Traumatic brain injury is a major health problem in all developed countries. The main aim of this review is to provide a short update on the most recent advances in our knowledge of the brains response to mechanical injuries, focusing on metabolic, cellular, subcellular, and molecular events that take place in severe head injuries. Knowledge of these events is essential for a better understanding of new pharmacological avenues and non-pharmacological strategies, such as moderate hypothermia, which are being developed to improve the outcome of this silent epidemic. We will focus on several topics that we consider to be the most significant: diffuse axonal injury, ischemia and the cascades it generates, metabolic derangements, excitotoxicity, oxidative stress, and other phenomena that have been included in the term tertiary injuries. Recent evidence has clearly demonstrated that traumatic brain lesions are highly dynamic and that the different lesions observed after closed head injury are not single events but processes set in motion by the mechanical impact. These processes are not finished until an unpredictable time after injury. We will discuss recent evidence showing that in diffuse axonal injury, primary immediate damage can coexist with axons that, although initially intact, may be evolving towards secondary disconnection. The concept of ischemic penumbra and the more recent concept of traumatic penumbra are discussed, together with recent experimental and clinical data that shed light on the non-ischemic forms of brain hypoxia. The role of excitotoxicity in mechanically-induced cell death and the molecular events that excessive release of glutamate induce, including apoptosis and delayed inflammatory processes, are reviewed. Finally, new knowledge on how central nervous system cells regulate their volume, the new family of channel water molecules known as aquaporins and their possible role in the physiopathology of the swollen brain are discussed. Basic and clinical investigations are still needed to translate the huge amount of pathophysiological knowledge acquired in the last decade into effective treatments for these patients.

The adequate management of cerebral perfusion pressure (CPP) continues to be a controversial issue in head-injured patients. The purpose of our study was to test two hypotheses. The first was that in patients with a CPP below 70 rom Hg, oxygen delivery is compromised and that therefore signs of tissue hypoxia would be reflected in low Pti02 measurements. The second hypothesis was that manipulating mean arterial blood pressure to increase CPP improves oxygen delivery, particularly in patients with a CPP below 70 rom Hg.Twenty-five moderately or severely head-injured patients were included in the study. In all of them Pti02 was monitored in the noninjured hemisphere using the Licox system (GMS, Kiel-Mielkendorf, Germany). Arterial hypertension was induced with phenylephrine 29 times. To quantify the effect of increasing mean arterial blood pressure (MABP) on oxygen delivery to the brain, the Pti02-BP index was calculated (Pti02-BP index = APti02/AMABP). In 16 tests (55%) baseline CPP was above or equal to 70 rom Hg and in the remaining 13 (45%) it was below 70 mm Hg. Mean increase in MABP after phenylephrine was 23.7 ± 10.2 rom Hg. Mean Pti02 was 29.5 ± 14.7 rom Hg in patients with a basal CPP of below 70 rom Hg and 28.9 ± 10.6 rom Hg in patients in the high CPP group. These differences being not statistically significant. The Pti02-BP index was 0.29 ± 0.23 in patients with a basal CPP of below 70 rom Hg and in patients with a CPP of above 70 rom Hg this index was 0.16 ± 0.11 Hg. These differences were not statistically significant (Student's t-test, P = 0.09). In our study a low Pti02 was not observed in patients with marginally low CPPs (48-70 mm Hg) and readings below 15 rom Hg were observed in cases with both normal or supranormal CPPs. We conclude that episodes oflow Pti02 could not be predicted on the basis of CPP alone. On the other hand, raising CPP did not increase oxygen availability in the majority of cases, even if the CPP was markedly improved.

To assess the safety and accuracy of the Camino intraparenchymal sensor, we prospectively evaluated hemorrhagic complications, zero-drift, infection, and system malfunction in 163 patients monitored after a severe head injury. Mean duration of intracranial pressure (ICP) monitoring was 5 +/- 2.2 days (range: 12 h to 11 days). Of the 141 patients with a control CT scan, four showed a 1-2-cc collection of blood at the catheter's end. When removed, the sensors underread the true ICP value (negative zero-drift) in 80 of the 126 sensors evaluated (63.5%). Fourteen sensors showed no zero-drift, and 32 sensors overread the true ICP value (positive zero-drift) (median: -1 mm Hg; interquartile range: -4 to +1 mm Hg). No significant relationship was found between zero-drift, the surgeon who implanted the sensor, intracranial hypertension, or duration of ICP monitoring. No clinical infections could be attributed to the devices. Sixteen patients (9.8%) required more than one ICP sensor due to malfunctioning of the system. In conclusion, continuous ICP monitoring using the Camino intraparenchymal sensor has a low complication rate. However, this sensor may underread the real ICP values in a high number of patients. The lack of correlation between duration of ICP monitoring and zero-drift suggests that, contrary to the recommendations of other reports, the intraparenchymatous Camino sensor can provide reliable readings after the fifth day of use.

A 36-year-old woman with high myopia had uneventful implantation of a phakic refractive lens (PRL) bilaterally. Two months postoperatively, the best corrected visual acuity (BCVA) in the right eye decreased to the preoperative level and the posterior chamber PRL disappeared from the anterior segment and was found lying in the vitreous cavity inferiorly. After lensectomy and pars plana vitrectomy, the PRL was removed through the initial clear corneal incision, improving the BCVA to 1.0. A zonular defect associated with high myopia, previously forgotten and unrecognized ocular trauma, or intraoperative manipulations may have resulted in the spontaneous dislocation of the PRL.

The Traumatic Coma Data Bank (TCDB) classification of CT (computed tomography) scan has been related to the general outcome and intracranial pressure evolution. Our aim was to analyse the relationship of this classification with neuropsychological outcome and late indices of ventricular dilatation. Fifty-seven patients with a moderate or severe head injury (mean admission Glasgow Coma Scale Score, 7.7) were studied from 122 consecutive cases. There were 49 males and 8 females (mean age, 27.7 years). Subjects were classified into TCDB categories on the basis of their most serious acute CT scan finding. From the last control CT scan image, performed at a mean of 6.12 months postinjury, several measures of ventricular dilatation were calculated. Neuropsychological assessment at 6-month included tests of verbal and visual memory, visuoconstructive functions, fine motor speed, and frontal lobe functions. Patients with diffuse injury type I showed better neuropsychological outcome than patients with more severe diffuse injuries and those with mass lesions. Within the diffuse injury groups, the degree of diffuse damage was related to measures of verbal memory and attention and cognitive flexibility. Ventricular enlargement was more evident in patients with mass lesions and it decreased in the remaining groups as the severity of diffuse injury diminished. These results show that there is a relationship between acute intracranial lesion diagnosis according to TCDB classification and neuropsychological results and ventricular dilatation indices at 6 months postinjury.