[Is it possible to extract intracranial pressure information based on the EEG activity?].

Introduction: The capability of the electroencephalography (EEG) of recording the bioelectrical activity of the brain has made of it a fundamental tool for the evaluation of the patient's neurological condition. In recent years, moreover, it has also begun to be used in obtaining information for other kind of variables, as the ones related with the cerebral hemodynamics.

Aim: To study the potential relationship between the EEG activity and the intracranial pressure (ICP) in patients suffering from traumatic brain injury and subarachnoid hemorrhage, during their stay at the intensive care unit.

Potential EEG biomarkers of sedation doses in intensive care patients unveiled by using a machine learning approach.

Objective: Sedation of neurocritically ill patients is one of the most challenging situation in ICUs. Quantitative knowledge on the sedation effect on brain activity in that complex scenario could help to uncover new markers for sedation assessment. Hence, we aim to evaluate the existence of changes of diverse EEG-derived measures in deeply-sedated (RASS-Richmond agitation-sedation scale  -4 and  -5) neurocritically ill patients, and also whether sedation doses are related with those eventual changes.

Identifying causal relationships between EEG activity and intracranial pressure changes in neurocritical care patients.

Objective: To explore and assess the relationship between electroencephalography (EEG) activity and intracranial pressure (ICP) in patients suffering from traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) during their stay in an intensive care unit.

Approach: We performed an observational prospective cohort study of adult patients suffering from TBI or SAH. Continuous EEG-ECG was performed during ICP monitoring.

Nasomaxillary reconstruction in Binder syndrome: bone versus cartilage grafts. A long-term intercenter comparison between Sweden and Mexico.

Maxillonasal dysplasia is characterized by a concave facial profile and a flat nose. The etiology of Binder syndrome is skeletal hypoplasia around the piriform aperture and excavations-fossae prenasales, bilaterally in the nasal floor-which are pathognomonic. There is no real shortage of the soft tissues.