Stroke is still a significant health problem that affects millions of people worldwide, as it is the second-leading cause of death and the third-leading cause of disability. Many changes have occurred in the treatment of acute ischemic stroke. Although the innovative concepts of neuroprotection and neurorecovery have been vigorously investigated in a substantial number of clinical studies in the past, only a few trials managed to increase the number of promising outcomes with regard to the multidimensional construct of brain protection and rehabilitation. In terms of pharmacological therapies with proven benefits in the post-ischemic process, drugs with neurorestorative properties are thought to be effective in both the acute and chronic phases of stroke. One significant example is Cerebrolysin, a combination of amino acids and peptides that mimic the biological functions of neurotrophic factors, which has been shown to improve outcomes after ischemic stroke, while preserving a promising safety profile. The purpose of this paper is to offer an overview on the role and impact of Cerebrolysin for ischemic stroke care, by touching on various aspects, from its complex, multimodal and pleiotropic mechanism of action, to its efficacy and safety, as well as cost effectiveness.

Patients with traumatic brain injury (TBI) of varying severities are experiencing adverse outcomes during and after rehabilitation. Besides depression and anxiety, post-traumatic stress disorder (PTSD) is highly encountered in civilian and military populations. As more prospective and retrospective studies – focused on evaluating new or old psychological therapies in inpatient, outpatient, or controlled environments, targeting patients with PTSD with or without a history of TBI – are carried out, researchers are employing various scales to measure PTSD as well as other psychiatric diagnoses or cognitive impairments that might appear following TBI. We aimed to explore the literature published between January 2010 and October 2021 by querying three databases. Our preliminary results showed that several scales – such as the Clinician-Administered PTSD Scale (CAPS), the Posttraumatic Stress Disorder Checklist Military Version (PCL-M) as well as Specific Version (PCL-S), and Civilian Version (PCL-C) – have been frequently used for PTSD diagnosis and symptom severity. However, heterogeneity in the scales used when assessing and evaluating additional psychiatric comorbidities and cognitive impairments are due to the study aim and therapeutic approaches. Therefore, conducting an intervention focusing on post-TBI PTSD patients requires increased attention to patients' medical history in capturing multiple cognitive impairments and affected neuropsychological processes when designing the study and including validated instruments for measuring primary and secondary neuropsychological outcomes.

Introduction: Post-stroke depression (PSD) has complex pathophysiology determined by various biological and psychological factors. Although it is a long-term complication of stroke, PSD is often underdiagnosed. Given the diagnostic role of quantitative electroencephalography (qEEG) in depression, it was investigated whether a possible marker of PSD could be identified by observing the evolution of the (Delta + Theta)/(Alpha + Beta) Ratio (DTABR), respectively the Delta/Alpha Ratio (DAR) values in post-stroke depressed patients (evaluated through the HADS-D subscale). Methods: The current paper analyzed the data of 57 patients initially selected from a randomized control trial (RCT) that assessed the role of N-Pep 12 in stroke rehabilitation. EEG recordings from the original trial database were analyzed using signal processing techniques, respecting the conditions (eyes open, eyes closed), and several cognitive tasks. Results: We observed two significant associations between the DTABR values and the HADS-D scores of post-stroke depressed patients for each of the two visits (V1 and V2) of the N-Pep 12 trial. We recorded the relationships in the Global (V1 = 30 to 120 days after stroke) and Frontal Extended (V2 = 90 days after stroke) regions during cognitive tasks that trained attention and working memory. For the second visit, the association between the analyzed variables was negative. Conclusions: As both our relationships were described during the cognitive condition, we can state that the neural networks involved in processing attention and working memory might go through a reorganization process one to four months after the stroke onset. After a period longer than six months, the process could localize itself at the level of frontal regions, highlighting a possible divergence between the local frontal dynamics and the subjective well-being of stroke survivors. QEEG parameters linked to stroke progression evolution (like DAR or DTABR) can facilitate the identification of the most common neuropsychiatric complication in stroke survivors.