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This meta-analysis was conducted to systematically review the efficacy and safety of the H-Wave (Electronic Waveform Lab, Inc, Huntington Beach, CA, USA) device and programme as a non-pharmacological analgesic treatment in chronic soft tissue inflammation and neuropathic pain.Five studies related to pain relief, reduction in pain medication and increased functionality obtained with the H-Wave device were included in the analysis. Data were analysed using the random effects model, including adjustment to evaluate variability, size of study and bias in effect size. A total of 6535 participants were included in the meta-analysis; there were 8065 participants' outcomes measured due to multiple measurements per participant.The H-Wave device decreased pain ratings across various chronic soft tissue inflammation and neuropathic pain conditions. The mean weighted effect size was 0.59, and the estimated effect size variance was 0.00003 (95% confidence intervals [CI]: 0.580, 0.600). The H-Wave device also decreased the intake of pain medication in patients with various chronic soft tissue inflammation and neuropathic pain conditions. The mean weighted effect size was 0.56, and the estimated effect size variance was 0.000013 (95% CI: 0.553, 0.567). Patient functionality was also improved with use of the H-Wave device. The mean weighted effect size was 0.70, and the estimated effect size variance was 0.00002 (95% CI: 0.691, 0.709). A chi-square test for homogeneous effect sizes found highly significant (P0.00001) variability, indicating a robust significant effect size for increased functionality relative to both pain relief and reduction in pain medication. There was little to no evidence of any adverse effects associated with the use of the H-Wave device.The findings indicate a moderate to strong effect of the H-Wave device in providing pain relief, reducing the requirement for pain medication and increasing functionality. The most robust effect was observed for improved functionality, suggesting that the H-Wave device may facilitate a quicker return to work and other related daily activities.

Multilevel fusions, the use of allograft bone, and smoking have been associated with an increased risk of nonunion after anterior cervical discectomy and fusion (ACDF) procedures. Pulsed electromagnetic field (PEMF) stimulation has been shown to increase arthrodesis rates after lumbar spine fusion surgery, but there are minimal data concerning the effect of PEMF stimulation on cervical spine fusion.To determine the efficacy and safety of PEMF stimulation as an adjunct to arthrodesis after ACDF in patients with potential risk factors for nonunion.A randomized, controlled, prospective multicenter clinical trial.Three hundred and twenty-three patients with radiographic evidence (computed tomography-myelogram [CT-myelo] or magnetic resonance imaging [MRI]) of a compressed cervical nerve root and symptomatic radiculopathy appropriate to the compressed root that had failed to respond to nonoperative management were enrolled in the study. The patients were either smokers (more than one pack per day) and/or were undergoing multilevel fusions. All patients underwent ACDF using the Smith-Robinson technique. Allograft bone and an anterior cervical plate were used in all cases.Measurements were obtained preoperatively and at each postoperative interval and included neurologic assessment, visual analog scale (VAS) scores for shoulder/arm pain at rest and with activity, SF-12 scores, the neck disability index (NDI), and radiographs (anteroposterior, lateral, and flexion-extension views). Two orthopedic surgeons not otherwise affiliated with the study and blinded to treatment group evaluated the radiographs, as did a blinded radiologist. Adverse events were reported by all patients throughout the study to determine device safety.Patients were randomly assigned to one of two groups: those receiving PEMF stimulation after surgery (PEMF group, 163 patients) and those not receiving PEMF stimulation (control group, 160 patients). Postoperative care was otherwise identical. Follow-up was carried out at 1, 2, 3, 6, and 12 months postoperatively.The PEMF and control groups were comparable with regard to age, gender, race, past medical history, smoking status, and litigation status. Both groups were also comparable in terms of baseline diagnosis (herniated disc, spondylosis, or both) and number of levels operated (one, two, three, or four). At 6 months postoperatively, the PEMF group had a significantly higher fusion rate than the control group (83.6% vs. 68.6%, p=.0065). At 12 months after surgery, the stimulated group had a fusion rate of 92.8% compared with 86.7% for the control group (p=.1129). There were no significant differences between the PEMF and control groups with regard to VAS pain scores, NDI, or SF-12 scores at 6 or 12 months. No significant differences were found in the incidence of adverse events in the groups.This is the first randomized, controlled trial that analyzes the effects of PEMF stimulation on cervical spine fusion. PEMF stimulation significantly improved the fusion rate at 6 months postoperatively in patients undergoing ACDF with an allograft and an anterior cervical plate, the eligibility criteria being patients who were smokers or had undergone multilevel cervical fusion. At 12 months postoperatively, however, the fusion rate for PEMF patients was not significantly different from that of the control group. There were no differences in the incidence of adverse events in the two groups, indicating that the use of PEMF stimulation is safe in this clinical setting.

Objectives:To evaluate the effect of prolonged infusion of 3% hypertonic saline (514 mEq/L) and sustained hypernatremia on refractory intracranial hypertension in pediatric traumatic brain injury patients.Design:A prospective study.Setting:A 24-bed Pediatric Intensive Care Unit (Level III) at Childr

✓ The boundaries of somatosensory cortex were localized noninvasively by means of a large-array biomagnetometer in six patients with mass lesions in or near eloquent cortex. The results were used by neurosurgeons and neurologists in preoperative planning and for reference in the operating room. The magnetic source imaging (MSI) localizations from somatosensory evoked potentials were used to predict the pattern of phase reversals measurable intraoperatively on the cortical surface, providing a quantitative comparison between the two measures. The magnetic localizations were found to be predictive in all six cases, with the two sets of localizations falling within an 8-mm distance on average. Somatosensory localizations using MSI offer accuracy in localizing somatosensory cortex stereotactically and in depicting its relationship to lesions. Such data are valuable preoperatively in assessing the risks associated with a proposed surgical procedure and for optimizing subsequent minimum-risk surgical strategy.

Infectious intracavernous carotid artery aneurysms usually present with ophthalmoplegia and/or signs of cavernous sinus thrombosis. We report an unusual case in which a patient with AIDS presented with intractable epistaxis secondary to rupture of a giant infectious intra-cavernous carotid artery aneurysm. Culture of the aneurysm grew mycobacterium avium intracellulare (MAI). The patient was treated successfully by excision of the aneurysm and reconstruction of the internal carotid artery with a saphenous vein interposition graft.

To monitor the course of infectious intracranial aneurysms, repeated cerebral angiography has been recommended every 2 weeks during intravenous antibiotic therapy until the aneurysm has resolved or an operation has been performed. However, serial cerebral angiograms are not without some risk to the patient. We have prospectively studied five patients harboring a total of six infectious intracranial aneurysms by sequential computed tomography (CT) and/or magnetic resonance imaging (MRI) studies. All infectious aneurysms were initially identified by cerebral angiography and were treated with 6 to 8 weeks of intravenous antibiotics. The aneurysm size ranged from 4 to 10 mm. Sequential CT scans and/or MRI studies were obtained at 2- to 3-week intervals to monitor the course of the aneurysms. Three aneurysms enlarged during antibiotic therapy, and one remained unchanged in size. These four aneurysms were treated surgically. The two remaining aneurysms resolved with intravenous antibiotic therapy. Cerebral angiograms were obtained routinely preoperatively and were used to verify the resolution of the infectious aneurysms when they were no longer visible on CT or MRI. On the basis of this prospective study, we conclude that sequential thin-slice CT and/or MRI can effectively and safely monitor the course of infectious intracranial aneurysms once identified by cerebral angiography. This may reduce the need for serial angiography and reduce the ultimate risk in the management of infectious intracranial aneurysms.

Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are classified on the basis of their activation by different agonists. The agonists kainate and alpha-amino-3-hydroxy-5-methyl-4-isoxasolepropionic acid define a class of glutamate receptors termed kainate receptors. We have isolated and sequenced a human glutamate receptor (GluHI) cDNA and determined the chromosomal localization of its gene. The DNA sequence of GluHI would encode a 907-amino acid protein that has a 97% identity to one of the rodent kainate receptor subunits. Many of the changes between the predicted amino acid sequence of GluHI and the most similar rodent kainate receptor (GluRI) occur in a region of the protein encoded in rodents by an alternatively spliced exon. The extreme conservation between the human and rat kainate receptor subunits suggests that a similar gene family will encode human kainate receptors. The GluHI mRNA is widely expressed in human brain. The human gene encoding the GluHI subunit is located at 5q33. While the GluHI gene is not located near a chromosomal region associated with any human neurogenetic disorders, the homologous region on mouse chromosome 11 contains the sites of five neurologic mutations.

A newborn presented with a skin-covered lumbar mass with a subcutaneous hemangioma and on a magnetic resonance image (MRI) revealed a tethered spinal cord with a local mass. The mass had signal characteristics compatible with a lipoma. An initial diagnosis of a lipomeningocele with tethered cord was made, and the patient underwent surgical exploration and subtotal resection of the mass. A follow-up MRI revealed that the cord was still tethered, but an additional mass was present. The initial mass with signal characteristics of lipomatous tissue was accompanied by a low-signal mass in the lumbosacral canal, ventral to the cord, and bilateral enlargement of the foramina at the lumbosacral level. Because of a concern for an intraspinal tumor, a second operative intervention was performed. Multiple biopsies of the mass inside the spinal cord, the nerve roots and at the level of the foramina revealed angiomas that had similiar pathology in all the specimens. A partial resection of the masses and a release of the tethered cord was performed by sectioning the thickened filum terminale. The diagnosis of Cobb’s syndrome was made. The unique association of a tethered cord and the Cobb syndrome is reported here.

Background Aging is marked by declines in levels of many sex hormones and growth factors, as well as in cognitive function. The P300 event-related potential has been established as a predictor of cognitive decline. We decided to determine if this measure, as well as 2 standard tests of memory and attention, may be correlated with serum levels of sex hormones and growth factors, and if there are any generalizations that could be made based on these parameters and the aging process. Findings In this large clinically based preliminary study several sex-stratified associations between hormone levels and cognition were observed, including (1) for males aged 30 to 49, both IGF-1 and IGFBP-3 significantly associated negatively with prolonged P300 latency; (2) for males aged 30 to 49, the spearman correlation between prolonged P300 latency and low free testosterone was significant; (3) for males aged 60 to 69, there was a significant negative correlation between P300 latency and DHEA levels; (4) for females aged 50 to 59 IGFBP-3 significantly associated negatively with prolonged P300 latency; (5) for females at all age periods, estrogen and progesterone were uncorrelated with P300 latency; and (6) for females aged 40 to 69, there was significant negative correlation between DHEA levels and P300 latency. Moreover there were no statistically significant correlations between any hormone and Wechsler Memory Scale-III (WMS-111). However, in females, there was a significant positive correlation between estrogen levels and the number of Attention Deficit Disorder (ADD) complaints. Conclusion Given certain caveats including confounding factors involving psychiatric and other chronic diseases as well as medications, the results may still have important value. If these results could be confirmed in a more rigorously controlled investigation, it may have important value in the diagnosis, prevention and treatment of cognitive impairments and decline.

Management of craniopharyngiomas and masses affecting the third ventricular chamber represents one of the most challenging problems confronting contemporary neurological surgeons. Given the devastating sequelae of surgical complications involved in approaches to the deep cerebral midline, surgical management requires a combination of sophisticated imaging, diagnostic pathology and surgical technique including ventricular microsurgery and stereotaxy and its attendant refinements. Surgical and nonsurgical management is based upon the structural presentation of these masses as defined by detailed imaging studies. Operative objectives include histological definition, maximally feasible excision, cerebral spinal fluid diversion and relief of neurologic deficits created by masses affecting the third venticular chamber.

✓ Thirteen patients with recurrent hemorrhages from angiographically occult vascular malformations are presented. Recurrent hemorrhages were indicated by the exacerbation of neurological deficits, the appearance of a new neurological deficit, or the onset of acute severe headache confirmed by evidence of recent hemorrhage on either computerized tomography or magnetic resonance imaging. Persistent neurological deficits correlated with an increased number of recurrent hemorrhages and their location. The median time from initial hemorrhage to the first recurrent hemorrhage was 12 months and the second rebleed generally occurred much earlier, with a median time of 2 months after the first. Eight patients underwent surgery with total excision and favorable results. One patient with a large pontine lesion underwent partial excision and has had a progressing neurological deficit from recurrent hemorrhages. Histopathological review confirmed the excised lesions to be cavernous angiomas. The authors conclude that angiographically occult vascular malformations are not the benign entity they were previously thought to be, and that they are prone to cause recurrent hemorrhages and persistent neurological deficits. Surgery can be effective and relatively safe in removing these lesions even in eloquent areas of the brain, but the necessity of occasional incomplete removal must be recognized in order to avoid creating an unacceptable neurological outcome.

Albino rabbits with experimental brain edema produced by a combined cryogenic left hemisphere lesion and metabolic 6-aminonicotinamide lesion were administered a 3-hour intravenous infusion of dimethyl sulfoxide (DMSO). Simultaneous recording of intracranial pressure (ICP), systolic arterial pressure (SAP), and central venous pressure (CVP) and electroencephalography were performed while the animals were being ventilated mechanically to produce a constant Pa CO2 value (38-42 torr). At the end of the infusion, the brain water and electrolyte contents were measured. There was a persistent and progressive reduction of ICP during the infusion, the nadir occurring at 3 hours (p less than 0.005 from zero time), with no change in SAP or CVP. There was a reduction of brain water in both hemispheres when compared to untreated controls, but this was significant for the right hemisphere only (p less than 0.005). There was a significant reduction of the brain sodium content for both hemispheres, but no significant change occurred in brain potassium content. The DMSO infusion was effective not only in reducing ICP, but also in sustaining this reduction for 3 hours.

Albino rabbits with a cryogenic lesion to the left parieto-occipital cortex had cerebral blood flow studies (CBF) with the hydrogen clearance technique 24 hours after the insult. Similar subgroups were treated with DMSO (1 g/kg) bolus, DMSO (2 g/kg) infusion, indomethacin (20 mg/kg) bolus, and indomethacin followed by DMSO. Following DMSO bolus administration there was an immediate rise in CBF over both hemispheres, with a significant paradoxical decrease at 30 minutes, followed by a second smaller rise at 60 minutes. With DMSO infusion, the rise in CBF was sustained throughout the infusion period with no paradoxical decrease. With indomethacin there was an initial decrease immediately following the drug, and at 60 minutes there was a rise in the insulted left hemisphere, more than the right one. Indomethacin administration 15 minutes prior to DMSO failed to halt the immediate increase in CBF noted following DMSO bolus injection. These results, together with the changes that occurred in intracranial pressure and brain water content, are analyzed.

Albino rabbits with experimental brain oedema produced by a combined cryogenic left hemisphere and a metabolic 6-aminonicotinamide lesion were given indomethacin (20 mg/kg) fifteen minutes prior to dimethyl sulfoxide (DMSO) treatment (1 g/kg bolus). Intracranial pressure (ICP), systolic arterial pressure (SAP), central venous pressure (CVP), and EEG were continuously measured while the animals were being mechanically ventilated at a constant PaCO2 (38-42 torr). At the end of the run, brain H2O and electrolytes were measured. There was no significant reduction in ICP at 5 minutes and 15 minutes after DMSO. This was strikingly different to what occurred when DMSO alone was administered, when a significant reduction was noted (p less than 0.05). At 30 minutes there was a reduction in ICP in both the DMSO and the DMSO/indomethacin groups, but in the former it was 50% of the pretreatment values while in the latter it was only 24%. Because indomethacin is a proven prostaglandin inhibitor, these results suggest that these substances may play a role in the mechanism of action of DMSO.

Background and hypothesis Based on neurochemical and genetic evidence, we suggest that both prevention and treatment of multiple addictions, such as dependence to alcohol, nicotine and glucose, should involve a biphasic approach. Thus, acute treatment should consist of preferential blocking of postsynaptic Nucleus Accumbens (NAc) dopamine receptors (D1-D5), whereas long term activation of the mesolimbic dopaminergic system should involve activation and/or release of Dopamine (DA) at the NAc site. Failure to do so will result in abnormal mood, behavior and potential suicide ideation. Individuals possessing a paucity of serotonergic and/or dopaminergic receptors, and an increased rate of synaptic DA catabolism due to high catabolic genotype of the COMT gene, are predisposed to self-medicating any substance or behavior that will activate DA release, including alcohol, opiates, psychostimulants, nicotine, gambling, sex, and even excessive internet gaming. Acute utilization of these substances and/or stimulatory behaviors induces a feeling of well being. Unfortunately, sustained and prolonged abuse leads to a toxic" pseudo feeling" of well being resulting in tolerance and disease or discomfort. Thus, a reduced number of DA receptors, due to carrying the DRD2 A1 allelic genotype, results in excessive craving behavior; whereas a normal or sufficient amount of DA receptors results in low craving behavior. In terms of preventing substance abuse, one goal would be to induce a proliferation of DA D2 receptors in genetically prone individuals. While in vivo experiments using a typical D2 receptor agonist induce down regulation, experiments in vitro have shown that constant stimulation of the DA receptor system via a known D2 agonist results in significant proliferation of D2 receptors in spite of genetic antecedents. In essence, D2 receptor stimulation signals negative feedback mechanisms in the mesolimbic system to induce mRNA expression causing proliferation of D2 receptors. Proposal and conclusion The authors propose that D2 receptor stimulation can be accomplished via the use of Synapatmine™, a natural but therapeutic nutraceutical formulation that potentially induces DA release, causing the same induction of D2-directed mRNA and thus proliferation of D2 receptors in the human. This proliferation of D2 receptors in turn will induce the attenuation of craving behavior. In fact as mentioned earlier, this model has been proven in research showing DNA-directed compensatory overexpression (a form of gene therapy) of the DRD2 receptors, resulting in a significant reduction in alcohol craving behavior in alcohol preferring rodents. Utilizing natural dopaminergic repletion therapy to promote long term dopaminergic activation will ultimately lead to a common, safe and effective modality to treat Reward Deficiency Syndrome (RDS) behaviors including Substance Use Disorders (SUD), Attention Deficit Hyperactivity Disorder (ADHD), Obesity and other reward deficient aberrant behaviors. This concept is further supported by the more comprehensive understanding of the role of dopamine in the NAc as a "wanting" messenger in the meso-limbic DA system.