Hagenmcknight8250

Background Persistent post-traumatic symptoms (PPS) after traumatic brain injury (TBI) can lead to significant chronic functional impairment. Pseudocontinuous arterial spin labeling (pCASL) has been used in multiple studies to explore changes in cerebral blood flow (CBF) that may result in acute and chronic TBI, and is a promising neuroimaging modality for assessing response to therapies. Methods Twenty-four subjects with chronic mild-moderate TBI (mmTBI) were enrolled in a pilot study of 10 days of computerized executive function training combined with active or sham anodal transcranial direct current stimulation (tDCS) for treatment of cognitive PPS. EED226 clinical trial Behavioral surveys, neuropsychological testing, and magnetic resonance imaging (MRI) with pCASL sequences to assess global and regional CBF were obtained before and after the training protocol. Results Robust improvements in depression, anxiety, complex attention, and executive function were seen in both active and sham groups between the baseline and post-treatment visits. Global CBF decreased over time, with differences in regional CBF noted in the right inferior frontal gyrus (IFG). Active stimulation was associated with static or increased CBF in the right IFG, whereas sham was associated with reduced CBF. Neuropsychological performance and behavioral symptoms were not associated with changes in CBF. Discussion The current study suggests a complex picture between mmTBI, cerebral perfusion, and recovery. Changes in CBF may result from physiologic effect of the intervention, compensatory neural mechanisms, or confounding factors. Limitations include a small sample size and heterogenous injury sample, but these findings suggest promising directions for future studies of cognitive training paradigms in mmTBI.A thinning of intraretinal layers has been previously described in Parkinson's disease (PD) patients compared to healthy controls (HCs). Few studies evaluated the possible correlation between retinal thickness and retinal microvascularization. Thus, here we assessed the thickness of retinal layers and microvascular pattern in early PD patients and HCs, using, respectively, spectral-domain optical coherence tomography (SD-OCT) and SD-OCT-angiography (SD-OCT-A), and more interestingly, we evaluated a possible correlation between retinal thickness and microvascular pattern. Patients fulfilling criteria for clinically established/clinically probable PD and HCs were enrolled. Exclusion criteria were any ocular, retinal, and systemic disease impairing the visual system. Retinal vascularization was analyzed using SD-OCT-A, and retinal layer thickness was assessed using SD-OCT. Forty-one eyes from 21 PD patients and 33 eyes from 17 HCs were evaluated. Peripapillary retinal nerve fiber layer (RNFL) and macular RNFL, ganglionic cell layer (GCL), inner plexiform layer (IPL), and inner nuclear layer (INL), resulted to be thinner in PD compared to HCs. Among PD patients, a positive correlation between RNFL, GCL, and IPL thickness and microvascular density was found in the foveal region, also adjusting by age, sex, and, especially, hypertension. Such findings were already present in the early stage of disease and were irrespective of dopaminergic treatment. Thus, the retina might be considered a biomarker of PD and could be a useful instrument for onset and disease progression.Mild traumatic brain injury (mTBI) is a significant public health problem. Insomnia is one of the most common symptoms of TBI, occurring in 30-50% of patients with TBI, and is more frequently reported in patients with mild as opposed to moderate or severe TBI. Although insomnia may be precipitated by mTBI, it is unlikely to subside on its own without specific treatment even after symptoms of mTBI reduce or remit. Insomnia is a novel, highly modifiable treatment target in mTBI, treatment of which has the potential to make broad positive impacts on the symptoms and recovery following brain injury. Cognitive-behavioral therapy for insomnia (CBT-I) is the front-line intervention for insomnia and has demonstrated effectiveness across clinical trials; between 70 and 80% of patients with insomnia experience enduring benefit from CBT-I and about 50% experience clinical remission. Examining an existing model of the development of insomnia in the context of mTBI suggests CBT-I may be effective for insomnia initiated or exacerbated by sustaining a mTBI, but this hypothesis has yet to be tested via clinical trial. Thus, more research supporting the use of CBT-I in special populations such as mTBI is warranted. The current paper provides a background on existing evidence for using CBT-I in the context of TBI, raises key challenges, and suggests considerations for future directions including need for increased screening and assessment of sleep disorders in the context of TBI, examining efficacy of CBT-I in TBI, and exploring factors that impact dissemination and delivery of CBT-I in TBI.Background Lacunar infarcts, white matter lesions, cerebral microbleed, enlarged perivascular space and brain atrophy are regarded as magnetic resonance imaging (MRI) manifestations of cerebral small vessel disease (cSVD). 24-hour blood pressure variability (BPV) has been reported to relate with cerebral small vessel disease, but the impact of 24-h BPV on the total MRI cSVD burden and its progression in inpatients with cerebrovascular disease has not been investigated yet. Methods We enrolled inpatients with cerebrovascular disease, who underwent the 24-h ambulatory blood pressure monitoring (ABPM) and the brain MRI scan at baseline and had the follow-up brain MRI images stored in the clinical information system of our hospital. BPV was quantified by the calculation of standard deviation (SD), coefficient of variation (CV), weighted standard deviation (wSD) of blood pressure record. We evaluated the total cSVD score on baseline MRI and the MRI followed-up to obtain the total burden of cSVD. The cSVD burden pr; SBP wSD OR = 2.248, 95% CI = 1.564-3.230 (per 5 mmHg increase in wSD), P less then 0.001)] and SBP wSD was a significant predictor for cSVD progression [OR = 2.990, 95% CI = 1.053-8.496 (per 5 mmHg increase in wSD), P = 0.040]. Conclusion Higher BPV were significantly related with total cSVD burden in inpatients with cerebrovascular disease. SBP SD during daytime and SBP wSD were independent risk factor for total cSVD burden and SBP wSD was an predictive factor for cSVD progression.