Ramsis F. Ghaly

Effects of Incremental Ketamine Hydrochloride Doses on Motor Evoked Potentials (meps) Following Transcranial Magnetic Stimulation: A Primate Study

Summary the cumulative dose effect of ketamine hydrochloride (KH) on transcranial magnetic-induced motor evoked potentials (MEPs) was examined in monkeys. Electromyographic (EMG) responses were recorded from the contralateral abductor pollicis brevis (APB) and abductor hallucis (AH) muscles. MEP brain stimulation threshold, latency, and amplitude values were studied. After obtaining baseline recordings, increments of KH (5 mg/kg every 15–20 min) were given i.v. (50 mg/kg total dose). MEPs were repeatedly recorded following KH injections. No loss of potentials was encountered in any animal. However, KH induced significant MEP latency delay in doses ≥35–40 mg/kg and amplitude depression in doses ≥15–20 mg/kg (p < 0.01). Under various KH doses, the amplitude depression ranged from 13.6 to 45.5% for APB and 57.3 to 82% for AH compared to the control values. The MEP latency prolongation ranged from 3.5 to 18% for APB and 4.2 to 13.1% for AH. The stimulation threshold rise ranged from 6.7 to 14.7% for APB and 7 to 17.9% for AH. Statistical correlation was closest between cumulative KH doses and MEP latency prolongation. We conclude that, in the primate model, reliable MEP recording is feasible under deep KH anesthesia. However, awareness of drug-induced response alterations is essential during interpretation of intraoperative MEP changes. Further investigation is warranted regarding the specific dose effect in humans and safety of magnetic stimulation.

Recovery after high-dose methylprednisolone and delayed evacuation: a case of spinal epidural hematoma.

Spinal epidural hematoma (SEH) is rare and not without serious sequelae. We report a patient who developed Brown-Séquard syndrome from SEH after fluoroscopic-guided cervical steroid injection and favorable response to methylprednisolone (MP). A 56-year-old man reported immediate sharp shooting pain to the upper extremities on introduction of epidural toughy needle. A total of 5 mL of 0.2% ropivacaine and 120 mg methylprednisolone acetate suspension was administered at the C6–7 interspace. Within half an hour, a neurologic deficit occurred at C7–8 and right Brown-Séquard syndrome developed. Once SEH was suspected (3 hours after onset of neurologic deficit), a protocol of high-dose MP intravenous infusion was initiated. Immediate incomplete recovery of motor, sensory, and sphincteric functions was noted within 30 minutes of infusion. Emergency spinal C6–T2 bilateral decompressive laminectomies and evacuation SEH were performed within an expected delay (10 hours from the onset of neurologic deficit). Fluoroscopic guidance does not take the place of adherence to meticulous technique. An unexplained neurologic deficit after invasive spinal procedures should raise the concern for SEH. Early recognition and emergent evacuation remain the mainstay management for SEH. This case suggests some neuroprotection from MP in cases of cervicothoracic cord compression secondary to traumatic SEH. When potential risks for SEH exist, it is advisable not to administer local anesthetic so as not to interfere with neurologic assessment and delaying the diagnosis.

A posterior tibial nerve neurilemoma unrecognized for 10 years: case report.

OBJECTIVE AND IMPORTANCE Neoplasms of peripheral nerves can be obscured, especially during the early phase. The author reports a patient with a posterior tibial nerve neurilemoma (schwannoma). For a decade, the tumor was misdiagnosed as nonspecific S1 radiculopathy and psychogenic chronic pain syndrome. The patient’s presentation and initial management are unique. CLINICAL PRESENTATION A 40-year-old woman reported severe left foot and calf pain, numbness, and weakness. The symptoms were evident during three pregnancies, and they gradually progressed. The neuropathic pain was protracted, despite implantation of a dorsal column stimulator and administration of a wide variety of medications and therapies. The symptoms were unresponsive to both inpatient and outpatient treatments, which resulted in a misdiagnosis of psychogenic pain for more than a decade. Diagnostic scans obtained by computed tomography, ultrasonography, and nuclear scintigraphy confirmed a popliteal fossa mass. INTERVENTIONA high, large posterior tibial nerve neurilemoma was found intraoperatively, positioned just below the sciatic nerve bifurcation with extensive degenerative features and hemorrhages. Surgical resection provided immediate recovery. CONCLUSIONPeripheral nerve tumors are rarely acknowledged clinical entities. Chronic unexplained foot and calf pain and a positive Tinel’s sign should raise suspicion of posterior tibial nerve neurilemoma. Even in patients who have had such tumors for a decade, surgical resection remains the treatment of choice.

Evoked potentials in head injury and states of increased intracranial pressure.

Recent clinical studies have addressed the utility of sensory evoked potentials (auditory, somatosensory, and visual) in head injury. The clinical significance of evoked potentials in head trauma, states of increased intracranial pressure, and post-traumatic syndrome is discussed. Emphasis is placed on up-to-date studies discussing evoked potential correlation with clinical findings, lesion localization, intracranial pressure, brain herniation, and prognosis.

The effect of an anesthetic induction dose of midazolam on motor potentials evoked by transcranial magnetic stimulation in the monkey

&NA; The effect of a hypnotic dose (0.5 mg/kg) of midazolam (MDZ) on motor evoked potentials (MEPs) was examined in 12 monkeys. MEPs were elicited by transcranial magenetic stimulation (TMS) and the resultant potentials recorded from abductor pollicis brevis (APB) and anterior tibialis (AT) muscles contralateral to the stimulation site. After administration of MDZ, sequential MEP recordings were obtained at postinduction, hypnosis, awakening, emergence, and recovery periods. The results were compared with control values using one-way analysis of variance and Tukeys post-hoc test. Under hypnosis, MEP reproducibility was problematic as the potentials were occasionally ill identified and questionable. MDZ resulted in marked MEP scalp field reduction, coil demography alteration, stimulation threshold elevation, and amplitude suppression (p <0.01). Latency response was unaltered. During hypnosis, awakening, and recovery periods, the mean APB and AT thresholds were elevated by 39, 23, and 0% and by 60, 34, and 4% respectively; while APB and AT amplitudes were depressed by 95, 86, and 53% and by 99, 91, and 60%, respectively. We conclude that an induction dose of MDZ can produce profound and prolonged attenuation of TMS MEPs. The drug inhibitory effect on MEPs may perist after recovery. Anesthetic doses of MDZ should cautiously be used in the settings of MEP monitoring.

The effect of nitrous oxide on transcranial magnetic-induced electromyographic responses in the monkey.

Summary Transcranial magnetic stimulation (TMS) to produce motor evoked potentials (MEPs) is a newly developed intraoperative modality to monitor functional integrity of the motor pathways. The present study was designed to examine the reliability of magnetic MEP recording under nitrous oxide (N2O) inhalation. Following ketamine injection (10 mg/kg i.m.) and endotracheal intubation, 16 monkeys were exposed to N2O:O2 mixture ratios 1:3, 1:1, and 3:1. Electromyographic (EMG) responses, evoked by pulsed magnetic fields applied extracranially to the scalp zone overlying motor cortex, were recorded from the contralateral fore- and hind limb flexor muscles. The scalp topography zone for contralateral muscle excitation was markedly reduced by 75 vol% N2O. Significant stimulation threshold elevation, latency prolongation, and amplitude depression were noted after inhalation of 75 vol% N2O (p <0.05) compared with ≤50 vol% N2O inhalation. The mean range of brain stimulation rise was 1%, 7–8%, and 13–20%, and MEP latency delay was 3%, 3–6%, and 7–11% on exposure to 25%, 50%, and 75 vol% N2O, respectively. The mean amplitude response first increased by 20% and 7% with 25% and 50% N2O, respectively, and then reduced by 60% with 75 vol%. We conclude that, in a primate model, while magnetic MEPs could reliably be recorded under 25–75% N2O, the evoked motor responses were least affected by ≤50 vol% inhalation. Knowledge of N2O-induced MEP alteration is essential when interpreting the response change while using this agent.

High-dose ketamine hydrochloride maintains somatosensory and magnetic motor evoked potentials in primates

Abstract Monitoring the descending neural motor volleys (MEPs), in comparison to muscle action potentials, allows sensitive motor assessment under anesthesia irrespective of the use of muscular blockade and status of skeletal musculature. Ketamine hydrochloride (KH) had preserved muscle MEPs on a pre-established primate model. The present work examines the effect of incremental hypnotic KH dosages thoracic neural on somatosensory (SEP) and MEPs recorded epidurally in response to transcranial magnetic stimulation (TMS). Through a small thoracic T11-T12 laminotomy, an insulated double bipolar electrode was inserted epidurally and cephalad in seven cynomolgus monkeys. Thoracic spinal TMS-MEPs, and SEPs, were tested against graded increase of KH doses (0.01, 0.018, 0.032, 0.056, 0.1, and 0.18 mg kg-1 min-1 i.v. infusion). The direct (D-) and indirect (I-) epidural MEP peaks were well-defined under sole KH infusion. The waveforms were consistent at various dosages. At the highest cumulative dose (0.18 mg kg-1 min-1, total 6.5 mg kg-1 over 150 min), I5 was host and I3 and I4 latencies were delayed. The scalp and spinal SEP showed no significant change. Recording of both neural D- and I- MEPs and SEPs is feasible under high sole i.v. KH. It is the first agent to maintain up to four later I1 peaks. The reproducibility of both modalities is unquestionable under KH-based deep anesthesia. This reflects the maintenance of state of neural excitability under KH. [Neurol Res 2001; 23: 881-886]

Endoscopic carpal tunnel release surgery: Report of patient satisfaction

Abstract Recently, a trend has developed to use an endoscope to achieve carpal tunnel release. Proponents of the endoscopic technique believe it has benefits to patients that include minimal incision, minimal pain and scarring, a shortened recovery period and a high level of patient satisfaction. To test these beliefs, a retrospective analysis of the first 42 cases that were done between May 1997 and June 1998 was completed. Endoscopic carpal tunnel release surgery was performed on patients with the classical clinical and neurophysiological findings of carpal tunnel syndrome. The procedure was performed in an outpatient surgery center under primarily local anesthesia and by the same neurosurgeon (RG), who was blind to data analysis. The biportal technique (Instratek Inc., Houston, TX, USA) was used as described by Brown. The first 42 patients (n = 35, seven patients had bilateral surgeries) were sent a survey (modified Health Outcomes Carpal Tunnel Questionnaire, Health Outcomes, Bloomington, MN, USA) that measured a wide spectrum of variables, with a year follow-up. Patient demography indicated wide patient selection. All subjects (100%) had claimed work-related injury. Patient satisfaction was reported in 86%. No or mild incisional pain, night pain, absent tingling, and improved grip strengthening were reported in 100%, 95%, 81%, and 85% respectively. The mean for return to daily activity and work was 14 and 25 days respectively. No recurrent hematoma, infection, or structure injury was reported. Endoscopic carpal tunnel release can be done safely and effectively with excellent self-reports of patient satisfaction. Reduced recovery period and hospitalization with minimal tissue violation and incisional pain can be expected. [Neurol Res 2000; 22: 551-555]

Etomidate dose-response on somatosensory and transcranial magnetic induced spinal motor evoked potentials in primates

There is growing interest and need to monitor reliably both motor (MEP) and somatosensory (SEP) evoked potentials under anesthesia. On a pre-established primate model, the present study examined the effect of incremental etomidate (ET) dosages on spinal neural MEPs to transcranial magnetic stimulation (TMS) and posterior tibial rate (PTN) SEPs. Through a small thoracic T11-T12 laminotomy, an insulated double bipolar electrode was inserted epidurally in seven cynomolgus monkeys. Spinal TMS-MEPs, PTN-SEPs, and frontal EEG were tested against graded increase of ET doses. Etomidate 0.5 mg kg-1 i.v. was initially given and followed by 30 min continuous infusion of 0.01 mg kg-1 min-1, 0.018, 0.032, 0.056, 0.1, and 0.18 mg kg-1 min-1 in that order. Measurable spinal MEPs and SEPs were recorded under deep ET anesthesia (total 12.38 mg kg-1 cumulative dose over 180 min). The EEG showed marked slow wave and graded burst suppression at cumulative dose of > or = 3.14 mg kg-1. The direct (D) and subsequent initial indirect (I) waves (I1, I2, I3) were reproducible at doses < 0.18 mg kg-1 min-1 infusion. The latter I-waves (I4 and I5) showed graded loss at infusion dosage 0.056 mg kg-1 min-1. Etomidate remains an anesthetic of attractive features in neuroanesthesia. In the primate model, neural MEPs-SEPs were reproducible despite the exceedingly high dose of ET and markedly depressed EEG. Moreover, MEP-SEP can be monitored during ET burst-suppressive neuroprotective state. The study may set a model in humans for intra-operative multi-modality neurophysiologic recording under ET-based anesthesia.

The effect of neuroleptanalgesia (droperiodol-fentanyl) on motor potentials evoked by transcranial magnetic stimulation in the monkey.

Motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) have been examined in 12 monkeys under neuroleptanalgesia (NLA). Compound muscle action potentials were recorded from abductor policis brevis (APB) and gastroncnemius (GN) muscles contralateral to the stimulation site. After obtaining baseline tracings during emergence from methohexitone, 10 mg/kg i.m., NLA was induced using droperiodol, 0.3 mg/kg i.v. followed by fentanyl, 0.006 mg/kg i.v. Sequential MEP recordings were obtained 10 min after i.v. droperiodol, 2, 8, and 16 min after i.v. fentanyl, and during recovery. Replicable TMS MEPs were consistently recorded under NLA. However, droperidol and fentanyl caused significant stimulation threshold elevation, amplitude depression, and latency delay compared to control values (p <0.01). Ten minutes after droperiodol administration, the APB-GN threshold, amplitude, and latency values (mean +/- SD) were 0.81 +/- 0.2-0.84 +/- 0.1 T (baseline 0.57 +/- 0.1-0.59 +/- 0.1 T), 3.4 +/- 2.1-4.0 +/- 2.5 mV (baseline 8.0 +/- 3.7-9.0 +/- 3.7 mV), and 15.8 +/- 1.3-21.1 +/- 1.2 ms (baseline 14.9 +/- 1.2-20.1 +/- 1.3 ms), respectively. Addition of fentanyl resulted in further response deterioration. Two minutes after fentanyl injection, the APB-GN threshold, amplitude, and latency values were 0.88 +/- 0.18-0.95 %% 0.15 T, 2.1 +/- 1.7-2.0 +/- 2.1 mV, and 16.0 +/- 1.4-21.9 +/- 1.3 ms, respectively. Subsequent MEPs revealed gradual response improvement but, in contrast to baseline, remained markedly altered (p <0.05). During the recovery period (53 +/- 6 min), the APB-GN threshold, amplitude, and latency measurements were 0.66 +/- 0.1-0.77 +/- 0.2 T, 4.4 +/- 3.1-4.2 +/- 2.9 mV, 15.5 %% 1.4-20.9 +/- 1.7 ms, respectively. We conclude that, in a primate model, NLA maintains measurable TMS MEPs. Nevertheless, droperiodol and fentanyl produce significant and prolonged response alterations. Knowledge of these changes, while administering NLA drugs intraoperatively, is essential to interpretation of MEP data.