Direct compression of parts of the plexus by adjacent skeletal anomalies (cervical rib, fascial bands, narrowed thoracic outlet) represents another, if somewhat controversial, category of brachial plexus injury. A subcutaneous or intramuscular injection of vaccine or foreign serum was in the past sometimes followed by a brachial plexopathy (due to the aforementioned serum sickness reaction), usually a partial plexopathy. There are also plexus lesions of presumed toxic nature, such as following distal intravenous heroin injection. Granulomatous diseases such as sarcoid and secondary inflammatory processes related to lymphoma may implicate a plexus and an ischemic condition resulting from thrombosis of the subclavian artery or vein (Paget-Schrötter syndrome) is known.
In assessing the type and degree of plexus injury, electrophysiologic testing is of particular importance. Early after a traumatic injury or other acute disease of the plexus, the only electrophysiologic abnormality may be an absence of late responses (F wave). After 7 to 10 days or more, as the process of wallerian degeneration proceeds, sensory potentials are progressively lost and the amplitudes of compound muscle action potentials are variably reduced. Fibrillation potentials, indicative of denervation, then begin to appear in the corresponding muscles. Even later, usually after several weeks, signs of reinnervation can be detected. In more chronic cases, all of these features are evident when the patient is first studied. The pattern of denervated muscles allows a distinction to be made between a plexopathy, radiculopathy, and mononeuritis multiplex based on the known patterns of muscle innervation. If denervation changes are found in the paraspinal muscles, the source of weakness and pain is in the intraspinal roots, proximal to the plexus. In this case, the sensory potentials are retained. MRI may expose metastatic deposits of the plexus, but small nodular lesions may escape detection and one then defers to the clinical data if the circumstances suggest an infiltrative or compressive lesion.
The anatomic plan of the brachial (and lumbosacral) plexus and their relations to blood vessels and bony structures (Fig. 43-5) and one of many detailed maps of the peripheral nerves should be consulted. We resort to the illustrations of individual nerves and plexuses that are well demonstrated in the monograph published by the
Guarantors of Brain.
For orientation, it is enough to remember that the brachial plexus is formed from the anterior and posterior divisions of cervical roots 5, 6, 7, and 8 and thoracic nerve root 1. The fifth and sixth cervical roots merge into the upper trunk, the seventh root forms the middle trunk, and the eighth cervical and first thoracic roots form the lower trunk. Each trunk divides into an anterior and posterior division. The posterior divisions of each trunk unite to form the posterior cord of the plexus. The anterior divisions of the upper and middle trunks unite to form the lateral cord. The anterior division of the lower trunk forms the medial cord. Two important nerves emerge from the upper trunk (dorsal scapular nerve to the rhomboid and levator scapulae muscles, and long thoracic nerve to the anterior serratus). The posterior cord gives rise mainly to the radial nerve. The medial cord gives rise to the ulnar nerve, medial cutaneous nerve to the forearm, and medial cutaneous nerve to the upper arm. This cord lies in close relation to the subclavian artery and apex of the lung and is the part of the plexus most susceptible to traction injuries and to compression by tumors that invade the costoclavicular space. The median nerve is formed by the union of parts of the medial and lateral cords.
Lesions of the Entire Brachial Plexus