Does Brain Swelling Increase Estimated Specific Gravity?

Objective  At the acute phase of traumatic brain injury (TBI), brain swelling contributes substantially to the development of secondary neurological lesions. Elucidating the pathophysiology of brain swelling is crucial to improve TBI management. In a previous study, specific gravity (SG) of the noncontused hemisphere, as estimated by computed tomography (CT), was higher in patients with high Marshall CT scores and severe brain swelling. The aim of this study was to investigate the relationship between estimated specific gravity (eSG) and clinical variable suggestive of brain swelling. Design  Retrospective study of data from a prospectively established database. Setting  Neurology ICU in a teaching hospital in Paris, France. Participants  We studied 20 patients with severe traumatic brain injury (TBI), 20 patients with high-grade subarachnoid hemorrhage (SAH) presenting similar brain-swelling criteria, 20 patients with low-grade SAH, and 20 healthy controls. Interventions  None. Measurements and Results  Estimated brain specific gravity was acquired from CT images obtained at ICU admission. eSG was estimated in the overall intracerebral content and in a region-of-interest composed of white matter and the diencephalon. eSG in the region of interest was significantly higher in the TBI patients than in the high-grade SAH patients (1.0350 ± 0.0041 vs. 1.0310 ± 0.0019 g/ml, P < 0.05). eSG was similar in the high-grade SAH, low-grade SAH, and control groups. Conclusions  Our findings do not support a causal link between brain swelling and eSG elevation. The eSG increase in severe TBI patients is not due to brain swelling.     

Microsurgical anatomy of the anterior choroidal artery

Microdissection of 100 hemispheres from human cadavers were performed in order to study the anatomic characteristics of the anterior choroidal artery (AChA). One AChA per hemisphere was found. In 98% of hemispheres the AChA arose from the internal carotid artery (ACI) 2.4mm distal to the origin of the posterior communicating artery (ACoP) and 4.7mm proximal to the carotid bifurcation. One or more perforating branches arose from communicating segment of ACI in 29% of hemispheres. The average calibre of the cisternal portion was 0.9mm and the plexal portion 0.7mm. The most frequent branches of the cisternal portion pass to the optic tract, cerebral peduncle, uncus and lateral geniculate body. Anastomosis were found between branches of the AChA and posterior cerebral artery, ACoP, middle cerebral artery and ACI. The results are discussed.     

Bony Protuberances on the Anterior and Posterior Clinoid Processes Lead to Traumatic Internal Carotid Artery Aneurysm Following Craniofacial Injury

Traumatic intracranial aneurysms are rare, comprising 1% or less of all cerebral aneurysms. The majority of these aneurysms arise at the skull base or in the distal anterior and middle cerebral arteries or their branches following direct mural injury or acceleration-induced shearing force. We present a 50-year-old patient in whom subarachnoid hemorrhage (SAH) was developed as a result of traumatic aneurysm rupture after a closed craniofacial injury. Through careful evaluation of the three-dimensional computed tomography and conventional angiographies, the possible mechanism of the traumatic internal carotid artery trunk aneurysm is correlated with a hit injury by the bony protuberances on the anterior and posterior clinoid processes. This traumatic aneurysm was successfully obliterated with clipping and wrapping technique. The possibility of a traumatic intracranial aneurysm should be considered when patient with SAH demonstrates bony protuberances on the clinoid process as a traumatic aneurysm may result from mechanical injury by the sharp bony edges.     

Analysis of Clip-induced Ischemic Complication of Anterior Choroidal Artery Aneurysms

Objective

The surgical approach is typically similar to those used for other supraclinoid internal carotid artery (ICA) lesions. However, the surgical clipping of this aneurysm is complicated and as a result, can result in postoperative ischemic complications. We studied to clarify the clip-induced ischemic complication risk of AChA aneurysm and to get the benefits for helping decision making.

Methods

We retrospectively investigated 53 cases (4.0%) of AchA aneurysm treated surgically. We divided the AChA aneurysm to 3 subtype according to the origin of aneurysmal neck; A type originating from the AChA itself, J type from junction of AChA and ICA, and I type from the ICA itself. We evaluated brain CT about 1 week post-operative day to confirm the low density in AChA territory.

Results

Ruptured aneurysm was 26 cases and unruptured aneurysm 27 cases. The aneurysmal subtype of A, J, and I was 13, 17, and 23 cases. Of the 53 cases who performed surgical neck clipping, twelve (22.6%) had postoperative AChA distribution infarcts. Increased infarct after neck clipping had statistic significance in non-I subtype (p=0.005).

Conclusion

It is easy to classify as "easy" surgery. But surgery for AChA aneurysms carries with it a significant risk of postoperative stroke. Don''t always stick to clipping only, especially in non-I type of incidental small aneurysm, which has high risk of post-clip ischemic complications.     

Photosensitivity as a symptom of maladapive plasticity in a patient with traumatic brain injury: Diffusion tensor imaging study

We report on a patient with traumatic brain injury who had photosensitivity as the presenting visual symptom and demonstrated axonal injury of the left optic radiation using diffusion tensor imaging. A 41-year-old man with traumatic brain injury began to complain of photosensitivity about 4 months after head trauma. The ophthalmic evaluation, including visual evoked potential study and conventional brain MRI, did not exhibit a pathologic basis for his photosensitivity. However, we did detect axonal injury in the left optic radiation on a diffusion tensor imaging study 36 months after onset. This lesion was almost recovered on 76-month diffusion tensor imaging study, however, the photosensitivity had continued. We suggest that the photosensitivity in this patient was caused by axonal injury of the left optic radiation and it seems to be a symptom of maladaptive plasticity that occurs during the recovery of the axonal injury of the left optic radiation.     

Temporal changes of neurogenesis in the mouse hippocampus after experimental subarachnoid hemorrhage

Abstract

Recent studies indicate the existence of progenitor cells and their potential for neurogenesis in the subventricular zone (SVZ) and the hippocampus dentate gyrus (DG) of normal adult mammalian brain. Increased neurogenesis has been shown following cerebral ischemia and traumatic brain injury; however, the involvement of neurogenesis in subarachnoid hemorrhage (SAH) has not been examined. Adult male CD-1 mice were subjected to SAH by endovascular perforation of the left anterior cerebral artery. Mice received intraperitoneal injections of the cell proliferation-specific marker 5 ′ -bromodeoxyuridine (BrdU) after SAH induction. BrdU incorporation was examined from 1 to 30 days after SAH by immunohistochemistry. The BrdU-positive cells were detected in SVZ and DG of normal control brain, and were significantly decreased in both areas three days after SAH. The number of these cells had recovered to its control level seven days after SAH. Double staining with BrdU and NeuN indicated that the majority of the BrdU-positive cells migrating into the granular cell layer of the DG became NeuN-positive 30 days after SAH. In conclusion, temporal changes of the neurogenesis as shown in the present study suggest that neurogenesis in the hippocampus may affect functional outcome after SAH. The induction of the neurogenesis can provide therapeutic value against SAH.     

Temporal changes of neurogenesis in the mouse hippocampus after experimental subarachnoid hemorrhage

Recent studies indicate the existence of progenitor cells and their potential for neurogenesis in the subventricular zone (SVZ) and the hippocampus dentate gyrus (DG) of normal adult mammalian brain. Increased neurogenesis has been shown following cerebral ischemia and traumatic brain injury; however, the involvement of neurogenesis in subarachnoid hemorrhage (SAH) has not been examined. Adult male CD-1 mice were subjected to SAH by endovascular perforation of the left anterior cerebral artery. Mice received intraperitoneal injections of the cell proliferation-specific marker 5'-bromodeoxyuridine (BrdU) after SAH induction. BrdU incorporation was examined from 1 to 30 days after SAH by immunohistochemistry. The BrdU-positive cells were detected in SVZ and DG of normal control brain, and were significantly decreased in both areas three days after SAH. The number of these cells had recovered to its control level seven days after SAH. Double staining with BrdU and NeuN indicated that the majority of the BrdU-positive cells migrating into the granular cell layer of the DG became NeuN-positive 30 days after SAH. In conclusion, temporal changes of the neurogenesis as shown in the present study suggest that neurogenesis in the hippocampus may affect functional outcome after SAH. The induction of the neurogenesis can provide therapeutic value against SAH.     

Treating Hyperglycemia in Neurocritical Patients: Benefits and Perils

There is growing debate over the value of intensive insulin therapy (IIT) in critically ill patients. Available trials have been performed in general medical or surgical intensive care units, and the results may not be directly applicable to patients with severe acute brain disease because these patients may have heightened susceptibility to hyperglycemia (HyperG) and hypoglycemia. Our objective was to review the pathophysiology and effects of HyperG and hypoglycemia in neurocritical patients and to analyze the potential role of IIT in this population. Source data were obtained from a PubMed search of the medical literature combining the terms HyperG, hypoglycemia, insulin, stroke, intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), spinal cord injury (SCI), and related diagnoses. Brain metabolism is highly dependent on constant supply of glucose. As a consequence, the acutely injured brain is particularly sensitive to hypoglycemia, which can induce a state of energy failure (metabolic crisis). Meanwhile, neurocritical patients have a high prevalence of HyperG, and its occurrence is associated with poor outcome after acute ischemic stroke, ICH, SAH, and TBI. It is unclear whether this association is due to direct detrimental effects exerted by HyperG or simply represents a marker of severe brain injury. Insulin has been shown to have various potentially pleiotropic neuroprotective properties in experimental models. However, the safety and efficacy of IIT in patients with critical brain disease have not been well studied. Available results do not support the use of IIT to maintain strict normoglycemia in this population. Patients with critical brain disease should have frequent glucose monitoring because severe HyperG and even modest hypoglycemia may be detrimental. Careful use of insulin infusion protocols appears advisable, but maintenance of strict normoglycemia cannot be recommended. Rigorous studies must be conducted to assess the value of insulin therapy and to determine the optimal blood glucose targets in patients with the most common acute vascular and traumatic brain insults.

     

Cost‐effectiveness of decompressive craniectomy in non‐traumatic neurological emergencies

Background: Decompressive craniectomy is used regularly in traumatic brain injury (TBI) and malignant middle cerebral artery infarction. Its benefits for other causes of non‐traumatic brain swelling, if any, are unclear, especially after a devastating primary event. Methods: We evaluated the outcomes as well as treatment costs of all emergency decompressive craniectomies performed between the 2000 and 2006 in a single institution to lower intractable intracranial pressure, excluding the standard indications TBI and malignant middle cerebral infarction. The health‐related quality of life (HRQoL) was evaluated on the Euroqol (EQ‐5D) scale, and cost of a quality‐adjusted life year (QALY) calculated. Results: The overall 3‐year mortality rate was 62% for subarachnoid haemorrhage (SAH, 29 patients) and 31% for other neurological emergencies (13 patients). Patients with SAH were on average 13 years older than the other indications mean. Of the non‐survivors, 45% died within a month and 95% within 1 year. Median EQ‐5D index values were poor (0.15 for SAH and 0.62 for the other emergencies, versus 0.85 for the normal population), but of the survivors, 73% and 89% were able to live at home. The cost of neurosurgical treatment for one QALY was 11 000 € for SAH and 2000 € for other emergencies. Conclusion: Mortality after non‐traumatic neurological emergencies leading to decompressive craniectomy was high, and the HRQoL index of the survivors was poor. Most survivors were, however, able to live at home, and the cost of neurosurgical treatment for a QALY gained was acceptable.     

Profound amnesia and confabulation following traumatic brain injury

Amnesia and confabulation may persist following acute aneurysmal hemorrhage of the anterior communicating artery, chronic alcoholic Korsakoff's syndrome, and late-stage dementia of the Alzheimer type. However, there is a paucity of information regarding the persistence of these symptoms following traumatic brain injury. We present the case of JL, a 43-year-old male with persistent and severe anterograde amnesia for verbal and visual information with co-occurring provoked confabulation which persists well into the chronic phase of recovery after a severe traumatic brain injury. Neuropsychological testing at 7 weeks post-injury demonstrated severe anterograde amnesia with co-occurring confabulation. Follow-up testing at 9.5 months post-injury showed persistent and severe anterograde amnesia and provoked confabulation despite superior non-verbal intelligence and above average attentional and perceptual abilities. Late computed tomography showed chronic hypodense regions in the temporal lobes, bilaterally (L > R), and in the region of the left ventrolateral frontal lobe. This case demonstrates that anterograde amnesia and provoked confabulation may persist long after the acute phase of recovery after traumatic brain injury, and also supports previous research which asserts that medial temporal lobe damage must be accompanied by ventral frontal lobe pathology to produce the amnestic-confabulatory syndrome.     

Effects of the Neurological Wake-Up Test on Intracranial Pressure and Cerebral Perfusion Pressure in Brain-Injured Patients

Objective  

To evaluate the effects of the neurological “wake-up test” (NWT), defined as interruption of continuous propofol sedation and evaluation of the patient’s level of consciousness, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in patients with severe subarachnoid hemorrhage (SAH) or traumatic brain injury (TBI).     

Vulnerability of the anterior commissure in moderate to severe pediatric traumatic brain injury

In relation to the adult brain, the immature brain might be more vulnerable to damage during and following traumatic brain injury, particularly in white-matter tracts. Given well-established evidence of corpus callosum atrophy, we hypothesized that anterior commissure volume (using quantitative magnetic resonance imaging [MRI]) in this structure would be decreased in children with moderate to severe traumatic brain injury relative to typically developing children. Second, given the purported role of the anterior commissure in interhemispheric axon conveyance between temporal lobes, we hypothesized that temporal lobe white matter, temporal lesion volume, and injury severity (Glasgow Coma Scale score) would be predictive of decreased anterior commissure cross-sectional volume in patients with traumatic brain injury. Finally, we wished to establish the relationship between the anterior commissure and the temporal stem, a major white-matter tract into the temporal lobes, using diffusion tensor imaging fiber-tracking maps for each patient. We also hypothesized that children with traumatic brain injury would exhibit decreased fractional anisotropy in relation to typically developing children in a fiber system including the anterior commissure and the temporal lobes. Decreased anterior commissure cross-sectional volume was observed in patients with traumatic brain injury, and, as predicted, anterior commissure and temporal white-matter volumes were positively related to each other and to higher Glasgow Coma Scale scores. Lesion volume was not independently predictive of anterior commissure volume in the overall model. Diffusion tensor imaging fractional anisotropy values differed between the groups for the temporal stem-anterior commissure system, with the traumatic brain injury group exhibiting decreased fractional anisotropy. The anterior commissure, like the corpus callosum, appears to be highly vulnerable to white-matter degenerative changes resulting from mechanisms such as the direct impact of trauma, progressive axonal injury as tissue in other brain regions atrophies, or myelin degeneration. This is the first systematic examination of anterior commissure atrophy following traumatic brain injury using in vivo quantitative MRI and diffusion tensor imaging fiber tracking in pediatric subjects.     

Investigation of the effect of dietary intake of omega-3 polyunsaturated fatty acids on trauma-induced white matter injury with quantitative diffusion MRI in mice

Previous studies suggest that long-term supplementation and dietary intake of omega-3 polyunsaturated fatty acids (PUFAs) may have neuroprotective effects following brain injury. The objective of this study was to investigate potential neuroprotective effects of omega-3 PUFAs on white matter following closed-head trauma. The closed-head injury model of engineered rotational acceleration (CHIMERA) produces a reproducible injury in the optic tract and brachium of the superior colliculus in mice. Damage is detectable using diffusion tensor imaging (DTI) metrics, particularly fractional anisotropy (FA), with sensitivity comparable to histology. We acquired in vivo (n = 38) and ex vivo (n = 41) DTI data in mice divided into sham and CHIMERA groups with two dietary groups: one deficient in omega-3 PUFAs and one adequate in omega-3 PUFAs. We examined injury effects (reduction in FA) and neuroprotection (FA reduction modulated by diet) in the optic tract and brachium. We verified that diet did not affect FA in sham animals. In injured animals, we found significantly reduced FA in the optic tract and brachium (~10% reduction, p < 0.001), and Bayes factor analysis showed strong evidence to reject the null hypothesis. However, Bayes factor analysis showed substantial evidence to accept the null hypothesis of no diet-related FA differences in injured animals in the in vivo and ex vivo samples. Our results indicate no neuroprotective effect from adequate dietary omega-3 PUFA intake on white matter damage following traumatic brain injury. Since damage from CHIMERA mainly affects white matter, our results do not necessarily contradict previous findings showing omega-3 PUFA-mediated neuroprotection in gray matter.     

Pituitary dysfunction after aneurysmal subarachnoid hemorrhage

Abstract

Patients recovering from aneurysmal SAH often complain about weakness, fatigue and impaired cognitive skills. Pituitary dysfunction might be one possible reason for these complaints, as in patients with traumatic brain injury, hypopituitarism is known to be a common complication. There are only a few studies dealing with this problem in SAH patients, but these studies suggest that pituitary disturbances are very frequent after aneurysmal SAH. But anterior pituitary lobe disturbances might not be the only one responsible for some complaints or complications in patients suffering from aneurysmal SAH. Hyponatremia in the early state after SAH could be a hint for posterior pituitary lobe dysfunction.     

Tracking posttraumatic hemianopia

Hemianopia after traumatic brain injury is not infrequent and results from retro-chiasmatic lesions. Differentiating optic pathway lesions can be challenging with classic imaging. Advanced imaging techniques as an investigational tool for posttraumatic hemianopia are discussed and their pitfalls highlighted through an illustrative case study. In a patient with posttraumatic hemianopia, MRI at 8 weeks and 2 years after trauma were analyzed. Diffusion tensor imaging (DTI) and morphometric analysis of the primary visual cortex (V1) were performed. Optical coherence tomography (OCT) was performed 2 years after trauma. DTI at 8 weeks showed a decrease in fractional anisotropy (FA) of the left optic tract together with a decrease in FA in the right optic tract and optic radiation. At 2 years, an isolated decrease of the left optic tract FA values was noticed together with signs of Wallerian degeneration on classic MR imaging. OCT showed thinning of the retina congruent with the visual field deficit. While DTI abnormalities were also present in the early scan, they were more diffuse and also encompassed functionally intact structures. Results of advanced imaging techniques need to be interpreted with caution and can vary according to the timing of imaging due to Wallerian degeneration.     

CT血管造影对重型颅脑创伤的早期监测及预后判定

目的 探讨CT血管造影(CTA)对重型颅脑创伤早期监测及预后判定的作用.方法 对58例重型颅脑创伤患者术前及术后使用128层螺旋CT行头颅CTA动态检查.结果 重型颅脑创伤后CTA显示脑血管主要发生五种变化:血管移位、动脉痉挛或闭塞、动脉穿支减少、脑深静脉狭窄或闭塞、大脑浅静脉狭窄或闭塞.大动脉痉挛或闭塞者预后差,大脑深静脉如大脑内静脉和基底静脉同时闭塞者预后极差,大脑浅静脉的狭窄或闭塞反映了颅内压的变化.结论 CTA可用于重型颅脑创伤的早期监测及预后判定.     

Concentration of brain free magnesium following severe brain injury correlates with neurologic motor outcome

Recent studies have shown that brain intracellular free magnesium concentration significantly declines following mild to severe, focal and diffuse traumatic brain injury. However, little is known about how this decline or its attenuation by magnesium salts relates to neurologic outcome. This study uses phosphorus magnetic resonance spectroscopy and rotarod tests to characterise the relationship between brain free magnesium concentration and neurologic motor scores following severe, diffuse traumatic brain injury in rats. An intravenous bolus of MgSO(4) or MgCl(2) (100 mumoles/kg) at 30 min following brain injury significantly attenuated the postinjury brain free magnesium decline. This improved magnesium homeostasis was sustained for the entire postinjury monitoring period (1 week). There was an associated significant improvement in neurologic motor function in magnesium treated rats. Moreover, the brain free magnesium concentration over the one week period was linearly correlated with the neurologic motor function (r=0.70; P < 0.001) as assessed on a daily basis. We propose that brain free magnesium concentration may be used as a prognostic indicator of neurologic motor function after traumatic brain injury.     

Optic radiation injury following traumatic epidural hematoma: Diffusion tensor imaging study

Little is known about optic radiation (OR) injury in patients with traumatic brain injury (TBI). We report on a patient who showed an OR injury on diffusion tensor imaging (DTI) following traumatic epidural hematoma (EDH). A 38 year-old man with TBI and 7 age-matched normal subjects were enrolled in this study. The patient had fallen down stairs while in an alcohol intoxicated state. He underwent a craniotomy following diagnosis of traumatic EDH in the left temporo-parietal lobe on brain CT. He complained of right bilateral homonymous hemianopsia, which was confirmed on the Humphrey visual field test. No lesion on the left OR was observed during brain MRI. We were not able to reconstruct the fiber tractography for the left OR in this patient. We found that the left OR had been injured most severely around the midportion between the lateral geniculate body and occipital pole. We determined that DTI would be a useful technique for detection of an OR injury in patients with TBI. Therefore, we believe that DTI should be performed along with conventional brain MRI for patients with visual field defects following TBI.