The Role of Depression in Verbal Memory Following Traumatic Brain Injury

The purpose of this study was to characterize the relationship between verbal memory and depression scores on the Personality Assessment Inventory following traumatic brain injury. Depression was associated with diminished delayed recall and recognition on the California Verbal Learning Test-II (CVLT-II), even after controlling for a neuropsychological composite score and/or a measure of motivation (i.e., the TOMM). There was no relationship between depression and recall on Verbal Paired Associates or Logical Memory when controlling for the same covariates. The findings were most consistent with depressed subjects failing to utilize the semantic organization of the CVLT-II list to enhance their learning.     

Mild Traumatic Brain Injury and Subsequent Acute Pulmonary Inflammatory Response

ObjectiveThe influence of moderate-to-severe traumatic brain injury (TBI) on acute pulmonary injury is well established, but the association between acute pulmonary injury and mild TBI has not been well studied. Here, we evaluated the histological changes and fluctuations in inflammatory markers in the lungs to determine whether an acute pulmonary inflammatory response occurred after mild TBI. MethodsMouse models of mild TBI (n=24) were induced via open-head injuries using a stereotaxic impactor. The brain and lungs were examined 6, 24, and 72 hours after injury and compared to sham-operated controls (n=24). Fluoro-Jade B staining and Astra blue and hematoxylin staining were performed to assess cerebral neuronal degeneration and pulmonary histological architecture. Quantitative real-time polymerase chain reaction analysis was done to measure inflammatory cytokines. ResultsIncreased neuronal degeneration and the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and transforming growth factor (TGF)-β were observed after mild TBI. The IL-6, TNF-α, and TGF-β levels in mice with mild TBI were significantly different compared to those of sham-operated mice 24 hours after injury, and this was more pronounced at 72 hours. Mild TBI induced acute pulmonary interstitial edema with cell infiltration and alveolar morphological changes. In particular, a significant infiltration of mast cells was observed. Among the inflammatory cytokines, TNF-α was significantly increased in the lungs at 6 hours, but there was no significant difference 24 and 72 hours after injury. ConclusionMild TBI induced acute pulmonary interstitial inflammation and alveolar structural changes, which are likely to worsen the patient’s prognosis.     

Intensive Insulin Therapy After Severe Traumatic Brain Injury: A Randomized Clinical Trial

Introduction  To investigate the risks and possible benefits of routine versus intensive insulin therapy, assessed by the frequency of hypoglycemic events defined as a glucose concentration less than 80 mg/dl (<4.44 mmol/l) in patients admitted to the intensive care unit (ICU) after severe traumatic brain injury (TBI). Methods and Results  Ninety-seven patients admitted after severe TBI, were enrolled and randomly assigned to two groups of target glycemia. Insulin was infused at conventional rates when blood glucose levels exceeded 220 mg/dl (12.22 mmol/l) or at intensive rates, to maintain glycemia at 80–120 mg/dl (4.44–6.66 mmol/l). The following primary and outcome variables were measured during follow-up: hypoglycemic episodes, duration of ICU stay, infection rate, and 6-month mortality and neurologic outcome measured using the Glasgow Outcome Scale (GOS). Episodes of hypoglycemia (defined as blood glucose <80 mg/dl or 4.44 mmol/l) were significantly higher in patients receiving intensive insulin therapy: median (min–max) conventional insulin therapy 7 (range 0–11) vs. intensive insulin therapy 15 (range 6–33); P<0.0001. Duration of ICU stay was shorter in patients receiving intensive insulin therapy (7.3 vs. 10.0 days; P < 0.05); while infection rates during ICU stay (25.0% vs. 38.8%, P = 0.15), and GOS scores and mortality at 6 months were similar in the two groups. Conclusions  Intensive insulin therapy significantly increases the risk of hypoglycemic episodes. Even though patients receiving intensive insulin therapy have shorter ICU stays and infection rates similar to those receiving conventional insulin therapy, both groups have similar follow-up mortality and neurologic outcome. Hence if intensive insulin therapy is to be used, great effort must be taken to avoid hypoglycemia. This work was done in the Department of Neuroanaesthesia, University of Rome “La Sapienza”, Rome, Italy, and was in part presented at the Euroanaesthesia 2006 meeting Madrid, Spain.     

High-dose Dexmedetomidine-induced Hypertension in a Child with Traumatic Brain Injury

Introduction  Dexmedetomidine is a centrally acting α₂-adrenergic agonist which is currently FDA-approved for the short-term (less than 24 h) sedation of adults during mechanical ventilation. Discussion  Given its beneficial physiologic properties, there has been increasing use of this agent in the pediatric population. As with any agent used for sedation in the Pediatric ICU setting, dose escalations may be necessary. Unlike benzodiazepines and opioids, there are limited data regarding the administration of dexmedetomidine above the current package insert dosing recommendations of 0.7 μg/kg/h. Results  We report a 2-year-old child with traumatic brain injury who developed hypertension following the administration of a dexmedetomidine infusion at 4 μg/kg/h for several hours. Investigation into the etiology of the hypertension was negative and the blood pressure returned to baseline with a decrease in the infusion rate. Conclusion  Subsequent to this, no further issues with hypertension were noted.     

Analysis of Complications Following Decompressive Craniectomy for Traumatic Brain Injury

Objective

Adequate management of increased intracranial pressure (ICP) is critical in patients with traumatic brain injury (TBI), and decompressive craniectomy is widely used to treat refractory increased ICP. The authors reviewed and analyzed complications following decompressive craniectomy for the management of TBI.

Methods

A total of 89 consecutive patients who underwent decompressive craniectomy for TBI between February 2004 and February 2009 were reviewed retrospectively. Incidence rates of complications secondary to decompressive craniectomy were determined, and analyses were performed to identify clinical factors associated with the development of complications and the poor outcome.

Results

Complications secondary to decompressive craniectomy occurred in 48 of the 89 (53.9%) patients. Furthermore, these complications occurred in a sequential fashion at specific times after surgical intervention; cerebral contusion expansion (2.2 ± 1.2 days), newly appearing subdural or epidural hematoma contralateral to the craniectomy defect (1.5 ± 0.9 days), epilepsy (2.7 ± 1.5 days), cerebrospinal fluid leakage through the scalp incision (7.0 ± 4.2 days), and external cerebral herniation (5.5 ± 3.3 days). Subdural effusion (10.8 ± 5.2 days) and postoperative infection (9.8 ± 3.1 days) developed between one and four weeks postoperatively. Trephined and post-traumatic hydrocephalus syndromes developed after one month postoperatively (at 79.5 ± 23.6 and 49.2 ± 14.1 days, respectively).

Conclusion

A poor GCS score (≤ 8) and an age of ≥ 65 were found to be related to the occurrence of one of the above-mentioned complications. These results should help neurosurgeons anticipate these complications, to adopt management strategies that reduce the risks of complications, and to improve clinical outcomes.     

Pediatric Severe Traumatic Brain Injury : Updated Management

Traumatic brain injury (TBI) is the leading cause of death and disability in children. Survivors of severe TBI are more susceptible to functional deficits, resulting in disability, poor quality of life, cognitive decline, and mental health problems. Despite this, little is known about the pathophysiology of TBI in children and how to manage it most effectively. Internationally, efforts are being made to expand knowledge of pathophysiology and develop practical clinical treatment recommendations to improve outcomes. Here we discuss recently updated evidence and management of severe pediatric TBI.     

Patterns of Increased Intracranial Pressure After Severe Traumatic Brain Injury

Introduction  Secondary brain injury due to increased intracranial pressure (ICP) contributes to post-traumatic morbidity and mortality. Although it is often taught that increased ICP begins early after traumatic brain injury, some patients develop increased ICP after the first 3 days post-injury. We examined our data to describe temporal patterns of increased ICP. Methods  This is a retrospective review of prospectively collected physiologic and demographic data. Results  Seventy-seven patients were included. We identified four patterns of increased ICP: beginning within 72 h (early), beginning after 72 h (late), early increases with resolution, and then a second rise after 72 h (bimodal), and continuously increased ICP. Late increases in ICP occur in 17% of this cohort. Peak day of swelling was day 7 for the “late” rise group and day 4 for the other patients with increased ICP. Forty-four percent of patients showed enlargement of cerebral contusions on follow-up imaging at 24 h post-injury. Conclusions  Late rises in ICP were not rare in this cohort. This is clinically relevant as it may impact decisions about ICP monitor removal. Differences between groups in age, CT patterns of injury, fluid therapy, osmotic use, and fever were not statistically significant. Portions of this work were presented in poster form at the 5th Annual Neurocritical Care Society Meeting in Las Vegas, NV, on November 2, 2007.     

Operating Characteristics of Executive Functioning Tests Following Traumatic Brain Injury

The primary purposes of this study were to determine if controls, and mild and moderate/severe traumatic brain injury (TBI) patients performed differently on a battery of executive functioning (EF) tests, and to identify the operating characteristics of EF tests in this population. Participants consisted of 46 brain-injured individuals and 24 healthy controls. All participants completed an extensive battery of EF tests. Results showed that mild TBI participants performed worse than controls on the Trail Making Test Part B, and that moderate/severe TBI participants consistently performed worse than either group on a variety of EF measures. Tests of EF exhibited a wide range of operating characteristics, suggesting that some EF tests are better than others in identifying TBI-related neurocognitive impairment. Predictive values were better for individuals with moderate/severe TBI than mild TBI. Overall, the Digit Span Backward Test showed the best positive predictive power in differentiating TBI. Our results provide useful data that may guide test selection in evaluating EF in patients with traumatic brain injury.     

外伤后颅内进展性出血性损伤106例分析

目的探讨颅脑损伤后进展性出血性损伤（PHI）的发生及影响预后的相关因素。方法对2007年颅脑损伤后出现PHI的106例患者的临床资料进行回顾性分析,并与同期无PHI患者进行对照研究。结果颅脑损伤后是否出现PHI与患者的年龄是否超过50岁（P〈0．05）、血浆纤维蛋白原水平是否低于2g／L（P〈0．01）及有无蛛网膜下腔出血（SAH）（P〈0．05）密切相关。PHI患者的预后与年龄是否超过50岁（P〈0．01）、血浆纤维蛋白原水平是否低于2g／L（P〈0．01）、有无SAH（P〈0．01）及入院时的GCS评分（P〈0．01）密切相关。结论PHI最常出现于颅脑伤后12h内,好发于着力点的对冲部位,以额颞部为主,与患者的年龄、血浆纤维蛋白原水平及是否伴有SAH等因素密切相关;其预后与患者的年龄是否超过50岁、入院时GCS评分、血浆纤维蛋白原水平是否低于正常及是否伴有SAH密切相关。     

Pediatric Traumatic Brain Injury : The Epidemiology in Korea

Traumatic brain injury (TBI) is one of the leading causes of death in the pediatric population in Korea. In addition, it can cause disability in children and adolescents, with physical and mental consequences. This causes a substantial burden on the health care system and occurs globally and not just in Korea. We searched and reviewed current data on the epidemiologic characteristics of pediatric TBI in Korea. Our review provides the recent epidemiological trend mainly focusing on incidence and mortality along with worldwide reported data. This review will be helpful to understand the global epidemiology of pediatric TBI and its differences between countries.