Introduction: Neutrophil-lymphocyte count ratio (NLCR) is a simple and low-cost marker of inflammatory response. NLCR has shown to be a sensitive marker of clinical severity in inflammatory-related tissue injury, and high value of NLCR is associated with poor outcome in traumatic brain injured (TBI) patients. The purpose of this study was to retrospectively analyze NLCR and its association with outcome in a cohort of TBI patients in relation to the type of brain injury. Methods: Adult patients admitted for isolated TBI with Glasgow Coma Score lower than eight were included in the study. NLCR was calculated as the ratio between the absolute neutrophil and lymphocyte count immediately after admission to the hospital, and for six consecutive days after admission to the intensive care unit (ICU). Brain injuries were classified according to neuroradiological findings at the admission computed tomography (CT) as DAI—patients with severe diffuse axonal injury; CE—patients with hemispheric or focal cerebral edema; ICH—patients with intracerebral hemorrhage; S-EH/SAH—patients with subdural and/or epidural hematoma/subarachnoid hemorrhage. Results: NLCR was calculated in 144 patients. Admission NLCR was significantly higher in the non-survivors than in those who survived at 28 days (p < 0.05) from admission. Persisting high NLCR value was associated with poor outcome, and admission NLCR higher than 15.63 was a predictor of 28-day mortality. The highest NLCR value at admission was observed in patients with DAI compared with other brain injuries (p < 0.001). Concussions: NLCR can be a useful marker for predicting outcome in TBI patients. Further studies are warranted to confirm these results.

Measurement of cerebral oximetry by near-infrared spectroscopy provides continuous and non-invasive information about the oxygen saturation of haemoglobin in the central nervous system. This is especially important in the case of patients with traumatic brain injuries. Monitoring of cerebral oximetry in these patients could allow for the diagnosis of inadequate cerebral oxygenation caused by disturbances in cerebral blood flow. It could enable identification of episodes of hypoxia and cerebral ischemia. Continuous bedside measurement could facilitate the rapid diagnosis of intracranial bleeding or cerebrovascular autoregulation disorders and accelerate the implementation of treatment. However, it should be remembered that the method of monitoring cerebral oximetry by means of near-infrared spectroscopy also has its numerous limitations, resulting mainly from its physical properties. This paper summarizes the usefulness of monitoring cerebral oximetry by near-infrared spectroscopy in patients with traumatic brain injury, taking into account the advantages and the disadvantages of this technique.

Organism survival depends on oxygen delivery and utilization to maintain the balance of energy and toxic oxidants production. This regulation is crucial to the brain, especially after acute injuries. Secondary insults after brain damage may include impaired cerebral metabolism, ischemia, intracranial hypertension and oxygen concentration disturbances such as hypoxia or hyperoxia. Recent data highlight the important role of clinical protocols in improving oxygen delivery and resulting in lower mortality in brain-injured patients. Clinical protocols guide the rules for oxygen supplementation based on physiological processes such as elevation of oxygen supply (by mean arterial pressure (MAP) and intracranial pressure (ICP) modulation, cerebral vasoreactivity, oxygen capacity) and reduction of oxygen demand (by pharmacological sedation and coma or hypothermia). The aim of this review is to discuss oxygen metabolism in the brain under different conditions.

Hyperosmotic therapy is commonly used to treat intracranial hypertension in traumatic brain injury patients. Unfortunately, hyperosmolality also affects other organs. An increase in plasma osmolality may impair kidney, cardiac, and immune function, and increase blood–brain barrier permeability. These effects are related not only to the type of hyperosmotic agents, but also to the level of hyperosmolality. The commonly recommended osmolality of 320 mOsm/kg H₂O seems to be the maximum level, although an increase in plasma osmolality above 310 mOsm/kg H₂O may already induce cardiac and immune system disorders. The present review focuses on the adverse effects of hyperosmolality on the function of various organs.

Background: Fingolimod is a drug administered orally to adult patients treated for relapsing remitting course of multiple sclerosis (MS). Mode of action of fingolimod is based on intense S1P1 receptor stimulation and “arresting” lymphocytes in lymphatic organs. Objective of the research was to assess changes in the frequencies of basic lymphocyte subsets in patients treated for multiple sclerosis with the use of fingolimod. Material and methods: Study group comprised of 25 previously untreated adult patients with MS. Venous blood samples were collected from each patient before and one month, three months and six months after treatment initiation. Peripheral blood lymphocyte immunophenotype was assessed with a set of monoclonal antibodies bounded to appropriate fluorochromes and flow cytometer FACSCalibur. Statistical analysis of the results was conducted using Statistica 9.0 software. Results: Before fingolimod administration median of lymphocyte subsets percentage in each patient was in reference range. After 1 month of treatment we noticed significant changes in frequencies of following lymphocyte subsets: NK cells – 51.22% (p = 0.016), T CD4+ cells – 11.58% (p = 0.01), T CD4+:T CD8+ cells ratio – 0.61 (p = 0.005). After 3 and 6 months of treatment there was further increase of deviation from normal state. Conclusions: The use of fingolimod is associated with profound changes in lymphocyte subsets distribution, which might bear a risk of the development of cellular immune deficiency symptoms.