The Development of Sewing Board Media to Optimize the Fine Motor Abilities of Students with Cerebral Palsy

Disability can be classified into two types, namely disorders of the function of the orthopedic limb (orthopedic disability) and disorders of the function of the nerve (neurological disability). The purpose of this study was to optimize the fine motor skills of students with cerebral palsy at TKLB SLB D YPAC, South Jakarta, through sewing board media. In this study, the ADDIE Approach (Analysis-Design-Develop-ImplementEvaluate) was used. The sewing board media developed in this study were shown to be effective and can be used in optimizing the fine motor skills of students with cerebral palsy. Keywords: children with special needs, cerebral palsy, fine motor, sewing board media

What are the effects of scuba diving-based interventions for clients with neurological disability, autism or intellectual disability? A systematic review

Introduction: Recreational scuba diving has existed for over 70 years with organisations emerging that teach individuals with disabilities to dive. It is unclear what the physical and psychosocial effects of scuba interventions might be. This systematic review explores evidence for the effects of scuba diving in individuals with neurological disability, intellectual disability and autism. Methods: The databases Medline, EMBASE, Ovid Emcare, and SportDiscus were searched. Included papers described a scuba-based intervention for clients with a neurological disability, intellectual disability and autism, with physical or psychosocial outcomes explored in the paper. Quality of the included papers was assessed using the McMaster Appraisal Tools, with descriptive data synthesis completed to explore the physical and psychosocial effects of the interventions. Results: Four papers met the inclusion criteria: a cross-sectional investigation, a phenomenological study, a case-control study and a multiple case study. The quality of the papers was low to moderate. Papers addressed the psychosocial effects of scuba diving, including motivation to participate, participant experiences, the effect on cognition and physical self-concept. One study reported an increase in self-concept for the majority of participants. An increase in understanding instructions and in visual attention was reported in another. Enjoyment of the activity was reported and motivators to be involved in scuba diving for people with disabilities included fun and excitement. No papers addressed functional outcomes. Conclusions: Whilst scuba diving interventions appear to enhance physical self-concept and are enjoyable, conclusive evidence regarding effectiveness could not be determined. Research in this area is extremely limited.

Oligodendrocytes, BK channels and the preservation of myelin

Oligodendrocytes wrap multiple lamellae of their membrane, myelin, around axons of the central nervous system (CNS), to improve impulse conduction. Myelin synthesis is specialised and dynamic, responsive to local neuronal excitation. Subtle pathological insults are sufficient to cause significant neuronal metabolic impairment, so myelin preservation is necessary to safeguard neural networks. Multiple sclerosis (MS) is the most prevalent demyelinating disease of the CNS. In MS, inflammatory attacks against myelin, proposed to be autoimmune, cause myelin decay and oligodendrocyte loss, leaving neurons vulnerable. Current therapies target the prominent neuroinflammation but are mostly ineffective in protecting from neurodegeneration and the progressive neurological disability. People with MS have substantially higher levels of extracellular glutamate, the main excitatory neurotransmitter. This impairs cellular homeostasis to cause excitotoxic stress. Large conductance Ca2+-activated K+ channels (BK channels) could preserve myelin or allow its recovery by protecting cells from the resulting excessive excitability. This review evaluates the role of excitotoxic stress, myelination and BK channels in MS pathology, and explores the hypothesis that BK channel activation could be a therapeutic strategy to protect oligodendrocytes from excitotoxic stress in MS. This could reduce progression of neurological disability if used in parallel to immunomodulatory therapies.

Neurological outcomes after traumatic cardiopulmonary arrest: a systematic review

BackgroundDespite appropriate care, most patients do not survive traumatic cardiac arrest, and many survivors suffer from permanent neurological disability. The prevalence of non-dismal neurological outcomes remains unclear.ObjectivesThe aim of the current review is to summarize and assess the quality of reporting of the neurological outcomes in traumatic cardiac arrest survivors.Data sourcesA systematic review of Embase, Medline, PubMed, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and ProQuest databases was performed from inception of the database to July 2020.Study eligibility criteriaObservational cohort studies that reported neurological outcomes of patients surviving traumatic cardiac arrest were included.Participants and interventionsPatients who were resuscitated following traumatic cardiac arrest.Study appraisal and synthesis methodsThe quality of the included studies was assessed using ROBINS-I (Risk of Bias in Non-Randomized Studies - of Interventions) for observational studies.ResultsFrom 4295 retrieved studies, 40 were included (n=23 644 patients). The survival rate was 9.2% (n=2168 patients). Neurological status was primarily assessed at discharge. Overall, 45.8% of the survivors had good or moderate neurological recovery, 29.0% had severe neurological disability or suffered a vegetative state, and 25.2% had missing neurological outcomes. Seventeen studies qualitatively described neurological outcomes based on patient disposition and 23 studies used standardized outcome scales. 28 studies had a serious risk of bias and 12 had moderate risk of bias.LimitationsThe existing literature is characterized by inadequate outcome reporting and a high risk of bias, which limit our ability to prognosticate in this patient population.Conclusions or implications of key findingsGood and moderate neurological recoveries are frequently reported in patients who survive traumatic cardiac arrest. Prospective studies focused on quality of survivorship in traumatic arrest are urgently needed.Level of evidenceSystematic review, level IV.PROSPERO registration numberCRD42020198482.

Brain Natriuretic Peptide as a Marker of Adverse Neurological Outcomes Among Survivors of Cardiac Arrest

Background Neurological prognosis after cardiac arrest remains ill-defined. Plasma brain natriuretic peptide (BNP) may relate to poor neurological prognosis in brain-injury patients, though it has not been well studied in survivors of cardiac arrest. Methods We performed a retrospective review and examined the association of BNP with mortality and neurological outcomes at discharge in a cohort of cardiac arrest survivors enrolled from January 2012 to December 2016 at the Wake Forest Baptist Hospital, in North Carolina. Cerebral performance category (CPC) and modified Rankin scales were calculated from the chart based on neurological evaluation performed at the time of discharge. The cohort was subdivided into quartiles based on their BNP levels after which multivariable adjusted logistic regression models were applied to assess for an association between BNP and poor neurological outcomes as defined by a CPC of 3 to 4 and a modified Rankin scale of 4 to 5. Results Of the 657 patients included in the study, 254 patients survived until discharge. Among these, poor neurological status was observed in 101 (39.8%) patients that had a CPC score of 3 to 4 and 97 patients (38.2%) that had a modified Rankin scale of 4 to 5. Mean BNP levels were higher in patients with poor neurological status compared to those with good neurological status at discharge ( P = .03 for CPC 3-4 and P = .02 for modified Rankin score 4-5). BNP levels however, did not vary significantly between patients that survived and those that expired ( P = .22). BNP did emerge as a significant discriminator between patients with severe neurological disability at discharge when compared to those without. The area under the curve for BNP predicting a modified Rankin score of 4 to 5 was 0.800 (95% confidence interval [CI] 0.756-0.844, P < .001) and for predicting CPC 3 to 4 was 0.797 (95% CI 0.756-0.838, P < .001). BNP was able to significantly improve the net reclassification index and integrated discriminatory increment ( P < .05). BNP was not associated with long-term all-cause mortality ( P > .05). Conclusions In survivors of either inpatient or out-of-hospital cardiac arrest, increased BNP levels measured at the time of arrest predicted severe neurological disability at discharge. We did not observe an independent association between BNP levels and long-term all-cause mortality. BNP may be a useful biomarker for predicting adverse neurological outcomes in survivors of cardiac arrest.

Oligodendrocytes, BK channels and remyelination

Oligodendrocytes wrap multiple lamellae of their membrane, myelin, around axons of the central nervous system (CNS), to improve impulse conduction. Myelin synthesis is specialised and dynamic, responsive to local neuronal excitation. Subtle pathological insults are sufficient to cause significant neuronal metabolic impairment, so myelin preservation is necessary to safeguard neural networks. Multiple sclerosis (MS) is the most prevalent demyelinating disease of the CNS. In MS, inflammatory attacks against myelin, proposed to be autoimmune, cause myelin decay and oligodendrocyte loss, leaving neurons vulnerable. Current therapies target the prominent neuroinflammation but are mostly ineffective in protecting from neurodegeneration and the progressive neurological disability. People with MS have substantially higher levels of extracellular glutamate, the main excitatory neurotransmitter. This impairs cellular homeostasis to cause excitotoxic stress. Large conductance Ca2+-activated K+ channels (BK channels) could preserve myelin or allow its recovery by protecting cells from the resulting excessive excitability. This review evaluates the role of excitotoxic stress, myelination and BK channels in MS pathology, and explores the hypothesis that BK channel activation could be a therapeutic strategy to protect oligodendrocytes from excitotoxic stress in MS. This could reduce progression of neurological disability if used in parallel to immunomodulatory therapies.