Object
Although nucleus ventralis intermedius stimulation has been shown to be safe and efficacious in the treatment of essential tremor, there is a subset of patients who eventually lose benefit from their stimulation. Proposed causes for this phenomenon include tolerance, disease progression, and suboptimal location. The goal of this study was to assess the factors that may lead to both stimulation failure, defined as loss of meaningful tremor relief, and less satisfactory outcomes, defined as leads requiring voltages > 3.6 V for effective tremor control.
Methods
The authors present their clinical outcomes from 31 leads in 27 patients who had effective tremor control for > 1 year following nucleus ventralis intermedius stimulation. All patients postoperatively had a mean decrease in both the writing and drawing subscales of the Fahn-Tolosa-Marin Tremor Rating Scale (p < 0.001).
Results
After a mean follow-up of 40 months, 22 patients continued to have tremor control with stimulation. Four patients eventually lost efficacy of their stimulation at a mean of 39 months. There was no difference in age, duration of disease, or disease severity between the groups. Examination of perioperative factors revealed that suboptimal anteroposterior positioning as evidenced on intraoperative fluoroscopy occurred significantly more frequently in patients with stimulation failure (p = 0.018). In patients with less satisfactory outcomes, no difference was seen between group demographics. Fluoroscopy again revealed suboptimal positioning more frequently in these patients (p = 0.005).
Conclusions
This study provides further evidence that suboptimal lead position in combination with disease progression or tolerance may result in less satisfactory long-term outcomes.
Total intravenous anesthesia (TIVA) with propofol and opioids is frequently utilized for spinal surgery when somatosensory evoked potentials (SSEPs) and transcranial motor evoked potentials (tcMEPs) are monitored. Many anesthesiologists would prefer to utilize low dose halogenated anesthetics (e.g. 1/2 MAC). We examined our recent experience using 3% desflurane or TIVA during spine surgery to determine the impact on propofol usage and on the evoked potential responses. After institutional review board approval we conducted a retrospective review of a 6 month period for adult spine patients who were monitored with SSEPs and tcMEPs. Cases were included for the study if anesthesia was conducted with propofol-opioid TIVA or 3% desflurane supplemented with propofol or opioid infusions as needed. We evaluated the propofol infusion rate, cortical amplitudes of the SSEPs (median nerve, posterior tibial nerve), amplitudes and stimulation voltage for eliciting the tcMEPs (adductor pollicis brevis, tibialis anterior) and the amplitude variability of the SSEP and tcMEP responses as assessed by the average percentage trial to trial change. Of the 156 spine cases included in the study, 95 had TIVA with propofol-opioid (TIVA) and 61 had 3% expired desflurane (INHAL). Three INHAL cases were excluded because the desflurane was eliminated because of inadequate responses and 26 cases (16 TIVA and 10 INHAL) were excluded due to significant changes during monitoring. Propofol infusion rates in the INHAL group were reduced from the TIVA group (average 115-45 μg/kg/min) (p<0.00001) with 21 cases where propofol was not used. No statistically significant differences in cortical SSEP or tcMEP amplitudes, tcMEP stimulation voltages nor in the average trial to trial amplitude variability were seen. The data from these cases indicates that 1/2 MAC (3%) desflurane can be used in conjunction with SSEP and tcMEP monitoring for some adult patients undergoing spine surgery. Further studies are needed to confirm the relative benefits versus negative effects of the use of desflurane and other halogenated agents for anesthesia during procedures on neurophysiological monitoring involving tcMEPs. Further studies are also needed to characterize which patients may or may not be candidates for supplementation such as those with neural dysfunction or who are opioid tolerant from chronic use.
To provide an educational service to the intraoperative neurophysiologist community by publishing a position statement by the American Society of Neurophysiological Monitoring on the recommended appropriate and correct use of somatosensory evoked potentials as an intraoperative neurophysiological monitoring tool to protect patient well-being during surgery. This position statement presents the somatosensory evoked potential utilization basis, relevant anatomy, patient preparation, important systemic factors, anesthesia considerations, safety and technical considerations, documentation requirements, neurophysiologist credentials and staffing practice patterns, and monitoring applications for protecting brain, spinal nerve root, peripheral nerve, plexus and spinal cord function. In conclusion, a summary of major recommendations regarding the use of somatosensory evoked potentials in intraoperative neurophysiological monitoring is presented.
We have studied the effect of i.v. midazolam on median nerve somatosensory evoked potentials (SSEP) in 10 unpremedicated adults. Anaesthesia was induced with midazolam by bolus administration (0.2 mg kg-1) followed by infusion (5 mg h-1). The latency and amplitudes of the SSEP responses over the second cervical vertebrae (SC2) and sensory cortex (P17, N20, P25) were recorded before and for 10 min after induction. Data were analysed over that period for time-related alterations. Small but statistically significant increases in latency of the cortical N20 (P less than 0.005) and P25 (P less than 0.001) waves and interwave conduction times of SC2 to P25 (P less than 0.005) and N20 to P25 (P less than 0.021) were observed. Cortical amplitude (N20-P25) decreased significantly (P less than 0.012), to approximately 60% of baseline. These results demonstrated that midazolam produced a depression of cortical SSEP amplitude without clinically significant alterations in latency.
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