A 32-year-old woman was referred to our neuromuscular clinic with a one-year history of bilateral scapular winging, a presumed diagnosis of brachial neuritis, and left arm numbness and paraesthesias with use, which had developed more recently. The brachial neuritis had started approximately 2 weeks after temporomandibular joint surgery, and she presented with severe, bilateral shoulder pain that woke her from sleep. The pain subsided after 2-3 weeks; however, she was left with bilateral weakness and scapular winging. As she started physiotherapy, she developed paraesthesias only in the left arm. Her past medical history included acid reflux and irritable bowel syndrome. Her only medication was gabapentin 600 mg twice daily. She had a magnetic resonance imaging (MRI) of her cervical spine prior to the referral, which was unremarkable.
Her nerve conduction study approximately one year after onset of the brachial neuritis was fairly unremarkable, with borderline low sensory nerve action potentials over the median nerve to the thumb, and ulnar nerve to the fourth and fifth digits on the left. Needle electromyography exam showed 1+ polyphasics and decreased recruitment in the right serratus anterior, but normal studies for the left serratus anterior, trapezius, deltoid, and biceps.
The weakness on her right side improved with time, but worsened on the left. In addition, her paraesthesias worsened, so that when she abducted her left shoulder to 45  or more paraesthesias occurred. She also developed paraesthesias with any pressure over her pectoralis muscles or scalenes, including pressure from wearing a seatbelt, or even tight clothing. The paraesthesias were localized to her hand and forearm, but she had pain more proximally in her shoulder and neck. Now she was also having difficulty performing activities of daily living (ADLs), playing with her young children, and driving, secondary to these symptoms. The working diagnosis at this time was history of bilateral brachial neuritis plus left thoracic outlet syndrome.
An initial MRI of her left brachial plexus showed increased T2 signal in the C8 root, superior trunk, and posterior cord. Over the next 2 years several treatments were tried, including a course of prednisone, baclofen, and gabapentin, none of which improved her symptoms. A trial of an ultrasound-guided botulinum toxin injection to the left anterior scalene was also undertaken, which provided no benefit. A subsequent MRI of the brachial plexus was ordered, but now with her arm in full abduction. This MRI (Fig. 1) showed that the superior trunk separates from the inferior and middle trunks and takes a 90  turn and kinks as it travels toward the costoclavicular space, where it has mildly elevated T2 signal. It also showed the posterior cord travelling through the proximal costoclavicular space, which is markedly narrowed compared with the other side, and has an increased T2 signal here compared with the arm in the neutral position.
Because of the kinking, as well as the asymmetrically narrowed costoclavicular space, and in the setting of unsuccessful conservative management, surgical management was pursued. A supraclavicular technique was used. A segment of fascia constricting a portion of the brachial plexus was released and a small portion of the anterior scalene was excised. There was no rib removal.
After the operation, the patient's symptoms improved by at least 80%. She became independent in ADLs, was not taking any medication for neuropathic pain, and was able to drive without problems. She reported ongoing paraesthesias if her arm was held abducted to 150  or with prolonged pressure over her anterior scalenes or pectoralis, but had improved significantly.
Repeat MRI 2.5 years after her operation showed almost complete resolution of the T2 hyperintense signal and thickening of the distal superior trunk and proximal posterior cord of the brachial plexus. The superior trunk of the brachial plexus continued to demonstrate a kink upon shoulder abduction, although it was less conspicuous.