 |
|
Volume
12 Spring 1999
Pages 40-44 |
|
|
From the
Department of Orthopaedic Surgery, University of Pennsylvania School of
Medicine, Philadelphia, PA. Address correspondence
to: Ernest J. Gentchos, M.D., F.A.C.S., Department of Orthopaedic Surgery,
3400 Spruce Street, Philadelphia, PA 19104.
Shoulder
pain, weakness, and instability are common findings of nerve entrapment
and traumatic and inflammatory lesions of the brachial plexus. These disorders
can be properly diagnosed with careful clinical examination and electrophysiologic
testing. An understanding of the kinesiology of muscles acting on the
scapula aids in the diagnosis of patients presenting with muscle atrophy
and scapular winging. This article reviews the kinesiology of the muscles
acting on the scapula, the clinical manifestation of isolated peripheral
nerve lesions of the brachial plexus, and the indications for clinical
observation and rehabilitation as well as for surgical treatment of established
lesions.
As a multiarticulated
joint system, the upper extremity is a delivery system to position the
hand in space for its prehensile function (grasp, pinch, and hook) and
as a tactile organ. To fulfill its function, this system requires both
a stable and mobile base. The scapula is superbly positioned phylogenetically
to serve this purpose. It is positioned dorsally and rotated laterally
35 to 40 degrees from the frontal plane to accommodate the upright position
of the bipedal primate [17]. The glenohumeral
joint behaves as a ball-and-socket joint. Although there are differences
in size between the glenoid (average 25 mm in diameter) and the humeral
head (average 48 mm in diameter), as a unit, they form a functional congruous
joint. The radii of curvature of the cartilaginous surfaces approach 99%
[33] and the center of rotation is functionally fixed to minimize
translation of the humeral head [33]. The resultant forces are
compressive rather than shearing in nature. These forces are dissipated
in a ball-and-socket joint, like that of a hip [33]. Only imbalance
created either by loss of the rotator cuff muscles (which act to dynamically
compress and rotate the humeral head) or the scapular stabilizer muscles
(which serve to dynamically position and stabilize the glenoid) can disrupt
this fine, elegant balance of the scapular humeral rhythm [17,33].
As a result, shearing forces, which are so destructive to joint function,
are minimized [33]. The nomenclature
of scapular motion about the thorax is described as elevation, depression,
adduction (retraction), abduction (protraction), medial rotation of the
inferior angle of the scapula, lateral rotation of the inferior angle
of the scapula, and anterior and posterior tilting [11,17]. Upward
rotation of the scapula is most important for arm elevation. The upward
rotator muscles of the scapula are the trapezius and the serratus anterior
muscles. However, Inman et al. [17] have also included the levator
scapula. Maximum scapular rotations can only occur when the trapezius
and the serratus anterior muscles function normally. To understand
the effects of peripheral nerve injuries of the brachial plexus on shoulder
girdle function, it is crucial to realize that muscles do not act independently.
Each muscle is a component of a muscle force couple that executes normal
shoulder motion [17]. This concept is reinforced and painfully
realized when a single muscle transfer is attempted to compensate for
a loss of multiple muscle units or when there is diffuse brachial plexus
injury. Isolated
peripheral nerve injuries of the brachial plexus present as common clinical
manifestations: pain, weakness, and instability. These complaints are
common to all dysfunctions of the shoulder girdle and may be misdiagnosed
and mistreated as disorders of the glenohumeral joint [30]. A
detailed history and physical examination is imperative. Although a thorough
clinical neurologic examination may have been performed, the true diagnoses
can easily be missed. For example, the differential diagnosis of shoulder
pain with atrophy of the supraspinatus and infraspinatus muscles may be
due to either a compressive lesion secondary to a suprascapular nerve
ganglion or to a chronic rotator cuff tear [14]. In addition,
as part of the differential diagnosis, it must also be realized that these
two lesions may also coexist [29]. The true diagnosis can only
be ascertained by electrodiagnostic testing and shoulder magnetic resonance
imaging. Unfortunately, delay and misdiagnosis is the norm in identifying
peripheral nerve lesions of the shoulder. An understanding of the dynamic
causes of winging of the scapulae in conjunction with timely electrophysiologic
studies will direct physicians, in many instances, to the true nature
of the illness. The long
thoracic nerve of Bell is derived from ventral rami C5, C6, and C7. Its
course runs downward and passes either in front of or behind the middle
scalene muscle. Then, it reaches the upper slip of the serratus anterior
muscle and descends along its anterior surface. The mechanisms
of injury to this nerve may be as a result of viral illnesses, repetitive
trauma or stretching, general anesthesia, or surgical procedures [10,20,33].
The clinical result of this injury is winging of the scapulae without
any muscular atrophy in the shoulder girdle. Most patients will have a
great deal of disability due to this nerve injury. Functional loss will
include the inability to lift and pull heavy objects, to play sports such
as tennis or golf, and to perform tasks involving reaching above the shoulder
level. This functional impairment results from the limited upward rotation
of the scapulae and anterolateral positioning around the chest wall. These
movements are essential to perform functions that demand elongation of
the arm, such as pushing or pulling. With the loss of these three scapulae
functions (i.e., fixation to the chest wall, rotation, and protraction),
the upper limb will appear to hang from the scapulae, accentuating pain
and cosmetic deformity. In the absence
of a normal muscle force coupling with the trapezius, the scapula will
medially rotate, wing-out, and its spine will be elevated [11,16--18].
The deformity will be accentuated on forward elevation, because the trapezius
alone will function as the sole rotator. With complete paralysis, there
is marked weakness and inability to elevate the arm above 130 degrees. In the majority
of cases of closed injuries, recovery will be spontaneous although function
may not return for up to a year. If there is no clinical or electrophysiologic
evidence of recovery within 6 months to a year, surgery should be considered.
However, exploration of the nerve in closed injuries is almost never warranted. In 1979,
Gregg et al. [11] reported winging of the scapula in a series
of 10 young patients with traction injury to the long thoracic nerve of
Bell. The average recovery time was 9 months and functional recovery was
good. Foo and Swann [9] reported on 20 patients with winging of
the scapula. The majority of the subjects experienced spontaneous onset
of pain followed by deformity and associated loss of function. History
of trauma was elicited in only three patients. Their functional recovery
occurred within 2 years without any specific treatment. However, patients
in both series displayed a mild degree of residual weakness [11]. Iannotti
et al. [15] reported on 15 patients with injuries to the long
thoracic nerve of Bell. Nine patients underwent reconstructive procedures
utilizing a pectoralis major muscle transfer with a fascia lata tubular
graft attached to the inferior border of the scapula. These patients were
reported to have good results [9,16,18,21,29]. Iceton and Harris
[16] reported on 15 patients with winged scapulae who were followed
for 1--16 years after surgical treatment with pectoralis major muscle
transfers. The results were good in nine patients, fair in two, and poor
in four. These four patients were reoperated on for avulsed fascia lata
(one patient) and for scarring of the fascia lata graft (three patients).
Furthermore, in this group, two patients had other muscle paralysis. No
cause could be ascertained in the other two patients. In 1995,
Post [29] reported on eight patients with 1--5-year follow-up
after pectoralis major transfer for winging of the scapula. The results
for these patients were excellent. They returned to work with full, pain-free,
motion, but did experience slight weakness on elevation of the arm. However,
it is of interest to note that in this small series, three patients were
previously misdiagnosed and had four prior operations including cervical
spine fusion, teres minor release for quadrilateral space syndrome, first
rib resection, and an acromioplasty with lateral clavicle resection. The spinal
accessory nerve is a cranial nerve whose spinal portion is derived from
four to five rootlets of the medulla oblongata and motor cells in the
anterior gray column as low as the fifth cervical segment. The spinal
portion of the nerve enters the foramen magnum and exits the jugular foramen
where it travels beneath the sternomastoid muscle. This nerve proceeds
superficially over the levator scapula muscle, innervating this muscle
in the posterior triangle of the neck. It remains quite superficial and
innervates the trapezius muscle [2,35]. Injury to
the spinal accessory nerve (cranial nerve XI) is commonly due to a stab
wound, surgery in the posterior triangle of the neck such as a lymph node
biopsy, blunt trauma to the top of the shoulder, or to prolonged pressure
on the shoulder [31,35]. The patient presents with pain and is
often misdiagnosed as having a rotator cuff injury. With delay in diagnosis,
secondary signs will appear such as drooping of the shoulder, asymmetry
of the neckline, and winging of the scapulae. This type of scapula winging
is not as prominent as that seen with long thoracic nerve injuries. Scapulae
winging is accentuated with abduction, especially with elevation beyond
90 degrees [2]. This type
of scapulae winging will reflect the loss of muscle force coupling with
the serratus anterior [11,17]. Paralysis of the upper portion
of the trapezius will cause the loss of the ability to shrug and suspend
the scapula as well as rotation upward. Loss of the middle portion will
cause weakness of medial adduction and rotation of the inferior angle
of the scapula. Loss of the lower segment will result in an inability
to maintain the scapula to the chest wall and will also compromise rotation.
As a result, the scapula is depressed, droops, and is laterally rotated,
but winging is minimal. The functional deficit is weakness in the forward
elevation and abduction of the shoulder. The drooping of the shoulder
may cause brachial plexus nerve irritation, subacromial impingement, and
may result in a thoracic outlet syndrome. The disability
and disfigurement from an accessory nerve injury are not as debilitating
when the nerve is severed at its high proximal location such as during
a lymph node resection, as when the incision is placed distally along
the lateral border of the sternocleidomastoid muscle. Some suspensory
trapezius function from accessory nerve branches proximal to the injury
site may be preserved. Because the
diagnosis of accessory nerve injury is difficult and often missed, electrophysiologic
testing is essential [2]. Non-operative treatment is advised in
closed injuries. With open injuries, however, exploration, neurolysis,
and grafting may be required [31]. Ogino et al. [27] reported
on a series of 10 patients with accessory nerve injury: three had transection
treated by primary end-to-end repair and five had segmental loss that
required cable nerve grafting. The elapsed time period from injury to
repair was longer than 6 months in five of the patients. Delay in diagnosis
of accessory nerve injury as a common problem was reported by Hudson [13]
in 60 patients who presented with pain and shoulder dysfunction after
posterior cervical lymph node biopsy. The average delay in diagnosis was
14 months. Reconstructive surgical treatment should be offered to patients
who suffer from pain and disfigurement secondary to brachial plexus traction,
subacromial impingement, and thoracic outlet syndrome. Bigliani
et al. [2] reported on treatment of 18 patients with trapezius
paralysis, nine of which were misdiagnosed. One patient was treated successfully
surgically and 10 underwent the Eden-Lange surgical procedure. The seven
patients followed for 10 years had the following results: five had excellent
results, one had a good result, and one had an unsatisfactory result.
All patients had the deformity corrected with good function and six patients
had their pain relieved. In a recent
retrospective article on seven patients with accessory nerve injuries,
Nakamichi and Tachibana [24] reported on six patients who sustained
lacerations of the spinal accessory nerve following cervical node biopsy,
which were subsequently treated by primary repair. Four patients fully
recovered and two had residual stiffness of the shoulder. The seventh
patient's mechanism of injury was a gunshot wound. He was treated with
neurolysis and sustained some residual stiffness of the shoulder. The origin
of the dorsal scapular nerve is the fifth cervical nerve root. This nerve
is found just proximal to the upper trunk of the brachial plexus. After
piercing the scalenus medius muscle, it passes posteriorly beneath the
levator scapula, which it innervates, and begins its descent to innervate
the rhomboid major and minor muscles. Injury to
the dorsal scapular nerve is rare. In the differential diagnosis of medial
scapulae border pain, one must consider not only C5 root cervical radiculopathy,
but also dorsal scapular nerve injury. Examination of the back will demonstrate
atrophy of the rhomboid major and minor muscles. Scapulae winging will
be minimal at rest and may appear like winging associated with paralysis
of the trapezius on static examination. With dynamic testing, the scapulae
will translate laterally with minimal inferior angle rotation. Winging
is more noticeable when the arm is lowered from the forward elevated position.
Weakness and atrophy can further be noticed when patients place their
hands on their hips and attempt to push backward against resistance. Treatment
should only be considered when patients suffer from chronic debilitating
pain. Then, the Dickson fascial sling operation can be performed [6]. The suprascapular
nerve is derived from the upper trunk of the brachial plexus and receives
its fibers from C5 and C6 [1]. It contains both the sensory and
motor components, but does not innervate skin. Sensory branches innervate
the glenohumeral and acromioclavicular joint [1]. This nerve courses
downward and laterally, deep to the omohyoid and trapezius muscles, as
it runs posteriorly beneath the trapezius. It reaches the suprascapular
notch along with the suprascapular artery and vein. The artery is located
above the transverse scapular ligament, the nerve beneath it. The suprascapular
nerve may be entrapped at the suprascapular notch as it enters beneath
the transverse scapular ligament. At this site, entrapment can be caused
by a ganglionic cyst, the transverse scapular ligament, or by repetitive
use of the upper extremity. Entrapment at this site will cause painful
paralysis of the supraspinatus and infraspinatus muscles because the sensory
branches to the posterior capsule of the glenohumeral joint arise at this
site. The other site of entrapment is at the spinoglenoid notch, where
the infraspinatus muscle may be singularly paralyzed. Entrapment of the
spinalglenoid site can be due to ganglionic cysts [14] or by the
spinoglenoid ligament. Cummins et al. [5] found that the spinoglenoid
ligament occurred in 80% of their dissections of 112 shoulders in 76 cadavers. Pain and
weakness in external rotation and abduction of the glenohumeral joint
accompanied by atrophy of the supraspinatus and infraspinatus muscles
may misdirect one to the incorrect diagnosis of a complete rotator cuff
tear [9,14]. Electrophysiologic testing will affirm the diagnosis
as well as define the site of entrapment. MRI should be performed for
further anatomic evaluation. When a mass lesion is identified, surgery
should be performed within 6 months. The axillary
and radial nerves originate from the posterior cord of the brachial plexus
arising from the C5 and C6 nerve roots. The axillary nerve can be found
immediately posterior to the coracoid process and conjoint tendon where
it runs along the anterior surface of the subscapularis muscle and courses
along the inferior border of the shoulder capsule. It enters the quadrilateral
space with the posterior humeral circumflex artery. The axillary nerve
then passes around the cervical neck of the humerus in a spiral fashion.
It innervates the teres minor and then divides into anterior and posterior
branches to innervate the posterior, middle, and anterior deltoid muscle.
In addition, it provides sensation to the glenohumeral joint and the skin
overlying the deltoid muscle. Injury to
the axillary nerve can occur close to the inferior capsule of the glenohumeral
joint, where it is susceptible to direct trauma secondary to glenohumeral
dislocation, laceration during surgery, as well as to direct compression
such as during the misuse of crutches [1,25]. Entrapment of this
nerve can also occur at the quadrilateral space [4,10,28]. Injuries
to the axillary nerve at the quadrilateral space can occur as a result
of stretching or crushing. Although compression of the posterior humeral
circumflex artery has been implicated by Cahill and Palmar [4],
this remains to be proven. This diagnosis is usually made on clinical
grounds. Originally, they described this syndrome in a subset of patients
whose symptoms were originally attributed to thoracic outlet syndrome.
These patients described poorly localized shoulder pain, paresthesias
in a nondermatomal distribution, point tenderness in the quadrilateral
space, and had an arteriogram demonstrating compression of the posterior
circumflex humeral artery when the shoulder was abducted. The axillary
nerve palsy causing dysfunction of the deltoid muscle is a catastrophic
event to the shoulder girdle. Forward elevation can be limited to 33 degrees
(range of 0 to 75 degrees). With this degree of loss of motion, attempts
at elevation and abduction will result in superior subluxation of the
humeral head. The patient, however, may use "trick movements" to achieve
full elevation of the arm by rotating the scapula, contracting the rotator
cuff, long head of the biceps, and clavicular portion of the pectoralis
major muscle [34]. There is no good surgical treatment to compensate
for the loss of function of the deltoid muscle. Treatment of axillary
nerve injuries either by closed nerve graft or neurolysis has been encouraging
[3,4,10,28]. Cahill and
Palmar [4] reported on 18 patients with axillary nerve entrapment,
16 of whom underwent operative decompression of the nerve at the quadrilateral
space. Eight patients improved dramatically, eight patients improved markedly,
and two patients showed no improvement (an 89% improvement). Francel et
al. [10] presented a series of five patients with axillary nerve
entrapment at the quadrilateral space treated by operative decompression.
All patients resolved their sensory deficit and showed some improvement
in active motion of the shoulder. In three patients, however, functional
return was minimal. Petrucci et al. [28] reported on 21 cases
of axillary nerve injuries treated by nerve grafting and neurolysis. Fifteen
patients with transection of the axillary nerve required sural nerve grafting
and six patients were treated with neurolysis alone. These patients were
operated on within 6 months. The most frequent site of injury was the
quadrilateral space. Of the 12 patients examined 1 year or more after
surgery, 5 recovered normal function, 6 showed good recovery, and 1 displayed
fair return of shoulder abduction due to axillary nerve function. The clinical
evaluation of shoulder pain is often complicated by the wide array of
possible differential diagnoses. The overlapping symptoms of multiple
possible conditions make diagnosing injuries to the peripheral nerves
of the brachial plexus challenging. Electrophysiologic testing is indispensable
in the diagnosis of these conditions. As a result, predictable surgical
results can only be ascertained by the accuracy of the diagnosis.
Pages 40-44
Abstract: