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Editor,—Spinal cord stimulation has been used for pain relief in patients with painful diabetic neuropathies.1 Coeliac disease is associated with varied neurological complications (5–8%) including ataxia, peripheral neuropathy, myelopathy, myopathy, and dementia.2 We report the novel use of electrical spinal cord stimulation for the management of chronic painful peripheral neuropathy secondary to coeliac disease.
A 47 year old man presented to the pain clinic with an 11 year history of generalised aches and pains in the lower limbs. However, they were now becoming more symptomatic and shooting in character. This generalised body pain resulted in his inability to work as a bank official. During the previous year he suffered from nausea, vomiting and weight loss, and a subsequent jejunal biopsy specimen yielded a diagnosis of coeliac disease. An initial impression was that of peripheral neuropathy secondary to coeliac disease. Nerve conduction studies showed no evidence of large fibre peripheral neuropathy. Bone biochemistry confirmed vitamin D deficiency, secondary hyperparathyroidism and a notable increase in bone turnover. After a year on a gluten-free diet these indexes returned to normal; however, the patient still suffered from severe neuropathic pain in the lower extremities and was unable to resume full employment.Letters, Book review, Notes, Corrections
Initial pharmacological therapy for this painful neuropathy included trials of intravenous lignocaine and oral gabapentin which were without therapeutic benefit. In view of his ongoing symptoms and decreasing physical function, a spinal cord stimulator (Medtronic I TREL III system) was implanted and neuropathic pain relief was assessed by visual analogue scale. Pain was reduced by about 60–70%, and within two months the patient was able to return to full employment. This pain relief is sustained to date.
Although painful diabetic neuropathies have been treated with spinal cord stimulation,1 to our knowledge this is the first case of a painful peripheral neuropathy secondary to coeliac disease being treated in this way. The aetiology of neurological dysfunction in coeliac disease is poorly understood and research has largely concentrated on vitamin deficiencies (B12, E, D, folic acid, and pyridoxine) as a result of malabsorption. However, vitamin replacement rarely improves the neurological deficit or neuropathic symptoms.3 We suggest that implantation of a spinal cord stimulator may result in improved physical function and decreased pain in patients with painful peripheral neuropathies secondary to malabsorption syndromes. Further studies to elucidate these mechanisms might allow spinal cord stimulation to be exploited more effectively in painful disorders that are currently refractory to conventional treatment modalities.