Peripheral Nerve Stimulation for Refractory Trigeminal Pain: Recent Single-Institution Case Series With Long-Term Follow-Up and Review of the Literature.

BACKGROUND: Peripheral neurostimulation (PNS) for medically refractory trigeminal pain is an emerging alternative to traditional surgical approaches, with safety and efficacy demonstrated in several retrospective series and a prospective trial currently in progress. Many existing studies suffer from relatively small numbers and short or inconsistent follow-up, making balanced treatment assessment difficult. MATERIALS AND METHODS: Consecutive cases of trial and permanent placement of trigeminal branch stimulation electrodes by a single surgeon from May 2014 through January 2019 were retrospectively reviewed from a prospectively collected database, following the PROCESS guidelines for surgical case series. Outcomes were assessed at six months and at last follow-up. RESULTS: Ninteen patients underwent trial electrode placement, with 15 patients undergoing permanent system placement. The most common diagnoses were idiopathic trigeminal neuralgia Type 2 (N = 8) and trigeminal neuropathic pain (N = 7). Median follow-up was 14 months (range 6-58 months). At last follow-up, 12 of 15 implanted patients (80%) were still receiving stimulation, with mean (median) pain reduction of 52.3% (47.5%). Infection and revision rates were high, although erosion and migration, which have typically plagued trigeminal PNS surgery, did not occur. Implanted systems were well-tolerated, with excellent cosmetic outcomes and high patient satisfaction that proved durable over long follow-up. CONCLUSIONS: We present a single-institution series of PNS for complex craniofacial pain involving the trigeminal nerve. The procedure is safe, effective and durable over at least one year in the large majority of a well-selected patient population.

Cortical gene expression: prognostic value for seizure outcome following temporal lobectomy and amygdalohippocampectomy.

Whole genome analyses were performed to test the hypothesis that temporal cortical gene expression differs between epilepsy patients rendered seizure-free versus non-seizure-free following anterior temporal lobectomy with amygdalohippocampectomy (ATL/AH). Twenty four patients underwent ATL/AH to treat medically intractable seizures of temporal lobe origin (mean age 35.5 years, mean follow-up 42.2 months); they were then dichotomized into seizure-free and non-seizure-free groups. Tissue RNA was isolated from the lateral temporal cortex and gene expression analysis was performed. Whole genome data were analyzed for prognostic value for seizure-free outcome following ATL/AH by logistic regression. Genes that could distinguish seizure outcome groups were identified based on providing an accuracy of >0.90 judging by area under the receiver operating characteristic curve, AUC, with a P value of the slope coefficient of <0.05. Four genes and seven RNA probes were with prognostic value for post-operative seizure-free outcome. Gene expression associated with seizure-free outcome included relative down-regulation of zinc finger protein 852 (ZNF852), CUB domain-containing protein 2 (CDCP2), proline-rich transmembrane protein 1 (PRRT1), hypothetical LOC440200 (FLJ41170), RNA probe 8047763, RNA probe 8126238, RNA probe 8113489, RNA probe 8092883, RNA probe 7935228, RNA probe 806293, and RNA probe 8104131. This study describes the predictive value of temporal cortical gene expression for seizure-free outcome after ATL/AH. Four genes and seven RNA probes were found to predict post-operative seizure-free outcome. Future prospective investigation of these genes and probes in human brain tissue and blood could establish new biomarkers predictive of seizure outcome following ATL/AH.

Cortical gene expression correlates of temporal lobe epileptogenicity.

INTRODUCTION: Despite being one of the most common neurological diseases, it is unknown whether there may be a genetic basis to temporal lobe epilepsy (TLE). Whole genome analyses were performed to test the hypothesis that temporal cortical gene expression differs between TLE patients with high vs. low baseline seizure frequency. METHODS: Baseline seizure frequency was used as a clinical measure of epileptogenicity. Twenty-four patients in high or low seizure frequency groups (median seizures/month) underwent anterior temporal lobectomy with amygdalohippocampectomy for intractable TLE. RNA was isolated from the lateral temporal cortex and submitted for expression analysis. Genes significantly associated with baseline seizure frequency on likelihood ratio test were identified based on >0.90 area under the ROC curve, P value of <0.05. RESULTS: Expression levels of forty genes were significantly associated with baseline seizure frequency. Of the seven most significant, four have been linked to other neurologic diseases. Expression levels associated with high seizure frequency included low expression of Homeobox A10, Forkhead box A2, Lymphoblastic leukemia derived sequence 1, HGF activator, Kelch repeat and BTB (POZ) domain containing 11, Thanatos-associated protein domain containing 8 and Heparin sulfate (glucosamine) 3-O-sulfotransferase 3A1. CONCLUSIONS: This study describes novel associations between forty known genes and a clinical marker of epileptogenicity, baseline seizure frequency. Four of the seven discussed have been previously related to other neurologic diseases. Future investigation of these genes could establish new biomarkers for predicting epileptogenicity, and could have significant implications for diagnosis and management of temporal lobe epilepsy, as well as epilepsy pathogenesis.

Brain tumors enhance plasmatic coagulation: the role of hemeoxygenase-1.

BACKGROUND: Patients with brain tumors suffer significant thrombotic morbidity and mortality. In addition to increased thrombin generation via tumor release of tissue factor-bearing microparticles and hyperfibrinogenemia, brain tumors and surrounding normal brain likely generate endogenous carbon monoxide (CO) via the hemeoxygenase-1 (HO-1) system. CO has been shown to enhance plasmatic coagulation via formation of carboxyhemefibrinogen (COHF). Thus, our goals in this study were to determine whether patients with brain tumors had increased HO-1 upregulation/CO production, plasmatic hypercoagulability, and formation of COHF. METHODS: Patients with brain tumors (N = 20) undergoing craniotomy had blood collected for determination of carboxyhemoglobin as a marker of HO-1 activity, plasmatic hypercoagulability (defined as clot strength > 95% confidence interval value of normal subject plasma), and COHF formation (determined with a thrombelastograph-based assay). Plasma obtained from commercially available normal subjects (N = 30) was used for comparison with brain tumor patient samples. RESULTS: Brain tumor patients had carboxyhemoglobin concentrations of 1.5% ± 0.5% (mean ± SD), indicative of HO-1 upregulation. Compared with normal subject plasma, brain tumor patient plasma had significantly (P < 0.0001) greater clot formation velocity (5.2 ± 1.5 vs 9.5 ± 2.3 dynes/cm/s, respectively) and significantly (P = 0.00016) stronger final clot strength (166 ± 28 vs 230 ± 78 dynes/cm, respectively). Ten of the brain tumor patients had plasma clot strength that exceeded the 95% confidence interval value observed in normal subjects, and 12 of the brain tumor patients had COHF formation. Five of the brain tumor patients in the hypercoagulable subgroup had COHF formation. Last, 5 of the hypercoagulable patients had primary brain tumors, whereas the other 5 patients had metastatic tumors or an inflammatory mass lesion. CONCLUSIONS: A subset of patients with brain tumors has increased endogenous CO production, plasmatic hypercoagulability, and COHF formation. Future investigation of the role played by HO-1 derived CO in the pathogenesis of brain tumor-associated thrombophilia is warranted.

Subdural hematoma, retinal hemorrhage, and fracture triad as a clinical predictor for the diagnosis of child abuse.

OBJECTIVE: Nonaccidental trauma (NAT) is a major cause of traumatic death during infancy and early childhood. Several findings are known to raise the index of clinical suspicion: subdural hematoma (SDH), retinal hemorrhage (RH), fracture, and external trauma. Combinations of certain injury types, determined via statistical frequency associations, may assist clinical diagnostic tools when child abuse is suspected. The present study sought to assess the statistical validity of the clinical triad (SDH + RH + fracture) in the diagnosis of child abuse and by extension pediatric NAT. METHODS: A retrospective review of The University of Arizona Trauma Database was performed. All patients were evaluated for the presence or absence of the components of the clinical triad according to specific International Classification of Diseases (ICD)-10 codes. Injury type combinations included some variation of SDH, RH, all fractures, noncranial fracture, and cranial fracture. Each injury type was then correlated with the ICD-10 codes for child abuse or injury comment keywords. Statistical analysis via contingency tables was then conducted for test characteristics such as sensitivity, specificity, positive predictive value, and negative predictive value. RESULTS: There were 3149 patients younger than 18 years of age included in the quantitative analysis, all of whom had at least one component of the clinical triad. From these, 372 patients (11.8%) had a diagnosis of child abuse. When compared to a single diagnosis of either SDH, RH, all fractures, noncranial fracture, or cranial fracture, the clinical triad had a significantly greater correlation with the diagnosis of child abuse (100% of cases) (p < 0.0001). The dyad of SDH + RH also had a significantly greater correlation with a child abuse diagnosis compared to single diagnoses (88.9%) (p < 0.0001). The clinical triad of SDH + RH + fracture had a sensitivity of 88.8% (95% CI 87.6%-89.9%), specificity of 100% (95% CI 83.9%-100%), and positive predictive value of 100% (95% CI 99.9%-100%). The dyad of SDH + RH had a sensitivity of 89.1% (95% CI 87.9%-90.1%), specificity of 88.9% (95% CI 74.7%-95.6%), and positive predictive value of 99.9% (95% CI 99.6%-100%). All patients with the clinical triad were younger than 3 years of age. CONCLUSIONS: When SDH, RH, and fracture were present together, child abuse and by extension pediatric NAT were highly likely to have occurred.

Curcuminoids limit neutrophil-mediated reperfusion injury in experimental stroke by targeting the endothelium.

OBJECTIVE: We sought to test the hypothesis that turmeric-derived curcuminoids limit reperfusion brain injury in an experimental model of stroke via blockade of early microvascular inflammation during reperfusion. METHODS: Male Sprague Dawley rats subjected to MCAO/R were treated with turmeric-derived curcuminoids (vs. vehicle) 1 hour prior to reperfusion (300 mg/kg ip). Neutrophil adhesion to the cerebral microcirculation and measures of neutrophil and endothelial activation were assayed during early reperfusion (0-4 hours); cerebral infarct size, edema, and neurological function were assessed at 24 hours. Curcuminoid effects on TNFα-stimulated human brain microvascular endothelial cell (HBMVEC) were assessed. RESULTS: Early during reperfusion following MCAO, curcuminoid treatment decreased neutrophil rolling and adhesion to the cerebrovascular endothelium by 76% and 67% and prevented >50% of the fall in shear rate. The increased number and activation state (CD11b and ROS) of neutrophils were unchanged by curcuminoid treatment, while increased cerebral expression of TNFα and ICAM-1, a marker of endothelial activation, were blocked by >30%. Curcuminoids inhibited NF-κB activation and subsequent ICAM-1 gene expression in HBMVEC. CONCLUSION: Turmeric-derived curcuminoids limit reperfusion injury in stroke by preventing neutrophil adhesion to the cerebrovascular microcirculation and improving shear rate by targeting the endothelium.

Outcomes following therapeutic intervention of post-traumatic vasospasm: A systematic review and meta-analysis.

BACKGROUND: Vasospasm occurrence following traumatic brain injury may impact neurologic and functional recovery of patients, yet treatment of post-traumatic vasospasm (PTV) has not been well documented. This systematic review and meta-analysis aims to assess the current evidence regarding favorable outcome as measured by Glasgow Outcome Scale (GOS) scores following treatment of PTV. METHODS: A systematic review of PubMed, Ovid MEDLINE, and Ovid EMBASE was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Included manuscripts were methodically scrutinized for quality; occurrence of PTV; rate of favorable outcome following each treatment modality; and follow-up duration. Treatments evaluated were calcium channel blockers (CCBs), endovascular intervention, and dopamine-induced hypertension. Outcomes were compared via the random-effects analysis. RESULTS: Fourteen studies with 1885 PTV patients were quantitatively analyzed: 982 patients who received tailored therapeutic intervention and 903 patients who did not receive tailored therapy. For patients undergoing treatment, the rate of favorable outcome was 57.3 % (500/872 patients; 95 % CI 54.1 - 60.6 %) following administration of CCBs, 94.1 % (16/17 patients; 95 % CI 82.9 - 100.0 %) following endovascular intervention, and 54.8 % (51/93 patients; 95 % CI 44.7 - 65.0 %) following dopamine-induced hypertension. Of note, the endovascular group had the highest rate of favorable outcome but was also the smallest sample size (n = 17). Patients who received tailored therapeutic intervention for PTV had a higher rate of favorable outcome than patients who did not receive tailored therapy: 57.7 % (567/982 patients; 95 % CI 54.1 - 60.8 %) versus 52.0 % (470/903 patients; 95 % CI 48.8 - 55.3 %), respectively. CONCLUSIONS: The available data suggests that tailored therapeutic intervention of PTV results in a favorable outcome. While endovascular intervention of PTV had the highest rate of favorable outcome, both CCB administration and dopamine-induced hypertension had similar lower rates of favorable outcome.

Three-Dimensional Printing in Neurosurgery Residency Training: A Systematic Review of the Literature.

BACKGROUND: The use of three-dimensional (3D) printing in neurosurgery has become more prominent in recent years for surgical training, preoperative planning, and patient education. Several smaller studies are available using 3D printing; however, there is a lack of a concise review. This article provides a systematic review of 3D models in use by neurosurgical residents, with emphasis on training, learning, and simulation. METHODS: A structured literature search of PubMed and Embase was conducted using PRISMA guidelines to identify publications specific to 3D models trialed on neurosurgical residents. Criteria for eligibility included articles discussing only neurosurgery, 3D models in neurosurgery, and models specifically tested or trialed on residents. RESULTS: Overall, 40 articles were identified that met inclusion criteria. These studies encompassed different neurosurgical areas including aneurysm, spine, craniosynostosis, transsphenoidal, craniotomy, skull base, and tumor. Most articles were related to brain surgery. Of these studies, vascular surgery had the highest overall, with 13 of 40 articles, which include aneurysm clipping and other neurovascular surgeries. Twenty-two articles discussed cranial plus tumor surgeries, which included skull base, craniotomy, craniosynostosis, and transsphenoidal. Five studies were specific to spine surgery. Subjective outcome measures of neurosurgical residents were most commonly implemented, of which results were almost unanimously positive. CONCLUSIONS: 3D printing technology is rapidly expanding in health care and neurosurgery in particular. The technology is quickly improving, and several studies have shown the effectiveness of 3D printing for neurosurgical residency education and training.

Leukocyte expression profiles reveal gene sets with prognostic value for seizure-free outcome following stereotactic laser amygdalohippocampotomy.

Among patients with intractable epilepsy, the most commonly performed surgical procedure is craniotomy for amygdalohippocampectomy (AH). Stereotactic laser amygdalohippocampotomy (SLAH) has also been recently employed as a minimally invasive treatment for intractable temporal lobe epilepsy (TLE). Among patients treated with AH and SLAH approximately 65% and 54% of patients become seizure-free, respectively. Therefore, selection criteria for surgical candidates with improved prognostic value for post-operative seizure-free outcome are greatly needed. In this study, we perform RNA sequencing (RNA-Seq) on whole blood leukocyte samples taken from 16 patients with intractable TLE prior to SLAH to test the hypothesis that pre-operative leukocyte RNA expression profiles are prognostic for post-operative seizure outcome. Multidimensional scaling analysis of the RNA expression data indicated separate clustering of patients with seizure free (SF) and non-seizure-free (NSF) outcomes. Differential expression (DE) analysis performed on SF versus NSF groups revealed 24 significantly differentially expressed genes (≥2.0-fold change, p-value < 0.05, FDR <0.05). Network and pathway analyses identified differential activation of pathways involved in lipid metabolism, morphology of oligodendrocytes, inflammatory response, and development of astrocytes. These results suggest that pre-operative leukocyte expression profiles have prognostic value for seizure outcome following SLAH.

Altered expression of signaling pathways regulating neuronal excitability in hippocampal tissue of temporal lobe epilepsy patients with low and high seizure frequency.

Despite recent advances in our understanding of synaptic transmission associated with epileptogenesis, the molecular mechanisms that control seizure frequency in patients with temporal lobe epilepsy (TLE) remain obscure. RNA-Seq was performed on hippocampal tissue resected from 12 medically intractable TLE patients with pre-surgery seizure frequencies ranging from 0.33 to 120 seizures per month. Differential expression (DE) analysis of individuals with low (LSF, mean = 4 seizure/month) versus high (HSF, mean = 60 seizures/month) seizure frequency identified 979 genes with ≥2-fold change in transcript abundance (FDR-adjusted p-value ö0.05). Comparisons with post-mortem controls revealed a large number of downregulated genes in the HSF (1676) versus LSF (399) groups. More than 50 signaling pathways were inferred to be deactivated or activated, with Signal Transduction as the central hub in the pathway network. While neuroinflammation pathways were activated in both groups, key neuronal system pathways were systematically deactivated in the HSF group, including calcium, CREB and Opioid signaling. We also infer that enhanced expression of a signaling cascade promoting synaptic downscaling may have played a key role in maintaining a higher seizure threshold in the LSF cohort. These results suggest that therapeutic approaches targeting synaptic scaling pathways may aid in the treatment of seizures in TLE.

Predicting functional gains in a stroke trial.

BACKGROUND AND PURPOSE: A number of therapies in development for patients with central nervous system injury aim to reduce disability by improving function of surviving brain elements rather than by salvaging tissue. The current study tested the hypothesis that, after adjusting for a number of clinical assessments, a measure of brain function at baseline would improve prediction of behavioral gains after treatment. METHODS: Twenty-four patients with chronic stroke underwent baseline clinical and functional MRI assessments, received 6 weeks of rehabilitation therapy with or without investigational motor cortex stimulation, and then had repeat assessments. Thirteen baseline clinical/radiological measures were evaluated for ability to predict subsequent trial-related gains. RESULTS: Across all patients, bivariate analyses found that greater trial-related functional gains were predicted by (1) smaller infarct volume, (2) greater baseline clinical status, and (3) lower degree of activation in stroke-affected motor cortex on baseline functional MRI. When these 3 variables were further assessed using multivariate linear regression modeling, only lower motor cortex activation and greater clinical status at baseline remained significant predictors. Note that lower baseline motor cortex activation was also associated with larger increases in motor cortex activation after treatment. CONCLUSIONS: Lower motor cortex activity at baseline predicted greater behavioral gains after therapy, even after controlling for a number of clinical assessments. The boosts in cortical activity that paralleled behavioral gains suggest that in some patients, low baseline cortical activity represents underuse of surviving cortical resources. A measure of brain function might be important for optimal clinical decision-making in the context of a restorative intervention.

Time from ictal subdural EEG seizure onset to clinical seizure onset: an electrocorticographic time factor associated with temporal lobe epileptogenicity.

Long-term subdural video/electroencephalographic (EEG) monitoring was performed in a series of patients with medically intractable complex partial seizures, in a study of diagnostic accuracy, to test the hypothesis that the time from ictal subdural EEG seizure onset to clinical seizure onset (ECOT) is correlated with temporal lobe epileptogenicity and confirm measures of validity of ECOT for predicting seizure-free outcome following anterior temporal lobectomy and amygdalohippocampectomy (ATL/AH). In 34 patients with refractory temporal lobe epilepsy, subdural EEG monitoring localized the ictal epileptogenic focus to a single temporal lobe. In each patient, ECOT was analysed for correlation with temporal lobe epileptogenicity as measured by seizure interval in hours. Patients in whom ECOT was equal to or less than the mean (i.e. subdural EEG seizure onset preceding clinical seizure onset by at least 11.7 seconds) had a significantly greater likelihood of becoming seizure-free following ATL/AH compared to patients in whom ECOT was greater than the mean (i.e. subdural EEG seizure onset preceding clinical seizure onset by less than 11.7 seconds) (x(2) = 5.78, p<0.05). The validity of ECOT for predicting seizure-free outcome following ATL/AH is confirmed to have sensitivity of 55.0%, specificity of 85.7%, false positive rate of 15.4%, false negative rate of 42.9%, diagnostic value of 84.6% and diagnostic accuracy of 67.6%. In addition, a significant correlation, described by a second order polynomial relationship, was found between the natural exponential function of ECOT and seizure interval [f(x=0.415x(2) -25.554x + 267.036, r= 0.731, df= 32, t =6.05, p<0.001, where f(x)=e(ECOT) and x= seizure interval). This result provides the epileptologist with a quantitative tool capable of predicting seizure interval based on ECOT. The capability of ECOT to predict seizure interval may allow the patient and epileptologist to anticipate future seizure onset based on ECOT, potentially facilitating accurate timing of ictal seizure focus localization techniques and clinical intervention to abort seizure onset using various available central and peripheral nervous system stimulation therapeutic strategies. The results suggest a relationship between ECOT and seizure interval. Fundamental pathophysiologic processes involved in the transition from ictal EEG to clinical seizure onset may be responsible for temporal lobe epileptogenicity.

Correlation of electrocorticographic to clinical seizure onset and interhemispheric propagation times in temporal lobe epilepsy.

This study was performed to test the hypothesis that, in human temporal lobe epilepsy, electrocorticographic time factors involved in the ictal EEG to clinical ictal transition (electrocorticographic to clinical seizure onset time, ECOT) and the interhemispheric propagation of epileptic activity (interhemispheric propagation time, IHPT), which are independently correlated with temporal lobe epileptogenicity and predictive of seizure-free outcome following temporal lobectomy, are correlated with one another in a quantitative fashion. A series of 37 patients with medically intractable temporal lobe seizures was studied with long-term subdural videoelectroencephalographic monitoring. Temporal lobe seizure interhemispheric propagation time (IHPT) was found to be a negative, exponential function of electrocorticographic to clinical seizure onset time (ECOT) (f(x)=8.201x10(-0.016x), r=0.347, d.f.=35, t=2.19, p<0.05, where f(x)=IHPT and x=ECOT). A small increase in ECOT was associated with a substantial decrease in IHPT and vice versa. The results suggest the electrophysiological time factor, ECOT, involved in the transition from ictal EEG seizure onset to clinical seizure onset, may determine the speed of interhemispheric propagation of established epileptic activity. The results suggest the interesting hypothesis that, in human temporal lobe epilepsy and, perhaps, under non-pathological circumstances, the human temporal lobe might possess a "time-labeling" function amenable to quantitative analysis.

Use of functional MRI to guide decisions in a clinical stroke trial.

BACKGROUND AND PURPOSE: An investigational trial examined safety and efficacy of targeted subthreshold cortical stimulation in patients with chronic stroke. The anatomical location for the target, hand motor area, varies across subjects, and so was localized with functional MRI (fMRI). This report describes the experience of incorporating standardized fMRI into a multisite stroke trial. METHODS: At 3 enrollment centers, patients moved (0.25 Hz) the affected hand during fMRI. Hand motor function was localized at a fourth center guiding intervention for those randomized to stimulation. RESULTS: The fMRI results were available within 24 hours. Across 12 patients, activation site variability was substantial (12, 23, and 11 mm in x, y, and z directions), exceeding stimulating electrode dimensions. CONCLUSIONS: Use of fMRI to guide decision-making in a clinical stroke trial is feasible.

Surgical treatment of peripheral neuropathy: outcomes from 100 consecutive decompressions.

Since 1992 it has been reported that patients with diabetes mellitus recover sensibility and obtain relief of pain from neuropathy symptoms by decompression of lower-extremity peripheral nerves. None of these reports included a series with more than 36 diabetic patients with lower-extremity nerves decompressed, and only recently has a single report appeared of the results of this approach in patients with nondiabetic neuropathy. No previous report has described a change in balance related to restoration of sensibility. A prospective study was conducted of 100 consecutive patients (60 with diabetes and 40 with idiopathic neuropathy) operated on by a single surgeon, other than the originator of this approach, and with the postoperative results reviewed by someone other than these two surgeons. Each patient had neurolysis of the peroneal nerve at the knee and the dorsum of the foot, and the tibial nerve released in the four medial ankle tunnels. After at least 1 year of follow-up, 87% of patients with preoperative numbness reported improved sensation, 92% with preoperative balance problems reported improved balance, and 86% whose pain level was 5 or greater on a visual analog scale from 0 (no pain) to 10 (the most severe pain) before surgery reported an improvement in pain. Decompression of compressed lower-extremity nerves improves sensation and decreases pain, and should be recommended for patients with neuropathy who have failed to improve with traditional medical treatment.

Prognostic value of concordant seizure focus localizing data in the selection of temporal lobectomy candidates.

This study was performed to test the hypotheses that (a) resection of the temporal lobe epileptic focus, amenable to noninvasive as opposed to invasive localization, is associated with superior seizure outcome and (b) that quadruple (versus lesser degrees of) concordance of seizure focus localizing data predicts superior seizure-free outcome. Eighty-three patients underwent invasive (subdural-EEG) and/or noninvasive (video/scalp-EEG, SPECT, PET, MRI, neuropsychological testing) evaluation. All patients underwent anterior temporal lobectomy and amygdalohippocampectomy (ATL/AH) and seizure outcome was assessed at minimum one-year follow-up. At 34.8 +/- 2.5 months following ATL/AH, outcome was superior for patients in whom the seizure focus was amenable to noninvasive compared to invasive localization (80% versus 40% seizure-free, X2 = 14.03, p < 0.05). Seizure outcome was superior for patients with quadruple, compared to all lesser degrees of, concordance of seizure focus localizing data (85% versus 51% seizure-free, X2 = 7.34, p < 0.05). Post-ATL/AH, seizure outcome is superior in patients (1) harboring an epileptic focus amenable to noninvasive localization and (2) with quadruple concordance of seizure focus localizing data. These findings support the development of temporal lobectomy selection criteria including up to four invasive and/or noninvasive concordant seizure focus localizing techniques.

Integration of Perceptual and Mnemonic Dysfunction: Sensory Auras Are Associated with Left Hemispheric Memory Impairment.

Memory function during the intracarotid amobarbital test was studied to test the hypothesis that left hemisphere memory impairment is associated with sensory auras. In a series of 37 patients undergoing preoperative evaluation for epilepsy surgery, the quantitative memory scores during amobarbital inactivation of right and left hemisphere were analyzed for correlation with habitual epileptic auras classified as either (a) experiential, forced emotion, or whole-body dysphoria or (b) sensory hallucinations and/or illusions or localized dysesthesias. The left hemispheric memory score impairment was significantly worse in association with auras classified as sensory hallucinations and/or illusions or localized dysesthesias compared with auras classified as experiential, forced emotion, or whole-body dysphoria (P < 0.05). This finding may assist in predicting left-sided hemispheric memory dysfunction in patients with seizures beginning as auras involving sensory material. The results suggest an integration of perceptual and mnemonic dysfunction in which sensory auras are associated with left hemispheric memory impairment.

Normalization of periictal bihemispheric cerebral perfusion in temporal lobe epilepsy.

Under normal circumstances, cerebral blood flow (CBF), between the two hemispheres is coupled in a direct (i.e. positive slope), linear fashion. However, in temporal lobe epilepsy, the relationship between the two temporal cortices, during the interictal and postictal periods, is the inverse of normal (i.e. correlation is with negative slope and linear). Long-term combined temporal lobe thermal diffusion flowmetry (TDF) subdural regional cerebral blood flow and electroencephalographic (EEG) recording was performed to test the hypothesis that, during the 10min periictal period (i.e. 5min before and 5min following clinical seizure onset), the cerebral perfusion relationship between epileptic and nonepileptic cortex returns to normal (i.e. becomes direct, with positive slope, and linear). A consecutive series of 13 patients with complex partial epilepsy was studied. During continuous monitoring of clinical phenomenology in time sequence with subdural CBF/EEG, the 10min periictal period was characterized by a direct, linear correlation between epileptic and nonepileptic temporal cortical blood flow ( [Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text] ). The fact that this pertubation in the CBF relationship between the bilateral temporal cortices begins prior to and continues for 5min following clinical and subdural EEG seizure onset raises the interesting possibility that normalization of periictal bilateral cerebral perfusion may be associated with temporal lobe epileptogenesis.

Thyrocervical trunk-external carotid artery bypass for positional cerebral ischemia due to common carotid artery occlusion. Report of three cases.

Medically refractory positional cerebral ischemia and concomitant orthostatic hypotension associated with chronic common carotid artery (CCA) occlusion are rare. The authors detail their experience with three cases treated exclusively by an extracranial bypass in which the thyrocervical trunk was used as the donor vessel. Postoperatively grafts were patent and symptoms resolved in all three patients, although orthostatic hypotension remained. Postural cerebral ischemia due to CCA occlusion can be treated by extracranial bypass surgery. The thyrocervical trunk is a suitable donor for reconstruction of the external carotid artery in these cases.

Spinal cord stimulation with implanted epidural paddle lead relieves chronic axial low back pain.

INTRODUCTION: Spinal cord stimulation (SCS) provides significant relief for lumbosacral radiculopathy refractory to both medical and surgical treatment, but historically only offers limited relief for axial low back pain (LBP). We aim to evaluate the response of chronic axial LBP treated with SCS using a surgically implanted epidural paddle lead. MATERIALS AND METHODS: This is a retrospective review of a consecutive series of patients with exclusive LBP or predominant LBP associated with lower extremity (LE) pain evaluated and treated with SCS using an implanted paddle lead within the dorsal thoracic epidural space. Baseline LBP, and if present LE pain, were recorded using the visual analogue scale (VAS) at an initial evaluation. At a follow-up visit (a minimum of 12 months later), LBP and LE pain after a spinal cord stimulator implantation were again recorded using the VAS. Patients were also asked to estimate total LBP pain relief achieved. RESULTS: Patients with either exclusive (n=7) or predominant (n=2) axial LBP were treated with SCS by implantation of a paddle lead at an average spine level of T9. The baseline VAS score for LBP was 7.2; after a follow-up of 20 months, the score decreased to 2.3 (P=0.003). The LE pain VAS score decreased from 7.5 to 0.0 (P=0.103). Patients also reported a subjective 66.4% decrease of their LBP at follow-up. There were no surgical complications. CONCLUSIONS: Axial LBP is refractory to many treatments, including SCS. SCS using a surgically implanted paddle electrode provides significant pain relief for chronic axial LPB, and is a safe treatment modality.