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 Parry ³ 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 Sindou ⁶ 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.