Arrow Research search

Author name cluster

Michael T. Jurkiewicz

Possible papers associated with this exact author name in Arrow. This page groups case-insensitive exact name matches and is not a full identity disambiguation profile.

3 papers
1 author row

Possible papers

3

YNICL Journal 2022 Journal Article

The role of the temporal pole in temporal lobe epilepsy: A diffusion kurtosis imaging study

  • Loxlan W. Kasa
  • Terry Peters
  • Seyed M. Mirsattari
  • Michael T. Jurkiewicz
  • Ali R. Khan
  • Roy A.M Haast

This study aimed to evaluate the use of diffusion kurtosis imaging (DKI) to detect microstructural abnormalities within the temporal pole (TP) and its temporopolar cortex in temporal lobe epilepsy (TLE) patients. DKI quantitative maps were obtained from fourteen lesional TLE and ten non-lesional TLE patients, along with twenty-three healthy controls. Data collected included mean (MK); radial (RK) and axial kurtosis (AK); mean diffusivity (MD) and axonal water fraction (AWF). Automated fiber quantification (AFQ) was used to quantify DKI measurements along the inferior longitudinal (ILF) and uncinate fasciculus (Unc). ILF and Unc tract profiles were compared between groups and tested for correlation with disease duration. To characterize temporopolar cortex microstructure, DKI maps were sampled at varying depths from superficial white matter (WM) towards the pial surface. Patients were separated according to the temporal lobe ipsilateral to seizure onset and their AFQ results were used as input for statistical analyses. Significant differences were observed between lesional TLE and controls, towards the most temporopolar segment of ILF and Unc proximal to the TP within the ipsilateral temporal lobe in left TLE patients for MK, RK, AWF and MD. No significant changes were observed with DKI maps in the non-lesional TLE group. DKI measurements correlated with disease duration, mostly towards the temporopolar segments of the WM bundles. Stronger differences in MK, RK and AWF within the temporopolar cortex were observed in the lesional TLE and noticeable differences (except for MD) in non-lesional TLE groups compared to controls. This study demonstrates that DKI has potential to detect subtle microstructural alterations within the temporopolar segments of the ILF and Unc and the connected temporopolar cortex in TLE patients including non-lesional TLE subjects. This could aid our understanding of the extrahippocampal areas, more specifically the temporal pole role in seizure generation in TLE and might inform surgical planning, leading to better seizure outcomes.

YNICL Journal 2017 Journal Article

Neuromagnetic responses to tactile stimulation of the fingers: Evidence for reduced cortical inhibition for children with Autism Spectrum Disorder and children with epilepsy

  • William Gaetz
  • Michael T. Jurkiewicz
  • Sudha Kilaru Kessler
  • Lisa Blaskey
  • Erin S. Schwartz
  • Timothy P.L. Roberts

The purpose of this study was to compare somatosensory responses from a group of children with epilepsy and a group of children with autism spectrum disorder (ASD), with age matched TD controls. We hypothesized that the magnitude of the tactile "P50m" somatosensory response would be reduced in both patient groups, possibly due to reduced GABAergic signaling as has been implicated in a variety of previous animal models and in vivo human MRS studies. We observed significant (~ 25%) decreases in tactile P50m dipole moment values from the source localized tactile P50m response, both for children with epilepsy and for children with ASD. In addition, the latency of the tactile P50m peak was observed to be equivalent between TD and ASD groups but was significantly delayed in children with epilepsy by ~ 6 ms. Our data support the hypothesis of impaired GABAergic signaling in both children with ASD and children with epilepsy. Further work is needed to replicate these findings and directly relate them to both in vivo measures of GABA via e.g. magnetic resonance spectroscopy and psychophysical assessments of somatosensory function, and behavioral indices.

YNIMG Journal 2006 Journal Article

Post-movement beta rebound is generated in motor cortex: Evidence from neuromagnetic recordings

  • Michael T. Jurkiewicz
  • William C. Gaetz
  • Andreea C. Bostan
  • Douglas Cheyne

Voluntary movements are accompanied by amplitude changes in cortical rhythms presumably as a result of functional activation of sensorimotor areas. Recently, the location of the neural generators involved in increasing power within the beta (15–30 Hz) frequency band following movement (post-movement beta rebound, PMBR) has come into question [Parkes, L. M, Bastiaansen, M. C. M, Norris, D. G. , 2006. Combining EEG and fMRI to investigate the post-movement beta rebound. NeuroImage 29, 685–696. ]. We used the synthetic aperture magnetometry (SAM) spatial filtering method to identify the time course and location of oscillatory changes within the beta and mu (8–14 Hz) frequency bands during the performance of voluntary movements. Neuromagnetic activity was recorded from 10 adult subjects during abduction of the right index finger. Changes in beta and mu source power were calculated for periods during and following movement, relative to pre-movement baseline activity. Decreases in beta band activity (event-related desynchronization, ERD) were observed during movement, with a strong increase (PMBR) beginning 230±170 ms following movement, lasting for 680±170 ms. Mu band ERD was observed both during and following movement, with little to no post-movement rebound. Beta and mu ERD were localized bilaterally to the hand region of postcentral gyrus whereas PMBR was localized bilaterally to the hand region of precentral gyrus (motor cortex). Both PMBR and beta ERD were strongest contralateral to the side of movement. These results provide further evidence that movement influences independent cortical rhythms in sensorimotor areas, and confirm previous reports of precentral generators of PMBR in the region of motor cortex, with postcentral generators of beta and mu ERD during movement.

v2026.09.13