Persistent postictal hyperperfusion demonstrated with PET

Tatlidil, Rozet

doi:10.1016/s0920-1211(00)00135-2

Cited by 17 publications

(13 citation statements)

References 14 publications

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“…Prior to this report the direction of postictal hemodynamic changes was unclear since conflicting reports indicated either postictal hypoperfusion (Rowe et al, 1991; Newton et al, 1992; Leonhardt et al, 2005) or hyperperfusion (Fong et al, 2000; Tatlidil, 2000; Hassan et al, 2012). This discordance is most likely explained by the variable timing of the single postictal scans.…”

Section: Discussionmentioning

confidence: 97%

“…It is well established that there is a dramatic, transient increase in blood flow during seizures (Gibbs et al, 1934; Penfield et al, 1939) with a corresponding decrease in oxygenation that quickly recovers (Bahar et al, 2006; Suh et al, 2006). The few studies that investigated changes in blood flow during the postictal period have not yielded consistent observations with reports of local hypoperfusion (Rowe et al, 1991; Newton et al, 1992; Leonhardt et al, 2005) and hyperperfusion (Fong et al, 2000; Tatlidil, 2000; Hassan et al, 2012). These inconsistencies were likely due to the variable time-points after the seizure when blood flow was measured.…”

Section: Introductionmentioning

confidence: 87%

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Postictal behavioural impairments are due to a severe prolonged hypoperfusion/hypoxia event that is COX-2 dependent

Farrell

Gaxiola‐Valdez

Wolff

et al. 2016

eLife

110

213

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Seizures are often followed by sensory, cognitive or motor impairments during the postictal phase that show striking similarity to transient hypoxic/ischemic attacks. Here we show that seizures result in a severe hypoxic attack confined to the postictal period. We measured brain oxygenation in localized areas from freely-moving rodents and discovered a severe hypoxic event (pO2 < 10 mmHg) after the termination of seizures. This event lasted over an hour, is mediated by hypoperfusion, generalizes to people with epilepsy, and is attenuated by inhibiting cyclooxygenase-2 or L-type calcium channels. Using inhibitors of these targets we separated the seizure from the resulting severe hypoxia and show that structure specific postictal memory and behavioral impairments are the consequence of this severe hypoperfusion/hypoxic event. Thus, epilepsy is much more than a disease hallmarked by seizures, since the occurrence of postictal hypoperfusion/hypoxia results in a separate set of neurological consequences that are currently not being treated and are preventable.DOI: http://dx.doi.org/10.7554/eLife.19352.001

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 87%

Postictal behavioural impairments are due to a severe prolonged hypoperfusion/hypoxia event that is COX-2 dependent

Farrell

Gaxiola‐Valdez

Wolff

et al. 2016

eLife

110

213

View full text Add to dashboard Cite

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“…Previous studies that examined blood flow during the postictal period in persons with epilepsy yielded inconsistent observations, with some reporting local hypoperfusion and others local hyperperfusion . To better understand postictal perfusion, Farrell et al .…”

Section: The Postictal Hypoperfusion/hypoxia Phenomenon In People Witmentioning

confidence: 99%

Postictal hypoperfusion/hypoxia provides the foundation for a unified theory of seizure‐induced brain abnormalities and behavioral dysfunction

et al. 2017

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A recent article by Farrell et al. characterizes the phenomenon, mechanisms, and treatment of a local and severe hypoperfusion/hypoxia event that occurs in brain regions following a focal seizure. Given the well-established role of cerebral ischemia/hypoxia in brain damage and behavioral dysfunction in other clinical settings (e.g., stroke, cerebral vasospasm), we put forward a new theory: postictal hypoperfusion/hypoxia is responsible for the negative consequences associated with seizures. Fortunately, inhibition of two separate molecular targets, cyclooxygenase-2 (COX-2) and l-type calcium channels, can prevent the expression of postictal hypoperfusion/hypoxia. These inhibitors are important experimental tools used to separate the seizure from the resulting hypoperfusion/hypoxia and can allow researchers to address the contribution of this phenomenon to negative outcomes associated with seizures. Herein we address the implications of this postictal stroke-like event in acute behavioral dysfunction (e.g., Todd's paresis) and sudden unexpected death in epilepsy (SUDEP). Moreover, anatomic alterations such as increased blood-brain barrier permeability, glial activation, central inflammation, and neuronal loss could also be a consequence of repeated hypoperfusion/hypoxic events and, in turn, underlie chronic interictal cognitive and behavioral comorbidities (e.g., memory deficits, anxiety, depression, and psychosis) and exacerbate epileptogenesis. Thus these seemingly disparate and clinically important observations may share a common point of origin: postictal hypoperfusion/hypoxia.

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“…Focal hyperperfusion in 123 I‐IMP SPECT persisted even during an asymptomatic period. It lasted too long to be considered to be a result of myoclonus, though hyperperfusion can last for several days as a result of anaerobically glycolysed products in epilepsy . These data suggest that hyperactivity occurs insidiously without symptoms, and causes TMA and sometimes its recurrence.…”

Section: Discussionmentioning

confidence: 97%

Transient myoclonic state with asterixis presenting as persistent hyperperfusion on single‐photon emission computed tomography: A case report

Umemura

Oeda

Sawada

2014

Neurology & Clinical Neurosc

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Transient myoclonic state with asterixis is characterized by sudden onset generalized myoclonus and asterixis without consciousness impairment. Electrophysiological studies have shown that myoclonus correlates with cortical hyperexcitability localized in the primary motor cortex during the symptomatic period. However, it is unclear whether this excitability remains in the asymptomatic period. Here, we report a 79-year-old Japanese man who presented with transient myoclonic state with asterixis. He had been diagnosed with progressive non-fluent aphasia and he suffered from rhythmic myoclonus; predominantly in the neck, shoulders and upper extremities. Asterixis was observed in the forearms. Brain 123 I-iodoamphetamine single-photon emission computed tomography showed focal hyperperfusion in the bilateral precentral gyri even at 3 months after remission of the myoclonus. These data suggest that cortical hyperactivity was persistent without symptoms and led to transient myoclonic state with asterixis, which could have been due to the underlying neurodegenerative disorder of progressive non-fluent aphasia.

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Persistent postictal hyperperfusion demonstrated with PET

Cited by 17 publications

References 14 publications

Postictal behavioural impairments are due to a severe prolonged hypoperfusion/hypoxia event that is COX-2 dependent

Postictal behavioural impairments are due to a severe prolonged hypoperfusion/hypoxia event that is COX-2 dependent

Postictal hypoperfusion/hypoxia provides the foundation for a unified theory of seizure‐induced brain abnormalities and behavioral dysfunction

Transient myoclonic state with asterixis presenting as persistent hyperperfusion on single‐photon emission computed tomography: A case report

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