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It is a prospective study of 41 cases of traumatic brain stem injury cases whose medico legal autopsy was done in the Institute of Forensic Medicine, at the Madras Medical College and Government General Hospital, Chennai from December 2007 to June 2008. In the 41 cases, 16 cases, (39.02%) were primary brain stem injury and 25 cases, (60.98) were secondary brain stem injury. The mean ages of cases with primary and secondary brainstem injuries were respectively 55.7 and 36.2. Male victims outnumbered the female victims with male female sex ratio of 13:1. Road traffic accidents involving mainly pedestrians and two wheelers were the most common cause for traumatic brain injury.

The brainstem conveys sensory and motor inputs between the spinal cord and the brain, and contains nuclei of the cranial nerves. It controls the sleep-wake cycle and vital functions via the ascending reticular activating system and the autonomic nuclei, respectively. Brainstem dysfunction may lead to sensory and motor deficits, cranial nerve palsies, impairment of consciousness, dysautonomia, and respiratory failure. The brainstem is prone to various primary and secondary insults, resulting in acute or chronic dysfunction. Of particular importance for characterizing brainstem dysfunction and identifying the underlying etiology are a detailed clinical examination, MRI, neurophysiologic tests such as brainstem auditory evoked potentials, and an analysis of the cerebrospinal fluid. Detection of brainstem dysfunction is challenging but of utmost importance in comatose and deeply sedated patients both to guide therapy and to support outcome prediction. In the present review, we summarize the neuroanatomy, clinical syndromes, and diagnostic techniques of critical illness-associated brainstem dysfunction for the critical care setting.

Background Many of the deaths that occur shortly after injury or in hospitals are caused by mild trauma. Slight morphological changes are often found in the brain stems of these patients during autopsy. The purpose of this study is to investigate the histopathological changes involved in primary brain stem injuries (PBSI) and their diagnostic significance. Methods A total of 65 patients who had died of PBSI and other conditions were randomly selected. They were divided into 2 groups, an injury group (25 cases) and a control group (20 cases). Slides of each patient’s midbrain, pons, and medulla oblongata were prepared and stained with HE, argentaffin, and immunohistochemical agents (GFAP, NF, amyloid-ß, MBP). Under low power (×100) and NF staining, the diameter of the thickest longitudinal axon was measured at its widest point. Ten such diameters were collected for each part of the brain (midbrain, pons, and medulla oblongata). Data were recorded and analyzed statistically. Results Brain stem contusions, astrocyte activity, edema, and pathological changes in the neurons were visibly different in the injury and control groups ( P  < 0.05). Characteristic changes occurred in the neural axons, axon diameter varied from axon to axon and even over different segments of one axon, and several pathological phenomena were observed. These included segmental thickening and curving, wave-like processing, disarrangement, and irregular swelling. A few axons ruptured and intumesced into retraction balls. Immunohistochemical MBP staining showed enlargement and curving of spaces between the myelin sheaths and axons in certain areas. The myelin sheaths lining the surfaces of the axons were in some cases incomplete and even exfoliated, and segmentation disappeared. These pathological changes increased in severity over time ( P  < 0.05). Conclusions These histopathological changes may prove beneficial to the pathological diagnosis of PBSI during autopsy. The measurement of axon diameters provides a referent quantitative index for the diagnosis of the specific causes of death involved in PBSI. Virtual Slides The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1345298818712204

Combinations of biomaterials and cells can effectively target delivery of cells or other therapeutic factors to the brain to rebuild damaged nerve pathways after brain injury. Porous collagen-chitosan scaffolds were prepared by a freeze-drying method based on brain tissue engineering. The scaffolds were impregnated with rat bone marrow mesenchymal stem cells. A traumatic brain injury rat model was established using the 300 g weight free fall impact method. Bone marrow mesenchymal stem cells/collagen-chitosan scaffolds were implanted into the injured brain. Modified neurological severity scores were used to assess the recovery of neurological function. The Morris water maze was employed to determine spatial learning and memory abilities. Hematoxylin-eosin staining was performed to measure pathological changes in brain tissue. Immunohistochemistry was performed for vascular endothelial growth factor and for 5-bromo-2-deoxyuridine (BrdU)/neuron specific enolase and BrdU/glial fibrillary acidic protein. Our results demonstrated that the transplantation of bone marrow mesenchymal stem cells and collagen-chitosan scaffolds to traumatic brain injury rats remarkably reduced modified neurological severity scores, shortened the average latency of the Morris water maze, increased the number of platform crossings, diminished the degeneration of damaged brain tissue, and increased the positive reaction of vascular endothelial growth factor in the transplantation and surrounding areas. At 14 days after transplantation, increased BrdU/glial fibrillary acidic protein expression and decreased BrdU/neuron specific enolase expression were observed in bone marrow mesenchymal stem cells in the injured area. The therapeutic effect of bone marrow mesenchymal stem cells and collagen-chitosan scaffolds was superior to stereotactic injection of bone marrow mesenchymal stem cells alone. To test the biocompatibility and immunogenicity of bone marrow mesenchymal stem cells and collagen-chitosan scaffolds, immunosuppressive cyclosporine was intravenously injected 12 hours before transplantation and 1-5 days after transplantation. The above indicators were similar to those of rats treated with bone marrow mesenchymal stem cells and collagen-chitosan scaffolds only. These findings indicate that transplantation of bone marrow mesenchymal stem cells in a collagen-chitosan scaffold can promote the recovery of neuropathological injury in rats with traumatic brain injury. This approach has the potential to be developed as a treatment for traumatic brain injury in humans. All experimental procedures were approved by the Institutional Animal Investigation Committee of Capital Medical University, China (approval No. AEEI-2015-035) in December 2015.

Background Recovery of functional independence is possible in patients with brainstem traumatic axonal injury (TAI), also referred to as “grade 3 diffuse axonal injury,” but acute prognostic biomarkers are lacking. We hypothesized that the extent of dorsal brainstem TAI measured by burden of traumatic microbleeds (TMBs) correlates with 1-year functional outcome more strongly than does ventral brainstem, corpus callosal, or global brain TMB burden. Further, we hypothesized that TMBs within brainstem nuclei of the ascending arousal network (AAN) correlate with 1-year outcome. Methods Using a prospective outcome database of patients treated for moderate-to-severe traumatic brain injury at an inpatient rehabilitation hospital, we retrospectively identified 39 patients who underwent acute gradient-recalled echo (GRE) magnetic resonance imaging (MRI). TMBs were counted on the acute GRE scans globally and in the dorsal brainstem, ventral brainstem, and corpus callosum. TMBs were also mapped onto an atlas of AAN nuclei. The primary outcome was the disability rating scale (DRS) score at 1 year post-injury. Associations between regional TMBs, AAN TMB volume, and 1-year DRS score were assessed by calculating Spearman rank correlation coefficients. Results Mean ± SD number of TMBs was: dorsal brainstem = 0.7 ± 1.4, ventral brainstem = 0.2 ± 0.6, corpus callosum = 1.8 ± 2.8, and global = 14.4 ± 12.5. The mean ± SD TMB volume within AAN nuclei was 6.1 ± 18.7 mm 3 . Increased dorsal brainstem TMBs and larger AAN TMB volume correlated with worse 1-year outcomes ( R  = 0.37, p  = 0.02, and R  = 0.36, p  = 0.02, respectively). Global, callosal, and ventral brainstem TMBs did not correlate with outcomes. Conclusions These findings suggest that dorsal brainstem TAI, especially involving AAN nuclei, may have greater prognostic utility than the total number of lesions in the brain or brainstem.

Purpose Diffuse axonal injury (DAI) is the rupture of multiple axons due to acceleration and deceleration forces during a closed head injury. Most traumatic brain injuries (TBI) have some degree of DAI, especially severe TBI. Computed tomography (CT) remains the first imaging test performed in the acute phase of TBI, but has low sensitivity for detecting DAI, since DAI is a cellular lesion. The aim of this study is to search in the literature for CT signs, in the first 24 h after TBI, that may help to differentiate patients in groups with a better versus worst prognosis. Methods We searched for primary scientific articles in the PubMed database, in English, indexed since January 1st, 2000. Results Five articles were selected for review. In the DAI group, traffic accidents accounted 70% of the cases, 79% were male, and the mean age was 41 years. There was an association between DAI and intraventricular hemorrhage (IVH) and traumatic subarachnoid hemorrhage (tSAH); an association between the IVH grade and number of corpus callosum lesions; and an association between blood in the interpeduncular cisterns (IPC) and brainstem lesions. Conclusion In closed TBI with no tSAH, severe DAI is unlikely. Similarly, in the absence of IVH, any DAI is unlikely. If there is IVH, patients generally are clinically worse; and the more ventricles affected, the worse the prognosis.

Despite the association between brainstem lesions and coma, a mechanistic understanding of coma pathogenesis and recovery is lacking. We developed a coma model in the rat mimicking human brainstem coma, which allowed multimodal analysis of a brainstem tegmentum lesion's effects on behavior, cortical electrophysiology, and global brain functional connectivity. After coma induction, we observed a transient period (∼1h) of unresponsiveness accompanied by cortical burst-suppression. Comatose rats then gradually regained behavioral responsiveness concurrent with emergence of delta/theta-predominant cortical rhythms in primary somatosensory cortex. During the acute stage of coma recovery (∼1–8h), longitudinal resting-state functional MRI revealed an increase in functional connectivity between subcortical arousal nuclei in the thalamus, basal forebrain, and basal ganglia and cortical regions implicated in awareness. This rat coma model provides an experimental platform to systematically study network-based mechanisms of coma pathogenesis and recovery, as well as to test targeted therapies aimed at promoting recovery of consciousness after coma. [Display omitted] •ET-1-induced diffuse brainstem injury produced rat coma mimicking human brainstem coma.•The Rat Coma Scale and LFP track acute recovery of neurological function in comatose rats.•Rat-MRI characterized the anatomical lesion and functional restoration after coma.•The cortex reactivates as subcortical centers regain functional connectivity.

Background Spinal imaging has been a neglected part of abusive head trauma (AHT) imaging. As most of the radiographs and CT spine are negative in AHT in infants, the cervical spine is assumed to be normal. There is increasing evidence in the role of injury to brainstem and cervical cord in the pathogenesis of AHT. In addition, in courts of law, there is fierce debate about AHT, its mimics and other disparate nontraumatic diagnoses explaining the neuroradiological and skeletal findings. However, this discussion ignores the evidence and significance of spinal injury. We sought to study the cervical spine in an AHT cohort to understand the true prevalence of spinal injuries in AHT and contrast it with cohorts of accidental and nontraumatic groups to give the clinicians a robust diagnostic tool in evaluating AHT. Objective The purpose of this study is to compare the relative incidence of spinal ligamentous and soft-tissue abnormalities on spinal MRI among three groups of children ages <48 months: 1) those with AHT, 2) those with accidental trauma, and 3) those with nontraumatic conditions. Materials and methods This comparative study included 183 children who underwent spine MRI: 67 with AHT, 46 with accidental trauma and a clinical suspicion of spinal injury, and 70 with nontraumatic conditions. Clinical and radiographic findings were collected in all cases and were analyzed retrospectively to identify MRI evidence of traumatic spinal injuries. The incidence of spinal injuries among the three groups was compared. The incidence of spinal ligamentous injuries was calculated for those with and without radiographic evidence of hypoxic-ischemic encephalopathy. All comparisons were performed using Fisher exact test with P  < 0.05 considered statistically significant. Results Cervical spine ligamentous injuries (predominantly the nuchal, atlanto-occipital and atlanto-axial ligaments) were present in 78% of the AHT group, 46% of the accidental trauma group and 1% of the nontraumatic group; all of these differences were statistically significant. Among the AHT group, ligamentous injuries were statistically correlated with evidence of brain ischemia. Conclusion Injury to the cervical spinal posterior ligamentous complex is common in AHT and even more prevalent than in clinically symptomatic traumatic cases. The high correlation between the radiographic findings of occipitocervical ligamentous injuries and hypoxic-ischemic brain injury is consistent with an interpretation that transient upper occipitocervical spinal cord injury in AHT leads to disordered breathing and results in hypoxic-ischemic encephalopathy. We recommend imaging the entire spine in AHT to properly identify and classify these injuries.

Traumatic brain injury is an increasingly common affliction, although many of its serious repercussions are still underappreciated. A frequent consequence is the development of light-induced pain, or ‘ photalgia’, which can often lead to prolonged debilitation. The mechanism underlying the sensitivity to light, however, remains unresolved. Since tissue oedema (swelling) is a common feature of traumatic brain injury, we propose that the brainstem oedema, in particular, might sensitize the brainstem trigeminal complex to signals from ocular mechanisms activated in bright light. To assess this hypothesis, we ran high-resolution Magnetic Resonance Imaging of the brainstems of concussion groups with mild and severe photalgia, without photalgia, and healthy controls. The 3D configuration of the brainstem was determined by Tensor-Based Morphometry (TBM) for each participant. The TBM revealed significant deviations in the brainstem morphology of all concussion groups, with a characteristic signature for each group. In particular, concussion without photalgia showed bilateral expansion at the pontine/medulla junction, whereas concussion with photalgia showed mid-pontine shrinkage, consistent with degeneration of nuclei of the trigeminal complex. These results support the hypothesis that brainstem shrinkage/degeneration represents a morphological substrate of the photalgic sensitization of the trigeminal pathway.

Background Patients with primary posterior fossa catastrophic lesions may clinically meet brain death criteria, but may retain supratentorial brain function or blood flow. These patients could be declared brain-dead in the United Kingdom (UK), but not in the United States of America (USA). We report the outcome of adult patients with primary posterior fossa lesions without concurrent major supratentorial injury. Methods Henry Ford Hospital database was reviewed over a period of 88 months in order to identify all adult patients with isolated brainstem or posterior fossa lesions. We excluded patients with concurrent significant supratentorial pathology potentially confounding the clinical brain death examination. One more patient from a different hospital meeting these criteria was also included. Results Three patients out of 161 met inclusion criteria (1.9% of all brain deaths during this period). With the addition of a fourth patient from another hospital, 4 patients were analyzed. All four patients had catastrophic brainstem and cerebellar injuries meeting the clinical criteria of brain death with positive apnea test in the UK. All had preserved supratentorial blood flow, which after a period of 2 h to 6 days disappeared on repeat testing, allowing declaration of brain death by US criteria in all four. One patient became an organ donor. Conclusions Patients with primary posterior fossa catastrophic lesions, who clinically seem to be brain-dead, evolve from retaining to losing supratentorial blood flow. If absent cerebral blood flow is used as an additional criterion for the declaration of death by neurological criteria, these patients are not different than those who become brain death due to supratentorial lesions.