Partial lateralization of the nasopalatine nerve at the incisive foramen for ridge augmentation in the anterior maxilla prior to placement of dental implants: a retrospective case series evaluating self-reported data and neurosensory testing

The objective of this study was to assess implant therapy after a staged guided bone regeneration procedure in the anterior maxilla by lateralization of the nasopalatine nerve and vessel bundle. Neurosensory function following augmentative procedures and implant placement, assessed using a standardized questionnaire and clinical examination, were the primary outcome variables measured. This retrospective study included patients with a bone defect in the anterior maxilla in need of horizontal and/or vertical ridge augmentation prior to dental implant placement. The surgical sites were allowed to heal for at least 6 months before placement of dental implants. All patients received fixed implant-supported restorations and entered into a tightly scheduled maintenance program. In addition to the maintenance program, patients were recalled for a clinical examination and to fill out a questionnaire to assess any changes in the neurosensory function of the nasopalatine nerve at least 6 months after function. Twenty patients were included in the study from February 2001 to December 2010. They received a total of 51 implants after augmentation of the alveolar crest and lateralization of the nasopalatine nerve. The follow-up examination for questionnaire and neurosensory assessment was scheduled after a mean period of 4.18 years of function. None of the patients examined reported any pain, they did not have less or an altered sensation, and they did not experience a "foreign body" feeling in the area of surgery. Overall, 6 patients out of 20 (30%) showed palatal sensibility alterations of the soft tissues in the region of the maxillary canines and incisors resulting in a risk for a neurosensory change of 0.45 mucosal teeth regions per patient after ridge augmentation with lateralization of the nasopalatine nerve. Regeneration of bone defects in the anterior maxilla by horizontal and/or vertical ridge augmentation and lateralization of the nasopalatine nerve prior to dental implant placement is a predictable surgical technique. Whether or not there were clinically measurable impairments of neurosensory function, the patients did not report them or were not bothered by them.

Anterior superior alveolar nerve (ASAN): A morphometric-anatomical Analysis

The anterior superior alveolar nerve (ASAN) is a branch of the infraorbital nerve. Only few studies have morphometrically evaluated the course of the ASAN. Midfacial segments of ten hemisectioned fresh adult cadaver heads were dissected to uncover the anterior wall of the maxilla. Specimens were subsequently decalcified and the bone overlying the ASAN was removed under a microscope to expose the ASAN. Its branching pattern from the infraorbital nerve was recorded, and the course of the ASAN within the anterior wall of the maxillary sinus was morphometrically assessed measuring distances to predefined landmarks using a digital caliper. A distinct ASAN was observed in all specimens. It arose lateral (six cases) or inferior (four cases) from the infraorbital nerve. The point of origin was located at a mean distance of 12.2 ± 5.79 mm posterior to the infraorbital foramen. The ASAN was located on average 2.8 ± 5.13 mm lateral to the infraorbital foramen. After coursing medially, the ASAN ran inferior to the foramen at a mean distance of 5.5 ± 3.07 mm. When approaching the nasal aperture, the loop of the ASAN was on average 13.6 ± 3.07 mm above the nasal floor. The horizontal mean distance from the ASAN to the nasal aperture was 4.3 ± 2.74 mm halfway down from the loop, and 3.3 ± 2.60 mm at the floor of the nose, respectively. In conclusion, the present study evaluated the course of the ASAN relative to the infraorbital foramen and nasal aperture. This information is helpful to avoid damage to this anatomical structure during interventions in the infraobrital region of the maxilla. Further, knowledge of the course of the ASAN and of its bony correlate (canalis sinuosus) may be valuable in interpreting anesthetic or radiologic findings in the anterior maxilla.

Tibial Nerve Stimulation for Treating Neurogenic Lower Urinary Tract Dysfunction: A Systematic Review

CONTEXT Tibial nerve stimulation (TNS) is a promising therapy for non-neurogenic lower urinary tract dysfunction and might also be a valuable option for patients with an underlying neurological disorder. OBJECTIVE We systematically reviewed all available evidence on the efficacy and safety of TNS for treating neurogenic lower urinary tract dysfunction (NLUTD). EVIDENCE ACQUISITION The review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement. EVIDENCE SYNTHESIS After screening 1943 articles, 16 studies (4 randomized controlled trials [RCTs], 9 prospective cohort studies, 2 retrospective case series, and 1 case report) enrolling 469 patients (283 women and 186 men) were included. Five studies reported on acute TNS and 11 on chronic TNS. In acute and chronic TNS, the mean increase of maximum cystometric capacity ranged from 56 to 132mL and from 49 to 150mL, and the mean increase of bladder volume at first detrusor overactivity ranged from 44 to 92mL and from 93 to 121mL, respectively. In acute and chronic TNS, the mean decrease of maximum detrusor pressure during the storage phase ranged from 5 to 15cm H2O and from 4 to 21cm H2O, respectively. In chronic TNS, the mean decrease in number of voids per 24h, in number of leakages per 24h, and in postvoid residual ranged from 3 to 7, from 1 to 4, and from 15 to 55mL, respectively. No TNS-related adverse events have been reported. Risk of bias and confounding was high in most studies. CONCLUSIONS Although preliminary data of RCTs and non-RCTs suggest TNS might be effective and safe for treating NLUTD, the evidence base is poor, derived from small, mostly noncomparative studies with a high risk of bias and confounding. More reliable data from well-designed RCTs are needed to reach definitive conclusions. PATIENT SUMMARY Early data suggest tibial nerve stimulation might be effective and safe for treating neurogenic lower urinary tract dysfunction, but more reliable evidence is required.

Transcutaneous Electrical Nerve Stimulation for Treating Neurogenic Lower Urinary Tract Dysfunction: A Systematic Review

CONTEXT Transcutaneous electrical nerve stimulation (TENS) is a promising therapy for non-neurogenic lower urinary tract dysfunction and might also be a valuable option in patients with an underlying neurological disorder. OBJECTIVE We systematically reviewed all available evidence on the efficacy and safety of TENS for treating neurogenic lower urinary tract dysfunction. EVIDENCE ACQUISITION The review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement. EVIDENCE SYNTHESIS After screening 1943 articles, 22 studies (two randomised controlled trials, 14 prospective cohort studies, five retrospective case series, and one case report) enrolling 450 patients were included. Eleven studies reported on acute TENS and 11 on chronic TENS. In acute TENS and chronic TENS, the mean increase of maximum cystometric capacity ranged from 69ml to 163ml and from 4ml to 156ml, the mean change of bladder volume at first detrusor overactivity from a decrease of 13ml to an increase of 175ml and from an increase of 10ml to 120ml, a mean decrease of maximum detrusor pressure at first detrusor overactivity from 18 cmH20 to 72 cmH20 and 8 cmH20, and a mean decrease of maximum storage detrusor pressure from 20 cmH20 to 58 cmH2O and from 3 cmH20 to 8 cmH2O, respectively. In chronic TENS, a mean decrease in the number of voids and leakages per 24h ranged from 1 to 3 and from 0 to 4, a mean increase of maximum flow rate from 2ml/s to 7ml/s, and a mean change of postvoid residual from an increase of 26ml to a decrease of 85ml. No TENS-related serious adverse events have been reported. Risk of bias and confounding was high in most studies. CONCLUSIONS Although preliminary data suggest TENS might be effective and safe for treating neurogenic lower urinary tract dysfunction, the evidence base is poor and more reliable data from well-designed randomised controlled trials are needed to make definitive conclusions. PATIENT SUMMARY Early data suggest that transcutaneous electrical nerve stimulation might be effective and safe for treating neurogenic lower urinary tract dysfunction, but more reliable evidence is required.

Inflammation and Optic Nerve Regeneration

Neuroinflammation has long been studied for its connection to the development and progression of Multiple Sclerosis. In recent years, the field has expanded to look at the role of inflammatory processes in a wide range of neurological conditions and cognitive disorders including stroke, amyotrophic lateral sclerosis, and autism. Researchers have also started to note the beneficial impacts of neuroinflammation in certain diseases. Neuroinflammation: New Insights into Beneficial and Detrimental Functions provides a comprehensive view of both the detriments and benefits of neuroinflammation in human health. Neuroinflammation: New Insights into Beneficial and Detrimental Functions opens with two chapters that look at some fundamental aspects of neuroinflammation in humans and rodents. The remainder of the book is divided into two sections which examine both the detrimental and beneficial aspects of inflammation on the brain, spinal cord and peripheral nerves, on various disease states, and in normal aging. These sections provide a broad picture of the role neuroinflammation plays in the physiology and pathology of various neurological disorders. Providing cross-disciplinary coverage, Neuroinflammation: New Insights into Beneficial and Detrimental Functions will be an essential volume for neuroimmunologists, neurobiologists, neurologists, and others interested in the field.

Sural nerve conduction studies using ultrasound-guided needle positioning: Influence of age and recording location.

INTRODUCTION The aim of this study was to compare orthodromic sural nerve conduction study (NCS) results using ultrasound-guided needle positioning (USNP) to surface electrode recordings. METHODS 51 healthy subjects aged 24 - 80 years, divided into 5 age groups, were examined. Electrical stimuli were applied behind the lateral malleolus. Sensory nerve action potentials (SNAPs) were recorded 8 and 15 cm proximally with surface and needle electrodes. RESULTS Mean SNAP amplitudes in µV (surface/needle electrodes) averaged 12.7 (SD 7.6)/40.6 (SD 20.8), P<0.001, for subjects aged 20-29 years, and 5.0 (SD 2.4)/19.8 (SD 9.8), P<0.01, for subjects aged > 60 years. SNAP amplitudes were smaller at the proximal recording location. DISCUSSION NCS using USNP yield higher amplitude responses than surface electrodes in all age groups at all recording sites. SNAP amplitudes are smaller at proximal recording locations due to sural nerve branching. This article is protected by copyright. All rights reserved.

Effects of Vasoactive Intestinal Peptide and Nerve Growth Factor on Rat Osteosarcoma Cells

Submitted in partial fulfillment of the requirements for a Certificate in Orthodontics, Dept. of Orthodontics, University of Connecticut Health Center, 1986

Inner-Hair Cells Parameterized-Hardware Implementation for Personalized Auditory Nerve Stimulation

In this paper the hardware implementation of an inner hair cell model is presented. Main features of the design are the use of Meddis’ transduction structure and the methodology for Design with Reusability. Which allows future migration to new hardware and design refinements for speech processing and custom-made hearing aids

Expression of B-nerve growth factor in rabbit male tract and seminal plasma

Nerve growth factor (NGF) has been recently identified as an ovulation inductor factor (OIF) in the seminal plasma (SP) (Ratto et al. PNAS 2012; 109:15042-7). The presence of OIF in rabbit has been suggested but this protein has not yet been identified. Our aim was to study the mRNA expression in the rabbit male reproductive tract and to identify the protein β-NGF in the SP.

Induction of ovulation in rabbit does using purified nerve growth factor and camel seminal plasma

The presence of an ovulation-inducing factor (OIF) in the seminal plasma (SP) of several species with spontaneous and induced ovulation, including the rabbit, has been documented. Recent studies have demonstrated that the OIF in the SP of camels (SPCAM) is a nerve growth factor (β-NGF). The aim of this study was to determine if purified β-NGF from mouse submandibular glands or SPCAM could provoke ovulation induction in the rabbit doe. A total of 35 females were synchronized with 25 IU of equine chorionic gonadotropin (Serigan, Laboratorios Ovejero, Spain) and allocated into 4 groups. Forty-eight hours later (Day 0), does were given a single dose (IM) of 1 mL of saline solution (SS; n = 8); 1 mL of gonadorelin (GnRH; Inducel, Laboratorios Ovejero, Spain; n = 9); 24 µg of β-NGF (2.5S-NGF; Promega, USA; n = 10); or 1 mL of centrifuged raw camel SP (SPCAM; 127 pg mL–1 NGF; n = 8). After treatment, an empty catheter was introduced through the vagina to simulate the nervous/mechanical stimulus of coitus (4 animals per group). Plasma LH concentrations were determined in blood samples taken 30 min before treatment and at 0, 30, 60, 90, and 120 min after injection. Progesterone concentrations were assessed at 0 and 120 min and every 2 days until Day 6 after treatment. Concentrations of β-NGF in camel SP and hormone determinations were made by enzyme immunoassay. Ovulation rate (OR) was determined after euthanasia on Day 7.

A nerve growth factor mimetic TrkA antagonist causes withdrawal of cortical cholinergic boutons in the adult rat

Cholinergic neurons respond to the administration of nerve growth factor (NGF) in vivo with a prominent and selective increase of choline acetyl transferase activity. This suggests the possible involvement of endogenous NGF, acting through its receptor TrkA, in the maintenance of central nervous system cholinergic synapses in the adult rat brain. To test this hypothesis, a small peptide, C(92-96), that blocks NGF-TrkA interactions was delivered stereotactically into the rat cortex over a 2-week period, and its effect and potency were compared with those of an anti-NGF monoclonal antibody (mAb NGF30). Two presynaptic antigenic sites were studied by immunoreactivity, and the number of presynaptic sites was counted by using an image analysis system. Synaptophysin was used as a marker for overall cortical synapses, and the vesicular acetylcholine transporter was used as a marker for cortical cholinergic presynaptic sites. No significant variations in the number of synaptophysin-immunoreactive sites were observed. However, both mAb NGF30 and the TrkA antagonist C(92-96) provoked a significant decrease in the number and size of vesicular acetylcholine transporter–IR sites, with the losses being more marked in the C(92-96) treated rats. These observations support the notion that endogenously produced NGF acting through TrkA receptors is involved in the maintenance of the cholinergic phenotype in the normal, adult rat brain and supports the idea that NGF normally plays a role in the continual remodeling of neural circuits during adulthood. The development of neurotrophin mimetics with antagonistic and eventually agonist action may contribute to therapeutic strategies for central nervous system degeneration and trauma.

Nerve growth factor inhibits sympathetic neurons’ response to an injury cytokine

Axonal damage to adult peripheral neurons causes changes in neuronal gene expression. For example, axotomized sympathetic, sensory, and motor neurons begin to express galanin mRNA and protein, and recent evidence suggests that galanin plays a role in peripheral nerve regeneration. Previous studies in sympathetic and sensory neurons have established that galanin expression is triggered by two consequences of nerve transection: the induction of leukemia inhibitory factor (LIF) and the reduction in the availability of the target-derived factor, nerve growth factor. It is shown in the present study that no stimulation of galanin expression occurs following direct application of LIF to intact neurons in the superior cervical sympathetic ganglion. Injection of animals with an antiserum to nerve growth factor concomitant with the application of LIF, on the other hand, does stimulate galanin expression. The data suggest that the response of neurons to an injury factor, LIF, is affected by whether the neurons still receive trophic signals from their targets.

Phosphatidylcholine-specific phospholipase C regulates glutamate-induced nerve cell death

Phosphatidylcholine-specific phospholipase C (PC-PLC) is a necessary intermediate in transducing apoptotic signals for tumor necrosis factor and Fas/Apo-1 ligands in nonneuronal cells. The data presented here show that PC-PLC also is required in oxidative glutamate-induced programmed cell death of both immature cortical neurons and a hippocampal nerve cell line, HT22. In oxidative glutamate toxicity, which is distinct from excitotoxicity, glutamate interferes with cystine uptake by blocking the cystine/glutamate antiporter, indirectly causing a depletion of intracellular glutathione. A PC-PLC inhibitor blocks oxidative glutamate toxicity, and exogenous PC-PLC potentiates glutamate toxicity. The inhibition of PC-PLC uncouples the cystine uptake from glutamate inhibition, allowing the maintenance of glutathione synthesis and cell viability. These data suggest that PC-PLC modulates neuronal cell death through a mechanism that is distinct from that involved in nonneuronal apoptosis.