No abstract

The effect of blast on biological tissue is well documented for particular organ systems such as the lung. This is not the case for the CNS, where the mechanism of CNS injury following a detonation and blast wave is unclear. The effect of blast on traumatic brain injury (TBI) has come into particular focus with the Global War on Terror and Operation Iraqi Freedom, and Operation Enduring Freedom where TBI has become known as the signature injury of these conflicts. The reason for the prominence of TBI in these particular conflicts as opposed to others is unclear, but may result from the increased survivability of blast due to improvements in body armor. In this review, we trace the historical context of blast injury and develop current concepts from this framework, in addition to highlighting many remaining unsolved questions.

There is ample evidence that the retinal pigment epithelium (RPE) is affected in diabetes, and that epitheliopathy may be among the early changes. The fast oscillation (FO) of the electro-oculogram (EOG) reflects the activity of the RPE, most notably the mechanisms responsible for pumping fluid and ions in the retina-to-choroid direction. The FO was measured in three groups of subjects: normal controls, eyes of diabetic individuals with no evidence of retinopathy, and eyes of diabetics with mild background retinopathy. FO amplitude, light trough voltage and dark peak voltage in both diabetic groups were all significantly reduced, independent of retinopathy status. The peak to trough ratio was unaffected. These changes, reduced voltages and smaller light-evoked voltage changes, are consistent with a decrease in the resistance of the RPE and may relate to accumulation of fluid in the sub-retinal space.