Cranial Motor Research Articles

Persistent Feeding and Swallowing Deficits in a Mouse Model of 22q11.2 Deletion Syndrome.

Disrupted development of oropharyngeal structures as well as cranial nerve and brainstem circuits may lead to feeding and swallowing difficulties in children with 22q11. 2 deletion syndrome (22q11DS). We previously demonstrated aspiration-based dysphagia during early postnatal life in the LgDel mouse model of 22q11DS along with disrupted oropharyngeal morphogenesis and divergent differentiation and function of cranial motor and sensory nerves. We now ask whether feeding and swallowing deficits persist in adult LgDel mice using methods analogous to those used in human patients to evaluate feeding and swallowing dysfunction. Compared to wild-type mice, videofluoroscopic swallow study revealed that LgDel mice have altered feeding and swallowing behaviors, including slower lick rates, longer inter-lick intervals, and longer pharyngeal transit times with liquid consistency. Transoral endoscopic assessment identified minor structural anomalies of the palate and larynx in one-third of the LgDel mice examined. Video surveillance of feeding-related behaviors showed that LgDel mice eat and drink more frequently. Furthermore, LgDel animals engage in another oromotor behavior, grooming, more frequently, implying that divergent craniofacial and cranial nerve structure and function result in altered oromotor coordination. Finally, LgDel mice have significantly increased lung inflammation, a potential sign of aspiration-based dysphagia, consistent with results from our previous studies of early postnatal animals showing aspiration-related lung inflammation. Thus, oromotor dysfunction, feeding, and swallowing difficulties and their consequences persist in the LgDel 22q11DS mouse model. Apparently, postnatal growth and/or neural plasticity does not fully resolve deficits due to anomalous hindbrain, craniofacial, and cranial nerve development that prefigure perinatal dysphagia in 22q11DS. This new recognition of persistent challenges with feeding and swallowing may provide opportunities for improved therapeutic intervention for adolescents and adults with 22q11DS, as well as others with a history of perinatal feeding and swallowing disorders.

Corticomotor control of airway calibre in obstructive sleep apnoea syndrome.

Corticomotor control of airway calibre in obstructive sleep apnoea syndrome.

Prevalence of profound laryngeal sensory neuropathy in head and neck cancer survivors with feeding tube-dependent oropharyngeal dysphagia.

Laryngopharyngeal sensory neuropathy (LSN) has been observed to be a contributing factor to swallowing dysfunction in head and neck cancer (HNC) survivors. Retrospective review of 43 tube-dependent HNC survivors was conducted. LSN was assessed with direct palpation of the aryepiglottic fold and by traversing the true vocal folds without eliciting a cough reflex with a flexible laryngoscope. The primary tumor sites were oropharynx (51%), larynx (14%), nasopharynx (4.7%), oral cavity (14%), thyroid (4.7%), unknown primary (9.3%), and esophagus (2.3%). The prevalence of profound LSN was 79.1%. Objective fluoroscopic parameters contributing to swallowing dysfunction were diminished laryngohyoid elevation (100%), pharyngeal weakness (67%), and reduced lateral PES opening (37%). The prevalence of LSN in HNC survivors with feeding tube-dependent dysphagia is high (79.1%). The data suggest that LSN, in addition to fibrosis, pharyngoesophageal stenosis, and cranial nerve motor deficits contributes to swallowing dysfunction in these patients.

BDNF and NGF signals originating from sensory ganglia promote cranial motor axon growth.

After exiting the hindbrain, branchial motor axons reach their targets in association with sensory ganglia. The trigeminal ganglion has been shown to promote motor axon growth from rhombomeres 2/3 and 4/5, but it is unknown whether this effect is ganglion specific and through which signals it is mediated. Here, we addressed these questions by co-cultures of ventral rhombomere 8 explants with cranial and spinal sensory ganglia in a collagen gel matrix. Our results show that all cranial sensory ganglia and even a trunk dorsal root ganglion can promote motor axon growth and that ganglia isolated from older embryos had a stronger effect on the axonal growth than younger ones. We found that brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are necessary and sufficient for this effect. Altogether, our results demonstrate that the promoting effect of sensory ganglia on cranial motor axon growth is stage dependent, but not ganglion specific and is mediated by BDNF and NGF signals.

Neuroanatomical relationship between the cholinergic and tachykininergic systems in the adult human brainstem: An immunohistochemical study

The cholinergic system plays an important role in brain homeostasis and interacts with the neuropeptidergic systems, and the functional relationships between both systems are well known. However, in the brainstem the possible physiological interactions between neurokinins and acetylcholine are unknown, although both substances have been detected in the same brainstem nuclei and have been implicated in similar functions controlled from brainstem regions such as some cranial motor nuclei. The aim of this work is to determine whether these possible physiological interactions might have a neuroanatomical basis by means of the double immunohistochemical detection of neurokinins (NK) and the enzyme choline acetyl-transferase (ChAT) in the human brainstem. No double-labelled structures were detected, although both NK and ChAT were observed in cell bodies and fibers of the same brainstem nuclei. The distribution of immunoreactive fibers is widespread, and NK and ChAT were observed in several motor cranial nerves as well as in the substantia nigra. The results obtained in the present work provide a neuroanatomical basis for possible physiological interactions between NK and ChAT that may be carried out by volume-transmission mechanisms. These interactions might participate in motor regulation or in limbic pathways as well as influence on other neurotransmitter systems such as the dopaminergic system.

Cranial nerve injuries in adult faciomaxillary trauma: prospective study in a tertiary referral centre

<p class="abstract"><strong>Background:</strong> Cranial nerve injury is often an overlooked aspect of faciomaxillary trauma. Most of these injuries do require active intervention in the acute stage. Cranial nerve injuries require long-term management, repeated surgical procedures or reconstructive measures.</p><p><strong>Methods:</strong> The study was conducted for one-year prospective study of clinical evaluation of 180 patients with faciomaxillary injuries from May 2017 to May 2018 at tertiary care hospital. There were 154 male patients (86.3%) and 26 (13.7%) female patients. The patients from the age of 18 onwards were included in the study group after obtaining consent. A number of parameters, including age, gender, injury of cranial nerve injuries, sensory and motor deficit in relation to soft tissue trauma and bone fracture were evaluated. The objective of the present study is to evaluate early management and document the frequency of cranial nerve injuries associated with maxillofacial trauma.<strong></strong></p><p class="abstract"><strong>Results:</strong> In 180 cases of faciomaxillary trauma, 60 patients presented with cranial nerve injuries including olfactory, optic, trigeminal, facial, vestibulocochlear, abducens nerve either as an isolated or combined cranial nerve injuries. Out of which most common nerve to get injured was trigeminal followed by facial nerve observed in our study.</p><p><strong>Conclusions:</strong> Cranial nerve injury in maxillofacial trauma is significant and it should be addressed at the time of treatment so that quality of life of patient is improved by getting back his sensory and motor functions of the injured nerves.</p>

Giant intracranial aneurysms of the posterior circulation and their relation to the brainstem: analysis of risk factors for neurological deficits.

Giant posterior circulation aneurysms (GPCirAs) usually cause substantial mass effect on the brainstem, which may lead to neurological deficits. So far, there has been no systematic investigation of factors associated with such deficits in GPCirA. The authors aim to examine the risk factors for cranial nerve deficit (CND), motor deficit, and disability in patients with GPCirA. Using MR images obtained in 30 patients with unruptured GPCirA, the authors examined GPCirA volume, presence of hydrocephalus or partial thrombosis (PT) of the aneurysm, and the degree of brainstem displacement measured by the distance between the McRae line and the tip of the GPCirA (∆MT). They evaluated associations between these factors and neurological deficits. Thirty GPCirAs in 30 patients were included. The prevalence of CNDs was 50%. Patients with CNDs significantly differed from those without CNDs in terms of age (mean 51.0 years [SD 15.0 years] vs 69.0 years [SD 21.0 years], p = 0.01) and in ∆MT (median 50.7 mm [IQR 39.2-53.9 mm] vs 39.0 mm [IQR 32.3-45.9 mm], p = 0.02). The prevalence of motor deficits was 33.3%. Patients with motor deficits showed a larger ∆MT (median 50.5 mm [IQR 40.8-54.6 mm]) compared with those without (∆MT: median 39.1 mm [IQR 32.8-50.5 mm], p = 0.04). GPCirA volume was larger in patients with poor modified Rankin Scale (mRS) scores (median 14.9 cm3 [IQR 8.6-18.7 cm3]) than in those with mRS scores of 0-2 (median 6.8 cm3 [IQR 4.4-11.7 cm3], p = 0.03). After adjusting for patient age and the occurrence of hydrocephalus or PT, the authors found that higher degrees of disability were significantly associated with aneurysm volume (OR 1.13, 95% CI 1.0-1.3; p = 0.04), but not with ∆MT. The occurrence of CND or motor deficit was not associated with any of the examined variables. There was no correlation between GPCirA volume and ∆MT (rs = 0.01, p = 0.96). The prevalence of neurological deficits did not differ between GPCirA at the basilar apex, the basilar trunk, the vertebrobasilar junction, or the vertebral artery. In this study, the neurological condition of the patients was associated only with GPCirA volume and not with the degree of brainstem displacement, the occurrence of PT or hydrocephalus, or the exact location of the GPCirA. These findings highlight the clinical relevance of GPCirA volume and suggest that factors such as brainstem displacement or PT should play less of a role when finding arguments for or against treatment of GPCirA.Clinical trial registration no.: NCT02066493 (clinicaltrials.gov).

Stem cell-derived cranial and spinal motor neurons reveal proteostatic differences between ALS resistant and sensitive motor neurons.

In amyotrophic lateral sclerosis (ALS) spinal motor neurons (SpMN) progressively degenerate while a subset of cranial motor neurons (CrMN) are spared until late stages of the disease. Using a rapid and efficient protocol to differentiate mouse embryonic stem cells (ESC) to SpMNs and CrMNs, we now report that ESC-derived CrMNs accumulate less human (h)SOD1 and insoluble p62 than SpMNs over time. ESC-derived CrMNs have higher proteasome activity to degrade misfolded proteins and are intrinsically more resistant to chemically-induced proteostatic stress than SpMNs. Chemical and genetic activation of the proteasome rescues SpMN sensitivity to proteostatic stress. In agreement, the hSOD1 G93A mouse model reveals that ALS-resistant CrMNs accumulate less insoluble hSOD1 and p62-containing inclusions than SpMNs. Primary-derived ALS-resistant CrMNs are also more resistant than SpMNs to proteostatic stress. Thus, an ESC-based platform has identified a superior capacity to maintain a healthy proteome as a possible mechanism to resist ALS-induced neurodegeneration.

Clinical diagnosis-part I: what is really caused by Chiari I.

Chiari malformation is a group of congenital malformations involving the brainstem, cerebellum, and upper spinal cord, frequently identified in both young adults and in children. Chiari I malformation (CM1), classically defined as a caudal displacement of the cerebellar tonsils through the foramen magnum into the spinal cord, is the most common clinical type. A syringomyelia can be associated at the time of the diagnosis or appear secondarily and manifest with medullary symptoms. The aim of this paper is to update the knowledge on clinical manifestations specifically related to Chiari I malformation with or without syringomyelia in the pediatric population. Current literature with focus on relevant clinical pediatric issues is reviewed and discussed, comparing with those related to adults; we include the results of a 10-year single-center experience on 600 CM1 patients. Herniation of the cerebellar tonsils may lead to significant clinical symptoms, including neck and cervical pain, short-lasting occipital "cough" headache, dizziness, and gait impairment; in children younger than 3 years, oropharyngeal symptoms are prevalent (sleep apnea, feeding problems) whereas in those older than 3 years, a higher incidence of cough headache and scoliosis is reported. CM1 clinical features, both in children and in adults, have in common the presence of anatomical deformities of the brainstem and cerebellum. Clinical myelopathy (sensory/autonomic disorders, motor weakness) can result from direct compression of the cervical spinal cord by the herniated cerebellar tonsils or can be due to the presence of a syrinx, reported in association with Chiari I between 35 and 75% of pediatric patients. Similarly, in our series (440 females, 160 males, 98% > 18 years), syringomyelia associated with Chiari I was ranging from 40 to 60% (respectively in asymptomatic and symptomatic groups); headache was reported in 65%. Sensory disturbances (48%), cranial nerve deficits (45%), motor weakness (32%), and autonomic disorders (35%) were the most frequent neurological signs in our cohort. In Chiari I malformation, cervical pain and occipital cough headache are the most characteristic presenting symptoms, both in old children and in adults; however, headache is often multifactorial, and CM1 patients can report a wide variety of non-specific symptoms and signs. Clinical diagnostic CM1 criteria, shared at the national and international level, are recommended with the aim to avoid consequent controversies on diagnosis and on surgical decision making.

Facial Nerve Translocation for Low Tension Neurorrhaphy to Masseteric Nerve.

The techniques of facial reanimation are continually evolving in search of the ideal method for rehabilitating the paralyzed face. In the past, alternative cranial nerve motor nuclei have been used to power facial musculature. The trigeminal nerve is gaining popularity as a promising nerve to drive facial motion, particularly in the lower face. This article describes a low-tension technique of using the transposed facial nerve to the trigeminal nerve (masseteric branch) for facial reanimation. Six patients over 2.5 years were treated with facial nerve translocation with division at the geniculate and direct neurorrhaphy to the motor branch of the masseter. Patients were evaluated by physical examination, measurement of oral commissure excursion using MEEI FACE-gram software, video assessment, Sunnybrook Facial Grading System, Facial Disability Index, and Facial Clinimetric Evaluation Scale (FaCE). Patients demonstrated early motion within 4 months postoperatively and were placed into facial physical therapy. All demonstrated improvements in oral competence, strong oral commissure excursion with good symmetry, speech improvements, and variable results in facial tone. Synkinesis to the smile antagonists in the lower face was noted and treated with chemodenervation in three of six. No upper division synkinesis was noted. The motor branch of the trigeminal nerve is an effective option for facial reanimation via facial nerve translocation and end-to-end neurorrhaphy. Variable results in facial tone were noted with excellent oral commissure excursion. This procedure is safe in the reoperated mastoid.

Videolaryngoscope-Aided Electrode Placement for Lower Cranial Nerve Monitoring in a Child with Tonsillar Enlargement

AbstractIntraoperative neuromonitoring for tumor resection near brain stem consists of monitoring the lower cranial nerves (CNs) and motor evoked potentials to check for integrity of CN and corticospinal pathway. Usually CN mapping of CN VII (orbicularis oris/oculi and frontalis bilaterally), CN IX, CN X (posterior pharyngeal wall and soft palate bilaterally, vocal cords), CN XI (sternomastoid bilaterally), and CN XII (tongue bilaterally) is done. An intraoral pathology such as tonsillar enlargement especially in pediatric patients can pose a challenge to placement of the electrodes for CN monitoring. Videolaryngoscope will aid in better visualization and safe and precise placement of electrodes in the posterior pharyngeal wall, soft palate, vocal cords, and tongue. Thus, integration of different technologies aims to provide a safer and scientifically sound anesthetic technique and improves the outcome even in challenging situations.

Excitation-inhibition balance regulates the patterning of spinal and cranial inspiratory motor outputs in rats in situ

Spinal phrenic nerve activity (PNA) drives the diaphragm but cranial hypoglossal nerve activity (HNA) also expresses synchronous activity during inspiration. Here, we investigated the effects of local disinhibition (bilateral microinjections of bicuculline) of the nucleus tractus solitarius (NTS), the pre-Bötzinger complex and Bötzinger complex core circuit (pre-BötC/BötC) and the Kölliker-Fuse nuclei (KFn) on the synchronization of PNA and HNA in arterially-perfused brainstem preparations of rats. To quantitatively analyze the bicuculline effects on a putatively distributed inspiratory central pattern generator (i-CPG), we quantified the phase synchronization properties between PNA and HNA. The analysis revealed that bicuculline-evoked local disinhibition significantly reduced the strength of phase synchronization between PNA and HNA at any target site. However, the emergence of desynchronized HNA following disinhibition was more prevalent after NTS or pre-BötC/BötC microinjections compared to the KFn. We conclude that the primary i-CPG is located in a distributed medullary circuit whereas pontine contributions are restricted to synaptic gating of synchronous HNA and PNA.

Conversion of Human Induced Pluripotent Stem Cells (iPSCs) into Functional Spinal and Cranial Motor Neurons Using PiggyBac Vectors.

We describe here a method to obtain functional spinal and cranial motor neurons from human induced pluripotent stem cells (iPSCs). Direct conversion into motor neuron is obtained by ectopic expression of alternative modules of transcription factors, namely Ngn2, Isl1 and Lhx3 (NIL) or Ngn2, Isl1 and Phox2a (NIP). NIL and NIP specify, respectively, spinal and cranial motor neuron identity. Our protocol starts with the generation of modified iPSC lines in which NIL or NIP are stably integrated in the genome via a piggyBac transposon vector. Expression of the transgenes is then induced by doxycycline and leads, in 5 days, to the conversion of iPSCs into MN progenitors. Subsequent maturation, for 7 days, leads to homogeneous populations of spinal or cranial MNs. Our method holds several advantages over previous protocols: it is extremely rapid and simplified; it does not require viral infection or further MN isolation; it allows generating different MN subpopulations (spinal and cranial) with a remarkable degree of maturation, as demonstrated by the ability to fire trains of action potentials. Moreover, a large number of motor neurons can be obtained without purification from mixed populations. iPSC-derived spinal and cranial motor neurons can be used for in vitro modeling of Amyotrophic Lateral Sclerosis and other neurodegenerative diseases of the motor neuron. Homogeneous motor neuron populations might represent an important resource for cell type specific drug screenings.

Conversion of Human Induced Pluripotent Stem Cells (iPSCs) into Functional Spinal and Cranial Motor Neurons Using PiggyBac Vectors

Conversion of Human Induced Pluripotent Stem Cells (iPSCs) into Functional Spinal and Cranial Motor Neurons Using PiggyBac Vectors

The Role of Nesprin in the Facial Branchiomotor Neuron (FBMN) Migration of Danio rerio (zebrafish) development

Nuclear envelope spectrin‐repeat proteins (Nesprins) are part of the LINC (LInker of Nucleoskeleton and Cytoskeleton) complex, which plays a vital role in the binding of F‐actin cytoskeleton to the nuclear envelope. Nesprins are crucial in maintaining the integrity of the nuclear membrane. Nuclear membrane movement is a fundamental aspect in cell migration and muscle development. Previous work has demonstrated that Nesprins may be associated with myosin‐dependent tension, which has implications in muscular dystrophy due to the role that nesprins play in muscle cells. We hypothesize that expressing dominant‐negative nesprin in Danio rerio (zebrafish) embryos would result in defects in the migration of facial branchiomotor neurons and also cause disruptions in nuclear positioning in multinucleated muscle cells. To test this hypothesis, we use transient transgenic expression of dominant Nesprin in cranial motor neurons using the islet1 promoter. We quantify the extent of migration in neurons with inactive Nesprin. In addition, we express dominant‐negative Nesprin in muscle cells using a heat shock promoter and explore the positioning of nuclei in developing skeletal muscle myofibrils. Our preliminary data shows that transgenic zebrafish embryos with expression of dominant‐negative nesprin have disruptions and defects in tangential FBMN migration. However, with further experimentation and data collection in progress, we hope to analyze our findings for statistical significance. Our goal is to gain insight into the function of Nesprins in embryo development to better devise therapeutic strategies for patients with mutations in Nesprins.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Method of preoperative labeling of lymph nodes affected by thyroid cancer metastases to facilitate their intraoperative identification

Objective. In surgical treatment of thyroid cancer, the appropriate resection of lymph nodes affected by metastases is mandatory. Minimally invasive inter­vention for metastatic process in thyroid cancer is alternative method of treatment in case of solitary neck metastases. The specific complications associa­ted with surgical trauma occur in cases of repeated interventions, namely the damage of Х, ХІ, and ХІІ pairs of cranial nerves, motor and sensory fibers of the cervical and brachial plexus, lymphorrhea. Complications associated with dissection of lymph drainage collectors lead to prolongation of post­operative stay in hospital. Thus, the need to minimize surgery risk and to increase efficacy of lymp­ha­den­e­ctomies in primary and repea­ted neck dissections emerges. The aim is to develop method of preoperative la­­beling of lymph nodes affected by thyroid cancer metastases to facilitate their intraoperative identi­fication. Materials and methods. The methylene blue dye for biological tissue labeling was used. In preoperative period, 24 hours before surgery FNAP was performed under the ultrasonography control with the purpose of metastatic lesion verification and then the 1 % solution of methylene blue dye was injected directly to affected node. During the dissection the labeled node was identified by its blue color. Results and discussion. Lymph nodes of different collector groups were labeled in 10 patients. The visual intraoperative identification of lymph node was feasible in all patients. The operation time was shortened in 9 patients (90 %). The mean decrease of operation time was 31.2 ± 7.6 min (p ≤ 0.05). The consecutive patho­logical investigation of all removed labelled lymph nodes confirmed the presence of metastatic thyroid cancer. Conclusion. The preoperative labeling of affected lymph nodes 24 hours ahead surgery is efficient, easy to use and cost-saving method of visualization which allows to mitigate excessive surgical traumatization during the lymph neck dissection and to decrease the operation time.

Death by neurologic criteria: pathophysiology, definition, diagnostic criteria and tests.

Death by neurologic criteria is an irreversible sequence of events culminating in permanent cessation of cerebral functions. In this context, there are no responses arising from the brain, no cranial nerve reflexes nor motor responses to pain stimuli, and no respiratory drive. The diagnosis of death by neurologic criteria implies that there is clinical evidence of the complete and irreversible cessation of brainstem and cerebral functions. The diagnosis, confirmation, and certification of death are core skills for medical practitioners. The aim of this review is to discuss the pathophysiology and definition of death by neurological criteria, describing the clinical assessment, and the use of ancillary tests for the diagnosis of brainstem death.

Using Pupillometry to Assess the Atypical Pupillary Light Reflex and LC-NE System in ASD.

With recent advances in technology, there has been growing interest in use of eye-tracking and pupillometry to assess the visual pathway in autism spectrum disorder (ASD). Within emerging literature, an atypical pupillary light reflex (PLR) has been documented, holding potential for use as a clinical screening biomarker for ASD. This review outlines dominant theories of neuropathology associated with ASD and integrates underlying neuroscience associated with the atypical PLR through a reciprocal model of brainstem involvement and cortical underconnectivity. This review draws from animal models of ASD demonstrating disruption of cranial motor nuclei and brain imaging studies examining arousal and the influence of the locus coeruleus norepinephrine (LC-NE) system on the pupillary response. Pupillometry methods are explained in relation to existing data examining the PLR in ASD and pupillary parameters of constriction latency and tonic pupil diameter as key parameters for investigation. This focused review provides preliminary data toward future work developing pupillometry metrics and offers direction for studies aimed at rigorous study replication using pupillometry with the ASD population. Experimental conditions and testing protocol for capturing pupil parameters with this clinical population are discussed to promote clinical research and translational application.

Genioglossus activation during maximal sniff manoeuvres: Is upper airway function relevant in the clinical assessment of inspiratory and expiratory muscle strength?

Genioglossus activation during maximal sniff manoeuvres: Is upper airway function relevant in the clinical assessment of inspiratory and expiratory muscle strength?

GH deficiency in patients with spinal cord injury: efficacy/safety of GH replacement, a pilot study.

ObjectiveGrowth hormone (GH) was shown to stimulate proliferation, migration and survival of neural cells in animal models. GH deficiency (GHD) was reported following traumatic brain lesions; however, there are not available data in spinal cord injury (SCI) patients. The aim of the study was to evaluate (1) the frequency of GHD in chronic SCI population; (2) the efficacy/safety of GH replacement in patients with SCI and suboptimal GH secretion.Design and methodsNineteen consecutive patients with chronic thoracic complete SCI (AIS-A) were studied. Patients with low GH secretion were randomized in a double-blind, placebo-controlled study to receive either subcutaneous placebo injections or GH combined with physical therapy, for 6 months. Baseline cranial MRI, AIS motor and sensory scale, quality of life (spinal cord impact measurement) and modified Ashworth spasticity scale, quantitative sensory testing and neurophysiological exploration were assessed at baseline, 1, 3 and 6 months following treatment.ResultsThirteen had GH deficiency. Seven received GH, five placebo and one dropped out. Both groups were similar according to clinical and demographical data at baseline, except for greater GH deficiency in the GH treatment group. At 6th month, patients treated with GH showed a significant improvement in SCIM-III score and in electrical perception threshold up to the 5th level below SCI, on both sides compared to baseline.ConclusionsGHD seems to be frequent in traumatic SCI and GH replacement is safe without side effects. GH combined with physical therapy can improve quality of life of SCI patients and, strikingly, the sensory perception below lesion level.