Abstract
To optimize the technique of implanting laminotomy plate electrodes for spinal cord stimulation and to minimize the discomfort of the patients during surgery. This operation is often performed while the patient is under local anesthesia, which is very stressful for the patient, or under general anesthesia, which precludes the use of test stimulation. An alternative approach is to perform the implantation with a spinal anesthetic and to examine whether stimulation-induced paresthesiae can still be evoked to guide the positioning of the electrode. Spinal anesthesia was induced by bupivacaine (12.5-20 mg), which produced complete motor block and anesthesia up to a midthoracic level. After a single-level laminotomy (thoracic vertebrae 9-11) a four-pole plate electrode was inserted into the epidural space. Stimulation was applied with commonly used parameters, and the electrode was positioned so that the paresthesiae covered the painful region. In 19 patients (20 procedures) with different forms of neuropathic pain, implantation of laminotomy plate electrodes could be performed under spinal anesthesia without problems. In all patients, it was possible to evoke paresthesiae, the distribution of which could be reproduced postoperatively. The paresthesia thresholds during surgery were only moderately higher than those recorded after implantation (mean, 3.1 versus 2.1 V, respectively). During an interview after the intervention, no patient reported that he or she had experienced surgery as painful or uncomfortable. Implantation of laminotomy electrodes can be performed conveniently with spinal anesthesia because it minimizes discomfort for the patient and enables the use of intraoperative test stimulation to guide the positioning of the electrode. In spite of the total motor block and anesthesia, paresthesiae representing the activation of the dorsal columns can be evoked and are well perceived, and the thresholds are not abnormally high. This observation supports the notion that the subarachnoidal anesthetic agent acts predominantly on the spinal rootlets rather than on the spinal afferent pathways.
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