flexion
Triceps transfer may be indicated if weakness of biceps greater than triceps to prevent extension contracture and restore flexion
Transfers around the shoulder® little functional improvement and arthrodesis may be indicated if serratus and trapezius functioning to enable scapulo-thoracic movement

Amputation may be indicated for a permanently flail and anaesthetic arm but this is unlikely to be successful in eliminating pain, if pain is a feature
Pain may be improved following successful grafting (improves in 60% with positive motor results) otherwise try to control with medications
Anti-epileptic drugs such as clonazepam or carbamazepine can control medulla, thalamic or cortical epileptic activity that is responsible for the impression of electric shocks and paroxysmal pain. Tricyclic antidepressants also have an analgesic effect which may assist in relief of pain. If successful this medication should be continued for 6 - 12 months
Mental techniques and distractions also may improve pain perception
DREZ (dorsal root entry zone) lesions may improve pain in refractory cases but not without complications
In birth injuries Gilbert et al suggest repair should be carried out if there has been no recovery of biceps function by three months

 

Prognosis

Brooks (1954) found that spontaneous recovery was good in lesions of the roots of C5 and C6 or of the upper trunk, fair in lesions of the posterior cord and poor in those in C8 and T1 or the medial cord
Birth palsy usually® spontaneous recovery in 1 week to 18 months

 

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Obstetric Brachial Plexus Palsy

Affected babies are usually larger averaging 2 pounds heavier than normal and delivery is usually difficult
Experimental studies on the tensile strength of the brachial plexus® disruption of the lower plexus components occurs with approximately half the force required to disrupt the components of the upper plexus

Clinically

The limb lies motionless at the side and the elbow in extension
Horner's syndrome may be present
There may be supraclavicular swelling and tenderness

Erb's Palsy

Affects C5 & C6 and C7 may be slightly affected
The abductors and external rotators of the shoulder, elbow flexors and the forearm supinators are paralysed® the arm held to the side internally rotated and pronated® fixed internal rotation deformity
Most cases (75%) recover without treatment
If contracture threatens splintage and daily stretching are important

Klumpke Palsy

Rare palsy which follows breach delivery with the arm above the head
Affects predominantly C8 and T1 may® flexion contracture of the elbow and posterior subluxation / dislocation of the radial head
Wrist flexors and long flexors of the fingers as well as the intrinsic muscles of the hand are paralysed
May be sensory loss on the ulnar forearm and hand and sometimes a Horner's syndrome
Fingers should be kept mobile in the hope of recovery
Splints and operations of little use

Entire Plexus Palsy

The entire arm is paralysed and the upper limb is almost completely flaccid and there is often extensive sensory loss

Prognosis

Degree and rate of recovery varies with the type and severity of paralysis and it is difficult to estimate the end point as maximal spontaneous recovery may take 1 - 18 months
In general patients with involvement of the entire plexus or lower plexus have a slower and more incomplete return than do those with only upper plexus involvement

 

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Peripheral Nerve Injuries

Median nerve

Low lesions

thenar wasting, opponens paralysis, sensory loss

High lesions

front of forearm wasted; thumb, indexand middle flexors, FCR, and pronators paralysed. Often the hand is held with th ulnar fingers flexed and the index straight (pointing index) - the middle finger may be flexed as its deep flexor, although paralysed, is joined to the unparalysed ulnar half of FDP

Management


splintage to prevent deformity
if no recovery- severe disability with sensory loss and loss of pinch
if sensation recovers but not opposition, sublimis®opponens transfer

 

Ulnar nerve

eg open wound, # medial epicondyle, # lateral condyle- if ununited®tardy palsy with progression of valgus. Bilat. lesions occur in leprosy

Low lesions (wrist)

hand is clawed, ring and little fingers hyperextended at the MCP jts and flexed at the IP jts.
Wasting of intrinsics- esp 1st cleft; interosseous paralysis; Sensory loss

High lesions (eg elbow)

the visible deformity is less marked in that the terminal jts of ring and littleare not flexed as the ulnar 1/2 of FDP is also paralysed (loss of active flexion of the DIP jt of the little finger is a good test)
-otherwise as for low lesions

Management

Transposition- when lesion is at the elbow
splintage to prevent deformity
if recovery does not occur- hand still has good function
Zancollis operation -through 4 longitudinal palmar incisions the volar capsule of each MCP jt is shortened by proximal advancement of a distally based flap

 

Radial nerve

Low lesions (post inteross n)- posterior forearm looks flat
ECU,EDC,EDM,APL,EPB,EPL,EI paralysis
high lesions (elbow)-also ECRB,ECRL,BR,Supinator paralysis ; sensory loss
v. high lesions (axilla)-also triceps paralysis

Radial Neuropathy Associated with Humeral Fractures

Only 8% of patients require exploration and nerve repair
This should be done at three to four months after the injury if there is still no clinical evidence of recovery

 

Sciatic nerve

-rare eg open wounds, traction in hip dislocations
Clinically- calf, leg thin; foot drop - all muscles below knee paralysed; weak knee flesion
sensation absent below knee except medially- trophic ulcer risk
Management- AFO/below knee iron and toe raising spring
-pressure careto avoid ulcers

Lateral popliteal nerve

eg damage at neck of fibula, correction of valgus, skin traction or pressure from splint

High lesion (common peroneal nerve)

outer leg wasted, foot drop- unable to DF or evert
sensory loss- front +outer 1/2 of leg +dorsum of foot +toes

Low lesion (superficial peroneal nerve)

  1. peroneal paralysis + wasting®dorsiflexion into varus
    sensory loss
  2. deep peroneal n-paralysis of tib ant, EDL® dorsiflexion into eversion
    sensory loss

Management

splint to avoid deformity
tendon transfer eg tib post transfer
arthrodesis if required

Medial popliteal nerve

complete lesion

thin calf , heel valgus, unable to plantar flex, intrinsic paralysis® claw toes
sensory loss- sole of foot and part of calf

lesion of post. tibial branch alone

less calf wasting , plantar flexion good, claw toes from intrinsic paralysis
sensory loss- sole of foot (sural n intact)

Management

splint to prevent over dorsiflexion in complete lesion
pressure care

 

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Tunnel Syndromes

Wherever peripheral nerves traverse fibro-osseous tunnels they are at risk of compression especially if the soft tissues increase in bulk as they may in pregnancy, myxoedema or with rheumatoid arthritis
The underlying pathology is probably not simple compression but an ischaemic neuropathy due to venous stasis and impedance of arterial flow
Common sites are the median nerve (carpal tunnel), the epicondylar tunnel at the elbow (ulnar nerve) and the inguinal ligament (lateral cutaneous nerve of the thigh)
Sensory disturbance and pain usually occur with involvement of a mixed nerve
Patient complains of tingling and numbness distal to the point of compression
Typically symptoms occur at night and relief obtained by movement of the joint "to get the circulation going"
Nerve conduction is slowed and® typical EMG findings
Symptoms relieved by decompression

Entrapment syndromes include

The long thoracic nerve® pain in the shoulder radiating to the arm and neck accompanied with winging of the scapula
The suprascapular nerve® weakness of abduction and external rotation
The axillary nerve in the quadrilateral space which may follow shoulder dislocation
Median nerve due to a supracondylar process or ligament of Struthers® high median nerve compression with weakness of wrist and finger flexors as well as the thenar muscles (95% are due to compression at the wrist)
Pronator syndrome due to entrapment of the median nerve as it passes through the pronator teres® weakness of long flexors but not pronator teres as the branch to this muscle comes off proximally (usually occurs in males) but resisted pronation® pain
Anterior interosseous nerve due to compression from pronator teres or compression beneath the fibrous arch of FDS® pain in the upper forearm followed by weakness of flexion of the thumb and index finger
Carpal Tunnel due to compression of the median nerve at the wrist and is associated with carpal dislocation, Colle's fracture, chronic tenosynovitis wrist arthritis, myxoedema, acromegaly, renal disease, amyloid, blood dyscrasias etc, said to be present in 21% of pregnancies and more likely in females in the age group 40 - 60 years. Phalen test where the wrist is maintained in full flexion for at least 60 seconds® aggravation of sensory symptoms in the hand
Posterior Interosseous nerve due to compression along its passage through the supinator muscle® nocturnal upper forearm pain and local tenderness and weakness of muscles supplied by it (extensors or the wrist and fingers)
Ulnar nerve may be compressed at the elbow or in the wrist® different pattern of weakness (long flexors at the elbow and intrinsics only at the wrist) 95% are due to pathology at the elbow
Thoracic outlet syndrome due to cervical rib or fibrous band® lower brachial plexus displaced upwards® neurological sequelae (may also be due to apical lung tumours)

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Regional Blockade Mode of action of drugs® low concentrations delay and in higher concentrations completely prevent the Na+ pump of the nerve cell membrane and the duration of the effect is dependant primarily on the perfusion of the tissue injected
Fine fibres are easier to block than coarser ones® sensibility lost before motor function
Toxic effects of local anaesthetic agents primarily involve the cardiovascular and central nervous system. Prilocaine associated with formation of methaemoglobin formation but due to rapid breakdown clinical toxicity is very low
Treatment of toxic effects® oxygen, anticonvulsants may be needed and cardiac support

Maximal dosages

Lignocaine2 - 3mg/kg
200mg in a 70kg man
20mls of 1% without adrenalin (50mls with)
Bupivacaine2 - 3mg/kg
40mls of 1% without adrenalin
Prilocaine4 - 6mg/kg
400 mg in 70kg man
40 mls 1% without adrenalin (60mls with)

Biers block

40mls 0.5% prilocaine (upper limb) and 60 - 80mls (lower limb)® satisfactory analgesia and muscular relaxation after 10 - 15 minutes
Cuff should not be deflated until at least 15 minutes have elapsed to allow tissue binding and prevent rapid IV purge of drug into circulation
There is rapid termination of anaesthesia once the cuff is deflated

Other blocks


ulnar nerve at elbow or wrist
Median nerve by infiltration just medial to the brachial artery or at the wrist by injecting between palmaris longus and FCR
Radial nerve can be blocked in the cubital fossa mid way between biceps and brachioradialis
The sciatic and femoral nerves can be blocked as can the lateral cutaneous nerve of the thigh and obturator nerve
The saphenous nerve can be blocked on the medial side of the knee immediately below sartorius tendon, the sural nerve between the Achilles tendon and the lateral malleolus, the posterior tibial behind the medial malleolus and peroneal nerve in front of the ankle joint
Caudal, epidural and spinal blocks using either narcotic or local anaesthetic agents by single injection, continuous infusion or PCA


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