Human studies have begun to show promising results with this method 78 - Of interest, fMRI changes during absence seizures include both increases and decreases in signal. In addition, the anatomical distribution of changes varies substantially from patient to patient. In the largest of these studies 79 , the cortex showed mainly decreases in fMRI signal, and the thalamus increases, although regions of opposite change as well were seen in some patients.
Regions of changes did not involve the whole brain homogenously; rather, focal, often bilateral frontal and parietal regions were involved, along with changes in the thalamus, while other regions were relatively spared. Further work will be needed to fully interpret the relationship of fMRI signal increases and decreases during absence seizures to the underlying changes in neuronal activity 29 , If the spike predominates in the average, this may lead to increases in CBF and metabolism seen on neuroimaging, while if the wave predominates, this many lead to decreases.
Of interest, in this model, fMRI measurements showed mainly increases both in thalamus and in cortex and few decreases. CBF variations are independent of arterial blood pressure fluctuations. Bilateral and relatively symmetrical increases in BOLD signal were present mostly in frontoparietal somatosensory cortex, thalamus, and brainstem nuclei, whereas temporal and occipital regions did not show significant changes. A: reproduced with permission from Human genetic studies have so far elucidated mutations in genes in only a few families or individuals with absence seizures.
These likely represent rare causes of absence seizures, and the search for additional genes continues. However, these early results demonstrate that changes in single genes important in neuronal signaling and excitability can generate absence seizures. One limitation of most of these mouse models is that the phenotype includes other features, such as ataxia and cerebellar degeneration, not typically seen in human absence epilepsy.
Klein et al. Increases in cortical Nav1. Working in the same model, Strauss et al. Voltage clamp recordings also showed enhanced excitability, and reduced I h in these neurons compared to nonepileptic control rats Reduced I h may enhance cortical excitability by increasing dendritic impedance, while increased Nav1. Anatomical locations of tissue plugs used for quantitative PCR analysis are indicated on inset drawing of rat brain.
Changes in neuronal activity in one part of the network can transform the rhythmic behavior of the entire network, for example, by switching between activation of GABA receptors with different pacemaker properties. Rather, selective thalamocortical networks are involved, while others are spared. As we move closer toward this goal, further investigations may provide more selectively targeted therapies, with fewer side effects and greater therapeutic efficacy. Novotny, Jr. Volume 46 , Issue s9.
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Figure 1 Open in figure viewer PowerPoint. Figure 2 Open in figure viewer PowerPoint. Figure 3 Open in figure viewer PowerPoint. Figure 4 Open in figure viewer PowerPoint. Figure 5 Open in figure viewer PowerPoint. Figure 6 Open in figure viewer PowerPoint. The electroencephalogram in epilepsy and in conditions of impaired consciousness. Arch Neruol Psychiat chic ; 34 : — Crossref Google Scholar. Google Scholar. Citing Literature. Psychophysiology 35, — Hanganu, I.
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Sleep spindles in rats with absence epilepsy
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NREM and REM Sleep: Complementary Roles in Recovery after Wakefulness
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- Neuroscience of sleep!
- Sleep (Chapter 91) - The Causes of Epilepsy.
- Traumziel Kajütboot: Von zweien, die auszogen, das Bootfahren zu lernen (German Edition);
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Related Chapter 004, Genetic Mechanisms Underlying Rhythmic EEG Activity during Sleep
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