AOSpine Consensus Paper on Nomenclature for Working-Channel Endoscopic Spinal Procedures.

STUDY DESIGN: International consensus paper on a unified nomenclature for full-endoscopic spine surgery. OBJECTIVES: Minimally invasive endoscopic spinal procedures have undergone rapid development during the past decade. Evolution of working-channel endoscopes and surgical instruments as well as innovation in surgical techniques have expanded the types of spinal pathology that can be addressed. However, there is in the literature a heterogeneous nomenclature defining approach corridors and procedures, and this lack of common language has hampered communication between endoscopic spine surgeons, patients, hospitals, and insurance providers. METHODS: The current report summarizes the nomenclature reported for working-channel endoscopic procedures that address cervical, thoracic, and lumbar spinal pathology. RESULTS: We propose a uniform system that defines the working-channel endoscope (full-endoscopic), approach corridor (anterior, posterior, interlaminar, transforaminal), spinal segment (cervical, thoracic, lumbar), and procedure performed (eg, discectomy, foraminotomy). We suggest the following nomenclature for the most common full-endoscopic procedures: posterior endoscopic cervical foraminotomy (PECF), transforaminal endoscopic thoracic discectomy (TETD), transforaminal endoscopic lumbar discectomy (TELD), transforaminal lumbar foraminotomy (TELF), interlaminar endoscopic lumbar discectomy (IELD), interlaminar endoscopic lateral recess decompression (IE-LRD), and lumbar endoscopic unilateral laminotomy for bilateral decompression (LE-ULBD). CONCLUSIONS: We believe that it is critical to delineate a consensus nomenclature to facilitate uniformity of working-channel endoscopic procedures within academic scholarship. This will hopefully facilitate development, standardization of procedures, teaching, and widespread acceptance of full-endoscopic spinal procedures.

Tandem interbody fusion grafting after cervical vertebrectomy.

STUDY DESIGN: A case is presented with clinical and radiologic follow-up assessment to evaluate the possible effectiveness of tandem interbody fusion grafting. OBJECTIVE: To design a technique for rescuing a long iliac crest bone autograft that is too short or must be shortened because of the undesirable shape some long iliac crest grafts can take. SUMMARY OF BACKGROUND DATA: Supplementing a larger piece of autograft with a smaller piece in tandem is suggested in this report as a potentially valuable technique for a surgeon presented with a large but inadequate piece of autograft. METHODS: Instead of requiring a second incision to remove iliac crest from the other side or an allograft, the technique described in this report uses a small piece of iliac crest laid in tandem with the original strut graft to span the vertebrectomy channel. RESULTS: A case of an anterior cervical vertebrectomy using a tandem strut graft resulted in good clinical and radiographic results. CONCLUSIONS: Tandem graft placement can salvage a graft that is of inadequate final length.

Postoperative epilepsy in patients undergoing craniotomy for glioblastoma multiforme.

Glioblastoma multiforme (GBM) has associated with it one of the poorest prognoses among brain tumors. Postoperative seizures and the side effects of anticonvulsants, routinely given for prophylactic purposes, add to patient morbidity. The primary goal of this study was to determine who, of those undergoing craniotomy for GBM resection, is at risk for epilepsy. We studied 72 consecutive patients who underwent craniotomy and palliative resection for GBM. Twenty-nine presented with seizures and 17 had postoperative seizures. All patients were treated with a postoperative anticonvulsant for at least six months; anticonvulsants were continued longer if there was a postoperative seizure. Patient factors examined for an association with risk for postoperative seizure included age, sex, tumor size, tumor location, adjuvant therapy, postoperative complications and history of preoperative seizures. The majority of patients with no prior seizure history and who seized postoperatively had their first seizure after withdrawal from their anticonvulsant medication. All, but one, of the patients with both pre- and postoperative seizures had their first postoperative seizure while still on anticonvulsants. Smaller tumor size and frontal resection were associated with an increased risk of postoperative seizures. Our data suggests that those who do not present with seizures and undergo GBM resection may still be prone to seize but more easily protected from postoperative seizures with anticonvulsant therapy than patients who present with seizures; resection of frontal tumors and smaller tumors seemed to indicate an increased risk for postoperative seizures.

Results and risk factors for anterior cervicothoracic junction surgery.

OBJECT: Stabilization of the cervicothoracic junction (CTJ) requires special attention to the operative approach and biomechanical requirements of the fixation construct. In this study the authors assess the morbidity associated with the anterior approach to the CTJ and define risks that may lead to construct failure after anterior CTJ surgery. METHODS: Data obtained for 14 patients (six men and eight women, mean age 50.1 years) who underwent surgical stabilization of the CTJ via an anterior cervical approach were retrospectively reviewed to assess the anterior approach-related morbidity and the risks of construct failure. The mean follow-up period was 21.1 months. Four patients (29%) had previously undergone CTJ surgery; in 11 patients (64%) more than one motion segment was involved (two levels, six patients; three levels, four patients; four levels, one patient); allograft was placed in three (21%) of 14 graft sites; and anterior plates were used for reconstruction augmentation in eight patients (57%). Postoperatively all patients improved, although four patients had residual deficits or pain. Graft/plate failure, requiring surgical revision and/or halo placement, occurred in five patients (36%). One patient experienced transient recurrent laryngeal nerve palsy. Postoperatively, the authors classified patients into one of two groups: those in whom surgery was successful (nine cases) and those in whom it had failed (five cases). Analysis of the characteristics of these two groups revealed that male sex (p < 0.0365), multiple levels of involvement (p < 0.0378), and the use of allograft as compared with autograft (p < 0.0088) were significant risk factors for construct failure. Prior CTJ surgery (p < 0.053) tended to be associated with graft failure. CONCLUSIONS: Findings of this study, in the setting of these factors, indicate that anterior reconstruction alone may not meet the biomechanical needs of this spinal region and that supplementary fixation may be considered to augment stabilization for fusion success.

Overexpression of GluR6 in rat hippocampus produces seizures and spontaneous nonsynaptic bursting in vitro.

We hypothesized that overexpression of specific glutamate receptors within the hippocampus would induce seizures and the associated cellular changes seen in temporal lobe epilepsy (TLE). The GluR6 kainate receptor was overexpressed by injecting rat hippocampi with HSVGluR6, a viral vector transducing fully edited GluR6. These animals experienced limbic seizures approximately 4 h following the injection. Control animals injected with HSVlac, a vector expressing beta-galactosidase, did not have seizures. Recordings from hippocampal CA1 pyramidal cells were performed 12 to 48 h and 1 week to 1 month postinjection. We observed nonsynaptic Na(+)-mediated bursting in 77.5% of cells 12 to 48 h following injection of HSVGluR6 but not HSVlac. The synaptic responses were normal in both groups. However, the physiological properties of cells from HSVGluR6-injected hippocampi changed over time. Two weeks following HSVGluR6 injection, synaptic bursts could be evoked, but intrinsic bursting became rare. These changes persisted for at least 1 month. We postulate that this transition from intrinsic to synaptic hyperexcitability may be important in the development of TLE.

Efficacy of unilateral deep brain stimulation of the thalamic ventralis intermedius nucleus in a patient with bipolar disorder associated with Klinefelter syndrome and essential tremor. Case report.

Deep brain stimulation (DBS) of the ventralis intermedius nucleus (Vim) is a safe and effective treatment for essential tremor. Bipolar disorder and essential tremor had each been reported to occur in association with Klinefelter syndrome but the three diseases have been reported to occur together in only one patient. The genetic basis and natural history of these disorders are not completely understood and may be related rather than coincidental. The authors report on a 23-year-old man with Klinefelter syndrome (47,XXY) and bipolar disorder who was treated successfully with unilateral DBS of the thalamic Vim for essential tremor.

Long-term deep brain stimulation in a patient with essential tremor: clinical response and postmortem correlation with stimulator termination sites in ventral thalamus. Case report.

Essential tremor can be suppressed with chronic, bilateral deep brain stimulation (DBS) of the ventralis intermedius nucleus (Vim), the cerebellar receiving area of the motor thalamus. The goal in this study was to correlate the location of the electrodes with the clinical efficacy of DBS in a patient with essential tremor. The authors report on a woman with essential tremor in whom chronic bilateral DBS directed to the ventral thalamus produced adequate tremor suppression until her death from unrelated causes 16 months after placement of the electrodes. Neuropathological postmortem studies of the brain in this patient demonstrated that both stimulators terminated in the Vim region of the thalamus, and that chronic DBS elicited minor reactive changes confined to the immediate vicinity of the electrode tracks. Although the authors could not identify neuropathological abnormalities specific to essential tremor, they believe that suppression of essential tremor by chronic DBS correlates with bilateral termination of the stimulators in the Vim region of the thalamus.

Epileptiform propagation patterns mediated by NMDA and non-NMDA receptors in rat neocortex.

PURPOSE: The neocortex can generate various forms of epileptiform activity, including one that depends on N-methyl-D-aspartate (NMDA)-type glutamate receptors (NMDARs), and another dependent on non-NMDA-type (AMPA) glutamate receptors (AMPARs). Previous work in vitro suggests that both forms of activity are initiated by neurons of layer 5, but the spatial patterns of horizontal propagation have been studied only for the AMPAR form. We have tested the hypothesis that both types of epileptiform activity spread via common pathways in one cortical layer, suggesting that lamina-specific intervention might selectively interrupt both. METHODS: Slices of rat somatosensory cortex were maintained in vitro and treated with the gamma-aminobutyric acid type A (GABA(A))-receptor antagonist picrotoxin. Single all-or-none epileptiform discharges were evoked with an electrical stimulus, and extracellular microelectrodes were used to track the vertical and lateral spread of the discharges. RESULTS: In both high and low concentrations of picrotoxin, the non-NMDAR antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) completely blocked propagation, whereas the NMDAR antagonist D-2-amino-5-phosphonovaleric acid (DAPV) only shortened the duration of discharges. When extracellular [Mg2+] was reduced in the presence of picrotoxin and CNQX, NMDAR-dependent epileptiform discharges could be initiated. NMDAR-dependent discharges spread at about one fifth the conduction velocity of AMPAR-dependent events. Analysis of spatiotemporal field-potential patterns suggested that both NMDAR- and AMPAR-mediated propagation involved early activity in layers 5 and 6, followed by larger-amplitude activity in upper cortical layers along the path of propagation. CONCLUSIONS: Our results imply that a common pathway mediates the propagation of these two forms of epileptiform activity, and suggests that lamina-specific surgical intervention might maximize anticonvulsant effect while minimally disrupting cortical function.

Lack of correlation between neuronal hyperexcitability and electrocorticographic responsiveness in epileptogenic human neocortex.

OBJECT: The purpose of this study was to determine whether intrinsic neuronal properties and synaptic responses differed between interictally active and inactive tissue removed in neocortical resections from patients undergoing surgical treatment for epilepsy. METHODS: Whole-cell patch recordings were performed in layer 2 or 3 and layer 5 pyramidal cells in neocortical slices obtained from tissue surgically removed from patients for the treatment of medically intractable seizures. Synaptic responses to stimulation at the layer 6-white matter border were used to classify cells as nonbursting if they responded with only a single action potential for all above-threshold stimuli (80%). These responses were usually followed by biphasic inhibitory postsynaptic potentials (IPSPs). Cells were classified as bursting if they fired at least three action potentials in response to synaptic stimulation (20%). These cells typically showed no IPSPs and responded in either an all-or-nothing or graded fashion. Approximately twice as many cells at layer 2 or 3 (29%) than cells at layer 5 (14%) fired synaptic bursts. Synaptic bursting was not associated with an alteration in a cell's response properties to gamma-aminobutyric acid. It was notable that, in tissue samples determined by electrocorticography (ECoG) to be either interictally active or not active, the proportion of cells that burst was exactly the same in both groups (24%). We found no cells with intrinsic burst firing. CONCLUSIONS: We conclude that synaptic bursting was characteristic of a small proportion of cells from epileptic tissue; however, this did not correlate with interictal spikes on ECoG.

Layer-specific pathways for the horizontal propagation of epileptiform discharges in neocortex.

PURPOSE: Epileptiform discharges that resemble interictal spikes can be generated by slices of neocortex treated with antagonists of gamma-aminobutyric acid A (GABA(A)) receptors. These discharges can propagate horizontally for long distances. We tested the hypothesis that propagation occurs through preferred horizontal pathways that lie in a particular cortical layer. METHODS: Slices were prepared from the primary somatosensory cortex of rats, maintained in vitro, and bathed with the GABA(A) receptor antagonist picrotoxin. Electrical stimuli were used to evoke single all-or-none paroxysmal field potentials (PFP) that were recorded with pairs or arrays of field potential electrodes. RESULTS: To test which laminae are necessary for propagation, vertical cuts were made to force the PFP to spread horizontally through particular layers. If slices were bathed in a high dose of picrotoxin (35 microM), a bridge of cortex 350 microm thick placed at any lamina was sufficient to support PFP propagation. However, in low picrotoxin doses (2.5 microM), similarly sized bridges had to include tissue from layers 4/5 or 5/6 to support propagation. When slices were cut horizontally (i.e., parallel to the pia) in strips. either upper-, middle-, or lower-layer strips were sufficient to support PFP propagation if the picrotoxin concentration was high; however, in low picrotoxin doses, only horizontal strips that included layer 5 could support propagation. Finally, in intact picrotoxin-treated slices, focal applications of GABA were systematically applied to different laminae as the PFP propagated past; GABA was most effective at blocking or delaying propagation when it was applied to layer 5b. CONCLUSIONS: We conclude that epileptiform propagation can occur through a variety of horizontal pathways when cortical inhibition is strongly impaired. However, when inhibition is reduced only moderately, axonal pathways in layer 5 are critical for seizure spread.

Prolonged GABA responses in dentate granule cells in slices isolated from patients with temporal lobe sclerosis.

1. Medial temporal lobe sclerosis is a common pathological finding in patients with medically intractable temporal lobe epilepsy. This disease is characterized by extensive cell loss in the hilus and the hippocampal CA1 and CA3 cell fields in addition to synaptic reorganization throughout the dentate gyrus. 2. The dentate granule cells from hippocampal slices of patients diagnosed with medial temporal lobe sclerosis exhibit reduced synaptic inhibition with concommitant hyperexcitability. These physiological changes were studied relative to the hippocampi of patients with temporal lobe tumors in which the cell loss and synaptic reorganization are not seen. 3. We attempted to determine if this disinhibition was because of changes in the postsynaptic sensitivity to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by studying the responses to exogenously applied transmitter. As in rodents, the GABA responses in human dentate granule cells studied at the resting membrane potential were depolarizing and were mediated primarily by GABAA receptors. In many cases, these depolarizing GABA responses could trigger action potentials. Thus in some situations, GABA could act as an excitatory neurotransmitter. 4. We found that GABAA receptor-mediated responses in the sclerotic hippocampi were approximately 80% longer than in the comparison population. This difference was not because of changes in either the GABA reversal potential or the GABA-induced conductance change. The data support the hypothesis that the GABA transport system is impaired in sclerotic tissue: application of the GABA uptake inhibitor NNC711 (a tiagibine derivative) greatly prolonged the GABA responses in the tumor-related temporal lobe epilepsy tissue, but had little effect on the sclerotic tissue.