Treatment Of Severe Brain Injury Research Articles

Diagnosis and Treatment of Severe Traumatic Brain Injury in Idiopathic Intracranial Hypertension Syndrome

A topic of current research is the development of a new approach to the diagnosis and treatment of severe brain injury taking into consideration its main pathophysiological mechanism-idiopathic intracranial hypertension syndrome. The goal of this study was to identify Doppler patterns of unfavorable craniocerebral injury conditions to form a consistent algorithm of treatment measures to reduce secondary brain damage in patients with severe craniocerebral trauma. Transcranial Doppler imaging is a prospective method, which allows quick and noninvasive assessment of the intracerebral blood flow dynamics right at the patient's bedside. Due to the operator-dependent nature of this method, clinical interpretation can often be contradictory. As a result, no clear criteria for therapy correction have yet been formulated based on this neuroimaging method. Analysis of the therapy performed allowed us to specify the options for the hyperosmolar solutions for the correction of idiopathic intracranial hypertension syndrome. No statistically significant difference in effectiveness was shown between mannitol and hypertonic saline solutions.

The S-100B level, intracranial pressure, body temperature, and transcranial blood flow velocities predict the outcome of the treatment of severe brain injury.

This study evaluates the applicability of S100B levels, mean maximum velocity (Vmean) over time, pulsatility index (PI), intracranial pressure (ICP), and body temperature (T) for the prediction of the treatment of patients with traumatic brain injury (TBI). Sixty patients defined by the Glasgow Coma Scale score ≤ 8 were stratified using the Glasgow Coma Scale into 2 groups: favorable (FG: Glasgow Outcome Scale ≥ 4) and unfavorable (UG: Glasgow Outcome Scale < 4). The S100B concentration was at the time of hospital admission. Vmean was measured using transcranial Doppler. PI was derived from a transcranial Doppler examination. T was measured in the temporal artery. The differences in mean between FG and UG were tested using a bootstrap test of 10,000 repetitions with replacement. Changes in S100B, Vmean, PI, ICP, and T levels stratified by the group were calculated using the one-way aligned rank transform for nonparametric factorial analysis of variance. The reference ranges for the levels of S100B, Vmean, and PI were 0.05 to 0.23 µg/L, 30.8 to 73.17 cm/s, and 0.62 to 1.13, respectively. Both groups were defined by an increase in Vmean, a decrease in S100B, PI, and ICP levels; and a virtually constant T. The unfavorable outcome is defined by significantly higher levels of all parameters, except T. A favorable outcome is defined by S100B < 3 mg/L, PI < 2.86, ICP > 25 mm Hg, and Vmean > 40 cm/s. The relationships provided may serve as indicators of the results of the TBI treatment.

The temporality of uncertainty in decision-making and treatment of severe brain injury.

The aim of the study is to investigate how time and uncertainties of clinical action and decision-making plays out in the practical work of early neurorehabilitation in order to present new analytical ways to understand the underlying logics and dynamic social processes that take place during professional treatment of patients with severe acquired brain injury. Drawing on ethnographic fieldwork in a Danish neuro-intensive step-down unit (NISU) specialising in early neurorehabilitation, we found that negotiation of futures takes place in the modern ICU in the present by strategically building upon past experiences. We have argued that the clinical programme therefore cannot be understood only from a "here and now perspective", since the early neurorehabilitation practice is embedded in overlapping temporalities of the past, the present, and desired futures. The study discusses the underlying logics-often hidden or unnoticed-that impact clinical practice of early neurorehabilitation, in what we have termed a logic of clinical reenactment, a logic of future negotiation and a logic of paradox.

RETRACTED: Routine parental request of organ donation in end-of-life care of children in the United Kingdom: Unresolved medical, legal, cultural and religious challenges.

The opt-out system (or presumed consent) for end-of-life organ donation is being widely adopted in the United Kingdom. Since presumed consent for organ donation applies only to adults, commentators have recommended the implementation of routine parental request and integration of organ donation in the end-of-life care of children to increase the donor pool and the supply of transplantable organs. The empirical data for this recommendation originated from a survey of parents of deceased children with severe congenital and acquired brain injuries. The demographics of the surveyed parents were not representative of the diverse ethnic and religious affiliations of British society. Here, it is argued that there are unresolved medical, legal, cultural and religious challenges to the routine integration of end-of-life organ donation that can result in harmful consequences for children and parents. To address these challenges: (1) paediatric practice guidelines should be updated to incorporate new advances in the diagnosis and the treatment of severe brain injuries to eliminate potential clinical errors from premature treatment discontinuation and/or incorrect diagnosis of brain(stem) death and (2) a broad societal debate on the legal, cultural and religious consequences of routine integration of end-of-life organ donation in children.

Surgical techniques for severe brain injury : With special emphasis on polytrauma

In Austria approximately 2000 people suffer from severe brain injury per year. Brain trauma is the most common cause of death under the age of 45years. In polytrauma patients the treatment and management of severe brain injury is particularly challenging because the life-threatening injuries of other organ systems significantly influence the timing of surgery and the outcome. The sequence of the necessary surgery is an interdisciplinary decision already made in the emergency room. The evacuation of space-occupying intracranial hemorrhage can be of secondary importance. The standard approach for acute subdural hematoma is a craniotomy using alarge question mark-shaped incision (trauma flap) and decompression. In acute epidural hematoma and impression fractures the localization of the lesion determines the surgical approach and evacuation. A variety of access procedures are available. Frontobasal injuries are extremely rarely an indication for an emergency operation for life-threatening injuries. Decompressive craniotomy is performed as for craniotomy for acute subdural hematoma by the standard trauma flap. Emergency room computed tomography provides fast and accurate information about the localization and extent of brain injury. The mortality of acute subdural hematoma ranges between 50-90% despite an adequate evacuation. Outcome of epidural hematoma has a much better prognosis (10% mortality). The results of decompressive craniectomy versus conservative treatment for moderate disability and good recovery are quite similar according to the randomized evaluation of surgery with craniectomy for uncontrolled elevation of intracranial pressure (RESCUE-ICP) study. Interdisciplinary cooperation and communication and well-trained trauma surgeons with experience in brain trauma are key factors in the treatment of severe brain injury in polytrauma patients.

Experience of treatment of severe brain injury, complicated by severe sepsis in department of anesthesiology and intensive care of Ternopil Medical University Hospital

Experience of treatment of severe brain injury, complicated by severe sepsis in department of anesthesiology and intensive care of Ternopil Medical University Hospital

Thiopental protects human neuroblastoma cells from apoptotic cell death - Potential role of heat shock protein 70.

Abstract Aims Thiopental, a general anesthetic, is recommended for the treatment of severe brain injury in the presence of intracranial hypertension and during surgical procedures where adequate perfusion of the brain may be at risk leading to neuronal programmed cell death, also known as apoptosis. The exact cellular mechanisms of the neuroprotective effects associated with thiopental in this context have not been identified yet. As we have previously shown that thiopental is able to protect human t lymphocytes from apoptosis by inducing heat shock protein-70, we hypothesized that the same mechanism may be responsible in a neuronal cell model. Main methods Human SK-N-SH neuroblastoma cells were preincubated with thiopental (100–500 μg/ml) before the induction of apoptosis (staurosporine, 2 μM). DNA-binding of heat shock factor (HSF)-1 was analyzed by electrophoretic mobility shift assay, mRNA-expression of heat shock protein (hsp)70 by Northern Blot, activity of caspase-3 by fluorogenic caspase activity assay and cleavage of pro-caspase-3 by Western blot. Apoptosis was assessed by flow cytometry after annexin V-fluorescein isothiocyanate staining. Induction of Hsp70 was inhibited using N-formyl-3,4-methylenedioxy-benzylidene-gamma-butyrolaetam. Data are given as mean ± standard deviation or median and 25/75% percentile. Key findings Dobutamine induced DNA-binding of HSF-1 and mRNA expression of hsp70. Pre-incubation with thiopental inhibited staurosporine-induced LDH release (p Significance Thiopental protects human neuroblastoma cells from apoptotic cell death possibly by the induction of Hsp70.

Recommendations of the jury of the third Italian consensus conference for treatment of severe brain injury

Recommendations of the jury of the third Italian consensus conference for treatment of severe brain injury

Application of continuous intracranial pressure monitoring in treatment of severe brain injury

Objective To explore the significance and clinical value of continuous intracranial pressure monitoting in the treatment of brain injury.Methods 60 patients with severe brain injury were randomly divided into group of 30 patients (conventional treatment + continuous intracranial pressure monitoring), control group 30 patients( conventional treatment) ,disability,rate of successful treatment and efficacy renal function were compared after given mannitol. Results The loss rate of the observation group was 13％, and was lower than that of the control group (33％) (P ＜0. 05) :The successful rate of the observation group was 20％ ,and was higher than that of the controlgroup( 10％ )( P ＜ 0. 05 ). Conclusion In patients with severe brain injury, intracranial pressure monitoring was effective to reduce renal damage and reduce the loss rate increase treatment efficacy. Key words: Intracranial pressure; Craniocerebral trauma

Neural Plasticity After Acquired Brain Injury: Evidence from Functional Neuroimaging

Abstract The reorganization of the adult central nervous system after damage is a relatively new area of investigation. Neuroimaging methods, such as functional magnetic resonance imaging, diffusion tensor imaging, and positron emission tomography, have the ability to identify, in vivo, some of the processes involved in these neuroplastic changes and can help with diagnosis, prognosis, and potentially treatment approaches. In this article, traumatic brain injury and stroke are used as examples in which neural plasticity plays an important role in recovery. Basic concepts related to brain remodeling, including spontaneous reorganization and training-induced recovery, as well as characteristics of reorganization in successful recovery, are reviewed. The microscopic and molecular mechanisms that underlie neural plasticity and neurogenesis are briefly described. Finally, exciting future directions for the evaluation, diagnosis, and treatment of severe brain injury are explored, with an emphasis on how neuroimaging can help to inform these new approaches.

Comparison of mannitol and hypertonic saline in the treatment of severe brain injuries

The purpose of this study was to compare the effects of mannitol and hypertonic saline in doses of similar osmotic burden for the treatment of intracranial hypertension in patients with severe traumatic brain injury. The authors used an alternating treatment protocol to compare the effect of hypertonic saline with that of mannitol given for episodes of increased intracranial pressure in patients treated for severe head injury at their hospital during 2006-2008. Standard guidelines for the management of severe traumatic brain injury were followed. Elevated intracranial pressure (ICP) was treated either with mannitol or hypertonic saline. Doses of similar osmotic burden (mannitol 20%, 2 ml/kg, infused over 20 minutes, or saline 15%, 0.42 ml/kg, administered as a bolus via a central venous catheter) were given alternately to the individual patient with severe brain injury during episodes of increased pressure. The dependent variables were the extent and duration of reduction of increased ICP. The choice of agent for treatment of the initial hypertensive event was determined on a randomized basis; treatment was alternated for every subsequent event in each individual patient. Reduction of ICP and duration of action were recorded after each event. Results obtained after mannitol administration were statistically compared with those obtained after hypertonic saline administration. Data pertaining to 199 hypertensive events in 29 patients were collected. The mean decrease in ICP obtained with mannitol was 7.96 mm Hg and that obtained with hypertonic saline was 8.43 mm Hg (p = 0.586, equal variances assumed). The mean duration of effect was 3 hours 33 minutes for mannitol and 4 hours 17 minutes for hypertonic saline (p = 0.40, equal variances assumed). No difference between the 2 medications could be found with respect to the extent of reduction of ICP or duration of action.

Cerebral oxygen metabolism and neuroelectrophysiology in a clinical study of severe brain injury and mild hypothermia

Mild hypothermia has an important role in the treatment of severe brain injury and there are therapeutic windows for this technique for patients with severe brain injury. We used a randomized, controlled, clinical study to investigate indexes of cerebral oxygen metabolism and neuroelectrophysiology to evaluate the efficacy of mild hypothermia treatment in severe brain injury. A total of 148 patients (106 males and 42 females), aged 18 to 64 years with acute severe brain injury were selected from June 1998 to June 2004 from the Department of Neurosurgery at The First Affiliated Hospital of Chongqing Medical University. All patients met the inclusion criteria: admission to hospital within 10 hours of injury; Glasgow Coma Scale (GCS) score ⩽ 8; age < 65 years; no other severe combined visceral injury; and no severe co-morbidities of the heart, lung, liver, kidney, or other visceral organs. Patients were divided into groups according to brain injury severity: GCS scores 7–8, 5–6, and 3–4. Patients in each GCS score group were randomly assigned to two subgroups: hypothermia and normothermia. Brain oxygen metabolism indexes (partial pressure of oxygen in brain tissue [P brO 2] and regional cerebral oxygen saturation [rSaO 2]) as well as neuroelectrophysiology indexes (short-latency somatosensory evoked potential [SLSEP] and brain-stem auditory evoked potential [BAEP]) were recorded in the normothermia and hypothermia subgroups (32–34 °C) prior to and after cooling for 5 days. Brain oxygen metabolism indexes (P brO 2 and rSaO 2) and neuroelectrophysiology indexes (SLSEP and BAEP) were also compared for patients who underwent mild hypothermia and those who did not. For patients with GCS 7–8, SLSEP, BAEP and rSaO 2 following cooling were significantly improved in the hypothermia subgroup and the P brO 2 was less in the hypothermia subgroup. For patients with GCS 5–6, the SLSEP, BAEP and rSaO 2 were improved following hypothermia on some days, and the PbrO 2 was greater in the hypothermia subgroup on some days. For patients with GCS 3–4, there was no difference between the hypothermia and normothermia subgroups. We conclude that hypothermia had a significant therapeutic effect on severe brain injury of patients with GCS 7–8, had no effect on patients with GCS 3–4, and an uncertain effect on patients with GCS 5–6. The indexes of cerebral oxygen metabolism and neuroelectrophysiology indicated primary and secondary brain injury, respectively, and provided an effective way to evaluate brain injury.

Bafflement in diagnosis and treatment of severe brain injuries

Bafflement in diagnosis and treatment of severe brain injuries

The influence of focal brain cooling on neurophysiopathology: validation for clinical application

Focal brain cooling has been recognized to have a suppressive effect on epileptiform discharges or a protective effect on brain tissue. However, the precise influence of brain cooling on normal brain function and histology has not yet been thoroughly investigated. The aim of this study was to investigate the neurophysiopathological consequences of focal cooling and to detect the threshold temperature that causes irreversible histological change and motor dysfunction. The experiments were performed in adult male Sprague-Dawley rats (weighing 250-350 g) after induction of halothane anesthesia. A thermoelectric chip (6 x 6 x 2 mm) was used as a cooling device and was placed on the surface of the sensorimotor cortex after a 10 x 8-mm craniotomy. A thermocouple was placed between the chip and the brain surface. Focal cooling of the cortex was performed at the temperatures of 20, 15, 10, 5, 0, and -5 degrees C for 1 hour (5 rats in each group). Thereafter, the cranial window was repaired. Motor function was evaluated using the beam-walking scale (BWS) every day for 7 days. The rats were killed 7 days after the operation for histological examination with H & E, Klüver-Barrera, glial fibrillary acidic protein, and terminal deoxynucleotidyl transferasemediated deoxyuridine triphosphate nick-end labeling stainings. The authors also euthanized some rats 24 hours after cooling and obtained brain sections by the same methods. The BWS score was decreased on the day after cooling only in the -5 degrees C group (p < 0.05), whereas the score did not change in the other temperature groups. Histologically, the appearance of cryoinjury such as necrosis, apoptosis, loss of neurons, and marked proliferation of astrocytes at the periphery of the lesion was observed only in the -5 degrees C group, while no apparent changes were observed in the other temperature groups. The present study confirmed that the focal cooling of the cortex for 1 hour above the temperature of 0 degrees C did not induce any irreversible histological change or motor dysfunction. These results suggest that focal brain cooling above 0 degrees C has the potential to be a minimally invasive and valuable modality for the treatment of severe brain injury or to assist in the examination of brain function.

Ethical Issues in the Treatment of Severe Brain Injury

Technological developments in functional neuroimaging have important ethical implications for the care of brain-injured patients. Patterns of fMRI and PET responses to stimuli may help clarify if a patient is utterly unaware, and thereby enhance a physician's confidence in reaching an accurate diagnosis of vegetative state or minimally conscious state. The analysis of similar responses may enhance a physician's confidence in pronouncing an accurate prognosis for functional recovery and help avoid committing the fallacy of the self-fulfilling prophesy. Surrogate decision making is necessary to secure consent for treatment decision in brain-injured patients and should attempt to reproduce the treatment decision the patient would have made. Physicians should manage irreducible clinical uncertainty by sharing their level of certainty of diagnosis and prognosis with the surrogate decision-maker. Shared decision making between the physician and surrogate is the current formulation of the doctrine of informed consent. Advance care planning can help inform surrogate decision making, but is available less commonly among young, previously healthy brain-injured patients. Functional neuroimaging technologies also impact on ethical issues of treatment, rehabilitation, and palliation. Families of brain-injured patients should be compassionately counseled that, despite provocative and highly publicized case reports, these technologies, while promising, are currently investigational and have not been sufficiently validated yet to be available for routine clinical use.

Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension.

Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease. The study focused on seven patients (mean age 30.6 +/- 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management. All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 +/- 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 +/- 11 mm Hg) and an increase in CPP (81 +/- 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 +/- 13.8 mm Hg to 45.5 +/- 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.

Cerebral hypoxia in severely brain-injured patients is associated with admission Glasgow Coma Scale score, computed tomographic severity, cerebral perfusion pressure, and survival.

The purpose of this study was to determine the relationship of cerebral hypoxia with admission Glasgow Coma Scale (GCS) score, brain computed tomographic (CT) severity, cerebral perfusion pressure (CPP), and survival in patients with severe brain injury. CPP and noninvasive transcranial oximetry (Stco2) were recorded hourly for 6 days in patients with a GCS score < or = 8 (3,722 observations). CT score was derived from midline shift (0/1) plus abnormal cisterns (0/1) plus subarachnoid hemorrhage (SAH) (0/1) (range, 0-3). Brain CT results were as follows: shift, 10 (56%); abnormal cisterns, 14 (78%); SAH, 9 (50%); epidural hematoma, 2 (11%); subdural hematoma, 11 (61%); and contusion, 17 (94%). The incidences of Stco2 < 60 were: GCS score 3-4, 26.5%; GCS score 5-7, 12.4%; and GCS score 8, 2.8% (p < 0.0001); CT score 2/3, 26.4%; and CT score 0/1, 10.0% (p < 0.0001); nonsurvivors 36.1%; and survivors 16.3% (p < 0.0001). For incidence of CPP < 70, the results were as follows: Stco2 < 60%, 33% of observations; Stco2 > or = 60%, 10% of observations (odds ratio, 4.3; p < 0.01). Despite CPP > or = 70, Stco2 < 60 incidence was 16% of observations. Cerebral hypoxia is common, even with CPP > or = 70, and is associated with GCS score, CT scan severity, and mortality. Cerebral hypoxia is related to cerebral hypoperfusion. Additional studies may prove that Stco2 monitoring will enhance the treatment of severe brain injury.

Active hypothermia in the management of head injuries.

For over half a century scientists and clinicians have been attempting to discover if moderate therapeutic hypothermia (32–34°C) is beneficial in the treatment of severe brain injury. Deep hypothermia (15–22°C) has long been recognized as one method of achieving neuroprotection, but is not without serious implications and risks to the patient. However, hyperthermia among headinjured patients is known to be associated with a worse outcome as compared to a normothermic cohort. Early work suggested that hypothermia could protect the brain after traumatic head injury.

Systemic Hypothermia in Treatment of Severe Brain Injury: A Review and Update

Laboratory studies of moderate hypothermia (30-33 degrees C) after injury show diminished neuronal loss after ischemia, diminished excessive neurotransmitter release after ischemia, prevention of blood-brain barrier disruption after ischemia and brain injury, and behavioral improvement after brain injury. Clinical literature suggests that brief periods of moderate hypothermia (> or = 30 degrees C) in humans are not associated with cardiovascular, hematologic, metabolic, or neurological toxicity. Clinical studies were, therefore, organized to investigate the potential application of moderate systemic hypothermia in patients after severe brain injury. A study of 21 elective craniotomy patients and 11 patients with severe brain injury led to the conclusion that 32 to 33 degrees C was the lowest safe temperature in patients with severe brain injury. A randomized study of moderate hypothermia in 46 patients with Glasgow Coma Score (GCS) 4-7 gave an indication of improved neurologic outcome in the hypothermia group. A multicenter, randomized protocol to test the effect of moderate systemic hypothermia in patients with severe brain injury is in progress. Funded by the National Institutes of Health, The National Acute Brain Injury Study: Hypothermia tests the hypothesis that systemic hypothermia to 32-33 degrees C if rendered within 6 h of injury improves Glasgow Outcome Scores (GOS) at 6 months after injury in patients with severe brain injury (GCS 3-8).

Systemic Hypothermia in Treatment of Severe Brain Injury

Department of Neurosurgery, The University of Texas Houston Health Science Center, Houston, Texas, U.S.A.