Neurotrauma reports最新文献

Major determinants of the biological background or reserve, such as age, biological sex, comorbidities (diabetes, hypertension, obesity, etc.), and medications (e.g., anticoagulants), are known to affect outcome after traumatic brain injury (TBI). With the unparalleled data richness of coronavirus disease 2019 (COVID-19; ∼375,000 and counting!) as well as the chronic form, long-COVID, also called post-acute sequelae SARS-CoV-2 infection (PASC), publications (∼30,000 and counting) covering virtually every aspect of the diseases, pathomechanisms, biomarkers, disease phases, symptomatology, etc., have provided a unique opportunity to better understand and appreciate the holistic nature of diseases, interconnectivity between organ systems, and importance of biological background in modifying disease trajectories and affecting outcomes. Such a holistic approach is badly needed to better understand TBI-induced conditions in their totality. Here, I briefly review what is known about long-COVID/PASC, its underlying-suspected-pathologies, the pathobiological changes induced by TBI, in other words, the TBI endophenotypes, discuss the intersection of long-COVID/PASC and TBI-induced pathobiologies, and how by considering some of the known factors affecting the person's biological background and the inclusion of mechanistic molecular biomarkers can help to improve the clinical management of TBI patients.

Glial fibrillary acidic protein (GFAP) has become the most promising biomarker for detecting traumatic abnormalities on head computed tomography (CT) in patients with traumatic brain injury (TBI), but most studies have not addressed the potential added value of combining the biomarker with clinical variables that confer risk for intracranial injuries. The Scandinavian Guidelines for Initial Management of Minimal, Mild, and Moderate Head Injuries in Adults were the first clinical decision rules in the field with an incorporated biomarker, the S100 astroglial calcium-binding protein B (S100B), which is used in the Mild (Low Risk) group defined by the guidelines. Our aim was to evaluate the performance of the guidelines when S100B was substituted with GFAP. The sample (N = 296) was recruited from the Tampere University Hospital's emergency department between November 2015 and November 2016, and there were 49 patients with available GFAP results who were stratified in the Mild (Low Risk) group (thus patients undergoing biomarker triaging). A previously reported cutoff of plasma GFAP ≥140 pg/mL was used. Within the Mild (Low Risk) group (n = 49), GFAP sensitivity (with 95% confidence intervals in parentheses) for detecting traumatic CT abnormalities was 1.0 (0.40-1.00), specificity 0.34 (0.19-0.53), the negative predictive value (NPV) 1.0 (0.68-1.00), and the positive predictive value (PPV) 0.16 (0.05-0.37). The sensitivity and specificity of the modified guidelines with GFAP, when applied to all imaged patients (n = 197) in the whole sample, were 0.94 (0.77-0.99) and 0.20 (0.15-0.28), respectively. NPV was 0.94 (0.80-0.99) and PPV 0.18 (0.13-0.25). In the Mild (Low Risk) group, none of the patients with GFAP results below 140 pg/mL had traumatic abnormalities on their head CT. These findings were derived from a small patient subgroup. Future researchers should replicate these findings in larger samples and assess whether GFAP has added or comparable value to S100B in acute TBI management.

Alcohol use disorder (AUD) increases risk of traumatic spinal cord injury (SCI) and is associated with depression, anxiety, and chronic pain. Given that these neuropsychiatric morbidities are frequently observed in SCI patients, the effects of pre-injury AUD on risk of depression, anxiety, or chronic pain were analyzed using an insurance claim database. Of 10,591 traumatic SCI patients, 507 had AUD-associated claims in a 12-month period before injury. Those AUD-positive SCI patients showed distinct demographic characteristics, including greater representation of men, younger age, more comorbidities, lower coverage by commercial insurance, and more cervical-level injuries. The AUD group also showed elevated pre-injury comorbidity of depression, anxiety, and chronic pain. However, multi-regression analysis revealed an increased odds ratio (OR) of de novo diagnosis of post-SCI depression in AUD patients 6 months (1.671; 95% confidence interval [CI]: 1.124, 2.483) and 1 year post-injury (1.511; 95% CI: 1.071, 2.131). The OR of de novo post-SCI anxiety was unaffected by pre-injury AUD. Finally, 1 year after SCI, pre-injury AUD increased the OR of de novo diagnosis of post-injury chronic pain (1.545; 95% CI: 1.223, 1.951). Thus, pre-injury AUD may be a risk factor for development of depression and chronic pain after traumatic SCI.

The majority of traumatic encephalopathy syndrome (TES) cases have been reported in former contact sport athletes. This is the first case with TES in a 19-year-old male patient with progressive cognitive decline after daily domestic physical violence through repeated hits to the head for 15 years. The patient presented with a moderate depressive episode and progressive cognitive decline. Tau positron emission tomography (PET) with 220 MBq of [¹⁸F]PI-2620 revealed increased focal signal at the frontal and parietal white/gray matter border. Brain magnetic resonance imaging (MRI) showed a cavum septum pellucidum, reduced left-sided hippocampal volume, and a left midbrain lesion. Cerebrospinal fluid results showed elevated total and p-tau. Neurocognitive testing at admission showed memory deficits clearly below average, and hampered dysfunctions according to the slow processing speed with a low mistake rate, indicating the acquired, thus secondary, attentional deficits. We diagnosed the patient with a TES suggestive of chronic traumatic encephalopathy and classified him as having subtle/mild functional limitation with a most likely transition to mild dementia within the TES criteria. This report underlines child abuse as a relevant criterion in diagnosing TES in cases with repetitive hits to the head. In addition to clinical markers, we show the relevance of fluid tau biomarkers and tau-PET to support the diagnosis of TES according to the recently published diagnosis criteria for TES.