PubMed Health⌕ Search

PubMed · 15379218

Randomization-based hypothesis testing from event-related data.

Abstract

Methods are described for non-parametric significance testing from event-related encephalographic data, using randomization tests. These methods may be applied in both signal space and source space. The methods include within-subject between-condition comparisons, paired and unpaired comparisons, and within-group and between-group comparisons. Test statistics are also derived for comparing the spatial or temporal response patterns, independent of specific changes at individual locations. Novel methods for testing peak-height significance, and also for making map-wide comparisons, are described. These methods have been validated using simulated data.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Richard E Greenblatt, Mark E Pflieger. 2004. Randomization-based hypothesis testing from event-related data.. https://doi.org/10.1023/b%3Abrat.0000032856.48286.18

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Observer-independent analysis of high-resolution MR images of the human cerebral cortex: in vivo delineation of cortical areas.

Using high-resolution MRI, it is now possible to examine the living human cortex down to a resolution of less than 300 mum. Thus, in vivo imaging is now approaching the resolution that has been successfully used in histological analysis of the cerebral cortex for many years, e.g., low-magnification light microscopy. This allows unprecedented views of cortical microstructure that reflect defined histological features, specifically, individual cortical layers. As in histological brain mapping, it is possible to use the changes in the cortical lamination patterns to define individual cortical areas. This allows in vivo neuroanatomical maps to be generated for individual subjects and precise correlation of the results from functional imaging studies in these subjects with their own microanatomical information. To this end, we adapted the well-established observer-independent cytoarchitectonic mapping techniques for defining cortical borders based on changes in cortical lamination for in vivo parcellation of high-resolution structural MR images.

Brain Mapping↗

Frontotemporal dementia and parkinsonism associated with the IVS1+1G->A mutation in progranulin: a clinicopathologic study.

We previously reported a kindred with three cases of dementia, in which the proband exhibited features typical of frontotemporal dementia and parkinsonism (FTDP). An arginine insertion at codon 352 (insR352) in the presenilin-1 (PSEN1) gene was identified in the proband, but analyses in plasma and CSF suggested a mechanism of neurodegeneration not directly related to amyloid pathophysiology. The proband was followed with yearly evaluations of functional, clinical, neuropsychologic, neuropsychiatric and radiologic status, which showed relatively linear change over the initial 4 years of assessment. Upon the proband's death at age 63, neuropathologic examination revealed frontotemporal lobar degeneration (FTLD) with ubiquitin-positive inclusions (FTLD-U). We recently identified several kindreds with familial FTDP associated with mutations in the progranulin (PGRN) gene, particularly in those cases with neuronal intranuclear inclusions. Our proband was indeed found to have such inclusions, and PGRN analysis in this proband revealed the G to A mutation in the exon 1 splice donor site (IVS1+1G-->A) which is predicted to destroy the 5'-splice site of exon 1 and remove the start methionine codon and hence completely block any PGRN protein from being generated. These findings suggest that the insR352 PSEN1 is not pathogenic, and the IVS1+1G-->A mutation in PGRN causes FTDP associated with FTLD-U pathology and represents a new class of neurodegenerative disease--the 'hypoprogranulinopathies'.

Brain Mapping↗

Stereotyped topography of different elevated contingent negative variation components in children with migraine without aura points towards a subcortical dysfunction.

Increased negativity during contingent negative variation (CNV) is thought to reflect abnormal neural activation in adult migraineurs' attention related processing. Findings in childhood and adolescence have yielded less clear results. This study characterizes the age-dependent development of CNV topography in migraine during childhood in order to elucidate the origin and cerebral generators of described CNV elevations. A large sample of children with primary headache (migraine with/without aura, tension type headache) and healthy controls aged 6-18 years was examined in a CNV paradigm using 64-channel high resolution DC-EEG. Patients were tested for diagnose-related topographic group differences of initial CNV (iCNV), late CNV (lCNV) and postimperative negative variation (PINV). All three CNV components of 6-11-year-old migraineurs without aura showed elevated negativity over the supplementary motor area (SMA) and around the vertex. Migraine children lacked age-dependent development of late CNV around Cz as previously reported. However, they showed a normal development of late CNV over pre-/primary motor cortex (MI). There was no marked elevation of iCNV amplitude over frontal areas (orienting reaction) nor specific amplitude elevations over "motor" or "sensory" areas during sustained attention (late CNV). Additional "pre-mature" activation e.g., in the locus coeruleus (leading to diffuse cortical activation summing up to a maximum over the vertex) or the basal ganglia (interacting with SMA) explained the rather stereotyped CNV elevation around the vertex better than a specific implication of the cortical systems responsible for orienting, motor preparation or sensory attention.

Brain Mapping↗