Poster No:
769
Submission Type:
Late-Breaking Abstract Submission
Authors:
Carmen Zheng1, Graeme Jackson2, Chris Tailby3
Institutions:
1University of Melbourne, Heidelberg, Victoria, 2The Florey Institute of Neuroscience and Mental Health, Melbourne, Australia, 3The Florey, Heidelberg, Victoria
First Author:
Co-Author(s):
Graeme Jackson
The Florey Institute of Neuroscience and Mental Health
Melbourne, Australia
Introduction:
Periventricular nodular heterotopia (PVNH) are malformations with epileptogenic potential, characterised as grey matter nodules lining the ependyma of the lateral ventricles. Previous studies have shown functional and structural connectivity between PVNH and the overlying cortex (Christodoulou et al., 2013; Deleo et al., 2020). Targeted task functional magnetic resonance imaging (fMRI) paradigms have been used to elicit within-nodule responses to basic sensory and cognitive processes (Janszky et al., 2003; Richardson et al., 1998). PVNH has been associated with alterations in cognition, such as reduced reading ability (Chang et al., 2005, 2007). Pertinent to surgical management, it is unclear whether PVNH are directly involved with cognition or indirectly interfere with established cognitive networks. In our study, this was tested using task fMRI to identify presence of task-modulated activation in PVNH that would be consistent with cognitive engagement.
Methods:
Adult PVNH participants (mean age= 32.3 years, standard deviation = 13.0 years) of the Australian Epilepsy Project all underwent nonword-rhyming (N = 17) and spatial N-back (N = 15) functional MRI paradigms. Lesion masks were manually traced based on high resolution T1-weighted structural MRI. For each individual in each paradigm, voxel-level (p < 0.001) and cluster-level (p < 0.05) thresholding were applied to t-statistic maps (voxel size: 3mm3) of task activations using SPM25. The number of task-active voxels intersecting with lesion was measured as a percentage against the total number of voxels in the corresponding lesion mask.
Results:
During nonword-rhyming task, 15 out of 17 individuals showed no activation in PVNH, the remaining two individuals showed activation in 0.4% of their lesion (1 out of 278 lesion voxels; 4 out of 1086 lesion voxels). During spatial N-back task, 13 of 15 individuals showed no activation in PVNH; one individual showed activation in 4.3% (1 out of 23 lesion voxels), and another showed activation in 0.3% (3 out of 869 lesion voxels) of PVNH. No participants showed evidence of lesion activation across both tasks.
Conclusions:
In this systematic study involving a large sample of PVNH cases, we observed no compelling evidence for the recruitment of PVNH tissue in language, visuospatial and attentional function. Our findings support the view that PVNH is unlikely to be directly engaged in high-order cognitive processes tested in this study. This also implies that resection of the PVNH tissue likely carries minimal cognitive risk.
Higher Cognitive Functions:
Higher Cognitive Functions Other 1
Language:
Language Other
Learning and Memory:
Working Memory
Modeling and Analysis Methods:
Activation (eg. BOLD task-fMRI) 2
Keywords:
ADULTS
Cognition
DISORDERS
Epilepsy
FUNCTIONAL MRI
1|2Indicates the priority used for review
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Please indicate below if your study was a "resting state" or "task-activation” study.
Task-activation
Healthy subjects only or patients (note that patient studies may also involve healthy subjects):
Patients
Was this research conducted in the United States?
No
Were any human subjects research approved by the relevant Institutional Review Board or ethics panel?
NOTE: Any human subjects studies without IRB approval will be automatically rejected.
Yes
Were any animal research approved by the relevant IACUC or other animal research panel?
NOTE: Any animal studies without IACUC approval will be automatically rejected.
Not applicable
Please indicate which methods were used in your research:
Functional MRI
For human MRI, what field strength scanner do you use?
3.0T
Provide references using APA citation style.
Chang, B., Katzir, T., Liu, T., Corriveau, K., Barzillai, M., Apse, K., Bodell, A., Hackney, D., Alsop, D., & Wong, S. (2007). A structural basis for reading fluency: White matter defects in a genetic brain malformation. Neurology, 69(23), 2146–2154.
Chang, B., Ly, J., Appignani, B., Bodell, A., Apse, K., Ravenscroft, R., Sheen, V., Doherty, M., Hackney, D., & O’connor, M. (2005). Reading impairment in the neuronal migration disorder of periventricular nodular heterotopia. Neurology, 64(5), 799–803.
Christodoulou, J. A., Barnard, M. E., Del Tufo, S. N., Katzir, T., Whitfield-Gabrieli, S., Gabrieli, J. D. E., & Chang, B. S. (2013). Integration of gray matter nodules into functional cortical circuits in periventricular heterotopia. Epilepsy & Behavior, 29(2), 400–406. https://doi.org/10.1016/j.yebeh.2013.08.028
Deleo, F., Hong, S.-J., Fadaie, F., Caldairou, B., Krystal, S., Bernasconi, N., & Bernasconi, A. (2020). Whole-brain multimodal MRI phenotyping of periventricular nodular heterotopia. Neurology, 95(17). https://doi.org/10.1212/WNL.0000000000010648
Janszky, J., Ebner, A., Kruse, B., Mertens, M., Jokeit, H., Seitz, R. J., Witte, O. W., Tuxhorn, I., & Woermann, F. G. (2003). Functional organization of the brain with malformations of cortical development. Annals of Neurology, 53(6), 759–767. https://doi.org/10.1002/ana.10545
Richardson, M. (1998). Cerebral activation in malformations of cortical development. Brain, 121(7), 1295–1304. https://doi.org/10.1093/brain/121.7.1295
Richardson, M., Koepp, M., Brooks, D., Coull, J., Grasby, P., Fish, D., & Duncan, J. (1998). Cerebral activation in malformations of cortical development. Brain: A Journal of Neurology, 121(7), 1295–1304.
Wagner, J., Elger, C. E., Urbach, H., & Bien, C. G. (2009). Electric stimulation of periventricular heterotopia: Participation in higher cerebral functions. Epilepsy & Behavior, 14(2), 425–428. https://doi.org/10.1016/j.yebeh.2008.11.006
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