Transient loss of inhibition precedes spontaneous seizures after experimental status epilepticus

Holtkamp, Martin; Matzen, Julia; Landeghem, Frank K.H. van; Buchheim, Katharina; Meierkord, Hartmut

doi:10.1016/j.nbd.2004.12.002

Cited by 24 publications

(18 citation statements)

References 45 publications

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“…Confirming previous results, we found decreased neuronal cell densities within the DG in all rats that had experienced SE (Fig. 5E) (Holtkamp et al, 2005). Importantly, the VPA-treated animals showed a comparable degree of neuronal degeneration in the dentate area as the untreated KA-injected animals (Fig.…”

Section: Neuronal Cell Death Does Not Appear To Be Affected By Vpasupporting

confidence: 92%

Epigenetic Modulation of Seizure-Induced Neurogenesis and Cognitive Decline

Jessberger¹,

Nakashima²,

Clemenson³

et al. 2007

J. Neurosci.

321

231

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The conceptual understanding of hippocampal function has been challenged recently by the finding that new granule cells are born throughout life in the mammalian dentate gyrus (DG). The number of newborn neurons is dynamically regulated by a variety of factors. Kainic acid-induced seizures, a rodent model of human temporal lobe epilepsy, strongly induce the proliferation of DG neurogenic progenitor cells and are also associated with long-term cognitive impairment. We show here that the antiepileptic drug valproic acid (VPA) potently blocked seizure-induced neurogenesis, an effect that appeared to be mainly mediated by inhibiting histone deacetylases (HDAC) and normalizing HDAC-dependent gene expression within the epileptic dentate area. Strikingly, the inhibition of aberrant neurogenesis protected the animals from seizure-induced cognitive impairment in a hippocampus-dependent learning task. We propose that seizure-generated granule cells have the potential to interfere with hippocampal function and contribute to cognitive impairment caused by epileptic activity within the hippocampal circuitry. Furthermore, our data indicate that the effectiveness of VPA as an antiepileptic drug may be partially explained by the HDAC-dependent inhibition of aberrant neurogenesis induced by seizure activity within the adult hippocampus.

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Section: Neuronal Cell Death Does Not Appear To Be Affected By Vpasupporting

confidence: 92%

Epigenetic Modulation of Seizure-Induced Neurogenesis and Cognitive Decline

Jessberger¹,

Nakashima²,

Clemenson³

et al. 2007

J. Neurosci.

321

231

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“…The study of Trevelyan et al (2007) is in keeping with such an assumption since in their experiments an increase in frequency of SLEs in low-Mg 2+ was associated with reduced feed-forward inhibition. Support of this finding comes also from the in vivo part of this study demonstrating progressive epileptogenesis in animals after SE (Holtkamp et al, 2005). Several studies have demonstrated progressive hyperexcitability in the DG following experimental SE in vivo (Gorter et al, 2002;Shirasaka and Wasterlain, 1994;Sloviter, 1991).…”

Section: Electrophysiological Featuressupporting

confidence: 77%

“…The in vivo experiments were carried out as described previously (Holtkamp et al, 2005). Male Wistar rats aged 10-12 weeks weighing 300-400 g at the time of SE were used in this study.…”

Section: Experiments In Vivomentioning

confidence: 99%

Status epilepticus induces increasing neuronal excitability and hypersynchrony as revealed by optical imaging

Holtkamp

Buchheim

Elsner

et al. 2011

Neurobiology of Disease

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“…[13] Deneysel hayvan modellerinde, uzamış elektrografik nö-bet aktivitesinin beyin hasarı yaptığı gösterilmiştir. [99] SE'nin prognozu altta yatan nedene, hastanın yaşına (>50 yaş), statusun tipi ve süresine bağlıdır. En yüksek mortalite semptomatik nedene bağlı status olgularında görülmektedir.…”

Section: Basamak Tedaviunclassified

Untitled

Akpınar¹,

Cengiz²

2014

Epilepsi

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SummaryStatus Epilepticus (SE) is a medical emergency that causes significant morbidity and mortality and requires prompt diagnosis and treatment. Although SE can be divided into two subgroups as convulsive and nonconvulsive, treatment principles are generally similar. Treatment should be prompt and underlying cause should be corrected. Although intravenous lorazepam is the first-line treatment due to a lower risk of relapse, diazepam becomes the first choice since loeazepan is not available in our country. Even though intravenous benzodiazepine stops seizures, intravenous antiepileptic drug (phenytoin, etc.) should be administered at a loading dose. Patients with refractory status epilepticus should be supported with respect to vital, respiratory, metabolic and hemodynamic aspects and followed up in an intensive care unit to monitor cerebral electrical activity. The most common cause in the etiology is the cessation of antiepileptic drugs. The aim of SE treatment is to stop seizures and prevent complications and recurrence. In this paper, current diagnosis, treatment and etiology of SE are reviewed.Key words: Aetiology; status epileptikus; diagnosis; treatment. ÖzetStatus epileptikus (SE) belirgin morbidite ve mortaliteye neden olan, hızlı tanı ve tedavi gerektiren acil bir durumdur. SE konvulziv ve nonkonvulziv olarak ikiye ayrılabilsede tedavi prensipleri genellikle benzerdir. Tedavi bir an önce başlanarak, altta yatan neden düzeltilmelidir. İlk basamak tedavi daha düşük relaps riski nedeniyle i.v lorezapam olsa da ülkemizde bulunmadığından ilk seçenek diazepamdır. İntravenöz (IV) benzodiazepin nöbeti durdursa bile IV antiepileptik ilaç (Fenitoin vb.) yükleme dozunda uygulanmalıdır. Dirençli SE hastası, vital, respiratuvar, metabolik ve hemodinamik yönden desteklenmeli ve serebral elektriksel aktivitenin izlenmesi için yoğun bakım ünitesinde takip edilmelidir. Etiyolojideki en sık neden antiepileptik ilacın kesilmesidir. SE tedavisi ile nöbetin durdurulması, nöbet tekrarı ve komplikasyonların önlenmesi amaçlanmaktadır. Bu yazıda SE'nin güncel tanı, tedavi ve etiyolojisi değerlendirilmiştir.

show abstract

Transient loss of inhibition precedes spontaneous seizures after experimental status epilepticus

Cited by 24 publications

References 45 publications

Epigenetic Modulation of Seizure-Induced Neurogenesis and Cognitive Decline

Epigenetic Modulation of Seizure-Induced Neurogenesis and Cognitive Decline

Status epilepticus induces increasing neuronal excitability and hypersynchrony as revealed by optical imaging

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