Leg pain after sacral neuromodulation: anatomical considerations

(Fig. 1). A comparison of the postoperative radiographs Case reports of the three patients with the cadaveric dissections showed equivalent lead positioning (Fig. 2). Thus we Sacral nerve stimulators were implanted in 13 women; three experienced distressing sensory symptoms in the suggest that it is legitimate to draw inferences from the findings at dissection. Analysis of the prosected speciipsilateral lower limb which commenced immediately after implantation. These three patients complained of mens confirmed that a stimulating lead passed through the S3 foramen could lie close to the S3 nerve root. It severe, ‘sciatica’-like pain, and one suCered loss of sensation to light touch in the foot. The last patient still was clear that this association becomes more intimate the more laterally in the S3 foramen the lead is placed takes regular analgesics 20 months after implantation. Another patient still complains of leg pain and continues (Fig. 3). An additional observation was the S3 dorsal ramus exiting the S3 foramen posteriorly in some of the to take analgesics intermittently 12 months after implantation. The third patient experienced leg pain for specimens. This small branch could possibly be damaged by the placement of a sacral lead in that foramen. 6 weeks after the operation, which then resolved. In all three patients the sensory symptoms persisted despite the temporary cessation of stimulation, suggesting that Comment the cause of the symptoms was not the stimulation. After a full neurological examination all three patients Neuromodulation of the sacral nerves by a permanently implanted sacral nerve stimulator has been shown to be underwent plain postero-anterior and lateral pelvic radiographs, and CT of the lumbosacral spine (MRI was an eCective therapy for treating various voiding disorders refractory to other treatment modalities [1–3] and it contraindicated because of the metallic implant). Clinical neurophysiological investigations included nerve conhas recently been granted a US Food and Drug Administration license for the treatment of urge duction studies, EMG sampling of lower limb muscles and tibial somatosensory evoked potentials. The radiographs confirmed the appropriate siting of electrodes according to the protocol. CT eliminated coexistent disk pathology in all three patients and the clinical neurophysiological investigations showed no abnormality; nerve conduction studies showed normal tibial motor conduction velocities, and ‘F’ waves recorded from flexor hallucis brevis were at a normal latency. The amplitudes of the sural and superficial peroneal nerve sensory action potentials were symmetrical between limbs. Concentric needle EMG sampling of L4-, L5and S1-innervated muscles showed no evidence of denervation. To better understand the anatomical relationships of the sacral foraminal lead when implanted, two cadavers were dissected, in addition to studying prosected specimens at The Royal College of Surgeons of England, London. The cadaveric dissections showed that there is Fig. 1. Dissection of the left hemipelvis with subsequent insertion a close association between the S3 nerve root and the of a sacral lead through the third sacral foramen. The probe is pointing to the third sacral root. sacral lead passed through the third sacral foramen