Sleep: big brain meets little brain

2001 Harcourt Publishers Ltd     

Measuring brain temperature while maintaining brain normothermia in patients with severe traumatic brain injury

The aim of this study was to evaluate the relationship between superficial temporal artery temperature (Tt), rectal temperature (Tr) and intracranial temperature (ICT) when attempting to keep the brain in a normothermic condition in patients with severe traumatic brain injury (TBI). We also compared the incidence of temperature gradient reversal in patients who survived (survivors) and patients who did not (non-survivors) and the difference in temperature gradient reversal between survivors and non-survivors. Tr is normally lower than and ICT and temperature gradient reversal, when Tr exceeds ICT, has been demonstrated to be an early sign of brain death. A total of 28 patients with severe TBI were enrolled retrospectively in our study between November 2008 and February 2010. Each patient’s Tt, Tr and ICT was recorded every hour for 4 days. Our results show that the frequency of brain hyperthermia in our participants (ICT > 38 °C) was 17.7%. Using a paired t-test and Bland-Altman plots, it was shown that a significant temperature difference existed between Tt, Tr and ICT (p < 0.001). The use of Spearman’s correlation method revealed that Tt, Tr and ICT were positively correlated (p < 0.001). Brain death occurred in five patients at a mean of 9.6 hours (range: 8-12 hours) after a temperature gradient reversal between Tt, Tr and ICT. Fisher’s exact test showed that there was a significant difference in the incidence of temperature gradient reversal between Tt, Tr and ICT in survivors and non-survivors (p < 0.001). We conclude that a significant temperature difference exists between Tt, Tr and ICT when maintaining brain normothermia. The daily practice of non-invasive Tt measurement may cause doctors to underestimate ICT; reversal of the ICT and Tt and/or Tr temperatures could be an early marker of a poor prognosis for patients with severe TBI.     

Repeat traumatic brain injury in the developing brain

The Center for Disease Control estimates that there are 1.7 million brain injuries in the US each year with 51% of these injuries occurring during periods of cerebral development. Among this population there is a growing population of individuals with repeat traumatic brain injury (RTBI). While the exact incidence is unknown, estimates range from 5.6 to 36% of the TBI population. This review summarizes the clinical problems/challenges and experimental research models that currently exist. It is intended to reveal the critical areas that need to be addressed so that age-relevant clinical management guidelines can be established to protect this population.     

梗死灶切除治疗重型颅脑外伤合并大面积脑梗死

目的探讨重型颅脑外伤合并大面积脑梗死的最佳外科处理方式.方法对53例重型颅脑外伤病人行开颅血肿、挫伤脑组织清除术加去骨瓣减压术,其中31例未行梗死灶切除(第1组),22例行梗死灶切除(第2组).术后1个月、12个月评价两组的GOS,并行χ2检验.结果术后第1组死亡7例,植物生存5例,重残8例,轻残11例;第2组死亡1例,植物生存2例,重残9例,轻残10例.两组不良结果率(死亡 植物状态)有显著性差异,P＜0.05.结论对重型颅脑外伤合并大面积脑梗死的病人行挫伤脑组织和血肿加梗死灶切除,对降低病死率、提高有效生存率有明显作用.     

Clinical cerebral microdialysis: brain metabolism and brain tissue oxygenation after acute brain injury.

While continuous monitoring of brain tissue oxygenation (P(ti)O2) is known as a practicable, safe and reliable monitoring technology supplementing traditional ICP-CPP-monitoring, the impact of cerebral microdialysis, now available bedside, is not proven extensively. Therefore our studies focused on the practicability, complications and clinical impact of microdialysis during long term monitoring after acute brain injury, especially the analysis of the correlation between changes of local brain oxygenation and metabolism. Advanced neuromonitoring including ICP-CPP-p(ti)O2 was performed in 20 patients suffering from acute brain injury. Analysis of the extracellular fluid metabolites (glucose, lactate, pyruvate, glutamate) were performed bedside hourly. No catheter associated complications, like infection and bleeding, occurred. However, longterm monitoring was limited in 5 out of 20 patients caused by obliteration of the microdialysis catheter after 3-4 days. In the individual patients partly a correlation between increased lactate levels as well as lactate pyruvate ratios and hypoxic brain tissue oxygenation could be found. Analysing the data sets of all patients only a low correlation was detected indicating physiological and increased lactate and lactate/pyruvate ratio during sufficient brain oxygenation. Additionally, concentrations of excitatory amino acid glutamate were found in normal and elevated range during periods of hypoxic oxygenation (P(ti)O2 < 10 mmHg) and intracranial hypertension. Our data strongly suggest partly evidence of correlation between hypoxic oxygenation and metabolic disturbances after brain injury. On the other hand brain metabolism is altered without changes of cerebral oxygenation. Further studies are indicated to improve our pathophysiological knowledge before microdialysis is routinely useful in neurointensive care.     

Working memory brain activation following severe traumatic brain injury

Functional magnetic resonance imaging (fMRI) has shown that brain activation during performance of working memory (WM) tasks under high memory loads is altered in adults with severe traumatic brain injury (TBI) relative to uninjured subjects (Perlstein et al., 2004; Scheibel et al., 2003). Our study attempted to equate TBI patients and orthopedically injured (OI) subjects on performance of an N-Back task that used faces as stimuli. To minimize confusion in TBI patients that was revealed in pilot work, we presented the memory conditions in two separate tasks, 0- versus 1-back and 0- versus 2-back. In the 0- versus 1-back task, OI subjects activated bilateral frontal areas more extensively than TBI patients, and TBI patients activated posterior regions more extensively than OI subjects. In the 0- versus 2-back task, there were no significant differences between the groups. Analysis of changes in activation over time on 1-back disclosed that OI subjects had decreases in bilateral anterior and posterior regions, while TBI patients showed activation increases in those and other areas over time. In the 2-back condition, both groups showed decreases over time in fusiform and parahippocampal gyri, although the OI group also showed increases over time in frontal, parietal, and temporal areas not seen in the TBI patients. The greatest group differences were found in the 1-back condition, which places low demand on WM. Although the extent of activation in the 2-back condition did not differ between the two groups, deactivation in the 2-back condition was seen in the OI patients only, and both groups' patterns of activation over time varied, suggesting a dissociation between the TBI and OI patients in recruitment of neural areas mediating WM.     

Blood–brain barrier and traumatic brain injury

The blood–brain barrier (BBB) is an anatomical microstructural unit, with several different components playing key roles in normal brain physiological regulation. Formed by tightly connected cerebrovascular endothelial cells, its normal function depends on paracrine interactions between endothelium and closely related glia, with several recent reports stressing the need to consider the entire gliovascular unit in order to explain the underlying cellular and molecular mechanisms. Despite that, with regard to traumatic brain injury (TBI) and significant events in incidence and potential clinical consequences in pediatric and adult ages, little is known about the actual role of BBB disruption in its diverse pathological pathways. This Mini‐Review addresses the current literature on possible factors affecting gliovascular units and contributing to posttraumatic BBB dysfunction, including neuroinflammation and disturbed transport mechanisms along with altered permeability and consequent posttraumatic edema. Key mechanisms and its components are described, and promising lines of basic and clinical research are identified, because further knowledge on BBB pathological interference should play a key role in understanding TBI and provide a basis for possible therapeutic targets in the near future, whether through restoration of normal BBB function after injury or delivering drugs in an increased permeability context, preventing secondary damage and improving functional outcome. © 2013 Wiley Periodicals, Inc.     

Early brain stem auditory evoked potentials in brain death

Brain-stem auditory evoked potentials (BAEPs) are realized after the first flat EEG in 50 patients. BAEPs were absent in 70% of the patients. In 22% of the patients, one- or two-sided peak I persists. In 8% the peaks I, II and IV exist after the first flat EEG. BAEP evolution with the course of time is realized. A complete disappearance is established after 24 h. The useful advantage of BAEPs in the early diagnosis of brain death is discussed.     

Phenobarbital modifies seizure-related brain injury in the developing brain

To investigate the potential role of drug therapy in preventing or exacerbating seizure-related brain injury in the prepubescent brain, we administered kainic acid to rats at postnatal day 35. Therapy with daily phenobarbital was started directly before or 1 day after kainic acid was administered, and was continued through postnatal day 153. Rats receiving phenobarbital had therapeutic concentrations during most of the 24-hour dosing period, but also experienced supratherapeutic peak concentrations. The animals were subsequently tested using the water maze (a measure of visuospatial memory), open field (a measure of activity level), and handling tests (a measure of emotionality). The frequency of spontaneous recurrent seizures was monitored during and after phenobarbital therapy. Kainic acid resulted in status epilepticus on postnatal day 35 in all the rats that received it but those receiving phenobarbital first manifested a shorter and less severe status epilepticus as compared to the rats given kainic acid alone. Rats starting phenobarbital immediately before kainic acid was administered did not differ from control rats on behavioral testing and had no subsequent spontaneous recurrent seizures and no histological lesions. Rats receiving kainic acid alone performed significantly poorer than did control rats in the water maze, were more aggressive, had histological lesions, and manifested spontaneous recurrent seizures. As compared to the group treated only with kainic acid, rats receiving kainic acid followed by phenobarbital at postnatal days 36 to 153 manifested similar aggressiveness and histological lesions, similar frequency of spontaneous recurrent seizures after phenobarbital taper, and even greater disturbances in memory, learning, and activity level. These results demonstrate that kainic acid–related injury can be prevented by a medication working through inhibitory mechanisms; that structural and functional damage in the prepubescent brain can be prevented through strategically timed pharmacotherapy; and that treatment of spontaneous recurrent seizures alone with daily exposure to phenobarbital does not decrease, and may actually exacerbate, damage in the kainic acid model.     

Oxidative stress in immature brain after traumatic brain injury

High oxygen demand along with the abundance of readily oxidizable substrates yielding productive oxidative metabolism are required for the normal function of the brain. This necessitates the existence of the complex and multicomponent antioxidant system in the brain for protection against oxidative damage. However, during development, individual components of the antioxidant system are not equally expressed and not always sufficient to fulfill their tasks in a coordinated way. As a result, the developing brain may be more vulnerable to oxidative insults than the adult brain. Traumatic brain injury is one of the damaging acute impacts that challenge the brain antioxidant reserves by exposing them to a number of decompartmentalized prooxidant molecules. This review focuses on the sources and assessment of oxidative stress and the link between oxidative stress and cell death pathways in the immature brain after experimental and clinical traumatic brain injury.     

Discovering the individual brain: brain stimulation in psychiatry

European Archives of Psychiatry and Clinical Neuroscience -     

Adjuvant whole brain radiation following resection of brain metastases

Brain metastasis is a common complication of systemic cancer and significant cause of suffering in oncology patients. Despite a plethora of available treatment modalities, the prognosis is poor with a median survival time of approximately one year. For patients with controlled systemic disease, good performance status, and a limited number of metastases, treatment typically entails surgical resection or radiosurgery, followed by whole brain radiotherapy (WBRT) to control microscopic disease. WBRT is known to control the progression of cancer in the brain, but it can also have toxic effects, particularly with regard to neurocognition. There is no consensus as to whether the benefit of WBRT outweighs the potential harm. We review the evidence related to the question of whether patients undergoing surgical resection of brain metastases should receive adjuvant WBRT.