Coagulopathy after traumatic brain injury (TBI) is a frequent event and is associated with patients' prognosis. TBI is also associated with a stress response that includes hyperglycemia. This study investigated if coagulopathy occurrence is associated with admission blood glucose levels in patients with TBI. This study retrospectively evaluated patients with TBI who were admitted to a neurosurgical department over a 4-year period. Coagulopathy was defined as an aPTT >40 seconds and/or INR >1.2 and/or a platelet count <120*10(9) per litre. One-hundred and forty-nine patients were included in the study. Thirty-four patients developed coagulopathy. Patients with coagulopathy had significantly lower haemoglobin levels, increased INR and increased aPTT. Patients with severe TBI had more frequent coagulopathy. Patients with severe TBI had significant higher serum glucose levels compared to patients with mild TBI. Using ROC curves it was found that a serum glucose of 151 mg dl(-1) was the threshold for the discrimination of patients that developed coagulopathy. Logistic regression analysis revealed that serum glucose greater than 151 mg dl(-1) and haemoglobin levels lower than 12.4 mg dL(-1) were significantly associated with coagulopathy occurrence. Coagulopathy frequently occur after TBI. Patients with lower GCS score and lower haemoglobin levels and increased blood glucose levels at admission are at greater risk.

The aim of this work is to evaluate the outcome of patients treated with intrathecal colistin for meningitis/ventriculitis. This retrospective case series study included patients presenting with nosocomial meningitis/ventriculitis following neurosurgical interventions and having intravenous (IVC group) or intravenous and intrathecal/intraventricular colistin (ITC group) treatment between 2006 and 2014. Thirty-four patients presented nosocomial meningitis/ventriculitis; 11 (32.5 %) were included in the IVC group and 23 (67.6 %) in the ITC group. The most frequent isolated bacteria were Acinetobacter baumannii. The mean dose was 170,000 (±400) IU and the duration of intraventricular treatment was 16.0 (±8.3) days. The duration of intravenous treatment was 16.0 (±8.3) days in the ITC group and 15.3 ± 7.6 days in IVC group. Hospital mortality was significantly lower in the ITC group compared with the IVC group (13 vs. 72.7 %, p = 0.001). The combination of intravenous plus intraventricular (IV-IVT) colistin therapy may improve outcomes in patients attending with meningitis/ventriculitis due to multi-drug resistance infections.

Depression represents one of the most common non-motor disorders in Parkinson’s disease (PD) and it has been related to worse life quality, higher levels of disability, and cognitive impairment, thereby majorly affecting not only the patients but also their caregivers. Available pharmacological therapeutic options for depression in PD mainly include selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, and tricyclic antidepressants; meanwhile, agents acting on dopaminergic pathways used for motor symptoms, such as levodopa, dopaminergic agonists, and monoamine oxidase B (MAO-B) inhibitors, may also provide beneficial antidepressant effects. Recently, there is a growing interest in non-pharmacological interventions, including cognitive behavioral therapy; physical exercise, including dance and mind–body exercises, such as yoga, tai chi, and qigong; acupuncture; therapeutic massage; music therapy; active therapy; repetitive transcranial magnetic stimulation (rTMS); and electroconvulsive therapy (ECT) for refractory cases. However, the optimal treatment approach for PD depression is uncertain, its management may be challenging, and definite guidelines are also lacking. It is still unclear which of these interventions is the most appropriate and for which PD stage under which circumstances. Herein, we aim to provide an updated comprehensive review of both pharmacological and non-pharmacological treatments for depression in PD, focusing on recent clinical trials, systematic reviews, and meta-analyses. Finally, we discuss the pharmacological agents that are currently under investigation at a clinical level, as well as future approaches based on the pathophysiological mechanisms underlying the onset of depression in PD.

Background: There is increasing interest in the role of EEG in neurorehabilitation. We primarily aimed to identify the knowledge base through highly influential studies. Our secondary aims were to imprint the relevant thematic hotspots, research trends, and social networks within the scientific community. Methods: We performed an electronic search in Scopus, looking for studies reporting on rehabilitation in patients with neurological disabilities. We used the most influential papers to outline the knowledge base and carried out a word co-occurrence analysis to identify the research hotspots. We also used depicted collaboration networks between universities, authors, and countries after analyzing the cocitations. The results were presented in summary tables, plots, and maps. Finally, a content review based on the top-20 most cited articles completed our study. Results: Our current bibliometric study was based on 874 records from 420 sources. There was vivid research interest in EEG use for neurorehabilitation, with an annual growth rate as high as 14.3%. The most influential paper was the study titled “Brain-computer interfaces, a review” by L.F. Nicolas-Alfonso and J. Gomez-Gill, with 997 citations, followed by “Brain-computer interfaces in neurological rehabilitation” by J. Daly and J.R. Wolpaw (708 citations). The US, Italy, and Germany were among the most productive countries. The research hotspots shifted with time from the use of functional magnetic imaging to EEG-based brain–machine interface, motor imagery, and deep learning. Conclusions: EEG constitutes the most significant input in brain–computer interfaces (BCIs) and can be successfully used in the neurorehabilitation of patients with stroke symptoms, amyotrophic lateral sclerosis, and traumatic brain and spinal injuries. EEG-based BCI facilitates the training, communication, and control of wheelchair and exoskeletons. However, research is limited to specific scientific groups from developed countries. Evidence is expected to change with the broader availability of BCI and improvement in EEG-filtering algorithms.

Objective Severe traumatic brain injuries (TBIs) occur frequently. In some of these patients decompressive craniectomy (DC) must be performed. Posttraumatic hydrocephalus (PTH) can develop after TBI further damaging the brain. DC is considered to be one of the causes of PTH. This study defines the incidence of PTH in TBI patients who underwent DC and tries to determine associated factors. Materials and Methods We conducted a retrospective study (2009–2013) that included 126 patients with severe TBI and DC. The collected data were demographics, the craniectomy size, the presence or absence of hydrocephalus, the need for changing the opening pressure of the valve of the cerebrospinal fluid (CSF) shunt or replacing all or parts of the CSF shunt, and the interval between cranioplasty and shunt placement. We excluded patients with additional intraventricular hemorrhage and those with bilateral or bifrontal DC. Results Ten of the 126 patients (7.9%) developed PTH and were treated with a CSF shunt. There was no statistical correlation between development of PTH and age or sex, but a statistically significant correlation between development of PTH and the size of DC. Conclusion Our study suggests that PTH development is multifactorial and shows that PTH is not that rare. We showed a correlation between craniectomy size and the incidence of PTH.