Biomedical subjects

Anton Coenen

Publications and source records attributed to Anton Coenen.

3 recordsLinked to original sources

PubMed2006

Time-frequency analysis of spike-wave discharges using a modified wavelet transform.

The continuous Morlet wavelet transform was used for the analysis of the time-frequency pattern of spike-wave discharges (SWD) as can be recorded in a genetic animal model of absence epilepsy (rats of the WAG/Rij strain). We developed a new wavelet transform that allows to obtain the time-frequency dynamics of the dominating rhythm during the discharges. SWD were analyzed pre- and post-administration of certain drugs. SWD recorded predrug demonstrate quite uniform time-frequency dynamics of the dominant rhythm. The beginning of the discharge has a short period with the highest frequency value (up to 15 Hz). Then the frequency decreases to 7-9 Hz and frequency modulation occurs during the discharge in this range with a period of 0.5-0.7 s. Specific changes of SWD time-frequency dynamics were found after the administration of psychoactive drugs, addressing different brain mediator and modulator systems. Short multiple SWDs appeared under low (0.5 mg/kg) doses of haloperidol, they are characterized by a fast frequency decrease to 5-6 Hz at the end of every discharge. The frequency of the dominant frequency of SWD was not stable in long lasting SWD after 1.0 mg/kg or more haloperidol: then two periodicities were found. Long lasting SWD seen after the administration of vigabatrin showed a stable frequency of the discharge. The EEG after Ketamin showed a distinct 5 s quasiperiodicity. No clear changes of time-frequency dynamics of SWD were found after perilamine. It can be concluded that the use of the modified Morlet wavelet transform allows to describe significant parameters of the dynamics in the time-frequency domain of the dominant rhythm of SWD that were not previously detected.

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PubMed2005

Evolving concepts on the pathophysiology of absence seizures: the cortical focus theory.

Four main theories on the pathophysiology of generalized absence seizures have been proposed. The "centrencephalic" theory, proposed in 1954, suggested that discharges originate from a deep-seated diffusely projecting subcortical pacemaker in the midline thalamus. This concept was refined in 1991 with the "thalamic clock" theory, implying that the reticular thalamic nucleus contains the pacemaker cells for the thalamic clock, imposing its rhythm to the cortex. According to other investigators, however, the cortex seems to play a leading role. They suggested that spike-wave discharges have a focal onset in the cortex and are generalized through a rapid propagation. In the "corticoreticular" theory, postulated in 1968, spike-wave discharges are linked to the thalamocortical mechanisms that generate spindles. Rhythmic spindle oscillations generated in the thalamus are transformed into spike-wave discharges when the cortex is hyperexcitable. A 2002 study confirmed in epileptic rats that a functionally intact thalamocortical network is required for the generation of spike-wave discharges. The corticothalamic interrelationships were investigated by means of nonlinear association signal analyses of multiple spike-wave discharges. This showed a consistent focus within the perioral region of the somatosensory cortex. From this focus, seizure activity generalizes rapidly over the cortex. During the first cycles of the seizure the cortex drives the thalamus, while thereafter cortex and thalamus drive each other, thus amplifying and maintaining the rhythmic discharge. In this way the "cortical focus" theory for generalized absence epilepsy bridges cortical and thalamic theories.

Animals↗

PubMed2004

Chromosomal mapping of genetic loci controlling absence epilepsy phenotypes in the WAG/Rij rat.

PURPOSE: The WAG/Rij rat is among the most appropriate models for the study of spontaneous childhood absence epilepsy, without complex neurologic disorders that are associated with some mouse models for absence epilepsy. Previous studies have allowed the identification of distinct types of spike-wave discharges (SWDs) characterizing seizures in this strain. The purpose of this study was to investigate the genetic basis of electroencephalographic (EEG) properties of SWDs. METHODS: An intercross was derived from WAG/Rij and ACI inbred strains that are known to differ substantially in the number of SWDs. Phenotypic analyses based on 23-h EEG recording in all progenies allowed the quantification of type I and type II SWD phenotypes. A genome-wide scan was performed with 145 microsatellite markers, which were used to test for evidence of genetic linkage to SWD quantitative phenotypes. RESULTS: We were able to map quantitative trait loci independently, controlling type I and type II SWD variables to rat chromosomes 5 and 9. Strongest linkages were obtained for D5Mgh15 and total duration of type II SWD (lod, 3.64) and for D9Rat103 and the average duration of type I SWD (lod, 3.91). These loci were denoted T2swd/wag and T1swd/wag, respectively. CONCLUSIONS: The independent genetic control of type I and type II SWDs underlines the complexity of the molecular mechanisms participating in SWDs. The identification of these genetic loci represents an important step in our fundamental knowledge of the architecture of SWDs and may provide new insights for resolving the genetic heterogeneity of absence epilepsy.

Animals↗