Corticosteroids including ACTH for childhood epilepsy other than epileptic spasms

Gayatri, NA; Ferrie, Colin D.; Cross, Helen HJ

doi:10.1002/14651858.cd005222.pub2

Cited by 26 publications

(27 citation statements)

References 19 publications

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“…This positive global outcome was associated with reductions in both seizure frequency and interictal EEG abnormalities. Although the Cochrane review on corticosteroids for childhood epilepsy other than epileptic spasms found no evidence for their efficacy or safety in treating childhood epilepsies (Gayatri et al, 2007), our results, along with those of other case reports and retrospective studies on this therapeutic option (Aykut-Bingol et al, 1996;Tsuru et al, 2000;Okuyaz et al, 2005; Steroid pulse therapy in epilepsy © C I C E d i z i o n i I n t e r n a z i o n a l i Sevilla-Castillo et al, 2009;Lichtenfeld et al, 2010;Heyman et al, 2012), confirm the usefulness of this approach. In particular, Heyman et al (2012) found clinical and electroencephalographic improvements in more than 50% of patients; both Aykut-Bingol et al (1996) and Tsuru et al (2000) reported suppression of EEG abnormalities and language improvement in Landau-Kleffner patients.…”

Section: Discussionmentioning

confidence: 99%

Intravenous methylprednisolone pulse therapy for children with epileptic encephalopathy

Pera

Randazzo

Masnada

et al. 2015

Functional Neurology

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SummaryThe aim of this retrospective study of children affected by epileptic encephalopathy was to evaluate seizure frequency, electroencephalographic pattern and neuropsychological status, before and after intravenous methylprednisolone therapy. Eleven children with epileptic encephalopathy were administered one cycle of intravenous methylprednisolone (15-30 mg/kg/day for three consecutive days, once a month for four months) in addition to constant dosages of their regular antiepileptic drugs. The treatment resulted in statistically significant reductions of generalized slow spike-and-wave discharges (p<0.0028) and seizure frequency (p<0.013), which persisted even after methylprednisolone pulse therapy was stopped. A globally positive outcome was noted in 9/11 patients (81.8%). This methylprednisolone treatment regimen did not cause significant or persistent adverse effects. We suggest that children with epileptic encephalopathy without an underlying structural lesion could be the best candidates for intravenous methylprednisolone pulse therapy.

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Section: Discussionmentioning

confidence: 99%

Intravenous methylprednisolone pulse therapy for children with epileptic encephalopathy

Pera

Randazzo

Masnada

et al. 2015

Functional Neurology

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“…164 Well-controlled, blinded studies have been published for the use of ACTH and steroids for infantile spasms; 161,170–172 however, a Cochrane Collaboration review on the use of ACTH for other childhood epilepsies, published in 2007, found only a single randomized controlled trial, which only included five patients. 173 The authors of this review concluded that, at present, no evidence exists to support either the safety or the efficacy of ACTH for general pediatric epilepsies. 173 …”

Section: Immune and Anti-inflammatory Therapiesmentioning

confidence: 96%

“…173 The authors of this review concluded that, at present, no evidence exists to support either the safety or the efficacy of ACTH for general pediatric epilepsies. 173 …”

Section: Immune and Anti-inflammatory Therapiesmentioning

confidence: 96%

The role of inflammation in epilepsy

French²,

et al. 2010

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Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the ≈30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators—released by brain cells and peripheral immune cells—in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis.

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“…Exogenous melanocortins may markedly influence the behavior, although the role of endogenous melanocortins is doubtful in this respect (Bertolini et al 2009). These extra-adrenal effects of ACTH are worth to consider not only for research purposes, but also during the increasing number of diagnostic and therapeutic usage of ACTH, e.g., infant spasm (Mikati et al 2002), epilepsy (Gayatri et al 2007), and lipid-lowering activity (Thorisdottir et al 2009). …”

Section: Acth-independent Regulation Of the Corticosterone Secretionmentioning

confidence: 99%

The Vasopressin-Deficient Brattleboro Rat: Lessons for the Hypothalamo–Pituitary–Adrenal Axis Regulation

et al. 2012

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Adaptation to stress is indispensable to life and the hypothalamo-pituitary-adrenocortical axis is one of the major components of the adaptation. The hypothalamic component consists of corticotropin-releasing hormone and arginine vasopressin, with a questionable contribution of the latter. Vasopressin was more important in the regulation of the adrenocorticotropin secretion in the perinatal vasopressin-deficient Brattleboro rats than in adulthood, where its role depended on the nature of the stressor encountered. In adults, the vasopressin deficiency did not influence the development of chronic stress response. In the neonatal rats, the role of vasopressin was supported by the inhibitory action of a V1b antagonist and vasopressin antiserum. As the corticosterone response to stress did not follow the adrenocorticotropin levels, we assume the presence of an adrenocorticotropin independent adrenal gland regulation in the neonates. We have shown that the apparent dissociation of the corticosterone and adrenocorticotropin responses is not due to the different time course of the two hormone responses, to different level of the corticosterone binding globulin or to changes in the adrenal gland sensitivity. In vitro experiments point to the contribution of beta-adrenoceptors in the process. It was also confirmed by in vivo tests using the vasopressin-deficient Brattleboro pup as a model organism, where corticosterone levels may rise without adrenocorticotropin level changes. Another important question is the role of adrenocorticotropin beyond the corticosterone secretion regulation, which could be supposed, e.g., in cardiovascular events, immunological processes, and metabolism. We can conclude that Brattleboro rats gave us much information about the stress-axis regulation far beyond the role of vasopressin itself.

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Corticosteroids including ACTH for childhood epilepsy other than epileptic spasms

Cited by 26 publications

References 19 publications

Intravenous methylprednisolone pulse therapy for children with epileptic encephalopathy

Intravenous methylprednisolone pulse therapy for children with epileptic encephalopathy

The role of inflammation in epilepsy

The Vasopressin-Deficient Brattleboro Rat: Lessons for the Hypothalamo–Pituitary–Adrenal Axis Regulation

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