Transabdominal motor evoked potential neuromonitoring of lumbosacral spine surgery.

Background Context: Transcranial Motor Evoked Potentials (TcMEPs) can improve intraoperative detection of femoral plexus and nerve root injury during lumbosacral spine surgery. However, even under ideal conditions, TcMEPs are not completely free of false-positive alerts due to the immobilizing effect of general anesthetics, especially in the proximal musculature. The application of transcutaneous stimulation to activate ventral nerve roots directly at the level of the conus medularis (bypassing the brain and spinal cord) has emerged as a method to potentially monitor the motor component of the femoral plexus and lumbosacral nerves free from the blunting effects of general anesthesia.

Misconceptions in IONM Part III: Stimulation Repetition Rate Effects on Intraoperative Somatosensory Evoked Potential Amplitude and Latency.

The rate at which stimulation is applied to peripheral nerves is critical to generating high-quality intraoperative somatosensory evoked potentials (SSEPs) in a timely manner. Guidelines based on a limited study and anecdotal evidence present differing, incorrect, or incomplete stimulation rate recommendations. We examined the effect stimulating the ulnar and tibial nerves at 1.

Misconceptions in IONM Part II: Does Anodal Blocking Occur and Is Bipolar Stimulation Necessary with Intraoperative Somatosensory Evoked Potentials?

Current intraoperative somatosensory evoked potential (SSEP) guidelines recommend bipolar stimulation with the anode at or near the crease of the wrist and the cathode 2-4 cm proximal to the anode for median nerve SSEPs. The rationale for this cathode proximal bipolar configuration appears to be the avoidance of anodal blocking; however, there is a paucity of experimental support for the existence of anodal blocking. Evidence that bipolar stimulation preferentially drives stimulation from the cathode better than monopolar cathodal or monopolar anodal in peripheral nerves in human neurophysiology is also lacking.

Intraoperative transabdominal MEPs: four case reports.

Four recent cases utilizing transabdominal motor-evoked potentials (TaMEPs) are presented as illustrative of the monitoring technique during lumbosacral fusion, sciatic nerve tumor resection, cauda equina tumor resection, and lumbar decompression. Case 1: In a high-grade lumbosacral spondylolisthesis revision fusion, both transcranial motor-evoked potentials (TcMEPs) and TaMEPs detected a transient focal loss of left tibialis anterior response in conjunction with L5 nerve root decompression. Case 2: In a sciatic nerve tumor resection, TcMEPs responses were lost but TaMEPs remained unchanged, the patient was neurologically intact postoperatively.

Misconceptions in IONM Part I: Interleaved Intraoperative Somatosensory Evoked Potential Stimulation.

A misconception in the field of intraoperative neurophysiological monitoring (IONM) is that continuous, multi-nerve (four-limb), interleaved somatosensory evoked potential (SSEP) stimulation, while advantageous, is not universally utilized due to variety of misunderstandings regarding this approach to SSEP stimulation. This article addresses the rationale for this misconception. We find that continuous, multi-nerve, interleaved SSEP stimulation is superior to all other stimulation paradigms in most operative scenarios, allowing the fastest acquisition of SSEPs at low stimulation repetition rates, which generate the highest amplitude cortical responses.

Lateral mass screw stimulation thresholds in posterior cervical instrumentation surgery: a predictor of medial deviation.

OBJECTIVE Normative data exists for stimulus-evoked pedicle screw electromyography (EMG) current thresholds in the lumbar spine, and is routinely referenced during spine surgeries to detect a screw breach, prevent injury of neural elements, and ensure the most biomechanically sound instrumentation construct. To date, similar normative data for cervical lateral mass screws is limited, thus the utility of lateral mass screw testing remains unclear. To address this disparity, in this study the authors describe cumulative lateral mass screw stimulation threshold data in patients undergoing posterior cervical instrumentation with lateral mass screws.

Use of Posterior Root-Muscle Reflexes in Peripheral Nerve Surgery: A Case Report.

It is well established that a mixed-agent general anesthetic regimen of volatile gas and intravenous anesthetic or total intravenous anesthetic (TIVA) is required to obtain adequate transcranial motor-evoked potentials (TcMEPs) to detect and hopefully prevent injury during brain, spinal cord, and peripheral nerve surgery. But even under ideal general anesthetic conditions, TcMEPs are not always detectable in every muscle monitored, and are prone to anesthetic fade, especially when neuropathic or injured tissue is monitored. TcMEP sensitivity to general anesthesia can be especially problematic during peripheral nerve surgery where there is often only one or a few essential muscles required to provide adequate monitoring; thus, maximum fidelity is essential.

Vasculopathy, Ischemia, and the Lateral Lumbar Interbody Fusion Surgery: Report of Three Cases.

Multi-modal neurophysiologic monitoring consisting of triggered and spontaneous electromyography and transcranial motor-evoked potentials may detect and prevent both acute and slow developing mechanical and vascular nerve injuries in lateral lumbar interbody fusion (LLIF) surgery. In case report 1, a marked reduction in the transcranial motor-evoked potentials on the operative side alerted to a 28% decrease in mean arterial blood pressure in a 54-year-old woman during an L3-4, L4-5 LLIF. After hemodynamic stability was regained, transcranial motor-evoked potentials returned to baseline and the patient suffered no postoperative complications.

Anesthesia considerations for monitoring TCMEPs in adults diagnosed with poliomyelitis as children: a case report.

Unlabelled: The use of transcranial motor evoked potentials (TCMEPs) to detect and hopefully prevent injury to the brain, spinal cord, and peripheral nerves intraoperatively has increased greatly in recent years. It is well established that in addition to certain anesthetic agents, patient factors such as advanced age, obesity, diabetes, hypertension, and a collection of neurological and neuromuscular diseases and disorders can greatly reduce or completely eliminate the ability to monitor TCMEPs effectively. One such disease, poliomyelitis (polio), is a highly contagious viral disease that has been mostly forgotten since its near-eradication through vaccination.

The role of connexin-36 gap junctions in alcohol intoxication and consumption.

Ventral tegmental area (VTA) GABA neurons appear to be critical substrates underlying the acute and chronic effects of ethanol on dopamine (DA) neurotransmission in the mesocorticolimbic system implicated in alcohol reward. The aim of this study was to examine the role of midbrain connexin-36 (Cx36) gap junctions (GJs) in ethanol intoxication and consumption. Using behavioral, molecular, and electrophysiological methods, we compared the effects of ethanol in mature Cx36 knockout (KO) mice and age-matched wild-type (WT) controls.

Mefloquine effects on ventral tegmental area dopamine and GABA neuron inhibition: a physiologic role for connexin-36 GAP junctions.

Connexin-36 (Cx36) gap junctions (GJs) appear to be involved in the synchronization of GABA interneurons in many brain areas. We have previously identified a population of Cx36-connected ventral tegmental area (VTA) GABA neurons that may regulate mesolimbic dopamine (DA) neurotransmission, a system implicated in reward from both natural behaviors and drugs of abuse. The aim of this study was to determine the effect mefloquine (MFQ) has on midbrain DA and GABA neuron inhibition, and the role Cx36 GJs play in regulating midbrain VTA DA neuron activity in mice.

Ventral tegmental area BDNF induces an opiate-dependent-like reward state in naive rats.

The neural mechanisms underlying the transition from a drug-nondependent to a drug-dependent state remain elusive. Chronic exposure to drugs has been shown to increase brain-derived neurotrophic factor (BDNF) levels in ventral tegmental area (VTA) neurons. BDNF infusions into the VTA potentiate several behavioral effects of drugs, including psychomotor sensitization and cue-induced drug seeking.

Acute and chronic ethanol modulate dopamine D2-subtype receptor responses in ventral tegmental area GABA neurons.

Background: Ventral tegmental area (VTA) gamma-aminobutyric acid (GABA) neurons appear to be critical substrates underlying the acute and chronic effects of ethanol on dopamine (DA) neurotransmission in the mesocorticolimbic system implicated in drug reward. VTA GABA neuron firing rate is reduced by acute ethanol and enhanced by DA via D2 receptor activation. The objective of this study was to evaluate the role of D2 receptors in acute ethanol inhibition of VTA GABA neuron activity, as well as the adaptation of D2 receptors by chronic ethanol consumption.

Cocaine disinhibits dopamine neurons in the ventral tegmental area via use-dependent blockade of GABA neuron voltage-sensitive sodium channels.

The aim of this study was to evaluate the effects of cocaine on gamma-aminobutyric acid (GABA) and dopamine (DA) neurons in the ventral tegmental area (VTA). Utilizing single-unit recordings in vivo, microelectrophoretic administration of DA enhanced the firing rate of VTA GABA neurons via D2/D3 DA receptor activation. Lower doses of intravenous cocaine (0.

Dehydroepiandrosterone sulfate and estrone sulfate reduce GABA-recurrent inhibition in the hippocampus via muscarinic acetylcholine receptors.

Several recent studies have established a role for estrogens in ameliorating specific neurodegenerative disorders, mainly those associated with the cholinergic neurons of the basal forebrain and their targets in the cortex and hippocampus. We have previously demonstrated that endogenous and exogenous application of the neurosteroid dehydroepiandrosterone sulfate (DHEAS) markedly reduces GABA-mediated recurrent inhibition and synchronizes hippocampal unit activity to theta rhythm (Steffensen (1995) Hippocampus 5:320-328). In this study, we evaluated the role of muscarinic receptors in mediating the effects of DHEAS and estrone sulfate (ES), the principal circulating estrogen in humans, on short-latency-evoked potential responses, paired-pulse inhibition (PPI), paired-pulse facilitation, and GABA interneuron activity in the dentate gyrus and CA1 subfields of the rat hippocampus.

Connexin-36 gap junctions mediate electrical coupling between ventral tegmental area GABA neurons.

Communication between neurons in the mammalian brain is primarily through chemical synapses; however, evidence is accumulating in support of electrical synaptic transmission between some neuronal types in the mature nervous system. The authors have recently demonstrated that the gap junction (GJ) blocker quinidine suppresses stimulus-induced and dopamine-evoked coupling of gamma amino butyric acid (GABA) neurons in the ventral tegmental area (VTA) of mature rats (Stobbs et al., 2004).

Frontal sinus fractures in children.

Objective: To review the epidemiologic characteristics, clinical course, and management of pediatric patients with frontal sinus fractures.

Methods: Retrospective review of 120 patients with maxillofacial fractures who presented to a tertiary children's hospital from 1998 to 2003 revealed 11 patients with frontal sinus fractures.

Results: The study group included 9 males and 2 females with a mean age of 9.

Ethanol suppression of ventral tegmental area GABA neuron electrical transmission involves N-methyl-D-aspartate receptors.

Ventral tegmental area (VTA) GABA neurons are critical substrates modulating the mesocorticolimbic dopamine system implicated in natural and drug reward. The aim of this study was to evaluate the effects of ethanol on glutamatergic and GABAergic modulation of VTA GABA neuron electrical synaptic transmission. We evaluated the effects of systemic ethanol (0.

Targeted disruption of RC3 reveals a calmodulin-based mechanism for regulating metaplasticity in the hippocampus.

We used homologous recombination in the mouse to knock-out RC3, a postsynaptic, calmodulin-binding PKC substrate. Mutant brains exhibited lower immunoreactivity to phospho-Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) but had the same synaptic density as wild type and did not exhibit a gross neuroanatomical phenotype. Basal excitatory synaptic transmission in CA1 was depressed, long-term potentiation (LTP) was enhanced, and the depressant effects of the metabotropic glutamate receptor (mGluR) agonist (RS)-3,5-dihydroxyphenylglycine was occluded compared with littermate controls.