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Nerve Lesion (nerve + lesion)
Selected AbstractsTransection of the sciatic nerve and reinnervation in adult rats: muscle and endplate morphologyEQUINE VETERINARY JOURNAL, Issue S33 2001J. IJKEMA-PAASSEN Summary The functional recovery after peripheral nerve lesions is generally poor. We studied whether changes in muscles after reinnervation might explain such disappointing results. The functional recovery after peripheral nerve lesions is generally poor. Changes in muscle morphology and neuromuscular innervation might partly explain this lack of compensation. In order to test this hypothesis, we studied muscular differentiation in the soleus, gastrocnemius and tibialis anterior muscles at 7, 15 and 21 weeks after a sciatic nerve lesion in adult rats. In the gastrocnemius and tibialis muscles the percentages of type II muscles fibres were decreased at 7 and 15 weeks but at 21 weeks they again approached normal values. The soleus muscle, however, was permanently decreased in size and this muscle, in contrast to the normal soleus muscle, contained mainly type II fibres. The morphology of the endplates showed distinct stages of degeneration and reinnervation. Two weeks after denervation, in rats in which reinnervation was prevented, all 3 muscles contained considerable numbers of morphologically abnormal endplates and, after 7 weeks, no endplates were detected. During reinnervation, endplates showing signs of acetylcholinesterase activity were observed in all 3 muscles from 7 weeks. At later ages a shift towards morphologically normal endplates occurred, but complete recovery was not observed. Endplates in all 3 muscles were polyneurally innervated at 7 weeks. Although these percentages decreased over age, polyneural innervation was still present at 21 weeks. We conclude that the changes in the distribution of fibre types, abnormal endplate morphology and polyneural innervation may in part explain the poor functional recovery after peripheral nerve lesions. [source] High prevalence of vasomotor reflex impairment in newly diagnosed leprosy patientsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2005X. Illarramendi Abstract Background, Initial nerve damage in leprosy occurs in small myelinated and unmyelinated nerve fibers. Early detection of leprosy in the peripheral nervous system is challenging as extensive nerve damage may take place before clinical signs of leprosy become apparent. Patients and methods, In order to determine the prevalence of, and factors associated with, peripheral autonomic nerve dysfunction in newly diagnosed leprosy patients, 76 Brazilian patients were evaluated prior to treatment. Skin vasomotor reflex was tested by means of laser Doppler velocimetry. Blood perfusion and reflex vasoconstriction following an inspiratory gasp were registered on the second and fifth fingers. Results, Vasomotor reflex was impaired in at least one finger in 33/76 (43%) patients. The fifth fingers were more frequently impaired and suffered more frequent bilateral alterations than the second fingers. Multivariate regression analysis showed that leprosy reaction (adjusted odds ratio = 8·11, 95% confidence interval: 1·4,48·2) was associated with overall impaired vasomotor reflex (average of the four fingers). In addition, palmar erythrocyanosis and an abnormal upper limb sensory score were associated with vasomotor reflex impairment in the second fingers, whereas anti-phenolic glycolipid-I antibodies, ulnar somatic neuropathy and a low finger skin temperature were associated with impairment in the fifth fingers. Conclusions, A high prevalence of peripheral autonomic dysfunction as measured by laser Doppler velocimetry was observed in newly diagnosed leprosy patients, which is clinically evident late in the disease. Autonomic nerve lesion was more frequent than somatic lesions and was strongly related to the immune-inflammatory reaction against M. leprae. [source] Cloning and characterization of SDF-1,, a novel SDF-1 chemokine transcript with developmentally regulated expression in the nervous systemEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2000Marc Gleichmann Abstract The cytokines SDF-1, and -1, are two alternatively spliced variants of the CXC (,) chemokines that are highly conserved among species. SDF-1, was shown to function as a B-cell maturation factor, a ligand for the CXCR4 (LESTR/fusin) chemokine receptor, thereby inhibiting replication of T cell-tropic HIV-1 strains and inducing cell death in human neuronal cell lines. In this report the cloning of the rat SDF-1, cDNA and a new SDF-1 isoform, SDF-1,, are presented. Using Northern blot analysis, the expression pattern of both isoforms was studied in different tissues and it is shown that during postnatal development of the central and peripheral nervous system SDF-1,- and SDF-1,-mRNA expression is inversely regulated. Whilst SDF-1,-mRNA is the predominant isoform in embryonic and early postnatal nerve tissue, SDF-1,-mRNA is expressed at higher levels in adulthood. After peripheral nerve lesion a transient increase in SDF-1,-mRNA expression is observed. As revealed by in situ hybridization, neurons and Schwann cells are the main cellular sources of both SDF-1, and SDF-1, mRNAs in the nervous system. Computer-assisted analysis revealed that both transcripts encode secreted peptides with putative proteolytic cleavage sites which might generate novel neuropeptides. [source] Abnormal substance P release from the spinal cord following injury to primary sensory neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2000Marzia Malcangio Abstract The neuropeptide substance P (SP) modulates nociceptive transmission within the spinal cord. Normally, SP is uniquely contained in a subpopulation of small-calibre axons (A,- and C-fibres) within primary afferent nerve. However, it has been shown that after nerve transection, besides being downregulated in small axons, SP is expressed de novo in large myelinated A,-fibres. In this study we investigated whether, following peripheral nerve injury, SP was released de novo from the spinal cord after selective activation of A,-fibres. Spinal cords with dorsal roots attached were isolated in vitro from rats 2 weeks following distal sciatic axotomy or proximal spinal nerve lesion (SNL). The ipsilateral dorsal roots were electrically stimulated for two consecutive periods at low- or high-threshold fibre strength, spinal cord superfusates were collected and SP content was determined by radioimmunoassay. SNL, but not axotomized or control rat cords, released significant amounts of SP after selective activation of A,-fibres. Not only do these data support the idea that A, myelinated fibres contribute to neuropathic pain by releasing SP, they also illustrate the importance of the proximity of the lesion to the cell body. [source] Involvement of gp130-associated cytokine signaling in Müller cell activation following optic nerve lesionGLIA, Issue 7 2010Matthias Kirsch Abstract Ciliary neurotrophic factor (CNTF) and the related cytokine leukemia inhibitory factor (LIF) have been implicated in regulating astrogliosis following CNS lesions. Application of the factors activates astrocytes in vivo and in vitro, and their expression as well as their receptors is upregulated after brain injury. Here, we investigated their function by studying Müller cell activation induced by optic nerve crush in CNTF- and LIF-deficient mice, and in animals with deficiencies in cytokine signaling pathways. In the retina of CNTF,/, mice, basal GFAP expression was reduced, but unexpectedly, injury-induced upregulation in activated Müller cells was increased during the first 3 days after lesion as compared to wild-type animals and this corresponded with higher phosphorylation level of STAT3, an indicator of cytokine signaling. The observation that LIF expression was strongly upregulated in CNTF,/, mice but not in wild-type animals following optic nerve lesion provided a possible explanation. In fact, additional ablation of the LIF gene in CNTF/LIF double knockout mice almost completely abolished early lesion-induced GFAP upregulation in Müller cells and STAT3 phosphorylation. Early Müller cell activation was also eliminated in LIF,/, mice, despite normal CNTF levels, as well as in mutants deficient in gp130/JAK/STAT signaling and in conditional STAT3 knockout mice. Our results demonstrate that LIF signaling via the gp130/JAK/STAT3 pathway is required for the initiation of the astrogliosis-like reaction of retinal Müller cells after optic nerve injury. A potential role of CNTF was possibly masked by a compensatory increase in LIF signaling in the absence of CNTF. © 2010 Wiley-Liss, Inc. [source] Loss of translation elongation factor (eEF1A2) expression in vivo differentiates between Wallerian degeneration and dying-back neuronal pathologyJOURNAL OF ANATOMY, Issue 6 2008Lyndsay M. Murray Abstract Wallerian degeneration and dying-back pathology are two well-known cellular pathways capable of regulating the breakdown and loss of axonal and synaptic compartments of neurons in vivo. However, the underlying mechanisms and molecular triggers of these pathways remain elusive. Here, we show that loss of translation elongation factor eEF1A2 expression in lower motor neurons and skeletal muscle fibres in homozygous Wasted mice triggered a dying-back neuropathy. Synaptic loss at the neuromuscular junction occurred in advance of axonal pathology and by a mechanism morphologically distinct from Wallerian degeneration. Dying-back pathology in Wasted mice was accompanied by reduced expression levels of the zinc finger protein ZPR1, as found in other dying-back neuropathies such as spinal muscular atrophy. Surprisingly, experimental nerve lesion revealed that Wallerian degeneration was significantly delayed in homozygous Wasted mice; morphological assessment revealed that ~80% of neuromuscular junctions in deep lumbrical muscles at 24 h and ~50% at 48 h had retained motor nerve terminals following tibial nerve lesion. This was in contrast to wild-type and heterozygous Wasted mice where < 5% of neuromuscular junctions had retained motor nerve terminals at 24 h post-lesion. These data show that eEF1A2 expression is required to prevent the initiation of dying-back pathology at the neuromuscular junction in vivo. In contrast, loss of eEF1A2 expression significantly inhibited the initiation and progression of Wallerian degeneration in vivo. We conclude that loss of eEF1A2 expression distinguishes mechanisms underlying dying-back pathology from those responsible for Wallerian degeneration in vivo and suggest that eEF1A2 -dependent cascades may provide novel molecular targets to manipulate neurodegenerative pathways in lower motor neurons. [source] Recovery of touch after median nerve lesion and subsequent repairMICROSURGERY, Issue 1 2003M.F. Meek M.D., Ph.D. Many techniques have been developed for the evaluation of peripheral nerve function. Consequently, physicians use different techniques in the clinic. This study describes the evaluation of touch after median nerve lesions in the forearm and repair. In order to evaluate touch, 25 patients, aged 11,51 years (mean, 29 years), were evaluated 3,10.5 years (mean, 5 years) after median nerve repair. The evaluation included the moving two-point discrimination test and Semmes-Weinstein monofilaments. We showed that 32% good,excellent results can be obtained with difficult nerve lesions. The results could have been improved if a sensory reeducation regime had been applied. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:2,5 2003 [source] Tissue engineering of peripheral nerves: Epineurial grafts with application of cultured Schwann cellsMICROSURGERY, Issue 1 2003H. Fansa M.D., Ph.D. After a simple nerve lesion, primary microsurgical suture is the treatment of choice. A nerve gap has to be bridged, with a nerve graft sacrificing a functioning nerve. Alternatively, tissue engineering of nerve grafts has become a subject of experimental research. It is evident that nerve regeneration requires not only an autologous, allogenous, or biodegradable scaffold, but additional interactions with regeneration-promoting Schwann cells. In this study, we compared epineurial and acellularized epineurial tubes with and without application of cultured Schwann cells as alternative grafts in a rat sciatic nerve model. Autologous nerve grafts served as controls. Evaluation was performed after 6 weeks; afterwards, sections of the graft and distal nerve were harvested for histological and morphometrical analysis. Compared to controls, all groups showed a significantly lower number of axons, less well-shaped remyelinizated axons, and a delay in clinical recovery (e.g., toe spread). The presented technique with application of Schwann cells into epineurial tubes did not offer any major advantages for nerve regeneration. Thus, in this applied model, neither the implantation of untreated nor the implantation of acellularized epineurial tubes with cultured Schwann cells to bridge nerve defects was capable of presenting a serious alternative to the present gold standard of conventional nerve grafts for bridging nerve defects in this model. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:72,77 2003 [source] Myoclonus of the scapula after acute long thoracic nerve lesion: A case report,MOVEMENT DISORDERS, Issue 1 2006Filippo Camerota MD Abstract We describe a patient who presented myoclonus in the left scapula 3 months after a traumatic lesion of the left long thoracic nerve. Myoclonic activity was recorded as pseudorhythmic electromyographic bursts repeated at a frequency of 2 to 4 Hz, each lasting between 100 and 200 msec, in the left serratus,dorsalis muscle region, trapezius, and deltoid muscles. A combination of peripheral and central mechanisms may have induced the myoclonus in this case. © 2005 Movement Disorder Society [source] Atypical double nerve lesion after humeral fracture: Diagnosis by ultrasoundMUSCLE AND NERVE, Issue 2 2010Giovanna Liotta MD No abstract is available for this article. [source] Nerve-terminal and Schwann-cell response after nerve injury in the absence of nitric oxideMUSCLE AND NERVE, Issue 2 2006Maria Julia Marques PhD Abstract Dystrophic muscles show alterations in the dystrophin,glycoprotein complex and a lack of neuronal nitric oxide (NO) synthase. In mdx mice, presynaptic expression of neuronal NO synthase is decreased, suggesting that presynaptic signaling may be altered in dystrophic muscle. In this study, we examined the nerve-terminal and Schwann-cell responses after a crush lesion in control and NO-deficient mice. Seven days after nerve crush, 24% of control neuromuscular junctions (n = 200) showed ultraterminal sprouts, whereas in NO-deficient mice this frequency was 28.5% (n = 217; P > 0.05 compared to controls; chi-square test). Schwann-cell response did not change in the absence of NO, after a nerve lesion of 7-day duration. Fourteen days after the lesion, nerve terminals sprouted and Schwann cells showed an extensive network of processes away from the synaptic site in controls. In the absence of NO, there was a dramatic decrease in nerve-terminal sprouting and Schwann-cell processes failed to extend away from the endplate. These results show that NO is involved in the nerve-terminal and Schwann-cell response to nerve injury. They also suggest that presynaptic molecular signaling may be impaired in dystrophic muscles, and this could influence the innervation and survival of newly formed myofibers generated by cell-mediated therapies. Muscle Nerve, 2006 [source] Neurophysiological testing in anorectal disordersMUSCLE AND NERVE, Issue 3 2006Jean-Pascal Lefaucheur MD, PhDArticle first published online: 15 JUL 200 Abstract The neurophysiological techniques currently available to evaluate anorectal disorders include concentric needle electromyography (EMG) of the external anal sphincter, anal nerve terminal motor latency (TML) measurement in response to transrectal electrical stimulation or sacral magnetic stimulation, motor evoked potentials (MEPs) of the anal sphincter to transcranial magnetic cortical stimulation, cortical recording of somatosensory evoked potentials (SEPs) to anal nerve stimulation, quantification of electrical or thermal sensory thresholds (QSTs) within the anal canal, sacral anal reflex (SAR) latency measurement in response to pudendal nerve or perianal stimulation, and perianal recording of sympathetic skin responses (SSRs). In most cases, a comprehensive approach using several tests is helpful for diagnosis: needle EMG signs of sphincter denervation or prolonged TML give evidence for anal motor nerve lesion; SEP/QST or SSR abnormalities can suggest sensory or autonomic neuropathy; and in the absence of peripheral nerve disorder, MEPs, SEPs, SSRs, and SARs can assist in demonstrating and localizing spinal or supraspinal disease. Such techniques are complementary to other methods of investigation, such as pelvic floor imaging and anorectal manometry, to establish the diagnosis and guide therapeutic management of neurogenic anorectal disorders. Muscle Nerve, 2005 [source] Simplified orthodromic inching test in mild carpal tunnel syndromeMUSCLE AND NERVE, Issue 12 2001Paul Seror MD Abstract This prospective study was undertaken to determine the clinical relevance, reliability, sensitivity, and specificity of the orthodromic inching test with 2-cm incremental study of the median nerve over the four intracarpal centimeters in 50 control and 50 successive (unselected) patient wrists with mild carpal tunnel syndrome (CTS). In controls, the mean maximum conduction delay per 2 cm (CD/2cm) was 0.445 ± 0.04 ms, and abnormality was defined as at least one CD/2cm exceeding the mean + 2.5 SD of the normal CD/2cm. This yielded a specificity of 98%. In patients with mild unselected CTS, this simplified orthodromic inching test (SOIT) detected the median nerve lesion at the wrist in 47 cases (sensitivity = 94%). The SOIT detected 15 more CTS cases than did the orthodromic median-ulnar latency difference of the 4th digit (Chi square = 13; P = .002). Thus, the SOIT was as effective as an incremental study every centimeter over 10 cm, and the time required for the test allows its routine use when other electrodiagnostic tests fail to reveal any median nerve impairment. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 1595,1600, 2001 [source] Effect of weak, interrupted sinusoidal low frequency magnetic field on neural regeneration in rats: Functional evaluationBIOELECTROMAGNETICS, Issue 5 2005Marijan Bervar Abstract A study of the effect of weak, interrupted sinusoidal low frequency magnetic field (ISMF) stimulation on regeneration of the rat sciatic nerve was carried out. In the experiment, 60 Wistar rats were used: 24 rats underwent unilateral sciatic nerve transection injury and immediate surgical nerve repair, 24 rats underwent unilateral sciatic nerve crush injury, and the remaining 12 rats underwent a sham surgery. Half of the animals (n,=,12) with either sciatic nerve lesion were randomly chosen and exposed between a pair of Helmholtz coils for 3 weeks post-injury, 4 h/day, to an interrupted (active period to pause ratio,=,1.4 s/0.8 s) sinusoidal 50 Hz magnetic field of 0.5 mT. The other half of the animals (n,=,12) and six rats with sham surgery were used for two separate controls. Functional recovery was followed for 6 weeks for the crush injuries and 7½ months for the transection injuries by video assisted footprint analysis in static conditions and quantified using a recently revised static sciatic index (SSI) formula. We ascertained that the magnetic field influence was weak, but certainly detectable in both injury models. The accuracy of ISMF influence detection, determined by the one-way repeated measures ANOVA test, was better for the crush injury model: F(1, 198),=,9.0144, P,=,.003, than for the transection injury model: F(1, 198),=,6.4826, P,=,.012. The Student,Newman,Keuls range test for each response day yielded significant differences (P,<,.05) between the exposed and control groups early in the beginning of functional recovery and later on from the points adjacent to the beginning of the plateau, or 95% of functional recovery, and the end of observation. These differences probably reflect the ISMF systemic effect on the neuron cell bodies and increased and more efficient reinnervation of the periphery. Bioelectromagnetics 26:351,356, 2005. © 2005 Wiley-Liss, Inc. [source] Clinical significance of suprascapular nerve mobilizationCLINICAL ANATOMY, Issue 8 2005Kale D. Bodily Abstract The anatomy of the suprascapular nerve is important to surgeons when focal nerve lesions necessitate surgical repair. Recent experience with a patient who had a complete suprascapular nerve lesion in the retroclavicular region (combined with axillary and musculocutaneous nerve lesions) is presented to illustrate that successful direct nerve repair is possible despite resection of a neuroma. Specifically, we found that neurolysis and mobilization of the suprascapular nerve and release of the superior transverse scapular ligament provided the necessary nerve length to achieve direct nerve repair after the neuroma was removed. A combined supraclavicular and infraclavicular approach to the suprascapular nerve provided excellent visualization, especially in the retroclavicular region. Postoperatively, the patient recovered complete shoulder abduction and external rotation with the direct repair, an outcome uncommonly achieved with interpositional grafting. Based on our operative experience, we set out to quantify the length that the suprascapular nerve could be mobilized with neurolysis. Mobilization of the nerve and release of the superior transverse scapular ligament generated an average of 1.6 cm and 0.7 cm of extra nerve length respectively, totaling 2.3 cm of additional usable nerve length overall. The ability to expose the suprascapular nerve in the retroclavicular/infraclavicular region and to mobilize the suprascapular nerve for possible direct repair has not been previously emphasized and is clinically important. This surgical approach and technique permits direct nerve repair after resection of a focal neuroma in the retroclavicular or infraclavicular region, thus avoiding interpositional grafting, and improving outcomes. Clin. Anat. 18:573,579, 2005. © 2005 Wiley-Liss, Inc. [source] Transection of the sciatic nerve and reinnervation in adult rats: muscle and endplate morphologyEQUINE VETERINARY JOURNAL, Issue S33 2001J. IJKEMA-PAASSEN Summary The functional recovery after peripheral nerve lesions is generally poor. We studied whether changes in muscles after reinnervation might explain such disappointing results. The functional recovery after peripheral nerve lesions is generally poor. Changes in muscle morphology and neuromuscular innervation might partly explain this lack of compensation. In order to test this hypothesis, we studied muscular differentiation in the soleus, gastrocnemius and tibialis anterior muscles at 7, 15 and 21 weeks after a sciatic nerve lesion in adult rats. In the gastrocnemius and tibialis muscles the percentages of type II muscles fibres were decreased at 7 and 15 weeks but at 21 weeks they again approached normal values. The soleus muscle, however, was permanently decreased in size and this muscle, in contrast to the normal soleus muscle, contained mainly type II fibres. The morphology of the endplates showed distinct stages of degeneration and reinnervation. Two weeks after denervation, in rats in which reinnervation was prevented, all 3 muscles contained considerable numbers of morphologically abnormal endplates and, after 7 weeks, no endplates were detected. During reinnervation, endplates showing signs of acetylcholinesterase activity were observed in all 3 muscles from 7 weeks. At later ages a shift towards morphologically normal endplates occurred, but complete recovery was not observed. Endplates in all 3 muscles were polyneurally innervated at 7 weeks. Although these percentages decreased over age, polyneural innervation was still present at 21 weeks. We conclude that the changes in the distribution of fibre types, abnormal endplate morphology and polyneural innervation may in part explain the poor functional recovery after peripheral nerve lesions. [source] Peripheral Neuropathy in Acrodermatitis Chronica Atrophicans , Effect of TreatmentJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2003E Kindstrand Forty-seven patients with the late borrelial manifestation acrodermatitis chronica atrophicans (ACA) and with objective neurological and/or neurophysiological findings were followed up after antibiotic treatment with dermatological, serological, neurological and neurophysiological controls. Despite a good therapeutic effect on ACA lesions, specific antibody values and symptoms of irritative nerve lesions, the objective neurological and neurophysiological findings of nerve deficit remained unchanged. There was no progress of neuropathy findings during the follow-up time. Our interpretation of the results is that the remaining neuropathy signs after treatment of ACA are neurological sequelae and not manifestations of persisting Borrelia infection. [source] Recovery of touch after median nerve lesion and subsequent repairMICROSURGERY, Issue 1 2003M.F. Meek M.D., Ph.D. Many techniques have been developed for the evaluation of peripheral nerve function. Consequently, physicians use different techniques in the clinic. This study describes the evaluation of touch after median nerve lesions in the forearm and repair. In order to evaluate touch, 25 patients, aged 11,51 years (mean, 29 years), were evaluated 3,10.5 years (mean, 5 years) after median nerve repair. The evaluation included the moving two-point discrimination test and Semmes-Weinstein monofilaments. We showed that 32% good,excellent results can be obtained with difficult nerve lesions. The results could have been improved if a sensory reeducation regime had been applied. © 2003 Wiley-Liss, Inc. MICROSURGERY 23:2,5 2003 [source] Descriptions of Cervical Dystonia by Sir Charles BellMOVEMENT DISORDERS, Issue 3 2010Pedro Gonzalez-Alegre MD Abstract Sir Charles Bell is better known among neurologists for his descriptions of the clinical consequences of facial nerve lesions. However, as an accomplished physician, anatomist, and artist, he made many other contributions to the fields of neurology and neuroscience. Among those, his descriptions of patients with what we now know as cervical dystonia have not received much attention. In this report, Bell's depictions of patients presenting with a syndrome consistent with cervical dystonia will be discussed, including the identification of many of the different clinical features we currently use for the diagnosis of this disorder and his thoughts about its pathogenesis. © 2010 Movement Disorder Society [source] Postoperative complications after extracapsular dissection of benign parotid lesions with particular reference to facial nerve functionTHE LARYNGOSCOPE, Issue 3 2010Nils Klintworth MD Abstract Objectives/Hypothesis: The desirable extent of surgical intervention for benign parotid tumors remains a matter of controversy. Superficial or total parotidectomy as a standard procedure is often said to be the gold standard; however, with it the risk of intraoperative damage to the facial nerve cannot be ignored. For some time now, extracapsular dissection without exposure of the main trunk of the facial nerve has been favored as an alternative for the treatment of discrete parotid tumors. Data on the incidence of facial nerve lesions and other acute postoperative complications of extracapsular dissection have been lacking until now. Study Design: Retrospective analysis. Methods: We performed a retrospective analysis of the data from patients in whom extracapsular dissection of a benign parotid tumor had been performed under facial nerve monitoring and as a primary intervention in our department between 2000 and 2008. Results: A total of 934 patients were operated on for a newly diagnosed benign tumor of the parotid gland. Three hundred seventy-seven patients (40%) underwent extracapsular dissection as a primary intervention. The most common postoperative complication was hypoesthesia of the cheek or the earlobe, as reported by 38 patients (10%). Eighteen patients (5%) developed a seroma and 13 patients (3%) a hematoma. A salivary fistula formed in eight patients (2%). Secondary bleeding occurred in three patients (0.8%). In 346 patients (92%) facial nerve function was normal (House-Brackmann grade I) in the immediate postoperative period, whereas 23 patients (6%) showed temporary facial nerve paresis (House-Brackmann grade II or III) and eight patients (2%) developed permanent facial nerve paresis (seven patients House-Brackmann grade II, one patient House-Brackmann grade III). Conclusions: Extracapsular dissection of benign parotid tumors is associated with a low rate of postoperative complications, a fact that is confirmed by the available literature. We therefore recommend that use of this technique always be considered as a means of treating benign parotid tumors as conservatively, that is, as uninvasively, as possible. Laryngoscope, 2010 [source] Current density threshold for the stimulation of neurons in the motor cortex areaBIOELECTROMAGNETICS, Issue 6 2002T. Kowalski Abstract The aim of this study was to determine a current density threshold for exciting the motor cortex area of the brain. The current density threshold for excitation of nerve fibres (20 ,m in diameter) found in the literature is approximately 1 A/m2 at frequencies lower than 1 kHz. In consideration of a safety factor of 100, the International Commission on Non-Ionizing Radiation Protection (ICNIRP) recommends to restrict the exposure to 0.01 A/m2. The electromagnetic stimulation of neurons in the motor cortex is used in the clinical diagnosis of nerve lesions and neuropathy by means of magnetic or electrical transcranial stimulation. Combining medical data from clinical studies and technical specifications of the Magstim® Model 200 stimulator, we were able to compute the current density threshold for the excitation of the human motor cortex by means of the finite element method (FEM). A 3D-CAD head model was built on the basis of magnetic resonance imaging (MRI) slices and segmented into four anatomical structures (scalp, skull, brain, and ventricular system) with different conductivities. A current density threshold for the stimulation of the motor cortex area of the upper limbs of 6 and 2.5 A/m2 at 2.44 kHz and 50 Hz, respectively, was calculated. As these values lie above the recommended ICNIRP values by two orders of magnitude there is no need for lower safety standards with regard to stimulation of the brain. Bioelectromagnetics 23:421,428, 2002. © 2002 Wiley-Liss, Inc. [source] Clinical significance of suprascapular nerve mobilizationCLINICAL ANATOMY, Issue 8 2005Kale D. Bodily Abstract The anatomy of the suprascapular nerve is important to surgeons when focal nerve lesions necessitate surgical repair. Recent experience with a patient who had a complete suprascapular nerve lesion in the retroclavicular region (combined with axillary and musculocutaneous nerve lesions) is presented to illustrate that successful direct nerve repair is possible despite resection of a neuroma. Specifically, we found that neurolysis and mobilization of the suprascapular nerve and release of the superior transverse scapular ligament provided the necessary nerve length to achieve direct nerve repair after the neuroma was removed. A combined supraclavicular and infraclavicular approach to the suprascapular nerve provided excellent visualization, especially in the retroclavicular region. Postoperatively, the patient recovered complete shoulder abduction and external rotation with the direct repair, an outcome uncommonly achieved with interpositional grafting. Based on our operative experience, we set out to quantify the length that the suprascapular nerve could be mobilized with neurolysis. Mobilization of the nerve and release of the superior transverse scapular ligament generated an average of 1.6 cm and 0.7 cm of extra nerve length respectively, totaling 2.3 cm of additional usable nerve length overall. The ability to expose the suprascapular nerve in the retroclavicular/infraclavicular region and to mobilize the suprascapular nerve for possible direct repair has not been previously emphasized and is clinically important. This surgical approach and technique permits direct nerve repair after resection of a focal neuroma in the retroclavicular or infraclavicular region, thus avoiding interpositional grafting, and improving outcomes. Clin. Anat. 18:573,579, 2005. © 2005 Wiley-Liss, Inc. [source] |