Transcranial Magnetic Motor-evoked Potentials Research Articles

Enhancement of motor functional recovery in thoracic spinal cord injury: voluntary wheel running versus forced treadmill exercise.

JOURNAL/nrgr/04.03/01300535-202503000-00028/figure1/v/2024-06-17T092413Z/r/image-tiff Spinal cord injury necessitates effective rehabilitation strategies, with exercise therapies showing promise in promoting recovery. This study investigated the impact of rehabilitation exercise on functional recovery and morphological changes following thoracic contusive spinal cord injury. After a 7-day recovery period after spinal cord injury, mice were assigned to either a trained group (10 weeks of voluntary running wheel or forced treadmill exercise) or an untrained group. Bi-weekly assessments revealed that the exercise-trained group, particularly the voluntary wheel exercise subgroup, displayed significantly improved locomotor recovery, more plasticity of dopaminergic and serotonin modulation compared with the untrained group. Additionally, exercise interventions led to gait pattern restoration and enhanced transcranial magnetic motor-evoked potentials. Despite consistent injury areas across groups, exercise training promoted terminal innervation of descending axons. In summary, voluntary wheel exercise shows promise for enhancing outcomes after thoracic contusive spinal cord injury, emphasizing the role of exercise modality in promoting recovery and morphological changes in spinal cord injuries. Our findings will influence future strategies for rehabilitation exercises, restoring functional movement after spinal cord injury.

Transcranial magnetic motor evoked potentials and magnetic resonance imaging findings in paraplegic dogs with recovery of motor function.

BackgroundTranscranial magnetic motor evoked potentials (TMMEP) are associated with severity of clinical signs and magnetic resonance imaging (MRI) findings in dogs with spinal cord disease.HypothesisThat in initially paraplegic dogs with thoracolumbar intervertebral disc herniation (IVDH), MRI findings before surgery and TMMEPs obtained after decompressive surgery are associated with long‐term neurological status and correlate with each other.AnimalsSeventeen client‐owned paraplegic dogs with acute thoracolumbar IVDH.MethodsProspective observational study. TMMEPs were obtained from pelvic limbs and MRI (3T) of the spinal cord was performed at initial clinical presentation. Follow‐up studies were performed ≤ 2 days after reappearance of motor function and 3 months later. Ratios of compression length, intramedullary hyperintensities' length (T2‐weighted hyperintensity length ratio [T2WLR]), and lesion extension (T2‐weighted‐lesion extension ratio) in relation to the length of the 2nd lumbar vertebral body were calculated.ResultsTMMEPs could be elicited in 10/17 (59%) dogs at 1st and in 16/17 (94%) dogs at 2nd follow‐up. Comparison of TMMEPs of 1st and 2nd follow‐up showed significantly increased amplitudes (median from 0.19 to 0.45 mV) and decreased latencies (from 69.38 to 40.26 ms; P = .01 and .001, respectively). At 2nd follow‐up latencies were significantly associated with ambulatory status (P = .024). T2WLR obtained before surgery correlated with latencies at 2nd follow‐up (P = .04).ConclusionsTMMEP reflect motor function recovery after severe spinal cord injury.

Correlation between severity of clinical signs and transcranial magnetic motor evoked potentials in dogs with intervertebral disc herniation

Transcranial magnetic motor evoked potentials (TMMEPs) can assess the functional integrity of the spinal cord descending motor pathways. In intervertebral disc herniation (IVDH), these pathways are compromised to varying degrees reflected by the severity of neurological deficits. The hypotheses of this study were as follows: (1) TMMEPs differ in dogs with IVDH and healthy control dogs; (2) TMMEPs reflect different severities of neurological signs; and (3) TMMEPs can document functional motor improvement and therefore monitor recovery of function. TMMEPs were recorded in 50 dogs with thoracolumbar IVDH. Clinical signs ranged from spinal hyperesthesia to non-ambulatory paraparesis in 19 dogs and paraplegia with/without deep pain sensation in 31 dogs. In these 31 paraplegic dogs, transcranial magnetic stimulation (TMS) was repeated during follow-up examinations. Ten healthy Beagle dogs served as controls.There was a significant increase in onset latency and decrease in peak-to-peak amplitude in the pelvic limb TMMEPs of dogs with spinal hyperesthesia to severe paraparesis compared to control dogs. Waveforms in dogs with IVDH were predominantly polyphasic in contrast to the biphasic waveforms of the control dogs. TMMEPs could not be generated in the pelvic limbs of paraplegic dogs. However, TMMEPs with markedly increased onset latencies and decreased peak-to-peak amplitudes reappeared in the pelvic limbs of dogs that were paraplegic before surgery and showed functional motor improvement during follow-up. The severity of neurological deficits was reflected by TMMEP findings, which could be used to document functional motor recovery in IVDH. TMS could therefore be used as an ancillary test to monitor response to therapy in dogs during rehabilitation.

Transcranial magnetic stimulation with acepromazine or dexmedetomidine in combination with levomethadone/fenpipramide in healthy Beagle dogs

The aim of this study was to evaluate the influence of two sedation protocols on transcranial magnetic motor evoked potentials (TMMEPs) after transcranial magnetic stimulation in medium sized dogs. Onset latencies and peak-to-peak amplitudes, elicited in the extensor carpi radialis and cranial tibial muscles, were analysed in 10 healthy Beagles that received either acepromazine or dexmedetomidine in combination with levomethadone/fenpipramide, in a crossover design. Similar TMMEP recordings could be made using both sedation protocols at 80–90% stimulation intensity; however, there were significantly shorter onset latencies with the acepromazine-levomethadone/fenpipramide protocol at 100% stimulation intensity. Reference values were established and it was concluded that both drug combinations are feasible for measuring TMMEPs in medium sized dogs.

Improved differentiation of oligodendrocyte precursor cells and neurological function after spinal cord injury in rats by oscillating field stimulation

Oscillating field stimulation (OFS) has been used in attempts to treat spinal cord injury (SCI) and has been shown to improve remyelination after SCI in rats. However, some controversies regarding the effects of OFS have been presented in previous papers. Oligodendrocytes (OLs) are the main cell for remyelination and are derived from the differentiation of oligodendrocyte precursor cells (OPCs). To date, it has been unclear whether the differentiation of OPCs can be regulated by OFS. The goal of this study was to determine if OFS can improve the differentiation of OPCs and promote the recovery of neurological function after SCI in rats. Immature and mature OLs were observed in spinal cord slices through immunofluorescence staining. Levels of adenosine triphosphate (ATP) and the cytokine leukemia inhibitory factor (LIF) were detected by enzyme-linked immunosorbent assay (ELISA). Basso–Beattie–Bresnahan (BBB) scores and transcranial magnetic motor-evoked potentials (tcMMEPs) were used to evaluate the locomotor outcomes of rats after SCI. Our results showed a significant improvement in the differentiation of OPCs and the content of ATP and LIF in the injured spinal cord in the OFS group. Furthermore, BBB scores and tcMMEPs were significantly improved in the rats stimulated by OFS. These findings suggest that OFS can improve the differentiation of OPCs and promote the recovery of neurological function following SCI in rats.

Inhibition of LINGO-1 promotes functional recovery after experimental spinal cord demyelination

Blocking LINGO-1 has been shown to enhance remyelination in the rat lysolecithin-induced focal spinal cord demyelination model. We used transcranial magnetic motor-evoked potentials (tcMMEPs) to assess the effect of blocking LINGO-1 on recovery of axonal function in a mouse lysolecithin model at 1, 2 and 4weeks after injury. The role of LINGO-1 was assessed using LINGO-1 knockout (KO) mice and in wild-type mice after intraperitoneal administration of anti-LINGO-1 antagonist monoclonal antibody (mAb3B5). Response rates (at 2 and 4weeks) and amplitudes (at 4weeks) were significantly increased in LINGO-1 KO and mAb3B5-treated mice compared with matched controls. The latency of potentials at 4weeks was significantly shorter in mAb3B5-treated mice compared with controls. Lesion areas in LINGO-1 KO and mAb3B5-treated mice were reduced significantly compared with matched controls. The number of remyelinated axons within the lesions was increased and the G-ratios of the axons were decreased in both LINGO-1 KO and mAb3B5-treated mice compared with matched controls. These data provide morphometric and functional evidence of enhancement of remyelination associated with antagonism of LINGO-1.

Transcranial magnetic motor evoked potentials in Great Danes with and without clinical signs of cervical spondylomyelopathy: Association with neurological findings and magnetic resonance imaging

Transcranial magnetic motor evoked potentials (TMMEPs) assess the functional integrity of the descending motor pathways, which are typically compromised in canine cervical spondylomyelopathy (CSM). The objective of this prospective study was to establish the reference ranges of TMMEP latency and amplitude in clinically normal (control) Great Danes (GDs), compare TMMEPs obtained in GDs with and without CSM, and determine whether there is any association between TMMEP data and severity of neurological signs or magnetic resonance imaging (MRI) findings. Twenty-nine client-owned GDs were enrolled (15 controls, 14 CSM-affected). All dogs underwent TMMEPs under sedation, and latencies and amplitudes were recorded from the extensor carpi radialis (ECR) and cranial tibial (CT) muscles. MRI of the cervical vertebral column was performed to evaluate the presence and severity of spinal cord (SC) compression, and the presence of SC signal changes.ECR and CT latencies were significantly longer in CSM-affected than control GDs. No significant differences between groups were found for amplitudes or neuronal path lengths. For the CT TMMEPs, CSM-affected GDs with moderate and severe clinical signs had significantly longer latencies than those with mild clinical signs. Significantly longer CT latencies were found in dogs with moderate and severe SC compression compared with dogs with mild compression. CT TMMEPs could not be recorded in 7/9 CSM-affected GDs with SC signal changes. These results provide a reference range for TMMEPs of clinically normal GDs. The use of TMMEPs is a valid ancillary test to assess the integrity of motor pathways in GDs with CSM.

Effects of Prophylactic and Therapeutic Teriflunomide in Transcranial Magnetic Stimulation–Induced Motor-Evoked Potentials in the Dark Agouti Rat Model of Experimental Autoimmune Encephalomyelitis

Teriflunomide is a once-daily oral immunomodulatory agent recently approved in the United States for the treatment of relapsing multiple sclerosis (RMS). This study investigated neurophysiological deficits in descending spinal cord motor tracts during experimental autoimmune encephalomyelitis (EAE; a model of multiple sclerosis) and the functional effectiveness of prophylactic or therapeutic teriflunomide treatment in preventing the debilitating paralysis observed in this model. Relapsing-remitting EAE was induced in Dark Agouti rats using rat spinal cord homogenate. Animals were treated with oral teriflunomide (10 mg/kg daily) prophylactically, therapeutically, or with vehicle (control). Transcranial magnetic motor-evoked potentials were measured throughout the disease to provide quantitative assessment of the neurophysiological status of descending motor tracts. Axonal damage was quantified histologically by silver staining. Both prophylactic and therapeutic teriflunomide treatment significantly reduced maximum EAE disease scores (P < 0.0001 and P = 0.0001, respectively) compared with vehicle-treated rats. Electrophysiological recordings demonstrated that both teriflunomide treatment regimens prevented a delay in wave-form latency and a decrease in wave-form amplitude compared with that observed in vehicle-treated animals. A significant reduction in axonal loss was observed with both teriflunomide treatment regimens compared with vehicle (P < 0.0001 and P = 0.0014, respectively). The results of this study suggest that therapeutic teriflunomide can prevent the deficits observed in this animal model in descending spinal cord motor tracts. The mechanism behind reduced axonal loss and improved motor function may be primarily the reduced inflammation and consequent demyelination observed in these animals through the known effects of teriflunomide on impairing proliferation of stimulated T cells. These findings may have significant implications for patients with RMS.

Major ozonated autohemotherapy promotes the recovery of upper limb motor function in patients with acute cerebral infarction.

Major ozonated autohemotherapy is classically used in treating ischemic disorder of the lower limbs. In the present study, we performed major ozonated autohemotherapy treatment in patients with acute cerebral infarction, and assessed outcomes according to the U.S. National Institutes of Health Stroke Score, Modified Rankin Scale, and transcranial magnetic stimulation motor-evoked potential. Compared with the control group, the clinical total effective rate and the cortical potential rise rate of the upper limbs were significantly higher, the central motor conduction time of upper limb was significantly shorter, and the upper limb motor-evoked potential amplitude was significantly increased, in the ozone group. In the ozone group, the National Institutes of Health Stroke Score was positively correlated with the central motor conduction time and the motor-evoked potential amplitude of the upper limb. Central motor conduction time and motor-evoked potential amplitude of the upper limb may be effective indicators of motor-evoked potentials to assess upper limb motor function in cerebral infarct patients. Furthermore, major ozonated autohemotherapy may promote motor function recovery of the upper limb in patients with acute cerebral infarction.

Characterizing Phospholipase A2-Induced Spinal Cord Injury—A Comparison with Contusive Spinal Cord Injury in Adult Rats

To assess whether phospholipase A2 (PLA2) plays a role in the pathogenesis of spinal cord injury (SCI), we compared lesions either induced by PLA2 alone or by a contusive SCI. At 24-h post-injury, both methods induced a focal hemorrhagic pathology. The PLA2 injury was mainly confined within the ventrolateral white matter, whereas the contusion injury widely affected both the gray and white matter. A prominent difference between the two models was that PLA2 induced a massive demyelination with axons remaining in the lesion area, whereas the contusion injury induced axonal damage and myelin breakdown. At 4 weeks, no cavitation was found within the PLA2 lesion, and numerous axons were myelinated by host-migrated Schwann cells. Among them, 45% of animals had early transcranial magnetic motor-evoked potential (tcMMEP) responses. In contrast, the contusive SCI induced a typical centralized cavity with reactive astrocytes forming a glial border. Only 15% of rats had early tcMMEP responses after the contusion. BBB scores were similarly reduced in both models. Our study indicates that PLA2 may play a unique role in mediating secondary SCI likely by targeting glial cells, particularly those of oligodendrocytes. This lesion model could also be used for studying demyelination and remyelination in the injured spinal cord associated with PLA2-mediated secondary SCI.

Effects of syringomyelia on electrodiagnostic test results in Cavalier King Charles Spaniels

To determine the effects of syringomyelia on electromyography (EMG) findings, somatosensory-evoked potentials (SEPs), and transcranial magnetic motor-evoked potentials (TMMEPs) in Cavalier King Charles Spaniels (CKCSs). 27 client-owned CKCSs that underwent prebreeding magnetic resonance imaging screening or investigation of clinical signs consistent with syringomyelia. In dogs with (n = 11) and without (16) magnetic resonance imaging-confirmed syringomyelia, the median nerve in each thoracic limb was stimulated and SEPs were recorded over the C1 vertebra; onset latency and latency and amplitude of the largest negative (N1) and positive (P1) peaks were measured. The TMMEPs were recorded bilaterally from the extensor carpi radialis and tibialis cranialis muscles; onset latencies in all 4 limbs were measured. Bilateral systematic needle EMG examination was performed on the cervical epaxial musculature, and the number of sites with spontaneous activity was recorded. In dogs with syringomyelia, amplitudes of N1 and P1 and the amplitude difference between P1 and N1 were significantly smaller than those recorded for dogs without syringomyelia (approx 2-fold difference). No difference in SEP latencies, TMMEP latencies, or the proportion of dogs with > 2 sites of spontaneous activity detected during EMG examination was detected between groups. Results indicated that SEP amplitude at the C1 vertebra was a more sensitive measure of spinal cord function in CKCSs with syringomyelia, compared with results of EMG or TMMEP assessment. Measurement of SEP amplitude may have use as an objective assessment of the evolution and treatment of this disease.

Transplantation of ciliary neurotrophic factor-expressing adult oligodendrocyte precursor cells promotes remyelination and functional recovery after spinal cord injury.

Demyelination contributes to the dysfunction after traumatic spinal cord injury (SCI). We explored whether the combination of neurotrophic factors and transplantation of adult rat spinal cord oligodendrocyte precursor cells (OPCs) could enhance remyelination and functional recovery after SCI. Ciliary neurotrophic factor (CNTF) was the most effective neurotrophic factor to promote oligodendrocyte (OL) differentiation and survival of OPCs in vitro. OPCs were infected with retroviruses expressing enhanced green fluorescent protein (EGFP) or CNTF and transplanted into the contused adult thoracic spinal cord 9 d after injury. Seven weeks after transplantation, the grafted OPCs survived and integrated into the injured spinal cord. The survival of grafted CNTF-OPCs increased fourfold compared with EGFP-OPCs. The grafted OPCs differentiated into adenomatus polyposis coli (APC(+)) OLs, and CNTF significantly increased the percentage of APC(+) OLs from grafted OPCs. Immunofluorescent and immunoelectron microscopic analyses showed that the grafted OPCs formed central myelin sheaths around the axons in the injured spinal cord. The number of OL-remyelinated axons in ventrolateral funiculus (VLF) or lateral funiculus (LF) at the injured epicenter was significantly increased in animals that received CNTF-OPC grafts compared with all other groups. Importantly, 75% of rats receiving CNTF-OPC grafts recovered transcranial magnetic motor-evoked potential and magnetic interenlargement reflex responses, indicating that conduction through the demyelinated axons in VLF or LF, respectively, was partially restored. More importantly, recovery of hindlimb locomotor function was significantly enhanced in animals receiving grafts of CNTF-OPCs. Thus, combined treatment with OPC grafts expressing CNTF can enhance remyelination and facilitate functional recovery after traumatic SCI.

Anatomical and Functional Outcomes following a Precise, Graded, Dorsal Laceration Spinal Cord Injury in C57BL/6 Mice

To study the pathophysiology of spinal cord injury (SCI), we used the LISA-Vibraknife to generate a precise and reproducible dorsal laceration SCI in the mouse. The surgical procedure involved a T9 laminectomy, dural resection, and a spinal cord laceration to a precisely controlled depth. Four dorsal hemisection injuries with lesion depths of 0.5, 0.8, 1.1, and 1.4 mm, as well as normal, sham (laminectomy and dural removal only), and transection controls were examined. Assessments including the Basso Mouse Scale (BMS), footprint analysis, beam walk, toe spread reflex, Hargreaves' test, and transcranial magnetic motor-evoked potential (tcMMEP) analysis were performed to assess motor, sensorimotor, and sensory function. These outcome measures demonstrated significant increases in functional deficits as the depth of the lesion increased, and significant behavioral recovery was observed in the groups over time. Quantitative histological examination showed significant differences between the injury groups and insignificant lesion depth variance within each of the groups. Statistically significant differences were additionally found in the amount of ventral spared tissue at the lesion site between the injury groups. This novel, graded, reproducible laceration SCI model can be used in future studies to look more closely at underlying mechanisms that lead to functional deficits following SCI, as well as to determine the efficacy of therapeutic intervention strategies in the injury and recovery processes following SCI.

The co-transplantation of human bone marrow stromal cells and embryo olfactory ensheathing cells as a new approach to treat spinal cord injury in a rat model

Both bone marrow stromal cells (BMSC) and olfactory ensheathing cells (OEC) have been demonstrated experimentally as promising for therapy of spinal cord injury (SCI). However, clinical use may be constrained by the margin neuronal differentiation capacity of BMSC as well as the limited number of isolatable OEC. This study therefore tested the efficacy of co-grafting human BMSC and OEC in treating thoracic SCI. Rat SCI models were created with cushion forces. OEC were labeled with Hoechst 33342 and BMSC with BrdU or GFP. BMSC, OEC and BMSC plus OEC were injected into the injured sites of rat spinal cords. Histologic, electrophysiologic and functional approaches were applied to assess the effects of transplantation of these cell types. Behavioral evaluation showed an improvement in animals with all cell-based treatments. The co-graft led to significantly higher gait scaling. The latency of transcranial magnetic motor-evoked potential (tcMMEP) responses was also better restored in the co-graft group. Larger numbers and sizes of axon bundles through the transitional zone between the normal and injured regions were observed in the co-graft animals in comparison with all other animals. Transplanted bone marrow stromal cells were identified as neurofilament-positive in the co-grafted animals although the number of glial fibrillary acidic protein-positive cells remained the same in all groups. Taken together, our results suggest that the combined use of BMSC and OEC may provide an improved approach for the treatment of SCI.

Annexin A1 Reduces Inflammatory Reaction and Tissue Damage Through Inhibition of Phospholipase A2 Activation in Adult Rats Following Spinal Cord Injury

Annexin A1 (ANXA1) has been suggested to be a mediator of the anti-inflammatory actions of glucocorticoids and more recently an endogenous neuroprotective agent. In the present study, we investigated the anti-inflammatory and neuroprotective effects of ANXA1 in a model of contusive spinal cord injury (SCI). Here we report that injections of ANXA1 (Ac 2-26) into the acutely injured spinal cord at 2 concentrations (5 and 20 microg) inhibited SCI-induced increases in phospholipase A2 and myeloperoxidase activities. In addition, ANXA1 administration reduced the expression of interleukin-1beta and activated caspase-3 at 24 hours, and glial fibrillary acidic protein at 4 weeks postinjury. Furthermore, ANXA1 administration significantly reversed phospholipase A2-induced spinal cord neuronal death in vitro and reduced tissue damage and increased white matter sparing in vivo, compared to the vehicle-treated controls. Fluorogold retrograde tracing showed that ANXA1 administration protected axons of long descending pathways at 6 weeks post-SCI. ANXA1 administration also significantly increased the number of animals that responded to transcranial magnetic motor-evoked potentials. However, no measurable behavioral improvement was found after these treatments. These results, particularly the improvements obtained in tissue sparing and electrophysiologic measures, suggest a neuroprotective effect of ANXA1.

Objective assessment of cervical spinal cord injury levels by transcranial magnetic motor-evoked potentials

Background The neurologic examination serves as the optimal method to record the level of spinal cord injury (SCI). However, this test is subject to interexaminer variability. To address this shortcoming, we describe a technique that uses transcranial magnetic motor-evoked potentials (tcMMEPs) and dermatomal somatosensory-evoked potentials (d-SSEPs) to more accurately measure the precise level of SCI. Methods Two groups of subjects were studied: (1) complete cervical SCI (n = 10) and (2) neurologically intact volunteers (n = 10). Two additional patients were evaluated: one with a cervical central spinal cord syndrome and another with a head injury with a suspected cervical SCI. Each subject underwent upper extremity tcMMEPs and d-SSEPs. Results Transcranial magnetic motor-evoked potentials were elicited from all upper limb myotomes (C4-T1, bilaterally) in neurologically intact volunteers (20 sides). The level of injury was determined using tcMMEPs by observing the lowest level of measurable response. The level of injury obtained using tcMMEPs was the same as that determined by neurologic examination in 13 (65%) of the 20 sides. In 7 sides, tcMMEP responses were obtained 1 level lower than that assessed by physical examination. Dermatomal somatosensory-evoked potentials were obtained from all dermatomes of volunteers tested in the laboratory compared with only 5 of the 9 patients with SCI who underwent d-SSEP testing. Conclusion Testing using tcMMEPs provides an objective supplement to the neurologic examination after acute cervical SCI. Dermatomal somatosensory-evoked potentials were of limited value in determining the level of cervical SCI.

Correlation of motor evoked potentials with magnetic resonance imaging and neurologic findings in Doberman Pinschers with and without signs of cervical spondylomyelopathy

To establish the reference ranges for motor evoked potential (MEP) latency and amplitude in clinically normal Doberman Pinschers, compare the MEPs of Doberman Pinschers with and without clinical signs of cervical spondylomyelopathy (CSM; wobbler syndrome), and determine whether MEP data correlate with neurologic or magnetic resonance imaging (MRI) findings. 16 clinically normal and 16 CSM-affected Doberman Pinschers. Dogs were classified according to their neurologic deficits. After sedation with acepromazine and hydromorphone, transcranial magnetic MEPs were assessed in each dog; latencies and amplitudes were recorded from the extensor carpi radialis and cranial tibial muscles. Magnetic resonance imaging was performed to evaluate the presence and severity of spinal cord compression. Significant differences in cranial tibial muscle MEP latencies and amplitudes were detected between clinically normal and CSM-affected dogs. No differences in the extensor carpi radialis MEP were detected between groups. There was a significant correlation (r = 0.776) between the cranial tibial muscle MEP latencies and neurologic findings. Significant correlations were also found between MRI findings and the cranial tibial muscle MEP latencies (r = 0.757) and amplitudes (r = -0.453). Results provided a reference range for MEPs in clinically normal Doberman Pinschers and indicated that cranial tibial muscle MEP latencies correlated well with both MRI and neurologic findings. Because of the high correlation between cranial tibial muscle MEP data and neurologic and MRI findings, MEP assessment could be considered as a screening tool in the management of dogs with spinal cord disease.

Motor Cortical Excitability in Depressive Patients After Electroconvulsive Therapy and Repetitive Transcranial Magnetic Stimulation

Electroconvulsive therapy (ECT) and repetitive transcranial magnetic stimulation (rTMS) of the dorsolateral prefrontal cortex are brain stimulation techniques that are used as therapeutic interventions in major depression. However, the exact therapeutic mode of action needs further clarification. In this case report, we describe the impact of these stimulation techniques on motor cortical excitability, as revealed by transcranial magnetic stimulation-elicited motor-evoked potentials in 2 patients who received consecutively both rTMS and ECT. Both patients showed a decrease in motor cortical excitability after response to antidepressant brain stimulation, whereas parameters of motor cortical excitability remained unchanged after the first non-successful intervention. These results suggest that both ECT and rTMS may have an impact on parameters of motor cortical neuronal excitability. Furthermore, measurement of motor cortical excitability may be a useful tool for investigating and monitoring inhibitory brain effects of different antidepressant stimulation techniques.

Plasticity in the descending motor pathways after spinal cord hemisection

The present study evaluates the motor functional recovery after C2 spinal cord hemisection combined with contralateral brachial root transection, which causes a condition that is similar to the crossed phrenic phenomenon (CPP). Descending motor pathways, including the reticulospinal extrapyramidal tract and corticospinal pyramidal tracts, were evaluated by transcranial magnetic motor-evoked potentials (mMEPs) and direct cortical electrical motor-evoked potentials (eMEP), respectively. All MEPs recorded from the left forelimb were abolished immediately after the left C2 hemisection. Left mMEPs recovered dramatically immediately after contralateral right brachial root transection. Corticospinal eMEPs never recovered, regardless of transection. The facilitation of mMEPs in animals that had undergone combined contralateral root transection was well correlated with open-field behavioral motor performance.

Functional and electrophysiological changes after graded traumatic spinal cord injury in adult rat

A graded contusion spinal cord injury (SCI) was created in the adult rat spinal cord using the Infinite Horizons (IH) impactor to study the correlation between injury severity and anatomical, behavioral, and electrophysiological outcomes. Adult Fisher rats were equally divided into five groups and received contusion injuries at the ninth thoracic level (T9) with 100, 125, 150, 175, or 200 kdyn impact forces, respectively. Transcranial magnetic motor-evoked potentials (tcMMEPs) and BBB open-field locomotor analyses were performed weekly for 4 weeks postinjury. Our results demonstrated that hindlimb locomotor function decreased in accordance with an increase in injury severity. The locomotor deficits were proportional to the amount of damage to the ventral and lateral white matter (WM). Locomotor function was strongly correlated to the amount of spared WM, which contains the reticulospinal and propriospinal tracts. Normal tcMMEP latencies were recorded in control, all of 100-kdyn-injured and half of 125-kdyn-injured animals. Delayed latency responses were recorded in some of 125-kdyn-injured and all of 150-kdyn-injured animals. No tcMMEP responses were recorded in 175- and 200-kdyn-injured animals. Comparison of tcMMEP responses with areas of WM loss or demyelination identified the medial ventrolateral funiculus (VLF) as the location of the tcMMEP pathway. Immunohistochemical and electromicroscopic (EM) analyses showed the presence of demyelinated axons in WM tracts surrounding the lesion cavities at 28 days postinjury. These data support the notion that widespread WM damage in the ventral and lateral funiculi may be a major cause for locomotor deficits and lack of tcMMEP responses after SCI.