Detection of subclinical brain electrical activity changes in Huntington's disease using artificial neural networks

Tommaso, Marina de; Carlo, Francesco De; Difruscolo, Olimpia; Massafra, Raffaella; Sciruicchio, Vittorio; Bellotti, R.

doi:10.1016/s1388-2457(03)00074-9

Cited by 37 publications

(45 citation statements)

References 24 publications

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“…Our findings of reduced alpha power confirm similar findings of previous EEG studies in HD [16][17][18][19] and in vascular (multi-infarct) dementia and Alzheimer's disease (AD) [37,39,40,65]. The origin of the alpha rhythm is still unclear, but the abnormality may be associated with a dysfunction primarily affecting the cortex or a dysfunction of subcortical structures which modulate cortical activity, mainly the thalamus.…”

Section: Discussionsupporting

confidence: 90%

“…The lower the alpha-2 power in the frontal, limbic and occipital lobes, the higher the UHDRS motor score disruption of the cortico-striato-thalamocortical circuits causing a decrease in thalamic alpha activity [66,67]. Therefore, the results can be interpreted as an effect of an abnormal subcortical modulation of the alpha rhythm due to dysfunctional action of the thalamus on the cortical activities [18,19,67]. The decrease in alpha power in our patients was found all over the cortex, affecting nearly every voxel.…”

Section: Discussionmentioning

confidence: 99%

“…But routine EEGs have also been reported as abnormal [16][17][18][19][20][21][22][23][24][25]. EEG patterns differ extensively among HD patients, but the most frequent electroencephalographic abnormality described in HD is an amplitude reduction or suppression of alpha activity [16][17][18][19]. Even in the EEG of preclinical mutation carriers for HD, reduced alpha activity was found [19].…”

Section: Introductionmentioning

confidence: 99%

“…The severity of neurological impairment was correlated with increased beta power and faster delta frequency, and poor cognitive performance was correlated with reductions in delta power, less theta power, reduced alpha power and increased beta power over frontal and temporal regions [17]. On the other hand, using artificial neural networks Tommaso et al [19] reported that absolute alpha power was not correlated with cognitive decline.…”

Section: Introductionmentioning

confidence: 99%

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EEG low-resolution brain electromagnetic tomography (LORETA) in Huntington’s disease

et al. 2010

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Previous studies have shown abnormal electroencephalography (EEG) in Huntington's disease (HD). The aim of the present investigation was to compare quantitatively analyzed EEGs of HD patients and controls by means of low-resolution brain electromagnetic tomography (LORETA). Further aims were to delineate the sensitivity and utility of EEG LORETA in the progression of HD, and to correlate parameters of cognitive and motor impairment with neurophysiological variables. In 55 HD patients and 55 controls a 3-min vigilance-controlled EEG (V-EEG) was recorded during midmorning hours. Power spectra and intracortical tomography were computed by LORETA in seven frequency bands and compared between groups. Spearman rank correlations were based on V-EEG and psychometric data. Statistical overall analysis by means of the omnibus significance test demonstrated significant (p < 0.01) differences between HD patients and controls. LORETA theta, alpha and beta power were decreased from early to late stages of the disease. Only advanced disease stages showed a significant increase in delta power, mainly in the right orbitofrontal cortex. Correlation analyses revealed that a decrease of alpha and theta power correlated significantly with increasing cognitive and motor decline. LORETA proved to be a sensitive instrument for detecting progressive electrophysiological changes in HD. Reduced alpha power seems to be a trait marker of HD, whereas increased prefrontal delta power seems to reflect worsening of the disease. Motor function and cognitive function deteriorate together with a decrease in alpha and theta power. This data set, so far the largest in HD research, helps to elucidate remaining uncertainties about electrophysiological abnormalities in HD.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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EEG low-resolution brain electromagnetic tomography (LORETA) in Huntington’s disease

et al. 2010

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“…The EEG has been shown to exhibit amplitude reduction in Huntington patients. De Tomasso et al (2003) used a neural network classifier with a 16-dimensional vector (output from 16 electrodes) to classify the level of functioning of Huntington subjects to evaluate the alpha, beta, theta, and delta ranges. Alpha was shown to be the most discriminating rhythm.…”

Section: Huntington'smentioning

confidence: 99%

Neural Signal Processing

Hudson

Cohen

Bioelectric Engineering

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An autoimmune biliary disease mouse model for primary biliary cirrhosis: Something for everyone

Mason

2006

Hepatology

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Primary biliary cirrhosis (PBC) is an autoimmune disease with a strong genetic component characterized by biliary ductular inflammation with eventual liver cirrhosis. The serologic hallmark of PBC is antimitochondrial antibodies that react with the pyruvate dehydrogenase complex, targeting the inner lipoyl domain of the E2 subunit (anti‐PDC‐E2). Herein we demonstrate that NOD.c3c4 mice congenically derived from the non‐obese diabetic strain develop an autoimmune biliary disease (ABD) that models human PBC. NOD.c3c4 (at 9‐10 wk, before significant biliary pathology) develop antibodies to PDC‐E2 that are specific for the inner lipoyl domain. Affected areas of biliary epithelium are infiltrated with CD3+, CD4+, and CD8+ T cells, and treatment of NOD.c3c4 mice with monoclonal antibody to CD3 protects from ABD. Furthermore, NOD.c3c4‐scid mice develop disease after adoptive transfer of splenocytes or CD4+ T cells, demonstrating a central role for T cells in pathogenesis. Histological analysis reveals destructive cholangitis, granuloma formation, and eosinophilic infiltration as seen in PBC, although, unlike PBC, the extrahepatic biliary ducts are also affected. Using a congenic mapping approach, we define the first ABD (Abd) locus, Abd1. These results identify the NOD.c3c4 mouse as the first spontaneous mouse model of PBC.

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Detection of subclinical brain electrical activity changes in Huntington's disease using artificial neural networks

Cited by 37 publications

References 24 publications

EEG low-resolution brain electromagnetic tomography (LORETA) in Huntington’s disease

EEG low-resolution brain electromagnetic tomography (LORETA) in Huntington’s disease

Neural Signal Processing

An autoimmune biliary disease mouse model for primary biliary cirrhosis: Something for everyone

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