**4. Medical treatment**

This kind of pain, particularly in case of nerve root avulsions, is difficult to treat due to partial responses and frequent relapses [5, 6, 17]. The response to pharmacological treatments decreases when the pain intensity increases [6].

The non-steroidal anti-inflammatory drugs (NSAIDs) are of little help in the chronic phase [17, 30].

**5. Surgical treatment**

central nervous system procedures [114, 115].

**5.1. Neuromodulation procedures**

reducing the side effects, particularly muscle spasms [122].

Brachial plexus injury repair by direct suture, by grafts or by nerve transfers, particularly sensory nerve transfers, minimizes the incidence and severity of neuropathic pain [4, 26, 34, 67, 104–109], and the sooner the repair is done the better [25, 67]. CRPS is the exception as further surgery outside trapped nerve decompression seems to have a negative impact on the outcome [101]. In these cases either an interscalene [102] or stellate ganglion block [110] or a cervical spinal cord stimulator [111–113] is recommended instead. The phantom limb pain only improves with

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There are two main roads of action: neuromodulation and ablative procedures. The first group relies on applying electric impulses to different areas of the central or peripheral nervous system, aiming to block the transmission of the nerve impulses that are finally interpreted as pain in the sensory motor cortex. They are particularly effective for continuous pain but less so for paroxysmal painful discharges [84]. The ablative procedures aim to destroy the posterior horn spinal cord neurons that start to fire in an abnormal way after being disconnected from their peripheral

*Peripheral nerve stimulation* provides 50–83% pain relief in 65–80% of the patients [116–120], and the affected limb preserves the residual function remaining after the injury [121]. Allodynia and neuropathic pain are controlled with mild improvement in the sensory function [116, 118]. The results are stable long-term [118, 119, 121]. The electrodes can be implanted with an open surgical procedure [117, 119] or percutaneously under ultrasound guidance [116, 120]. Unfortunately lead fracture, displacement or infection can spoil an initial successful result [116, 120]. A further refinement is to apply the stimulating electrodes not through a cuff around the affected nerve but by direct selective nerve fascicle stimulation [122]. In this way only the affected sensory fascicles are stimulated and not the motor ones, improving the results and

*Cervical spinal cord stimulation* stops the transmission of the abnormal electrical impulses coming from the deafferented posterior spinal cord horn neurons [123], controlling the pain with preservation of the remaining upper limb function [112, 124, 125]. Its success rate in the treatment of neuropathic pain associated with brachial plexus injuries is 50% [51, 111–113, 124–129]. It is particularly useful in CRPS [112] but it also helpful in nerve root avulsions [129]. In cases of failed previous dorsal root entry zone (DREZ), lesioning can provide good pain control [113]. Contrariwise, when the spinal cord stimulation failed the DREZ-otomy through radiofrequency, it yields suboptimal results [130]. Nevertheless several research groups recommend to restrict the cervical spinal cord stimulation for failed previous DREZ-otomy due to its high economical costs [25, 131–133]. A trial period is needed before the definitive pulse generator implantation to predict the results [129]. The stimulation parameters can be modified according to the patient's individual needs through an external programming device. The electrodes can be implanted percutaneously or surgically. Lead fracture or dislocation

sensory input [25, 64–66], controlling paroxysmal pain better than continuous pain [84].

The first step is *tricyclic antidepressants (TCAs)* or *serotonin* and *noradrenaline reuptake inhibitors* [6, 57, 87]. Among TCAs, amitriptyline (25–125 mg/day) and venlafaxine (150–225 mg/day) are the most commonly used [6, 57]. They not only help with the pain but also with the accompanying nervous depression [57, 87]. A regular ECG surveillance is recommended as at high doses these drugs can induce cardiac arrhythmias [88]. Duloxetine, the most commonly used serotonin-noradrenaline reuptake inhibitor, is devoid of cholinergic or cardiac side effects [87].

The second step is the combination of the above-mentioned drugs with anti-epileptic agents [89], like *gabapentin* or *pregabalin* [6, 19, 27, 57, 87]. Clonazepam at night time is very effective, but it can induce drowsiness, and some patients find it difficult to tolerate [90]. Other antiepileptic drugs like topiramate, carbamazepine, oxcarbazepine and lamotrigine are also used but with limited success [57].

*Lidocaine* (lignocaine) 5% patches applied to the painful area are the third line of medical treatment [27, 91, 92]. It controls the cold allodynia but not the mechanical one [73].

*Capsaicin* 8% patches are used but can cause severe local skin irritation [27].

*Oral cannabinoids*, which were successful in controlling brachial plexus injury pain in rats [70], have limited success in humans and are not currently recommended [93].

*Opioids* (tramadol [6, 89], morphine, oxycodone and tapentadol) are to be avoided as they are not very effective in the treatment of neuropathic pain [32] and because of their addictive properties [27, 57, 91, 92]. In any case the opioid dose should never exceed 180 mg/day of oral morphine equivalents [57] and should be complemented with TCAs and anti-epileptic drugs [89].

Other drugs have been tried experimentally in rats, like rapamycin [94], intrathecal Trichostatin A (TSA) [94] or intravenous immunoglobulin [95], but there are no reports of their use in humans.

*Transcutaneous electrical nerve stimulation* (TENS) has been used to control and prevent the development of neuropathic pain after brachial plexus injury [35, 96–98]. Its main advantage is that it can be self-applied by the patient. However, it needs constant application, and at times it can provoke local skin irritation [35, 96–98].

The common clinical features shared by neuropathic pain and CRPS hinder a pure clinical diagnosis [6]. Distinguishing between both of them is essential as the latter causes greater disabilities [99]. To differentiate them, an ultrasound examination can be performed, as the muscular architecture is preserved in neuropathic pain but not in CRPS [99].

Medical treatments can also classify the pain: *stellate ganglion blocks* will only relieve CRPS [6, 100, 101]. Other therapies for CRPS include *botulinum toxin*, which can be used to treat muscular trigger points [102] when found, and *electroacupuncture*, which has been found effective in controlling experimental brachial plexus pain in rats [103]. We have not found any publication reporting the use of electroacupuncture in human beings.
