Sources of spontaneous slow waves associated with brain lesions, localized by using the MEG

Vieth, J.; Kober, H.; Grummich, P.

doi:10.1007/bf01184772

Cited by 61 publications

(33 citation statements)

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“…High densities of focal generators of such slow wave activity have been found to be related to brain pathology or dysfunctional brain tissue as a result of metabolism and blood flow changes after an insult (e.g. Baayen et al 2003;de Jongh et al 2001;Niedermeyer & Lopes da Silva 1987;Vieth et al 1996) or deafferentation of neuronal networks cut off from major input sources (e.g. Amzica & Steriade 1997;Gloor et al 1977).…”

Section: Introductionmentioning

confidence: 99%

“…Amzica & Steriade 1997;Gloor et al 1977). For example, brain lesions are frequently accompanied by slow waves in deafferented regions after stroke (Meinzer et al 2004) or in circumscribed regions around a tumor (Baayen et al 2003;de Jongh et al 2001;Vieth et al 1996). Furthermore, even in the absence of structurally obvious lesions, focal slow wave generators are also abnormally distributed in psychiatric diseases such as depression, schizophrenia and post-traumatic stress disorder (Fehr et al 2001Fernández et al 2005;Kolassa et al 2007;Rockstroh et al 2007;.…”

Section: Introductionmentioning

confidence: 99%

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Changes in cortical slow wave activity in healthy aging

Leirer

Wienbruch

Kolassa³

et al. 2011

Brain Imaging and Behavior

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Enhanced slow wave activity has been found in stroke patients, schizophrenia, depression, Alzheimer's disease and post-traumatic stress disorder, but the relationship between slow wave activity and healthy aging is as yet unclear. We investigated the relationship between age and the frequency at which focal generators of delta waves appear in the healthy cerebral cortex, as well as whether this measure is associated with cognitive performance. Resting MEG was assessed in 53 healthy individuals aged 18-53. Focal slow wave generator dipole density decreased with age, but there was no relationship between dipole density and cognitive performance. These results emphasize the necessity of controlling for age in studies of slow wave activity in psychopathology.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Changes in cortical slow wave activity in healthy aging

Leirer

Wienbruch

Kolassa³

et al. 2011

Brain Imaging and Behavior

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“…If the neural generators are focally concentrated, slow wave rhythms appear in the vicinity of a structural lesion, that is, focal electromagnetic slow waves are generated in the surround of circumscribed lesions or neuronal tissue otherwise affected by pathology such as cerebral infarct, contusion, local infection, tumor, epileptic foci and subdural hematoma de Jongh et al, 2001ade Jongh et al, ,b, 2002de Jongh et al, , 2003Gallen et al, 1992Gallen et al, , 1993Tanaka et al, 1998;Vieth et al, 1998Vieth et al, , 1996Vieth et al, , 2001Walter, 1936). Furthermore, reduced levels of neurotransmitters (e.g.…”

Section: Introductionmentioning

confidence: 99%

Abnormal slow wave mapping (ASWAM)—A tool for the investigation of abnormal slow wave activity in the human brain

Wienbruch¹

2007

Journal of Neuroscience Methods

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Slow waves in the delta and theta frequency range, normal signs of deactivated networks in sleep stages, are considered 'abnormal' when prominent in the waking state and when generated in circumscribed brain areas. Structural cortical lesions, e.g. related to stroke, tumors, or scars, generate focal electric and magnetic slow wave activity in the penumbra. Focal concentrations of slow wave activity exceeding those of healthy subjects have also been found in individuals suffering from psychiatric disorders without obvious structural brain damage. Hence, identification and mapping of abnormal slow wave activity might contribute to the investigation of cortical indications of psychopathology.Here I propose a method for abnormal slow wave mapping (ASWAM), based on a 5 min resting magnetoencephalogramm (MEG) and equivalent current dipole fitting to sources in the 1-4 Hz frequency band (delta) in anatomically defined cortical regions. The method was tested in a sample of 116 healthy subjects (59 males), with the aim to provide a basis for later comparison with patient samples. As to be expected, delta dipole density was low in healthy subjects. However, its distribution differed between genders with fronto-central > posterior dipole density in male and posterior dominance in female participants, which was not significantly related to either age or headsize. Results suggest that this method allows the identification of ASWA, so that comparison against Z-scores from a larger normal control group might assist diagnostic purposes in patient groups. As specific distributions seem to reflect differences between genders, this should be considered also in the analysis of patient samples.

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“…MEG was also found to be more sensitive than conventional MRI or EEG in detecting abnormalities in mTBI patients (Lewine et al, 1999(Lewine et al, , 2007. Unlike normal resting-state MEG data, which is dominated by neuronal activity with frequencies above 8 Hz, injured neuronal tissues (due to head trauma, brain tumors, stroke, and epilepsy) generate abnormal focal or multi-focal lowfrequency neuronal magnetic signals (delta-band 1-4 Hz, or theta-band 5-7 Hz) that can be directly measured and localized using MEG de Jongh et al, 2003;Decker and Knott, 1972;Lewine et al, 1999;Lewine and Orrison, 1995;Nagata et al, 1985;Vieth et al, 1996). While TBI is not the only neurological disorder that generates abnormal slow-wave, in practice, brain tumors, stroke, and epilepsy can be easily ruled out based on structural imaging (i.e., CT and MRI for tumor and stroke) and medical history (for epilepsy).…”

mentioning

confidence: 99%

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

Huang

Risling

Baker

2016

Psychoneuroendocrinology

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SummaryBackground: Pervasive use of improvised explosive devices (IEDs), rocket-propelled grenades, and land mines in the recent conflicts in Iraq and Afghanistan has brought traumatic brain injury (TBI) and its impact on health outcomes into public awareness. Blast injuries have been deemed signature wounds of these wars. War-related TBI is not new, having become prevalent during WWI and remaining medically relevant in WWII and beyond. Medicine's past attempts to accurately diagnose and disentangle the pathophysiology of war-related TBI parallels current lines of inquiry and highlights limitations in methodology and attribution of symptom etiology, be it organic, psychological, or behavioral. New approaches and biomarkers are needed. Preclinical: Serological biomarkers and biomarkers of injury obtained with imaging techniques represent cornerstones in the translation between experimental data and clinical observations. Experimental models for blast related TBI and PTSD can generate critical data on injury threshold, for example for white matter injury from acceleration. Carefully verified and validated models can be evaluated with gene expression arrays and proteomics to identify new candidates for serological biomarkers. Such models can also be analyzed with diffusion MRI and microscopy in order to identify criteria for detection of diffuse white matter injuries, such as DAI (diffuse axonal injury). The experimental models can also be analyzed with focus on injury outcome in brain stem regions, such as locus coeruleus or nucleus raphe magnus that can be involved in response to anxiety changes. * Corresponding author at: UCSD Radiology Imaging Laboratory, San Diego, CA 92121, USA. Tel.: +1 858 534 1254; fax: +1 8585346046. E-mail address: mxhuang@ucsd.edu (M. Huang). Clinical: Mild (and some moderate) TBI can be difficult to diagnose because the injuries are often not detectable on conventional MRI or CT. There is accumulating evidence that injured brain tissues in TBI patients generate abnormal low-frequency magnetic activity (ALFMA, peaked at 1-4 Hz) that can be measured and localized by magnetoencephalography (MEG). MEG imaging detects TBI abnormalities at the rates of 87% for the mild TBI, group (blast-induced plus non-blast causes) and 100% for the moderate group. Among the mild TBI patients, the rates of abnormalities are 96% and 77% for the blast and non-blast TBI groups, respectively. There is emerging evidence based on fMRI and MEG studies showing hyper-activity in the amygdala and hypo-activity in prefrontal cortex in individuals with PTSD. MEG signal may serve as a sensitive imaging marker for mTBI, distinguishable from abnormalities generated in association with PTSD. More work is needed to fully describe physiological mechanisms of post-concussive symptoms.Published by Elsevier Ltd. BackgroundBlast injuries are deemed the signature wounds of the first wars (Afghanistan and Iraq) of the 21st century (Lancet, 2007;Galarneau et al., 2008). According to a recent U.S. Department Veterans Affairs (DVA) ...

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Sources of spontaneous slow waves associated with brain lesions, localized by using the MEG

Cited by 61 publications

References 14 publications

Changes in cortical slow wave activity in healthy aging

Changes in cortical slow wave activity in healthy aging

Abnormal slow wave mapping (ASWAM)—A tool for the investigation of abnormal slow wave activity in the human brain

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

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