Intensive task-specific rehabilitative training, such as robotic BWSTT, can promote supraspinal plasticity in the motor centers known to be involved in locomotion. Furthermore, improvement in over-ground locomotion is accompanied by an increased activation of the cerebellum.

Background/Objective: To develop and test a clinically relevant model for predicting the recovery of over ground walking speed after 36 sessions of progressive body weight-supported treadmill training (BWSTT) in individuals with motor incomplete spinal cord injury (SCI). Design: A retrospective review and stepwise regression analysis of a SCI clinical outcomes data set. Setting: Outpatient SCI laboratory. Subjects: Thirty individuals with a motor incomplete SCI who had participated in locomotor training with BWSTT. Eight individuals with similar diagnoses were used to prospectively test the prediction model. Main Outcome Measures: Over ground walking speed was assessed using the 10-m walking test. Methods: The locomotor training program consisted of 36 sessions of sequential comprehensive training comprised of robotic assisted BWSTT, followed by manual assisted BWSTT, and over ground walking. The dose of locomotor training was standardized throughout the protocol. Results: Clinical characteristics with predictive value for walking speed were time from injury onset, the presence or absence of voluntary bowel and bladder voiding, a functional spasticity assessment, and over ground walking speed before locomotor training. The model identified that these characteristics accounted for 78.3% of the variability in the actual final over ground walking speed after 36 sessions of locomotor training. The model was successful in prospectively predicting over ground walking speed in the 8 test participants within 4.15 6 2.22 cm/s in their recovered walking speed.Conclusions: This prediction model can identify individuals who are most likely to experience success using locomotor training by determining an expected magnitude of training effect, thereby allowing individualized decisions regarding the use of this intensive approach to rehabilitation.

Background Arginase 1 Deficiency (ARG1‐D) is a rare autosomal recessive urea cycle disorder (UCD) characterized by pathologic elevation of plasma arginine and debilitating manifestations. Based on clinical commonalities and low disease awareness, ARG1‐D can be diagnosed as hereditary spastic paraplegia (HSP), leading to treatment delays. Cases A Hispanic woman with unremarkable medical history experienced progressive lower‐limb spasticity in her 20s and received a diagnosis of HSP. She developed significant gait abnormalities and is unable to walk without assistance. More recently, two Hispanic brothers with childhood‐onset manifestations including lower‐limb spasticity, developmental delays, and seizures presented with suspected HSP. All three patients were ultimately diagnosed with ARG1‐D based on plasma arginine several‐fold above normal levels and loss‐of‐function ARG1 variants. Disease progression occurred before ARG1‐D was correctly diagnosed. Literature Review Retrospective analyses demonstrate that diagnostic delays in ARG1‐D are common and can be lengthy. Because of clinical similarities between ARG1‐D and HSP, such as insidious onset and progressive spasticity, accurate diagnosis of ARG1‐D is challenging. Timely ARG1‐D diagnosis is critical because this UCD is a treatable genetic cause of progressive lower‐limb spasticity. Conclusions Arginase 1 Deficiency should be considered in HSP differential diagnosis until biochemically/genetically excluded, and should be routinely included in HSP gene panels.