Brachial plexus injury, etiology, pathogenesis, terminology, anatomy, cutaneous innervation of the arm and forearm, anatomical and pathological basis, symptoms and signs, neuralgic amyotrophy, neoplasm and radiotherapy, thoracic outlet syndromes, hyperabduction syndrome, costoclavicular syndrome, management

1. BRACHIAL PLEXUS INJURY
AND COSTOCLAVICULAR
SYNDROME
DR BHAVIN MANDOWARA

2. ANATOMY OF BRACHIAL PLEXUS

4. ANATOMY AND PATHOLOGIC BASIS
 The plexus can be divided into regions that include (from proximal
to distal) trunks, divisions, cords, branches, and nerves. Trunks and
divisions are further subdivided with a nomenclature based on
overall relationships with other upper extremity anatomic structures
and include upper, lower, and middle trunks, and posterior and
anterior cords.
 The pathologic basis and histologic changes seen with brachial
plexus lesions vary with the underlying cause, which include
compression, transection, ischemia, inflammation, metabolic
abnormalities, neoplasia, and radiation therapy.

5. SYMPTOMS AND SIGNS
 The onset of symptoms from brachial plexopathies may vary from acute to
insidious. Acute onset is usually characterized by pain in the shoulder or
upper arm, while insidious onset can manifest as progressive pain, evolving
numbness, weakness of selected muscles, or any combination. Acute onset,
in the absence of trauma, favors a metabolic or inflammatory process
 Chronic progression of symptoms in patients with a history of cancer and
radiation treatment suggests either as a cause. Clinical signs include muscle
weakness, atrophy, and sensory loss
 The primary pathologic lesion in most plexopathies is axonal loss, with
demyelination and conduction block as secondary processes

6. ETIOLOGY
 Traumatic injuries are the most common cause of brachial plexus
lesions in children and adults. Motor vehicle accidents, industrial
accidents, falls, objects falling on a shoulder, and sports injuries are
among the many causes of closed brachial plexus trauma
 Open traumatic brachial plexus injuries result from gunshot wounds,
lacerations, and animal bites. Open injuries are frequently associated
with secondary injury from expanding hematomas,
pseudoaneurysms, and arteriovenous fistulas
 Nontraumatic brachial plexopathies include neuralgic amyotrophy,
hereditary brachial plexopathy, neoplastic and radiation induced
plexopathy, thoracic outlet syndrome, and brachial plexopathy
related to diabetes

7. NEURALGIC AMYOTROPHY
Neuralgic amyotrophy is characterized clinically by the
onset of severe pain followed by patchy weakness in the
distribution of the upper and/or middle brachial plexus,
usually involving winging of the scapula. The time to onset
of weakness is highly variable. Sensory symptoms occur in
a majority of patients, most commonly manifesting as
hypesthesia and/or paresthesia, and usually involving the
lateral shoulder and arm and/or the hand

8. Hereditary brachial plexopathy
 Hereditary brachial plexopathy is a rare autosomal dominant
disorder characterized by recurrent, painful brachial
plexopathies. In some families the cause has been identified as
mutations in the SEPT9 gene

9. NEOPLASM AND RADIOTHERAPY
 Breast and lung cancers are the most frequent neoplasms leading
to brachial plexopathy. Pain in the shoulder and axilla is the most
common presenting symptom of neoplastic brachial plexopathy.
Invasion of the lower plexus (inferior trunk and medial cord)
occurs more frequently than invasion of the upper trunk
 Radiation-induced brachial plexopathy is a consideration in
patients with cancer who develop plexopathy after radiation
therapy in the vicinity of the brachial plexus. Either cancer
recurrence or radiation therapy can cause a brachial plexopathy in
this setting.

10. THORACIC OUTLET SYNDROMES
 Thoracic outlet syndrome (TOS) is a term used to denote
a variety of upper extremity syndromes, with only a
small number having a neurologic basis. TOS is generally
divided into true neurogenic TOS, vascular TOS (with
arterial vascular and venous vascular subtypes), and
disputed (nonspecific) TOS

11. DIABETIC PLEXOPATHY
 Plexopathies related to diabetes mellitus usually involve the
lumbosacral plexus, but upper extremity involvement has also
been observed as part of the syndrome. In contemporary
series, upper extremity involvement occurs in up to one-third
of patients and may be in the form of mononeuropathies of
the ulnar and median nerves, or at more proximal sites in the
brachial plexus

12. IATROGENIC BRACHIAL PLEXOPATHIES
 Iatrogenic brachial plexopathies related to surgery and other
medical procedures account for approximately 7 to 10 percent
of all brachial plexopathies. Examples include classic
postoperative paralysis, postmedian sternotomy plexopathy,
and medial fascial compartment syndrome

13. THORACIC OUTLET SYNDROMES
 Thoracic outlet syndrome (TOS) refers to a constellation of signs and
symptoms that arise from compression of the neurovascular bundle by
various structures in the area just above the first rib and behind the
clavicle, within the confined space of the thoracic outlet
 several names have been coined to describe pathology involving the
thoracic outlet which are
• cervical rib syndrome
• scalene anticus syndrome
• costoclavicular syndrome
• hyperabduction syndrome
The term “thoracic outlet syndrome” was coined to collectively encompass
the spectrum of syndromes related to the general region of the thoracic
outlet

14. TERMINOLOGY OF TOS
 Neurogenic (nTOS) from brachial plexus compression(95%)
 Venous (vTOS) from subclavian vein compression (3%)
 Arterial (aTOS) from subclavian artery compression(1%)
Compression of the brachial plexus leads to upper extremity numbness,
dysesthesia and weakness
Venous compression may cause deep vein thrombosis and extremity
swelling
Arterial compression can lead to distal thromboembolism, arm pain with
exertion (‘claudication’) or acute arterial thrombosis

16. ETIOPATHOGENESIS
 Thoracic outlet syndromes are due to rib anomalies, muscular
anomalies, or a result of injury. Cervical ribs predispose the patient
to TOS after hyperextension-flexion (whiplash) injury. The absence
of a rib anomaly makes the diagnosis of arterial thoracic outlet
syndrome less likely. Many patients with nTOS have a prior history
of neck trauma or repetitive occupational physical stress. Similarly,
vTOS is highly associated with repetitive movements, particularly
with repetitive overhead upper extremity movements

17. CLINICAL EXAMINATION
 Symptoms of neurogenic TOS include upper extremity pain,
dysesthesia, weakness, and numbness in the hand, arm, or
shoulder. Progressive unilateral atrophic weakness of the
hypothenar hand muscles and numbness in the distribution of the
ulnar nerve and medial antebrachial cutaneous nerves can occur,
but very rarely. Tenderness over the scalene muscles is often
present
 Arterial TOS typically presents as thromboembolism to the hand or
arm. Features of arm/hand ischemia include pain, paresthesia,
pallor, and coolness
 Venous TOS is easily differentiated from the other forms of TOS
because venous compression may lead to upper extremity venous
thrombosis, swelling, and cyanosis even in the absence of
thrombosis. Due to swelling, some patients may complain of hand
paresthesias

18. DIAGNOSIS
 Diagnosis of nTOS is often clinical, but electrodiagnostic and
imaging can exclude other diagnosis
 Arterial or venous duplex ultrasounds are the initial diagnostic
tests for aTOS or vTOS, respectively
 The role for computed tomographic or magnetic resonance
imaging is evolving and provides important diagnostic
information especially when ultrasound results are equivocal
 Conventional arteriography (aTOS) and venography (vTOS)
remain useful diagnostic modalities especially when initiation
of thrombolysis is considered

19. MANAGEMENT
 Patients with nTOS should be managed conservatively with physical
therapy and weight loss supplemented by medical therapy unless
they have progressive neurologic weakness or disabling pain and
paresthesia. Patients who have not responded to conservative
treatment may become candidates for thoracic outlet
decompression; however, the patient needs to understand that the
long-term success rates for thoracic outlet decompression for nTOS
diminish over time.
 For patients with deep vein thrombosis due to vTOS, thrombolysis
and early thoracic outlet decompression are performed to relieve
extrinsic vein compression. In properly selected patients, long-term
outcomes are excellent following thrombolysis and thoracic outlet
decompression

20. MANAGEMENT (contd…)
 Patients with aTOS are treated according to the nature of their
symptoms and initial presentation. Patients with signs and
symptoms of upper extremity thromboembolism undergo
thoracic outlet decompression in conjunction with
embolectomy, thrombolytic therapy, or anticoagulation.
Arterial TOS is nearly always associated with a correctable
anatomic bony abnormality, and, without decompression, the
rate of recurrent thromboembolism is high. The
supraclavicular approach offers direct access to the subclavian
artery. Occasionally, arterial reconstruction (ie, surgical bypass)
may be needed.

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