![]() ![]() SIDS and SUDEP victims are often found deceased in bed, in the prone position, and sometimes in soft bedding, focusing attention on exposure to elevated CO 2 concentrations associated with these conditions during sleep ( 6, 7). The focus on high CO 2 arises from the circumstances normally associated with SIDS or postictal cessation of breathing in epilepsy. Here, we evaluate the role of the cerebellum in mediating the consequences of exposure to one exogenous stressor, increased levels of environmental carbon dioxide (CO 2 hypercapnia). Although an inability to respond to severe, transient hypotension is a strong possibility ( 3, 4), the circumstances surrounding both SIDS and SUDEP conditions suggest an unknown brain abnormality that results in an inability to appropriately compensate for, or recover from, exposure to an intrinsic or exogenous stressor ( 5). ![]() A defect in breathing, or deficient responses to a ventilatory challenge is suspected in both SIDS and SUDEP. Sudden death in epilepsy (SUDEP), appears in adults as well as older children, often occurs during sleep, but leaves few signs of mechanisms operating to induce a fatal event. Sudden infant death syndrome (SIDS) is one such syndrome the condition occurs in infants <1 year of age, often during sleep, and with victims succumbing suddenly with major causes excluded even after autopsy and a thorough investigation ( 1, 2). Sudden unexpected death occurs in several syndromes, with mechanisms underlying the fatal event not yet understood. Multiple disorders, including sudden infant death syndrome (SIDS) and sudden unexpected death in epilepsy (SUDEP), appear to involve both cardiorespiratory failure and loss or injury to cerebellar Purkinje cells the findings support the concept that such neuropathology may precede and exert a prominent role in these fatal events. These data implicate cerebellar Purkinje cells in the ability to recover from hypercarbia, suggesting that neuropathologic changes or loss of these cells contribute to inadequate ventilatory recovery to increased environmental CO 2. Developmental cerebellar Purkinje cell loss significantly affects compensatory breathing patterns following mild CO 2 exposure, possibly by inhibiting recovery from elevated CO 2. Additionally, mutant mice exhibited signs of post-sigh disordered breathing during recovery following each exposure. However, during recovery, EEP durations significantly lengthened in mutants, compared to WT mice, following the relatively low levels of CO 2 exposure. No baseline genotypic differences emerged. Breath-by-breath patterns, including depth of breathing and end-expiratory pause (EEP) durations during recovery, were recorded. Six mutant and six WT mice were exposed to 4-min blocks of increasing CO 2 (2, 4, 6, and 8%), separated by 4-min recovery intervals in room air. We evaluated breathing patterns in 12 wild-type (WT) and Lurcher mutant mice with 100% developmental cerebellar Purkinje cell loss under baseline (room air), and recovery from hypercapnia, a concern in sudden death events. Purkinje cell alterations or loss appear in sudden infant death and sudden death in epilepsy victims, possibly contributing to the fatal event. ![]() The cerebellum assists coordination of somatomotor, respiratory, and autonomic actions. 4Department of Psychological Science, Ball State University, Muncie, IN, USA.3Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, BC, Canada.2Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.1Department of Psychology, The University of Memphis, Memphis, TN, USA.Harper 2 Dan Goldowitz 3 Guy Mittleman 4* ![]()
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