Pediatric spina bifida (SB) and spinal cord injury (SCI) are unfortunately common in our society, and their unique findings and comorbidities warrant special consideration. This manuscript will discuss the epidemiology, pathophysiology, prevention, and management strategies for children growing and developing with these unique neuromuscular disorders. Growth and development of the maturing child places them at high risk of spinal cord tethering, syringomyelia, ascending paralysis, pressure injuries, and orthopedic abnormalities that must be addressed frequently and judiciously. Similarly, proper neurogenic bladder and neurogenic bowel management is essential not just for medical safety, but also for optimal psychosocial integration into the child’s expanding social circle.

Traumatic brain injury (TBI) remains a major cause of morbidity and death among the pediatric population. Timely diagnosis, however, remains a complex task because of the lack of standardized methods that permit its accurate identification. The aim of this study was to determine whether serum levels of brain injury biomarkers can be used as a diagnostic and prognostic tool in this pathology. This prospective, observational study collected and analyzed the serum concentration of neuronal injury biomarkers at enrollment, 24h and 48h post-injury, in 34 children ages 0–18 with pTBI and 19 healthy controls (HC). Biomarkers included glial fibrillary acidic protein (GFAP), neurofilament protein L (NfL), ubiquitin-C-terminal hydrolase (UCH-L1), S-100B, tau and tau phosphorylated at threonine 181 (p-tau181). Subjects were stratified by admission Glasgow Coma Scale score into two categories: a combined mild/moderate (GCS 9–15) and severe (GCS 3–8). Glasgow Outcome Scale-Extended (GOS-E) Peds was dichotomized into favorable (≤4) and unfavorable (≥5) and outcomes. Data were analyzed utilizing Prism 9 and R statistical software. The findings were as follows: 15 patients were stratified as severe TBI and 19 as mild/moderate per GCS. All biomarkers measured at enrollment were elevated compared with HC. Serum levels for all biomarkers were significantly higher in the severe TBI group compared with HC at 0, 24, and 48h. The GFAP, tau S100B, and p-tau181 had the ability to differentiate TBI severity in the mild/moderate group when measured at 0h post-injury. Tau serum levels were increased in the mild/moderate group at 24h. In addition, NfL and p-tau181 showed increased serum levels at 48h in the aforementioned GCS category. Individual biomarker performance on predicting unfavorable outcomes was measured at 0, 24, and 48h across different GOS-E Peds time points, which was significant for p-tau181 at 0h at all time points, UCH-L1 at 0h at 6–9 months and 12 months, GFAP at 48h at 12 months, NfL at 0h at 12 months, tau at 0h at 12 months and S100B at 0h at 12 months. We concluded that TBI leads to increased serum neuronal injury biomarkers during the first 0–48h post-injury. A biomarker panel measuring these proteins could aid in the early diagnosis of mild to moderate pTBI and may predict neurological outcomes across the injury spectrum.

Acute intermittent porphyria (AIP) is an uncommon metabolic disease that impacts multiple organs and can manifest in many ways. It is often misdiagnosed due to its nonspecific symptoms. Neurovisceral signs and symptoms should alert physicians to consider AIP in the differential after excluding more common causes. Identifying the underlying cause is critical in preventing acute attacks, and trigger avoidance is the optimal approach to managing AIP. Medications that are contraindicated should be reviewed thoroughly. Prompt intravenous hematin administration is the primary treatment for acute attacks, and additional pharmacological therapies may be necessary to treat concurrent symptoms. A severe neurological manifestation of AIP is flaccid paralysis or severe motor weakness, which can develop into total quadriplegia and respiratory insufficiency. A comprehensive rehabilitation program is an integral aspect of the treatment plan. Since the incidence of this disease is low, functional prognosis is not well-known. As a result, it is challenging to determine the most appropriate structure, intensity, and duration of rehabilitation therapy. By extending the treatment plan, individuals with tetraplegia due to AIP can continue to make functional gains years after the onset of weakness. Understanding the disease’s functional prognosis will aid in coordinating resources and improving healthcare expenditures.

The novel coronavirus 2019 pandemic has led to new dilemmas in medical education because of an initial shortage of personal protective equipment, uncertainty regarding disease transmission and treatments, travel restrictions, and social distancing guidelines. These new problems further compound the already existing problem of limited medical student exposure to the field of physical medicine and rehabilitation, particularly for students in medical schools lacking a department of physical medicine and rehabilitation, approximately 50% of medical schools. A virtual medical student physical medicine and rehabilitation rotation was created to mitigate coronavirus 2019–related limitations and impact on medical education. Using audiovisual technology, students had the opportunity to participate in clinical inpatient and outpatient care, live-streamed procedures, and virtual didactics, develop and showcase their clinical knowledge and reasoning skills, and become familiar with the culture of the physical medicine and rehabilitation residency program. Adaptive educational approaches, including integration of the flipped classroom model, success, pitfalls, and areas for improvement will be described and discussed. Providing nontraditional methods for physical medicine and rehabilitation education and exposure to medical students is crucial to maintain and promote growth of the field in this unprecedented and increasingly virtual era.

Introduction: Dual diagnosis (DD) with traumatic brain injury (TBI) and spinal cord injury (SCI) poses clinical and rehabilitation challenges. While comorbid TBI is common among adults with SCI, little is known about the epidemiology in the pediatric population. The primary objective of this study was to evaluate the prevalence of TBI among children in the United States hospitalized with SCI. Secondary objectives were to compare children hospitalized with DD with those with isolated SCI with regards to age, gender, race, hospital length of stay, and hospital charges.Methods: A retrospective analysis of hospital discharges among children aged 0–18 years occurring between 2016–2018 from U.S. hospitals participating in the Kids’ Inpatient Database. ICD-10 codes were used to identify cases of SCI, which were then categorized by the presence or absence of comorbid TBI.Results: 38.8% of children hospitalized with SCI had a co-occurring TBI. While DD disproportionately occurred among male children (67% of cases), when compared with children with isolated SCI, those with DD were not significantly more likely to be male. They were more likely to be Caucasian. The mean age of children with DD (13.2 ± 5.6 years) was significantly less than that of children with isolated SCI (14.4 ± 4.3 years). DD was associated with longer average lengths of stay (6 versus 4 days) and increased mean total hospital charges ($124,198 versus $98,089) when compared to isolated SCI.Conclusion: Comorbid TBI is prevalent among U.S. children hospitalized with SCI. Future research is needed to better delineate the impact of DD on mortality, quality of life, and functional outcomes.

Traumatic brain injury (TBI) is one of the leading causes of death and neurological disability worldwide. The search for biomarkers that indicate TBI severity and prognosis with greater accuracy is ongoing. This study aimed to evaluate the significance of several neuroinflammatory cytokines and chemokines, assessing their potential as biomarkers in pediatric TBI (pTBI). This was an exploratory analysis of inflammatory cytokines and chemokines measured in a subset of 26 children aged 0–18 years with TBI and 21 controls. TBI severity was determined by GCS. The functional outcome was measured via the GOS-E score at 6 weeks and 3, 6, 9, and 12 months post-injury. Serum samples were analyzed for ICAM-1, VCAM-1, SAA, CRP, IFN-g, IL-10, IL-12p70, IL-13, IL-1b, IL-2, IL-4, IL-6, IL-8, TNF-a, TNF-b, eotaxin, eotaxin-3, IP-10, MCP-1, MCP-4, MDC, MIP-1a, MIP-1b and TARC. Levels of IL-6, IL-10, IL-13, IL-16, MDC, and GM-CSF were increased, and IFN-γ, IL-5, IL-8, and eotaxin-3 were decreased at enrollment when compared with controls. Elevated IL-6 and IL-10 at enrollment were associated with severe TBI (AUC of 1, p = 0.0002 and p = 0.8, suggesting biomarker potential. Our data indicate that several cytokines and chemokines measured after TBI may aid in the assessment of pTBI severity and prognosis. IL-6, IL-10, and IL-16 may show potential as biomarkers for pTBI severity and outcomes.