Diffusional kurtosis imaging of cingulate fibers in Parkinson disease: Comparison with conventional diffusion tensor imaging

Diffusion Kurtosis Imaging Detects Microstructural Alterations in Brain of α-Synuclein Overexpressing Transgenic Mouse Model of Parkinson’s Disease: A Pilot Study

“…Using the ROI-based analysis, we found an increase in kurtosis metrics in SN, striatum, sensorimotor cortex, and thalamus regions known to show a-synuclein accumulation in our PD model. Our findings thus accord with the results of Wang et al (2011), and are in line with the hypothesis that the pathology induced by a-synuclein accumulation may result in microstructural changes that cause a decrease in free diffusion of water and hence are expressed by an increase in kurtosis metrics and decrease in diffusivity (Giannelli et al 2012;Wang et al 2011 (Kamagata et al 2013(Kamagata et al , 2014. Unlike those authors, we have found an increase in MK in white matter in TNWT-61 mice.…”

“…Unlike those authors, we have found an increase in MK in white matter in TNWT-61 mice. The reason for this discrepancy in direction of described changes might be due to the fact that our mice model is particularly characterized by overexpression of a-synuclein (Delenclos et al 2014;Watson et al 2012;Wang et al 2011), while DKI as well as DTI changes described by Kamagata et al in humans might be caused particularly by brain neurodegeneration (loss of neurons) and white matter tracts disruption (Kamagata et al 2013;Schwarz et al 2013).…”

“…Specifically, preclinical DKI studies with mice and rats revealed changes in the microstructural complexity of the brain in the mouse model of Alzheimer's disease (Vanhoutte et al 2013), Huntington's disease (Blockx et al 2012), traumatic brain injury model (Zhuo et al 2012), chronic mild stress model of depression (Delgado y Palacios et al 2011), experimental model of ischemia and stroke (Hui et al 2012;Cheung et al 2012) and in cuprizone-induced corpus callosum demyelination model (Falangola et al 2014). In addition, DKI studies in PD patients have found significant changes of MK in the caudate nucleus, putamen, ipsilateral SN (Wang et al 2011), and in the frontal, parietal, occipital, right temporal white matter, and lastly in anterior cingulate fiber as compared to those in the healthy controls (Kamagata et al 2013(Kamagata et al , 2014; however, the direction of these changes remains controversial and the underlying pathological mechanisms for these changes are not well understood.…”

A longitudinal evaluation of diffusion kurtosis imaging in patients with mild traumatic brain injury

“…patients with mTBI may continue to evolve well past the 6 month time frame, which suggests that longer longitudinal evaluations are needed to fully characterize the recovery from injury [26,27]. Furthermore, given that axonal injury is likely both spatially and temporally dependent, differences in results may stem from differences in mechanical impact following injury in addition to the difference in post-injury time points examined [25].…”

“…DKI has also demonstrated changes in both grey and white matter, as Falangola et al [20] found that grey and white matter MK undergoes changes over an individual's lifetime, presumably due to changes in glial cell packing and myelination. MK in the anterior cingulum has also been identified to have better diagnostic performance than FA for Parkinson's disease [25]. Finally, an animal study performed by this group using a controlled cortical impact experimental model of TBI demonstrated that DKI is capable of detecting white and gray matter changes in the acute and sub-acute stages of mTBI.…”