Background
Traumatic brain injuries (TBI) are associated with complex inflammatory pathways that lead to the development of secondary injuries such as cerebral ischemia, elevated intracranial pressure, and cognitive deficits. The association between intracellular danger signaling involving nuclear chromatin-binding factor, high mobility group box-1 (HMGB1), and inflammatory pathways following TBI has not yet been fully understood.
Primary Objective
To comprehensively review the available literature regarding the potential diagnostic, prognostic and therapeutic use of HMGB1 in TBI.
Methods
A systematic literature review of studies available in PubMed using human and animal subjects was performed. A total of eight studies were included in our results.
Conclusions
Comprehensive review of these reports demonstrated that following TBI, HMGB1 is released from damaged neurons and is elevated in patient’s serum and CSF. Furthermore, these studies showed the potential for HMGB1 to serve as a prognostic biomarker and therapeutic target in patients with TBI. Thus, HMGB1 is a prospective candidate for future studies as it shows promise in treating and/or predicting the sequelae of TBI.
The incidence of spinal cord injuries (SCI) is high every year. As the spinal cord is the highway that allows for the brain to control the rest of the body, spinal cord injuries greatly impact the quality of life of the patients. The SCI include the primary response consisting of the initial accident-induced damage and the secondary response that is characterized by damage due to inflammation and biological responses. Astrocytes are the first to act at the site of the injury, forming a glial scar and attracting immune cells. The immune system plays a role in cleaning out the debris caused by the injury, as well as preventing neurons to grow and heal. The secondary injury caused by the inflammatory response is the major target to combat SCI. This article critically reviews the key players in the inflammatory SCI response and potential therapies, specifically targeting astrocytes, neutrophils, and macrophages. These cells are both beneficial and detrimental following SCI, depending on the released molecules and the types of cells infiltrated to the site of injury. Indeed, depending on the subtype of macrophages, M1 or M2, beneficial or detrimental response could be incited. Therapeutic strategies to regulate and manipulate the immune cells via increasing or decreasing their recruitment to the site of injury could be developed together with upregulating and downregulating the release of certain chemicals from the infiltrated cells.
A case of posttraumatic intradiploic meningoencephalocele is reported. The patient presented with a progressively enlarging lump in the left parietal area approximately 8 months after a blunt trauma. Magnetic resonance imaging showed an intradiploic cyst containing cerebrospinal fluid and brain tissue. These findings were confirmed at surgery. In addition, the cyst was found to have a lining of arachnoid membrane.
Computed tomography (CT) scans provide three-dimensional information about intracranial structures, which can be used to place stereotactically guided radiofrequency (RF) lesions and destroy a targeted volume of tissue. This technique was used for lesioning of the corpus callosum (CC) or the amygdala-hippocampus complex (AHC) in 9 patients with intractable seizures. The procedures were monitored by intraoperative CT scans. Lesions were made in the AHC in 7 patients and the CC in 2 patients. In addition, multiple subpial transection (MST) was performed in 6 patients. The longest follow-up is 29 months with a median of 19 months. Five patients (56%) are free of seizures, 3 patients (33%) have greater than 90% reduction in seizure activity and 1 patient (11%) has greater than 50 % but at most 90 % reduction in seizure activity. There were no complications except for temporary hemiparesis following MST in 1 patient. The results suggest that stereotactic volumetric RF lesioning of the AHC and the CC may be safe and effective in controlling intractable seizures.
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