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Types ofneurological injury
Spinal contusion
Functional continuity is not lost, paralysis below the
level of injury is incomplete and recovery may start
within a few hours. Full return of function is
possible.
Complete spinal cord injury
Loss of all neurological function below the level of
the injury is irrecoverable, as the axons within the
cord have no power of regeneration. There is an initial period of spinal shock with complete flaccid
paralysis, loss of tendon reflexes, atonicity of the
bladder (which becomes distended), faecal retention
priapism. This phase may last for a few days. The
and
cord below the level of injury then recovers reflex
function, and the paralysis becomes associated with
increased muscle tone (spasticity) and with muscle
spasms. The plantar responses become extensor, and
the bladder and bowel may begin to empty spontaneously (Box18.2).
Box 18.2 Components ofneurological injury
The neurological injury following spinal cord damage
can be divided into three components.
Sensory loss
Somatic and visceral sensations are lost below the
level of injury. Hyperaesthesia may be present at the
level of injury.
Motor loss
Spinal cord injuries result in an upper motor neurone
spastic paralysis with increased reflexes. Cauda
equina injuries, being injuries of nerve roots,
produce a lower motor neurone paralysis characterized by reduced tone and loss of reflexes.
Autonomic loss
Loss of sympathetic outflow results in hypotension
as a result of loss of vasomotor tone.
Thermoregulation, which also depends on
vasomotor activity, is also impaired. Sphincter
control is also autonomic. With injuries above the
level of the sacral outflow, the spinal reflex arc
triggering micturition remains intact so the bladder
can empty automatically. Injuries below this level
interrupt the reflex and an atonic bladder results.
Cauda equina injury
This may complicate fractures below the conus,
which is usually at the lower border of the first lumbar
vertebra. There is saddle anaesthesia (over the buttocks, anus and perineum), weakness of the lower leg
muscles, absent ankle reflexes and painless urinary
retention. The cauda equina are peripheral nerve
fibres and possess some regenerative potential
provided the continuity of the nerve root is not lost.
Recovery is rarely complete if compression is
prolonged.
Combined cord andcauda equina injury
As many spinal injuries take place at the thoracolumbar junction, there can be a combination of spinal
cord and nerve root injury. For example, a fracture
dislocation at the T12/L1junction may injure the cord
at the first sacral segment but clinical examination
may reveal paralysis being due to damage to the spinal roots as they pass the site of the fracture dislocation (Figure 18.3). In this instance, the roots may
recover with return of knee and hip movement,
although the sacral paralysis will be permanent.
Cord injury syndromes
Although other patterns of injury may occur, the three
most common syndromes of cord injury are as
follows.
Anterior cord syndrome
Injury to the anterior part of the spinal cord as a result
of hyperflexion or occlusion of the anterior spinal
artery causes paralysis below the injury (involvement
of the pyramidal tracts) with loss of pain and temperature sensation (involvement of the anterior spinothalamic tracts) but preserved touch, movement
and vibration sense (posterior column involvement).
Central cord syndrome
Occurs following ischaemia or trauma e.g. a hyperextension injury in the cervical spine in the elderly.
Sensory and motor fibres for the legs are situated
more peripherally in the cord than those for the arms,
so central cord swelling results in greater neurological
impairment in the arms than the legs. In the arms,
there is a mixture of upper and lower motor neurone
damage while in the legs the weakness is predominantly upper motor neurone (spastic paralysis).
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Vertebrae Nerve roots
T8
T9
T10
lesion (the spinothalamic tract). Such an injury is
often partial, and rarely occurs after a closed injury.
Treatment ofspinal injuries
The treatment of spinal injuries depends on whether
or not there has been neurological injury, and also
upon the stability of the fracture.
T11
T12
L1
L2
L3
L4
L5
Figure18.3 The relationship of the spinal cord
and nerve roots to the vertebrae. Because of the
disparity between the two, a fracture dislocation at
the thoracolumbar junction, shown here by the dotted
line may injure the sacral segments of the spinal cord
together with injury to the lumbar nerve roots.
Brown- Séquard syndrome
A unilateral penetrating injury of the spinal cord may
cause loss of power on the affected side (ipsilateral
pyramidal tract), loss of joint position and vibration
sense (ipsilateral dorsal column) and loss of pain and
temperature sensation on the opposite side to the
3
Charles Edward Brown- Séquard (1817–1894), born in
Mauritius, trained in Paris. Neurologist at the National
Hospital for Nervous Diseases, London, and later Professor
of Medicine at Harvard, Boston, MA, USA, and then the
Collège de France in Paris, France.
3
Immediate management
Spinal injury should be suspected in anyone following severe trauma or who is unconscious following
trauma. In addition, any patient with sensory or
motor symptoms following minor trauma should be
treated as having had a spinal injury until proved otherwise. Protection of the airway is paramount. Before
such a patient is moved, neck movements should be
minimized with a collar and the patient carefully
moved onto a properly designed stretcher for transfer.
Provided a patient is lying down, they will not come to
further harm. Patients should not lie on hard surfaces
for prolonged periods as their skin integrity may be
compromised.
Airway management and circulatory support are
the immediate considerations. The principles are the
same as those following head injury. In addition, following spinal cord injury, loss of sympathetic tone
may lead to vasodilation and hypotension, on top of
any blood loss that may result from trauma, and so
replacing circulating volume is important to prevent
ischaemia.
Treatment withno neurological
injury
Stable fractures of the spine are treated by a short
initial period of bed rest, to allow the associated soft
tissue injury to subside and pain to become manageable. Patients should be out of bed as soon as possible
with support from physiotherapists.
Potentially unstable fractures require more active
intervention in order to minimize the small risk of
secondary neurological injury and to reduce deformity. A fracture/dislocation with cord compression and
incomplete neurological injury is an indication for
urgent operative reduction and fixation.
Unstable cervical fractures should be managed by
open reduction and internal fixation when facilities
are available. Closed reduction and traction are no
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longer in widespread use in developed countries. A
Halo vest remains a good method of immobilizing the
cervical spine when internal fixation is either not possible or not available.
Thoracolumbar burst fractures are often treated by
operative reduction and internal fixation to relieve
pain, allow early mobilization and reduce the risk of
deformity.
Treatment ofparaplegia
ortetraplegia
The patient is transported in a neutral position to a
spinal or neurosurgical centre, the spine being supported by suitably arranged pillows and the patient
being moved from side to side to relieve pressure on
the skin. The distended bladder should be catheterized under full aseptic precautions to prevent
infection.
The following are the main principles of treatment.
Management of a complete spinal cord injury. A
•
complete injury is one where there is no motor or
sensory function below the level of the injury.
There will be no neurological recovery and there is
no indication for emergency intervention.
• Management of an incomplete spinal cord injury. If
the injury is incomplete and there is evidence of
spinal cord compression then decompression and
internal fixation should be organized as soon as
feasible but only when the patient is stable.
•
Management of the spinal column injury. Open
reduction and internal fixation of the fracture as
soon as the patient is haemodynamically stable
(i.e. urgent not emergency surgery) allows early
mobilization and reduces the risk of complications associated with prolonged bed rest.
Care of the skin. Pressure sores may develop very
•
quickly in the first weeks because of the combination of anaesthesia and immobilization. Two- hourly
turning and meticulous skin care are required.
• The bladder. In the initial phase of complete bladder
paralysis, acute urinary retention is common and
continuous catheter drainage by means of a urethral
catheter is necessary. The vast majority of patients
will need permanent urinary diversion usually
with a suprapubic catheter, intermittent selfcatheterization or an indwelling urethral catheter.
• The bowels. Acute spinal injury results in paralytic
ileus. Following recovery of motility, constipation
is common and is best managed by regular enemas.
Faecal impaction must be avoided and the rectum
emptied by digital evacuation.
Venous thromboembolism prophylaxis. Patients
•
with paralysis of the legs following spinal cord
injury are at risk of venous thrombosis and pulmonary emboli. Prophylaxis with subcutaneous low
molecular weight heparin should be instituted
and continued as long as necessary.
•
Rehabilitation. Active development of muscles
with an intact or partial innervation by expert
physiotherapy can restore mobility in many
patients with significant neurological injury.
Patients have complex rehabilitation and enablement needs, which are best delivered in dedicated
spinal cord injury centres.
Age- related (degenerative)
spinal disorders
Age- related spinal disorders arise from changes in the
intervertebral joints and intervertebral discs. Axial
spinal pain is multifactorial and poorly characterized.
Occasionally, agesion of the neural structures. These are the spinal cord
(myelopathy), nerve roots (radiculopathy) and cauda
equina (neurogenic claudication or cauda equina
syndrome).
Clinical presentations associated
withage- related changes
• Back or neck (axial) pain may be associated with
age- related changes but there is a very poor correlation between radiological findings and symptoms in patients with non- specific low back or
neck pain. Some patients develop an abnormal
curvature of the spine (scoliosis) which may be
associated with pain.
Radiculopathy, causing pain and lower motor
•
neurone symptoms, arises from compression of
nerve roots either in the spinal canal or as
they exit through the intervertebral foramina.
Compression may be due to disc prolapse, facet
joint hypertrophy, ligamentous thickening or
osteophytes.
• Degenerative cervical myelopathy causes upper
motor neurone symptoms and results from compression of the spinal cord. It can be caused by
related changes result in compres-
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prolapse of an intervertebral disc, ligamentous
and facet joint hypertrophy and osteophytes
encroaching into the spinal canal. Myelopathy
occurs more frequently in patients with congenital
narrowing of the spinal canal.
• Neurogenic claudication may arise as a result of
lumbar canal stenosis. Symptoms overlap with
those resulting from peripheral vascular disease.
There is usually bilateral leg pain with sensory disturbance that is worse when standing or walking
and relieved promptly by sitting down. Walking
distance may be reduced to less than 100m before
the patient has to sit or bend forwards to relieve
their symptoms. In contrast, symptoms of claudication from vascular disease are often unilateral,
worse when walking uphill and relieved by
standing.
Prolapsed intervertebral disc
Disc herniation (prolapse) comprises a protrusion of
disc material posteriorly into the spinal canal. Disc
prolapse is common and can be triggered by minor
events but is often associated with bending, lifting
and twisting. The most common levels in the lumbar
spine are between L4/L5 and L5/S1. Cervical disc
protrusions are most common at C5/C6 and C6/C7.
Disc prolapses occur more frequently in younger
patients and neurological symptoms in older patients
are more often associated with age- related changes in
the spine.
Lumbar disc herniation
Clinical features
The onset of symptoms is often with low back pain
and patients often report a specific time of onset following straining or heavy lifting. The majority of
patients complain of leg pain (sciatica) radiating
from the buttock down the back of the thigh and
knee and down the lateral side of the leg to the foot.
There may be paraesthesiae or altered sensation in
the foot. This pain is made worse by coughing, sneezing or straining (all of which raise intrathecal pressure) or by straight leg raising (which stretches the
inflamed nerve root across the disc prolapse).
Sometimes there may be motor weakness affecting
dorsiflexion (L5) or plantar flexion (S1). A central
lumbar disc prolapse, if large enough, can fill the
spinal canal causing compression of the cauda
equina with bilateral leg pain and disturbance of
bladder, bowel and sexual function (cauda equina
syndrome).
Examination may reveal flattening of the normal
lumbar lordosis, lateral curvature of the spine and
reduced spinal movements. The paraare in spasm and straight leg raising is limited and
painful. There may be weakness of the ankle and sensory loss on the medial side of the dorsum of the foot
and the great toe (L5) which suggests an L4/L5 disc
lesion. Sensory loss on the lateral side of the foot (S1)
and loss of the ankle reflex may occur in L5/S1 disc
lesions.
spinal muscles
Special investigations
• Magnetic resonance imaging (MRI) of the spine
will reveal vertebral fractures (common in elderly
osteoporotic spines), bone marrow changes (in
metastatic disease) and compression of the neural structures in the spinal canal or neural
foramina.
Computed tomography (CT) is the primary modality
•
for imaging patients following trauma.
Inflammatory markers including C- reactive pro-
•
tein (CRP) are normally raised in spinal infection.
Haematological and biochemical screening can
be helpful in detecting otherwise unsuspected
malignancy.
Differential diagnosis
This includes other causes of radicular pain including
lateral recess and lumbar canal stenosis, spondylolisthesis (ventral subluxation), spinal tumours and
rarely lesions affecting the sacral plexus such as
tumours of the prostate or rectum. Intermittent claudication can usually be differentiated by careful history, examination and a Doppler probe. An abdominal
aortic aneurysm may occasionally cause low back
pain.
Treatment
Severe acute pain is treated with analgesia including
anti- inflammatories and an initial period of rest. As
soon as the patient is more comfortable, gentle mobilization should start. Without treatment, most lumbar
disc prolapses will heal and the symptoms they cause
will resolve spontaneously. Most people get better
without any medical intervention and after three
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months seventy per cent of people will have had significant reduction in their leg pain. An epidural or
nerve root block may provide relief of symptoms during this period. A spinal injection cannot cure the
underlying pressure on the nerve, which is the cause
of the pain, but may provide significant pain relief
while waiting for the disc prolapse to heal. Operative
treatment of the prolapsed disc is indicated if conservative measures fail, if repeated attacks occur or if
the symptoms severely impair an individual’s quality
of life. If bladder sphincter disturbance occurs and an
MRI scan reveals a large central disc prolapse filling
the spinal canal with loss of CSF signal from the dural
sac, then surgical decompression with excision of the
prolapsed disc fragment must be performed without
avoidable delay.
Spinal stenosis
The cross- sectional area of the spinal canal follows
a normal distribution in the population. Patients
with congenital narrowing are more likely to
develop symptoms of spinal stenosis as the normal
age- related changes become superimposed on the
pre- existing narrowing. These changes include
thickening of the ligamentum flavum, over growth
of the facet joints and changes in vertebral
bodyalignment (spondylolisthesis). Symptomatic
lumbar canal stenosis only occurs with significant
reduction in the cross- sectional area to less than
20% of normal and most frequently occurs at L4/5
and L3/4.
The clinical features overlap with intermittent vascular claudication (see Chapter 12), but in spinal
claudication the patient presents with pain, numbness and weakness in the legs brought on by standing
or walking, and, in contrast to vascular claudication, it
is not relieved by standing still but by sitting down or
bending forwards. Neurological examination of the
legs is usually normal.
The diagnosis is confirmed by MRI (or CT if
patients are unable to have an MRI) which shows a
reduction of the cross- sectional area of the lumbar
spinal canal. Once stenosis is severe and symptomatic, decompression surgery will provide effective
relief of symptoms. Minimally invasive techniques
allow adequate decompression, minimize operative
morbidity and allow early mobilization and discharge from hospital.
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Cervical spondylosis
Cervical spondylosis refers to age- related (degenerative) changes that occur in the neck, with similar
pathological processes to those that occur in the lumbar spine. In the cervical spine, these changes can be
associated with spinal cord compression (myelopathy) and nerve root compression (radiculopathy).
Clinical features
Non- specific neck pain is common. Radicular symptoms include severe pain radiating into the arm
accompanied by sensory disturbance in a specific
dermatome. Patients with myelopathy often present
with numb, clumsy hands, impaired balance and difficulty walking. Occasionally, patients notice a change
in bladder function, most often urinary frequency
and urgency. Examination of the arms can reveal a
mixture of lower and upper motor neurone signs. In
cervical myelopathy, examination of the legs will
reveal upper motor neurone findings with increased
tone, leg weakness (especially hip flexion), brisk
reflexes and extensor plantars.
Differential diagnosis
The differential diagnosis of cervical myelopathy
includes spinal tumour, multiple sclerosis and motor
neurone disease. When arm pain alone is present, the
differential diagnosis includes a cervical rib, carpal
tunnel syndrome and angina pectoris.
Treatment
Radiculopathy usually settles with conservative treatment, including early rest and antimedication with gentle physiotherapy once the pain
begins to settle. The natural history and indications
for surgery are the same for a prolapsed cervical disc
as for a lumbar disc prolapse.
inflammatory
Spinal infection
An abscess in the extradural (epidural) spinal compartment can either be blood- borne infection as part
of a Staphylococcus aureus septicaemia or is often
associated with spondylodiscitis (osteomyelitis) of the
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spine. Diagnosis is often delayed due to an insidious
presentation in patients with other comorbidities.
Clinical features
Clinical features are progressive local pain, fever,
malaise and anorexia, and in rare cases, rapidly progressive paraplegia. The white blood cell count may
be raised, CRP and erythrocyte sedimentation rate
(ESR) are elevated and the diagnosis is confirmed
with contrast enhanced MRI.
Treatment
If there is an abscess in the spinal canal, then urgent
treatment is required to drain any pus usually via a
posterior or posterospinal infection, the causative organism should be
identified with repeated blood cultures and CTguided aspiration/biopsy. Prolonged intravenous
antibiotic therapy is started, preferably guided by the
results of culture and sensitivities. The involvement of
infectious diseases specialists is needed to guide antibiotic therapy. Patients with profound neurological
deficits can make a worthwhile recovery but delay in
diagnosis and treatment carries with it the risk of permanent cord damage.
Spinal tumours
Spinal tumours are conveniently classified, from
both the pathological and clinical points of view,
into those which occur outside the dura (extradural), those inside the dura but outside the spinal
cord (intradural, extramedullary) and those occurring within the substance of the spinal cord
(intramedullary).
The tumours most commonly encountered are the
following.
1
Extradural.
a Metastatic spinal tumours– are by far the most
common spinal tumour and are usually found
in the vertebral body. The primary is most
commonly the breast, kidney or prostate.
b Primary vertebral bony tumours– (e.g. osteo-
clastoma, chondrosarcoma, Ewing’s tumour
and osteosarcoma.).
c Haematological malignancies – Lymphoma
including Hodgkin’s disease and myeloma.
lateral approach. In patients with
2
Intradural extramedullary.
Meningioma.
a
b
Schwannoma.
3
Intramedullary (rare).
a
Astrocytoma.
Ependymoma.
b
c
Haemangioblastoma which can be sporadic or
be found in patients with von Hippel-
4
disease
.
Clinical features
The three groups of spinal tumours listed above each
tend to have a fairly distinctive clinical picture.
Metastatic tumours. Commonly there is a pre-
•
existing diagnosis of cancer. There can be weeks
or even months of back pain and sometimes
radicular pain. Progressive cord compression
leading to postural pain and paraplegia can
occur.
The intradural extramedullary tumours are usu-
•
ally slow growing and benign. As the tumour
increases in size, cord compression takes place
with neurological symptoms resulting in weakness with a sensory level at or below the site of
the tumour. Neurological examination reveals
upper motor neurone signs with increased tendon reflexes and extensor plantar responses.
Urinary symptoms are typically urgency and
frequency.
Cauda equina tumours cause lower motor neu-
rone signs with weakness, which may be radicular,
diminished reflexes and impairment of bladder
and bowel control.
• The intramedullary tumours may be accompanied
by axial pain and followed by a slow and delayed
onset of motor weakness below the lesion. There
may be a suspended (normal above and below the
lesion) dissociated sensory loss, with loss of pain
and temperature (spinothalamic tract) but preservation of vibration and position sense (dorsal
column) initially which may be lost later on in the
progress of the disease.
4
Eugen von Hippel (1867–1939), Professor of
Ophthalmology, Göttingen, Germany, described
haemangiomas in the eye; Arvid Lindau (1892–1958),
Pathologist, Lund, Sweden, described haemangioblastomas
in the brain and spinal cord of aected individuals.
Lindau
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Differential diagnosis
Spinal tumours are relatively uncommon and most
occur in patients over 60 years who are being investigated for gait disturbance. In this group, the main differential diagnosis is of agedegenerative cervical myelopathy and thoracic disc
prolapse. In younger patients, inflammatory lesions
such as multiple sclerosis may present with spinal
cord lesions but careful history taking often distinguishes these pathologies.
related disorders such as
Special investigations
• MRI with contrast enhancement is the definitive
investigation and provides precise localization of
the level of the tumour and its relationship to the
spinal cord and other structures.
• CT myelography may rarely be necessary in
patients who are unable to have an MRI scan.
•
X- rays of the spine are no longer indicated in
the investigation of patients with spinal pain/
symptoms.
Treatment
Many intradural tumours can be safely removed
using modern microsurgical techniques. Localization
of the correct spinal level is fundamental and is
achieved with intraoperative Xreferencing the MRI scan to these intraoperative
films. Wherever possible, the tumour is completely
excised and this can normally be achieved in meningiomas, schwannomas, ependymomas and haemangioblastomas. In meningiomas, careful consideration
needs to be given to excising the dural origin, which
reduces the risk of recurrence but increases morbidity
associated with a postoperative CSF leak.
In metastatic tumours, radiotherapy and chemotherapy are the mainstay of treatment in the majority
of patients. Surgery has a role in highly selected
patients with a good prognosis and postural pain.
rays and cross-
Additional resources
Case 36: A spinal abnormality in a newborn child
Case 37: Back injury
1919
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Peripheral nerve injuries
Ian Grant
Learning objectives
✓ To know the dierent types of acute and chronic peripheral nerve
injuries and their prognosis.
✓ To be able to recognize the pattern of symptoms and signs associated
with injury to the major peripheral nerves in the upper and lower limbs.
The central nervous system is protected by the bones
of the skull and spine. The peripheral nervous system
is vulnerable to acute and chronic injury as a consequence of compression, traction and division. The
potential for a peripheral nerve to recover from injury
is dependent upon the extent of the injury, and the
proximity of the injury to the target organ.
Classification
Acute peripheral nerve injuries
Acute peripheral nerve injuries are commonly the
result of laceration, traction (stretching) or compression (crush) injuries. There are three types of injury.
Neurapraxia. This is the mildest and most tran-
1
sient peripheral nerve injury. It is associated with
localized loss of the myelin around the axons of
the injured nerve (demyelination). As a consequence, the amplitude and velocity of electrical
conduction is greatly diminished causing temporary weakness or numbness which resolves in
most patients within 4–6weeks.
2 Axonotmesis. This is injury to the axon and myelin
sheath without disruption of the continuity of its
perineural sheath. The axons distal to the lesion
degenerate (Wallerian degeneration
endoneurium (the connective tissue around the
axons) as a scaffold. Axons and Schwann cells
migrate from the proximal injured nerve at
approximately 1mm/day; therefore, the time to
recovery depends upon the distance between the
injury and end organ. The rate of recovery can
be followed by tapping the path of the injured
nerve and at suitable intervals mapping the point
of maximal tenderness which represents the leading point of the advancing regenerating axons
(The Hoffmann-
3 Neurotmesis. This is the physical division of a
peripheral nerve. Regeneration will only occur if
the fascicles of the proximal and distal ends of the
nerve are in close intimacy (or are sutured together).
In the absence of treatment, most divided nerves
will produce a tender lump called a neuroma.
A peripheral nerve contains a large number of individual fibres, so it is quite possible in a nerve injury for
some fibres to suffer from a mixture of neurapraxia,
axonotmesis and neurotmesis.
Tinel sign).
1
) leaving the
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
1
Augustus Waller (1816–1870), a General Practitioner in
London, UK, for 10 years before working as a Physiologist in
Bonn, Germany, Paris, France and Birmingham, UK.
Peripheral nerve injuries 183
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Chronic peripheral nerve injuries
Chronic peripheral nerve injuries are commonly the
result of compression or traction over a period of
6 weeks or more. This can be a consequence of
entrapment below a ligament (e.g. carpal tunnel syndrome), or pressure from a prominent bone or soft
tissue structure (e.g. the median nerve neuropathy
occasionally seen after malunion of a distal radial
fracture), or persistent traction (e.g. the ulna nerve
neuropathy seen in throwing athletes as a consequence of repetitive elbow flexion).
Patients initially report episodic symptoms such as
tingling, pain, weakness and numbness. This is
thought to be caused by cycles of demyelination and
remyelination of the injured nerve. If the cause is left
untreated, the symptoms are likely to worsen and
become continuous, and eventually the disability
becomes irreversible.
Patients with systemic conditions affecting the
peripheral nerve system (such as insulin dependent diabetes) or with inherited neuropathies that
affect the ability to produce myelin (such as
Charcotto chronic peripheral nerve injuries.
Marie- Tooth disease) are more vulnerable
Special investigations
Electrophysiological studies assess the speed and
amplitude of electrical conduction through a peripheral nerve (nerve conduction studies) and the electrical activity with the target muscle (electromyography,
EMG). This can help localize the site of injury in a
symptomatic patient.
For an acute injury with a peripheral nerve thought
to be ‘inneurapraxia and axonotmesis. For a nerve that cannot be readily explored or imaged, it can help distinguish between axonotmesis and neurotmesis.
Neurapraxia andaxonotmesis
Those joints whose muscles have been paralysed
are splinted in the position of function to avoid
contractures. They are put through passive
movements several times a day so that, when
recovery ofthe nerve lesion occurs, the joints will be
fullymobile.
continuity’, it can help distinguish between
Neurotmesis
Best outcomes are achieved with early repair (ideally
within 4days of injury) of the divided nerve using an
operating microscope. The proximal and distal ends
of the nerve are sequentially resected until healthy
fascicles are visible before repair is started. The fascicles of the proximal and distal nerve ends are aligned
and the epineurium approximated using fine sutures.
If a tensionnerve graft may be required. This can be a section of
aless valuable nerve such as the sural nerve. Smaller
nerve gaps of <1cm can be bridged with a conduit
such as a section of vein or a commercial product.
Generally, the recovery of sensibility after nerve
repair is, at best, partial, and the muscle strength is
reduced.
free anastomosis is not possible, a
Nerve transfers
When a nerve is acutely injured proximally, the denervated target muscle will maintain the potential for
recovery for about one year. If the nerve does not
reach the target muscle within this period, the muscle
atrophies, motor end plates disappear and any capacity for regeneration is lost. Patients with proximal
nerve injuries can benefit from a nerve transfer in
which a branch of an unanastomosed distally to the nerve fascicles heading
towards the target muscle. For example, in a patient
with a proximal ulnar nerve injury in the upper arm,
the anterior interosseous branch of the median nerve
can be anastomosed to the side of the motor fascicle
of the ulnar nerve at the wrist. This gives early recovery of the intrinsic muscles of the hand which are supplied by the ulnar nerve (which would otherwise
atrophy due to the prolonged wait of over a year for
the regenerating axons of the injured ulnar nerve to
reach the hand).
injured adjacent nerve is
Tendon transfers
If restoration of nerve function cannot be achieved
after injury or where the prognosis for recovery is
poor, tendon transfers may allow the patient to perform movements that would otherwise be impossible. For example, wrist drop after a radial nerve lesion
may be treated by transposing the pronator teres
muscle (supplied by the median nerve) onto the dorsum of the wrist and connecting the tendon to the
paralysed wrist extensor tendons.
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It is beyond the scope of this chapter to discuss
lesions of all the individual nerves, but a few important peripheral nerve injuries will be mentioned.
Brachial plexus injuries
Upper trunk lesions
(Erb’sparalysis
An acute injury of the upper trunk of the brachial
plexus occurs when the patient’s head is forced away
from the shoulder, for example in a fall from a motor
cycle. It may also occur as an obstetric injury. Injury
to the upper trunk of the brachial plexus, or the C5
and C6nerve roots, results in paralysis of the biceps,
brachialis, brachioradialis, supinator, supraspinatus,
infraspinatus and deltoid. The limb will assume the
‘waiter’s tip’ position, being internally rotated with
the forearm pronated (owing to the loss of the powerful supinating action of biceps). The arm hangs vertically (deltoid paralysis) and the elbow cannot be
flexed (biceps and brachialis). There will be an area of
impaired sensation over the outer side of the upper
arm. Patients should be referred for assessment at a
specialist centre.
Patients that have sustained neurapraxia or axonotmesis have the potential for recovery. Patients that
have sustained neurotmesis can potentially benefit
from exploration of the injury and repair of the
divided nerves (usually with nerve grafts). In more
severe injuries in which the nerve roots are avulsed,
there is no potential for nerve repair. These patients
are dependent upon improvements achieved by
nerve and tendon transfers.
T1injury (Klumpke’s paralysis3)
This can be caused by acute forced abduction of the
shoulder for example when falling from a height and
reaching out to grasp and to attempt to prevent the fall,
or from an obstetric injury in a child delivered in a
breech position. Chronic injuries can be caused by
compression from structures in the neck such as a
2
Wilhelm Erb (1840–1921), Professor of Neurology,
Heidelberg, Germany.
3
Auguste Dejerine- Klumpke (1859–1927), Neurologist,
Paris, France.
2
)
cervical rib. The small muscles of the hand are wasted
and there is loss of sensation on the inner side of the
forearm. There may also be Horner’s syndrome owing
to associated damage of sympathetic fibres passing to
the inferior cervical ganglion (see later in this chapter).
Radial nerve injuries
(Figure19.1a)
The radial nerve is most commonly acutely injured by
a fracture of the humerus involving the spiral groove
where the nerve is closely applied to the posterior
aspect of themidshaft of the bone. The nerve supply
to the triceps comes off the radial nerve before it
enters the spiral groove, and the lesions distal to that
point will not affect extension of the elbow. The
patient will be unable to actively extend their wrist
(sometimes called wrist drop) because of paralysis of
the wrist extensors. If the nerve is divided or is
crushed as the consequence of a iatrogenic injury
from surgery to the fracture, the patient is best served
by urgent exploration and nerve repair. Acute traction
injuries associated with an absence of any loss of
nerve continuity usually recover spontaneously.
Median nerve injuries
(Figure19.1b)
The median nerve may be acutely injured in fractures
around the elbow joint (such as a supracondylar fracture of the distal humerus) or laceration of the forearm
or wrist. In proximal injuries above the elbow, the pronators of the forearm and flexors of the wrist and fingers
will be involved, with the exception of the flexor carpi
ulnaris and the medial half of the flexor digitorum profundus, which are supplied by the ulnar nerve and
which produce ulnar deviation of the wrist. Whether
the injury is in the forearm or wrist, there will be paralysis of the abductor pollicis muscle at the base of the
thumb, resulting in significant disability as the patient is
unable to lift their thumb to allow it to oppose to the
other digits. The associated sensory loss is significant,
as humans generally explore the world with the combination of the thumb, index and middle fingers. This pattern of numbness makes it difficult for fine movements
such as those required to fasten buttons.
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