Acta Neurochir (2005) [Suppl] 92: 33–34 6 Springer-Verlag 2005
Printed in Austria
Suprascapular nerve entrapment
L. Coro`, A. Azuelos, and A. Alexandre
EU.N.I. European Neurosurgical Institute, Treviso, Italy
Summary
It is important to be aware of neuropathy involving the supra- scapular nerve. While direct trauma to the suprascapular nerve is the usual cause (direct blow to the base of the neck or posterior shoulder, shoulder dislocation or fracture), the problem may result from over- use injuries (such as repetitive tennis serving or spiking of a volley ball), excessive horizontal adduction, weight lifting, backpacking or no apparent reason.
These last three years we have operated 8 cases of suprascapular nerve neurolysis at the level of suprascapular incision, and section of the transverse scapular ligament through the back supraspinal approach.
Keywords: Suprascapular nerve; neuropathy; neurolysis; supra- scapular notch.
Anatomy
The suprascapular nerve (SS) is a motor nerve orig- inating from C5 and C6 nerve roots. It is the only lat- eral branch of the lateral upper trunk of the brachial plexus. It passes through the suprascapular notch which is covered by the transverse scapular ligament into the supraspinous fossa where it supplies the su- praspinatus muscle.
The nerve continues around the lateral border of the spine of the scapula to supply also the infraspinatus.
Depending upon where the compression occurs (su- prascapular notch or spinoglenoid notch) either both or individual muscles may be involved.
It is noteworthy (see below) that after it leaves the suprascapular notch, it also passes the subacromial bursa and gives o¤ sensory fibers to the capsular and ligamentous structures of the shoulder and acromio- clavicular joint [6].
This area is moving continuously due to the scapular outing at every change of arm position. Therefore the SS nerve is subject to friction and thence to inflamma-
tory reaction with oedema and nerve compression just on the most critical point of its way (suprascapular notch) [2].
Clinic
The patient may present with only vague posterior or posterolateral shoulder pain or di¤use pain with weakness.
Inspection of the shoulder may show atrophy of either or both the infraspinatus and supraspinatus muscle. Atrophy of the infraspinatus is easier to detect because the supraspinatus is covered by the trapezius muscle.
Diagnosis can usually be confirmed by EMG and nerve conduction studies or by magnetic resonance imaging (MRI) [7].
The conservative treatment of the suprascapular injury is directed at rehabilitation (strengthening and flexibility) of the supraspinatus, infraspinatus, and scapular rotators. At times, surgical decompression may be necessary.
Physiopathology
There are numerous clinical and experimental studies [3, 5] showing the way the initial oedema gives rise to the following succession of events: slackening of blood circulation, increase of extra/intra fasciculate pressure following further progression of the oedema and the supervening ischemia, the activation of fibro- blasts epi/peri neural fibrosis and consequently a fur- ther increase of the oedema that augments the phe- nomenon just described.
Olsson [6] studied the anatomical details of nerve structure which may be the base for fibrotisation pro-
cesses. Epineurium is similar to other connective tissue rich parts in the body, and its extracellular fluid is free to di¤use [9]. The walls of the endoneurium are entirely covered by a basal lamina which surrounds the outer plasma membrane surface of the Schwann cells, the endoneurial vessels and the perineurial cells apparently forming a stabilizing structure.
Endoneurial fluid circulation depends on two major forces, net hydrostatic pressure and net osmotic pres- sure. The lack of lymphatics in nerve fascicles might render the removal of endoneurial fluid di‰cult. Peri- neurium creates a fluid environment around the nerve fibres of optimal composition for transmission of elec- trical impulses [1].
Early and late oedema of the vasogenic type is as- sociated with elevated endoneurial fluid pressure and microcirculatory disturbances. Proliferation of fibro- blasts, changes in the composition of the matrix and collagen formation may result in endoneurial fibrosis at the site of the lesion and distal to it.
Nerve damage due to an injury may be further ag- gravated by oedema increasing endoneurial pressure which might compromise blood flow in the fascicles.
All segmentary compressions in nerves are accom- panied by a component of ischemia.
In front of a progressive or repetitive deforming force, the nerve becomes mechanically ‘‘ribbon like’’
[8].
The increase of the intraneural pressure causes a ve- nous slow down with oedema of the a¤ected segment, adding a greater deforming pressure [4]. So the area a¤ected by oedema is invaded by fibroblasts that will produce a greater epineural and perineural fibrosis.
Case summary
These last three years we have operated 8 cases of SS neurolysis at the level of suprascapular incision and section of the transverse scapular ligament through the back supraspinal approach (4 patients were treated positively by conservative methods).
All patients were involved in professional and sport activities [10] which caused strong pressures on
the shoulder articulation: 2 road workers, 3 volleyball players, 2 rugby players, 1 climber.
From the clinical point of view there was a pain in- sisting in all cases in the shoulder region which was greatly augmented by some particular movements and the atrophy of the super/under spinal muscles combined with a partial deficiency of the abduction/
rotation of the shoulder.
EMG (before and after – about 4/6 months later – the surgical treatment) and RMI (before) studies have been applied to all patients.
Results
In 6 patients clinical symptoms were recovered (both pain and motion: M3! M4); one patient reached partial recovery only (M2! M3) while only one patient had no improvement at all (M2¼ M2).
References
1. Dahlin LB, Rydevik B, McLean WG (1984) Changes in fast axonal transport during experimental nerve compression at low pressures. Exp Neurol 84: 29–36
2. Kharrazian D (2000) The role of the transverse ligament in suprascapular nerve entrapments. Proceedings of the Annual Meeting of the ICAK-USA, vol 1. Palm Springs, CA, -01 3. Lopez Alonso A, Palazzi S (1990) Experimental study on com-
pressive neuropathies, personal communication 4. Millesi H (1997) Personal communication
5. Mumenthaler M, Schliack H (1974) La¨sionen Peripherer Nerven – Diagnostik und Therapie. Springer, Wien New York 6. Olsson Y (1990) Microenvironment of the peripheral nervous
system. Gut Rev Neurobiol 5: 265–311
7. Post M, Mayer J (1987) Suprascapular nerve entrapment, diag- nosis and treatment. Clin Orthop 223: 419–422
8. Ramon Y, Cajal S (1917) Degeneracion y regeneracion experi- mental de los nervios perifericos. Trab Lab Invest Biol XV: 301–
358
9. Rydevik B, Lundborg G (1977) Permeability of intraneural mi- crovessels and perineurium following acute, graded experimen- tal nerve compression. Scand J Plast Reconstr Surg 11: 179–187 10. Wang DH, Koehler SM (2000) Isolated infraspinatus atrophy in a collegiate volleyball player. Proceedings of the Annual Meet- ing of the ICAK-USA, vol 1. Palm Springs, CA, -01
11. Weiss P (1943) Endoneural edema in constricted nerves. Anat Rec 84: 491–522
Correspondence: Alberto Alexandre M.D., EU.N.I. European Neurosurgical Institute, Via Ghirada 2, 31100 Treviso, Italy. e-mail:
alexandre@eunionline.com
34 L. Coro` et al.: Suprascapular nerve entrapment
