A modified transcondylar screw to accommodate anatomical skull base variations.

BACKGROUND: Occipitocervical instability may be attributed to congenital, bony/ligamentous abnormalities, trauma, neoplasm, degenerative bone disease, and failed atlantoaxial fixation. Indications for occipitocervical fixation include the prevention of disabling pain, cranial nerve dysfunction, paralysis, or even sudden death. METHODS: The screw trajectory for the modified transcondylar screw (mTCS) is optimally planned utilizing a three-dimensional skull reconstructed image. RESULTS: The modified mTCS technique is helpful where there is a loss of bone, such as after prior suboccipital craniotomy and/or an inadequate occipital condyle. The new proposed technique is similar to the classical transcondylar screw placement but follows a deeper course along the bony lip of foramen magnum toward clivus from a dorsolateral approach. CONCLUSION: The modified mTCS technique allows for direct visualization and, therefore, helps to avoid damage to the hypoglossal nerve and lateral aspect of brain stem.

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. INTERVENTION: A 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. CONCLUSION: Peripheral 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.

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

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.

Endoscopic carpal tunnel release surgery: report of patient satisfaction.

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.

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.

Supraclavicular glomus tumor, 20 year history of undiagnosed shoulder pain: a case report.

A long-standing case of severe dysesthesia due to a supraclavicular glomus tumor is presented. Chronic pain caused by a subcutaneous glomus (non-chemodectoma) tumor is rare and usually misdiagnosed. The supraclavicular location, presentation, and coincidence of trauma history are unique in this case. A 62-year-old male complained of 20 years of intractable right shoulder and supraclavicular region pain, which started 6 months after a fall. The pain was unrelieved by repeated and extensive physical therapy, chiropractic manipulation, local steroid injections, and two shoulder operations. The cause of the condition remained undiagnosed and obscure. Local surgical exploration revealed a subcutaneous grayish mass with pathologically proven glomus tumor. Immediate alleviation of the pain and tenderness followed complete resection of the mass. The patient remained free of pain at a 2-year follow-up. Subcutaneous glomus (non-chemodectoma) tumors can occur in unusual sites, and should be considered in chronic regional pain syndromes. Immediate cure is generally achieved by local resection. Pertinent literature is reviewed.

Monitoring spinal cord motor and somatosensory evoked potentials in anesthetized primates.

Monitoring Motor Evoked Potential (MEP) to Transcranial Stimulation (TMS) monitoring (MEP) is a growing technique to assess motor function under anesthesia. The following primate study was conducted to analyze the non-myogenic spinal motor and sensory volleys and to examine their reproducibility under nitrous oxide-methohexidone anesthesia. The traveling periodic spinal descending MEP to TMS and ascending somatosensory (SEP) to posterior tibial nerve stimulation across the thoracic cord were recorded in 12 cynomolgus monkeys. Through a small T11-T12 laminotomy, an insulated stainless steel electrode was inserted into the epidural thoracic space. The potentials were analyzed under 50 vol% NO in O2 with methohexital (0.1-0.2 mg kg-1 min-1). A well-defined periodic TMS-MEPs and PTN-SEPs were recorded with high reproducibility and consistency in repeated trials under N2O-methohexital anesthesia. MEP tracing consisted of an initial peak (direct (D) wave), occurring at 2.43 (+/- 0.28) msec followed by subsequent five positive (indirect (I) waves). Spinal SEPs-MEPs were clearly defined, morphologically stable, and consistent over time under N2O-methohexitone anesthesia. The present primate study may set a model to monitor both modalities in anesthetized neurosurgical patients.

Spinal cervical infection: a case report and current update.

Cervical spine infection is a term used to encompass osteomyelitis, discitis and epidural abscess. Most cases are caused by Staphylococcus aureus but other organisms have been isolated. The most frequent source is hematogenous spread from a nearby or distant source. Diagnosis is often confusing. The most common symptom is worsening back or neck pain that increases with movement. Patients may have motor or sensory changes if there is compression of the nerve roots or spinal cord. If the condition is not treated promptly, it may progress to irreversible neurologic deficit. Positive blood cultures and an elevated erythrocyte sedimentation rate (ESR) may be seen. Radiologic findings may include a paravertebral swelling, a destruction of the vertebral end plates and adjacent portions of the bodies and disc space and the presence of an epidural mass. Treatment includes radical surgical intervention for debridement and decompression to stabilize the spine in conjunction with 8-12 weeks of intravenous antibiotics. Closed continuous local antibiotic irrigation with a gravity control outflow system has been used.

Effect of nitric oxide synthase inhibition on the cerebral vascular response to hypercapnia in primates.

BACKGROUND AND PURPOSE: The role of nitric oxide in cerebrovascular response to changes in PCO2 is unclear. In the present study, we assessed responses at two levels of hypercapnia in a primate model before and after blockade of nitric oxide synthesis. METHODS: We compared the effects of two levels of hypercapnia, defined as PCO2 of approximately 70 mm Hg (high-CO2 group, n = 5) and PCO2 of approximately 50 mm Hg (moderate-CO2 group, n = 6), on increases in regional cerebral blood flow (microspheres) before and after inhibition of nitric oxide synthase with N omega-nitro-L-arginine methyl ester (L-NAME; 60 mg.kg-1) in isoflurane-anesthetized cynomolgus monkeys (1.0% end-tidal concentration). RESULTS: Before L-NAME administration, hypercapnia increased flow in all regions (eg, forebrain, high-CO2 group 69 +/- 10 to 166 +/- 15 mL.min-1.100 g-1; moderate-CO2 group, 49 +/- 7 to 93 +/- 15 mL.min-1.100 g-1) and decreased cerebral vascular resistance (high-CO2, 1.1 +/- 0.1 to 0.4 +/- 0.1 mm Hg.mL-1.min.100 g; moderate-CO2, 1.4 +/- 0.1 to 0.7 +/- 0.1 mm Hg.mL-1.min.100 g). During normocapnia, L-NAME decreased cerebral blood flow (high-CO2, 37 +/- 9%; moderate-CO2, 40 +/- 6%) and increased cerebral vascular resistance (high-CO2, 93 +/- 33%; moderate-CO2, 88 +/- 20%). After L-NAME, hypercapnia still increased blood flow in all regions (eg, forebrain: high-CO2, 56 +/- 7 to 128 +/- 3 mL.min-1.100 g-1, moderate-CO2, 36 +/- 5 to 57 +/- 8 mL.min-1.100 g-1) and decreased vascular resistance (high-CO2, 1.5 +/- 0.1 to 0.6 +/- 0.1 mm Hg.mL-1.min.100 g; moderate-CO2, 2.0 +/- 0.3 to 1.2 +/- 0.1 mm Hg.mL-1.min.100 g). In both groups L-NAME attenuated hypercapnia hyperemia by approximately 30% in cortex but not in other regions. CONCLUSIONS: Nitric oxide contributes to basal vascular tone but is not a major contributor to the mechanism of hypercapnia-induced cerebral vasodilation, except in cortex, in primates.

Cerebral blood flow in primates is increased by isoflurane over time and is decreased by nitric oxide synthase inhibition.

BACKGROUND: Cerebral blood flow (CBF) decreases over time in dogs and goats during volatile anesthesia. In the current study, we determined CBF during administration of isoflurane for 4 h in cynomolgus monkeys. In addition, we determined if nitric oxide (NO) contributes to cerebrovascular tone during isoflurane anesthesia by determining the CBF (microsphere) response to inhibition of NO synthase with N omega-nitro-L-arginine methyl ester (L-NAME). METHODS: CBF was measured in five monkeys anesthetized with isoflurane (1.0% end-tidal). After 4 h of isoflurane (1.0% = 1 MAC), the effects of intravenous L-NAME (60 mg/kg over 10 min) followed by intravenous L-arginine (600 mg/kg over 10 min) on CBF were measured at constant cerebral perfusion pressure and arterial carbon dioxide tension. RESULTS: CBF was unchanged over time (4 h) in cerebellum but increased by 50 +/- 18% in both forebrain and hindbrain (P < 0.05). CBF decreased by 41-48% (P < 0.05) 20 min after L-NAME in forebrain, cerebellum, and hindbrain, at which time brain NO synthase activity was less than 10% of baseline. Twenty minutes after L-arginine, CBF was increased in cerebellum by 32 +/- 8% and in forebrain by 41 +/- 9% (P < 0.05). The cerebral metabolic rate of oxygen consumption was unaffected by time or by L-NAME or L-arginine. CONCLUSIONS: These data demonstrate that CBF increases over time during isoflurane anesthesia in primates. Tonic production of NO contributes to control of CBF in primates during isoflurane anesthesia. Increased CBF by L-arginine after L-NAME supports the hypothesis that L-NAME decreases CBF via a mechanism requiring NO synthesis.

Monitoring the intracranial aneurysm patient.

The perioperative management of aneurysmal subarachnoidal haemorrhage is challenging and often requires an extensive team work. Unfortunately, there is no uniform system applied for perioperative monitoring of patients with subarachnoid haemorrhage. The new developing technology enhances our monitoring capability with subsequent impact on patient's outcome. This article presents a review of current monitoring modalities applicable to patients with subarachnoid haemorrhage with emphasis on the central nervous system and some of the authors' experience.

Cerebral oxygen metabolism during hypothermic circulatory arrest in humans.

Profound hypothermia with circulatory arrest is an important surgical adjuvant that allows protected cessation of cerebral blood flow for a brief period. In seven patients undergoing this procedure, continuous spectroscopic measurement of cerebral hemoglobin oxygen saturation was performed. Circulatory arrest at 18 degrees C was associated with a significant progressive desaturation (p < 0.01) of residual cerebral hemoglobin. Arrest time varied based on operative complexity (range 10 to 65 minutes), and a negative linear correlation between arrest time (y) and oxygen saturation (x) was noted (y = -0.87 x + 64). Five patients whose saturation remained above 35% had no neurological injury attributable to hypoxia. One patient (Hunt and Hess Grade 0) whose saturation fell below 35% had evidence of a global hypoxic injury at postmortem examination. Spectroscopically measured cerebral hemoglobin saturation (cerebral oximetry) may be used to monitor metabolic activity during circulatory arrest. Although the clinical utility of such monitoring cannot be established at this time, the potential may exist to prolong the safe duration of induced circulatory arrest for cerebral protection.

A comparative analysis of enflurane anesthesia on primate motor and somatosensory evoked potentials.

The effect of increasing enflurane concentration on magnetic-induced myogenic cranial (Cr) and peripheral (Pr) motor evoked potentials (MEPs), and electrically induced median (MN) and posterior tibial (PTN) somatosensory evoked potentials (SEPs) was studied in 10 monkeys. MEP, recorded from abductor pollicis brevis and abductor hallucis muscles, and SEP (short- and long-latency scalp recorded potentials) variables were examined at 0.25, 0.5, 0.75, 1.0 MAC enflurane concentrations. Cr-MEPs progressively attenuated (P less than 0.01) with 0.25 MAC and were abolished (greater than or equal to 0.75 MAC) by graded enflurane concentration. Stimulation threshold for Cr-MEP was progressively elevated (P less than 0.01), and eventually reliable responses were lost (greater than or equal to 0.75 MAC). Marked scalp zone reduction to obtain Cr-MEP responses was noted with increasing enflurane concentration. Pr-MEPs and most SEP peaks maintained good replicability but showed significant amplitude reduction (P less than 0.01). MEP and SEP latency values were not significantly delayed as long as the wave form remained identifiable. We conclude that enflurane has a differential influence on Cr-MEPs and SEPs. Administration of enflurane should be discouraged while monitoring myogenic Cr-MEPs since even a subanesthetic concentration is profoundly detrimental.

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.

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

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 magnetic 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 Tukey's 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 persist after recovery. Anesthetic doses of MDZ should cautiously be used in the settings of MEP monitoring.

The effect of etomidate on motor evoked potentials induced by transcranial magnetic stimulation in the monkey.

Etomidate (ET) is a known hypnotic agent in neuroanesthesia. This study was designed to examine the reliability of motor evoked potentials (MEPs) after transcranial magnetic stimulation in monkeys anesthetized intravenously with ET. The ET regimen was as follows: an initial dose (0.5 mg/kg) followed by 13 doses (0.2 mg/kg every 6-12 min; mean, 8.0 +/- 1.3 min). The total dose administered was 3.1 mg/kg. The magnetic coil was placed over the MEP scalp stimulation region. Evoked electromyographic responses were recorded from the contralateral abductor pollicis brevis (APB) and abductor hallucis (AH) muscles of the fore- and hindlimbs, respectively. Reproducible MEP responses were consistently recorded while the animal was under total ET anesthesia. The coil demography was altered and the MEP scalp topography was moderately reduced by ET injections. Significant threshold elevation was noted after a total dose of 1.7 mg/kg for APB responses and 0.5 mg/kg for AH responses (P less than 0.05). Marked prolongation of latency was observed after a dose of 0.5 mg/kg for APB MEPs and 2.5 mg/kg for AH MEPs (P less than 0.05). MEP amplitude responses showed marked variability. Repeated doses of ET produced a mean threshold rise of 14 to 28% for the APB and 19 to 29% for the AH. The mean latency delay was 5 to 11% for the APB and 0.5 to 8% for the AH, while the mean amplitude depression was 24 to 59% for the APB and 15 to 50% for the AH. Apparent seizure activity or abnormalities in behavior and feeding were not noted over a 1-year period.(ABSTRACT TRUNCATED AT 250 WORDS)