Neuroimaging of status epilepticus

Meletti, Stefano; Monti, Giulia; Mirandola, Laura; Vaudano, Anna Elisabetta; Giovannini, Giada

doi:10.1111/epi.14499

Cited by 45 publications

(57 citation statements)

References 34 publications

(34 reference statements)

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“…This retrospective long‐term follow‐up MRI study evaluated the timeline of MRI abnormalities in adult NORSE patients. The percentage of MRI abnormalities in NORSE patients in our study (82%) and other, previous studies (62%‐100%), 2,6–10 was higher than in the general population of SE patients (25%) 11 …”

Section: Discussioncontrasting

confidence: 44%

The timelines of MRI findings related to outcomes in adult patients with new‐onset refractory status epilepticus

et al. 2020

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Objective: To identify the timelines of magnetic resonance imaging (MRI) abnormalities and their relationships with the clinical outcomes of patients with new-onset refractory status epilepticus (NORSE). Methods: This retrospective observational study enrolled patients with NORSE who were admitted from March 2008 to July 2018. MRI abnormalities were analyzed visually with the readers blinded to the clinical characteristics of the patients. Poor functional outcome was defined as a Glasgow Outcome Scale score ≤ 3 at discharge. Subsequent pharmacoresistant epilepsy was defined as seizures not controlled by two or more anti-seizure medications 6 months after discharge. Results: Among 39 patients with NORSE, 32 (82.1%) exhibited an MRI abnormality. The most common abnormalities were persisting mesial temporal lobe signal abnormality (51.3%); initial diffuse leptomeningeal enhancement within 16 days from seizure onset (15/35, 42.9%); and hippocampal atrophy, which started to appear 26 days after seizure onset (15/26, 57.7%). Only three patients had claustrum abnormalities. Patients with insular involvement had longer treatment delay than those without (24.0 vs 5.5 hours, respectively, P = .02). Duration of status epilepticus (SE) tended to have a linear association with hippocampal atrophy (P = .055). Patients with diffuse leptomeningeal enhancement were more likely to have a poor functional outcome and to develop subsequent pharmacoresistant epilepsy than those without this finding (93.3% vs 15.0%, P < .001; 75.0% vs 22.2%, P = .004, respectively); the results were significant even after adjusting for age, sex, and duration of SE. Hippocampal atrophy and diffuse cortical atrophy were also significantly associated with poor functional outcomes (P = .001 and P = .002, respectively), and patients with these conditions were more likely to develop subsequent pharmacoresistant epilepsy than those without these conditions, after adjusting for age and sex (P = .035 and P = .048, respectively), but not after adjusting for duration of SE. Significance: Initial diffuse leptomeningeal enhancement and later hippocampal atrophy were associated with a poor functional outcome and subsequent pharmacoresistant epilepsy.

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Section: Discussioncontrasting

confidence: 44%

The timelines of MRI findings related to outcomes in adult patients with new‐onset refractory status epilepticus

et al. 2020

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“…66 Distinguishing clinically between postictal activity and nonconvulsive status epilepticus can be difficult, because clinical signs are often subtle and nonspecific and can occur both ictally and postictally. 80 Furthermore, in some critically ill patients, the transition from the ictal to the postictal state is more gradual, and patients can even enter a state known as the "ictal-interictal-continuum." 81 If the EEG shows focal or generalized periodic discharges with a frequency lower than 2.5 Hz or intermittent bursts of generalized spike-waves, postictal activity or nonconvulsive status epilepticus is not obvious, and evaluating the clinical response to antiepileptic medication is generally advised.…”

Section: Differentiation Bet Ween the Ictal Interictal And Postictal Statesmentioning

confidence: 99%

“…10,84,85 In one study, ictal hyperperfusion was followed by postictal hypoperfusion (T1). 10 Ictal hyperperfusion has been related to increased glucose and oxygen demand, 80 which sometimes also manifested postictally, leading to contradicting findings. 86 In a patient with epilepsy after encephalitis and postictal psychosis, hyperperfusion in the right temporal lobe and left basal ganglia manifested, indicating the possible relevance of increased cerebral blood flow in postictal psychosis (T2).…”

Section: Spectmentioning

confidence: 99%

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The postictal state — What do we know?

et al. 2020

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This narrative review provides a broad and comprehensive overview of the most important discoveries on the postictal state over the past decades as well as recent developments. After a description and definition of the postictal state, we discuss postictal sypmtoms, their clinical manifestations, and related findings. Moreover, pathophysiological advances are reviewed, followed by current treatment options. K E Y W O R D S epilepsy, postictal suppression, postictal symptoms, postictal treatment, SUDEPThis is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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“…It has been theorized that the damage induced by SE is caused not only by the excessive neuronal activation directly leading to excitotoxicity, but may also be due to an imbalance between oxygen and glucose requirements and su cient brain perfusion during SE [7]. Perfusion-weighted magnetic resonance imaging (MRI) may be used to investigate perfusion changes during SE in patients or animal models [7], but needs to be performed under general anesthesia during data acquisition to immobilize the subject. As anesthesia is known to in uence brain perfusion [8], this most probably in uences study outcome.…”

Section: Introductionmentioning

confidence: 99%

99mTc-HMPAO SPECT imaging reveals brain hypoperfusion during status epilepticus

Bascuñana

Wolf

Jahreis

et al. 2020

Preprint

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Status epilepticus (SE) is a clinical emergency with high mortality. SE can trigger neuronal death or injury and alteration of neuronal networks resulting in long-term cognitive decline or epilepsy. Among the multiple factors contributing to this damage, imbalance between oxygen and glucose requirements and brain perfusion during SE has been proposed. Herein, we aimed to quantify by neuroimaging the spatiotemporal course of brain perfusion during and after lithium-pilocarpine-induced SE in rats. To this purpose, animals underwent 99mTc-HMPAO SPECT imaging at different time points during and after SE using a small animal SPECT/CT system. 99mTc-HMPAO regional uptake was normalized to the injected dose. In addition, voxel-based statistical parametric mapping was performed. SPECT imaging showed an increase of cortical perfusion before clinical seizure activity onset followed by regional hypo-perfusion starting with the first convulsive seizure and during SE. Twenty-four hours after SE, brain 99mTc-HMPAO uptake was widely decreased. Finally, chronic epileptic animals showed regionally decreased perfusion affecting hippocampus and cortical sub-regions. Despite elevated energy and oxygen requirements, brain hypo-perfusion is present during SE. Our results suggest that insufficient compensation of required blood flow might contribute to the neuronal damage and neuroinflammation, and ultimately to chronic epilepsy generated by SE.

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Neuroimaging of status epilepticus

Cited by 45 publications

References 34 publications

The timelines of MRI findings related to outcomes in adult patients with new‐onset refractory status epilepticus

The timelines of MRI findings related to outcomes in adult patients with new‐onset refractory status epilepticus

The postictal state — What do we know?

99mTc-HMPAO SPECT imaging reveals brain hypoperfusion during status epilepticus

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