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The serratus anterior is supplied by the long thoracic nerve from C5,6 and 7. Long thoracic nerve palsy may follow traction injury, viral neuritis or nerve entrapment. Paralysis of the serratus anterior leads to winging of the scapula with poor scapula elevation, poor scapula control and impaired upper limb function, particularly with the arm in the forward elevated position. Exploration and decompression in the [osterior triangle of the neck, at the lateral border of the upper ribs or within the axilla may identify a cause of dysfunction that may be amenable to decompression. This is described elsewhere on OrthOracle. Failed recovery following decompression or persistent dysfunction at 6 months may be treated with a distal nerve transfer from the thoracodorsal nerve to the lower serratus anterior. Nerve transfer offers a reliable method of reinnervating paralysed muscles and utilises the proximity and redundancy of adjacent motor nerves close to the motor point of the paralysed muscle. Reinnervation distances are typically short resulting in good functional outcomes even when there is a delay to presentation or when other initial treatment modalities have failed.

INDICATIONS:
The long thoracic nerve arises from the C5,C6 and C7 nerve roots and has a long course from the posterior triangle of the neck, through the costoclavicular space to the axilla and the lateral chest wall where it supplies the serratus anterior which arises from the ribs 1-8. There are a number of innervation variants and the well described pattern of individual root contributions combining to a common trunk in the neck is only seen in approximately 1/3 of cases. Common variants are low contributions from the C7 within the costoclavicular space, contributions from the dorsal scapular nerve and aberrant innervation including contributions from C8.
The main indication for exploration of the long thoracic nerve is a persistent dysfunction with altered scapulothoracic motion and scapula winging. Entrapment of the long thoracic nerve can occur in the scalenus medius due to fibrous bands, aberrant vascular pedicles, points of tether from variant innervation patterns, at the lateral border of the first rib or in the axilla.
Loss of long thoracic nerve function may follow injury to the nerve, entrapment or viral neuropathy. The result is winging of the medial border of the scapula due to paralysis of the serratus anterior. This results in loss of scapula stability, control and elevation. Winging due to long thoracic nerve palsy should be distinguished from winging due to spinal accessory palsy or from loss of dorsal scapular nerve function. Poor scapula control may be associated with myopathic changes rather than neurogenic features and consideration should be given to rare conditions including facioscapulohumeral dystrophy.
Serratus anterior dysfunction from neurogenic causes may be amenable to physiotherapy rehabilitation, however persistent denervation on electromyography and persistent motor dysfunction may suggest nerve entrapment and consideration should be given to decompression in the neck, at the lateral border of the upper ribs and the axilla. Absent function after decompression and denervation for at least six months can be salvaged with a distal nerve transfer from the thoracodorsal nerve.
SYMPTOMS & ASSESSMENT:
There is a paralysis of the long thoracic nerve resulting in scapula winging and impaired scapula elevation. There is prominence of the scapula when the arm is lifted, incomplete abduction and forward elevation plus limited endurance with the arm elevated. A viral prodrome should be sought in the history with a typical history of severe neuropathic pain. A history of injury, traction or compression from carrying heavy shoulder bags may be elicited. The patient may report pain deep in the posterior triangle, high in the axilla or in the lateral chest wall.
Pain may be elicited when tapping over the course of the nerve, particularly at points of entrapment. There is no cutaneous innervation and so no sensory symptoms are reported.
INVESTIGATION:
MRI scan of the brachial plexus and cervical spine can exclude other causes of upper cervical root dysfunction including cervical root compression, tumours and some anatomical variants. Unfortunately not all anatomical variants are apparent on imaging and fibrous bands, intramuscular course of nerves and aberrant vascular pedicle compression are really only made during surgical exploration.
Neurophysiological investigations including electromyography (EMG) are essential components of the preoperative assessment of patients prior to consideration of nerve transfer surgery. EMG recording from the serratus anterior carries a small risk of pneumothorax and patients should be informed of this prior to referral for investigation. Electromyography can assess the extent of denervation of the potential target muscle as well as the integrity of the function within the donor. This is important when the cause is unknown and can confirm neurogenic pathology isolated to the LTN or part of a wider pattern typical of a brachial plexopathy or viral brachial neuritis.
OPERATIVE ALTERNATIVES:
The alternatives to nerve transfer surgery include simple decompression for an entrapment neuropathy, musculo-tendinous transfer or the lower pectoralis major to stabilise the scapula or scapulothoracic arthrodesis.
NON-OPERATIVE ALTERNATIVES:
Non-operative treatment strategies include physiotherapy rehabilitation to strengthen any residual serratus anterior function and restoration of normal rhthym through recruitment of accessory scapula stabilising muscles.
CONTRAINDICATIONS:
The main contraindication to nerve transfer surgery is a muscle that has been denervated for too long, typically between 9 and 12 months for a lower motor neurone complete injury and no donor muscle of sufficient strength in the vicinity with an intact nerve supply available for nerve transfer. Patients must be able to understand the planned treatment and be able to comply with the extensive period of post operative rehabilitation necessary to achieve a good functional outcome.

The patient is under general anaesthesia without neuromuscular blockade. The arm is placed on a side table and the chest elevated with a gel pad under the ipsilateral scapula. The chest wall is prepped and included in the surgical field as well as the whole upper limb.
In addition to basic instruments, a deep-jawed self-retaining retractor is required.
An operating microscope, nerve sloops, microinstruments, serrated nerve scissors, jeweller’s forceps and nerve stimulator plus needle are essential.
Tisseel fibrin glue may be used to support the neurorraphy.
Bipolar diathermy is needed for cautery near the nerves. In the superficial part of the wound monopolar diathermy may be used and so a diathermy plate should be placed on the patient in addition to an electrode to complete the nerve stimulator circuit.

A waterproof dressing with absorbent pad is applied to the wound. The wound should be kept clean and dry for 7 days after which the patient can shower then replace the dressing. A polysling is applied to the upper limb with a torso strap around the waist before the patient wakes from surgery. The polysling and torso strap should be maintained for 3 weeks to prevent excessive passive movement at the shoulder.
During this phase the patient is encouraged to maintain isometric contraction of the donor latissius dorsi muscle in the sling and to visualise the combination of latissimus contraction an shoulder stabilisation and elevation.
Nerve transfer rehabilitation involves a 6-phase programme of activity developed at the Centre for Nerve Injury and Paralysis, Birmingham, UK.
Phase 1 – Pre-operative phase: Education and donor optimisation. Introduction to trophic stimulation and the concept for functional electrical stimulation (FES).
Phase 2 – Protection phase: During the immediate post-operative period the nerve transfer is protected from inadvertent injury with the arm immobilised. Isometric contraction of the donor and visualisation of the combination donor-recipient action is performed during this period which typically lasts 3 weeks.
Phase 3 – Prevention phase: During this phase the arm is mobilised and neural gliding is commenced. Joint range of motion exercises (active and passive) are commenced to prevent joint contractures developing. The isometric exercises are continued and isotonic and eccentric exercises are commenced for the donor muscle to maintain function and restore strength. Functional stimulation can be commenced on the donor muscle. Trophic stimulation can be maintained on the recipient muscle.
Phase 4 – Power phase: During this period the donor muscle is strengthened and the recipient muscle starts to respond. Typically the first sign of reinnervation is a tender muscle squeeze sign due to small fibre reinnervation. Typically this is 3 months following transfer but is affected by the distance of the co-aptation from the recipient motor point.Visible flickers of contraction follow within 6 weeks and donor activation potentiate the recipient response. FES continues and the phase lasts for approximately 6-12 months during which useful motor grade returns: Medical Research Council – (MRC) Grade 3-4.
Phase 5 – Plasticity: During this phase the patient works on activation of the recipient muscle without activation of the donor. This phase can overlap with phase 4 and is guided by a therapist specialised in nerve transfer rehabilitation.
Phase 6 – Purpose: During this phase the patient introduces function tasks discussed as objectives during the pre-operative phase. This period of training is tailored to the individual and includes work hardening. Improvements are typically found in power and functional performance for at least 2 years following nerve transfer surgery.

Author’s note:
Th eTDN transfer is a useful method of restoring function to the lower 2/3 of the serratus after axonal degeneration. It can be combined with a decompression when there is insufficient time for full reinnervation. The optimum time to undertake the nerve transfer is when it is established that there is no spontaneous recovery after 6 months and before 9 months to allow sufficient time for the nerve transfer to reinnervate the lower serratus anterior.
References:
1: Raksakulkiat R, Leechavengvongs S, Malungpaishrope K, Uerpairojkit C, Witoonchart K, Chongthammakun S. Restoration of winged scapula in upper arm type brachial plexus injury: anatomic feasibility. J Med Assoc Thai. 2009 Dec;92 Suppl 6:S244-50
2: Uerpairojkit C, Leechavengvongs S, Witoonchart K, Malungpaishorpe K, Raksakulkiat R. Nerve transfer to serratus anterior muscle using the thoracodorsal nerve for winged scapula in C5 and C6 brachial plexus root avulsions. J Hand Surg Am. 2009 Jan;34(1):74-8
3: Ray WZ, Pet MA, Nicoson MC, Yee A, Kahn LC, Mackinnon SE. Two-level motor nerve transfer for the treatment of long thoracic nerve palsy. J Neurosurg. 2011 Oct;115(4):858-64
4: Noland SS, Krauss EM, Felder JM, Mackinnon SE. Surgical and Clinical Decision Making in Isolated Long Thoracic Nerve Palsy. Hand (N Y). 2017 Oct 1:1558944717733306. doi: 10.1177/1558944717733306
5: Novak CB, Mackinnon SE. Surgical treatment of a long thoracic nerve palsy. Ann Thorac Surg. 2002 May;73(5):1643-5
Reference
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