Learning the neurobiology of pain: A scoping review of pain education from an instructional design perspective

ObjectivesLearning modern pain biology concepts can improve important clinical outcomes for people with chronic pain. The primary purpose of this scoping review is to examine and report characteristics of chronic musculoskeletal pain education programs from an instructional design perspective.MethodsFollowing PRISMA-ScR guidelines, PubMed, Medline, and CINAHL databases were systematically searched. Articles included expert recommendations and those reporting pain education programs used in clinical trials enrolling adults with chronic neuromusculoskeletal pain and published in English between 1990 and 2021. Three authors independently evaluated articles for eligibility through title, abstract, and full text review. Instructional design characteristics such as learning outcomes, support materials, learning assessment methods, and key concepts communicated were summarized.ResultsThe search revealed 5260 articles of which 40 were included: 27 clinical studies, 7 expert recommendations, and 6 articles reporting on pain education from participant perspectives. Detailed reporting of instructional design characteristics informing replication in subsequent studies is sparse. Most included trials used only lecture and did not assess participant learning.ConclusionsMore comprehensive reporting of pain education programs is needed to facilitate replicability.Practical implicationsThis article proposes detailed and standardized reporting of trials using pain education programs employing a modified version of the TIDieR checklist.     

Gut memories: towards a cognitive neurobiology of irritable bowel syndrome

The brain and the gut are engaged in continual crosstalk along a number of pathways collectively termed the ‘brain-gut axis’. Over recent years it has become increasingly clear that dysregulation of the axis at a number of levels can result in disorders such as irritable bowel syndrome (IBS). With recent advances in neuroimaging technologies, insights into the neurobiology of IBS are beginning to emerge. However the cognitive neurobiology of IBS has remained relatively unexplored to date. In this review we summarise the available data on cognitive function in IBS. Moreover, we specifically address three key pathophysiological factors, namely; stress, immune activation and chronic pain, together with other factors involved in the manifestation of IBS, and explore how each of these components may impact centrally, what neurobiological mechanisms might be involved, and consider the implications for cognitive functioning in IBS. We conclude that each factor addressed could significantly impinge on central nervous system function, supporting the view that future research efforts must be directed towards a detailed assessment of cognitive function in IBS.     

Convulsing toward the pathophysiology of autism

The autisms and epilepsies are heterogeneous disorders that have diverse etiologies and pathologies. The severity of impairment and of symptoms associated with autism or with particular epilepsy syndromes reflects focal or global, structurally abnormal or dysfunctional neuronal networks. The complex relationship between autism and epilepsy, as reflected in the autism–epilepsy phenotype, provides a bridge to further knowledge of shared neuronal networks that can account for both the autisms and the epilepsies. Although epilepsy is not a causal factor for autism, increased understanding of common genetic and molecular biological mechanisms of the autism–epilepsy phenotype has provided insight into the pathophysiology of the autisms. The autism–epilepsy phenotype provides a novel model to the study of interventions that may have a positive modulating effects on social cognitive outcome.     

Cortical inhibitory dysfunction in epilepsia partialis continua: A high frequency oscillation somatosensory evoked potential study

ObjectiveThe pathophysiology of epilepsia partialis continua (EPC) is still unclear, a thalamo-cortical circuit dysfunction has been hypothesized.The aim of present study is the functional evaluation of the thalamo-cortical network in EPC by means of the study of low- and high-frequency somatosensory evoked potentials (LF-SEP and HF-SEP).MethodsMedian LF-SEP and HF-SEP were recorded in 3 patients with EPC and in 2 patients with rolandic lesions without EPC (non-EPC). Recording electrodes were placed on P3, C3, F3 and P4, C4, F4 of scalp regions. HF-SEP were obtained by an offline 400–800 Hz filtering of P3-F3 and P4-F4 traces.ResultsIn EPC patients, we found a significant suppression of post-synaptic HF-SEP burst and an amplitude reduction of the P24 wave of the LF-SEPs. Both these components are related to cortical inhibitory interneuron activity. HF-SEP and LF-SEP were normal in non-EPC patients.ConclusionThe different results obtained in patients with a rolandic lesion with and without EPC supports the hypothesis that EPC might be correlated to a dysfunction of gabaergic interneurons of a cortical sensory-motor network.SignificanceOur results might contribute to the understanding of the physiological basis of the cortical dysfunction causing epilepsia partialis continua.     

Anti-ganglioside antibodies in multiple sclerosis

Serological activity against several purified brain gangliosides has been demonstrated in sera of a proportion of multiple sclerosis patients, but not in normal individuals. The activity was determined by the capacity of the sera to bring about complement-dependent lysis of liposomes containing the respective ganglioside in their lipid bilayer. An apparent correlation is indicated between the severity of the disease and the extent of liposome lysis. Cerebrospinal fluid of the patients did not induce lysis, probably due to low antibody concentration.