LAUSR

Dear Editor We read with great interest the case report by Majmundar et al.1 recently published in British Journal of Pain. In this article, the authors reported for the first time the occurrence of chest wall and cardiac paraesthesias after cephalad lead migration reaching T1-T3 level during high-frequency spinal cord stimulation (HF-10 SCS). HF-10 SCS is a relatively new paraesthesia-free stimulation paradigm and little is known about the physiological mechanisms underlying its effect in pain reduction compared to conventional SCS. In this article, the authors considered the asynchronous firing as a possible explanation of paraesthesia onset after supra-threshold stimulation of nerve fibres with HF-10 SCS. We need to specify that the results obtained in the cited computational model2 are based on monophasic and rectangular HF-10 SCS waveform stimulation in spite of biphasic pulses that are commonly used in clinical setting. Moreover, as recently reported in a preclinical study by McMahon and Smith,3 no evidence of asynchronous firing or dorsal column fibre conduction block or latency change was noted even after prolonged HF-10 SCS stimulation. These findings are in line with the clinical observation, confirmed also by an animal study,4 that no sensory modifications or disturbance occurs during HF10-SCS. Consequently, the differential blocking hypothesis2,5 that the induced depolarization and blockage of lower-threshold large-diameter dorsal column fibres (vibration and pressure information) can avoid paraesthesia production should be regarded very cautiously. A male patient with failed back surgery syndrome (FBSS), treated with HF-10 SCS, recently come to our attention after a post-traumatic lead displacement. The patient developed acute parascapular and dorsal pain associated with lateral chest numbness and pain. These painful experiences immediately disappeared after the HF-10 SCS stimulation was stopped. The spine computed tomography (CT) revealed a foraminal and cranial (T5 level) HF-10 SCS lead displacement (Figure 1). Pain relief was promptly restored after surgical revision with a reposition of the lead to the appropriate location. In our case, the lateral displacement of the lead induced an activation of dorsal root ganglia due to the current–distance relationship6 and to the smaller threshold of this neural structure. An activation of the dorsal root entry zone is unlikely High-frequency spinal cord stimulation can induce numbness and painful dysaesthesia after lateral and cranial lead displacement 823807 BJP British Journal of PainLeoni and Micheli