Neuropathic pain in children: Case

This girl has complex regional pain syndrome of the right lower limb, complicated by opioid escalation, functional decline, and a fixed dystonic posture. Her pain is disproportionate to a minor injury that has long since healed, and she has the full clinical picture: allodynia in the flinching from light touch and the provocation by the bedclothes and the shower water, hyperalgesia in the burning quality, vasomotor and sudomotor change in the cool, swollen, dark-red foot, and a motor change in the fixed dystonic posture of the toes. The Mesaroli five-year review establishes that complex regional pain syndrome predominates in adolescent girls, affects the lower limb, and is accompanied by a movement disorder such as dystonia in a significant minority, and this girl fits that picture exactly. Her management has gone wrong in the directions that most often cause harm: immobilisation through rest and a compression bandage, and opioid escalation. The task now is to reverse both and to build the rehabilitation plan that should have been the foundation from the outset. [9]

Confirming the diagnosis and excluding dangerous alternatives

The first task is to confirm the diagnosis and exclude the dangerous alternatives. The diagnosis of complex regional pain syndrome is clinical, built on regional pain disproportionate to an inciting event, accompanied by sensory, vasomotor, sudomotor, and motor changes, and this girl has each of these. On the NeuPSIG grading system her pain is at least possible neuropathic pain, with a neuroanatomic distribution in the affected limb and a plausible injury. [1]

The most important alternative to exclude is infection, because a warm, swollen, painful limb in a febrile or unwell child is septic arthritis or osteomyelitis until proven otherwise. This girl is afebrile and well, and her inflammatory markers and full blood count are normal, which makes infection unlikely, but the exclusion is documented actively rather than assumed. A structural lesion of the nervous system is excluded by the red-flag screen: there is no progressive pain, no focal deficit, no sphincter disturbance, and no systemic features, and the neurological examination is normal, so urgent magnetic resonance imaging is not required. The fixed dystonic posture is the movement disorder of complex regional pain syndrome rather than a primary neurological lesion, and the diagnosis is secure. [9]

Reversing the opioid escalation and the immobilisation

The two errors that have driven this girl's deterioration are opioid escalation and immobilisation, and both must be reversed. Opioids have no place in the routine management of complex regional pain syndrome because neuropathic pain responds poorly to opioids and the escalating doses carry a high risk of dependence, sedation, and opioid-induced hyperalgesia, in which the opioids themselves increase the sensitivity of the nervous system and worsen the very pain they are meant to treat. I would plan a structured wean of the oxycodone, with a clear written schedule and the involvement of the family and the general practitioner, warning the family that the pain may transiently worsen during the wean and that this is expected. No rehabilitation plan works while escalating opioids continue, so the wean is the foundation of the plan. [3]

Immobilisation is the second error. Rest, a compression bandage, and the avoidance of weight-bearing have deepened the disuse and sensitisation that drive complex regional pain syndrome, and the fixed dystonic posture of the toes is the consequence of prolonged disuse. I would remove the compression bandage, commit to a graded return to weight-bearing and movement, and treat the dystonia as a target of the rehabilitation rather than as a reason to rest the limb further. [9]

Building the intensive rehabilitation plan

The core of the management is an intensive, function-focused exercise-based rehabilitation programme, and I would refer this girl urgently to physiotherapy and to a tertiary paediatric pain service for intensive multidisciplinary input. The classic series by Sherry and colleagues demonstrated excellent short- and long-term outcomes for children with complex regional pain syndrome treated with exercise therapy, and the principle is that the nervous system is retrained through movement rather than rested. The programme includes graded desensitisation of the allodynic skin, progressive weight-bearing, functional exercise, and, for the dystonic posture, targeted movement and motor retraining. Graded motor imagery and mirror therapy are valuable adjuncts. [6]

Because this girl has missed six weeks of school, sleeps poorly, and describes low mood, cognitive behavioural therapy and psychological support are core treatments and not optional extras. Cognitive behavioural therapy helps her reframe the pain, reduce the fear of movement that drives the disuse, and address the anxiety and low mood that amplify the nervous system's gain. I would quantify her disability with a validated paediatric pain and quality-of-life measure and repeat it at each visit, because improvement is measured by what she can do rather than by the pain score. I would counsel the family that the goal is a return to function and school, that the prognosis with intensive rehabilitation is good, and that relapses during stress are expected and manageable. [9]

The cautious role of gabapentin and the evidence base

Given the severity of her pain and its interference with participation in the rehabilitation programme, I would add gabapentin as an adjunct, with explicit acknowledgement to the family that it is being used off-label. I would start it low, at about 10 mg per kg per day in divided doses, given as a single night-time dose initially, and titrate over one to two weeks from once daily to twice daily to three times daily toward a usual effective range of 25 to 35 mg per kg per day in three divided doses. I would reduce the dose if her renal function were impaired, because gabapentin is excreted unchanged by the kidney, and I would warn the family that it must never be stopped abruptly, tapering it over at least a week because abrupt withdrawal can precipitate seizures. The oxycodone wean and the gabapentin titration are coordinated so that the gabapentin is built up as the opioid is weaned. [3]

If her sleep disturbance and low mood remained prominent and the baseline electrocardiogram were normal, I would consider amitriptyline as an alternative or adjunct, started at 0.1 to 0.2 mg per kg at night and titrated to a maximum of about 0.5 to 1 mg per kg per day, with a repeat ECG after dose increases. A fellowship-level answer must confront the evidence base: the 2017 Cochrane review by Cooper and colleagues found insufficient evidence for antiepileptic drugs in chronic non-cancer pain in children, and the GABA-1 trial was established precisely because gabapentin was used off-label without reliable evidence. The realistic framing is that gabapentin is a plausible adjunct borrowed from the adult evidence, used cautiously, and judged on function rather than pain intensity. [3] [4]

Prognosis and follow-up

The prognosis for this girl is good but depends on reversing the opioid escalation and the immobilisation and on building the intensive rehabilitation plan. I would review her in clinic at two to four weeks with the physiotherapy and psychology teams, tracking her function, her sleep, her mood, and her school attendance rather than the pain score alone. I would address the fixed dystonic posture aggressively within the rehabilitation programme, because it becomes harder to reverse the longer it persists. I would counsel the family that the goal is a return to school and to walking, that the prognosis with intensive rehabilitation is good, and that the gabapentin is weaned once the function is restored and the pain has settled. I would arrange a structured transition to a tertiary paediatric pain service for the intensive multidisciplinary input her severity requires, and I would ensure that the opioid wean is completed and not reopened. [6] [9]