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Introduction: Alzheimer's disease (AD), primary age-related tauopathy (PART), and chronic traumatic encephalopathy (CTE) all feature hyperphosphorylated tau (p-tau)-immunoreactive neurofibrillary degeneration, but differ in neuroanatomical distribution and progression of neurofibrillary degeneration and amyloid beta (Aβ) deposition.

Methods: We used Nanostring GeoMx Digital Spatial Profiling to compare the expression of 70 proteins in neurofibrillary tangle (NFT)-bearing and non-NFT-bearing neurons in hippocampal CA1, CA2, and CA4 subregions and entorhinal cortex of cases with autopsy-confirmed AD (n = 8), PART (n = 7), and CTE (n = 5).

Results: There were numerous subregion-specific differences related to Aβ processing, autophagy/proteostasis, inflammation, gliosis, oxidative stress, neuronal/synaptic integrity, and p-tau epitopes among these different disorders.

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Among the myriad of complications associated with traumatic brain injury (TBI), impairments in social behaviors and cognition have emerged as a significant area of concern. Animal models of social behavior are necessary to explore the underlying brain mechanisms contributing to chronic social impairments following brain injury. Here, we utilize large-scale brain recordings of local field potentials to identify neural signatures linked with social preference deficits following frontal brain injury.

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Primary Objectives: Annually, millions of Americans sustain mild traumatic brain injuries (mTBI), and some may experience neurobehavioral symptoms (NBS), like slow processing speed that persist chronically or longer than 6 months post injury. In turn, cognitive processes like language comprehension may be compromised. This study investigates the relationship between NBS and language comprehension in individuals with mTBI history and low or high NBS.

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Acute astrocytic and neuronal regulation of glutamatergic protein expression following blast.

Neurosci Lett

December 2024

School of Biomedical Engineering and Sciences, Virginia Tech, Blacksburg, VA, USA; Department of Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg, VA, USA; Veterans Affairs Medical Center, Salem, VA, USA. Electronic address:

Regulation of glutamate through glutamate-glutamine cycling is critical for mediating nervous system plasticity. Blast-induced traumatic brain injury (bTBI) has been linked to glutamate-dependent excitotoxicity, which may be potentiating chronic disorders such as post-traumatic epilepsy. The purpose of this study was to measure changes in the expression of astrocytic and neuronal proteins responsible for glutamatergic regulation at 4-, 12-, and 24 h in the cortex and hippocampus following single blast exposure in a rat model for bTBI.

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Background: Aneurysmal subarachnoid hemorrhage (aSAH) carries a high economic cost and clinical morbidity in the United States. Beyond prolonged admissions and poor post-injury functional status, there is an additional cost of chronic shunt-dependent hydrocephalus for many aSAH patients. Adjuvant lumbar drain (LD) placement has been hypothesized to promote clearance of subarachnoid blood from the cisternal space, with an ultimate effect of decreasing shunt placement rates.

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