- Email: [email protected]
Mechanisms of brachial plexus lesions
ClinicalNeurology and Neurasurgery, 9.5 (Suppl.) (1993) S24-S29 0 1993 Elsevier Sciecne Publishers B.V. All rights reserved O303-8467/93/%06.00 CLINEU cm250
mechanisms of brachial plexus lesions L.N.J.E.M. Coene Dqartment
of Orthopedic
Surgery, Municipal Hospital Leyenburg, The Hague, The Netherlands
Key words: Brachial plexus lesions; Trauma mechanisms Summary
The main causes of brachial plexus palsies are traction, due to extreme movements, and heavy impact. In downward traction of the arm and forcible widening of the shoulder-neck angle the lesion will occur in the upper roots and trunk. Forcible upward traction will cause avulsion of Tl and Cg. The most violent trauma will result in a lesion at all levels. Rupture of the cords and/or individual infraclavicular nerves will be produced by traction and/or forcible widening of the scapulohumeral angle. Vascular structures are subjected to the same mechanism and injuries of these structures give information about the site and severity of nerve lesions; fractures of the skull, cervical spine, clavicle, first rib or arm yield further data on the mechanism of trauma that has produced the brachial plexus palsy. Heavy impact or crush lesions are caused by direct trauma to the (supra)clavicular region and are nearly always associated with fracture of the clavicle.
Introduction
Brachial plexus (BP) lesions are, gross0 modo, seen in 3 groups of patients: (A) a large group of patients over 40 years of age who sustain glenohumera~ dislo~tion or humeral neck Fracture by a minor trauma like a fall. The lesion is mostly infraclavicular and always concerns the axillary nerve. Those palsies recover spontaneously in about 90% of the cases [l]. However, prognosis with regard to functional recovery is worse in elderly patients due to traumatic degenerative cuff - and capsular - lesions and less compensatory capacity. (B) Patients under 40 years of age who are involved in serious accidents. They are generally multi~auma~s~ patients with lesions of the head, arm and/or thorax. Rupture of nerve structures is frequently present. (C) Young patients who sustain minor shoulder trauma such as shoulder dislocation or humeral neck fracture. Neurapraxia of some infraclavicular nerves may occur but nerve rupture is very rare. The important physical role of traction in BP injuries was first described by Flaubert in 1827 [2]. He noticed at autopsy that violent reduction of a shoulder dislocation had resulted in avulsion of nerve roots from the spine. Several cadaver experiments have been reported trying to prove that plexus
Correspondence to: LN.J.E.M. Coene, Department of Ortbopaedic Surgery, Municipal Hospital Leyenburg, Lqweg 275,2545 CHTbe Hague, l%e Netherlands. Phone: (+31)-70-3592ooO; FAX: (+31)-70-3295046.
lesions were caused by forcible widening of the shoulderneck angle, as observed in birth lesions, and by dislocation of the shoulder. Horsley [3] lifted corpses to the ceiling of his laboratory, letting them drop down on the shoulder and head and in his macabre experjment found this assumption to be correct. Delbe and Cauchoix [4] noticed that dislocation of the shoulder could produce an infraclavicular plexus lesion. The effect of stretch on individual nerves has been studied in laboratory experiments by Haftek [5], Lundborg [6] and Sunderland [7] (Fig. 1). The main cause of BP palsies is forceful stretch together with extreme movements. Traction on the arm with the trunk fixed, such as occurs in deliveries in transverse presentation or pull on an outstretched arm during reduction of a dislocated shoulder, in cadaver experiments mainly produces root lesions. When the arm is fixed and traction is on the trunk, such as occurs in a falling person who grabs something, this mechanism remains the same (Fig. 2a and c). In clinical situations movement beyond the physiological limits is encountered under two conditions: forcible widening of the shoulder-neck angle, and forcible widening of the s~pulohumeral angle. The former frequency occurs in motor cyclists who are thrown onto the road (Fig. 2f-h). Forcible depression of the shoulder, for example by a falling tree, has the same effect (Fig. 2b). Since there is no osseous connection between the shoulder girdle and the spine, widening of the shoulder-neck angle is limited by the skin, muscles, fascia, the first rib (because it obstructs the clavicle)
s25 NERVE
NERVE FBRE
traumatic closed injuries, one should bear in mind that nerves tend to be tom between two points of anchorage and that the nerve injury may extend over a considerable distance. only violent trauma can cause nerve rupture. Accompanying lesions like vascular rupture or skeletal fractures yield a clue about the violence of the trauma, the site of the nerve lesion, the mechanism and the prognosis. There may be two levels of injury just as there may be two (or more) mechanisms of trauma.
Mechanisms
Fig. 1. Effect of stretch on a nerve and its nerve fibres, according to Haftek [5]. lhe histological events, occurring in one nerve fibre, are schematically sketched on the right. During progressive stretch, diameters of the axon (a) with myelin sheath (m) and of the epineurium (E) gradually decrease (p = perineurium). The first 2 diagrams represent the first stage, the 3rd diagram the 2nd stage, the 4th diagram represents the moment of epineurial rupture, the 5th diagram the moment of perineurial rupture, and the 6th diagram represents complete rupture of the nerve fibre.
and the neurovascular bundle, which is the weakest structure. Increasing the acromio-mastoid distance beyond physiological limits overstretches the supraclavicular BP structures. Forcible widening of the scapulohumeral angle produces tension on the infraclavicular neurovascular bundle. Shoulder dislocations and humeral fractures are produced by this mechanism (Figs. 3 and 4). In heavy impact BP lesions, constituting another mechanism of trauma, usually the supraclavicular region is directly hit. These lesions are often accompanied by fracture of the clavicle. Finally, plexus lesions may be caused by compression or stretch by fractured or dislocating bones. In clinical situations, these mostly are the fractured clavicle or the (fractured) humeral head or neck. Gradual compression by post-traumatic oedema or fibrosis occurs, but plays a less important role [6]. In analysing the mechanisms of nerve injury in acute
of root lesions
At the level of the vertebral foramen, the anterior and posterior rootlets, originating from the spinal cord, come together in a cone shaped dural envelope. This envelope continues as the epineurium of the spinal nerve. When traction is applied to a spinal nerve, this force is transmitted to the rootlets and the dural cone. The dura may rupture in some instances, while the rootlets, due to their elasticity, still resist the traction. This mechanism is called the peripheral mechanism by Sunderland [8]. A meningocele may be seen on myelography while the rootlets are intact. The second mechanism, called the central mechanism by Sunderland, is caused by forcible inclination of the cervical spine to the opposite side. Due to translation of the spinal cord to the opposite side, tension is applied on the ipsilateral rootlets. In this case roots rupture before the dural cone does. Progressive traction causes rootlets to rupture or to avulse from the spinal cord. The anterior rootlets, being shorter than the posterior ones, rupture first. The weak origin of the rootlets at the spinal cord is not only protected against traction by the cone-shaped dura but also by the so called root ligaments. The epineurium of the spinal nerve is flbrously attached to the related transverse process. The cervical fascia extends from the spine distally as a fibrous sheath around the neurovascular bundle and is another protection against traction. The higher incidence of avulsion of C8 and Tl as compared with CS, C6 and less so C7 is due to the lack of root ligaments in C8 and Tl. At the C5 and C6 levels, rupture of the spinal nerves occurs more frequently while the roots remain intact. C7 occupies an intermediate position [8]. When the plexus is pulled down by depression of the shoulder or inclination of the cervical spine, the rootlets of C5 and C6 in particular change direction while entering the intervertebral canal. The spinal nerves C5 and C6 ride over the transverse process downwards. This Z arrangement adds to the fixation of the roots C5 and C6 [9]. Fracture of the transverse process diminishes the protective function of the root ligaments and can be associated with root avulsion. Forcible downward traction in cadaver experiments may produce avulsion of C5 (infrequently), C6 and, to a lesser
S26
Fig. 2. Trauma
extent, C7, but C8 and Tl remain more or less relaxed [l&13]. On the other hand, forcible upward traction of the plexus in the cadaver produced avulsion of Tl and C8, being unprotected by root ligaments. Single avulsion of C7 may occur due to the short course of this root. Mechanisms In clinical
of supraclavicular practice,
plexus lesions
supraclavicular
plexus
lesions
are
caused by traction on the arm or widening of the shoulderneck angle. The structures of the plexus are stretched between two fixed points, such as on the one hand, attachments of CS and C6 to the transverse process, and on the other hand the point where the upper trunk starts to divide into cords. Another example is the origin of the medial cord and the point where it turns around the coracoid. In cadaver experiments forcible widening of the shoulderneck angle caused almost the same lesion as is produced by forcible downward traction of the arm.
Fig. 3. Relationships between the axillary nerve, the intiaclavicular neurovascular bundle and the humeral head in internal (A and C) and external (B and D) rotation. A and B are frontal, C and D are caudal views. In internal rotation the inferior glenohumeral ligament prevents further abduction. Both axillary nerve and neurovascular bundle are caudal to the humeral head and stretched over it In external rotation, the neurovascular bundle is ventral to the humeral head. Only extension will stretch it in this position. The axillary nerve runs from a ventral subcoracoid position to the dorsal side of the humeral neck and is the only nerve stretched during e.g. dislocation. The glenohumeral ligament does not prevent further abduction. Note that the humerus is in 30% retroflexion to the scapular plane (C and D), and the humeral head projects ca. 50% ventral to the anterior glenoid rim.
Fig. 4. Skeletal injuries. When a person falls sideways on the extended and internally rotated arm, the impact is initially on the hand, forearm and/or elbow. The mass of the torso causes hyperabduction of the glenohumeral joint, and forcible separation of the humems and scapula. The impact is all on one side. and the thorax hits the solid ground. Forced inclination of the scapula is blocked by the ground, and humerus and scapula are subsequently separated with more force. This mechanism nay produce injury to the hand, forearm, elbow, shoulder, scapula and ribs, successively. A dislocation or humeral neck fracture may occur.
S27
Fig. 3.
Fig. 5. Top: fall on the backward
extended elbow (A) or arm (B) produces stretch of the neurovascular
bundle over the humeral head. ‘Ihe humeral neck is
blocked by the acromion/spina scapulae and dislocation, humeral neck fracture, etc., may occur. Bottom: extension in 90’ abduction. The neurovascular is stretched over the humeral head, and excessive widening of the scapulohumeral angle occurs (A and B). (C) Caudal view into the axilla.
, Stretch lesions of the supraclavicular brachial plexus nearly always concern the upper and middle trunk, in contin ity with the lateral and posterior cords. Lower trunk lesi,“bns are very rare, because traction applied to this level results rather in avulsion of roots C8 and Tl. Traction on the abducted arm produces equally divided tension on all roots, trunks and cords. The first structure to rupture is the cervical fascia, followed by the epineurium, and subsequently the epineurial blood vessels around the cords. Further increase of tension produces progressive laceration of the epineurium, the perineurium and rupture of some fascicles at various levels, and finally severance of the three cords. Forcible downward traction results in laceration of the cervical fascia around the upper spinal nerves and subsequently of the epineurium, epineurial blood vessels, perineurium and superior trunk fascicles. Subsequently, the spinal nerve C5 ruptures, followed by C6 and occasionally C7. At this stage C8 remains more or less relaxed, but Tl becomes flattened over the first rib. Further increase of traction force results in definite rupture or avulsion of C7 and laceration of C8 and Thl. The spinal nerves and trunks of the lower plexus bend over the first rib, and the posterior cord, in particular, is crushed between the clavicle and first
bundle
or second rib. This type of injury frequently occurs in motor cyclists who are thrown onto the road. According to Barnes [14] most stress is on the upper roots, when the arm is held in a ventral position along the side of the body. When the arm is behind the trunk, all plexus roots are under extreme tension [3,10-151 (Fig. 2). In traffic accidents, however, traction is not slow but very fast. This produces lesions over \ relatively short distances. Bending over a bony structure, such as the clavicle, transverse process or first rib, facilitates more localized lesioning as well. Nonetheless, at a microscopical level the injury may extend over a considerable distance. One may encounter naked fasciculi without any epineurium but also “empty” epineurial sleeves with complete rupture of the neural content. Factors such as intrafascicular and interplexual crossing-over, and the changing amount of connective tissue throughout the plexus [9] differ greatly in individuals and clarify the wide variety of supraclavicular BP traction injuries. Mechanisms
of infi-aclavicular
The different
pathogenesis
plexus lesions of infraclavicular
injuries
is
s29
due to the close relationship of the neurovascular bundle with the glenohumeral joint and to the proximity of the distal anchorage points of the infraclavicular plexus. This makes these structures susceptible to stretch lesions when skeletal injuries occur in the area (Fig. 3). Experimentally produced traction with the arm along the side produces no significant tension on the infraclavicular plexus. Traction in abduction, however, produces more or less equal tension on all infraclavicular nerves. Additional endorotation of the arm increases tension in the axillary nerve, radial nerve and posterior cord, just as additional exorotation does in the musculocutaneous nerve [ 161. Movements beyond the physiological limits of motion of the glenohumeral joint have been studied by several authors
A final word should be devoted to the suprascapular nerve. This nerve is fixed in the scapular notch. During normal abduction of the arm the scapula moves away from the cervical spine. It rotates and turns around the thorax. The scapular nerve is put under tension by this normal movement. This accounts for the chronic suprascapular nerve lesions encountered in volleyball or tennis players. It is easy to understand that the suprascapular nerve is stretched or ruptured at the notch during abnormal traction or abduction
in cadaver experiments [ 1,4,13,16]. When the 90” abducted arm is extended behind the frontal plane of the body, the infraclavicular plexus is stretched over the humeral head. Also hyperabduction combined with internal rotation of the humerus produces stretch of the infraclavicular plexus over the humeral head. The latter mechanism occurs when one falls on the laterally outstretched arm and the movement of the scapula is blocked by the ground (Fig. 4). In these experiments, the highest tension arises in those nerves which have their distal anchorage points closest to the glenohumeral joint. This means that in a person falling on his outstretched arm or on an arm extended beyond the frontal plane the highest tension occurs in the axillary nerve or posterior cord. Subsequently, tension is to be borne by the musculocutaneous and radial nerves. The ulnar and the median nerves or, in specific anatomical situations, the medial cord are structures which bear less tension during these mechanisms and will rupture last. Nerves to latissimus dorsi, teres major and great pectoral muscles may also be stretched during this type of trauma. These experimental findings indeed fit in fairly accurately with the findings seen at exploration of infraclavicular brachial plexus lesions. It is nearly always the posterior cord or the axillary nerve that has suffered most in infraclavicular cases. According to the severity of the trauma mechanisms, ruptures of the musculocutaneous, the radial and, less frequently, the median and the ulnar nerves, can be seen. The axillary artery, which is relatively fixed by the acromiothoracic trunk, is subject to the same trauma mechanism. Rupture of this artery therefore occurs in 50% of serious infraclavicular plexus lesions.
References
movements of the scapula [ 171. In supraclavicular as well as in infraclavicular cases, an additional suprascapular nerve lesion is encountered frequently.
Coene, L.N. (1985) Axillary nerve lesion and associated injuries. Thesis, Leiden. Flaubert, M. (1827) Memoire sur plusieurs cas de luxation. Rep. Gen. Anat. Physiol. Pathol., 3: 5%9. Horsley, V. (1899) On injuries to peripheral nerves. Pratt., 63: 131-144. Delbet, P. and Cauchoix, A. (1910) Les paralysies darts les luxations de I’epaule. Rev. Chir., 41: 327-352 and 667-687. Haftek, J. (1970) Stretch injury of peripheral nerve, acute effects of stretching on rabbit nerve. J. Bone Joint Surg., 52B: 354-365. Lundborg, G. and Rydevik, B. (1973) Effect of stretching of the tibia1 nerve of the rabbit, a preliminary study of the intraneural circulation and the barrier function of the epineurium. J. Bone Joint Surg., 55B: 390401. Sunderland, S. (1978) Nerves and nerve injuries, 2nd edn. Churchill Livingstone, Edinburgh. Sunderland, S. (1974) Mechanisms of cervical root avulsion. J. Neurosurg., 41: 704-714. Bonnel, F. and Rabischong, P. (1981) Anatomy and systematisation of the brachial plexus in the adult. Anat. Clin., 2: 289-298. 10 Duval, P. and Guillain, G. (1898) Pathog6nie des accidents nerveux consecutifs aux luxations et traumatismes de I’bpaule. Arch. GCn. Med., 2: 143-191. 11 Frykholm, R (1952) The mechanism of cervical radicular lesions resulting from friction or forceful traction. Acta Chir. Stand., 102: 93-98. 12 Stevens, J. (1943) Brachial plexus paralysis. In: Codman, EA. (Ed.), The Shoulder, Thomas Todd, Boston, MA. 13 Gariepy, R., Derome, A. and Lamin, C. (1962) Bra&al plexus paralysis following shoulder dislocation. Can. J. Surg., 5: 418-421. 14 Barnes, R. (1949) Traction injuries of the brachial plexus in adults. J. Bone Joint Surg., 31B: 1: 10-16. 15 fieux, G. (1894) De la pathogenic des paralysies bra&ales chez le nouveau-nb; paralysies obst&ricales. Ann. GynCml. Obst&., 47: 52-64. 16 Milton, G.W. (1954) The circumflex nerve and dislocation of the shoulder. Br. J. Phys. Med., 17: 136-138. 17 Kopell, H.P. and Thompson, W.A.L. (1963) Peripheral entrapment neuropathies, Williams and Wilkins Co., Baltimore, MD.
mechanisms of brachial plexus lesions L.N.J.E.M. Coene Dqartment
of Orthopedic
Surgery, Municipal Hospital Leyenburg, The Hague, The Netherlands
Key words: Brachial plexus lesions; Trauma mechanisms Summary
The main causes of brachial plexus palsies are traction, due to extreme movements, and heavy impact. In downward traction of the arm and forcible widening of the shoulder-neck angle the lesion will occur in the upper roots and trunk. Forcible upward traction will cause avulsion of Tl and Cg. The most violent trauma will result in a lesion at all levels. Rupture of the cords and/or individual infraclavicular nerves will be produced by traction and/or forcible widening of the scapulohumeral angle. Vascular structures are subjected to the same mechanism and injuries of these structures give information about the site and severity of nerve lesions; fractures of the skull, cervical spine, clavicle, first rib or arm yield further data on the mechanism of trauma that has produced the brachial plexus palsy. Heavy impact or crush lesions are caused by direct trauma to the (supra)clavicular region and are nearly always associated with fracture of the clavicle.
Introduction
Brachial plexus (BP) lesions are, gross0 modo, seen in 3 groups of patients: (A) a large group of patients over 40 years of age who sustain glenohumera~ dislo~tion or humeral neck Fracture by a minor trauma like a fall. The lesion is mostly infraclavicular and always concerns the axillary nerve. Those palsies recover spontaneously in about 90% of the cases [l]. However, prognosis with regard to functional recovery is worse in elderly patients due to traumatic degenerative cuff - and capsular - lesions and less compensatory capacity. (B) Patients under 40 years of age who are involved in serious accidents. They are generally multi~auma~s~ patients with lesions of the head, arm and/or thorax. Rupture of nerve structures is frequently present. (C) Young patients who sustain minor shoulder trauma such as shoulder dislocation or humeral neck fracture. Neurapraxia of some infraclavicular nerves may occur but nerve rupture is very rare. The important physical role of traction in BP injuries was first described by Flaubert in 1827 [2]. He noticed at autopsy that violent reduction of a shoulder dislocation had resulted in avulsion of nerve roots from the spine. Several cadaver experiments have been reported trying to prove that plexus
Correspondence to: LN.J.E.M. Coene, Department of Ortbopaedic Surgery, Municipal Hospital Leyenburg, Lqweg 275,2545 CHTbe Hague, l%e Netherlands. Phone: (+31)-70-3592ooO; FAX: (+31)-70-3295046.
lesions were caused by forcible widening of the shoulderneck angle, as observed in birth lesions, and by dislocation of the shoulder. Horsley [3] lifted corpses to the ceiling of his laboratory, letting them drop down on the shoulder and head and in his macabre experjment found this assumption to be correct. Delbe and Cauchoix [4] noticed that dislocation of the shoulder could produce an infraclavicular plexus lesion. The effect of stretch on individual nerves has been studied in laboratory experiments by Haftek [5], Lundborg [6] and Sunderland [7] (Fig. 1). The main cause of BP palsies is forceful stretch together with extreme movements. Traction on the arm with the trunk fixed, such as occurs in deliveries in transverse presentation or pull on an outstretched arm during reduction of a dislocated shoulder, in cadaver experiments mainly produces root lesions. When the arm is fixed and traction is on the trunk, such as occurs in a falling person who grabs something, this mechanism remains the same (Fig. 2a and c). In clinical situations movement beyond the physiological limits is encountered under two conditions: forcible widening of the shoulder-neck angle, and forcible widening of the s~pulohumeral angle. The former frequency occurs in motor cyclists who are thrown onto the road (Fig. 2f-h). Forcible depression of the shoulder, for example by a falling tree, has the same effect (Fig. 2b). Since there is no osseous connection between the shoulder girdle and the spine, widening of the shoulder-neck angle is limited by the skin, muscles, fascia, the first rib (because it obstructs the clavicle)
s25 NERVE
NERVE FBRE
traumatic closed injuries, one should bear in mind that nerves tend to be tom between two points of anchorage and that the nerve injury may extend over a considerable distance. only violent trauma can cause nerve rupture. Accompanying lesions like vascular rupture or skeletal fractures yield a clue about the violence of the trauma, the site of the nerve lesion, the mechanism and the prognosis. There may be two levels of injury just as there may be two (or more) mechanisms of trauma.
Mechanisms
Fig. 1. Effect of stretch on a nerve and its nerve fibres, according to Haftek [5]. lhe histological events, occurring in one nerve fibre, are schematically sketched on the right. During progressive stretch, diameters of the axon (a) with myelin sheath (m) and of the epineurium (E) gradually decrease (p = perineurium). The first 2 diagrams represent the first stage, the 3rd diagram the 2nd stage, the 4th diagram represents the moment of epineurial rupture, the 5th diagram the moment of perineurial rupture, and the 6th diagram represents complete rupture of the nerve fibre.
and the neurovascular bundle, which is the weakest structure. Increasing the acromio-mastoid distance beyond physiological limits overstretches the supraclavicular BP structures. Forcible widening of the scapulohumeral angle produces tension on the infraclavicular neurovascular bundle. Shoulder dislocations and humeral fractures are produced by this mechanism (Figs. 3 and 4). In heavy impact BP lesions, constituting another mechanism of trauma, usually the supraclavicular region is directly hit. These lesions are often accompanied by fracture of the clavicle. Finally, plexus lesions may be caused by compression or stretch by fractured or dislocating bones. In clinical situations, these mostly are the fractured clavicle or the (fractured) humeral head or neck. Gradual compression by post-traumatic oedema or fibrosis occurs, but plays a less important role [6]. In analysing the mechanisms of nerve injury in acute
of root lesions
At the level of the vertebral foramen, the anterior and posterior rootlets, originating from the spinal cord, come together in a cone shaped dural envelope. This envelope continues as the epineurium of the spinal nerve. When traction is applied to a spinal nerve, this force is transmitted to the rootlets and the dural cone. The dura may rupture in some instances, while the rootlets, due to their elasticity, still resist the traction. This mechanism is called the peripheral mechanism by Sunderland [8]. A meningocele may be seen on myelography while the rootlets are intact. The second mechanism, called the central mechanism by Sunderland, is caused by forcible inclination of the cervical spine to the opposite side. Due to translation of the spinal cord to the opposite side, tension is applied on the ipsilateral rootlets. In this case roots rupture before the dural cone does. Progressive traction causes rootlets to rupture or to avulse from the spinal cord. The anterior rootlets, being shorter than the posterior ones, rupture first. The weak origin of the rootlets at the spinal cord is not only protected against traction by the cone-shaped dura but also by the so called root ligaments. The epineurium of the spinal nerve is flbrously attached to the related transverse process. The cervical fascia extends from the spine distally as a fibrous sheath around the neurovascular bundle and is another protection against traction. The higher incidence of avulsion of C8 and Tl as compared with CS, C6 and less so C7 is due to the lack of root ligaments in C8 and Tl. At the C5 and C6 levels, rupture of the spinal nerves occurs more frequently while the roots remain intact. C7 occupies an intermediate position [8]. When the plexus is pulled down by depression of the shoulder or inclination of the cervical spine, the rootlets of C5 and C6 in particular change direction while entering the intervertebral canal. The spinal nerves C5 and C6 ride over the transverse process downwards. This Z arrangement adds to the fixation of the roots C5 and C6 [9]. Fracture of the transverse process diminishes the protective function of the root ligaments and can be associated with root avulsion. Forcible downward traction in cadaver experiments may produce avulsion of C5 (infrequently), C6 and, to a lesser
S26
Fig. 2. Trauma
extent, C7, but C8 and Tl remain more or less relaxed [l&13]. On the other hand, forcible upward traction of the plexus in the cadaver produced avulsion of Tl and C8, being unprotected by root ligaments. Single avulsion of C7 may occur due to the short course of this root. Mechanisms In clinical
of supraclavicular practice,
plexus lesions
supraclavicular
plexus
lesions
are
caused by traction on the arm or widening of the shoulderneck angle. The structures of the plexus are stretched between two fixed points, such as on the one hand, attachments of CS and C6 to the transverse process, and on the other hand the point where the upper trunk starts to divide into cords. Another example is the origin of the medial cord and the point where it turns around the coracoid. In cadaver experiments forcible widening of the shoulderneck angle caused almost the same lesion as is produced by forcible downward traction of the arm.
Fig. 3. Relationships between the axillary nerve, the intiaclavicular neurovascular bundle and the humeral head in internal (A and C) and external (B and D) rotation. A and B are frontal, C and D are caudal views. In internal rotation the inferior glenohumeral ligament prevents further abduction. Both axillary nerve and neurovascular bundle are caudal to the humeral head and stretched over it In external rotation, the neurovascular bundle is ventral to the humeral head. Only extension will stretch it in this position. The axillary nerve runs from a ventral subcoracoid position to the dorsal side of the humeral neck and is the only nerve stretched during e.g. dislocation. The glenohumeral ligament does not prevent further abduction. Note that the humerus is in 30% retroflexion to the scapular plane (C and D), and the humeral head projects ca. 50% ventral to the anterior glenoid rim.
Fig. 4. Skeletal injuries. When a person falls sideways on the extended and internally rotated arm, the impact is initially on the hand, forearm and/or elbow. The mass of the torso causes hyperabduction of the glenohumeral joint, and forcible separation of the humems and scapula. The impact is all on one side. and the thorax hits the solid ground. Forced inclination of the scapula is blocked by the ground, and humerus and scapula are subsequently separated with more force. This mechanism nay produce injury to the hand, forearm, elbow, shoulder, scapula and ribs, successively. A dislocation or humeral neck fracture may occur.
S27
Fig. 3.
Fig. 5. Top: fall on the backward
extended elbow (A) or arm (B) produces stretch of the neurovascular
bundle over the humeral head. ‘Ihe humeral neck is
blocked by the acromion/spina scapulae and dislocation, humeral neck fracture, etc., may occur. Bottom: extension in 90’ abduction. The neurovascular is stretched over the humeral head, and excessive widening of the scapulohumeral angle occurs (A and B). (C) Caudal view into the axilla.
, Stretch lesions of the supraclavicular brachial plexus nearly always concern the upper and middle trunk, in contin ity with the lateral and posterior cords. Lower trunk lesi,“bns are very rare, because traction applied to this level results rather in avulsion of roots C8 and Tl. Traction on the abducted arm produces equally divided tension on all roots, trunks and cords. The first structure to rupture is the cervical fascia, followed by the epineurium, and subsequently the epineurial blood vessels around the cords. Further increase of tension produces progressive laceration of the epineurium, the perineurium and rupture of some fascicles at various levels, and finally severance of the three cords. Forcible downward traction results in laceration of the cervical fascia around the upper spinal nerves and subsequently of the epineurium, epineurial blood vessels, perineurium and superior trunk fascicles. Subsequently, the spinal nerve C5 ruptures, followed by C6 and occasionally C7. At this stage C8 remains more or less relaxed, but Tl becomes flattened over the first rib. Further increase of traction force results in definite rupture or avulsion of C7 and laceration of C8 and Thl. The spinal nerves and trunks of the lower plexus bend over the first rib, and the posterior cord, in particular, is crushed between the clavicle and first
bundle
or second rib. This type of injury frequently occurs in motor cyclists who are thrown onto the road. According to Barnes [14] most stress is on the upper roots, when the arm is held in a ventral position along the side of the body. When the arm is behind the trunk, all plexus roots are under extreme tension [3,10-151 (Fig. 2). In traffic accidents, however, traction is not slow but very fast. This produces lesions over \ relatively short distances. Bending over a bony structure, such as the clavicle, transverse process or first rib, facilitates more localized lesioning as well. Nonetheless, at a microscopical level the injury may extend over a considerable distance. One may encounter naked fasciculi without any epineurium but also “empty” epineurial sleeves with complete rupture of the neural content. Factors such as intrafascicular and interplexual crossing-over, and the changing amount of connective tissue throughout the plexus [9] differ greatly in individuals and clarify the wide variety of supraclavicular BP traction injuries. Mechanisms
of infi-aclavicular
The different
pathogenesis
plexus lesions of infraclavicular
injuries
is
s29
due to the close relationship of the neurovascular bundle with the glenohumeral joint and to the proximity of the distal anchorage points of the infraclavicular plexus. This makes these structures susceptible to stretch lesions when skeletal injuries occur in the area (Fig. 3). Experimentally produced traction with the arm along the side produces no significant tension on the infraclavicular plexus. Traction in abduction, however, produces more or less equal tension on all infraclavicular nerves. Additional endorotation of the arm increases tension in the axillary nerve, radial nerve and posterior cord, just as additional exorotation does in the musculocutaneous nerve [ 161. Movements beyond the physiological limits of motion of the glenohumeral joint have been studied by several authors
A final word should be devoted to the suprascapular nerve. This nerve is fixed in the scapular notch. During normal abduction of the arm the scapula moves away from the cervical spine. It rotates and turns around the thorax. The scapular nerve is put under tension by this normal movement. This accounts for the chronic suprascapular nerve lesions encountered in volleyball or tennis players. It is easy to understand that the suprascapular nerve is stretched or ruptured at the notch during abnormal traction or abduction
in cadaver experiments [ 1,4,13,16]. When the 90” abducted arm is extended behind the frontal plane of the body, the infraclavicular plexus is stretched over the humeral head. Also hyperabduction combined with internal rotation of the humerus produces stretch of the infraclavicular plexus over the humeral head. The latter mechanism occurs when one falls on the laterally outstretched arm and the movement of the scapula is blocked by the ground (Fig. 4). In these experiments, the highest tension arises in those nerves which have their distal anchorage points closest to the glenohumeral joint. This means that in a person falling on his outstretched arm or on an arm extended beyond the frontal plane the highest tension occurs in the axillary nerve or posterior cord. Subsequently, tension is to be borne by the musculocutaneous and radial nerves. The ulnar and the median nerves or, in specific anatomical situations, the medial cord are structures which bear less tension during these mechanisms and will rupture last. Nerves to latissimus dorsi, teres major and great pectoral muscles may also be stretched during this type of trauma. These experimental findings indeed fit in fairly accurately with the findings seen at exploration of infraclavicular brachial plexus lesions. It is nearly always the posterior cord or the axillary nerve that has suffered most in infraclavicular cases. According to the severity of the trauma mechanisms, ruptures of the musculocutaneous, the radial and, less frequently, the median and the ulnar nerves, can be seen. The axillary artery, which is relatively fixed by the acromiothoracic trunk, is subject to the same trauma mechanism. Rupture of this artery therefore occurs in 50% of serious infraclavicular plexus lesions.
References
movements of the scapula [ 171. In supraclavicular as well as in infraclavicular cases, an additional suprascapular nerve lesion is encountered frequently.
Coene, L.N. (1985) Axillary nerve lesion and associated injuries. Thesis, Leiden. Flaubert, M. (1827) Memoire sur plusieurs cas de luxation. Rep. Gen. Anat. Physiol. Pathol., 3: 5%9. Horsley, V. (1899) On injuries to peripheral nerves. Pratt., 63: 131-144. Delbet, P. and Cauchoix, A. (1910) Les paralysies darts les luxations de I’epaule. Rev. Chir., 41: 327-352 and 667-687. Haftek, J. (1970) Stretch injury of peripheral nerve, acute effects of stretching on rabbit nerve. J. Bone Joint Surg., 52B: 354-365. Lundborg, G. and Rydevik, B. (1973) Effect of stretching of the tibia1 nerve of the rabbit, a preliminary study of the intraneural circulation and the barrier function of the epineurium. J. Bone Joint Surg., 55B: 390401. Sunderland, S. (1978) Nerves and nerve injuries, 2nd edn. Churchill Livingstone, Edinburgh. Sunderland, S. (1974) Mechanisms of cervical root avulsion. J. Neurosurg., 41: 704-714. Bonnel, F. and Rabischong, P. (1981) Anatomy and systematisation of the brachial plexus in the adult. Anat. Clin., 2: 289-298. 10 Duval, P. and Guillain, G. (1898) Pathog6nie des accidents nerveux consecutifs aux luxations et traumatismes de I’bpaule. Arch. GCn. Med., 2: 143-191. 11 Frykholm, R (1952) The mechanism of cervical radicular lesions resulting from friction or forceful traction. Acta Chir. Stand., 102: 93-98. 12 Stevens, J. (1943) Brachial plexus paralysis. In: Codman, EA. (Ed.), The Shoulder, Thomas Todd, Boston, MA. 13 Gariepy, R., Derome, A. and Lamin, C. (1962) Bra&al plexus paralysis following shoulder dislocation. Can. J. Surg., 5: 418-421. 14 Barnes, R. (1949) Traction injuries of the brachial plexus in adults. J. Bone Joint Surg., 31B: 1: 10-16. 15 fieux, G. (1894) De la pathogenic des paralysies bra&ales chez le nouveau-nb; paralysies obst&ricales. Ann. GynCml. Obst&., 47: 52-64. 16 Milton, G.W. (1954) The circumflex nerve and dislocation of the shoulder. Br. J. Phys. Med., 17: 136-138. 17 Kopell, H.P. and Thompson, W.A.L. (1963) Peripheral entrapment neuropathies, Williams and Wilkins Co., Baltimore, MD.