Proton magnetic resonance spectroscopy study of bilateral thalamus in juvenile myoclonic epilepsy

Haki, Cemile; Gumustas, Oguzhan Guven; Bora, İbrahim; Gümüştaş, Ayşem U.; Parlak, Müfıt

doi:10.1016/j.seizure.2007.02.017

Cited by 34 publications

(36 citation statements)

References 35 publications

(43 reference statements)

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“…23,24 Thalamocortical dysfunction is considered to be the major mechanism of JME. MRS studies have reported reduced NAA in the frontal lobe and thalamus, 9,10 consistent with the results reported in the present article. The involvement of these regions may be related to the pathomechanisms of seizure generation in this form of generalized epilepsy.…”

Section: Discussionsupporting

confidence: 92%

“…The spatial distribution of FA reduction in this study reflects a disruption to the architecture of the anterior and ventral thalamic circuits, which are regions that have strong reciprocal projections with the prefrontal cortex. 27 Disruption to these projections, as suggested by the results presented here and in previous MRS studies, [8][9][10]28 may explain frontal lobe dysfunction in patients with JME, which is frequently reported. [29][30][31][32][33][34] In particular, it has been shown that patients with JME scored significantly below age-, education-, and gendermatched controls on neuropsychological measures of attention, immediate verbal memory, mental flexibility, control of inhibition, working memory, processing speed, and verbal fluency.…”

Section: Discussionsupporting

confidence: 68%

See 1 more Smart Citation

Nerve fiber impairment of anterior thalamocortical circuitry in juvenile myoclonic epilepsy

Deppe¹,

Kellinghaus²,

Duning³

et al. 2008

Neurology

119

112

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 68%

Nerve fiber impairment of anterior thalamocortical circuitry in juvenile myoclonic epilepsy

Deppe¹,

Kellinghaus²,

Duning³

et al. 2008

Neurology

119

112

View full text Add to dashboard Cite

show abstract

“…However, glutamine and glutamate are not easily quantifiable at field strengths below 4 Tesla when their overlapping peaks start to separate and GABA measurement requires additional editing. In contrast, the neuronal marker N ‐acetyl aspartate‐glutamate (NAA) is quantifiable even at lower field strengths, and reduced NAA was observed in brain structures that are involved in epilepsy . Only few studies measured in vivo concentrations of GABA or glutamate and glutamine separately (Glx as sum of both, Glx) in patients with JME .…”

mentioning

confidence: 99%

Frontal and thalamic changes of GABA concentration indicate dysfunction of thalamofrontal networks in juvenile myoclonic epilepsy

et al. 2014

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SUMMARYObjective: Juvenile myoclonic epilepsy (JME) has been considered to be a frontal variant of thalamocortical network dysfunction in epilepsy. Changes of c-aminobutyric acid (GABA)ergic neurotransmission may play a key role in this dysfunction. Magnetic resonance spectroscopy (MRS) is the only noninvasive method to measure GABA concentrations in different brain regions. We measured GABA and other metabolite concentrations in the thalamus and frontal lobe of patients with JME. Methods: A specific protocol was used for determining GABA concentrations in the thalamus, frontal lobe, and motor cortex contralateral to the handedness in 15 patients with JME and 15 age-matched controls. In addition, we measured concentrations of glutamate and glutamine, N-acetyl-aspartate (NAA), myoinositol, creatine, and choline using MRS with short echo time. JME-related concentration changes were analyzed comparing patients to controls, also considering potential effects of antiepileptic drugs. Results: In patients with JME, GABA and NAA were reduced in the thalamus (p = 0.03 and p = 0.02), whereas frontal GABA and glutamine were elevated (p = 0.046 and p = 0.03). MRS revealed reduced NAA in the thalamic gray matter contralateral to the handedness (p = 0.04 each). These changes were found consistently in patients treated with new antiepileptic drugs and with valproate, although the extent of metabolic changes differed between these treatments. Significance: Decreased thalamic and increased frontal GABA suggest a dysfunction of GABAergic neurotransmission in these brain regions of patients with JME. The NAA decrease in the gray matter of the thalamus may hint to a damage of GABAergic neurons, whereas frontal increase of GABA and its precursor glutamine may reflect increased density in GABAergic neurons due to subtle cortical disorganization in the thalamofrontal network.

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“…Recent advances in quantitative neuroimaging enable detailed investigation of the brain in vivo. A few studies in single voxel magnetic resonance spectroscopy (MRS) or magnetic resonance spectroscopic imaging (MRSI) have provided evidence of both cortical and deep gray matter (GM) abnormalities, particularly in frontal lobe and thalamus, in IGE patients (Savic et al., 2000; Bernasconi et al., 2003; Mory et al., 2003; Savic et al., 2004; Helms et al., 2006; Haki et al., 2007; Lin et al., 2009; Doelken et al., 2010). However, findings in IGE using MRI volumetry and voxel‐based morphometry (VBM) methods on T 1 ‐weighted images have been inconsistent.…”

mentioning

confidence: 99%

Distinct white matter abnormalities in different idiopathic generalized epilepsy syndromes

et al. 2011

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SUMMARYPurpose: By definition idiopathic generalized epilepsy (IGE) is not associated with structural abnormalities on conventional magnetic resonance imaging (MRI). However, recent quantitative studies suggest white and gray matter alterations in IGE. The purpose of this study was to investigate whether there are white and/or gray matter structural differences between controls and two subsets of IGE, namely juvenile myoclonic epilepsy (JME) and IGE with generalized tonic-clonic seizures only (IGE-GTC). Methods: We assessed white matter integrity and gray matter volume using diffusion tensor tractography-based analysis of fractional anisotropy and voxel-based morphometry, respectively, in 25 patients with IGE, all of whom had experienced generalized tonic-clonic convulsions. Specifically, 15 patients with JME and 10 patients with IGE-GTC were compared to two groups of similarly matched controls separately. Correlations between total lifetime generalized tonic-clonic seizures and fractional anisotropy were investigated for both groups. Key Findings: Tractography revealed lower fractional anisotropy in specific tracts including the crus of the fornix, body of corpus callosum, uncinate fasciculi, superior longitudinal fasciculi, anterior limb of internal capsule, and corticospinal tracts in JME with respect to controls, whereas there were no fractional anisotropy differences in IGE-GTC. No correlation was found between fractional anisotropy and total lifetime generalized tonic-clonic seizures for either JME or IGE-GTC. Although false discovery rate-corrected voxel-based morphometry (VBM) showed no gray matter volume differences between patient and control groups, spatial extent cluster-corrected VBM analysis suggested a trend of gray matter volume reduction in frontal and central regions in both patient groups, more lateral in JME and more medial in IGE-GTC. Significance: The findings support the idea that the clinical syndromes of JME and IGE-GTC have unique anatomic substrates. The fact that the primary clinical difference between JME and IGE-GTC is the occurrence of myoclonus in the former raises the possibility that disruption of white matter integrity may be the underlying mechanism responsible for myoclonus in JME. The cross-sectional study design and relatively small number of subjects limits the conclusions that can be drawn here; however, the absence of a correlation between fractional anisotropy and lifetime seizures is suggestive that the white matter abnormalities observed in JME may not be secondary to seizures.

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Proton magnetic resonance spectroscopy study of bilateral thalamus in juvenile myoclonic epilepsy

Cited by 34 publications

References 35 publications

Nerve fiber impairment of anterior thalamocortical circuitry in juvenile myoclonic epilepsy

Nerve fiber impairment of anterior thalamocortical circuitry in juvenile myoclonic epilepsy

Frontal and thalamic changes of GABA concentration indicate dysfunction of thalamofrontal networks in juvenile myoclonic epilepsy

Distinct white matter abnormalities in different idiopathic generalized epilepsy syndromes

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