Nerve anatomy
Peripheral nerves consist of axones, myelin sheath, connective tissue and blood vessels. Nerve function can be disrupted by anomalies in any of these structures.
Each nerve is divided anatomically into individual fascicles, each surrounded by a dense connective tissue, the epineurium. Under the epineurium is the perineurium, which is an extension of the pia mater and the arachnoid tissue, acting as a protective membrane. The endoneurium is the axonal interstitial connective tissue.
The internal structure of an axon is made up of linear microtubules which are essential to the axoplasmic flow, and microfilaments. Any interruption to this flow leads to dysfunction and even axonal demise with distal degeneration.24-26
Peripheral nerves are well-vascularised structures. The endoneurial vessels are normally impermeable, but following trauma their permeability can increase, leading to an endoneurial edema, which can interfere with nerve function. This is a sign of an irreversible lesion.27
Nerve lesions
The type of nerve damage significantly affects future prognosis with, potentially, differing degrees of nerve repair depending on the situation. There are various classifications:
According to anatomic nerve lesions
There are two main acute classifications: Seddon’s classification and Sunderland’s classification. Both are based on the different nerve structures affected and are closely correlated. Seddon’s classification28 uses the terms neurapraxia, axonotmesis and neurotmesis. Sunderland’s classification26 uses a scale of degrees from one to five:
• Neurapraxia or stage 1 refers to a conduction block, meaning that the nerve and its axon are intact, but are not conducting action potentials;
• Axonotmesis includes an axonal rupture. Neighboring Schwann cells are preserved in stage 2;
• In stage 3, there is also rupture of the Schwann cells surrounding the endoneurium;
• In stage 4, there is a total fascicular rupture, including the perineural casing.
Functional nerve recovery is possible with neurapraxia and axonotmesis
• Neurotmesis or stage 5 refers to a complete rupture of the nerve, resulting in a permanent loss of nerve function unless reparatory surgery is carried out.26
Sunderland Classification
Seddon Classification Lesion Clinical signs Recovery
Sunderland I Neuropraxia Intrafascicular edema Segment
Sunderland II Axonotmesis Axon affected Endoneurial tube
Sunderland III Axonotmesis Endoneurial tube
damaged Paresthesia,
Sunderland V Neurotmesis Loss of continuity Anesthesia, complete paresis
None without surgical repair
Table 1: Sunderland and Seddon Classifications 26,28
Wallerian degeneration (degeneration of the part of the cell which doesn’t contain the nucleus, i.e. the axonal extension of the nerve cell) occurs in all axonotmesis and neurotmesis type lesions.26 Clinical differentiation between neurapraxia, axonotmesis and neurotmesis is difficult, particularly in the early stages.
According to the mechanism of nerve lesion
Nerve section: this can be partial or complete and straight or rough (knife wounds, gunshot wounds…).
Damage by stretching – as found in displaced fractures, for example. The degree of neurological deficit depends on the degree of stretching. During traction, the perineurium extends and the axon, which was previously wavy, stretches out.
Intraneural pressure exacerbates damage to the neurovascular bundle. This type of lesion can lead to a permanent neuroma. If the extension is continued, the axon stretches even further and starts to present tears, as do the perineurium and epineurium. This type of lesion can occur acutely or chronically.
Nerve compression: can be intrinsic (tumors) or extrinsic (neighboring or external structures). This mechanism leads to either direct or indirect compression of the nerve. In cases of direct compression, there is damage to the myelin casing or to the axon itself, thereby restricting nerve conduction. In cases of indirect compression, the lesion is caused by vascular compression, leading to an endoneurial edema, which affects the nerve function directly, by modifying the axonal flow, or indirectly by increasing the pressure of the endoneurial fluid (similar to a compartment syndrome).
These perturbations (edema and microcirculatory problems) combined with chronic irritation, lead to fibrosis and other intra- and extra-neural scarring.
Nerve friction: this occurs when there is continuous or intermittent dynamic pressure, leading to friction between the nerve and its annexes. This irritation stimulates the
fibroblasts in the epineurium, leading to fascicular compression within the epineurium itself.
Modifications in pressure in anatomic tunnels: this situation is found in the ulnar tunnel, for example, where an increase in the pressure within the ulnar nerve occurs when the elbow is flexed.
Nerve constriction: this mechanism is rare and its pathophysiology somewhat unclear. This type of lesion is, however, similar to a complete section (Sunderland stage V).
Limits of these classifications
The Sunderland classification allows a clear description of the anatomic lesions but does not consider certain pre-operative factors which can affect recovery (e.g.
substance loss, local ischemia, burns, infections…). Likewise, the patient’s age, smoking status or delay in treatment can significantly delay or reduce recovery for an identical lesion. For this reason, Goubier et al. proposed a scale to predict final prognosis for nerve lesions.29
Table 2: Nerve injury severity scale. 29
It should be noted that this scale is approximate and that it is still difficult to attribute a clear score for each characteristic, but this scale does at least take account of the other factors influencing nerve recovery.29
Miniature compartment syndrome
Acute compressions, by a tourniquet, for example, are linked to edema with a no-reflow phenomenon. Chronic lesions can be reversed easily with surgical nerve decompression. This suggests that there is a metabolic block, the origin of which could be a temporary microcirculatory disorder in the region compressed, in addition to the myelin alterations described above.
The epineurial blood vessels are sensitive to compression and respond to variations in intraneural pressure by changing their vascular permeability. The perineurium forms a selective barrier for the endoneurium, which has no lymph vessels.
Endoneurial drainage is therefore difficult and a miniature compartment syndrome is formed.30
Nerve damage due to compression is not therefore solely the result of a structural modification in the myelin or the axon. It would appear that hemodynamic factors based on microvascular dysfunction, with formation of an endoneurial edema, play a pathogenic role in nerve damage. The immediate relief following nerve decompression is probably due to a rapid improvement in the intraneural microvascular flow.30
There are several recovery mechanisms following motor nerve damage: conduction block resolution in neuropraxia and axonotmesis, collateral intramuscular reinnervation in partial axonotmesis and axonal regeneration from the site of the lesion in partial and complete axonotmesis and in neurotmesis.31
Illustration 1: Recovery of strength over time, following nerve damage (according to Robinson).31
The following explanation may help to understand the poor functional recovery described above: in cases of axonotmesis, axonal continuity is lost, but the structures supporting the nerve are preserved. Axonal degeneration occurs in the distal part of the axon from the site of the lesion. Preservation of the endoneurial tube, however, allows axons to direct their regeneration pedicles towards the organ originally innervated. This type of lesion should have a relatively good prognosis, however the distance between the lesion and the organ innervated can vary. As the axon only grows at an average rate of 1mm per day, distally, the motor plate and muscle fibers start to atrophy before the axon reaches them. And finally, the Schwann cells in the basal membrane degenerate after long periods and the chances of an axon reaching the target organ are limited for lesions situated further away.32
Time sensitivity also limits the potential for regeneration. If the axon has not reached the motor plate within two years, the degree of atrophy and scarring of the target
muscle is so great that restoring its motor function will probably be impossible.25 If the motor plate is damaged, a sufficient number of axons would be needed for the muscles to be clinically functional. There is not, therefore, always a parallel between electrical and clinical recovery. It would appear that for electrical reinnervation to be effective, it needs to occur early – otherwise, recovery remains insufficient to restore functionality.
Brachial plexus lesions
The brachial plexus is formed from the coalescence of the ventral rami of the lower four cervical (C5 through C8) and first thoracic (T1) spinal nerves as they emerge from their respective neural foramina. The C5 and C6 nerves merge to form the superior trunk, and the C8 and T1 nerves merge to form the inferior trunk. The C7 nerve continues laterally as the middle trunk.33
Neurologic lesions during shoulder surgery are more likely due to indirect mechanisms.34,35 But, there is potential for direct nerve damage during shoulder surgery procedures, as the brachial plexus and its terminal nerve branches are in close proximity to the glenohumeral joint.
Nerve injuries occurring in the context of RSA mainly concern two nerves: the axillary nerf and the suprascapular nerve. For this reason, we will not focus on injuries to the other nerves of the brachial plexus which remain extremely rare.
Axillary nerve
The susceptibility of the axillary nerve to sustain direct or traction injury during surgical procedures has been well documented.34,36-40
However, no explanation was found for the higher prevalence of neurological lesions of the axillary nerve compared with the remainder of the brachial plexus. The anatomical position of the axillary nerve could make it more specifically vulnerable to injury due to lengthening of the arm and eventually to compression in cases of secondary impingement. The axillary nerve can be in close proximity to the glenoid rim, and thus to prosthetic components used in reverse shoulder arthroplasty.
Previous studies have demonstrated that the mean distance between the axillary nerve and the glenoid rim is between 3.2 mm and 12.4 mm.38,41-44 Therefore, the nerve is sufficiently distant from the glenoid component of the prosthesis to avoid any impingement (illustration 2).
Illustration 2: Course of the axillary nerve, in relation to the lower rim of the glenoid.
A cadaveric study examined the relationship of the axillary nerve to the prosthesis following RSA. No relationship was demonstrated between an inferior overhang of the glenosphere greater than or equal to 5 mm and the development of neurological impairment (P = 1.000).45 The axillary nerve is not in close proximity to the
the normal anatomic position relative to the glenoid, the hypothesis of the nerve’s impingement is not supported; inferior glenosphere overhang does not appear to decrease the distance to the axillary nerve. Therefore, the position of the glenosphere in the vertical plane is probably not related to the development of a neurological lesion due to direct contact.45
The nerve then exits posteriorly through the lateral axillary space and gives the anterior and posterior branches to muscles, capsule, and skin.46 Here, however, the axillary nerve runs close to the humeral component, which can lead to lesions, depending on the cup height or retroversion (illustration 3).
Illustration 3: Proximity of the axillary nerve to the prosthetic components.
Posterior view of right shoulder showing in detail the lateral axillary space after implantation of a reverse shoulder arthroplasty. The main anterior circumflex branch of the axillary nerve courses distally around the metaphysis and is in close contact with the humeral trial liners. (AN [black arrows]: main anterior circumflex branch of the axillary nerve; *: blue humeral liners; D: deltoid muscle; TB: long head of the triceps brachii muscle; TM: teres minor).45
Suprascapular nerve
The suprascapular nerve is a mixed motor and sensory nerve that is made up of contributions from the ventral rami of spinal nerves C5 and C6 predominantly, and C4 occasionally, as part of the upper trunk of the brachial plexus. From an anatomic
coracoid groove and distributes branches into the supraspinous fossa before reaching the posterior glenoid. It is then held in the spinoglenoid groove by the ligament of the same name, before reaching its destination under the scapular spine.
The motor component innervates the supraspinatus and infraspinatus muscles.47 The sensory branch innervates the posterior capsule of the glenohumeral joint.
Nerves Lesion before RSA Lesion during RSA Lesion after RSA
Axillary nerve Previous cervical radiculopathy 48
fixating baseplates 55 - Lengthening of the arm 52
Ulnar nerve Previous cervical radiculopathy 48
Median nerve Previous carpal tunnel syndrome 56
Radial nerve Previous cervical radiculopathy 48
- Lengthening of the arm 51,52
Table 3: Summary of the nerves affected in reverse shoulder arthroplasty (RSA) and the mechanism of these injuries.