Latency Conduction Research Articles

Delayed Axillary Nerve Motor Conduction Latency and Reduced CMAP Amplitudes in the Paretic Limbs of Patients With a Cerebrovascular Episode

Delayed Axillary Nerve Motor Conduction Latency and Reduced CMAP Amplitudes in the Paretic Limbs of Patients With a Cerebrovascular Episode

Orderly recruitment of motor units under optical control in vivo

A drawback of electrical stimulation for muscle control is that large, fatigable motor units are preferentially recruited before smaller motor units by the lowest-intensity electrical cuff stimulation. This phenomenon limits therapeutic applications because it is precisely the opposite of the normal physiological (orderly) recruitment pattern; therefore, a mechanism to achieve orderly recruitment has been a long-sought goal in physiology, medicine and engineering. Here we demonstrate a technology for reliable orderly recruitment in vivo. We find that under optical control with microbial opsins, recruitment of motor units proceeds in the physiological recruitment sequence, as indicated by multiple independent measures of motor unit recruitment including conduction latency, contraction and relaxation times, stimulation threshold and fatigue. As a result, we observed enhanced performance and reduced fatigue in vivo. These findings point to an unanticipated new modality of neural control with broad implications for nervous system and neuromuscular physiology, disease research and therapeutic innovation.

Quantification of Rossolimo reflexes: A sensitive marker for spondylotic myelopathy

Prospective study. To assess and quantify Rossolimo reflexes using an electrophysiological test, and correlate the findings with the severity of spinal cord dysfunction in cervical and thoracic spondylotic myelopathy (CTSM). A university neurorehabilitation center. We enlisted 42 patients with CTSM between the fifth cervical and the ninth thoracic cord levels. Using electrophysiological assessments, Rossolimo reflexes were evaluated in all patients. Conduction latencies and amplitude of muscle action potentials (MAPs) of the reflexes were measured, analyzed and compared with the grading of spinal cord dysfunction and the cord compression ratios. We found a high diagnostic sensitivity of quantified Rossolimo reflex in patients with CTSM. A positive correlation exists between the MAP amplitude of Rossolimo reflexes and the different grades of spinal cord dysfunction. A negative linear relationship was found between the MAP amplitude of Rossolimo reflexes and the cord compression ratios in CTSM patients. Rossolimo reflexes can be measured by electrophysiological assessments, and we demonstrate a quantification method for an established neurological sign. Not only is the Rossolimo reflex found to be a highly sensitive test in clinical neurological examination but the electrophysiological assessment for this reflex can also serve as an objective marker for evaluation of the severity of spinal cord dysfunction in CTSM.

Enhancement of regeneration with glia cell line–derived neurotrophic factor–transduced human amniotic fluid mesenchymal stem cells after sciatic nerve crush injury [RETRACTED

Object Human amniotic fluid–derived mesenchymal stem cells (AFMSCs) have been shown to promote peripheral nerve regeneration, and the local delivery of neurotrophic factors may additionally enhance nerve regeneration capacity. The present study evaluates whether the transplantation of glia cell line–derived neurotrophic factor (GDNF)–modified human AFMSCs may enhance regeneration of sciatic nerve after a crush injury. Methods Peripheral nerve injury was produced in Sprague-Dawley rats by crushing the left sciatic nerve using a vessel clamp. Either GDNF-modified human AFMSCs or human AFMSCs were embedded in Matrigel and delivered to the injured nerve. Motor function and electrophysiological studies were conducted after 1 and 4 weeks. Early or later nerve regeneration markers were used to evaluate nerve regeneration. The expression of GDNF in the transplanted human AFMSCs and GDNF-modified human AFMSCs was monitored at 7-day intervals. Results Human AFMSCs were successfully transfected with adenovirus, and a significant amount of GDNF was detected in human AFMSCs or the culture medium supernatant. Increases in the sciatic nerve function index, the compound muscle action potential ratio, conduction latency, and muscle weight were found in the groups treated with human AFMSCs or GDNF-modified human AFMSCs. Importantly, the GDNF-modified human AFMSCs induced the greatest improvement. Expression of markers of early nerve regeneration, such as increased expression of neurofilament and BrdU and reduced Schwann cell apoptosis, as well as late regeneration markers, consisting of reduced vacuole counts, increased expression of Luxol fast blue and S100 protein, paralleled the results of motor function. The expression of GDNF in GDNF-modified human AFMSCs was demonstrated up to 4 weeks; however, the expression decreased over time. Conclusions The GDNF-modified human AFMSCs appeared to promote nerve regeneration. The consecutive expression of GDNF was demonstrated in GDNF-modified human AFMSCs up to 4 weeks. These findings support a nerve regeneration scenario involving cell transplantation with additional neurotrophic factor secretion.

Nerve conduction in relation to vibration exposure - a non-positive cohort study

BackgroundPeripheral neuropathy is one of the principal clinical disorders in workers with hand-arm vibration syndrome. Electrophysiological studies aimed at defining the nature of the injury have provided conflicting results. One reason for this lack of consistency might be the sparsity of published longitudinal etiological studies with both good assessment of exposure and a well-defined measure of disease. Against this background we measured conduction velocities in the hand after having assessed vibration exposure over 21 years in a cohort of manual workers.MethodsThe study group consisted of 155 male office and manual workers at an engineering plant that manufactured pulp and paper machinery. The study has a longitudinal design regarding exposure assessment and a cross-sectional design regarding the outcome of nerve conduction. Hand-arm vibration dose was calculated as the product of self-reported occupational exposure, collected by questionnaire and interviews, and the measured or estimated hand-arm vibration exposure in 1987, 1992, 1997, 2002, and 2008. Distal motor latencies in median and ulnar nerves and sensory nerve conduction over the carpal tunnel and the finger-palm segments in the median nerve were measured in 2008. Before the nerve conduction measurement, the subjects were systemically warmed by a bicycle ergometer test.ResultsThere were no differences in distal latencies between subjects exposed to hand-arm vibration and unexposed subjects, neither in the sensory conduction latencies of the median nerve, nor in the motor conduction latencies of the median and ulnar nerves. Seven subjects (9%) in the exposed group and three subjects (12%) in the unexposed group had both pathological sensory nerve conduction at the wrist and symptoms suggestive of carpal tunnel syndrome.ConclusionNerve conduction measurements of peripheral hand nerves revealed no exposure-response association between hand-arm vibration exposure and distal neuropathy of the large myelinated fibers in a cohort of male office and manual workers.

NOVEL COMPOUND HETEROZYGOUS ALS2 MUTATIONS CAUSE JUVENILE AMYOTROPHIC LATERAL SCLEROSIS IN JAPAN

Homozygous mutations in ALS2 on chromosome 2q33 are responsible for autosomal recessive, early-onset forms of upper motor neuron diseases such as infantile ascending hereditary spastic paraplegia (IAHSP) and juvenile primary lateral sclerosis (JPLS).1 These mutations are rarely associated with lower motor neuron involvement in juvenile amyotrophic lateral sclerosis (JALS).2 Seventeen mutations from 16 families have been reported, but the phenotype–genotype correlation remains unclear.3–5 We searched for ALS2 mutations in 2 Japanese siblings presenting with infantile-onset ascending spastic paraplegia, pseudobulbar palsy, and amyotrophy of the extremities. ### Case reports. The older sibling was a 32-year-old Japanese man who started walking on tiptoes at 13 months of age and had never run. He developed dysarthria at 11 years of age and lost the ability to speak at 14. He displayed spasticity predominantly in the lower limbs, bilateral extensor plantar responses, and complete paralysis of the tongue without atrophy or fasciculation at 32 years of age. He also had discrete signs of lower motor neuron involvement manifesting as muscular atrophy of the distal upper and lower limbs. However, he was ambulatory with support and there was no evidence of cognitive dysfunction. Brain and spinal MRI showed no abnormalities. The peripheral nerve conduction velocities and latencies were …

Patterns of activity-dependent conduction velocity changes differentiate classes of unmyelinated mechano-insensitive afferents including cold nociceptors, in pig and in human

Activity-dependent slowing of conduction velocity (ADS) differs between classes of human nociceptors. These differences likely reflect particular expression and use-dependent slow inactivation of axonal ion channels and other mechanisms governing axonal excitability. In this study, we compared ADS of porcine and human cutaneous C-fibers. Extracellular recordings were performed from peripheral nerves, using teased fiber technique in pigs and microneurography in humans. We assessed electrically-induced conduction changes and responsiveness to natural stimuli. In both species, the group of mechano-insensitive C-fibers showed the largest conduction slowing (∼30%) upon electrical stimulation (2 Hz for 3 min). In addition, we found mechano-insensitive cold nociceptors in pig that slowed only minimally (<10% at 2 Hz), and a similar slowing pattern was found in some human C-fibers. Mechano-sensitive afferents showed an intermediate conduction slowing upon 2 Hz stimulation (pig: 14%, human 23%), whereas sympathetic efferent fibers in pig and human slowed only minimally (5% and 9%, respectively). In fiber classes with more pronounced slowing, conduction latencies recovered slower; i.e. mechano-insensitive afferents recovered the slowest, followed by mechano-sensitive afferents whereas cold nociceptors and sympathetic efferents recovered the fastest. We conclude that mechano-insensitive C-fiber nociceptors can be differentiated by their characteristic pattern of ADS which are alike in pig and human. Notably, cold nociceptors with a distinct ADS pattern were first detected in pig. Our results therefore suggest that the pig is a suitable model to study nociceptor class-specific changes of ADS.

Effects of ropivacaine dosage on electrophysiologic changes of the sciatic nerve in diabetic rats

Objective To observe the effects of clinical routine dasages 0.375% and 0.5% ropivacaine on electrophysiologic of changes of the sciatic nerve in diabetic rats. Methods Twelve healthy rsts and 12 rats with streptozotocin (STZ) induced diabetic peripheral,neuropathy were:used and further divided to 2 groups.Both sciatic nerves were exposed under general anesthesia.0.5 ml of either 0.375% or 0.5% ropivacaine wasiniected in close proximity to the right seiatic nerve which was the experimental side.0.5 ml of 0.9% sodium chloride was iniected in close proximity to the left sciatic nerve which served as control.Motor nerve conduction velocity(MNCV),amplitude (AMP) and latency (LAT) of compound muscle action potential were recorded before injection,at the moment of injection,at one minute intervals for to 15 minutes and 48 hours after the injection. Results MNCV,AMP and LAT didn't change at all the observed time points of the 0.9% sodium chloride iniected control side in either healthy rats or diabetic rats.MNCV and AMP in normal rats injected with 0.375% ropivaeaine began to decrease at average 4 minutes and became zero at 10 minutes,while they began to decrease at average 3 minutes and dropled to zero at average 9 minutes while injected with 0.5% ropivacaine.These parameters returned to baseline levels after 48 hours.MNCV and AMP in diabetic rats injected with 0.375% ropivacaine began to decrease at average one minute and became zero at 7 minutes,while they began to decrease at average one minute and dropped to zero at 6 minutes with 0.5% ropivacaine injection.The time course had statistically significant difference between diabetic and normal rats.LAT had the same change pattern as MNCV and AMP.After 48 hours.MNCV in 0.375% ropivacaine diabetic group was not different from baseline value(P＜0.05),but AMP and LAT Were still significantly different from baseline levels.MNCV, AMP and LAT in 0.5% ropivacaine diabetic group had significant difference comparing to baseline levels and levels of 0.375% ropivaeaine diabetic group(P＜0.05). Conclusion Either 0.375% or 0.5% ropivacaine may deteriorate the diabetic peripheral nerve injury,the latter more remarkable. Key words: Anesthetics; Diabetic neuropathies; Neural conduction

Dietary supplement with fermented soybeans, natto, improved the neurobehavioral deficits after sciatic nerve injury in rats

Clearance of fibrin and associated inflammatory cytokines by tissue-type plasminogen activator (t-PA) is related to improved regeneration in neurological disorder. The biological activity of fermented soybean (natto) is very similar to that of t-PA. We investigated the effect of the dietary supplement of natto on peripheral nerve regeneration. The peripheral nerve injury was produced by crushing the left sciatic nerve with a vessel clamp in Sprague–Dawley rats. The injured animals were fed orally either with saline or natto (16 mg/day) for seven consecutive days after injury. Increased functional outcome such as sciatic nerve functional index, angle of ankle, compound muscle action potential and conduction latency were observed in natto-treated group. Histological examination demonstrated that natto treatment improved injury-induced vacuole formation, S-100 and vessel immunoreactivities and axon loss. Oral intake of natto prolonged prothrombin time and reduced fibrinogen but did not change activated partial thromboplastin time and bleeding time. Furthermore, natto decreased injury-induced fibrin deposition, indicating a tolerant fibrinolytic activity. The treatment of natto significantly improved injury-induced disruption of blood–nerve barrier and loss of matrix component such as laminin and fibronectin. Sciatic nerve crush injury induced elevation of tumor necrosis factor α (TNF-α) production and caused apoptosis. The increased production of TNF-α and apoptosis were attenuated by natto treatment. These findings indicate that oral intake of natto has the potential to augment regeneration in peripheral nerve injury, possibly mediated by the clearance of fibrin and decreased production of TNF-α.

Autonomic dysfunction in experimental allergic neuritis.

Beat-to-beat variation (R-R variation) in the electrocardiogram was studied in experimental allergic neuritis in the Sprague-Dawley rat. Reduced R-R variations were found in 2 of 10 animals, probably as a sign of autonomic dysfunction. The vagal nerves from these two animals, studied in vitro, showed disturbed conduction. In one animal prolonged conduction latencies to supramaximal electrical stimuli were found. Vagal nerves from controls and from animals without clinical symptoms showed normal conduction. Histologically, the vagal nerves from affected animals showed a slight inflammatory cell infiltration and signs of demyelination but there was no evidence of involvement of the brainstem vasomotor nuclei. Thus, we suggest that the autonomic dysfunction in experimental allergic neuritis, measured as reduced R-R variations, is caused by a peripheral vagal neuropathy.

Re‐emerging microneurography

Re‐emerging microneurography

Tarsal tunnel syndrome: Assessment of treatment outcome with an anatomic pain intensity scale

Assessment of treatment outcomes for tarsal tunnel syndrome may be improved with a standardized pain rating scale using a descriptive anatomical foot model for pretreatment and post-treatment plantar foot pain analysis. Prospective evaluation of 46 consecutive patients (56 feet) who had non-operative and surgical treatment for tarsal tunnel syndrome. Pain intensity was documented before and after treatment with the Wong-Baker FACES Pain Rating Scale applied to the anatomic nerve regions of the plantar aspect of the foot. In patients who had successful non-operative treatment, overall pain intensity was significantly improved in the medial calcaneal, medial plantar, and lateral plantar nerve regions. In patients who had ongoing symptoms despite non-operative treatment, surgical treatment resulted in significant pain improvement in the medial calcaneal and medial plantar, but not lateral plantar, nerve regions. Pretreatment motor nerve conduction latency was significantly greater in patients who had surgical treatment than those who had only non-operative treatment. Anatomic pain intensity rating models may be useful in the pretreatment and follow-up evaluation of tarsal tunnel syndrome. Predictors of failed non-operative treatment included longer motor nerve conduction latency and greater predominance of foot comorbidities.

Oligodendrocytes Changing the Rules: Action Potentials in Glia and Oligodendrocytes Controlling Action Potentials

Two long-standing rules in cellular neuroscience must now be amended with the publication of two studies on myelin-forming glia in the CNS: 1) Neurons can no longer be considered the only cells that fire electric impulses in the brain. 2) Synapses between neurons are not the only way electrical information is regulated as it propagates through neural circuits: oligodendrocytes can cause rapid activity-dependent changes in spike latency. A category of oligodendrocyte precursor cells (OPCs) has been identified that can fire action potentials, and their excitation is driven by synapses from axons. This finding has relevance to excitotoxicity in ischemia, but the normal function may be to regulate myelination according to functional activity in axons. A second study reveals that action potential propagation through CNS axons can be rapidly regulated by oligodendrocytes. Mature oligodendrocytes in the rat hippocampus are depolarized by theta burst stimulation of axons, and when the oligodendrocytes are depolarized by current injection in paired whole-cell recordings with CA1 pyramidal neurons, the latency of impulse conduction through the axons it ensheathes rapidly decreases. This unprecedented finding suggests a dynamic role for myelin in regulating impulse transmission through axons, promoting neural synchrony among the multiple axons under the domain of an individual oligodendrocyte.

Test of sensory nerve in patients with Kennedy disease

To study the electrophysiological and pathological features of Kennedy disease (KD) and to make sure the functional and anatomical change of the sensory nerve of KD patients. Electrophysiological and pathological tests were performed in 14 KD patients, including electromyogram, conduction velocities of median, ulnar, peroneal, tibial, and sural nerves, trigemino-cervical reflex (TCR), contact heat evoked potential (CHEP), and biopsy of the sural nerves. During TCR, the patients lay on the back, holding the heads slightly raised to make the sternocleidomastoid muscles contract slightly. Electrical stimuli were applied to the infraorbital nerves and recording electrodes were placed in the sternocleidomastoid muscles. For CHEP, contact heat was delivered via a circular thermode to excite selectively nociceptors with a rapid rising time at 70 degrees C/s to elicit pain and CHEP. Thermal stimuli were sent at 54.5 degrees C to three body sites: skin of back of hand, proximal volar forearm, and C7. The CHEPs were recorded from Cz and Pz. The sensory conduction velocity and latency were almost normal, while the amplitude of the sensory nerve action potential (SNAP) declined to 0.65 - 2.85 microV. The latency of trigemino-cervical reflex was longer than normal with the onset peak latency of (38.9 +/- 7.0) ms. The configuration was asymmetric. The onset peak latencies when the skin of the back of hand, volar surface of forearm, and C7 were stimulated were (613 +/- 57), (595 +/- 32), and (489 +/- 37) ms respectively. Biopsy of the sural nerves showed that the large myelinated nerve fiber was decreased. Sensory nerve is involved in the patients with Kennedy disease, including the large and small fibers.

Enhanced regeneration in spinal cord injury by concomitant treatment with granulocyte colony-stimulating factor and neuronal stem cells

Granulocyte colony-stimulating factor (G-CSF) inhibits programmed cell death and stimulates neuronal progenitor differentiation. Neuronal stem cells transplanted into injured spinal cord can survive, differentiating into astroglia and oligodendroglia, and supporting axon growth and myelination. Herein, we evaluate the combined effects of G-CSF and neuronal stem cells on spinal cord injury. For 40 Sprague-Dawley rats ( n = 10 in each group) transverse spinal cord resections at the T8–9 level were carried out, leaving an approximately 2-mm gap between the distal and proximal ends of the cord. Neuronal stem cells embedded in fibrin glue treated with or without G-CSF (50 μg/kg × 5 days) (groups III and IV) or fibrin glue with or without G-CSF (50 μg/kg × 5 days) (groups I and II) were transplanted into the gap in the injured spinal cord. Spinal cord regeneration was assessed using a clinical locomotor rating scale scores and electrophysiological, histological and immunohistochemical analysis 3 months after injury. Regeneration was more advanced in group IV than in groups III or II according to the clinical motor score, motor evoked potential, and conduction latency. Most advanced cord regeneration across the gap was observed in group IV rats. Higher densities of bromodeoxyuridine in the injured area and higher expression levels of Neu-N and MAP-2 over the distal end of the injured spinal cord were observed in group IV compared with groups II or III, but there was no significant difference in expression of glial fibrillary acid protein. This synergy between G-CSF and neuronal stem cells may be due to increased proliferation of progenitor cells in the injured area and increased expression of neuronal stem cell markers extrinsically or intrinsically in the distal end of injured cord.

Amelioration effect of Zhenqing Capsule on peripheral neuropathy in type 1 diabetic rats

To investigate the effects of Zhenqing Capsule (ZQC), a compound traditional Chinese herbal medicine, in treating type 1 diabetic rats with peripheral neuropathy. Type 1 diabetes was induced by caudal vein injection of high-dose streptozotocin in 30 male Wistar rats. The thirty diabetic rats were randomly divided into three groups: ZQC-treated group, untreated group and aminoguanidine-treated group. Another group of 10 rats was taken as normal control. After 10-week treatment, the changes of body weight and fasting plasma glucose level were measured, and the serum MDA level and the changes of neurological electrophysiology were analyzed. The samples of sciatic nerve in diabetic rats were taken for morphological observation. The MDA level in type 1 diabetic rats was notably reduced in ZQC-treated group as compared with the untreated group (P<0.01). Compared with the untreated group, ZQC could improve the electrophysiology of sciatic nerve including conduction velocity (P<0.05), latency (P<0.01) and wave amplitude (P<0.05). The nerve myelin staining results showed that segmental demyelination of the nerve fibers in ZQC-treated group was not as serious as that in the untreated group. ZQC can obviously ameliorate the neurological electrophysiological function and the pathological changes of peripheral nerve in type 1 diabetic rats through the removal of free radical and resistance of lipid peroxidation.

Imbalance in multiple sclerosis: A result of slowed spinal somatosensory conduction

Balance problems and falls are common in people with multiple sclerosis (MS) but their cause and nature are not well understood. It is known that MS affects many areas of the central nervous system that can impact postural responses to maintain balance, including the cerebellum and the spinal cord. Cerebellar balance disorders are associated with normal latencies but reduced scaling of postural responses. We therefore examined the latency and scaling of automatic postural responses, and their relationship to somatosensory evoked potentials (SSEPs), in ten people with MS and imbalance and ten age-, sex-matched, healthy controls. The latency and scaling of postural responses to backward surface translations of five different velocities and amplitudes, and the latency of spinal and supraspinal somatosensory conduction, were examined. Subjects with MS had large, but very delayed automatic postural response latencies compared to controls (161 ± 31 ms vs. 102 ± 21 ms, p < 0.01) and these postural response latencies correlated with the latencies of their spinal SSEPs (r = 0.73, p < 0.01). Subjects with MS also had normal or excessive scaling of postural response amplitude to perturbation velocity and amplitude. Longer latency postural responses were associated with less velocity scaling and more amplitude scaling. Balance deficits in people with MS appear to be caused by slowed spinal somatosensory conduction and not by cerebellar involvement. People with MS appear to compensate for their slowed spinal somatosensory conduction by increasing the amplitude scaling and the magnitude of their postural responses.

Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the central nervous system

BackgroundCancer treatment with a variety of chemotherapeutic agents often is associated with delayed adverse neurological consequences. Despite their clinical importance, almost nothing is known about the basis for such effects. It is not even known whether the occurrence of delayed adverse effects requires exposure to multiple chemotherapeutic agents, the presence of both chemotherapeutic agents and the body's own response to cancer, prolonged damage to the blood-brain barrier, inflammation or other such changes. Nor are there any animal models that could enable the study of this important problem.ResultsWe found that clinically relevant concentrations of 5-fluorouracil (5-FU; a widely used chemotherapeutic agent) were toxic for both central nervous system (CNS) progenitor cells and non-dividing oligodendrocytes in vitro and in vivo. Short-term systemic administration of 5-FU caused both acute CNS damage and a syndrome of progressively worsening delayed damage to myelinated tracts of the CNS associated with altered transcriptional regulation in oligodendrocytes and extensive myelin pathology. Functional analysis also provided the first demonstration of delayed effects of chemotherapy on the latency of impulse conduction in the auditory system, offering the possibility of non-invasive analysis of myelin damage associated with cancer treatment.ConclusionsOur studies demonstrate that systemic treatment with a single chemotherapeutic agent, 5-FU, is sufficient to cause a syndrome of delayed CNS damage and provide the first animal model of delayed damage to white-matter tracts of individuals treated with systemic chemotherapy. Unlike that caused by local irradiation, the degeneration caused by 5-FU treatment did not correlate with either chronic inflammation or extensive vascular damage and appears to represent a new class of delayed degenerative damage in the CNS.

Effect of early onset otitis media on brainstem and cortical auditory processing

BackgroundOtitis media (OM) leads to significant reduction in the hearing sensitivity. The reduced auditory input, if in the early years of life when the auditory neural system is still maturing, may adversely influence the structural as well as functional development of the system. Past research has reported abnormalities in both the structure and function of brainstem nuclei following auditory deprivation, but, it has not necessarily focused on children who had OM in their first year of life. It can also be said that if auditory processing is affected at the brainstem level because of early onset OM (reduced auditory input in the crucial periods of neural development), then, it may be said that auditory processing is also affected at the cortical level because it receives distorted input from the brainstem. Therefore, the purpose of this study was to document the effects of early onset OM on auditory processing, if any, at the brainstem as well as at cortical levels. A related purpose of the study was to investigate the persistence of the effects of early onset OM, if any, on auditory processing.MethodsA cross sectional approach and a standard group comparison design was used in the study. Thirty children, who had OM between 6 and 12 months of age and who were in the age range of 3.1 – 5.6 years participated in the study. Children with OM were divided into 3 groups based on their age. Click evoked auditory brainstem responses (ABRs) and late latency responses (LLRs) were recorded from these children, and the responses were compared with those from age and gender matched normal children without any history of OM. The data from the 2 groups was statistically analyzed through independent t test. Pearson's Product Moment correlation was computed to examine the relationship between results of ABR and LLR in children with early onset OM.ResultsThe mean central conduction time was significantly increased and the mean amplitude of wave I and III of ABRs was significantly reduced in children with early onset OM compared to normal children. Also, the latency of all LLR waves was significantly less in children with early onset OM than in normal children. However, significant differences in mean values of either ABR or LLR (latencies or interwave intervals as the case may be) were observed only in 3-year old children. There was a significant, but negative association between central conduction time and latency of LLRs.ConclusionOM in the first year of life leads to negative effects on brainstem signal processing even if it has occurred only for a short duration (maximum of 3 months). In such a situation, auditory cortical structures probably show compensatory changes through central gain to offset the prolonged central conduction time. Although the results of the present study showed that the negative effects of early onset OM (occurring in the first year of life) on auditory processing disappeared by the time the children were 4.1 years, there is need for longitudinal studies on this to confirm the findings.

Post-injury regeneration in rat sciatic nerve facilitated by neurotrophic factors secreted by amniotic fluid mesenchymal stem cells

Amniotic fluid mesenchymal stem cells have the ability to secrete neurotrophic factors that are able to promote neuron survival in vitro. The purpose of this study was to evaluate the effects of neurotrophic factors secreted by rat amniotic fluid mesenchymal stem cells on regeneration of sciatic nerve after crush injury. Fifty Sprague–Dawley rats weighing 250–300 g were used. The left sciatic nerve was crushed with a vessel clamp. Rat amniotic fluid mesenchymal stem cells embedded in fibrin glue were delivered to the injured nerve. Enzyme-linked immunosorbent assay (ELISA) and immunocytochemistry were used to detect neurotrophic factors secreted by the amniotic fluid mesenchymal stem cells. Nerve regeneration was assessed by motor function, electrophysiology, histology, and immunocytochemistry studies. Positive CD29/44, and negative CD11b/45, as well as high levels of expression of brain-derived neurotrophic factor, glia cell line-derived neurotrophic factor, ciliary neurotrophic factor (CNTF), nerve growth factor, and neurotrophin-3 (NT-3) were demonstrated in amniotic fluid mesenchymal stem cells. Motor function recovery, the compound muscle action potential, and nerve conduction latency showed significant improvement in rats treated with amniotic fluid mesenchymal stem cells. ELISA measurement in retrieved nerves displayed statistically significant elevation of CNTF and NT-3. The immunocytochemical studies demonstrated positive staining for NT-3 and CNTF in transplanted cells. The histology and immunocytochemistry studies revealed less fibrosis and a high level of expression of S-100 and glial fibrillary acid protein at the crush site. Rat amniotic fluid mesenchymal stem cells may facilitate regeneration in the sciatic nerve after crush injury. The increased nerve regeneration found in this study may be due to the neurotrophic factors secreted by amniotic fluid mesenchymal stem cells.