Electrophysiologic Effects of γ‐Vinyl GABA and Carbamazepine

Mervaala, Esa; Partanen, Juhani; Nousiainen, Unto; Sivenius, Juhani; Riekkinen, Paavo

doi:10.1111/j.1528-1157.1989.tb05453.x

Cited by 40 publications

(26 citation statements)

References 28 publications

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“…However, VGB treatment had no effect on the EEG recordings from control rats (Supplemental Figures 4C and D) and did not suppress the slow waves of NREM sleep in these rats (Supplemental Figures 4B vs 4D). The latter results are in keeping with earlier studies that showed VGB has little or no effect on normal EEG activity in humans (Hammond and Wilder, 1985, Mervaala et al , 1989, Marciani et al , 1997). …”

Section: Resultssupporting

confidence: 93%

Vigabatrin therapy implicates neocortical high frequency oscillations in an animal model of infantile spasms

Frost

Lee

et al. 2015

Neurobiology of Disease

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Abnormal high frequency oscillations (HFOs) in EEG recordings are thought to be reflections of mechanisms responsible for focal seizure generation in the temporal lobe and neocortex. HFOs have also been recorded in patients and animal models of infantile spasms. If HFOs are important contributors to infantile spasms then anticonvulsant drugs that suppress these seizures should decrease the occurrence of HFOs. In experiments reported here, we used long-term video/EEG recordings with digital sampling rates capable of capturing HFOs. We tested the effectiveness of vigabatrin (VGB) in the TTX animal model of infantile spasms. VGB was found to be quite effective in suppressing spasms. In 3 of 5 animals, spasms ceased after a daily two week treatment. In the other 2 rats, spasm frequency dramatically decreased but gradually increased following treatment cessation. In all animals, hypsarrhythmia was abolished by the last treatment day. As VGB suppressed the frequency of spasms, there was a decrease in the intensity of the behavioral spasms and the duration of the ictal EEG event. Analysis showed that there was a burst of high frequency activity at ictal onset, followed by a later burst of HFOs. VGB was found to selectively suppress the late HFOs of ictal complexes. VGB also suppressed abnormal HFOs recorded during the interictal periods. Thus VGB was found to be effective in suppressing both the generation of spasms and hypsarrhythmia in the TTX model. Vigabatrin also appears to preferentially suppress the generation of abnormal HFOs, thus implicating neocortical HFOs in the infantile spasms disease state.

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Section: Resultssupporting

confidence: 93%

Vigabatrin therapy implicates neocortical high frequency oscillations in an animal model of infantile spasms

Frost

Lee

et al. 2015

Neurobiology of Disease

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“…For vigabatrin (VGB), the absence of cognitive side effects (compared with the existing first‐line drugs) is claimed, but the data come from only one center: Riekinnen et al in Finland (28,29), and are not based on high‐powered studies. A few additional studies did, however, not pass our aforementioned criteria, mostly because they were carried out in polytherapy designs.…”

Section: Newer Antiepileptic Drugsmentioning

confidence: 99%

Effects of Antiepileptic Drugs on Cognition

Aldenkamp

2001

Epilepsia

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“…Clinical and laboratory tests, including the serum concentrations of other antiepileptic drugs, were done at least every 3 months during the first 2 years of vigabatrin treatment and every 6 months thereafter. Electroencephalography Electroencephalograms (eight-, 16-, or 21-channel) that includ¬ ed photic stimulation and hyperventilation were evaluated before initiation of vigabatrin therapy; 7,12, and 24 months after the be¬ ginning of vigabatrin treatment; and when a patient was exclud¬ ed from the study. In addition to epileptiform activity, changes in the dominant occipital rhythm and the amounts of alpha, theta, and delta activities were assessed.…”

Section: Patients and Administration Of Vigabatrinmentioning

confidence: 99%