Band 33, Heft 2

The piriform cortex is rich in recurrent excitatory synaptic connections between pyramidal neurons. We asked how such connections could shape cortical responses to olfactory lateral olfactory tract (LOT) inputs. For this, we constructed a computational network model of anterior piriform cortex with 2000 multicompartment, multiconductance neurons (500 semilunar, 1000 layer 2 and 500 layer 3 pyramids; 200 superficial interneurons of two types; 500 deep interneurons of three types; 500 LOT afferents), incorporating published and unpublished data. With a given distribution of LOT firing patterns, and increasing the strength of recurrent excitation, a small number of firing patterns were observed in pyramidal cell networks: first, sparse firings; then temporally and spatially concentrated epochs of action potentials, wherein each neuron fires one or two spikes; then more synchronized events, associated with bursts of action potentials in some pyramidal neurons. We suggest that one function of anterior piriform cortex is to transform ongoing streams of input spikes into temporally focused spike patterns, called here “cell assemblies”, that are salient for downstream projection areas.

Post-traumatic hydrocephalus (PTH) following traumatic brain injury (TBI) may develop within or beyond the acute phase of recovery. Recognition and subsequent treatment of this condition leads to improved neurologic outcomes. In this scoping review, we identify statistically significant demographic, clinical, radiographic, and surgical risk factors as well as a predictive time frame for the onset of PTH in order to facilitate timely diagnosis. Two researchers independently performed a scoping review of the PubMed and Cochrane databases for articles relevant to risk factors for PTH. Articles that met inclusion and exclusion criteria underwent qualitative analysis. Twenty-seven articles were reviewed for statistically significant risk factors and a proposed time frame for the onset of PTH. Variables that could serve as proxies for severe brain injuries were identified as risk factors. The most commonly identified risk factors included either very young or old age, intracranial hemorrhage including intraventricular hemorrhage, hygroma, and need for decompressive craniectomy. Although the timeframe for diagnosis of PTH varied widely from within one week to 31.5 months after injury, the first 50 days were more likely. Established risk factors and timeframe for PTH development may assist clinicians in the early diagnosis of PTH after TBI. Increased consistency in diagnostic criterion and reporting of PTH may improve recognition with early treatment of this condition in order to improve outcomes.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is identified as the cause of coronavirus disease 2019 (COVID-19), and is often linked to extreme inflammatory responses by over activation of neutrophil extracellular traps (NETs), cytokine storm, and sepsis. These are robust causes for multi-organ damage. In particular, potential routes of SARS-CoV2 entry, such as angiotensin-converting enzyme 2 (ACE2), have been linked to central nervous system (CNS) involvement. CNS has been recognized as one of the most susceptible compartments to cytokine storm, which can be affected by neuropilin-1 (NRP-1). ACE2 is widely-recognized as a SARS-CoV2 entry pathway; However, NRP-1 has been recently introduced as a novel path of viral entry. Apoptosis of cells invaded by this virus involves Fas receptor–Fas ligand (FasL) signaling; moreover, Fas receptor may function as a controller of inflammation. Furthermore, NRP-1 may influence FasL and modulate cytokine profile. The neuroimmunological insult by SARS-CoV2 infection may be inhibited by therapeutic approaches targeting soluble Fas ligand (sFasL), cytokine storm elements, or related viral entry pathways. In the current review, we explain pivotal players behind the activation of cytokine storm that are associated with vast CNS injury. We also hypothesize that sFasL may affect neuroinflammatory processes and trigger the cytokine storm in COVID-19.

Error monitoring allows for the efficient performance of goal-directed behaviors and successful learning. Furthermore, error monitoring as a metacognitive ability may play a crucial role for neuropsychological interventions, such as rehabilitation. In the past decades, research has suggested two electrophysiological markers for error monitoring: the error-related negativity (ERN) and the error positivity (Pe), thought to reflect, respectively, error detection and error awareness. Studies on several neurological diseases have investigated the alteration of the ERN and the Pe, but these findings have not been summarized. Accordingly, a systematic review was conducted to understand what neurological conditions present alterations of error monitoring event-related potentials and their relation with clinical measures. Overall, ERN tended to be reduced in most neurological conditions while results related to Pe integrity are less clear. ERN and Pe were found to be associated with several measures of clinical severity. Additionally, we explored the contribution of different brain structures to neural networks underlying error monitoring, further elaborating on the domain-specificity of error processing and clinical implications of findings. In conclusion, electrophysiological signatures of error monitoring could be reliable measures of neurological dysfunction and a robust tool in neuropsychological rehabilitation.

Stroke is a major reason for disability and the second highest cause of death in the world. When a patient is admitted to a hospital, it is necessary to identify the type of stroke, and the likelihood for development of a recurrent stroke, vascular dementia, and depression. These factors could be determined using different biomarkers. Metabolomics is a very promising strategy for identification of biomarkers. The advantage of metabolomics, in contrast to other analytical techniques, resides in providing low molecular weight metabolite profiles, rather than individual molecule profiles. Technically, this approach is based on mass spectrometry and nuclear magnetic resonance. Furthermore, variations in metabolite concentrations during brain ischemia could alter the principal neuronal functions. Different markers associated with ischemic stroke in the brain have been identified including those contributing to risk, acute onset, and severity of this pathology. In the brain, experimental studies using the ischemia/reperfusion model (IRI) have shown an impaired energy and amino acid metabolism and confirmed their principal roles. Literature data provide a good basis for identifying markers of ischemic stroke and hemorrhagic stroke and understanding metabolic mechanisms of these diseases. This opens an avenue for the successful use of identified markers along with metabolomics technologies to develop fast and reliable diagnostic tools for ischemic and hemorrhagic stroke.

Early recanalization of the occluded vessel is the only efficient intervention that improves outcome after ischemic stroke. In contrast, interventions for chronic issues facing stroke patients are limited. Recent clinical and preclinical studies have shown a correlation between upregulated immune responses to brain antigens and post-stroke recrudescence (PSR), post-stroke fatigue (PSF), and dementia (PSD); all of which are associated with poor long-term stroke outcome. Recent retrospective studies have demonstrated a strong correlation between the onset of PSR and acute infection during acute stroke, suggesting some adaptive immune system mediated pathology. This review will discuss the mechanisms and epidemiology of PSR based on the current clinical and pre-clinical evidence. Accordingly, PSR does appear correlated with populations that are prone to autoimmunity, infection, and subsequent triggers, which corroborate autoimmune responses to self-brain antigens as an underlying mechanism. Moreover, PSR as well as PSF and PSD seem to be partly explained by the development of a neuro-inflammatory response to brain antigens. Therefore, the future of improving long-term stroke outcome could be bright with more accurate pre-clinical models focusing on the role of adaptive immune-mediated post stroke neuroinflammation and more clinical studies of PSR.

Parkinson’s disease (PD) is the second most common neurological disease affecting the elderly population . Pharmacological and surgical interventions usually employed for PD treatment show transient effectiveness and are associated with the insurgence of side effects. Therefore, motor rehabilitation has been proposed as a promising supplement in the treatment of PD, reducing the global burden of the disease and improving patients quality of life. The present systematic review aimed to critically analyse the literature concerning MRI markers of brain functional and structural response to motor rehabilitation in PD. Fourteen out of 1313 studies were selected according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria. Despite the limited number of retrieved studies coupled with their heterogeneity prevent ultimate conclusions from being drawn, motor rehabilitation seems to have beneficial effects on PD as measured both with clinical outcomes and MRI derived indices. Interestingly, consistent results seem to indicate that motor rehabilitation acts via a dual mechanism of strengthening cortico-subcortical pathways, restoring movements automaticity, or activating compensatory networks such as the fronto-parietal one. The employment of more advanced and quantitative MRI methods is warranted to establish and validate standardized metrics capable of reliably determining the changes induced by rehabilitative intervention.