Introduction

Traumatic brachial plexus injuries result in the development of chronic pain in up to 90% of patients. This chapter will focus on the clinical characteristics, pathophysiology, and management of pain following brachial plexus injuries. Emphasis will be placed on avulsion pain and the technique of radiofrequency thermocoagulation lesioning of the dorsal root entry zone (DREZ).

Musculoskeletal pain

The majority of patients with brachial plexus injuries will experience musculoskeletal pain. The weight of a flail limb creates strain on muscles of the neck, upper back, and shoulder girdle, and results in muscle spasms and constant aching pain. Weakness of the shoulder girdle, deltoid, supraspinatus, and upper limb strap muscles leaves the glenohumeral joint susceptible to subluxation or dislocation, as it counteracts the force of gravity on the limb. Partial injuries may alter the balance of force across joints to result in muscle spasms, joint stiffness, and the development of contractures. The approach to managing musculoskeletal pain focuses on restoring muscle function, providing external support via orthoses, and maintaining full range of motion in all joints. Anti-inflammatory and anti-spasmotic agents may provide symptomatic relief. Exercise and physical therapy aids in relief by maximizing function, improving flexibility, and maintaining passive range of motion. Maintaining passive range of motion of all affected joints will decrease the risk of pain.

Neuropathic pain

Neuropathic pain is common in patients with postganglionic injuries. Severe pain may arise in the distribution of injured elements of the brachial plexus. As the axons regenerate, paraesthesias or dyaesthesias may travel in the direction of regeneration. Sprouting of spared nerve fibers into denervated cutaneous territories may result in hypersensitivity. Axons that fail to regenerate to their targets may form painful neuromas at the site of injury or along the course of the nerves. Patients may experience spontaneous shooting electrical pains or hypersensitivity to stimulation of the skin in the distribution of the injured nerve. Palpation of the skin overlying a neuroma produces lancinating pain in the distribution of the injured nerve. First line therapy consists of anticonvulsants, tricyclic antidepressants, and opiate analgesics. Following brachial plexus repair, neuropathic pain subsides in the majority of patients. The timing of pain relief often correlates with recovery of motor function and may precede recovery of cutaneous sensation.¹

Avulsion pain

Avulsion pain arises in about 90% of patients with nerve root avulsions and persists as severe chronic pain in about 30%.² The initiation of pain may be immediate or delayed up to 3 months after injury, and then often becomes progressively severe. Description of the pain is consistent in all patients – a constant burning, crushing feeling in the deafferented hand. Patients frequently describe feeling like their hand is being crushed in a vice, or immersed in boiling water. As one of our patients described it, “It feels like someone parked a moving van on my hand and then lit the van on fire.” The pain is unrelenting, present day and night, and often awakens patients from sleep. Most patients also experience unpredictable paroxysms of electric shocks or stabbing pain that shoot through their arms causing them to wince or cry out in pain.

Conventional therapies for pain management usually fail to provide adequate relief for avulsion pain. Opiate analgesics may provide limited relief. Other medications that often ameliorate neuropathic pain, such as gabapentin, carbamazepine, tricyclic antidepressants, and nonopiate analgesics, are rarely effective. Some patients report pain improvement with alcohol or cannabis. We have not seen much benefit from accupuncture, physical therapy, or other alternative therapies. Distraction, including attempting to perform activities of daily living despite the pain, helps some patients cope. Wynn Parry³ championed transcutaneous electrical nerve stimulation (TENS) and reported clear benefits when TENS was applied using a strict protocol combined with intense inpatient rehabilitation. Unfortunately, the use of TENS without such a strict protocol has not proven effective, and thus it has fallen out of favor. Neurostimulation procedures including spinal cord, deep brain, and motor cortex stimulation, and neuroablative procedures including anterolateral cordotomy, spinothalamic tractotomy, and medial thalamotomy, have not proven beneficial. Neurotization procedures including replantation of avulsed roots⁴ and late intercostal nerve transfers⁵ have demonstrated some benefit in select patients.

DREZ lesioning is the one intervention that provides lasting, albeit incomplete, pain relief in the majority of cases. DREZ lesioning was introduced by Sindou⁶ for treatment of central pain from a pancoast tumor in 1972, and adapted for brachial plexus avulsion pain by Nashold.⁷ Surgical techniques including microsurgical bipolar coagulation,⁸ laser,⁹ and ultrasonic¹⁰ probes have since been developed to create DREZ lesions. Regardless of the technique used, the success of DREZ lesioning across several large series has been 70–90%. The amount of pain relief tends to decline over years following the procedure, but even at long-term follow-up the successful outcomes are maintained in 60–70% of patients. We have had a similar experience with almost complete immediate relief in the majority of patients. With time, some of the pain gradually returns, but it usually plateaus at a level that is tolerable and controllable with medications (approximately 20% of the original pain).

Several lines of evidence implicate dorsal horn neurons as the primary pain generators in avulsion pain. In animal models, cervical dorsal rhizotomy produces epileptogenic hyperactivity in dorsal horn neurons and self-mutilation behaviors believed to be due to spontaneous pain.¹¹ This hyperactivity may be facilitated by avulsion-induced loss of input from the dorsal columns, via a gating mechanism, and descending inhibitory tracts. Lesioning of the DREZ in these animal models eliminates dorsal horn hyperactivity and ameliorates self-mutilation. Intraoperative recordings using floating microelectrodes inserted into the dorsal horn of patients undergoing DREZ lesioning have shown the presence of hyperactive neurons.¹² The robust effect of DREZ lesioning in both animal models and patients further supports the dorsal horn as the primary pain generator. The rare failure of DREZ lesioning or relapse of pain may be due to the development of loci of pain generation at higher levels in the neuraxis. This is supported by animal studies demonstrating that hyperactivity develops in thalamic nuclei after cervical rhizotomy.¹³ DREZ lesioning may facilitate this effect by further damaging ascending sensory tracts and altering the input to higher level neurons.