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Results: 4

1.

Figure. From: Traumatic brain injury: Can the consequences be stopped?.

Figure 2: Computed tomography scans of the brain of a 35-year-old man showing normal anatomy and normal-sized ventricles (left) and a 25-year-old man involved in a motor vehicle crash (right), showing frontal contusions, a depressed skull fracture and compressed ventricles (arrow) from cerebral edema and raised intracranial pressure.

Eugene Park, et al. CMAJ. 2008 April 22;178(9):1163-1170.
2.

Figure. From: Traumatic brain injury: Can the consequences be stopped?.

Figure 3: Magnetic resonance images of the brain of a 38-year-old woman (left) and 35-year-old male passenger in a motor vehicle crash (right) with extensive injury to the corpus callosum (a major tract of white matter between the left and right cerebral cortex) (white arrow). The yellow arrow in the left panel shows an area of the corpus callosum with no edema or disruption.

Eugene Park, et al. CMAJ. 2008 April 22;178(9):1163-1170.
3.
Box 1

Box 1. From: Traumatic brain injury: Can the consequences be stopped?.

In general, the ongoing sequelae of damage to nervous tissue is perpetuated by the early failure of neuronal energy, glial injury and dysfunction (swelling of astrocytic foot processes, reversal of neurotransmitter reuptake and reactive astrocytosis), inflammation (invasion of the injury site by microglia and release of proinflammatory cytokines), destruction and stenosis of microvasculature, excitotoxicity and aberrant ionic homeostasis in neurons, and progressive white matter deterioration (Box 1).

Eugene Park, et al. CMAJ. 2008 April 22;178(9):1163-1170.
4.

Figure. From: Traumatic brain injury: Can the consequences be stopped?.

Figure 1: The major pathways associated with the progression of secondary injury after a traumatic brain injury. Microcirculatory derangements involve stenosis (1) and loss of microvasculature, and the blood–brain barrier may break down as a result of astrocyte foot processes swelling (2). Proliferation of astrocytes (“astrogliosis”) (3) is a characteristic of injuries to the central nervous system, and their dysfunction results in a reversal of glutamate uptake (4) and neuronal depolarization through excitotoxic mechanisms. In injuries to white and grey matter, calcium influx (5) is a key initiating event in a molecular cascades resulting in delayed cell death or dysfunction as well as delayed axonal disconnection. In neurons, calcium and zinc influx though channels in the AMPA and NMDA receptors results in excitotoxicity (6), generation of free radicals, mitochondrial dysfunction and postsynaptic receptor modifications. These mechanisms are not ubiquitous in the traumatized brain but are dependent on the subcellular routes of calcium influx and the degree of injury. Calcium influx into axons (7) initiates a series of protein degradation cascades that result in axonal disconnection (8). Inflammatory cells also mediate secondary injury, through the release of proinflammatory cytokines (9) that contribute to the activation of cell-death cascades or postsynaptic receptor modifications.

Eugene Park, et al. CMAJ. 2008 April 22;178(9):1163-1170.

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