Faculty Bibliography

Sudden Unexplained Death in Childhood (SUDC) is the unexpected death of a child over age 12 months that remains unexplained after a thorough case investigation, including review of the child's medical history, circumstances of death, a complete autopsy and ancillary testing (1). First defined in 2005, SUDC cases are more often male, with death occurring during a sleep period, being found prone, peak winter incidence, associated with febrile seizure history in ~28% of cases and mild pathologic changes insufficient to explain the death (1, 2). There has been little progress in understanding the causes of SUDC and no progress in prevention. Despite reductions in sudden unexpected infant death (SUID) and other causes of mortality in childhood, the rate of SUDC has increased during the past two decades (3-5). In Ireland, SUID deaths were cut in half from 1994 to 2008 while SUDC deaths more than doubled (4). Surveillance issues, including lack of standardized certification practices, affect our understanding of the true magnitude of unexplained child deaths. Mechanisms underlying SUDC, like SUID, remain largely speculative. Limited and inconsistent evidence implicates abnormalities in brainstem autonomic and serotonergic nuclei, critical for arousal, cardiorespiratory control, and reflex responses to life-threatening hypoxia or hypercarbia in sleep (6). Abnormalities in medullary serotonergic neurons and receptors, as well as cardiorespiratory brainstem nuclei occur in some SUID cases, but have never been studied in SUDC. Retrospective, small SUDC studies with non-standardized methodologies most often demonstrate minor hippocampal abnormalities, as well as focal cortical dysplasia and dysgenesis of the brainstem and cerebellum. The significance of these findings to SUDC pathogenesis remains unclear with some investigators and forensic pathologists labeling these findings as normal variants, or potential causes of SUDC. The development of preventive strategies will require a greater understanding of underlying mechanisms.

Neurologic infections during pregnancy represent a significant cause of maternal and fetal morbidity and mortality. Immunologic alterations during pregnancy increase the susceptibility of the premature brain to damage. This chapter summarizes the epidemiology, pathophysiology, and clinical manifestations in the pregnant woman and the infant, and the diagnosis, treatment, and prevention of the major viral, parasitic, and bacterial infections known to affect pregnancy. These organisms include herpes virus, parvovirus, cytomegalovirus, varicella, rubella, Zika virus, toxoplasmosis, malaria, group B streptococcus, listeriosis, syphilis, and tuberculosis. There is an emphasis on the important differences in diagnosis, treatment, and fetal outcome between trimesters. An additional overview is provided on the spectrum of neurologic sequelae of an affected infant, which ranges from developmental delay to hydrocephalus and seizures.

Objectives: Anhedonia, or the inability or the loss of the capacity to experience pleasure, is a core feature of several psychiatric disorders. Different types of anhedonia have been described including social and physical anhedonia, appetitive or motivational anhedonia, consummatory and anticipatory anhedonia. Musical anhedonia is a rare condition where individuals derive no reward responses from musical experience. Methods: We searched the PubMed electronic database for all articles with the search term "musical anhedonia". Results: A final set of 12 articles (six original research articles and six clinical case reports) comprised the set we reviewed. Conclusions: Individuals with specific musical anhedonia show normal responses to other types of reward, suggesting a specific deficit in musical reward pathways. Those individuals are not necessarily affected by psychiatric conditions, have normal musical perception capacities, and normal recognition of emotions depicted in music. Individual differences in the tendency to derive pleasure from music are associated with structural connections from auditory association areas in the superior temporal gyrus to the anterior insula. White matter connectivity may reflect individual differences in the normal variations of reward experiences in music. The moderate amount of heterogeneity between the reviewed studies is a limitation to the generalizability of our conclusions. (PsycInfo Database Record (c) 2021 APA, all rights reserved)

Background/UNASSIGNED:Spine surgeons encounter occasional complex cerebrospinal fluid fistulas/dural tears (CSF/DT) during lumbar spinal surgery. In some cases, these leaks are found during the index procedure, but others may appear postoperatively, or in the course of successive procedures. Here we asked, whether these complex CSF fistulas/DT could be more readily repaired utilizing a "bone suture anchor" technique, particularly where there is no residual dural margin/remnant. Methods/UNASSIGNED:With the combined expertise of the orthopedist and neurosurgeon, mini/micro bone suture anchors, largely developed for hand surgery, facilitated repair of complex DT occurring during lumbar spine surgery. This technique was utilized to suture in place fascia, periosteal, or muscle grafts, and was followed by the application of microfibrillar collagen, and a fibrin sealant. Results/UNASSIGNED:This mini/micro suture anchor technique has now been utilized to repair multiple significant intraoperative and/or postoperative recurrent DT, largely avoiding the need to place lumbar drains and/or lumbo- peritoneal shunts. Conclusions/UNASSIGNED:Here, we reviewed how to directly suture dural grafts utilizing a mini/micro bone suture anchor technique to repair complex intraoperative primary/recurrent DT occurring during lumbar spine surgery. The major advantages of this technique, in addition to obtaining definitive occlusion of the DT, largely avoids the need to place lumbar drains and/or lumbo-peritoneal shunts with their attendant risks and complications.

BACKGROUND:Depression is associated with a broad range of cognitive deficits, including processing speed (PS) and executive functioning (EF). Cognitive symptoms commonly persist with the resolution of affective symptoms and increase risk of relapse and recurrence. The cognitive control network is comprised of brain areas implicated in EF and mood regulatory functions. Prior research has demonstrated the effectiveness of computerized cognitive training (CCT) focused on PS and EF in mitigating both cognitive and affective symptoms of depression. METHODS:Ninety participants aged 18-29 with a current diagnosis of major depressive disorder or persistent depressive disorder, or a Hamilton Depression Rating Scale score ≥12, will be randomized to either PS/EF CCT, verbal CCT, or waitlist control. Participants in the active groups will complete 15 min of training 5 days/week for 8 weeks. Clinical and neuropsychological assessments will be completed at baseline, week 4, week 8, and 3-month follow-up. Structural and functional magnetic resonance imaging (fMRI) will be completed at baseline and week 8. We will compare changes in mood, cognition, daily functioning, and fMRI data. We will explore cognitive control network functioning using resting-state and task-based fMRI. RESULTS:Recruitment began in October 2019; we expect to finish recruitment by April 2022 and subsequently begin data analysis. CONCLUSIONS:This study is innovative in that it will include both active and waitlist control conditions and will explore changes in neural activation. Identifying the neural networks associated with improvements following CCT will allow for the development of more precise and effective interventions. TRIAL REGISTRATION/BACKGROUND:ClinicalTrials.gov NCT03869463; https://clinicaltrials.gov/ct2/show/NCT03869463.