Demonstration of Traumatic Subarachnoid Hemorrhage from the Anterior Choroidal Artery

We present a case of angiographically confirmed transection of the cisternal segment of the anterior choroidal artery (AChA) associated with a severe head trauma in a 15-year old boy. The initial brain computed tomography scan revealed a diffuse subarachnoid hemorrhage (SAH) and pneumocephalus with multiple skull fractures. Subsequent cerebral angiography clearly demonstrated a complete transection of the AChA at its origin with a massive extravasation of contrast medium as a jet trajectory creating a plume. We speculate that severe blunt traumatic force stretched and tore the left AChA between the internal carotid artery and the optic tract. In a simulation of the patient''s brain using a fresh-frozen male cadaver, the AChA is shown to be vulnerable to stretching injury as the ipsilateral optic tract is retracted. We conclude that the arterial injury like an AChA rupture should be considered in the differential diagnosis of severe traumatic SAH.     

The dynamic triple peak impact factor in traumatic brain injury influences native protein structures in gray and white matter as measured with computational simulation

Abstract

Background: Traumatic brain injuries (TBIs) cause a substantial burden to the patient, relatives, and the society as a whole. Much experience and knowledge during the last two decades have improved the neurosurgical treatment as well as the outcome. However, there is still much debate on what actually happens when external kinetic energy is transferred to the head immediately after a TBI. Better knowledge about the cascades of mechanical events at the time of accident is a prerequisite to further reduce the burden in all categories and improve the neurosurgical care of TBI patients.

Methods: In the present study, we use the finite element modeling of the human brain to numerically simulate impact velocities of 10, 6, and 2 m/s to clarify some of the immediate consequences of the external kinetic energy transfer focusing on the gray (GM) and white matters (WM).

Results: The numerical simulation was focused on the external kinetic energy transfer with a level of 227·3 J reaching the head, intracranial pressure (ICP), strain energy density, 1st principal strain level, and their respective impacts on the brain tissue. The results show that, for a 10 m/s impact, a total internal potential energy of 208·6 J was absorbed, of which 14·3% (29·81 J) was absorbed by the scalp, 22·05% (46·0 J) by the outer compact bone, 17·12% (35·72 J) by the porous bone, 27·44% (57·23 J) by the inner compact bone, and 7·31% (15·24 J) by the facial bone. The rest of the internal potential energy was defined to reach the GM (3·6%, 7·51 J) and the WM 1·59% (3·31 J). Also, the ICP, strain energy density, and 1st principal strain levels, defined as the dynamic triple peak impact factor, influenced the GM and WM with their own impact peaks during the first 10 ms after the accident and were the highest for the 10 and 6 m/s impacts, while the 2 m/s impact had only a slight influence on the GM and WM structures.

Conclusions: The present study shows for the first time that following an impact of 10 m/s, 88·31% of the calculated external kinetic energy was absorbed by the external parts of the head before the remaining energy of 5·19% reached the GM and WM. GM absorbed about twice as much of the energy compared to the WM. It is suggested that the dynamic triple peak impact factor may have a profound effect on native protein structures in the cerebral metabolism after a TBI.     

Cognitive deficits develop 1 month after diffuse brain injury and are exaggerated by microglia-associated reactivity to peripheral immune challenge

Traumatic brain injury (TBI) elicits immediate neuroinflammatory events that contribute to acute cognitive, motor, and affective disturbance. Despite resolution of these acute complications, significant neuropsychiatric and cognitive issues can develop and progress after TBI. We and others have provided novel evidence that these complications are potentiated by repeated injuries, immune challenges and stressors. A key component to this may be increased sensitization or priming of glia after TBI. Therefore, our objectives were to determine the degree to which cognitive deterioration occurred after diffuse TBI (moderate midline fluid percussion injury) and ascertain if glial reactivity induced by an acute immune challenge potentiated cognitive decline 30 days post injury (dpi). In post-recovery assessments, hippocampal-dependent learning and memory recall were normal 7 dpi, but anterograde learning was impaired by 30 dpi. Examination of mRNA and morphological profiles of glia 30 dpi indicated a low but persistent level of inflammation with elevated expression of GFAP and IL-1β in astrocytes and MHCII and IL-1β in microglia. Moreover, an acute immune challenge 30 dpi robustly interrupted memory consolidation specifically in TBI mice. These deficits were associated with exaggerated microglia-mediated inflammation with amplified (IL-1β, CCL2, TNFα) and prolonged (TNFα) cytokine/chemokine expression, and a marked reactive morphological profile of microglia in the CA3 of the hippocampus. Collectively, these data indicate that microglia remain sensitized 30 dpi after moderate TBI and a secondary inflammatory challenge elicits robust microglial reactivity that augments cognitive decline.Statement of SignificanceTraumatic brain injury (TBI) is a major risk factor in development of neuropsychiatric problems long after injury, negatively affecting quality of life. Mounting evidence indicates that inflammatory processes worsen with time after a brain injury and are likely mediated by glia. Here, we show that primed microglia and astrocytes developed in mice 1 month following moderate diffuse TBI, coinciding with cognitive deficits that were not initially evident after injury. Additionally, TBI-induced glial priming may adversely affect the ability of glia to appropriately respond to immune challenges, which occur regularly across the lifespan. Indeed, we show that an acute immune challenge augmented microglial reactivity and cognitive deficits. This idea may provide new avenues of clinical assessments and treatments following TBI.     

Self-reported exposure to severe events on the labour ward among Swedish midwives and obstetricians: A cross-sectional retrospective study

BackgroundThe process of delivery entails potentially traumatic events in which the mother or child becomes injured or dies. Midwives and obstetricians are sometimes responsible for these events and can be negatively affected by them as well as by the resulting investigation or complaints procedure (clinical negligence).ObjectiveTo assess the self-reported exposure rate of severe events among midwives and obstetricians on the delivery ward and the cumulative risk by professional years and subsequent investigations and complaints.DesignCross-sectional survey.ParticipantsMembers of the Swedish Association of Midwives (SFB) and the Swedish Society of Obstetrics and Gynaecology (SFOG).MethodsA questionnaire covering demographic characteristics, experiences of self-reported severe events on the delivery ward, and complaints of medical negligence was developed. Potential consequences of the complaint was not reported. A severe event was defined as: 1) the death of an infant due to delivery-related causes during childbirth or while on the neonatal ward; 2) an infant being severely asphyxiated or injured at delivery; 3) maternal death; 4) very severe or life threatening maternal morbidity; or 5) other stressful events during delivery, such as exposure to violence or aggression.ResultsThe response rate was 39.9% (n = 1459) for midwives and 47.1% (n = 706) for obstetricians. Eighty-four percent of the obstetricians and almost 71% of responding midwives had experienced one or more self-reported severe obstetric event with detrimental consequences for the woman or the new-born. Fourteen percent of the midwives and 22.4% of the obstetricians had faced complaints of medical negligence from the patient or the family of the patient.ConclusionsA considerable proportion of midwives and obstetricians will, in the course of their working life, experience severe obstetric events in which the mother or the new-born is injured or dies. Preparedness for such exposure should be part of the training, as should managerial and peer support for those in need. This could prevent serious consequences for the health care professionals involved and their subsequent careers.     

The natural history of post-traumatic hypopituitarism: implications for assessment and treatment

Purpose

Hypopituitarism has been reported in up to half of long-term survivors of traumatic brain injury. We attempted to define the natural history of post-traumatic hypopituitarism to devise guidelines for the optimal timing of patients’ assessment and hormone replacement.

Subjects and methods

Fifty consecutive patients with severe or moderate head trauma were enrolled in a prospective study of pituitary function during the acute phase, at 6 months, and at 12 months after injury. Growth hormone and adrenocorticotropin hormone reserves were assessed using the glucagon stimulation test. Baseline serum concentrations of other anterior pituitary hormones were measured. Results were compared with normative data obtained from matched healthy controls.

Results

Nine patients (18%) had growth hormone deficiency in the acute phase; at 6 months, 5 patients recovered function and 2 new deficiencies were detected; at 12 months, 1 patient recovered, leaving 5 patients (10%) with growth hormone deficiency. Eight patients (16%) showed subnormal cortisol response in the acute phase; at 6 months, 4 patients had recovered and 5 new deficiencies were detected; all 9 patients had persistent abnormalities at 2 months. Forty patients (80%) had gonadotropin deficiency in the acute phase, of whom 29 (73%) recovered by 6 months and 34 (85%) recovered by 12 months. Thyrotropin deficiency was present in 1 patient in the acute phase, who recovered by 6 months; 1 new case was diagnosed at 6 months, which persisted at 12 months.

Conclusion

After traumatic brain injury, early neuroendocrine abnormalities are sometimes transient, whereas late abnormalities present during the course of rehabilitation. A follow-up strategy with periodic evaluation is a necessary part of the optimal care for patients with traumatic brain injury.     

创伤性肺栓塞应用华法林治疗前后的血流动力学变化研究

目的：探讨创伤性肺栓塞患者使用华法林治疗后,血流动力学变化特征。方法将该院2013年10月—2014年10月收纳的36例创伤性肺栓塞患者设为观察组;另选取同期于该院接受体检的36名健康体检者设为对照组。对比两组研究对象不同时期的血流动力学变化值。结果相较于对照组,观察组患者治疗前MAP、CI、SV、SI、PAWP明显更低,HR、SVR、TFC、PVR明显更高,组间对比差异有统计学意义（P＜0.05）。结论华法林治疗创伤性肺栓塞会引起血流动力学变化,临床可根据该监测指标对患者对患者病情与治疗紧张进行准确评估。     

Mild Traumatic Brain Injury and Substance Use

An evidence review of mild TBI (mTBI) sequela was undertaken to explore associations between mTBI and substance use in college students. The pilot study included a convenience sample of college students. The results did not support a statistically significant relationship between mTBI and substance use disorders (SUDs). These findings were contradictory from existing and emerging evidence; however, the magnitude of this relationship remains unclear and further supports the need for continued research.