The early-infantile epileptic encephalopathy with suppression-burst: Developmental aspects

Ohtahara, Shunsuke; Ohtsuka, Yoko; Yamatogi, Yasuko; Oka, Eiji

doi:10.1016/s0387-7604(87)80110-9

Cited by 131 publications

(74 citation statements)

References 1 publication

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“…To ensure that all of our experiments began with comparable magnitude perturbation to brain activity, we began each series of experiments with an isoflurane concentration of 1.75%, which reliably produced burst suppression, a pathological pattern of activity seen after trauma (2), anesthesia (11), hypothermia (12), encephalopathy (13), hypoxia (14), and others (e.g., Fig. 1A, blue trace).…”

Section: Significancementioning

confidence: 99%

Recovery of consciousness is mediated by a network of discrete metastable activity states

Hudson

Calderon

Pfaff

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

156

175

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It is not clear how, after a large perturbation, the brain explores the vast space of potential neuronal activity states to recover those compatible with consciousness. Here, we analyze recovery from pharmacologically induced coma to show that neuronal activity en route to consciousness is confined to a low-dimensional subspace. In this subspace, neuronal activity forms discrete metastable states persistent on the scale of minutes. The network of transitions that links these metastable states is structured such that some states form hubs that connect groups of otherwise disconnected states. Although many paths through the network are possible, to ultimately enter the activity state compatible with consciousness, the brain must first pass through these hubs in an orderly fashion. This organization of metastable states, along with dramatic dimensionality reduction, significantly simplifies the task of sampling the parameter space to recover the state consistent with wakefulness on a physiologically relevant timescale.anesthesia | state transitions | spectral analysis | emergence T he brain exhibits a remarkable ability to recover normal function associated with wakefulness, even after large perturbations to its activity. Two well-known examples of this are anesthesia and brain injury (1, 2). How the brain recovers from large perturbations currently is unknown. Given the number of neurons involved, the potential space of activity is huge. Thus, it is not clear how the brain samples the vast parameter space to discover patterns of activity that are consistent with consciousness after a large perturbation.The simplest possibility for the recovery of consciousness (ROC) is that, driven by noise inherent in many aspects of neuronal activity (3), the brain performs a random walk through the parameter space until it eventually enters the region that is consistent with consciousness. An alternative possibility is that although the motion through the parameter space is not random, the trajectory nonetheless is smooth. Lastly, it is possible that en route to ROC, the brain passes through a set of discrete metastable states-that is, a series of jumps between long-lived activity configurations.The utility of metastable intermediates to the problem of ROC is well illustrated by analogy with protein folding. Levinthal's paradox (4) refers to the implausibility of a denatured protein recovering its native fold conformation by random walk alone, as the time required to randomly explore the conformational space will rapidly exceed the age of the universe, even for a small number of residues. (ii), a "small-world" structure, in which most states are connected only locally whereas a few central hub states connect widely, allowing rapid long-distance travel through the network; and (iii) a lattice structure, in which all states have approximately the same connectivity, allowing multiple routes to ROC.In this report, we demonstrate that in rats under isoflurane anesthesia, ROC occurs after the brain traverses a series of metastable in...

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Section: Significancementioning

confidence: 99%

Recovery of consciousness is mediated by a network of discrete metastable activity states

Hudson

Calderon

Pfaff

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

156

175

View full text Add to dashboard Cite

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“…Accurate classification of children with newly diagnosed epilepsy into epilepsy syndromes has repeatedly proved to be feasible in >90% of cases (18,(86)(87)(88). Syndromes that carry the highest risk of refractoriness and are recognizable early include Ohtahara syndrome in neonates (89), West syndrome and severe myoclonic epilepsy in infants (90,91), myoclonic-astatic epilepsy (92), Lennox-Gastaut syndrome (93), Rasmussen encephalitis (94), and partial epilepsies due to malformations of cortical development whatever the age (95).…”

Section: Pediatric Issuesmentioning

confidence: 99%

Is Refractory Epilepsy Preventable?

et al. 2002

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Summary: About a third of the patients diagnosed with epilepsy will not be fully controlled with antiepileptic drugs (AEDs), and many of them will have frequent and disabling seizures. These patients will undergo multiple drug trials, most often without complete seizure remission. Moreover, refractory epilepsy is associated with increased morbidity (from seizures and medications), social isolation, unemployment, and overall reduced quality of life. There is evidence that refractory epilepsy can be a progressive disorder, which, if controlled early, might never develop into a full syndrome with all of its associated sequelae. The difficulty lies in identifying at an early stage patients who are likely to progress to intractability. No currently known markers enable clinicians to make this identification with confidence. Advances in pharmacogenomics and our understanding of pharmacologic responsiveness in epilepsy may change this situation. Even now, we are able to identify many patients with a poor prognosis earlier than before, particularly in the pediatric population, in which syndromic classification may provide an approach to predict intractability. The early initiation of aggressive therapy may improve outcome and overall quality of life.

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“…The EEG characterized by burst suppression pattern, with periods of suppression (4-12 sec) that are seen during sleep (68) . The etiology may be related to inborn error of metabolism especially propionic academia, non ketotic hyperglycinemia and D-glyceric acidemia (68)(69)(70) . The seizures are resistant to treatment, the infants are severely neurologically abnormal and they may die early in the first year of life.…”

Section: Causesmentioning

confidence: 99%

Neonatal Seizures

Al-Zwaini¹

2011

Epilepsy in Children - Clinical and Social Aspects

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The early-infantile epileptic encephalopathy with suppression-burst: Developmental aspects

Cited by 131 publications

References 1 publication

Recovery of consciousness is mediated by a network of discrete metastable activity states

Recovery of consciousness is mediated by a network of discrete metastable activity states

Is Refractory Epilepsy Preventable?

Neonatal Seizures

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