An EEG severity index of traumatic brain injury

EEG spectral analyses were conducted from 19 scalp locations for patients with mild (n=40), moderate (n=25), and severe (n=43) traumatic brain injury (TBI), 15 days to 4 years after injury. Severity of TBI was judged by emergency hospital admission records (Glasgow Coma Score and duration of coma and amnesia). Highest-loading EEG variables on each factor that differed significantly between severe and mild TBI by univariate t-test were entered into a multivariate discriminant analysis, yielding 16 variables. Discriminant analysis between mild and severe TBI groups showed classification accuracy of 96.39%, sensitivity 95.45%, and specificity 97.44%. The EEG discriminant score also measured intermediate severity in moderate TBI patients. Results were cross-validated in 503 VA patients. Significant correlations between EEG discriminant scores, emergency admission measures, and post-trauma neuropsychological test scores validated the discriminant function as an index of severity of injury and a classifier of the extremes of severity.     

The Role of the Cerebellum in Degenerative Ataxias and Essential Tremor: Insights From Noninvasive Modulation of Cerebellar Activity

Over the last three decades, measuring and modulating cerebellar activity and its connectivity with other brain regions has become an emerging research topic in clinical neuroscience. The most important connection is the cerebellothalamocortical pathway, which can be functionally interrogated using a paired-pulse transcranial magnetic stimulation paradigm. Cerebellar brain inhibition reflects the magnitude of suppression of motor cortex excitability after stimulating the contralateral cerebellar hemisphere and therefore represents a neurophysiological marker of the integrity of the efferent cerebellar tract. Observations that cerebellar noninvasive stimulation techniques enhanced performance of certain motor and cognitive tasks in healthy individuals have inspired attempts to modulate cerebellar activity and connectivity in patients with cerebellar diseases in order to achieve clinical benefit. We here comprehensively explore the therapeutic potential of these techniques in two movement disorders characterized by prominent cerebellar involvement, namely the degenerative ataxias and essential tremor. The article aims to illustrate the (patho)physiological insights obtained from these studies and how these translate into clinical practice, where possible by addressing the association with cerebellar brain inhibition. Finally, possible explanations for some discordant interstudy findings, shortcomings in our current understanding, and recommendations for future research will be provided. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.     

Parkinson's disease,cortical dysfunction,and alpha‐synuclein

The ability to understand how Parkinson's disease neurodegeneration leads to cortical dysfunction will be critical for developing therapeutic advances in Parkinson's disease dementia. The overall purpose of this project was to study the small‐amplitude cortical myoclonus in Parkinson's disease as an in vivo model of focal cortical dysfunction secondary to Parkinson's disease neurodegeneration. The objectives were to test the hypothesis that cortical myoclonus in Parkinson's disease is linked to abnormal levels of α‐synuclein in the primary motor cortex and to define its relationship to various biochemical, clinical, and pathological measures. The primary motor cortex was evaluated for 11 Parkinson's disease subjects with and 8 without electrophysiologically confirmed cortical myoclonus (the Parkinson's disease + myoclonus group and the Parkinson's disease group, respectively) who had premortem movement and cognitive testing. Similarly assessed 9 controls were used for comparison. Measurements for α‐synuclein, Aβ‐42 peptide, and other biochemical measures were made in the primary motor cortex. A 36% increase in α‐synuclein was found in the motor cortex of Parkinson's disease + myoclonus cases when compared with Parkinson's disease without myoclonus. This occurred without significant differences in insoluble α‐synuclein, phosphorylated to total α‐synuclein ratio, or Aβ‐42 peptide levels. Higher total motor cortex α‐synuclein levels significantly correlated with the presence of cortical myoclonus but did not correlate with multiple clinical or pathological findings. These results suggest an association between elevated α‐synuclein and the dysfunctional physiology arising from the motor cortex in Parkinson's disease + myoclonus cases. Alzheimer's disease pathology was not associated with cortical myoclonus in Parkinson's disease. Cortical myoclonus arising from the motor cortex is a model to study cortical dysfunction in Parkinson's disease. © 2011 Movement Disorder Society     

Differential effects of sleep disordered breathing on polysomnographic characteristics in preschool and school aged children

ObjectiveChildhood sleep disordered breathing (SDB) peaks in the preschool years. We aimed to compare the effects of SDB on polysomnographic characteristics between preschool and school aged children.Participants and MethodsOne hundred and fifty-two preschool (3–5 y) and 105 school-aged (7–12 y) children, referred for assessment of SDB, plus controls (39, 3–5 y and 34, 7–12 y) with no history of snoring underwent overnight polysomnography. Subjects were grouped by their obstructive apnea hypopnea index (AHI) into those with primary snoring, mild obstructive sleep apnea (OSA), and moderate/severe OSA. The effects of SDB severity on sleep architecture and respiratory characteristics were compared between the age cohorts using quantile regression.ResultsThere was an average reduction in median sleep efficiency of 3.5% (p = 0.004) and an average increase in median WASO of 2% (p = 0.08) between the age cohorts across the severity groups, with sleep efficiency falling and WASO increasing with increasing SDB severity in the school-aged, but not the preschool, cohort. There was an average difference in median central AHI of 0.6 events/h (p < 0.001) between the age cohorts across the severity groups, with the 3–5 y old cohort but not the 7–12 y old cohort having more central apneas with increasing SDB severity.ConclusionsWe have demonstrated clinically important, age-related differences in sleep architecture in children with SDB. Preschool children with SDB maintain sleep efficiency and awaken fewer times throughout the night than do school aged children with a comparable severity of SDB, but experience more central apneas. This may have implications for the outcomes and treatment of SDB in children of different ages.