Recovery Of Sensory Function Research Articles

Lack of correlation between spinal microgliosis and long-term development of tactile hypersensitivity in two different sciatic nerve crush injury.

Microglia activation following peripheral nerve injury has been shown to contribute to central sensitization of the spinal cord for the development of neuropathic pain. In a recent study, we reported that the amount of nerve damage does not necessarily correlate with chronic pain development. Here we compared the response of spinal microglia, using immunohistochemistry as a surrogate of microglial activation, in mice with two different types of crush injury of the sciatic nerve. We confirmed that incomplete crush of the sciatic nerve (partial crush injury, PCI) resulted in tactile hypersensitivity after the recovery of sensory function (15 days after surgery), whereas the hypersensitivity was not observed after the complete crush (full crush injury, FCI). We observed that immunoreactivity for Iba-1, a microglial marker, was greater in the ipsilateral dorsal horn of lumbar (L4) spinal cord of mice 2 days after FCI compared to PCI, positively correlating with the intensity of crush injury. Ipsilateral Iba-1 reactivity was comparable between injuries at 7 days with a significant increase compared to the contralateral side. By day 15 after injury, ipsilateral Iba-1 immunoreactivity was much reduced compared to day 7 and was not different between the groups. Our results suggest that the magnitude of the early microgliosis is dependent on injury severity, but does not necessarily correlate with the long-term development of chronic pain-like hypersensitivity after peripheral nerve injury.

Recent advances in treatment of cerebral ischemic stroke

Ischemic stroke occurs when there is an obstruction or collapse of a blood vessel in the head or neck, which causes a lack of oxygen to the brain. Due to the lack of oxygen, detrimental motor and sensory deficits transpire in the areas of the brain that are affected. When an individual suffers an ischemic stroke, there is a specific time window and treatment regimen that is used to manage symptoms of a stroke. The principal concerns with stroke treatments are that don’t fully recover motor and sensory function lost during a stroke occurrence. With the use of stem cells from several sources, they can be reprogrammed and transplanted into the brain to facilitate full recovery of motor and sensory function. The purpose of this review article is to investigate the precursors, diagnostic methods, treatment techniques and new stem cell treatment research associated with ischemic stroke in anticipation to cure cognitive, sensory and motor dysfunction.

Cerium oxide nanoparticles as a new neuroprotective agent to promote functional recovery in a rat model of sciatic nerve crush injury

Background Peripheral nerve injury is a common clinical disorder. The aim of the present study was to investigate the role of cerium oxide nanoparticles on axonal regeneration and functional recovery of the sciatic nerve after a crush injury in the rat model. Method A total of 40 adult male Wistar rats were divided into four groups. The animals underwent deep anesthesia. Afterward, the right sciatic nerve of rats was exposed and crushed. In two experimental groups, rats were treated intraperitoneally with cerium oxide nanoparticles at the dosage of 20 or 80 mg/kg daily for 1 week. The control group was given a vehicle. Then, during the nerve regeneration motor and sensory function recovery tests, histomorphometric evaluations, histological assessment of gastrocnemius muscle, and gastrocnemius muscle wet weights tests were performed. Results Results demonstrated that the rate of nerve regeneration increased with the administration of cerium oxide nanoparticle in high doses. Also, the morphometric analysis showed that the number of myelinated fibers and myelin sheath thicknesses was significantly greater in the cerium oxide nanoparticle group versus the control group. Other parameters also improved in the cerium oxide nanoparticle treatment groups compared with the control group. Conclusion These data indicate that this nanoparticle has therapeutic potential and can be considered as a new treatment for nervous system regeneration.

Management of Radial Nerve Lesions after Trauma or Iatrogenic Nerve Injury: Autologous Grafts and Neurolysis.

Background: Proximal radial nerve lesions located between the brachial plexus and its division into the superficial and deep branches are rare but severe injuries. The majority of these lesions occur in association with humerus fractures, directly during trauma or later during osteosynthesis for fracture treatment. Diagnostics and surgical interventions are often delayed. The best type of surgical treatment and the outcome to be expected often is uncertain. Methods: Twelve patients with proximal radial nerve lesions due to trauma or prior surgery were included in this study and underwent neurolysis (n = 6) and sural nerve graft interposition (n = 6). Retrospective analysis of the collected patient data was performed and the postoperative course was systematically evaluated. The Disabilities of the Arm, Shoulder, and Hand (DASH) and the LSUHS (Louisiana State University Health Sciences) scores were used to determine regeneration after surgery. Comparison between the patients’ and calculated normative DASH scores was performed. Results: All patients had a traumatically or iatrogenically induced proximal radial nerve lesion and underwent secondary treatments. The average time from radial nerve lesion occurrence to surgical intervention was approximately four months (1.5–10 months). Eight patients (66.67%) had a humeral fracture. During follow up, no statistically significant difference between the calculated normative and the patients’ DASH scores was observed. The LSUHS scores were at least satisfactory. Conclusions: Neurolysis or sural nerve graft interposition performed within a specific period of time are the primary treatment options for radial nerve lesions. They should be performed depending on the lesion type. Regeneration to a satisfactory degree was observed in all patients, and the majority achieved full recovery of sensory and motor functions. This was the first study to highlight the efficiency of neurolysis and sural nerve graft interposition as secondary treatment interventions, especially for radial nerve lesions.

Neuromodulatory Interventions for Traumatic Brain Injury.

Neuromodulatory Interventions for Traumatic Brain Injury.

Fabrication of 3D Scaffolds Displaying Biochemical Gradients along Longitudinally Oriented Microchannels for Neural Tissue Engineering.

Biochemical and physical guidance cues are both pivotal for axonal guidance and nerve regeneration. However, fabrication of a platform that can integrate biochemical gradients and topographical guidance cues remains challenging, especially in a three-dimensional (3D) scaffold that closely mimics in vivo axonal outgrowth conditions and ready to be used for in vivo nerve repair. In this study, a new method was introduced to construct 3D scaffolds displaying continuous biochemical gradients along longitudinally oriented microchannels by combining the modified 3D printing and directional freezing techniques. Fluorescence analysis and ELISA results demonstrated that a continuous biochemical gradient was formed, and scanning electron microscopy revealed a longitudinally oriented microstructure. Dorsal root ganglia explants seeded on the longitudinal sections of the newly developed scaffold (scaffold with nerve growth factor gradient along oriented microstructure, G-NGF + OS) showed that 81.3 ± 4.5% of neurites oriented within ±10°, 0.3 ± 0.1 of guidance ratio, and 1.5-fold of the average length of neurites on the high-nerve growth factor (NGF) concentration side compared to that on the low-NGF concentration side, which were significantly higher than those in the other groups. In addition, the G-NGF + OS scaffold was used to repair a 15 mm sciatic nerve defect in rats. Immunofluorescence staining, Fluoro-Gold retrograde tracing, and transmission electron microscopy results confirmed that the G-NGF + OS scaffold enhanced nerve regeneration to the distal target and promoted myelination of regenerated axons. More importantly, the sciatic functional index and the von Frey test demonstrated that the G-NGF + OS scaffold accelerated sensory and motor functional recovery. These results provide new insights into the importance of combining topographical guidance cues with bioactive molecule gradient cues for neural tissue engineering. The 3D scaffold displaying biochemical gradients along longitudinally oriented microchannels represents a promising platform for the development of advanced devices for severe nervous system injuries.

CURIOUS CASE OF CAISSON DISEASE

SESSION TITLE: Medical Student/Resident Critical Care SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: Decompression sickness is caused by rapid changes in breath air pressure and increased amounts of oxygen and nitrogen in different body tissues. As stated by Henry’s law, at a constant temperature the amount of gas dissolved is proportional to its partial pressure above the liquid. As the diver rapidly ascends, the air pressure substantially decreases creating air bubbles that can obstruct different blood vessels creating a wide variety of complications, including ischemia. With more than 9.5 million licensed divers, only 1,000 approximate cases of decompression sickness are reported per year, making it a rare diagnosis. CASE PRESENTATION: A 33 years-old male scuba diver was brought to the ED by ambulance after being found unconscious on the beach shore. Medical history consistent with MDD and cocaine dependence. While en route to the ED, developed neck pain, loss of muscle strength with preserved consciousness. Symptoms developed after five consecutives dives at 115 feet of sea water (fsw) without safety stops nor surface intervals. Spinal MRI was performed with findings consistent with acute isquemia at C6-T2 level. At this point the diagnosis of severe Caisson’s disease was made. Physical exam consisted of severe sensory neurologic impairment at level of T4-T5 dermatome accompanied by motor deficit in the lower extremities and left upper extremity motor deficit at level C8-T1. Initial laboratories showed increased coagulation factors and serum pH of 7.2. Immediately after diagnosis Hyperbaric Oxygen Therapy (HBO) was initiated. During his first session the patient developed respiratory distress and required endotracheal intubation. Follow up spinal MRI showed significant improvement of edema, however, patient’s neurological deficit persisted despite receiving corticosteroids and five HBO sessions. At this point the decision to continue HBO was made. By day 10 in the hospital the patient’s respiratory symptoms improved significantly and MV was discontinued. The patient completed a total of 20 sessions and regained complete movement and sensation in his body. He was discharged for inpatient rehabilitation where he completed therapy. DISCUSSION: This case illustrates the potential complications of decompression sickness and the importance of a prompt identification and rapid treatment to diminish the neurological sequelae and irreversible damage. Identifying precipitant factors that could further aggravate the ischemic symptoms are essential to decide whether the patient will benefit from an extended treatment. The decision to lengthen therapy with hyperbaric oxygen was conclusively beneficial despite delayed neurological improvement. Ultimately minimizing the tissue damage and increasing the odds of motor and sensory function recovery. CONCLUSIONS: Prolonged hyperbaric oxygen therapy could be beneficial in some patients. However, decisions should be made case by case. Reference #1: Hallenbeck, J. M., A. A. Bove, and D. H. Elliott. "Mechanisms underlying spinal cord damage in decompression sickness." Neurology 25.4 (1975): 308-308. Reference #2: Bühlmann, Albert A. Decompression—Decompression Sickness. Springer Science & Business Media, 2013. Reference #3: Weathersby, P. K., L. D. Homer, and E. T. Flynn. "On the likelihood of decompression sickness." Journal of Applied Physiology 57.3 (1984): 815-825. DISCLOSURES: No relevant relationships by Felix Aponte Santos, source=Web Response No relevant relationships by Rosa Marrero-Fernandez, source=Web Response No relevant relationships by Nikita Rabelo-Pagán, source=Web Response No relevant relationships by Nicole Rassi, source=Web Response No relevant relationships by Jean Rodriguez/Agramonte, source=Web Response

Acute upper limb compartment syndrome in children: special focus on nerve recovery

BackgroundMany studies have discussed acute compartment syndrome in children associated with or without fractures and have given their visible perspectives. Little is known about the nerve involvement and the factors...

Neuroprotection in the Acute Stage Enables Functional Recovery Following Repair of Chronic Cervical Root Transection After a 3-Week Delay.

Preganglionic cervical root transection (PCRT) is the most severe type of brachial plexus injury. In some cases, surgical procedures must be postponed for ≥3 wk until electromyographic confirmation. However, research works have previously shown that treating PCRT after a 3-wk delay fails to result in functional recovery. To assess whether the immunosuppressive drug sirolimus, by promoting neuroprotection in the acute phase of PCRT, could enable functional recovery in cases of delayed repair. First, rats received a left 6th to 8th cervical root transection, after which half were administered sirolimus for 1 wk. Markers of microglia, astrocytes, neurons, and autophagy were assessed at days 7 and 21. Second, animals with the same injury received nerve grafts, along with acidic fibroblast growth factor and fibrin glue, 3 wk postinjury. Sirolimus was administered to half of them for the first week. Mechanical sensation, grasping power, spinal cord morphology, functional neuron survival, nerve fiber regeneration, and somatosensory-evoked potentials (SSEPs) were assessed 1 and 23 wk postinjury. Sirolimus was shown to attenuate microglial and astrocytic proliferation and enhance neuronal autophagy and survival; only rats treated with sirolimus underwent significant sensory and motor function recovery. In addition, rats who achieved functional recovery were shown to have abundant nerve fibers and neurons in the dorsal root entry zone, dorsal root ganglion, and ventral horn, as well as to have SSEPs reappearance. Sirolimus-induced neuroprotection in the acute stage of PCRT enables functional recovery, even if surgical repair is performed after a 3-wk delay.

Peripheral nerve regeneration in rats by chitosan/alginate hydrogel composited with Berberine and Naringin nanoparticles: in vitro and in vivo study

In the current study, we prepared chitosan (Cs)/Alginate (Alg) hydrogel containing Berberine (Ber)-loaded Cs nanoparticles (NPs) and Naringin (Nar)-loaded Cs NPs as the promising biomaterials for peripheral nerve regeneration. The Ber- and Ner-loaded NPs were synthesized via the ion gelation method and incorporated into Cs/Alg hydrogel. The characterizations of NPs showed that Ber-loaded NPs have an average size of 594 nm with the encapsulation efficacy (EE) of 51.6 ± 7.4%, and Nar-loaded NPs have an average size of 636 nm with EE of 47.1 ± 5.8%. The pore size of Cs/Alg hydrogel and Cs/Alg/Ber/Nar hydrogel were 22 ± 11 and 32 ± 13 μm, respectively. It was observed that the swelling and weight loss value of the prepared hydrogels were suitable for nerve regeneration. The compression strength of Cs/Alg hydrogel and Cs/Alg/Ber/Nar hydrogel were 39.7 ± 4.7 kPa and 32.08 ± 6.8 kPa. The releasing measurement showed a burst release at the first days following a sustained release of up to about 90% for 24 days. The in vitro studies illustrated that the hydrogels were hemo- and biocompatible with the significant proliferative effect on PC12 cells. The animal studies showed that the treatment using the hydrogels significantly promoted nerve regeneration. Treatment of the damaged nerve using Cs/Alg/Ber/Nar hydrogel resulted in the sensory function recovery (hot plate latency of 4.66 ± 0.57 s), the motor function recovery (sciatic index function of −14.6 ± 3.7) and anatomical healing (the gastrocnemius muscle cross-sectional area of 2509 ± 142 μm2). In conclusion, the results indicate that the prepared hydrogels possess promising characteristics and significantly enhanced sensory and motor functional recovery, as well as anatomical healing.

Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models.

Ischemic brain injury causes neuronal death and inflammation. Inflammation activates protein-tyrosine phosphatase 1B (PTP1B). Here, we tested the significance of PTP1B activation in glutamatergic projection neurons on functional recovery in two models of stroke: by photothrombosis, focal ischemic lesions were induced in the sensorimotor cortex (SM stroke) or in the peri-prefrontal cortex (peri-PFC stroke). Elevated PTP1B expression was detected at 4 days and up to 6 weeks after stroke. While ablation of PTP1B in neurons of neuronal knockout (NKO) mice had no effect on the volume or resorption of ischemic lesions, markedly different effects on functional recovery were observed. SM stroke caused severe sensory and motor deficits (adhesive removal test) in wild type and NKO mice at 4 days, but NKO mice showed drastically improved sensory and motor functional recovery at 8 days. In addition, peri-PFC stroke caused anxiety-like behaviors (elevated plus maze and open field tests), and depression-like behaviors (forced swimming and tail suspension tests) in wild type mice 9 and 28 days after stroke, respectively, with minimal effect on sensory and motor function. Peri-PFC stroke-induced affective disorders were associated with fewer active (FosB+) neurons in the PFC and nucleus accumbens but more FosB+ neurons in the basolateral amygdala, compared to sham-operated mice. In contrast, mice with neuronal ablation of PTP1B were protected from anxiety-like and depression-like behaviors and showed no change in FosB+ neurons after peri-PFC stroke. Taken together, our study identifies neuronal PTP1B as a key component that hinders sensory and motor functional recovery and also contributes to the development of anxiety-like and depression-like behaviors after stroke. Thus, PTP1B may represent a novel therapeutic target to improve stroke recovery. All procedures for animal use were approved by the Animal Care and Use Committee of the University of Ottawa Animal Care and Veterinary Service (protocol 1806) on July 27, 2018.

Numbers of Axons in Spared Neural Tissue Bridges But Not Their Widths or Areas Correlate With Functional Recovery in Spinal Cord-Injured Rats.

The relationships between various parameters of tissue damage and subsequent functional recovery after spinal cord injury (SCI) are not well understood. Patients may regain micturition control and walking despite large postinjury medullar cavities. The objective of this study was to establish possible correlations between morphological findings and degree of functional recovery after spinal cord compression at vertebra Th8 in rats. Recovery of motor (Basso, Beattie, Bresnahan, foot-stepping angle, rump-height index, and ladder climbing), sensory (withdrawal latency), and bladder functions was analyzed at 1, 3, 6, 9, and 12 weeks post-SCI. Following perfusion fixation, spinal cord tissue encompassing the injury site was cut in longitudinal frontal sections. Lesion lengths, lesion volumes, and areas of perilesional neural tissue bridges were determined after staining with cresyl violet. The numbers of axons in these bridges were quantified after staining for class III β-tubulin. We found that it was not the area of the spared tissue bridges, which is routinely determined by magnetic resonance imaging (MRI), but the numbers of axons in them that correlated with functional recovery after SCI (Spearman's ρ > 0.8; p < 0.001). We conclude that prognostic statements based only on MRI measurements should be considered with caution.

Galectin-3 protects against ischemic stroke by promoting neuro-angiogenesis via apoptosis inhibition and Akt/Caspase regulation

Post-stroke neurological deficits and mortality are often associated with vascular disruption and neuronal apoptosis. Galectin-3 (Gal3) is a potent pro-survival and angiogenic factor. However, little is known about its protective role in the cerebral ischemia/reperfusion (I/R) injury. We have previously shown significant up-regulation of Gal3 in the post-stroke rat brain, and that blocking of Gal3 with neutralizing antibody decreases the cerebral blood vessel density. Our current study demonstrates that intracerebral local delivery of the Gal3 into rat brain at the time of reperfusion exerts neuroprotection. Ischemic lesion volume and neuronal cell death were significantly reduced as compared with the vehicle-treated MCAO rat brains. Gal3 increased vessel density and neuronal survival after I/R in rat brains. Importantly, Gal3-treated groups showed significant improvement in motor and sensory functional recovery. Gal3 increased neuronal cell viability under in vitro oxygen–glucose deprivation conditions in association with increased phosphorylated-Akt, decreased phosphorylated-ERK1/2, and reduced caspase-3 activity. Gene expression analysis showed down regulation of pro-apoptotic and inflammatory genes including Fas-ligand, and upregulation of pro-survival and pro-angiogenic genes including Bcl-2, PECAM, and occludin. These results indicate a key role for Gal3 in neuro-vascular protection and functional recovery following ischemic stroke through modulation of angiogenic and apoptotic pathways.

Strychnos nux-vomica L. seed preparation promotes functional recovery and attenuates oxidative stress in a mouse model of sciatic nerve crush injury

BackgroundPeripheral nerve injury is a debilitating condition that may lead to partial or complete motor, sensory and autonomic function loss and lacks effective therapy until date. Therefore, it is quite imperative to explore impending remedies for rapid and accurate functional retrieval following such conditions. Natural product-based intervention can prove effective to facilitate the process of functions regain.MethodsHere, we investigated the effect of processed Strychnos nux-vomica seeds at a dose of 250 mg/kg body weight in a mouse model of induced Sciatic nerve lesion in promoting the recovery of the functions. A compression injury was induced in the Sciatic nerve of the right leg in the mice. Sensory function recovery was evaluated by hot-plate and formalin tests, whereas the motor function retrieval was assessed by measuring muscle grip strength, sciatic functional index, and muscle mass restoration. Oxidative stress and blood cell count were measured by biochemistry and haematological analyses.ResultsThis study indicates that Strychnos nux-vomica seeds enhance the rate of recovery of both sensory and motor functions. It helps restore the muscle mass, attenuates total oxidant status and enhances the total anti-oxidant capacity of the biological system. Moreover, the treated animals manifested an enhanced glucose tolerance aptitude and augmented granulocyte and platelet counts. Improved oxidant control, enhanced glucose sensitivity and amended granulocyte and platelet counts are likely to contribute to the advantageous effects of Strychnos nux-vomica, and warrant further in-depth studies for deciphering possible mechanisms and identification of active constituent(s) responsible for these effects.ConclusionStrychnos nux-vomica seed offers functional recovery promoting effects following a mechanical injury to the Sciatic nerve and the possible reasons behind this effect can be reduced oxidative stress and improved glycaemic control. Further and detailed investigations can unravel this mystery.

Chitosan/gelatin hydrogel and endometrial stem cells with subsequent atorvastatin injection impact in regenerating spinal cord tissue

Central nervous system trauma can cause loss of functional sensory neurons and motor functions that results in death of neuronal cells and axon degeneration. For this purpose, therapeutic approaches to enhance repair mechanisms spinal cord injury (SCI) is reflected to be a difficult task that requires thoughtful strategy. Hydrogel scaffolds in the presence of stem cells could repair damaged SCI due to their ability to support cellular viability, motility, and differentiation. In this study, we investigated the effectiveness of a biomimetic composite hydrogel of chitosan and gelatin containing endometrial stem cells (EnSCs) as a minimally invasive treatment of SCI in an animal model. Moreover, the simultaneous, effect of intraperitoneal injection of atorvastatin drug was assessed for animal models. From the results, morphological and cell viability studies demonstrated favorable seeding microenvironment and viability in the hydrogel. The transplanted hydrogel containing EnSCs into hemisected SCI rats showed recovery of sensory and motor functions by confirming locomotor activity evaluation using Basso, Beattie, and Bresnahan test. The growth of neuronal cells confirmed with immunohistochemical study. The findings in this study suggested that combination therapy using biomimetic hydrogel seeded with stem cells as well as atorvastatin injection has the potential to heal SCI through neuroinflammation attenuation, improvement of functional recovery, and limit the secondary damages.

The CD200/CD200R signaling pathway contributes to spontaneous functional recovery by enhancing synaptic plasticity after stroke

BackgroundSpontaneous functional recovery occurs during the acute phase after stroke onset, but this intrinsic recovery remains limited. Therefore, exploring the mechanism underlying spontaneous recovery and identifying potential strategies to promote functional rehabilitation after stroke are very important. The CD200/CD200R signaling pathway plays an important role in neurological recovery by modulating synaptic plasticity during multiple brain disorders. However, the effect and mechanism of action of the CD200/CD200R pathway in spontaneous functional recovery after stroke are unclear.MethodsIn this study, we used a transient middle cerebral artery occlusion (MCAO) model in rats to investigate the function of CD200/CD200R signaling in spontaneous functional recovery after stroke. We performed a battery of behavioral tests (Longa test, adhesive removal test, limb-use asymmetry test, and the modified grip-traction test) to evaluate sensorimotor function after intracerebroventricular (i.c.v.) injection with CD200 fusion protein (CD200Fc) or CD200R blocking antibody (CD200R Ab) post-stroke. Density and morphology of dendritic spines were analyzed by Golgi staining. Microglia activation was evaluated by immunofluorescence staining. Western blot was used to detect the levels of protein and the levels of mRNA were measured by qPCR.ResultsOur study demonstrated that sensorimotor function, synaptic proteins, and structures were gradually recovered and CD200R was transiently upregulated in ipsilateral cortex after stroke. Synapse-related proteins and dendritic spines were preserved, accompanied by sensorimotor functional recovery, after stereotaxic CD200Fc injection post-stroke. In addition, CD200Fc restrained microglia activation and pro-inflammatory factor release (such as Il-1, Tnf-α, and Il-6) after MCAO. On the contrary, CD200R Ab aggravated sensory function recovery in adhesive removal test and further promoted microglia activation and pro-inflammatory factor release (such as Il-1) after MCAO. The immune-modulatory effect of CD200/CD200R signaling might be exerted partly by its inhibition of the MAPK pathway.ConclusionsThis study provides evidence that the CD200/CD200R signaling pathway contributes to spontaneous functional recovery by enhancing synaptic plasticity via inhibition of microglia activation and inflammatory factor release.

Facial Sensory Restoration After Trigeminal Sensory Rhizotomy by Collateral Sprouting From the Occipital Nerves

Lesioning procedures are effective for trigeminal neuralgia (TN), but late pain recurrence associated with sensory recovery is common. We report a case of recurrence of type 1A TN and recovery of facial sensory function after trigeminal rhizotomy associated with collateral sprouting from upper cervical spinal nerves. A 41-yr-old woman presented 2 yr after open left trigeminal sensory rhizotomy for TN with pain-free anesthesia in the entire left trigeminal nerve distribution. Over 18 mo, she developed gradual recovery of facial sensation migrating anteromedially from the occipital region, eventually extending to the midpupillary line across the distribution of all trigeminal nerve branches. She reported recurrence of her triggered lancinating TN pain isolated to the area of recovered sensation with no pain in anesthetic areas. Nerve ultrasound demonstrated enlargement of ipsilateral greater and lesser occipital nerves, and occipital nerve block restored facial anesthesia and resolved her pain, indicating that recovered facial sensation was provided exclusively by the upper cervical spinal nerves. She underwent C2/C3 ganglionectomy, and ganglia were observed to be hypertrophic. Postoperatively, trigeminal anesthesia was restored with complete resolution of pain that persisted at 12-mo follow-up. This is the first documented case of a spinal nerve innervating a cranial dermatome by collateral sprouting after cranial nerve injury. The fact that typical TN pain can occur even when sensation is mediated by spinal nerves suggests that the disorder can be centrally mediated and late failure after lesioning procedures may result from maladaptive reinnervation.

Contribution of CD137-CD137L pathway in sciatic nerve crush-induced behavioral hypersensitivity and functional reduction

Abstract The T cell costimulatory molecule CD137L is involved in the development of neuropathic pain following peripheral nerve injury. Previously, our work has shown that absence or neutralization of CD137L reduces hypersensitivity, sensory and functional impairment following a sciatic nerve crush (SNC). CD137L activation utilizes both a CD137-dependent and a CD137-independent pathway. To further determine the contribution of these pathways, we examined pain-like and functional recovery-related behavioral responses following intrathecal injection (IT) of a CD137 neutralizing antibody (αCD137; daily days 3–10) after SNC in male and female B6 mice. Mice were randomly assigned to 1 of 4 groups: PBS, 0.5μg isotype control, 0.1 or 0.5μg of αCD137, and then were evaluated for sensitivity (von Frey, Hargreaves, &amp; cold plantar test), sensory (pin prick assay) and motor (hind limb grip strength, toe spread reflex and toe spacing score) functions before surgery and on post-surgery days 1–77. On post-SNC day 1, all groups showed changes in sensitivity and decreased sensory and motor functions. αCD137 treatment did not alter mechanical, heat or hypersensitivity compared to PBS- or isotype-treated controls. αCD137-treated groups showed faster sensory (pin prick score) and motor functional recovery (toe spread reflex, toe spacing), as well as slightly greater improvement in grip strength test compared to controls. Together, our results indicate partial involvement of the CD137-dependent pathway in SNC-induced sensory and motor function changes following peripheral nerve injury. (Supported by NIH/NINDS R01NS098426 (Cao))

Compensation of Ipsilateral Motor and Sensory Functions by Contralateral Uncrossed Pathway in a Stroke Patient With Half Brain.

This study reports a case of motor and sensory function recovery after massive left cerebral infarction in a young man, along with preserved function of the injured hemisphere. He received early rehabilitation therapy in a nerval care unit within 1 wk of surgery, and the rehabilitation lasted for more than 3 yrs. When he gradually recovered from coma, his motor, sensory, and speech functions improved significantly. Two years later, he was able to live independently and returned to work. The findings of functional magnetic resonance imaging, diffusion tensor imaging, somatosensory evoked potential, and motor evoked potential confirmed that there was a strong connection between his right brain and the right limbs. Thus, early rehabilitation is a promising approach for restoring motor and sensory function after massive brain injury or extensive brain tissue damage.

Vascular Endothelial Growth Factor-Transfected Bone Marrow Mesenchymal Stem Cells Improve the Recovery of Motor and Sensory Functions of Rats With Spinal Cord Injury.

Basic science. The aim of this study was to examine the effect of vascular endothelial growth factor (VEGF)-transfected bone marrow mesenchymal stem cells (BMSCs) on the recovery of motor and sensory functions of rats with spinal cord injury (SCI). There is no effective treatment to protect against SCI. BMSCs have been widely applied to the treatment of nervous system damage due to the function of prompt neurite growth and inhibition of demyelination following injury. VEGF-transfected BMSCs were injected to rats with SCI and the recovery of motor and sensory functions was observed. The Basso, Beattie, and Bresnahan, mechanical withdrawal threshold and thermal withdraw latency grading was conducted to assess the recovery status of motor and sensory functions of the SCI rats. The expression of VEGF, CD31, and NF200 was detected by immunofluorescence. The recovery of the rat motor and sensory functions in the VEGF-transfected BMSC (BMSC-VEGF) group was higher than those of the other groups with the exception of the Sham group (P < 0.05). The expression of the CD31 and NF200 proteins in the rat SCI regions was the highest in the BMSC-VEGF group, whereas the survival of BMSC in the BMSC-VEGF group was increased compared with that in the BMSC-Ad group. In addition, the injection of VEGF-transfected BMSCs can improve the angiogenesis of the injured area and retain the survival of injected cells and neurons. The injection of BMSC-VEGF improved the recovery of motor function in SCI rats. N/A.