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Reliable assessment of brachial plexus disorders can be challenging due to the complexity of the anatomy and variation of potential pathology. Electrodiagnostic testing can be both uncomfortable for the patient and inconclusive. Ultrasound can serve as a complement to clinical assessment, electrodiagnostic testing, and other imaging modalities. This study describes a systematic approach for performing neuromuscular ultrasound for suspected pathology in the brachial plexus. The literature regarding techniques for brachial plexus ultrasound was reviewed. A team composed of specialists in neurology, physiatry, anesthesiology, orthopedic surgery, and vascular surgery used this as the basis for describing standardized techniques for performing brachial plexus ultrasound. Four standard views, along with other supplemental views, are described for the evaluation of the brachial plexus. An illustrative case is presented. Ultrasound is a high-resolution point of care diagnostic tool that allows assessment of structural pathology affecting the brachial plexus. Muscle Nerve 58: 618-624, 2018.

Three individuals with C4 or C5 spinal cord injuries (SCI) were seen in follow-up for management of their late complications, which included impaired ventilation. Electrodiagnostic studies were performed on all three as part of the assessment of the function of their phrenic nerves and diaphragm muscles in relation to their need for mechanical ventilator support. Each patient had evidence of lower-motor neuron injury to the phrenic nerves. Two of the patients who initially displayed small-amplitude (<0.1 mV) compound muscle action potentials (CMAP) bilaterally were later reevaluated during the course of their observation in the outpatient rehabilitation clinic. The CMAP amplitude of the diaphragm increased in these two cases during the 3-11 mos after SCI. Evidence of nerve recovery occurred in parallel with improvements in pulmonary function testing and was followed by successful weaning from the ventilator. These individuals both gained ventilator independence after the CMAP amplitude of least one hemidiaphragm was >0.4 mV. In the third case, early failure of ventilator weaning was reported to the patient as a poor prognostic sign. At the time of our first evaluation 11 mos after injury, a CMAP of 1.0 mV was seen on the right, with an absent response on the left. In case 3, the needle electromyogram demonstrated voluntary active motor unit action potentials that provided additional electrophysiologic support for phrenic nerve function. Phrenic nerve-conduction studies can provide useful measures in assessing the recovery of lower-motor neuron diaphragm function in relation to impaired ventilation in individuals with C4- or C5-level SCI.

The patient's likely mechanism of injury occurred during delivery from external compression by the patient's dominant hand to the distal posterior thigh while under epidural anesthesia. Labor and delivery teams should be aware that nerve injury is also possible at the distal thigh with excessive external pressure.

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