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The impact of traumatic brain injury during the perinatal period, which coincides with glial cell (astrocyte and oligodendrocyte) maturation was assessed to determine whether a second insult, e.g., increased inflammation due to remote bacterial exposure, exacerbates the initial injury's effects, possibly eliciting longer-term brain damage. Thus, a murine multifactorial injury model incorporating both mechanisms consisting of perinatal penetrating traumatic brain injury, with or without intraperitoneal injection of lipopolysaccharide (LPS), an analog of remote pathogen exposure has been developed. Four days after injury, gene expression changes for different cell markers were assessed using mRNA in situ hybridization (ISH) and qPCR. Astrocytic marker mRNA levels increased in the stab-alone and stab-plus-LPS treated animals indicating reactive gliosis. Activated microglial/macrophage marker levels, increased in the ipsilateral sides of stab and stab-plus LPS animals by P10, but the differences resolved by P15. Ectopic expression of glial precursor and neural stem cell markers within the cortical injury site was observed by ISH, suggesting that existing precursors and neural stem cells migrate into the injured areas to replace the cells lost in the injury process. Furthermore, single exposure to LPS concomitant with acute stab injury affected the oligodendrocyte population in both the injured and contralateral uninjured side, indicating that after compromise of the blood-brain barrier integrity, oligodendrocytes become even more susceptible to inflammatory injury. This multifactorial approach should lead to a better understanding of the pathogenic sequelae observed as a consequence of perinatal brain insult/injury, caused by combinations of trauma, intrauterine infection, hypoxia and/or ischemia in humans.

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Introduction During the early stages, Parkinson’s disease (PD) is well recognized as an asymmetric disease with unilateral onset of resting tremor with varying degrees of rigidity, and bradykinesia. However, it remains unknown if other impairments, such as swallowing impairment (i.e., dysphagia), also present asymmetrically. Purpose The primary aim of this study was to examine muscle activity associated with swallow on the most affected side (MAS) and least affected side (LAS) in persons with PD. A secondary aim was to explore the relationship between differences in muscle activity associated with swallow and subjective reports of swallowing impairment and disease severity. Methods Function of muscles associated with swallowing was assessed using surface electromyography placed over the right and left submental and laryngeal regions during three swallows for a THIN and THICK condition. The Swallowing Quality of Life (SWAL-QOL) questionnaire and the Unified Parkinson’s Disease Rating Scale (UPDRS) were collected as measures of subjective swallow impairment and disease severity, respectively. Results Thirty-five participants diagnosed with idiopathic PD and on a stable antiparkinsonian medication regimen completed this study. Results revealed no significant mean difference in muscle activity during swallow between the more and less affected side. For the laryngeal muscle region, a significant difference in coefficient of variation between the MAS and LAS was revealed for peak amplitude for the THIN swallow condition. For the laryngeal muscle region, a significant association was revealed between muscle activity and disease severity but not subjective reports of swallowing impairment. Conclusion Superficially it appears that swallowing impairment present symmetrical during the early stages of PD, however, our variability data indicates otherwise. These results will be used to inform future studies in specific types of swallowing impairment (i.e., oral dysphagia, pharyngeal dysphagia, and esophageal dysphagia), disease progression, and overall asymmetry.

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