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changes in cortical processing of pain. The first is that of often there are overlapping features. In these situations,
persistent stimulation of free nerve endings at the site electrophysiologic studies and local anesthetic blocks
of injury with pain transmitted via the small diameter A are useful as diagnostic adjuncts. Electromyography and
delta and C fibers to the central somatosensory cortex. nerve conduction studies will usually establish if there
[5]
Following nerve injury, the proximal free nerve endings is a compressive element. Neuroma pain is significantly
are unmyelinated, and these small diameter fibers have reduced or diminished with infiltration of a small amount
increased electrical activity and are stimulated at lower of local anesthetic around the nerve proximal to the
thresholds. Spontaneous, mechanical and chemical activity suspected lesion.
has also been demonstrated within the neuroma. This is
accompanied by spontaneous activity in neurons of the Prevention
dorsal root ganglion, dorsal horn and more proximally Given the challenges of treating neuroma pain, the
within the central nervous system. In addition, it is importance of prevention must be stressed. Avoidance
believed that changes in the central processing of the of nerve injury seems obvious yet cannot be emphasized
somatosensory cortex result in amplification of the pain enough given that iatrogenic injuries are cited as a major
response and perpetuation of the pain process even after etiological source, especially with procedures such as
the injury is treated successfully by surgery. [6] ganglion resection, surgery for De Quervain’s syndrome
or procedures on ulnar head. It is imperative that once
[7]
The most severe pain occurs after partial injuries to the an injury is diagnosed an attempt at primary repair be
nerve trunks or injury to the terminal branches of the undertaken as soon as possible. The precise microsurgical
smaller cutaneous nerves such as the superficial radial coaptation of the epineurium has been shown to reduce
nerve, medial and lateral cutaneous nerves of the the incidence of neuroma formation. Providing the
[8]
forearm, palmar branch of the median nerve and the sural advancing axons are directed appropriately they may
and saphenous nerves of lower limbs. However, surgical reestablish connections with their end‑organs thereby
removal of these nerves for use as grafts for nerve restoring function in terms of muscle innervation and
reconstruction rarely leads to neuropathic pain. sensibility. If a nerve is found to be in‑continuity, it is
Presentation advised to perform an external neurolysis and to initiate
The patient describes sensory symptoms in the distribution early mobilization after surgery.
of the affected nerve. This is usually accompanied by a
history of previous injury or surgery in the vicinity of the TREATMENT STRATEGIES
nerve. Other pathologies causing neuropathic pain such as
nerve compression and complex regional pain syndrome Nonsurgical therapies
must be ruled out as these conditions can co‑exist with a It is difficult to treat pain from neuroma, and a wide range
neuroma. of surgical and nonsurgical therapies have been described.
Analgesia with or without supplementary neuropathic
Our unit previously described a simple assessment tool agents should be introduced early and prescribed to be
for grading pain from neuromas using characteristic taken regularly following any traumatic nerve injury. Early
symptoms: (1) baseline pain, (2) spontaneous spikes of aggressive medical treatment and preemptive analgesia
pain, (3) pain exerted by pressure over the nerve, (4) pain have both been shown to improve prognosis and reduce
on movement of the adjacent joints, and (5) cutaneous pain in upper limb pain conditions. [9,10]
“hyperesthesia”.
Medical management consists of four main classes of oral
Other clinical terms used to describe the pain medication: (1) antidepressants with reuptake blocking
are: (1) dysesthesia: any abnormal unpleasant sensation; effect, (2) anticonvulsants with sodium‑blocking action, (3)
(2) allodynia: pain from a stimulus that is, not normally anticonvulsants with calcium‑modulating actions, and (4)
painful; (3) hyperpathia: exaggerated pain from a normally opioids.
painful stimulus; (4) hyperesthesia‑an abnormal increase
in sensitivity to stimuli; and (5) paresthesia: an abnormal Topical treatments for patients experiencing cutaneous
sensation typically tingling or prickling “pins and needles”. hyperalgesia and allodynia include capsaicin and local
Localization of the symptoms guides the clinician to identify anesthetics administered as slow release patches. In many
the injured nerve. The range of symptoms varies from situations, an early combination of medications working
complete anesthesia distally (indicating nerve transection) at different levels of the pain pathway by different
to hyperesthesia or hyperpathia. Palpation of the neuroma mechanisms is useful. Current randomized controlled trials
bulb results in tenderness and light percussion over the provide general pain relief values for specific medications,
nerve elicits paresthesias in the distribution of the nerve. which may explain the failure to obtain complete pain
relief in neuropathic pain. A detailed review of medical
Neuropathic pain is intractable, severely debilitating, therapies for upper limb neuropathic pain is beyond the
and disproportionately intense in relation to the scope of this article but we would refer readers to the
initiating injury. Alongside sensory disturbances, there articles in the references. [11‑14]
may be motor disturbance and abnormal sympathetic
responses. In these cases, the distinction between Neuromodulation
neuroma pain and chronic regional pain syndrome or Our preferred next step in management is a trial of
a severe compressive neuropathy may be difficult and peripheral external electrical stimulation, also known as
166 Plast Aesthet Res || Vol 2 || Issue 4 || Jul 15, 2015