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Spinal cord injury is a devastating condition that is followed by long and often unsuccessful recovery after trauma. The state of the art approach to manage paralysis and concomitant impairments is rehabilitation, which is the only strategy that has proven to be effective and beneficial for the patients over the last decades. How rehabilitation influences the remodeling of spinal axonal connections in patients is important to understand, in order to better target these changes and define the optimal timing and onset of training. While clinically the answers to these questions remain difficult to obtain, rodent models of rehabilitation like bicycling, treadmill training, swimming, enriched environments or wheel running that mimic clinical rehabilitation can be helpful to reveal the axonal changes underlying motor recovery. This review will focus on the different animal models of spinal cord injury rehabilitation and the underlying changes in neuronal networks that are improved by exercise and rehabilitation.

Spinal cord injury is associated with chronic sensorimotor deficits due to the interruption of ascending and descending tracts between the brain and spinal cord. Functional recovery after anatomically complete spinal cord injury is limited due to the lack of long-distance axonal regeneration of severed fibers in the adult central nervous system. Most spinal cord injuries in humans, however, are anatomically incomplete. Although restorative treatment options for spinal cord injury remain currently limited, research from experimental models of spinal cord injury have revealed a tremendous capability for both spontaneous and treatment-induced plasticity of the corticospinal system that supports functional recovery. We review recent advances in the understanding of corticospinal circuit plasticity after spinal cord injury and concentrate mainly on the hindlimb motor cortex, its corticospinal projections, and the role of spinal mechanisms that support locomotor recovery. First, we discuss plasticity that occurs at the level of motor cortex and the reorganization of cortical movement representations. Next, we explore downstream plasticity in corticospinal projections. We then review the role of spinal mechanisms in locomotor recovery. We conclude with a perspective on harnessing neuroplasticity with therapeutic interventions to promote functional recovery.

Spinal cord injury (SCI) is a devastating lesion to the spinal cord, which determines the interruption of ascending/descending axonal tracts, the loss of supraspinal control of sensory-motor functions below the injured site, and severe autonomic dysfunctions, dramatically impacting the quality of life of the patients. After the acute inflammatory phase, the progressive formation of the astrocytic glial scar characterizes the acute-chronic phase: such scar represents one of the main obstacles to the axonal regeneration that, as known, is very limited in the central nervous system (CNS). Unfortunately, a cure for SCI is still lacking: the current clinical approaches are mainly based on early vertebral column stabilization, anti-inflammatory drug administration, and rehabilitation programs. However, new experimental therapeutic strategies are under investigation, one of which is to stimulate axonal regrowth and bypass the glial scar. One major issue in axonal regrowth consists of the different genetic programs, which characterize axonal development and maturation. Here, we will review the main hurdles that in adulthood limit axonal regeneration after SCI, describing the key genes, transcription factors, and miRNAs involved in these processes (seen their reciprocal influencing action), with particular attention to corticospinal motor neurons located in the sensory-motor cortex and subjected to axotomy in case of SCI. We will highlight the functional complexity of the neural regeneration programs. We will also discuss if specific axon growth programs, that undergo a physiological downregulation during CNS development, could be reactivated after a spinal cord trauma to sustain regrowth, representing a new potential therapeutic approach.

The corticoreticular tract （CRT） is known to be involved in walking and postural control. Using diffusion tensor tractography （DTT）, we investigated the relationship between the CRT and gait dysfunction, includ- ing trunk instability, in pediatric patients. Thirty patients with delayed development and 15 age-matched, typically-developed （TD） children were recruited. Fifteen patients with gait dysfunction （bilateral trunk instability） were included in the group A, and the other 15 patients with gait dysfunction （unilateral trunk instability） were included in the group B. The Growth Motor Function Classification System, Functional Ambulation Category scale, and Functional Ambulation Category scale were used for measurement of functional state. Fractional anisotropy, apparent diffusion coefficient, fiber number, and tract integrity of the CRT and corticospinal tract were measured. Diffusion parameters or integrity of corticospinal tract were not significantly different in the three study groups. However, CRT results revealed that both CRTs were disrupted in the group A, whereas CRT disruption in the hemispheres contralateral to clinical mani- festations was observed in the group B. Fractional anisotropy values and fiber numbers in both CRTs were decreased in the group A than in the group TD. The extents of decreases of fractional anisotropy values and fiber numbers on the ipsilateral side relative to those on the contralateral side were greater in the group B than in the group TD. Functional evaluation data and clinical manifestations were found to show strong correlations with CRT status, rather than with corticospinal tract status. These findings suggest that CRT status appears to be clinically important for gait function and trunk stability in pediatric patients and DTT can help assess CRT status in pediatric patients with gait dysfunction.

As most spinal cord injuries （SCIs） are incomplete, an important target for promoting neural repair and recovery of lost motor function is to promote the connections of spared descending spinal pathways with spinal motor circuits. Among the pathways, the corticospinal tract （CST） is most associated with skilled voluntary functions in humans and many animals. CST loss, whether at its origin in the motor cortex or in the white matter tracts subcortically and in the spinal cord, leads to movement impairments and paraly- sis. To restore motor function after injury will require repair of the damaged CST. In this review, I discuss how knowledge of activity-dependent development of the CST--which establishes connectional speci- ficity through axon pruning, axon outgrowth, and synaptic competition among CST terminals--informed a novel activity-based therapy for promoting sprouting of spared CST axons after injur in mature animals. This therapy, which comprises motor cortex electrical stimulation with and without concurrent trans-spi- nal direct current stimulation, leads to an increase in the gray matter axon length of spared CST axons in the rat spinal cord and, after a pyramidal tract lesion, restoration of skilled locomotor movements. I discuss how this approach is now being applied to a C4 contusion rat model.

Stroke causes long-term disability, and rehabilitative training is commonly used to improve the consecutive functional recovery. Following brain damage, surviving neurons undergo morphological alterations to reconstruct the remaining neural network. In the motor system, such neural network remodeling is observed as a motor map reorganization. Because of its significant correlation with functional recovery, motor map reorganization has been regarded as a key phenomenon for functional recovery after stroke. Although the mechanism underlying motor map reorganization remains unclear, increasing evidence has shown a critical role for axonal remodeling in the corticospinal tract. In this study, we review previous studies investigating axonal remodeling in the corticospinal tract after stroke and discuss which mechanisms may underlie the stimulatory effect of rehabilitative training. Axonal remodeling in the corticospinal tract can be classified into three types based on the location and the original targets of corticospinal neurons, and it seems that all the surviving corticospinal neurons in both ipsilesional and contralesional hemisphere can participate in axonal remodeling and motor map reorganization. Through axonal remodeling, corticospinal neurons alter their output selectivity from a single to multiple areas to compensate for the lost function. The remodeling of the corticospinal axon is influenced by the extent of tissue destruction and promoted by various therapeutic interventions, including rehabilitative training. Although the precise molecular mechanism underlying rehabilitation-promoted axonal remodeling remains elusive, previous data suggest that rehabilitative training promotes axonal remodeling by upregulating growth-promoting and downregulating growth-inhibiting signals.

•We investigate the usefulness of conventional magnetic resonance imaging (C-MRI) for diagnosing amyotrophic lateral sclerosis (ALS).•We focused corticospinal tract (CST) hyperintensity on C-MRI in patients with ALS.•Our results showed that the rate of CST positivity was higher in patients with definite-ALS than others.•C-MRI can play an important role in diagnosing ALS. The usefulness of conventional magnetic resonance imaging (C-MRI) for diagnosing amyotrophic lateral sclerosis (ALS) remains controversial. The aim of this study was to investigate the utility of C-MRI in identifying ALS, specifically the association between corticospinal tract (CST) hyperintensity on C-MRI and clinical characteristics in patients with ALS. Between June 2008 and April 2012, we retrospectively enrolled consecutive patients diagnosed with sporadic ALS who underwent C-MRI. Patients with ALS were classified as definite-phase ALS (D-ALS) and indefinite-phase ALS (ID-ALS). We focused on the hyperintensity of T2-weighted images in the CST in patients with ALS. Based on the MRI results, we divided patients into two groups: a positive CST group showing CST hyperintensity; and a negative CST group with no such findings. Clinical characteristics of the two groups were compared. Seventeen patients (median age, 62 years; 8 women, 9 men) were enrolled in this study, with D-ALS in eight (47%) and ID-ALS in nine (53%). Eight patients (47%) showed CST positivity. The rate of CST positivity was higher in patients with D-ALS (75%) than in patients with ID-ALS (22%, p=0.03). CST positivity appears significantly increased in D-ALS patients. C-MRI can play an important role in diagnosing ALS.

Major ozonated autohemotherapy has been shown to promote recovery of upper limb motor function in patients with acute cerebral infarction, but whether naajor ozonated autohelnotherapy affects remote in）ury remains poorly understood. Here, we assumed that major ozonated autohemotherapy contributes to recovery of clinical function, possibly by reducing remote injury after acute cerebral infarction. Sixty acute cerebral infarction patients aged 30-80 years were equally and randomly allocated to ozone treatment and control groups. Patients in the ozone treatment group received medical treatment and major ozonated autohemotherapy （47 mg/L, 100 mL ozone） for 10 ± 2 days. Patients in the control group received medical treatment only. National Institutes of Health Stroke Scale score, modified Rankin scale score, and reduced degree of fractional anisotropy values of brain magnetic resonance diffusion tensor imaging were remarkably decreased, brain function improved, clinical efficiency significantly increased, and no obvious adverse reactions detected in the ozone treatment group compared with the control group. These findings suggest that major ozonated autohemotherapy promotes recovery of neurological function in acute cerebral infarction patients by reducing re,note injury, and additionally, exhibits high safety.

The limited ability for injured adult axons to regenerate is a major cause for limited functional recovery after injury to the nervous system,motivating numerous efforts to uncover mechanisms capable of enhancing regeneration potential.One promising strategy involves deletion or knockdown of the phosphatase and tensin（PTEN） gene.Conditional genetic deletion of PTEN before,immediately following,or several months after spinal cord injury enables neurons of the corticospinal tract（CST） to regenerate their axons across the lesion,which is accompanied by enhanced recovery of skilled voluntary motor functions mediated by the CST.Although conditional genetic deletion or knockdown of PTEN in neurons enables axon regeneration,PTEN is a well-known tumor suppressor and mutations of the PTEN gene disrupt brain development leading to neurological abnormalities including macrocephaly,seizures,and early mortality.The long-term consequences of manipulating PTEN in the adult nervous system,as would be done for therapeutic intervention after injury,are only now being explored.Here,we summarize evidence indicating that long-term deletion of PTEN in mature neurons does not cause evident pathology; indeed,cortical neurons that have lived without PTEN for over 1 year appear robust and healthy.Studies to date provide only a first look at potential negative consequences of PTEN deletion or knockdown,but the absence of any detectable neuropathology supports guarded optimism that interventions to enable axon regeneration after injury are achievable.

[This corrects the article DOI: 10.3389/fnhum.2025.1598598.].