Laboratory investigationPathobiology of traumatically induced axonal injury in animals and man
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Cited by (218)
Circuit reorganization after diffuse axonal injury: Utility of the whisker barrel circuit
2022, Cellular, Molecular, Physiological, and Behavioral Aspects of Traumatic Brain InjuryCharacterization of neurite dystrophy after trauma by high speed structured illumination microscopy and lattice light sheet microscopy
2019, Journal of Neuroscience MethodsMicrostructural abnormalities in deep and superficial white matter in youths with mild traumatic brain injury
2019, NeuroImage: ClinicalCitation Excerpt :The majority of DTI studies in people with TBI have focused on alterations in microstructural features of deep white matter fibers (DWM) (Hulkower et al., 2013), the long-range fiber bundles that connect the different lobes and hemispheres of the brain, as well as carry signal from the peripheral nervous system into the brain. However, post-mortem studies have demonstrated that injured axons are often observed in areas of changing tissue density, such as the subcortical gray-white matter interface, where shorter superficial white matter fibers (SWM) mediate local connectivity (Catani et al., 2012; Grady et al., 1993; Peerless and Rewcastle, 1967; Povlishock, 1993). SWM fibers makeup 57% of cortical white matter volume (Schuz and Braintenberg, 2002) and mediate local connectivity in the form of U fibers or longer intralobar fibers (Catani et al., 2012; Yeterian et al., 2012).
The long-term consequences of repetitive head impacts: Chronic traumatic encephalopathy
2019, Handbook of Clinical NeurologyImmediate and Medium-term Changes in Cortical and Hippocampal Inhibitory Neuronal Populations after Diffuse TBI
2018, NeuroscienceCitation Excerpt :Traumatic brain injury (TBI) results from an impact to the head causing acceleration/deceleration stress effects and relative movement between brain and skull (Namjoshi et al., 2013; Xiong et al., 2013; McKee and Daneshvar, 2015). The most common form of TBI, diffuse TBI (dTBI) involves axonal stretch and shearing, produces pathophysiological changes (Blennow et al., 2012) at the cellular level such as axonal (Povlishock, 1993; Smith and Meaney, 2000; Greer et al., 2013) and dendritic injury (Cossart et al., 2001; Gao et al., 2011), osmotic irregularities (Werner and Engelhard, 2007), and triggers various primary and secondary injury processes (Davis, 2000; McKee and Daneshvar, 2015), all of which must contribute to changes in neuronal processing. We have carried out a series of detailed studies of neuronal function, in rodent somatosensory cortex, to show that starting with a suppression of cortical neuronal responses in layers 2–4 immediately after and at 4 days (Johnstone et al., 2013; Allitt et al., 2016b) post-dTBI, and by 2 weeks post-dTBI (Allitt et al., 2016a) this had spread in depth across all cortical columns to infragranular layer 5.
A hitchhiker's guide to lesion-behaviour mapping
2018, Neuropsychologia
Presented at the Neurotrauma: Concepts, Current Practice & Emerging Therapies symposium in Detroit, Michigan, June 1992.