Topographic mapping of the sensorimotor qualities of empathic reactivity: A psychophysiological study in people with spinal cord injuries.

The experience of empathy for pain is underpinned by sensorimotor and affective dimensions which, although interconnected, are at least in part behaviorally and neurally distinct. Spinal cord injuries (SCI) induce a massive, below-lesion level, sensorimotor body-brain disconnection. This condition may make it possible to test whether sensorimotor deprivation alters specific dimensions of empathic reactivity to observed pain. To explore this issue, we asked SCI people with paraplegia and healthy controls to observe videos of painful or neutral stimuli administered to a hand (intact) or a foot (deafferented). The stimuli were displayed by means of a virtual reality set-up and seen from a first person (1PP) or third person (3PP) visual perspective. A number of measures were recorded ranging from explicit behaviors like explicit verbal reports on the videos, to implicit measures of muscular activity (like EMG from the corrugator and zygomatic muscles that may represent a proxy of sensorimotor empathy) and of autonomic reactivity (like the electrodermal response and Respiratory Sinus Arrhythmia that may represent a general proxy of affective empathy). While no across group differences in explicit verbal reports about the pain stimuli were found, SCI people exhibited reduced facial muscle reactivity to the stimuli applied to the foot (but not the hand) seen from the 1PP. Tellingly, the corrugator activity correlated with SCI participants' neuropathic pain. There were no across group differences in autonomic reactivity suggesting that SCI lesions may affect sensorimotor dimensions connected to empathy for pain.

The prognosis and recovery of major postoperative neurological deficits after corrective surgery for scoliosis : an analysis of 65 cases at a single institution.

AIMS: The outcome following the development of neurological complications after corrective surgery for scoliosis varies from full recovery to a permanent deficit. This study aimed to assess the prognosis and recovery of major neurological deficits in these patients, and to determine the risk factors for non-recovery, at a minimum follow-up of two years. METHODS: A major neurological deficit was identified in 65 of 8,870 patients who underwent corrective surgery for scoliosis, including eight with complete paraplegia and 57 with incomplete paraplegia. There were 23 male and 42 female patients. Their mean age was 25.0 years (SD 16.3). The aetiology of the scoliosis was idiopathic (n = 6), congenital (n = 23), neuromuscular (n = 11), neurofibromatosis type 1 (n = 6), and others (n = 19). Neurological function was determined by the American Spinal Injury Association (ASIA) impairment scale at a mean follow-up of 45.4 months (SD 17.2). the patients were divided into those with recovery and those with no recovery according to the ASIA scale during follow-up. RESULTS: The incidence of major deficit was 0.73%. At six-month follow-up, 39 patients (60%) had complete recovery and ten (15.4%) had incomplete recovery; these percentages improved to 70.8% (46) and 16.9% (11) at follow-up of two years, respectively. Eight patients showed no recovery at the final follow-up. The cause of injury was mechanical in 39 patients and ischaemic in five. For 11 patients with misplaced implants and haematoma formation, nine had complete recovery. Fisher's exact test showed a significant difference in the aetiology of the scoliosis (p = 0.007) and preoperative deficit (p = 0.016) between the recovery and non-recovery groups. A preoperative deficit was found to be significantly associated with non-recovery (odds ratio 8.5 (95% confidence interval 1.676 to 43.109); p = 0.010) in a multivariate regression model. CONCLUSION: For patients with scoliosis who develop a major neurological deficit after corrective surgery, recovery (complete and incomplete) can be expected in 87.7%. The first three to six months is the time window for recovery. In patients with misplaced implants and haematoma formation, the prognosis is satisfactory with appropriate early intervention. Patients with a preoperative neurological deficit are at a significant risk of having a permanent deficit. Cite this article: Bone Joint J 2022;104-B(1):103-111.

Benefits of 1-Yr Home Training With Functional Electrical Stimulation Cycling in Paraplegia During COVID-19 Crisis.

ABSTRACT: The purpose of this observational study was to report the experience of a 1-yr home training with functional electrical stimulation cycling of a person with T4 American Impairment Scale A paraplegia for 9 yrs, homebound due to the COVID-19 health crisis. The 40-yr-old participant had a three-phase training: V1, isometric stimulation; V2, functional electrical stimulation cycling for 3 sessions/wk; and V3, functional electrical stimulation cycling for 2-4 sessions/wk. Data on general and physical tolerance, health impact, and performance were collected. Borg Scale score relating to fatigue was 10.1 before training and 11.8 after training. The average score for satisfaction at the end of sessions was 8.7. Lean leg mass increased more than 29%, although total bone mineral density dropped by 1.6%. The ventilatory thresholds increased from 19.5 to 29% and the maximum ventilatory peak increased by 9.5%. Rosenberg's Self-esteem Scale score returned to its highest level by the end of training. For the only track event on a competition bike, the pilot covered a distance of 1607.8 m in 17 mins 49 secs. When functional electrical stimulation cycling training is based on a clear and structured protocol, it offers the person with paraplegia the opportunity to practice this activity recreationally and athletically. In times of crisis, this training has proven to be very relevant.

Lipocalin 2 as a Putative Modulator of Local Inflammatory Processes in the Spinal Cord and Component of Organ Cross talk After Spinal Cord Injury.

Lipocalin 2 (LCN2), an immunomodulator, regulates various cellular processes such as iron transport and defense against bacterial infection. Under pathological conditions, LCN2 promotes neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes. Although it seems to have a negative influence on the functional outcome in spinal cord injury (SCI), the extent of its involvement in SCI and the underlying mechanisms are not yet fully known. In this study, using a SCI contusion mouse model, we first investigated the expression pattern of Lcn2 in different parts of the CNS (spinal cord and brain) and in the liver and its concentration in blood serum. Interestingly, we could note a significant increase in LCN2 throughout the whole spinal cord, in the brain, liver, and blood serum. This demonstrates the diversity of its possible sites of action in SCI. Furthermore, genetic deficiency of Lcn2 (Lcn2-/-) significantly reduced certain aspects of gliosis in the SCI-mice. Taken together, our studies provide first valuable hints, suggesting that LCN2 is involved in the local and systemic effects post SCI, and might modulate the impairment of different peripheral organs after injury.

Formation of a novel supraspinal-spinal connectome that relearns the same motor task after complete paralysis.

Having observed that electrical spinal cord stimulation and training enabled four patients with paraplegia with motor complete paralysis to regain voluntary leg movement, the underlying mechanisms involved in forming the newly established supraspinal-spinal functional connectivity have become of great interest. van den Brand et al. (Science 336: 1182-1185, 2012) subsequently, demonstrated the recovery, in response to spinal electro-neuromodulation and locomotor training, of voluntary stepping of the lower limbs in rats that received a lesion that is assumed to eliminate all long-descending cortical axons that project to lumbosacral segments. Here, we used a similar spinal lesion in rats to eliminate long-descending axons to determine whether a novel, trained motor behavior triggered by a unique auditory cue learned before a spinal lesion, could recover after the lesion. Hindlimb stepping recovered 1 mo after the spinal injury, but only after 2 mo, the novel and unique audio-triggered behavior was recovered, meaning that not only was a novel connectivity formed but also further evidence suggested that this highly unique behavioral response was independent of the recovery of the circuitry that generated stepping. The unique features of the newly formed supraspinal-spinal connections that mediated the recovery of the trained behavior is consistent with a guidance mechanism(s) that are highly use dependent.NEW & NOTEWORTHY Electrical spinal cord stimulation has enabled patients with paraplegia to regain voluntary leg movement, and so the underlying mechanisms involved in this recovery are of great interest. Here, we demonstrate in rodents the recovery of trained motor behavior after a spinal lesion. Rodents were trained to kick their right hindlimb in response to an auditory cue. This behavior recovered 2 mo after the paralyzing spinal cord injury but only with the assistance of electrical spinal cord stimulation.

Caffeine-induced hypokalemia: a case report.

BACKGROUND: With an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia. CASE PRESENTATION: A 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6-2.9 mmol/L) and low urine osmolality (100-130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized. CONCLUSIONS: An increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

Supraspinal nociceptive networks in neuropathic pain after spinal cord injury.

Neuropathic pain following spinal cord injury involves plastic changes along the whole neuroaxis. Current neuroimaging studies have identified grey matter volume (GMV) and resting-state functional connectivity changes of pain processing regions related to neuropathic pain intensity in spinal cord injury subjects. However, the relationship between the underlying neural processes and pain extent, a complementary characteristic of neuropathic pain, is unknown. We therefore aimed to reveal the neural markers of widespread neuropathic pain in spinal cord injury subjects and hypothesized that those with greater pain extent will show higher GMV and stronger connectivity within pain related regions. Thus, 29 chronic paraplegic subjects and 25 healthy controls underwent clinical and electrophysiological examinations combined with neuroimaging. Paraplegics were demarcated based on neuropathic pain and were thoroughly matched demographically. Our findings indicate that (a) spinal cord injury subjects with neuropathic pain display stronger connectivity between prefrontal cortices and regions involved with sensory integration and multimodal processing, (b) greater neuropathic pain extent, is associated with stronger connectivity between the posterior insular cortex and thalamic sub-regions which partake in the lateral pain system and (c) greater intensity of neuropathic pain is related to stronger connectivity of regions involved with multimodal integration and the affective-motivational component of pain. Overall, this study provides neuroimaging evidence that the pain phenotype of spinal cord injury subjects is related to the underlying function of their resting brain.

Extended post-exercise hyperthermia in athletes with a spinal cord injury.

OBJECTIVES: Determine the extent and underlying causes of post-exercise hyperthermia in athletes with a spinal cord injury following exercise. DESIGN: Observational. METHODS: Thirty-one males (8 with tetraplegia [TP; C5-C8], 7 with high paraplegia [HP; T1-T5], 8 with low paraplegia [LP; T6-L1] and 8 able-bodied [AB]), recovered in 35°C/50%RH for 45min after 30-min of exercise at a metabolic heat production (Hprod) of 4.0W/kg (AB vs TP) or 6.0W/kg (AB vs HP vs LP). Esophageal (Tes), gastrointestinal (Tgi) and skin temperatures, Hprod, local sweat rate (LSR) and mean arterial pressure were measured. RESULTS: TP maintained a higher Tes (38.05°C [95% CI: 37.83°C, 38.28°C], AB: 36.77°C [36.56°C, 36.98°C], p<0.001) and Tgi (TP: 38.36°C [38.15°C, 38.58°C], AB: 37.26°C [37.04°C, 37.47°C], p<0.001), with peak values observed 45min post-exercise. Core temperatures all declined in HP, LP and AB, but HP maintained a higher Tes than AB (p=0.030), and higher Tgi than LP and AB (p=0.019). No differences in post-exercise Hprod were observed between TP and AB (p=0.264), or HP, LP and AB (p=0.124). Evaporative heat loss was estimated to be zero in TP, while back LSR was greater in HP than LP (p=0.009). Minimal dry heat loss occurred in SCI groups (TP: 9W/m2 [6, 12], HP: 4W/m2 [1, 6], LP: 2W/m2 [0, 5]). CONCLUSIONS: Substantial post-exercise hyperthermia is evident in TP (∼1.4°C hotter than AB after 45min of post-exercise recovery) due to minimal evaporation. HP have delayed post-exercise thermoregulatory recovery whereas LP respond similarly to AB.

"Proximalization is Advancement"-Zone 3 Frozen Elephant Trunk vs Zone 2 Frozen Elephant Trunk: A Literature Review.

Over the decades, the Frozen Elephant Trunk (FET) technique has gained immense popularity allowing simplified treatment of complex aortic pathologies. FET is frequently used to treat aortic conditions involving the distal aortic arch and the proximal descending aorta in a single stage. Surgical preference has recently changed from FET procedures being performed at Zone 3 to Zone 2. There are several advantages of Zone 2 FET over Zone 3 FET including reduction in spinal cord injury, visceral ischemia, neurological and cardiovascular sequelae. In addition, Zone 2 FET is a technically less complicated procedure. Literature on the comparison between Zone 3 and Zone 2 FET is scarce and primarily observational and anecdotal. Therefore, further research is warranted in this paradigm to substantiate current surgical treatment options for complex aortic pathologies. In this review, we explore literature surrounding FET and the reasons for the shift in surgical preference from Zone 3 to Zone 2.

Cross training effects of non-paralytic dorsiflexion muscle strengthening exercise on paralytic dorsiflexor muscle activity, gait ability, and balancing ability in patients with chronic stroke: A randomized, controlled, pilot trial.

OBJECTIVE: To investigate the effects of non-paralytic dorsiflexion muscle strengthening exercise on functional abilities in chronic hemiplegic patients after stroke. METHODS: A total of 21 patients with chronic stroke underwent dorsiflexion muscle strengthening exercise (MST) 5 times a week for 6 weeks (the experimental group, MST to non-paralytic dorsiflexion muscles, n=11; the control group, MST to paralytic dorsiflexion muscles; n=10). Paralytic dorsiflexor muscle activities (DFA) and 10 m walking tests (10MWT) and timed up and go tests (TUG) were measured before and after intervention. RESULTS: A significant increase in DFA was observed after intervention in the experimental and control groups (p<0.05) (experimental 886.6% for reference voluntary contraction (RVC), control 931.6% for RVC). TUG and 10MWT results showed significant reductions post-intervention in the experimental and control groups (experimental group -5.6 sec, control -4.8 sec; experimental group -3.1 sec, control, -3.9 sec; respectively). No significant intergroup difference was observed between changes in DFA or between changes in TUG and 10MWT results after intervention (p>.05). CONCLUSION: Strengthening exercise performed on non-paralytic dorsiflexion muscles had positive cross-training effects on paralytic dorsiflexor muscle activities, balance abilities, and walking abilities in patients with chronic stroke.

Ddhd1 knockout mouse as a model of locomotive and physiological abnormality in familial spastic paraplegia.

We have previously reported a novel homozygous 4-bp deletion in DDHD1 as the responsible variant for spastic paraplegia type 28 (SPG28; OMIM#609340). The variant causes a frameshift, resulting in a functionally null allele in the patient. DDHD1 encodes phospholipase A1 (PLA1) catalyzing phosphatidylinositol to lysophosphatidylinositol (LPI). To clarify the pathogenic mechanism of SPG28, we established Ddhd1 knockout mice (Ddhd1[-/-]) carrying a 5-bp deletion in Ddhd1, resulting in a premature termination of translation at a position similar to that of the patient. We observed a significant decrease in foot-base angle (FBA) in aged Ddhd1(-/-) (24 months of age) and a significant decrease in LPI 20:4 (sn-2) in Ddhd1(-/-) cerebra (26 months of age). These changes in FBA were not observed in 14 months of age. We also observed significant changes of expression levels of 22 genes in the Ddhd1(-/-) cerebra (26 months of age). Gene Ontology (GO) terms relating to the nervous system and cell-cell communications were significantly enriched. We conclude that the reduced signaling of LPI 20:4 (sn-2) by PLA1 dysfunction is responsible for the locomotive abnormality in SPG28, further suggesting that the reduction of downstream signaling such as GPR55 which is agonized by LPI is involved in the pathogenesis of SPG28.

Feasibility of salvage decompressive surgery for pending paralysis due to metastatic spinal cord compression.

OBJECTIVE: Metastatic spinal cord compression (MSCC) is a frequent phenomenon in cancer disease, often leading to severe neurological deficits. Especially in patients with complete motor paralysis, regaining the ability to walk is an important treatment goal. Our study, therefore, aimed to assess the neurological outcome of patients with MSCC and complete motor paralysis after decompressive surgery. METHODS: Patients with MSCC and complete motor paralysis, surgically treated by decompressive surgery between 2004-2014 at a single institution were retrospectively analyzed. Clinical patient data were collected from medical records. To assess the neurological outcome, Frankel grade (FG) at admission and discharge were compared. Statistical analysis was performed to identify factors associated with an ambulatory status after surgery. RESULTS: Twenty-eight patients were included in this study. The majority of metastases (57 %) were located in the thoracic spine and 75 % showed extraspinal tumor spread. The median interval between loss of ambulation and surgery was 35 h (IQR: 29-70). Posterior circumferential decompression without stabilization was performed in all cases within 24 h of admission. Neurological function improved in 17 patients (63 %) and seven (26 %) even regained the ability to walk following surgery. The rate of complications was low (7%). In statistical analysis, only the Karnofsky Performance Index (KPI) displayed a significant predictive value for an ambulatory status at discharge. CONCLUSIONS: Our findings indicate that severely affected MSCC patients with complete motor paralysis might benefit from decompressive surgery even when the loss of ambulation occurred more than 24 h ago.

Spinal cord stimulation improves motor function and gait in spastic paraplegia type 4 (SPG4): Clinical and neurophysiological evaluation.

INTRODUCTION: Hereditary spastic paraplegia is a heterogeneous group of genetic disorders characterized by degeneration of the corticospinal tracts, coursing with progressive weakness and spasticity of the lower limbs. To date, there are no effective treatments for progressive deficits or disease-modifying therapy for those patients. We report encouraging results for spastic paraparesis after spinal cord stimulation. METHODS: A 51-year-old woman suffering from progressive weakness and spasticity in lower limbs related to hereditary spastic paraplegia type 4 underwent spinal cord stimulation (SCS) and experienced also significant improvement in motor function. Maximum ballistic voluntary isometric contraction test, continuous passive motion test and gait analysis using a motion-capture system were performed in ON and OFF SCS conditions. Neurophysiologic assessment consisted of obtaining motor evoked potentials in both conditions. RESULTS: Presurgical Spastic Paraplegia Rating Scale (SPRS) score was 26. One month after effective SCS was initiated, SPRS went down to 15. At 12 months follow up, she experienced substantial improvement in motor function and in gait performance, with SPRS scores 23 (OFF) and down to 20 (ON). There was an increased isometric muscle strength (knee extension, OFF: 41 N m; ON: 71 N m), lower knee extension and flexion torque values in continuous passive motion test (decrease in spastic tone) and improvement in gait (for example, step length increase). CONCLUSION: Despite being a case study, our findings suggest innovative lines of research for the treatment of spastic paraplegia.

Paraplegia Following Type B Acute Aortic Dissection Can Spare the Spinal Cord.

Ischemic lumbosacral plexopathy secondary to an acute aortic dissection is a rare condition that is usually unilateral and frequently accompanied by a simultaneous spinal cord infarction. The functional prognosis relies on the severity of the nervous system involvement being usually worse when the spinal cord is involved. We present a case of a 46-year-old man who suffered an acute type B aortic dissection presenting as acute paraplegia due to bilateral ischemic lumbosacral plexopathy treated with thoracic endovascular aortic repair. An up-to-date review of the literature on ischemic lumbosacral plexus injury is provided.

Tubercular longitudinally extensive transverse myelitis with lower motor neuron paralysis.

Transverse myelitis typically extends two or less spinal segments, whereas longitudinal extensive transverse myelitis (LETM) extends three or more spinal segments in length and may occasionally span all the segments of the spinal cord. We present a case of spinal tuberculosis presenting with LETM with true lower motor neuron-type flaccid paraplegia.

An investigation into the validity and reliability of the Chinese version of Spinal Cord Independence Measure III (SCIM III).

OBJECTIVE: To investigate the validity and reliability of a Chinese version of Spinal Cord Independence Measure III (SCIM III) in individuals with spinal cord injury. DESIGN: Study on psychometric properties. SETTING: An inpatient rehabilitation facility in China. SUBJECTS: 102 participants with spinal cord injury. Mean (SD) age was 48.8 (15.6) years; tetraplegia/paraplegia ratio was 50/52; median time post injury was 2 months. INTERVENTION: SCIM III was translated into Chinese. Chinese versions of Barthel Index and SCIM III were filled out for each participant by Rater 1. SCIM III was then administered by Rater 2 after 24 hours (n = 67) and 7 days (n = 65). MAIN MEASURES: Validity, inter-rater/test-retest reliability, and internal consistency of the Chinese version of SCIM III. RESULTS: The total scores between the two raters were similar (mean ± SD: 33.8 ± 25.8 vs 33.8 ± 25.5, P = 0.95). Total agreement between the raters in each item was >80%, with both Pearson and intraclass correlation coefficients >0.97 (P < 0.01) for each subscale and total score. The Pearson correlation coefficients of the two independent assessments performed by Rater 2 were also >0.97 (P < 0.01) for each subscale and the total score. Cronbach α was >0.7 for each subscale and the total score for both raters. High consistency was found between Barthel Index and SCIM III total scores (Pearson correlation coefficient = 0.88, P < 0.01). CONCLUSION: The Chinese version of SCIM III is valid and reliable for the functional assessment of patients with SCI.

Oxygen Uptake During Exoskeletal-Assisted Walking in Persons With Paraplegia.

OBJECTIVE: To determine the cardiometabolic demands associated with exoskeletal-assisted walking (EAW) in persons with paraplegia. This study will further examine if training in the device for 60 sessions modifies cost of transport (CT). DESIGN: Prospective cohort study. Measurements over the course of a 60-session training program, approximately 20 sessions apart. SETTING: James J. Peters Bronx Veterans Affairs Medical Center, Center for the Medical Consequences of Spinal Cord Injury Research Center. PARTICIPANTS: The participants' demographics (N=5) were 37-61 years old, body mass index (calculated as weight in kilograms divided by height in meters squared) of 22.7-28.6, level of injury from T1-T11, and 2-14 years since injury. INTERVENTIONS: Powered EAW. MAIN OUTCOME MEASURES: Oxygen consumption per unit time (V˙O2, mL/min/kg), velocity (m/min), cost of transport (V˙O2/velocity), and rating of perceived exertion (RPE). RESULTS: With training: EAW velocity significantly improved (Pre: 51±51m; 0.14±0.14m/s vs Post: 99±42m; 0.28±0.12m/s, P=.023), RPE significantly decreased (Pre: 13±6 vs Post: 7±4, P=.001), V˙O2 significantly improved (Pre: 9.76±1.23 mL/kg/m vs Post: 12.73±2.30 mL/kg/m, P=.04), and CT was reduced from the early to the later stages of training (3.66±5.2 vs 0.87±0.85 mL/kg/m). CONCLUSIONS: The current study suggests that EAW training improves oxygen uptake efficiency and walking velocities, with a lower perception of exertion.