Disease relevance of Contusions

• The authors conclude that there are discrete areas of uncoupling of cerebral blood flow and metabolism after head injury within 2 hours of cerebral contusion in the rat that cannot be explained by changes in cerebral glucose content in the majority of animals [1].
• Very-late-onset adrenoleukodystrophy: possible precipitation of demyelination by cerebral contusion [2].
• In addition, acute ethanol treatment reduced some of the histopathology that typically occurs following severe contusion of the medial frontal cortex but did not attenuate post-traumatic formation of edema [3].
• These results show that blockade of bradykinin B2 receptors is an effective approach to reduce cerebral edema and to improve neurological outcome after a focal contusion to the cranium [4].
• The amount of brain injury found at 2 weeks after injury, both at the contusion site and in the ipsilateral hippocampus, were inversely related to the dose of L-arginine administered [5].

Psychiatry related information on Contusions

• In contrast, kainic acid injections into L2 resulted in paraplegia with BBB scores similar to those following contusion injuries at either T9 or L2, without affecting tcMMEP response latencies [6].
• An eighteen-month-old Alaskan girl suffered transient coma with multiple superficial contusions when injured by her multiple personality disturbed caretaker [7].

High impact information on Contusions

• Immunization with myelin-associated antigens such as myelin basic protein (MBP) significantly promoted recovery after spinal cord contusion injury in the rat model [8].
• Furthermore, folic acid supplementation enhances neurological recovery from a spinal cord contusion injury, showing its potential clinical impact [9].
• Anesthetized adult Lewis rats subjected to spinal cord contusion at T7 or T9, using the New York University impactor, were injected systemically with anti-MBP T cells at the time of contusion or 1 week later [10].
• Passive or active immunization with myelin basic protein promotes recovery from spinal cord contusion [10].
• Both groups showed nitrotyrosine staining in the contusion, suggest ing that peroxynitrite is produced in contused brain [11].

Chemical compound and disease context of Contusions

• Histologic evaluation 72 h after trauma revealed that neuronal injury was confined exclusively to region A. The results indicate that compression contusion trauma produces a transient membrane depolarization associated with a pronounced cellular release of K+ and a massive Ca2+ entry into the intracellular compartment [12].
• Conspicuity of regions of microtrabecular trauma (bone contusions) was evaluated with conventional T2-weighted imaging in the sagittal plane, T2-weighted FSE imaging in the coronal plane, T2-weighted FS-FSE imaging in the sagittal plane, and conventional T1-weighted imaging in the sagittal plane [13].
• Microdialysis sampling combined with HPLC was used to assess spontaneous and d-amphetamine (AMPH)-evoked release of noradrenaline (NA) in the cerebellum 1 day after probe implantation and 1 day after contusion of the right sensorimotor cortex (SMCX) in rats [14].
• Treatment with N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl ketone for 72 h (480 ng/day) reduced contusion size and ipsilateral dorsal hippocampal tissue loss at 3 weeks but had no effect on functional outcome versus vehicle [15].
• Male rats received bilateral contusions of the medial prefrontal cortex and were given progesterone (4 mg/kg) or vehicle for 3 or 5 days postoperatively [16].

Biological context of Contusions

• CONCLUSION: Brain tissue (18)F-FDG kinetics in TBI patients were consistent with reduced hexokinase activity in the whole brain (including apparently uninjured cortex), whereas glucose transport was impaired only in the area immediately around the contusion [17].
• Our data suggest that chemokine antagonist infusion post-injury results in limiting the inflammatory response following spinal cord contusion injury, thereby attenuating neuronal loss, possibly due to decreased apoptosis [18].
• Allopregnanolone and progesterone decrease cell death and cognitive deficits after a contusion of the rat pre-frontal cortex [19].
• In addition to upregulation in the message levels of a number of chemokines, we have found up-regulation in the message levels of several chemokine receptors following spinal cord contusion injury [18].
• Our comparative analyses using semiquantitative reverse transcription polymerase chain reaction (RT-PCR) show an early and robust upregulation of IL-1beta, TNF-alpha, IL-6, and M-CSF mRNAs in spinal cord after contusion injury [20].

Anatomical context of Contusions

• TBI induced dramatic alterations in NF68, NF200, and MAP2 immunolabeling in dendrites within and beyond contusion sites ipsilateral and contralateral to the injury site [21].
• Using in situ hybridization, we found a selective increase of the subunits NR1 and NR2A mRNA at 24 h in ventral motor neurons (VMN) caudal to a standardized spinal cord contusion injury (SCI) [22].
• Macrophages and neurons are targets of retinoic acid signaling after spinal cord contusion injury [23].
• We further analyzed the effect of contusion on GFAP and S100beta immunoreactive astrocyte density at 96 h postlesion or postsham by double-label immunocytochemistry [24].
• Rats received modified-moderate contusion injuries at T8/9, and 9 days later, Fb-BDNF/NT3 or unmodified fibroblasts (OP-controls) were delivered into the cord [25].

Gene context of Contusions

• CONCLUSIONS: Presence of CAA in head injured cases was significantly associated with possession of an APOE epsilon 4 allele but not with the severity of contusions [26].
• To help in defining the role of MCP-1 in inflammation after SCI, we evaluated the time course of macrophage accumulation for 2 weeks following a midthoracic spinal cord contusion injury in mice lacking CCR2, a principal receptor for MCP-1 [27].
• Vascular endothelial growth factor improves functional outcome and decreases secondary degeneration in experimental spinal cord contusion injury [28].
• Increase of insulin-like growth factor (IGF)-1, IGF binding protein-2 and -4 mRNAs following cerebral contusion [29].
• We were unable to detect any changes in the type 1 IGF-receptor or IGF-2 mRNA following contusion [29].

Analytical, diagnostic and therapeutic context of Contusions

• During a consecutive 17 month period, 15 trauma patients were diagnosed as having a myocardial contusion on the basis of abnormal ECG in 14 patients, elevated creatinine phosphokinase (CPK) in 13 patients, and elevated CPK-Muscle Brain (CPK-MB) isoenzyme determination in 11 patients [30].
• Adult male rats received oral administration of ethanol or drinking water 2 h prior to surgery to produce a blood ethanol concentration of 100 mg% and then received bilateral contusion injuries of the medial prefrontal cortex [3].
• Intraspinal microinjection of 50 nmoles/19 micro g MDL28170, either 30 min prior to or 20 min following contusion injury, resulted in a more robust inhibition of total calpain activity and greater attenuation of alpha-spectrin breakdown and MAP2 proteolysis [31].
• Fifty five patients suffering from blunt chest trauma were studied to assess the diagnosis of myocardial contusion using thallium 201 myocardial scintigraphy [32].
• We tested this by administering dihydrokainic acid (DHK), a non-transported glutamate uptake blocker, into the rat spinal cord by microdialysis in association with contusion spinal cord injury [33].

References