A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus

doi:10.1016/0920-1211(90)90065-4

Epilepsy Research

Volume 5, Issue 1, January–February 1990, Pages 49-60

https://doi.org/10.1016/0920-1211(90)90065-4 Get rights and content

Abstract

Review of 60 electroencephalograms recorded during episodes of generalized convulsive status epilepticus suggested that there are 5 identifiable EEG patterns which occur in a predictable sequence during the course of generalized convulsive status epilepticus in man: (1) discrete seizures; (2) merging seizures with waxing and waning amplitude and frequency of EEG rhythms; (3) continuous ictal activity; (4) continuous ictal activity punctuated by low voltage ‘flat periods’: and (5) periodic epileptiform discharges on a ‘flat’ background. We confirmed our hypothesis that this sequence represents the natural history of electroencephalographic changes in untreated generalized convulsive status epilepticus by observing the same sequence in the EEGs of rats in which status epilepticus and been induced by 3 different methods; (1) systemic administration of kainic acid, (2) injection of homocysteine thiolactone to cobalt-lesioned rats; and (3) injection of lithium chloride followed 24 h later by injection of pilocarpine.

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Clinicians have treated super refractory status epilepticus (SRSE) with electroconvulsive therapy (ECT); however, data supporting the practice are scant and lack rigorous evaluation of continuous electroencephalogram (cEEG) changes related to therapy. This study aims to describe a series of patients with SRSE treated at our institution with ECT and characterize cEEG changes using a blinded review process.
We performed a single-center retrospective study of consecutive patients admitted for SRSE and treated with ECT from January 2014 to December 2022. Our primary outcome was the resolution of SRSE. Secondary outcomes included changes in ictal-interictal EEG patterns, anesthetic burden, treatment-associated adverse events, and changes in clinical examination. cEEG was reviewed pre- and post-ECT by blinded epileptologists.
Ten patients underwent treatment with ECT across 11 admissions (8 female, median age 57 years). At the time of ECT initiation, nine patients had ongoing SRSE while two had highly ictal patterns and persistent encephalopathy following anesthetic wean, consistent with late-stage SRSE. Super-refractory status epilepticus resolution occurred with a median time to cessation of 4 days (interquartile range [IQR]: 3–9 days) following ECT initiation. Background continuity improved in five patients and periodic discharge frequency decreased in six. There was a decrease in anesthetic use following the completion of ECT and an improvement in neurological exams. There were no associated adverse events.
In our cohort, ECT was associated with improvement of ictal-interictal patterns on EEG, and resolution of SRSE, and was not associated with serious adverse events. Further controlled studies are needed.
Is Socrates a cat? False EEG syllogisms in critically ill patients
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Progress in modelling of brain dynamics during anaesthesia and the role of sleep-wake circuitry
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General anaesthesia is used widely in surgery and during interventional medical procedures, but little is known about the exact neural mechanisms for how unconsciousness arises from administering an anaesthetic drug. Computational modelling of brain dynamics has already provided valuable insights into the neural circuitry involved in generating this state. Current theories for the origin of electroencephalographic (EEG) features in brain activity under GABAergic anaesthetic drugs have been proposed through modelling results. While much attention has been paid to describing alpha and delta oscillations, burst suppression, paradoxical excitation and the possibility of hysteresis during transitions to and from unconscious state, these models have focused only on the role of the thalamocortical system. Recent empirical findings suggest that anaesthetic drugs may act directly on the neural circuitry regulating sleep and wake states and circadian rhythms in the hypothalamus. Coupled with the common behavioural features found in physiological sleep and general anaesthesia, this evidence serves as a foundation for the ‘shared circuits hypothesis’ which proposes that anaesthetic-induced unconsciousness arises predominantly through modulation of the hypothalamic sleep-wake switch. This paper reviews the key findings from computational models describing brain states during the administration of anaesthetic drugs, with a focus on those enhancing GABAergic inhibition given their widespread use in practice and that almost all models of anaesthesia have focused on these drugs. We draw physiological and behavioural links between brain states during sleep and anaesthesia, and aim to highlight the importance of computational modelling in advancing our understanding of anaesthesia by considering sleep and circadian mechanisms in generating unconsciousness in future work.
Lateralized Periodic Discharges: Which patterns are interictal, ictal, or peri-ictal?
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There is an ongoing debate if Lateralized Periodic Discharges (LPDs) represent an interictal pattern reflecting non-specific but irritative brain injury, or conversely, is an ictal pattern. The challenge is: how to correctly manage these patients? Between this apparent dichotomous distinction, there is a pattern lying along the interictal-ictal continuum (IIC) that we may call “peri-ictal”. Peri-ictal means that LPDs are temporally associated with epileptic seizures (although not necessarily in the same recording). Their recognition should lead to careful EEG monitoring and longer periods of video-EEG to detect seizure activity (clinical and/or subclinical seizures). In order to distinguish which kind of LPDs should be considered as representing interictal/irritative brain injury versus ictal/peri-ictal LPDs, a set of criteria, with both clinical/neuroimaging and EEG, is proposed. Among them, the dichotomy LPDs-proper versus LPDs-plus should be retained. Spiky or sharp LPDs followed by associated slow after-waves or periods of flattening giving rise to a triphasic morphology should be included in the definition of LPDs-plus. We propose defining a particular subtype of LPDs-plus that we call “LPDs-max”. The LPDs-max pattern corresponds to an ictal pattern, and therefore, a focal non-convulsive status epilepticus, sometimes associated with subtle motor signs and epileptic seizures. LPDs-max include periodic polyspike-wave activity and/or focal burst-suppression-like patterns. LPDs-max have a posterior predominance over the temporo-parieto-occipital regions and are refractory to antiseizure drugs. Interpretations of EEGs in critically ill patients require a global clinical approach, not limited to the EEG patterns. The clinical context and results of neuroimaging play key roles.
The efficacy of fructose-1,6-bisphosphate in suppressing status epilepticus in developing rats
2020, Epilepsy Research
Treatment of pediatric status epilepticus (SE) remains challenging as up to 50 % of patients are refractory to conventional anti-seizure medications. The glycolytic intermediate, fructose-1,6-bisphosphate (FBP), has been reported to exert significant anticonvulsant effects in both adult animals and in in vitro models of seizures. This study aims to examine FBP efficacy in controlling seizures in a rat model of juvenile SE.
Sprague Dawley rats (P11-P17) were injected with pilocarpine (300 mg/kg, i.p.) to induce SE, which was monitored by video-electroencephalography (v-EEG). Thirty minutes into SE, FBP was administrated (500 or 1000 mg/kg, i.p.). v-EEG recording was continued for ∼60 additional minutes to assess the anticonvulsant effect of FBP, compared with vehicle (saline) treatment.
SE consistently occurred in rat pups 10−15 min after pilocarpine injection and persisted over the 90-min recording period. Neither saline nor a lower dose of FBP (500 mg/kg) treatment stopped behavioral and electrographic seizures. At higher doses (1000 mg/kg), FBP terminated SE in ∼15 min in 60 % (6 of 10) of the rat pups.
The endogenous glycolytic metabolite, FBP, promptly suppresses ongoing seizure activity and represents a potential alternative metabolic therapy to improve the treatment of SE in the juvenile age range.
Kainic acid-induced status epilepticus decreases mGlu<inf>5</inf> receptor and phase-specifically downregulates Homer1b/c expression
2020, Brain Research
Citation Excerpt :
Establishment of the SE was confirmed via behavioral output, such as head nodding, sniffing, behavioral arrest, wet dog shakes, excessive salivation and repetitive chewing, repeatedly interrupted by generalized convulsive seizures. Then, all the differential stages of SE were detected in the KA-induced rats via sequential electrographic patterns after a normal EEG; (i) discrete seizures with inter-ictal slowing, (ii) merging seizures with waxing and waning amplitude and frequency of EEG rhythm, (iii) continuous ictal activity, (iv) continuous ictal activity interrupted by low voltage flat periods and (v) periodic epileptiform discharges (Treiman et al., 1990) (data not shown). The EEGs were continuously recorded in the KA-induced SE animals until day 10 (T10; late latent phase), between day 49 and day 80 (T80; early exponential growth phase) or between day 89 and day 120 (T120; late exponential growth phase) post-SE.
Globally, over 50 million people are affected by epilepsy, which is characterized by the occurrence of spontaneous recurrent seizures. Almost one-third of the patients show resistance to current anti-epileptic drugs, making the exploration of new molecular targets necessary. An interesting target may be Homer1, due to its diverse roles in epileptogenesis and synaptic plasticity. Indeed, Homer1 regulates group I metabotropic glutamate (mGlu) receptors (i.e. mGlu₁ and mGlu₅) scaffolding and signaling in neurons. In the present work, using the systemic kainic acid (KA)-induced status epilepticus (SE) model in adult rats, we investigated the mRNA and protein expression patterns of the mGlu₅ receptor, Homer1a and Homer1b/c at 10, 80 and 120 days post-SE (i.e. T10, T80 and T120). Epileptogenesis was validated by electrophysiological recordings of seizures via electroencephalography (EEG) monitoring and through upregulation of glial fibrillary acidic protein. At the protein level, the mGlu₅ receptor was downregulated in the late latent phase (T10) and the early- and late exponential growth phase (T80 and T120, respectively), which was best observed in the hippocampal CA1 region. At mRNA level, significant downregulation of the mGlu₅ receptor was only detected in the late exponential growth phase. Homer1a expression did not change at any investigated time point. Interestingly, Homer1b/c was only downregulated in the late latent phase, a period where spontaneous seizures are extremely rare. Thus, this phase-specific downregulation may be indicative of an endogenous neuroprotective mechanism. In conclusion, these results suggest that Homer1b/c may be an interesting molecular target to prevent epileptogenesis and/or control seizures.

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^☆: Presented in part at the 39th Annual Meeting of the American Academy of Neurology, New York, NY, April 1987.

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Research reportA progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus☆

Abstract

Neuroscience

Epilepsy Res.

Brain Res. Bull.

Epilepsy Res.

Exp. Neurol.

A pneumoencephalographic demonstration of brain atrophy following status epilepticus

Dev. Med. Child. Neurol.

Convulsive status epilepticus in infants and children. A study of 239 cases

Epilepsia

A proposal for standard montages to be used in clinical EEG

J. Clin. Neurophysiol.

Effects of bicuculline-induced seizures on cerebral metabolism and circulation of rats rendered hypoglycemic by starvation

Ann. Neurol.

Research report
A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus☆