Síndromes da Traversa Cervico-Torácica

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Recent advance
Thoracic outlet syndromes. The so-called ‘‘neurogenic types’’
Syndromes du défilé cervico-thoraco-brachial. Formes dites « neurologiques »
J. Laulan
Hand Surgery Unit, Department of Orthopedic Surgery, Hôpital Trousseau, University Hospital of Tours, avenue de la République,
37170 Chambray-lès-Tours, France
Received 25 October 2015; received in revised form 22 January 2016; accepted 30 January 2016
Abstract
Neurogenic thoracic outlet syndrome (TOS) is one of the most controversial pain syndromes of the upper limbs. The controversies revolve
around both the diagnosis and treatment of the non-specific or subjective subtypes. Their diagnosis rests on a combination of history, suggestive
symptoms and clinical examination. Proximal pain is primarily muscular in origin, while distal symptoms may be the result of intermittent nerve
compression and/or myofascial pain syndrome. Stringent clinical criteria are required to confirm the diagnosis of subjective TOS. In reality,
multiple factors can be entangled, with TOS being one element within a multifactorial pain disorder; any musculotendinous pathology of the upper
limb and any peripheral nerve entrapment require screening for potential concomitant TOS. Surgery is indicated in most cases of true neurogenic
TOS, whereas rehabilitation is the standard treatment for subjective TOS.
# 2016 SFCM. Published by Elsevier Masson SAS. All rights reserved.
Keywords: Neurogenic thoracic outlet syndrome; Upper limb pain syndrome; Myofascial pain syndrome; Double-crush syndrome
Résumé
Les formes neurologiques de syndrome de la traversée cervico-thoraco-brachiale (STCTB) sont parmi les syndromes douloureux du membre
supérieur les plus controversés, les controverses concernant tant le diagnostic que le traitement des formes subjectives. Le diagnostic repose sur la
combinaison de l’histoire, de symptômes évocateurs et de l’examen clinique. Les douleurs proximales sont avant tout d’origine musculaire alors
que les symptômes distaux peuvent résulter de la compression nerveuse intermittente et/ou d’un syndrome myofascial. Ainsi, il faut exiger des
critères cliniques stricts pour retenir le diagnostic de STCTB subjectif. La chirurgie est indiquée dans la plupart des formes objectives, déficitaires,
alors que le traitement conservateur doit être la règle pour les formes subjectives.
# 2016 SFCM. Publié par Elsevier Masson SAS. Tous droits réservés.
Mots clés : Syndromes de la traversée neurologiques ; Syndrome douloureux du membre supérieur ; Syndrome myofascial ; Compressions nerveuses étagées
Available online at
ScienceDirect
www.sciencedirect.com
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1. Introduction
Neurogenic types constitute about 95% of thoracic outlet
syndrome (TOS) cases as a whole [1–3], but the very existence
of most cases is still controversial [4–7]. Clinical manifesta-
tions are usually limited to poorly defined subjective
E-mail address: j.laulan@chu-tours.fr.
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complaints that are difficult to attribute with certainty to
proximal nerve compression in the thoracic outlet (TO) [4].
A few forms of neurogenic TOS can lead to hand muscle
atrophy [8]. These subtypes of TOS associated with objective
physical findings are very uncommon but are paradigmatic and
help better define what can reasonably be considered as the
subjective form of TOS.
Neurogenic TOS has been incriminated in 5% to 10% of
painful conditions in the upper limb (UL) [7,9]. However, better
knowledge of central sensitization [10] and myofascial pain
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syndromes [11] requires reassessment of some subjective types
of TOS. Myofascial pain syndromes and their potential
interaction with neurogenic TOS may explain some of the
debate [12].
TOS remains extremely controversial with respect to
treatment, and is probably one of the most difficult UL
conditions to manage [13].
2. Different types of thoracic outlet syndrome
TOS refers to clinical manifestations resulting from
compression of the neurovascular bundle at the TO. Clinical
symptoms involving the UL may result from vascular and/or
neurological compression. Two main types can be defined:
vascular and neurogenic TOS. Vascular types are associated
with obvious signs, making diagnosis is straightforward [5].
Arterial subtypes account for 1% to 2% and venous subtypes for
2% to 3% of all TOS cases. Neurogenic TOSs are also to be
divided in 2 subtypes: true or objective, and disputed or
subjective TOS [6].
True neurogenic subtypes are responsible for obvious
clinical or, less conclusively, electrophysiological signs of
nerve compression. Annual incidence of true or objective
neurogenic TOS is estimated at 1 per 1,000,000 [14]. Because
of its rarity, there have been few dedicated publications and
diagnosis is often delayed [8]. The existence of ‘‘objective’’
types is vital, as it provides evidence of actual proximal nerve
compression at the TO. Furthermore, the topography of the
clinical signs and electrodiagnostic data show they are
systematically related to injury of the lower trunk of the
brachial plexus or its medial cord and branches [8,15], thereby
allowing the likely topography of clinical symptoms to be
determined relative to nerve compression at this level (Fig. 1).
Subjective subtypes account for the vast majority of
neurogenic TOS [1]. In these non-specific forms [7] where
clinical examination and electrophysiological findings are
Fig. 1. Drawing of the brachial plexus. The shaded region is the one involved in
true types of TOS. MN: median nerve; UN: ulnar nerve; MBCN: medial
brachial cutaneous nerve; MABCN: medial antebrachial cutaneous nerve.
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normal, two approaches are possible: either reject the diagnosis
and label the condition as ‘‘debatable’’ or ‘‘disputed’’ TOS [4], or
accept that dynamic, intermittent nerve compression can be
responsible for the painful symptomatology [16–18]. However,
recognizing the existence of subjective TOS types does not
justify this label being placed on all unexplained UL symptoms,
as tends to be the case when TOS is a ‘‘diagnosis of exclusion’’.
On the contrary, it is important to explore the possibility of TOS,
especially in a context of distal nerve entrapment syndrome or
painful dysfunction of the UL, to avoid pursuing an unsuitable
therapeutic approach [16–19]. There is no doubt in our mind that
these subjective types of TOS are real conditions; we have shown
that their presence influences outcomes after surgical treatment
of distal nerve compression [20,21].
‘‘Neurovascular’’ types of TOS are also reported in the
literature [9]. This concept can lead to biases, such as
diagnosing TOS in the presence of supposedly neurovascular
symptoms or choosing surgical treatment for a subjective type
on the basis of dynamic vascular compression. In subjective
TOS, vascular symptoms can be present but they are often non-
specific and consistent with autonomic symptoms [6,12,22],
which are also present in myofascial pain syndrome [11]. The
brachial plexus, and in particular its lower trunk, also carries
sympathetic fibers, which can explain the associated vasomotor
disorder [2,14,23]. Furthermore, there is no direct link between
the neurogenic and vasculartypes of TOS; neurological
symptoms and true vascular symptoms are rarely present
simultaneously [1,24,25].
3. Main anatomic features of the thoracic outlet
From the supraclavicular fossa to the axilla, the neurovas-
cular bundle travels through three successive outlets that are
potential sites of compression: the interscalene triangle (and the
fibrous structures of the pleural cupula), the costoclavicular
space, and the subpectoral tunnel (Fig. 2).
Fig. 2. The three main sites implicated in neurovascular compression in the
thoracic outlet. 1: interscalene triangle; 2: costoclavicular space; 3: subpectoral
tunnel.
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Fig. 3. The two main types of fibrous bands and their relationships with nerve
structures. a: fibrous band extending an incomplete cervical rib (type 1 of Roos);
b: costo-costal fibrous band (type 3 of Roos).
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The interscalene outlet has a triangular shape, bounded by
the dorsal edge of the anterior scalene muscle (ASM), the
anterior edge of the middle scalene muscle (MSM), and the
superior face of the first rib, which constitutes its base. It is
crossed by the three trunks of the plexus and the subclavian
artery, while the vein passes anteriorly to the ASM. There are
two other important neurological relationships: the phrenic
nerve, which crosses the anterior aspect of the ASM obliquely,
and the long thoracic nerve, which emerges from the MSM or
its posterior edge.
Before the interscalene triangle, the neurovascular bundle
crosses the pleural cupula, in which three fibrous structures can
cause compression: the transverse costoseptal ligament, taut
from C7 transverse to first rib, the costoseptocostal ligament
(Roos type III fibrous band) and the scalenus minimus muscle
or its fibrous equivalent (Roos types V and VI) [1,26].
Then, the neurovascular bundle crosses the costoclavicular
space. This outlet is bounded anteriorly by the clavicle and the
subclavius muscle in its medial part, and posteriorly by the 1st
rib and the scalene muscles. The nerve trunks and artery go
through its lateral part and the vein through its medial part. At
the back of the clavicle, brachial plexus trunks divide into three
cords. This space may be narrowed by backward and downward
movements of the shoulder or by trauma to the clavicle.
The subpectoral tunnel, or subcoracoid space, is bounded
anteriorly by the pectoralis minor muscle, which inserts
proximally on the coracoid process, posteriorly by the
subscapularis muscle and medially by the 2nd, 3rd and 4th
ribs. At this level, the plexus cords and terminal branches are
close to the axillary artery. This outlet was considered a
potential vascular compression site; however, recent publica-
tions also suggest possible neurological compression [27,28].
4. Etiologic forms
Although the pathophysiology is not always clear [24], three
main causes can be distinguished [7,18].
4.1. Structural abnormalities
Structural abnormalities are often reported, and can be
associated with traumatic or dysfunctional causes. These
developmental variants may involve the osseous, fibrous, and
muscular structures [1,6]. Two-thirds of the abnormalities
found during surgery are fibro-muscular [1].
Numerous variants have been reported for the scalene
muscles. For example, the upper roots can pass right through
the ASM. When a scalenus minimus muscle is present, it can
pass under or between the lower roots or between the lower
trunk and artery to insert on the suprapleural membrane.
Scalene muscle insertions on the first rib are also very variable;
in particular, they can interpenetrate, and even be connected by
a fascicle of muscle fibers (Roos type 4), forming a restraining
strap that can compress the lower trunk of the plexus and the
artery. Whereas surgeons’ interest was previously focused on
the pathogenic role of the ASM, Allieu et al. showed that the
MSM could exert a wedge effect under the lower trunk [29].
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Except for osteofibrous abnormalities, MSM dysplasia, in the
form of a forward extension of the costal insertion, is the main
abnormality we find in cases of true TOS [8].
Cervical ribs are encountered in 0.5% to 1.5% of the
population, and are bilateral in more than 50% of cases [7,23].
Only 5% to 10% of cervical ribs are associated with TOS [2,23].
Incomplete cervical ribs and hypertrophic transverse C7 processes
are usually prolonged by a fibrous band that is stretched under the
neurovascular bundle and is the main compressive structure [8].
Agenesia or hypoplasia of the 1st rib can also be responsible for
neurologic or vascular compression [30,31].
Variations in the fibrous bands were described by Roos and
Poitevin [1,26]. The main fibrous bands are those extending
from an incomplete cervical rib (type 1) or a hypertrophic
transverse process (type 2), crossing from underneath the C8-
T1 roots or the proximal part of the lower trunk (Fig. 3); the
costo-costal band (type 3) is taut in the concavity of the 1st rib,
which restrains the T1 root and increases the risk of nerve
damage during first rib resection.
Whereas structural abnormalities are found in all true
neurogenic types [8], it is necessary to relativize the role of
anatomical factors in subjective TOS. Abnormalities are more
common in patients who develop TOS [1,5], but the majority do
not give rise to symptoms [9,23]. In a cadaver study, Juvonen
et al. found normal anatomy on both sides in only 5 out of 50
cadavers [32]. While anatomic factors can play an inciting role,
subjective types of TOS are essentially related to cervicosca-
pulobrachial muscle imbalance or dysfunction [5].
4.2. Post-traumatic cases
Post-traumatic cases, after single or repeated trauma,
constitute the majority of operated cases in some studies
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Fig. 4. Appearance of intrinsic muscle atrophy in a case of true neurogenic
TOS. Muscle wasting predominates at thenar eminence and there is a claw-hand
deformity.
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[33,34]. The implication of trauma is obvious in cases of bone
damage: either clavicle fracture, leading to hypertrophic non-
union or a malunion, which shrinks the costoclavicular space,
or fracture of the 1st rib [1,34].
On the other hand, post-traumatic TOS without fracture
often raises medical and legal issues. It can develop after
cervicoscapular injury, in particular due to a whiplash
mechanism of injury. Trauma-induced fibrosis and chronic
scalene muscle spasm are implicated in the onset of secondary
TOS [7,33,34]. This mechanism, however, may also be
responsible for myofascial pain syndrome and central
sensitization [11,35].
4.3. Acquired ‘‘dysfunctional’’ causes
Acquired ‘‘dysfunctional’’ causes are by far the most
common and most controversial. This term is preferred to that
of ‘‘postural’’ [7], which is more restrictive and does not cover
the entire pathophysiology. In this group, patients should be
screened for scapulobrachial dysfunction and muscular
imbalance of the cervicoscapular region [5,17,18,34]. Imba-
lance may be the consequence of muscular hypotony or
hypotrophy, with secondary sloping shoulder [36], but can also
result from muscle tension, affecting the scalene muscles in
particular, secondary to occupational or psychological stressors
[37,38].
During the first half of the 20th century, it gradually came to
light that postural disorders could play a determining role, even
without anatomical abnormality [36]. The brachial plexus is
located between two mobilestructures, the cervical spine and
the UL [14], and can be compressed between the scalene
muscles or in the costoclavicular space, or stretched over the
first rib in case of sloping shoulder or 1st rib elevation. TO
muscles are accessory respiratory muscles, capable of
prolonged tonic contraction due to their high percentage of
type 1 muscle fibers (approximately 70%). Furthermore,
patients operated for TOS had a higher percentage of type 1
fibers in their ASM (85%) and after tenotomy the ASM was
enriched in type 2 fibers [39]. Thus, under the influence of
repeated muscle stimulation, adaptive enrichment in type 1
fibers may occur, aggravating the pathogenic effect of the
scalene muscles (direct nerve compression and indirect
compression by 1st rib elevation).
In certain occupations, symptoms suggestive of a cervico-
brachial origin are present in 45% of cases [40]: repetitive
overuse and certain working postures, particularly in occupa-
tions where the arms are used overhead, or with the head and
shoulders in a forward position (hairdressers, switchboard
operators, assembly line workers, keyboard operators, etc.)
[5,17,41]. Entanglement with unfavorable psychosocial factors
is frequent [7,37].
Proximal muscular imbalance is responsible for muscle pain
and intermittent nerve compression in TO [5,13]. It is important
to keep in mind that multiple factors may be entangled. Distal
nerve entrapment symptoms can be triggered by prior proximal
nerve compression, and vice versa [16,17,19,38]: i.e., double-
crush or reversed double-crush syndrome, respectively [42].
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Furthermore, Monsivais et al. showed that distal nerve
compression increased scalene muscle EMG activity [43].
Muscular dysfunction and the resulting repeated nociceptive
inputs of muscular and neurological origin may also lead to
central sensitization and myofascial pain syndrome. The latter
can also induce UL pain and paresthesia of the hand, and may be
associated with TOS [11,12,18]. Moreover, in a context of
chronic pain, clinical experience shows that muscular and
neurological factors are frequently associated and that TOS is
only one element within a multifactorial pain disorder
[12,18,41,44].
5. Clinical assessment and diagnosis
5.1. True types of TOS
In true TOS, symptomatology is dominated by progressive
muscle atrophy, which always begins in the lateral thenar
muscles and lasts a long time [8]. Atrophy may extend,
sometimes years later, to the other intrinsic muscles and induce
claw-hand deformity. Because of its insidious onset, muscle
wasting is often observed at the time of consultation, with the
hand appearing like in Duchenne–Aran disease [29] (Fig. 4).
Bilateral true TOS is rare but possible [8]. In 30 years’
experience, we encountered only one case of objective signs in
an initially subjective type of TOS.
Finally, pain and paresthesia are rarely at the forefront but,
when present, invariably involve the medial aspect of the UL,
ulnar fingers and volar aspect of the thenar eminence.
Sometimes clinical examination finds dysesthesia or hypoes-
thesia in the medial aspect of the forearm.
5.2. Subjective types of TOS
Although the existence of the subjective forms appears
indisputable, most symptoms reported in the literature are
vague and ill defined. Goeckel et al. [45] reported the most
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Fig. 5. Areas of referred pain in myofascial pain syndrome of the anterior
scalene muscle.
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frequent symptoms to be pain at rest (87%), numbness (66%)
and lack of power (55%). It is likely that heterogeneous entities
are grouped together under the label of TOS [25]. In our
opinion, the clinical approach has two essential components:
diagnosis must be based on stringent clinical criteria and
imposes to forget the scalpel!
Symptoms may be present for several years and the patient
may have gradually become disabled. There is sometimes a
trigger event, such as whiplash injury, carrying a backpack, or
prolonged activity with the arms overhead [5]. Mean patient age
is 40 years, but neurogenic TOS can be observed at any age;
females are affected in almost three quarters of cases [3,27].
Criteria that contribute to diagnosis of TOS are positional
exacerbation of symptoms, particularly when the arm is above
shoulder level or when the subject is carrying heavy weights with
the arm hanging down; pain or paresthesia involving the medial
aspect of the UL, two or three ulnar digits and the palmar aspect
of the thenar eminence; and pain or discomfort in the
supraclavicular hollow [13,17,30]. Cervical–scapular–brachial
pain and headache are mainly of muscular origin [5,11,18], and
the presence of paresthesia, or at least pain, in the C8-T1 nerve
root distribution is a prerequisite for diagnosis of TOS. Some
symptoms, such as pain at rest, feelings of heaviness in the UL
with loss of strength, or Raynaud phenomenon, are compatible
with diagnosis of neurogenic TOS [2,45], but lack specificity.
In contrast, other external signs are, in our opinion, not
directly connected to nerve compression in the TO: symptoms
in radial fingers, cervicofacial pain and/or paresthesia. All these
symptoms may result directly from cervicoscapular muscle
problems, although they are labelled by some authors as
‘‘proximal TOS’’. To our knowledge, compression of the upper
roots or trunks of the brachial plexus is rare [31], if it even
exists. Moreover, cutaneous hyperalgesia in the symptomatic
area is likely to implicate central sensitization, isolated or
associated with TOS [10–12].
None of the provocative tests used during physical examina-
tion are specific for diagnosis and all have a high percentage of
false positives [46,47]. They must therefore be interpreted
cautiously, especially in a context of distal nerve entrapment
[47]. Diagnosis is based on a range of clinical arguments, not on
the result of a single clinical test [3,6,13,18]. Two clinical
maneuvers are useful: the Roos test and the upper limb tension
test first described by Elvey and modified by Sanders [1,2].
Because of their lack of specificity [5,25,46], maneuvers that
look for a decrease or elimination of radial pulses serve only to
provide additional information and not to form the diagnosis of
neurogenic TOS [1,2]; they may however be taken into account if
they elicit pain on the symptomatic side [46].
Roos’s Elevated Arm Stress Test (EAST) or the Abduction
External Rotation Test (AERT) is performed by the patient in a
seated position with the shoulders in abduction and 908 external
rotation and the elbows in 908 flexion. The patient is asked to
alternately open and close his or her hands. The test is positive
if it reproduces the usual symptoms within 1 minute (and not
3 minutes, as initially described by Roos) [1,17,24]. With these
restrictions, this is likely the most appropriate maneuver to
establish diagnosis [2].
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For Elvey’s Upper Limb Tension Test (ULTT), as modified
by Sanders, the patient is in a seated position and executes the
maneuvers actively. The test is performed using three
successive maneuvers: in position 1, the shoulders are in 908
abduction, with the elbows in extension; then in position 2, the
wrists are held in active dorsi-flexion; and in position 3, the
head is tilted to the contralateral side. The test is positive if it
elicits pain down the arm, particularly in its medial aspect, and/
or paresthesia in the hand.
Palpation of the supraclavicular region is an essential stage
of the clinical examination. Palpation can perceive fullness or
even a hard mass caused by a cervical rib or prominenttransverse process; the elevated neurovascular bundle may even
be directly accessible to palpation, which sometimes reveals the
thrill of an arterial stenosis or a deep, hardened formation
related to a malignant tumor in the apex of the lung.
Physical examination must differentiate between localized
tenderness on palpation over the brachial plexus itself and
tenderness over the scalene muscles. Morley’s sign is positive if
pressure over the brachial plexus elicits pain radiating in the
medial aspect of the UL [30]. It is common for palpation over
the belly of one of the scalene muscles to evoke clear local pain;
sometimes, pressure can also elicit referred pain and/or
paresthesia in the UL, evidence of myofascial pain syndrome,
which may be isolated or associated with TOS [11,12] (Fig. 5).
Tinel’s sign should be sought after over the brachial plexus,
between the scalene muscles, just posterior to the clavicle.
Physical examination is completed by palpation over the
subpectoral space [27].
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It is common to find a postural disorder, such as lowered
rounded shoulders with an anterior tilt of the scapula and
restricted range of motion of the glenohumeral joint. Forward
head posture and even a lateral tilt towards the symptomatic
side, with painful scalene muscle spasm, are also common
findings [5,12,13,41,48].
Clinical examination must be completed by assessing the
cervical spine and by looking for signs of possible distal nerve
entrapment [5,13]. Clinical tests are often positive for a more
distal disorder, particularly in the medial aspect of the UL [41].
6. Supplementary investigations
The role of additional examinations is very limited in
subjective TOS. They are mainly indicated for vascular and true
neurogenic TOS cases or if surgery is considered. None are
really useful for the diagnosis of painful subjective TOS, but
they make it possible to rule out another diagnosis, and
generally screen for possible associated disorders.
Radiographs may show bony abnormalities, whether a
developmental variant or a traumatic sequela. CT in particular
allows better analysis of abnormal bone structures and can
identify abnormalities in 30% to 60% of cases [17]. But, once
again, structural abnormalities do not always underlie TOS.
MRI has limited benefit. A recent study comparing MRI data
with intraoperative findings showed that MRI had poor
sensitivity and specificity [49]. However, it can objectively
define fibrous bands or deviations of the brachial plexus, and
can be performed in association with postural maneuvers to
help locate a potential compression site [50]. These examina-
tions are essential, of course, if degenerative disease of the
cervical spine or cervicothoracic tumor is suspected. MR
neurography is a promising examination that allows not only
the fibrous bands, but also the neurological lesions themselves
to be visualized [51].
In this ‘‘neurological’’ context, dynamic vascular examina-
tions are of limited use. Postural anomalies of arterial flow
assessed by photoplethysmography at the digital level are present
in more than 60% of asymptomatic subjects [52]. Only complete
abolition of arterial flow indicates pathologic vascular compres-
sion [53]. In all cases, results must be interpreted cautiously
because, although vascular and neurological compressions can
occur together, there is no proven direct link between the two.
Therefore, it is not appropriate to take vascular signs into account
in diagnosing neurogenic TOS [2]. Doppler ultrasound screens
for static and dynamic vascular compression. If the location is
favorable, it may sometimes show nerve deviation or compres-
sion by an abnormal structure. CT- and MR angiography are
indicated only in vascular types of TOS [2].
Electrodiagnostic studies, on the other hand, are essential,
although they show abnormalities only in cases of permanent
nerve compression responsible for true TOS. Typical abnor-
malities comprise sensorimotor involvement for the ulnar nerve
and a sensorimotor dissociation for the median nerve
(preservation of the sensory contingent from C6-C7): reduction
or absence of compound muscle action potential of the ulnar
and median nerves with chronic denervation in the intrinsic
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muscles prevailing in the lateral thenar muscles; and reduction
of ulnar nerve SNAP whereas median nerve SNAP amplitude is
normal. The other abnormality that can be found at an early
stage is reduced amplitude or absence of MABCN SNAP [54].
These abnormalities are indicative of a C8-T1 postganglionic
lesion in the lower trunk of the brachial plexus or its medial
cord [15]. Somatosensory evoked potentials do not seem to
have any obvious interest [55].
Because neurogenic TOS usually results from a dynamic
process, electrodiagnostic testing is normal for proximal
exploration. However, it is useful for establishing differential
diagnosis and especially for screening associated nerve
compression syndromes [16,17,19].
7. Differential diagnosis
7.1. Other acquired causes that should be considered
The following conditions are rare but they must be
considered systematically as differential diagnoses: regional
tumor, hyperostosis, and osteomyelitis. Although Horner’s
syndrome was reported in association with TOS [8], it requires
screening for a tumor origin (Pancoast syndrome). Diagnosis
can be sometimes made by simple palpation of the
supraclavicular hollow. If there is any doubt, further
examinations (CT and/or MRI) will establish the diagnosis.
7.2. Other painful conditions of the upper limb
The diagnosis of cervical radiculopathy or carpal tunnel
syndrome (CTS) is not difficult. The problem is a little more
complex for cubital tunnel syndrome (CuTS) because
symptoms partially overlap. However, in TOS the topography
of paresthesia in the hand is less systematized and the territory
of the MABCN is also involved [25].
In practice, the challenge is not ruling out isolated distal nerve
entrapment, but dealing with the problem of double-crush
syndrome [38]. Between one-third and one-half of subjective
TOS cases are associated with signs of distal nerve entrapment,
and electrophysiological studies are positive in one-quarter of
cases [16,17,19]. Conversely, diagnostic TOS criteria are
positive before surgery in 40% of CTSs and 13% of CuTSs
seen in our department [20,21]. This ‘‘increased susceptibility’’
[42] of nerve fibers complicates the analysis of signs. In isolated
subjective TOS, clinical tests for distal nerve entrapment are
positive in two-thirds of cases, the Phalen test in 25%, and Tinel’s
sign in 8% [16,17]. Conversely, the rate of false positive tests
when looking for TOS was clearly higher in CTS patients [47].
Furthermore, concomitant subjective TOS impacts the surgical
outcome of distal nerve entrapment: persisting symptoms 8 years
after CTS surgery are significantly associated with the presence
of TOS at diagnosis [20]. Also, in this context of subjective TOS,
CuTS surgery is significantly associated with poorer subjective
results and muscular recovery [21].
TOS can also be observed in association with any painful
disorder of the UL, especially if symptoms are long lasting or
occur in an unfavorable psychosocial context [37,44]. Over
The so-called ‘‘neurogenic types’’. Hand Surg Rehab (2016), http://
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Fig. 6. Postural disorder of the shoulder associated with subjective TOS.
J. Laulan / Hand Surgery and Rehabilitation xxx (2016) xxx–xxx 7
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time, patients develop maladaptive muscular compensation,
with secondary dysfunction of thewhole UL. Secondary
cervicoscapular muscular imbalance can induce TOS, which in
return worsens the clinical picture and contributes to the
condition becoming chronic [18,44]. At this stage of chronic
maladaptive pain response, muscular imbalance is often
obvious as are major postural disorders of the shoulder (Fig. 6).
The diagnosis of TOS is above all positive, rather than by a
process of elimination. TOS should be considered in any case of
nerve entrapment and UL pain [16,17,19,38,41].
Myofascial pain syndrome can result from a single trauma or
from repetitive (notably occupational) overuse. It is characte-
rized by a trigger point within a taut muscular band [11]. These
trigger points, when active, can cause deep local somatic pain,
which is often poorly defined and activated by the slightest
muscular activity, but also referred pain with neuropathic
characteristics simulating nerve-related pain. In the absence of
TOS, myofascial pain syndrome of the ASM itself can induce
cervicobrachial pain and referred paresthesia in the hand
(Fig. 5). This fact justifies strict clinical criteria for diagnosing
TOS, as scalenectomy would be an unduly aggressive treatment
for myofascial pain syndrome of the ASM. However,
myofascial pain syndrome is frequently entangled with TOS,
activating other painful disorders or their consequences in a
context of central sensitization [10,11]. Cervicoscapular
muscle pain and myofascial pain syndromes are the main
causes of proximal TOS symptoms [5,6]. Examination of the
scalene and other cervicoscapular muscles often finds a trigger
point, palpation of which reproduces the cervicofacial or
scapular symptoms spontaneously felt by the patient. Myo-
fascial pain syndrome can partly explain the controversy
around what is considered to be neurogenic TOS and the
problems with the treatment results [12].
7.3. Other causes of intrinsic muscle atrophy [56]
When only the lateral thenar muscles are involved, thenar
hypoplasia is a possible diagnosis. Median nerve (MN)
compression is generally considered, either CTS or proximal
MN compression. The diagnosis of TOS must be considered if
EMG shows denervation in the abductor pollicis brevis muscle
without abnormalities in the other muscles innervated by the
MN, while nerve conduction is quite normal.
When atrophy affects the radial aspect of the hand, the
lateral thenar muscles and the 1st dorsal interosseous muscle
Please cite this article in press as: Laulan J. Thoracic outlet syndromes. 
dx.doi.org/10.1016/j.hansur.2016.01.007
(split-hand syndrome), a disease of the anterior horn, and more
particularly amyotrophic lateral sclerosis, must be considered
[57].
When hypothenar and interosseous muscles are involved but
there is no atrophy in the lateral thenar muscles, ulnar nerve
compression must be incriminated, in so far as true TOS always
affects the thenar muscles first [7,8].
When all the intrinsic muscles are involved, besides the
diagnosis of true TOS, concomitant entrapment of the median
and ulnar nerves or multifocal motor neuropathy with
conduction block must be considered.
In the presence of distal muscle atrophy, usually unilateral
and in a young male, Hirayama disease may be suspected. The
muscle atrophy affects the C7-T1 metameres and is described
as ‘‘oblique’’ because it does not involve the brachioradial
muscle (C6).
If the muscle atrophy is bilateral, a medullary origin must be
considered (cervical spondylotic myelopathy, syringomyelia).
In rare cases, it can be due to spinal amyotrophy caused by a
genetic mutation.
8. Treatment
8.1. Therapeutic methods
8.1.1. Physical therapy
Although physical therapy is the most widely used treatment
for subjective TOS [6,7,17,36], there is no scientific proof of
either the optimal method or its true efficacy, although it
appears to relieve symptoms and improve function [58]. The
aim of rehabilitation is mainly to correct muscle imbalances in
the cervicoscapular region [5]. Initially, muscle relaxation and
stretching exercises are performed to alleviate muscle
tightening, followed by postural correction exercises for the
cervical spine and shoulder girdle. In the last stage, an exercise
program is used to strengthen the weak shoulder muscles.
In 1997, Lindgren published the results of a multidisci-
plinary approach: with a mean follow-up of 2 years, the
satisfaction rate was 88% and 73% of patients had resumed
their work [59]. For 20 years, we have been using a
multifactorial approach for treating disabling TOS, as for
other chronic painful UL syndromes, after patient selection in
medical and surgical consultation [44]. To us, this appears to be
the best way to assess and take into account psychosocial and
emotional factors (psychological assessment or even psychia-
tric consultation), work on fitness (correct metabolic factors,
aerobic activities) and educate the patient (learn stretching
exercises, abdominal breathing and postural correction). The
objective is that, upon leaving the rehabilitation center, patients
can resume work in the same or a modified workplace.
8.1.2. Botulinum toxin injection in the ASM
We have only a limited experience with this treatment. Jones
reported particularly interesting results in the early phases, in
association with a stretching program [6]. Some authors use
botulinum toxin to relieve pain in elderly patients or to
postpone surgery [3]. It showed no significant effect over
The so-called ‘‘neurogenic types’’. Hand Surg Rehab (2016), http://
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placebo in terms of pain relief or improvement in disability, but
did significantly improve paresthesia at 6 months’ follow-up
[60].
8.1.3. Surgical treatment
At a first glance, two main surgical techniques can be
considered: transaxillary first rib resection, and transcervical
anterior scalenectomy [1,6,27,29,61]. The choice seems partly
conditioned by the surgeon’s pathophysiological concepts [7].
Some authors also take account of the result of Lidocaine
injections in the ASM [3,61]. More recently, a combined supra-
and infra-clavicular approach, allowing scalenectomy and first
rib resection with satisfactory exposure, was described [9,61].
Supraclavicular scalenotomy was promoted by Adson for
constitutional bone abnormalities, with the goal of widening the
interscalene triangle by transecting the ASM [23]. This
procedure was subsequently used in the absence of bony
abnormality, but ‘‘the enthusiasm was short-lived’’ [25]. It has
now been abandoned as an isolated treatment [7].
Because of the failures of simple scalenotomy, transaxillary
first rib resection was reintroduced in the 1960s, and
popularized by Roos [1]. Theoretically, it is able to control
and deal with all the potential causes of compression in the
interscalene and costoclavicular outlets [7]. It also decreases
tension in the neurovascular bundle by shortening the course.
During this procedure, the surgeon must ensure that no residual
connection remains between the two scaleni, as their proximal
translation could aggravate neurovascular compression due to a
hammock effect [9]. But even this technique can leave residual
compression. Furthermore, severe postoperative neurological
and vascular complications have been reported [62], and the
scope of indications has narrowed in favor of the supraclavi-
cular approach. The axillary approach remains indicated
particularly in vascular forms and for recurrence after
scalenectomy [61].
The rationale behind scalenectomy was that chronic ASM
contraction could induce direct neurovascular compression or
indirect tension secondarily to first rib proximal ascension [39].
However, the technique is not free from complications and is
not always regressive, in particular for the phrenic and long
thoracic nerves. Although rarer, venous vascular injury may
also ensue [61].
Because of insufficient resultswith anterior scalenectomy,
some surgeons perform double scalenectomy (AS and MS
muscles), while others associate first rib resection and
scalenectomy, either through a combined transaxillary and
transcervical approach or a supra- and infra-clavicular
approach through the same cutaneous incision [7,9,27,61].
There is no convincing proof of the superiority of one
technique over another [60]. Sanders and Pearce reported a
comparable success rate no matter which techniquewas used [61].
Furthermore, the success rate gradually decreased over the years,
from 90% to less than two-thirds of patients after 10 years [61].
In recent years, with renewed attention on the subpectoral
outlet, pectoralis minor tenotomy was also performed as an
isolated treatment or in combination with first rib resection and
double scalenectomy [27,28].
Please cite this article in press as: Laulan J. Thoracic outlet syndromes. 
dx.doi.org/10.1016/j.hansur.2016.01.007
8.2. Surgery indications
In recent cases of true neurogenic TOS, if muscle atrophy
appeared after unusual activity, rehabilitation while abstaining
from the activity allowed symptoms to regress [8]. In long-
standing painless cases, with stable atrophy present for many
years, surgery is not indicated. Otherwise it is systematic. At
present, we use the supraclavicular approach, because of the
constant presence of anatomical abnormalities, which are
always accessible by this route [8]. The result is essentially tied
to the duration of palsy. But even at advanced stages, despite
poor muscle recovery, surgery provides functional benefits in
most cases [8,12].
Surgery can be also indicated after failure of conservative
management when symptoms are limited to the territory of the
lower trunk with associated electrophysiological abnormalities
and predisposing anatomic factors.
For subjective TOS, surgery is usually considered in selected
patients after failure of conservative treatment, although there is
no scientific proof of the superiority of surgical treatment over
conservative management or even not performing treatment at
all [60]. Initially, good postoperative results range from 70% to
90%, but few patients (20% to 60%) are actually cured and
deterioration or even recurrence is common [45,61,63].
Furthermore, other dysfunctional disorders can appear secon-
darily [64].
We have operated on more than 100 patients for subjective
TOS. But given the absence of predictive criteria for success
and the deterioration of results over the years and onset of other
painful dysfunctional disorders, and given the favorable results
obtained with a comprehensive multidisciplinary approach in a
rehabilitation center, we hardly have any indications for surgery
anymore [18].
9. Conclusions
Diagnosis of true neurogenic TOS with intrinsic muscle
atrophy is generally obvious. Surgical treatment is usually
indicated. It leads to functional gains even in long-standing and
severe cases, if the palsy is incomplete [8,12].
Diagnosis of the subjective types of TOS is made clinically,
based on clinical history and physical examination [5,13]. Strict
criteria define clinical signs, which can reasonably be taken to
indicate TOS, and eliminate other causes of UL pain that often
occur simultaneously. In our opinion, subjective TOS is above
all of dysfunctional origin. The importance of psychosocial
factors in the chronic nature of the disorder and their
predominance over anatomical factors make surgical indica-
tions rare [18].
In cases of musculotendinous pathology of the UL and
peripheral nerve entrapment, concomitant TOS should be
considered and taken into account when informing and treating
the patient. In more or less diffuse chronic painful UL disorders,
TOS is often entangled with central sensitization and
myofascial pain syndrome of the cervicoscapular muscles. A
multidisciplinary approach to these entangled forms is essential
[12,18,44,59].
The so-called ‘‘neurogenic types’’. Hand Surg Rehab (2016), http://
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Given the multiplicity of surgical techniques, highly variable
results, deterioration over time and the risk of severe
complications, surgery should be considered only with the
greatest reserve. The best means of improving clinical
outcomes and avoiding complications is to limit surgery to
the rare cases in which it is actually justified [25].
Disclosure of interest
The author declare that they have no competing interest.
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	Thoracic outlet syndromes. The so-called “neurogenic types”
	1 Introduction
	2 Different types of thoracic outlet syndrome
	3 Main anatomic features of the thoracic outlet
	4 Etiologic forms
	4.1 Structural abnormalities
	4.2 Post-traumatic cases
	4.3 Acquired “dysfunctional” causes
	5 Clinical assessment and diagnosis
	5.1 True types of TOS
	5.2 Subjective types of TOS
	6 Supplementary investigations
	7 Differential diagnosis
	7.1 Other acquired causes that should be considered
	7.2 Other painful conditions of the upper limb
	7.3 Other causes of intrinsic muscle atrophy [56]
	8 Treatment
	8.1 Therapeutic methods
	8.1.1 Physical therapy
	8.1.2 Botulinum toxin injection in the ASM
	8.1.3 Surgical treatment
	8.2 Surgery indications
	9 Conclusions
	Disclosure of interest
	References