Lésions neurologiques après les prothèses totales inversées d’épaule

Thesis

Reference

Lésions neurologiques après les prothèses totales inversées d'épaule

NOWAK, Alexandra Nathalie

Abstract

De nos jours, il existe de plus en plus d'indications à la mise en place de prothèses totales inversées d'épaule. En effet, ce type de prothèse est non seulement utilisé pour les situations d'omarthrose avec lésion de la coiffe des rotateurs mais également lors d'échec de prothèses anatomiques, de fractures proximales et complexes de l'humérus, de mal-union de ces fractures, de polyarthrite rhumatoïde avec atteinte de la coiffe, de lésions massives et irréparables de la coiffe et des tumeurs. De par sa biomécanique particulière, la prothèse inversée d'épaule met à risque le plexus brachial. Le but de cette thèse est premièrement de revoir l'anatomie du plexus brachial et la physiopathologie de ces atteintes neurologiques.

Dans un deuxième temps, les moyens préventifs et traitements de ces lésions seront abordés en s'attardant sur les thérapies au stade de la recherche clinique mais qui s'annonce déjà prometteur dans un futur proche.

NOWAK, Alexandra Nathalie. Lésions neurologiques après les prothèses totales inversées d'épaule. Thèse de doctorat : Univ. Genève, 2020, no. Méd. 11020

DOI : 10.13097/archive-ouverte/unige:144378 URN : urn:nbn:ch:unige-1443780

Available at:

http://archive-ouverte.unige.ch/unige:144378

Disclaimer: layout of this document may differ from the published version.

Section de Médecine Clinique Département de chirurgie

orthopédique et de traumatologie Service de Chirurgie

Hôpitaux Universitaires de Genève ___________________________________________________________________

Lésions neurologiques après les prothèses totales inversées d’épaule

Thèse

présentée à la Faculté de Médecine de l'Université de Genève

pour obtenir le grade de Docteur en médecine par Alexandra NOWAK

De France

___________________________________________________________________

Directeur de thèse : PD Dr Alexandre LÄDERMANN Sous la supervision du Prof. Didier HANNOUCHE

Geneva

Table of Contents

1. Abbreviations……….4

2. Acknowledgment………..5

3. Disclaimer………...…6

4. French part……….7

Introduction……..………7

Discussion……….………..7

5. Introduction……….15

6. Pathoanatomy and Preferred Classification of Neurological Lesions….17 Nerve anatomy………..17

Nerve lesions………...17

According to anatomic nerve lesions……….18

According to the mechanism of nerve lesion………20

Limits of these classifications………..21

Miniature compartment syndrome………..23

Brachial plexus lesions……….25

Axillary nerve ……….26

Suprascapular nerve ………..…..29

7. Biomechanics of Reverse Shoulder Arthroplasty………..33

8. Prevalence of neurological lesions………43

Preoperatively………43

Intraoperatively ……….…44

Postoperatively………..45

9 Risk Factors and Causes of Neurological Lesions………...…47

Type of patient………...47

Risks associated with positioning and anesthesia………...47

Arm lengthening……….48

Direct damage………...….48

Postoperatory immobilization………...49

10 Clinical Presentation and Essential Physical Examination…………...…..50

11 Prevention……….52

Arm lengthening……….52

Prosthesis design………..…....54

Surgical approach………..56

Peri-operatory monitoring ………..…….56

12 Treatment Options………..57

Workup………57

Conservative treatment………57

Analgesic treatments………58

Vitamin treatments………58

Corticoid treatments……….59

Physical treatments……….…….59

Complementary therapies……….…..59

Alternative therapies……….……….…..60

Surgical treatments………..60

Neurolysis………..60

Sutures………...60

Grafts………..61

Locally-applied corticoids………61

Treatments currently in development………62

13. Conclusion………68

14. Appendices……….……..69

15. References………72

1. Abbreviations

PTIE: Prothèse totale inversée d’épaule CRPS: complex regional pain syndrom ENMG: Electroneuromyography

TENS: Transcutaneus electroneurostimulation TSA: Total shoulder arthroplasty

RSA: Reversed shoulder arthroplasty

2. Acknowledgment

First of all, I want to thank my parents who gave me a stable living environment and always pushed me to do better.

I also thank my supervisor, PD Dr. Alexandre Lädermann, who was behind this project and who accompanied me throughout it. I want to express my gratitude for the year of training I have spent by his side which allowed me to develop my knowledge in this vast field of shoulder surgery. I would also like to acknowledge Dr.

Maxime Grosclaude and Dr Jean-Luc Ziltener who gave me the desire to work in the domain of rehabilitation and physical medicine; I thank them for their advice. Finally, I thank Professor Didier Hannouche for his support and the time he spent supervising this thesis.

3. Disclaimer

The author certifies that neither they nor any members of their immediate families have funding or commercial associations (e.g., consultancies, stock ownership, equity interest, patent/licensing arrangements, etc.) that might pose a conflict of interest in connection with the present thesis.

4. French part

Introduction

Durant ces dernières années, j’ai eu la chance de travailler avec le PD Dr Alexandre Lädermann et ses collègues. J’ai ainsi pu approfondir mes connaissances sur l’épaule, et plus particulièrement sur les prothèses totales inversées d’épaule.

Avec les progrès réalisés, ce type de prothèse est de plus en plus proposé chez les personnes ayant une coiffe des rotateurs déficitaire. En effet, avec ce type de configuration, le deltoïde arrive à compenser la coiffe lésée et permet ainsi de retrouver une bonne fonction sans avoir à réparer la coiffe des rotateurs qui a été endommagée.

Ce type de prothèse offre de nombreux avantages par rapport aux prothèses anatomiques, éléments que nous avons étudié et publié ces dernières années, et sur lesquels je me suis basée pour rédiger cette thèse.

Discussion

Le but de cette thèse est d’analyser la biomécanique des prothèses totales inversées d’épaule afin d’étudier ses complications, notamment celles neurologiques. En comprenant les mécanismes à l’origine de ces lésions, on pourrait améliorer le type de design prothétique et ainsi limiter ces problèmes tout en améliorant la fonction de l’épaule.

Je vais donc m’appuyer sur mes différents travaux (Annexe 1 à 3) pour illustrer et

prothèses totales inversées d’épaule, mais aussi en montrant la complexité de cette biomécanique avec ses désavantages en fonction du sous-type de prothèses inversées. En effet, chaque détail a son importance (comme l’inclinaison humérale, la distance acromio-humérale…) et ses conséquences.

En cas de déficience de la coiffe des rotateurs (Annexe 1), le seul muscle restant capable d'élever le bras est le deltoïde. Afin de restaurer une élévation antérieure au- dessus de 90°, le rôle d'abduction du deltoïde doit être augmenté. Ceci peut être obtenu par plusieurs mécanismes, comme une ostéotomie de l’épine scapulaire¹ ou en médialisant le centre de rotation de l'articulation.² Le concept de chirurgie fonctionnelle est né de cette dernière option : en l'absence de solution anatomique efficace, la restauration de la fonction doit être proposé à travers une nouvelle morphologie. La prothèse totale inversée d'épaule (PTIE) a été développée pour médialiser et abaisser le centre de rotation gléno-humérale, augmentant ainsi le bras de levier du muscle deltoïde.³ Ce faisant, la PTIE permet de restaurer l'élévation antérieure active en l'absence d'une coiffe des rotateurs fonctionnelle.

La prothèse totale inversée d’épaule est un outil puissant qui a ouvert de nouvelles barrières, en particulier pour la chirurgie reconstructive de l'épaule. De nombreuses pathologies qui ne pouvaient pas être traitées auparavant ont trouvé une solution grâce à cette conception (Annexe 1), et les indications sont actuellement en expansion (Annexe 2). Il est maintenant utilisé pour diverses affections telles que l'échec des prothèses totales anatomiques d’épaule ou des hémiarthroplasties, les fractures humérales proximales complexes et la pseudarthrose, la polyarthrite

rhumatoïde avec lésions de la coiffe des rotateurs, les déchirures massives de la coiffe des rotateurs irréparables ou après échec de réparation, et les tumeurs.^4-20 Le suivi à long terme de plusieurs séries de PTIE a confirmé les résultats préliminaires : la fixation de la glénoïde est stable, on note une amélioration clinique postopératoire significative et un taux élevé de satisfaction des patients²¹.

Dans le premier article que j’ai rédigé (Annexe 1), l’influence de l’inclinaison humérale dans les prothèses totales inversées d’épaule a été évalué. On s’est par exemple rendu compte que la verticalisation de l’inclinaison humérale (c’est-à-dire une inclinaison plus anatomique) en passant de 155° à 135° permet une majoration de l’adduction et une diminution du conflit scapulaire (Table 2 de l’Annexe 1).

Table 2 de l’Annexe 1 : Amplitudes articulaires d’une épaule native et de 4 configurations prothétiques différentes.

En contrepartie, cette verticalisation de l’inclinaison humérale diminue l’abduction, engendrant cette fois-ci un conflit au niveau de la grande tubérosité contre l’acromion

Le but de cet article a donc été de comparer les avantages et inconvénients d’une prothèse totale inversée d’épaule avec un angle d’inclinaison élevé (155°) versus plus anatomique (135°) et de trouver le meilleur compromis, tout au moins théorique.

Le fait d’avoir une inclinaison plus anatomique va, entre autres, permettre une diminution de la distance acromio-humérale (Table 1 de l’Annexe 1) et donc une diminution de l’allongement du bras après la pose d’une prothèse totale inversée d’épaule, réduisant ainsi le risque de lésion neurologique.

Table 1 de l’Annexe 1 : Position humérale en fonction de 4 différentes configurations prothétiques

A noter que d’autres critères peuvent influencer cette distance acromio-humérale telle que la mise en place d’un réhausseur, un polyéthylène plus épais, une position de la glénosphère plus inférieure ou une glénosphère de plus grande taille.

Dans le deuxième article sur lequel je m’appuie pour cette thèse (Annexe 2), nous avons comparé deux voies d’abord différentes lors de la mise en place d’une prothèse totale inversée d’épaule : la première, traditionnelle, passant au travers du

deltoïde et du sous-scapulaire, et la deuxième préservant ces structures.

L’hypothèse alors avancée était que la deuxième voie d’abord permettrait une récupération fonctionnelle plus rapide en diminuant la prévalence de lésions neurologiques et en limitant l’immobilisation post-opératoire.

L’autre aspect étudié était le caractère financier : grâce à une hospitalisation moins longue dans le groupe préservant le sous-scapulaire, on note une diminution des coûts de la santé (de $5581), sans pour autant voir plus de complications ou de réhospitalisation par la suite. Le traitement physiothérapeutique a été quant à lui similaire dans les deux groupes de patients mais on note une meilleure fonction à 3 mois en termes d’élévation antérieure et au score de SANE (Single Assessment Numeric Evaluation) dans le groupe où le sous-scapulaire a été préservé.

La complexité des prothèses totales inversée d’épaule, en raison de son anatomie singulière, se reflète dans le grand nombre de problèmes et complications signalés. Comme défini par Zumstein et al., les problèmes peuvent être définis comme des événements intra ou post-opératoires qui ne sont pas susceptibles d'affecter le résultat final du patient.²² Cela inclut les hématomes, la phlébite, l'ossification hétérotopique, le syndrome douloureux complexe régional et ne sera pas couvert dans cette thèse. Les complications sont définies comme tout événement intra ou post-opératoire susceptible d'avoir une influence négative sur le résultat final du patient, comme une extravasation de ciment peropératoire, des fractures intra ou post-opératoires, des luxations prothétiques, des infections, des changements radiographiques tels que des lignes radiolucentes glénoïdiennes ou humérales, un conflit scapulaire, une fracture de stress, un descellement aseptique,

remplacement du composant), et lésions neurologiques. La situation dépendra également du nombre de chirurgies précédemment effectuées. Wall et al. ont rapporté 13% de complications dans les prothèses primaires et 37% dans les révisions.¹

Le troisième article cité (Annexe 3) et sur lequel je me suis basée pour ma thèse, compare deux types de prothèses totales inversée d’épaule : la première standard (Schéma C de la figure 2, Annexe 3) et la deuxième présentant une plus grande latéralisation de la glénoïde (et donc du centre de rotation) (Schéma B de la figure 2, Annexe 3).

Figure 2 de l’Annexe 3 : Position du centre de rotation en fonction du type de prothèse totale inversée. A) Epaule native. Le centre de rotation est au niveau de la tête humérale, et le niveau du bras ne permet pas le recrutement du deltoïde. B) Prothèse totale inversée d’épaule avec latéralisation de la glénoïde et médialisation de l’humérus. Cette configuration prothétique engendre une latéralisation du centre de rotation, diminuant ainsi le recrutement du deltoïde pour les rotations. C) Prothèse totale inversée d’épaule type Grammont avec latéralisation de l’humérus et médialisation de la glénoïde. La médialisation du centre de rotation et la latéralisation de l’humérus permettent un recrutement important du deltoïde.

L’hypothèse avancée dans cet article était que les prothèses inversées avec majoration de la latéralisation du centre de rotation permettraient de diminuer le conflit scapulaire, d’augmenter les amplitudes en rotation externe et en rotation interne, et de limiter les lésions neurologiques. Cette étude nous a permis de constater une amélioration de l’élévation antérieure et une amélioration du score de Constant (score d’évaluation fonctionnelle de l’épaule) avec la prothèse totale

n’avons pas non plus mis en évidence de différence concernant le conflit scapulo- huméral et le gain de rotation externe ou interne. En revanche, si le patient présente des tendons sous-scapulaire et sous-épineux intacts, la PTIE avec latéralisation du centre de rotation permet de diminuer le recrutement du deltoïde pour la rotation. A l’inverse, la PTIE avec médialisation du centre de gravité (type Grammont) permet de recruter plus facilement le deltoïde dans le cadre d’une lésion massive de la coiffe des rotateurs.

Cette thèse fournit une revue complète des concepts actuels relatifs aux lésions neurologiques supérieures après prothèse totale inversée d’épaule, y compris une revue des changements biomécaniques pertinents induits par l'implant, des techniques pour diagnostiquer les lésions neurologiques et les traiter. Enfin, cette thèse fournit des recommandations sur la tension idéale des tissus mous pour fournir le meilleur résultat fonctionnel sans augmenter le risque de lésion nerveuse.

5. Introduction

In rotator cuff deficiency (appendix 1), the only remaining muscle able to elevate the arm is the deltoid. In order to restore anterior elevation above 90°, the abduction role of the deltoid has to be increased. This can be obtained by several mechanisms, such as an osteotomy of the scapular spine² or by medializing the rotation center of the joint.³ The concept of functional surgery is born from the latter option: where no effective anatomic solution exists, restoration of function has to be proposed through a novel morphology. Reverse shoulder arthroplasty (RSA) was developed to medialize and lower the glenohumeral center of rotation, thereby increasing the lever arm of the deltoid muscle.⁴ In doing so, RSA allows restoration of active anterior elevation in the absence of a functional rotator cuff. The RSA is a powerful tool that has opened new barriers, especially for reconstructive shoulder surgery. Many pathologies that could not be treated previously found a solution through this design (appendix 1), and indications are currently expanding (appendix 2). It is now used for various conditions such as failed total shoulder arthroplasty or hemiarthroplasty, complex proximal humeral fractures and defective fracture union or nonunion, rheumatoid arthritis with rotator cuff lesions, failed or irreparable massive rotator cuff tears, and tumors.^1,5-20 Series of RSA with long term follow-up confirmed the preliminary results with stable glenoid fixation, significant postoperative improvement and high rate of patient satisfaction.²¹ However, the complexity of this procedure with regards to its singular anatomy is reflected by the large number of reported problems and complications. As defined by Zumstein et al., problems can be defined as intra- or postoperative events that are not likely to affect the patient’s final outcome.²² This includes hematomas, phlebitis, heterotopic ossification, CRPS and will not be

events that are likely to have a negative influence on the patient’s final outcome, such as intraoperative cement extravasation, intra- or postoperative fractures, prosthetic dislocations, infections, radiographic changes such as glenoid or humeral lucent lines, scapular notching, stress shielding, aseptic loosening, reinterventions (without replacement of the component) or revisions (with replacement of the component), and neurological lesions. The situation will also depend on the number of surgeries previously performed. Wall et al. reported 13% of complications in primary prostheses and 37% in revisions.¹

Neurological complications are not uncommon for numerous reasons.²³ Firstly, old, fragile and multiply-operated patients have a higher risk of pre-existing neurological lesions. Secondly, RSA is often used in patients with distorted anatomy. Exposure can be arduous, and traction on retractors important, particularly in revision surgery.

In such conditions, dissection might be dangerous due to aleatory nerve localization.

Thirdly, the prosthetic design can lead to arm lengthening and possibly to a humeral lateralization which increases the traction on the plexus (appendix 1). All these reasons imply physiological and biomechanical changes that may increase the potential for neurological complications.

This thesis provides a comprehensive review of current concepts pertaining to upper neurological lesions following RSA, including a review of pertinent biomechanical changes induced by the implant, techniques to diagnose neurological lesion, and to treat them. Lastly, this thesis provides recommendations on ideal soft-tissue tension to provide the best functional outcome without increasing the risk of nerve damage.

6. Pathoanatomy and Preferred Classification of Neurological Lesions

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 demyelination

Paresthesia, paresis (partial or complete)

Complete (1 day to 3 months)

Sunderland II Axonotmesis Axon affected Endoneurial tube

normal

Paresthesia, paresis (partial or complete)

Usually complete (1-6 months)

Sunderland III Axonotmesis Endoneurial tube

damaged Paresthesia,

dysesthesia, paresis (partial or complete)

Partial (12-24 months)

Sunderland IV Axonotmesis

Only the epineurium is normal (continuous

neuroma)

Hypoesthesia.

Dysesthesia, complete paresis

None without surgical repair

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

- Anesthetic bloc ⁴⁹ - Posterior impingement - Direct lesion with the scalpel or retractors ⁴⁹ - overstretching of the arm in external rotation and extension during the surgery ⁵⁰ -traction injury while implanting the glenosphere ⁵¹

- Lengthening of the arm ^51,52

Vascular

lesion/hematoma

49

Suprascapular nerve

- Previous cervical radiculopathy ⁴⁸ - Massive rotator cuff lesion ^53,54

- Anesthetic bloc ⁴⁹ - Direct injury with excessive length of the screws while

fixating baseplates ⁵⁵ - Lengthening of the arm ⁵²

Ulnar nerve Previous cervical radiculopathy ⁴⁸

- Anesthetic bloc ⁴⁹ - Lengthening of the arm ⁵²

Positioning of the elbow in flexed position post- operatively

Median nerve Previous carpal tunnel syndrome ⁵⁶

- Anesthetic bloc ⁴⁹ - Lengthening of the arm ⁵²

Positioning of the elbow in flexed position post- operatively

Radial nerve Previous cervical radiculopathy ⁴⁸

- Anesthetic bloc ⁴⁹ - Indirect traction injury ³⁵

- Lengthening of the arm ^51,52

- Periprothetic fracture ⁴⁹

- Ciment extrusion

49

Musculocutane ous nerve

Previous cervical radiculopathy ⁴⁸

- Anesthetic bloc ⁴⁹ - overstretching of the arm in external rotation and extension during the surgery ⁵⁰ - Indirect traction

- Lengthening of the arm ^51,52

Table 3: Summary of the nerves affected in reverse shoulder arthroplasty (RSA) and the mechanism of these injuries.

7. Biomechanics of Reverse Shoulder Arthroplasty

Firstly, medialization in the center of rotation doubles the lever arm of the deltoid muscle, allowing recruitment of more anterior and posterior deltoid fibers and therefore increasing deltoid abduction efficiency that compensate for a deficient rotator cuff. This phenomena is also responsible for impingement of the medial border of the humeral component on the scapular neck when the arm is adducted.⁵⁷ Repetitive contact between polyethylene and bone may result in polyethylene wear debris, chronic inflammation and osteolysis,^58,59 radiolucency around the glenoid component, loosening²⁰ of the glenoid component,⁶⁰ presence of an inferior bone spur and ossification in the glenohumeral space.^6,57,61 Effectively, changes on the humeral side such as osteolysis, osteopenia, the development of medial and lateral cortical bone narrowing associated with osteopenia, condensation lines around the tip of the stem, and a spot weld between the cortical bone and the stem, radiolucent lines and loosening have also been reported.^57,62 Therefore, the glenosphere has to be implanted on the lower part of the glenoid to avoid notching.^57,58

Secondly, the fixed nature of the glenosphere places torsional forces on the humerus that may affect humeral component instability.⁵⁷

Thirdly, the semi-constrained nature of the prosthesis created by the weight-bearing part being convex and the supported part concave (reversal of the ball and socket),⁵⁷ restores glenohumeral stability. The lever of the deltoid muscle is almost doubled with a RSA, as is, therefore, the abduction efficiency of the deltoid. Under such tension, the deltoid provides the stable fulcrum essential for shoulder active anterior

elevation and prosthesis stability.⁷ The increase in compressive force component has also a stabilizing effect on the humeral head.⁶³

Finally, and most relevant to this thesis, is lengthening of the arm which provides space for full range of motion of the proximal humerus, enhances stability, and retensions the deltoid (appendix 1). The type of glenosphere (size, eccentricity) allows for the adjustment of arm length by several millimeters (about 1% of arm length). Consequently, the only key factor for arm length is humerus length (including height of stem implantation, polyethylene thickness and spacer), as these factors permit the correction of arm length by several centimeters (about 10% of arm length).

Retension of the deltoid is critical due to the semi-constrained design of the prosthesis. The increase in compressive force between the humeral and glenoid components has a stabilizing effect.⁶³ This tension is determined by arm length (illustration 4).

Illustration 4: Influence of glenosphere position in the vertical plane:

A: superior implantation of the baseplate or the use of a non-eccentric glenosphere does not allow proper deltoid tensioning. B: Use of an eccentric glenosphere or inferior positioning of the glenosphere in the vertical plane allows satisfactory deltoid tensioning. From Lädermann et al. ⁶⁴

With the Grammont-type design, implantation of the humeral stem at the humeral cut then using the thickness of the polyethylene insert to obtain appropriate deltoid tension would seem to be a reasonable option.^65,66 However, a variety of RSA designs are currently available and each design has its own anatomic characteristics (e.g. humeral cut angle and lateralizing designs) that may affect arm length (appendix 1 et 3).

Typical postoperative lengthening of the arm, humerus, and subacromial space (acromiohumeral) with a Grammont style prosthesis is summarized in Table 4.

Table 4: Average lengthening of arm, humerus and subacromial space in millimeters.⁶⁴

Mean arm lengthening varies from 15 mm to 27 mm and mean humeral lengthening varies from -5 to 5 mm.⁶⁴ The humeral cut is typically more aggressive when a transdeltoid surgical approach is performed but this is compensated for by an increase in thickness of the polyethylene liner.

Failure to adequately tension the deltoid may result in prosthetic instability, the most common clinically significant complication.⁶⁶ Moreover, other complications following RSA, such as neurological lesions, fractures of the acromion, or permanent abduction of the arm,6,7,63,67,68, have also been described and could also be related to retensioning.⁶⁶

Postoperatively, the arm is lengthened by approximately 24 to 27 mm beyond normal length.65,66,69,70 Biomechanically, the tension on the deltoid and the acromion is therefore greater due to arm lengthening and longer lever arm.

Adequate deltoid tension is accepted as a key to prosthetic function and stability.^7,66,69 This tension is determined by arm length. The latter is dependent on 1) the position of the glenosphere in the frontal plane, 2) the size of the glenosphere, 3) the use of an eccentric or inferiorly tilted glenosphere, 4) the use of a spacer, 5) the thickness of the polyethylene, and 6) the height of humeral cut and stem implantation (Illustration 5).⁶⁴

Illustration 5: Influence of humeral cut on arm length:

(A) Preoperative status with a lack of deltoid tension. (B-C) A low humeral cut induces a low implantation of the stem with a lack of deltoid retensioning. (D-E) A high humeral cut leads to a high implantation of the prosthetic stem with adequate deltoid retensioning.⁶⁴

Different methods for measuring arm lengthening have been proposed (illustrations

6A

6B

Illustration 6: Technique proposed by Lädermann:

6A: Preoperative and postoperative true anteroposterior, bilateral, magnification- controlled radiographs of the humeri with neutral rotation and the patient standing.

6B: An epicondylar line (EL) defined as being between the most lateral part of the medial and lateral epicondyle. The diaphyseal axis (DI), is determined by a line drawn in the center of the proximal humeral medullary canal. The intersection between the epicondylar line and the diaphyseal axis represents the point C. The intersection between the diaphyseal axis and top of the humeral head is named H.

The point A is located at the intersection between the diaphyseal axis and a perpendicular line passing through the most lateral and inferior point of the acromion. A, C, and H are represented by small white points; large white points correspond to the magnification control marker adhered on the skin of the arm. A, acromion; C, condyles; H, head; EL, epicondylar line; DI, diaphyseal axis; preop, preoperative; contro, controlateral; EF, enlargement factor.⁶⁴

Illustration 7: Technique proposed by Jobin:

Radiographic measurements of the deltoid length from the inferolateral acromion tip to the midpoint of the deltoid tuberosity are shown (Left) preoperatively (d) and (Right) postoperatively (d’). ⁷¹

Illustration 8: Technique proposed by Renaud et al.:

Two main lines are placed for measurement; an acromial line that represents the superior cortex of the acromion, and a tangent line to the center of the prosthetic epiphysis or to the center of rotation of the humeral head perpendicular to the first line. The two latter lines represent the acromio–epiphyseal distance and are compared to provide a ratio of lengthening. ⁷²

Illustration 9: External measurement technique proposed by Boileau et al.

The distance between the acromion and olecranon with the elbow flexed is determined on non-operated (A) and operated (B) sides.⁷

8. Prevalence of neurological lesions

Potentially relevant neurological complications involving the brachial plexus or the axillary nerve are considered as rare.^6,73-76 However, Lädermann et al. compared prospectively the prevalence of neurological lesion after anatomic and reverse shoulder arthroplasty.²³ The conclusion of this study was that the occurrence of peripheral neurologic lesions following RSA is relatively common but usually transient, with arm lengthening as a main risk factor.

Preoperatively

Postoperative nerve injuries often reflect sub-clinical damage preoperatively. The prevalence of cervical, brachial plexus or carpal nerve damage in the general population is not as low as one may think. At the Mayo clinic, the average incidence of cervical radiculopathy between 1976 and 1990 was 83 per 100,000, with higher rates in men than in women.⁴⁸ The incidence was highest in people 50 to 54 years of age, with C6 and C7 root lesions making up 64 percent of all cases.

The incidence of brachial plexitis has also been studied through the Mayo Clinic records. Over a 12-year period, the annual incidence of this disorder was only 1.6 per 100,000 population.⁷⁷

Brachial plexus syndromes are rare, as illustrated by the prevalence of plexopathies associated with cancer (approximately 0.4 percent of patients with cancer) and those associated with radiation treatment (approximately 2 to 5 percent of those treated).⁷⁸ Idiopathic brachial plexopathy, or brachial amyotrophy, has an estimated annual

incidence of 2 to 3 per 100,000.⁷⁷ In one large series, the male to female ratio was 2:1.⁷⁹

Traumatic injuries are the most common cause of brachial plexus lesions in children and adults.⁸⁰ Motor vehicle accidents (particularly involving motorcycle riders), industrial accidents, falls, objects falling on a shoulder, sports injuries, and prolonged pressure on the plexus during deep sleep are among the many causes of closed brachial plexus trauma. Open traumatic brachial plexus injuries result from gunshot wounds, lacerations, and animal bites.⁸⁰ Open injuries are frequently associated with trauma to nearby blood vessels, with the result that the plexus suffers secondary injury from expanding hematomas, pseudoaneurysms, and arteriovenous fistulas.

In one population-based study in the Netherlands, clinical carpal tunnel syndrome was present in 3.4 percent of all people, and was likely present, although undiagnosed, in an additional 5.8 percent.⁵⁶

The disorder was much more common in women; the overall prevalence was only 0.6 percent in men. In another study from the Mayo Clinic, the annual incidence rate was only 99 per 100,000 (0.1 percent) with a female to male ratio of 3:1.⁸¹

Intraoperatively

The axillary nerve runs along the anterior then inferior surface of the subscapularis muscle, through the quadrilateral space, which exposes it to a risk of damage when using the anterior approach (deltopectoral approach) for the glenohumeral joint or the inferior capsule. One solution to reduce this risk is to locate the nerve and protect it, if

this approach is chosen.^82,83 Likewise, the axillary nerve can be protected if the lower third of the subscapularis muscle is left intact. If the capsule is incised, it is recommended that the arm be kept in external rotation, to keep the incision zone away from the nerve.^50,84

Nagda et al. Reported episodes of neurological problems in up to 57% of patients monitored during hemiarthroplasties and TSA.⁸⁵ They noted that 76.7% of alerts recorded had returned to normal after repositioning the arm in a neutral position perioperatively.

Postoperatively

Prevalence of clinically significant neurological damage was reported in 2% of cases following RSA and 1 to 4.3% of cases following anatomical TSA. Neurological lesions would appear, however, to be more frequent than previously thought and this type of damage is probably underestimated.²³ Another prospective study determined the electrodiagnostic occurrence of peripheral nerve lesions following RSA.²³ If subclinical deterioration of preoperative lesions is taken into account, 63% of patients in this study had postoperative neurologic lesions. However, only 5% of patients had a lesion that was present beyond 6 months postoperative. The prevalence of peripheral nerve lesions following primary RSA is thus common, but most lesions are subclinical and most clinically apparent lesions are temporary.

The retrospective study by Carofino et al.⁸⁶ refers to neurological lesions occurring during shoulder surgery, but unfortunately no statistics regarding RSA are included in

their iatrogenic injuries is not referred to at all, making any interpretation regarding the frequency of this type of injury during shoulder surgery impossible.

9. Risk Factors and Causes of Neurological Lesions

Although severe injuries can occur in any setting, their likelihood appears to be higher in certain scenarios.

Type of patient

Firstly, the patient pool for this type of surgery is patients at risk. RSA, often used in multiply-operated patients with distorted anatomy, imparts physiological and biomechanical changes that may increase the potential for complications.⁸⁷ Also, these are often patients suffering from cervical osteoarthritis. Theoretically, worsening of an entrapment neuropathy could be part of a double crush syndrome.

This was initially described by Upton and McComas in 1973,⁸⁸ whereby a proximal lesion along an axon predisposes it to injury at a more distal site along its course through impaired axoplasmic flow. Hence, a single lesion along the course of a nerve (like the presumed mechanism for the nerve lesions previously mentioned) predisposes that nerve to a second lesion further along its course (like an entrapment neuropathy).

Risks associated with positioning and anesthesia

Surgery usually involves a preoperatory interscalene block. Complications of regional anesthesia are also possible but are likely very rare. It is estimated, on the basis of two large prospective studies, that neurological injury results from three in 10,000 peripheral nerve blocks.^89-91 Arm positioning also places strain on the brachial plexus, and intraoperative neuromonitoring studies have demonstrated that nerve dysfunction may occur with extreme positions of the shoulder during arthroplasties

traction is applied.⁸⁵ The lateral decubitus position is riskier than the “beach-chair”

position.⁹² Nerve damage can be linked to arm positioning (abduction, external rotation and extension) or traction.^50,85

Arm lengthening

Lengthening of the arm during RSA, because of its nonanatomic design and/or maneuver of glenohumeral reduction, may be a major factor responsible for the increased prevalence of neurologic injury. Clinically relevant neurological complications involving the brachial plexus or the axillary nerve, however, are rare following RSA.^6,73-76

Direct damage

Neurological lesions could also theoretically occur from direct nerve damage during surgical dissection, compression secondary to retractors or postoperative hematoma, excess mobilization of the limb, vascular injury, humeral shaft fractures or cement extrusion.^85,93,94 In open surgery, retractors placed anterior to the subscapularis or medial to the glenoid can injure the brachial plexus, which is located just 10 to 25 mm medial to the glenoid. Caution should also be observed when reaming the metaphysis to avoid posterior humeral cortical violation, particularly when having a low humeral cut and using a large reamer. To prevent such lesions, the use of a combination of polyethylene adaptor systems that allow the use of a large glenosphere with a small metaphysis, might be an option. Another way to prevent excessive cortical reaming is to respect the natural version of the humerus and not to choose a fixed figure of retroversion (i.e. 20 or 30°), if the natural angle is smaller.

Lateral offset of glenosphere from the glenoid surface may be another possibility

since this approach provides sufficient stability without excessive lengthening. This approach may also theoretically relieve tension to the axillary nerve in the quadrilateral space. Further studies are needed to examine this relationship.

Postoperative immobilization

Postoperatively, the elbow brace (in flexion) should be removed as quickly as possible, to reduce the risk of decompensating a pre-existing carpal tunnel syndrome. The exact mechanism is still not known, but the lack of upper limb drainage and the 90° elbow position compressing vascular or neurologic structures could hypothetically be involved. Immediate mobilization is recommended, as is often the case in orthopedics ⁹⁵.

10. Clinical Presentation and Essential Physical Examination

Regardless of the perceived cause of injury, it is important that patients with postoperative neurological deficits be thoroughly and promptly evaluated. This is a very important point because the treatment options available to these patients are time-sensitive.⁹⁶

An additional radiological work-up is therefore necessary. Postoperative X-rays can rule out dislocations, humeral, acromial or scapular fractures and cement extravasation.

Depending on results and clinical suspicions, a myelography, myeloscan or MRI can be required. Electroneuromyography (ENMG) and a full neurological examination are essential to assess the degree of injury and propose a suitable treatment. It should be noted that these additional examinations must be performed at least 3 to 6 weeks after surgery, to reveal muscular fibrillation where denervation has occurred, following Wallerian degeneration. In radicular lesions, ENMG data can help identify the radicular topography of any motor deficit. Regular ENMGs should be carried out to monitor progress and guide reparatory surgery indications (neurolysis and/or nerve grafts) or palliative treatment (muscle transplants). They also allow the early signs of re-innervation to be detected and to evaluate the effects or physical therapy and rehabilitation.

Where postoperative or post-traumatic investigations reveal signs of acute or localized compression (hematoma, bone fragments, cerclage…), urgent

decompression is required. In the event of a peri-operatory nerve section, a suture will improve prognosis, especially in younger patients.

Indeed, irreversible changes occur at the motor end plate in a time-dependent manner so that reinnervation procedures are most successful if they are performed before six months.⁹⁶

11. Prevention

Arm lengthening

The risk of neurological lesions increases drastically above 4 cm of lengthening. A reasonable goal for arm lengthening should thus be between 0 and 2 cm. As a result, strategies have been developed to limit lengthening. In difficult cases with a high risk of dislocation, large glenoid size with shallow concave components, superior approach and prosthetic or bony lateralization of the glenosphere should be considered to avoid excessive tension.

A preoperative guide, useful in complex cases such as revision arthroplasty or post- traumatic arthritis where scar tissue and bone loss prevent making an accurate determination of humeral length, has thus been proposed (illustration 10).⁶⁶

Illustration 10: Proposition for determination of the height of the stem to restore humeral length, from Lädermann et al.

Proposition for determination of the height at which the prosthesis (Grammont-type) should be implanted by planning of the operation with a 10 centimeter marker: A

= corrected length of the contralateral humerus = CHcontro X 10: contro MF = 314 mm. B = corrected length of the preoperative humerus = CHipsi X 10: preop MF = 264 mm. A-B = the corrected length of the missing bone. PHipsi = A-B = 50 mm.

PHipsi is the exact distance in millimeters that we must measure at the time of implantation between the lateral cortex of the humerus (Hipsi) and the superolateral part of the metallic stem (P). A, acromion; C, condyles; H contro, head; EL, epicondylar line; DI, diaphyseal axis; pre-op, pre-operative; contro, contralateral; MF, enlargement factor.⁹⁷

Preoperative planning is probably not necessary in primary cases. Its use in revision cases, however, seems mandatory. To guarantee the best possible functional

goal.^69,71,72 Failure to restore sufficient deltoid tension may be responsible for poor anterior elevation and prosthetic instability.^66,69,87

Prosthesis design

The prosthetic design plays a major role, particularly regarding the neck-shaft angle (appendix 1). The acromiohumeral distance varied by 9.8 mm with the smallest occurring with the onlay 135° model and the largest occurring with the Grammont inlay 155° (Table 4). Compared to the inlay design, the onlay humeral design with the same 155° inclination decreased the acromiohumeral distance by 4.1 mm (appendix 1).^98,99

Table 5: Humeral position in relation to 4 different prosthetic configurations.¹⁰⁰

Likewise, humeral incline also leads to modifications in joint range of motion and position.

Humeral Offset (mm) Acromiohumeral distance (mm)

Inlay 155° Grammont stem 26.6 29.0

Onlay curve stem 155° 33.2 24.9

Onlay curve stem 145° 34.2 23.1

Onlay curve stem 135° 35.5 19.2

Illustration 11: Relationship between neck-shaft angle and acromiohumeral distance.⁹⁹

A steeper or more anatomic neck-shaft angle (Grammont-type 155° vs. 145° and 135° curved design in this example) leads to a decrease in the acromiohumeral distance (appendix 1).⁹⁹

Within the onlay design, incline had a slightly larger influence, with the acromiohumeral distance decreasing by an additional 5.7 mm when moving from 155° to 135°. As for humeral offset, a linear regression was found between acromiohumeral distance and the different inclinations of the onlay design.

Surgical approach

Another way to avoid axillary nerve lesion is to avoid subscapular cuts (appendix 2).

Recently, a novel approach that spare the deltoid and the subscapularis has been published. This technique that preserves the subscapularis improves the stability.

Consequently, deltoid retensionning is less necessary and the stress on the brachial plexus is decreased.^101,102

Intra-operative monitoring

It has been postulated that the high rates of clinically irrelevant neurologic abnormalities described in that study were due to alert criteria thresholds being relatively conservative (50% decrease in MEPs) which in retrospect has been shown to be unreliable when monitoring peripheral nerve.^103-106 The usefulness of this control remains controversial. It should probably be reserved for select situations, where there is a major risk of neurological damage.^32,107-109

12. Treatment Options

Treatment of neurological injuries remains complex, but when multidisciplinary treatment is provided quickly, the results are encouraging. Post-surgical follow-up must include particular monitoring to ensure the injury is recognized clinically, diagnosed quickly and assessed for severity of the neurological damage. While muscular and neurological evaluations are an important part of the physical workup, they are not always sufficiently precise to locate the nerve injury or determine its severity.

Workup

When a neurological lesion is identified, a radiological examination is required to rule out luxation of the prosthesis, cement leakage or excessive lengthening. An ENMG can help to locate the injury and identify its mechanism. It can also be useful in recognizing the nature and severity of the neurological condition. ENMG will also provide a prognosis for recovery from nerve damage, although this is not always precise. The initial follow-up ENMG should be carried out with in the first 3 to 6 weeks, then repeated every 6 months throughout neurological regrowth – i.e.

approximately 2 years.

Conservative treatment

Given that most neurological injuries resolve spontaneously following RSA,²³ conservative treatment is often preferable. Time is a treatment in itself. We often propose multidisciplinary care with physiotherapy (neurostimulation and TENS treatments), occupational therapy (desensitization, proprioceptive and sensory

rehabilitation of the limb), local and oral analgesia, but also cryotherapy, acupuncture, etc.…

Analgesic treatments:

Morphine derivatives are widely used in brachial plexus injuries, when mild analgesics are insufficient. If the morphine derivative is also ineffective, neuroleptics such as pregabalin (Lyrica ®), or gabapentin (Neurontin®) can be introduced, or certain antidepressants, notably duloxetine (Cymbalta®). If the side effects are not tolerated, local treatment by anesthetic patch (Neurodol patch®), anti-inflammatory patch (Flector patch®), or an anesthetic spray may be introduced. If the pain remains unbearable, a stellate ganglion block can be proposed, although this is only effective in 50 % of cases, and not without risk (Horner’s Syndrome, worsening of pain…).

Vitamin treatments:

The B vitamins are known for reducing degeneration of the nervous system, which is why they are often prescribed. A B12 (cobalamin) deficit leads to a deficit in methionine, which is necessary for phospholipid and myelin synthesis. Vitamin B12 is also believed to be an antioxidant,¹¹⁰ facilitating the elimination of free radicals, and would appear to be a neuroprotector.¹¹¹ In patients with alcohol or drug dependencies, and patients with a vitamin B12 deficiency, supplementation should be prescribed immediately. Of course, it is strongly recommended that patients be encouraged to wean of neurotoxic substances such as alcohol.