Postictal Effects Research Articles

Influence of Febrile Seizure in Children’s Neurodevelopment

Background: Febrile seizure is one of the most common diseases in early childhood. The impact of early-life Febrile Seizure on the developing brain is an important issue to detect.
 Objectives: To observe the neurodevelopment of children suffering from different types of febrile seizures.
 Methods: This was a prospective observational study; the study was conducted in Dhaka Shishu (Children) Hospital, Dhaka from July 2012 to August 2013. Total 71 children were included in the study who fulfilled the selection criteria. History was taken thoroughly. Rapid neurodevelopmental assessment (RNDA) was performed for initial assessment and subsequent follow up and was advised accordingly.
 Results: Total 71 cases were included where mean age was 17.76±8.03 months, median was 16 months; in both the group male child had slight high preponderance. Majority of seizures were <10 minutes duration in both group which was not statistically significant. Important postictal event was found, 12 cases (26.7%) in simple seizure and 16 cases (61.5%) in complex seizures which was found statistically significant, but there was no risk for further seizure. On follow up, RNDA detected risk of impairment in vision, cognition, speech and behavior. In complex group statistically significant association was found with impairment of cognition only at initial and follow up at 3 month.
 Conclusion: Neurodevelopment impairment is not influenced by types of febrile seizure but significant cognitive impairment was found in complex seizure.
 DS (Child) H J 2021; 37(1): 45-50

Edema Resolution and Clinical Assessment in Poor-Grade Subarachnoid Hemorrhage: Useful Indicators to Predict Delayed Cerebral Infarctions?

Background: The level of consciousness and cerebral edema are among the indicators that best define the intensity of early brain injury following aneurysmal subarachnoid hemorrhage (aSAH). Although these indicators are usually altered in patients with a poor neurological status, their usefulness for selecting patients at risk of cerebral infarction (CI) is not well established. Furthermore, little is known about the evolution of these indicators during the first week of post-ictal events. Our study focused on describing the association of the longitudinal course of these predictors with CI occurrence in patients with severe aSAH. Methods: Out of 265 aSAH patients admitted consecutively to the same institution, 80 patients with initial poor neurological status (WFNS 4–5) were retrospectively identified. After excluding 25 patients with early mortality, a total of 47 patients who underwent early CT (<3 days) and late CT (<7 days) acquisitions were included in the study. Early cerebral edema and delayed cerebral edema were calculated using the SEBES score, and the level of consciousness was recorded daily during the first week using the Glasgow Coma Scale (GCS). Results: There was a significant improvement in the SEBES (Early-SEBES median (IQR) = 3 (2–4) versus Delayed-SEBES = 2 (1–3); p = 0.001) and in GCS scores (B = 0.32; 95% CI 0.15–0.49; p = 0.001) during the first week. When comparing the ROC curves of Delayed-SEBES vs Early-SEBES as predictors of CI, no significant differences were found (Early-SEBES Area Under the Curve: 0.65; Delayed-SEBES: 0.62; p = 0.17). Additionally, no differences were observed in the relationship between the improvement in the GCS across the first week and the occurrence of CI (p = 0.536). Conclusions: Edema and consciousness level improvement did not seem to be associated with the occurrence of CI in a surviving cohort of patients with severe aSAH. Our results suggest that intensive monitoring should not be reduced in patients with a poor neurological status regardless of an improvement in cerebral edema and level of consciousness during the first week after bleeding.

Transcranial focal electrical stimulation via concentric ring electrodes in freely moving cats: Antiepileptogenic and postictal effects

Transcranial focal electrical stimulation (TFS) via tripolar concentric ring electrodes (TCRE), tripolar TFS, is proposed to treat pharmacoresistant epilepsy. We determined the effect of tripolar TFS on electrical amygdaloid kindling (AK) in freely moving cats. Fifteen cats were bilaterally implanted with electrodes in the amygdala (AM) and prefrontal cortex and assigned to three groups: the control group, which only received AK; the tripolar TFS before AK group, in which TCREs were placed over the vertex and tripolar TFS (300 Hz, 200 μs biphasic equal charge, square pulses) was delivered for 40 min just prior to AK; and the tripolar TFS after AK group, in which the TCREs were placed over the temporal bone ipsilateral to the kindled AM, while tripolar TFS was administered for 2 min just after AK onset for 40 days, and, thereafter, only AK was applied. AK was applied daily until all animals reached kindling stage VI. A three concentric spheres finite element cat head model was developed to analyze the electric fields caused by tripolar TFS. Tripolar TFS after AK inhibited kindling development. Animals with tripolar TFS after AK remained at the focal seizure stages for 20 days after tripolar TFS cessation and required 80.0 ± 15.42 AK stimulations to reach stage VI, significantly higher than TFS before AK, and control (P < .001). Tripolar TFS before AK did not show signs of protection against epileptogenesis. The finite modeling of tripolar TFS showed that the electric field is >0.3 mV/mm at depths less than approximately 12.6 mm in the cat brain, which should be strong enough to alter brain activity. In conclusion, tripolar TFS applied via a TCRE over the ipsilateral temporal area significantly delayed AK. This taken together with other reports of tripolar TFS aborting seizures in acute seizure models suggests that tripolar TFS is a promising new modality that should be considered for further testing.

Obstructive apnea due to laryngospasm links ictal to postictal events in SUDEP cases and offers practical biomarkers for review of past cases and prevention of new ones.

Seizure spread into autonomic and respiratory brainstem regions is thought to play an important role in sudden unexpected death in epilepsy (SUDEP). As the clinical dataset of cases of definite SUDEP available for study grows, evidence points to a sequence of events that includes postictal apnea, bradycardia, and asystole as critical events that can lead to death. One possible link between the precipitating seizure and the critical postictal sequence is seizure-driven laryngospasm sufficient to completely obstruct the airway for an extended period, but ictal laryngospasm is difficult to fully assess. Herein, we demonstrate in a rat model how the electrical artifacts of attempts to inspire during airway obstruction and features of the cardiac rhythm establish this link between ictal and postictal activity and can be used as practical biomarkers of obstructive apnea due to laryngospasm or other causes of airway obstruction.

Impairment of Dynamic Pressure Autoregulation Precedes Clinical Deterioration after Aneurysmal Subarachnoid Hemorrhage.

This study was designed to evaluate the potential of the dynamic autoregulation index (ARI) to serve as an early warning system for an imminent clinical deterioration after subarachnoid hemorrhage (SAH). All patients received a baseline digital subtraction angiography and a computed tomography (CT) prior to treatment. The clinical status, the ARI, and the transcranial Doppler (TCD) values were evaluated daily until discharge from the intensive care unit (ICU). A CT scan at least 10 days after the postictal event was used to determine the occurrence of delayed infarcts. 20 patients were prospectively included in the study. 3 refused further participation between days 2 and 3. Patients with no significant deteriorations of the clinical status and no proximal vasospasm (VS) in the middle cerebral artery (MCA)/delayed infarcts showed a significant positive linear regression of the ARI values in both hemispheres from day 1 till 11 (ARI right: 2.7 + .31/day, ARI left: 2.8 + .27/day; P < .01). All patients with angiographic VS of more than one-third in the MCA showed a corresponding drop of the ARI to values ≤1.7. The ARI drop occurred 2.5 (±1.3) days prior to significant deteriorations of the clinical status, increase of TCD values or the detection of angiographic cerebral VS/delayed infarcts in the corresponding hemispheres. The results demonstrate the capability of the ARI to serve as a reliable early warning system after SAH. Further trials with larger study populations are needed to validate these promising preliminary data.

Anesthesia for electroconvulsive therapy: A Noble approach

Electroconvulsive therapy (ECT) has always proved to be an effective mode of therapy in the field of Psychiatry. Modified ECT is applied in the form of electrical stimulus to the central nervous system; it is associated with acute physiologic response leading to autonomic nervous system stimulation with an initial parasympathetic stimulation followed by a more prominent sympathetic response as well as post-ictal effects like confusion and delirium. The factors governing the efficacy of Modified ECT are the strength of electrical current applied and the duration of the seizure activity. Modified ECT requires the use of general anesthesia and many of the anesthetic drugs also have an effect on the duration of seizure and could adversely affect the efficacy of the Modified ECT treatments. Therefore, there has to be a delicate balance between achieving an adequate anesthetic state and optimal duration of seizure activity.

Risk of severe and repetitive traumatic brain injury in persons with epilepsy: A population-based case–control study

BackgroundWhile traumatic brain injury (TBI) can lead to epilepsy, individuals with preexisting epilepsy or seizure disorder (ESD), depending on the type of epilepsy and the degree of seizure control, may have a greater risk of TBI from seizure activity or medication side effects. The joint occurrence of ESD and TBI can complicate recovery as signs and symptoms of TBI may be mistaken for postictal effects. Those with ESD are predicted to experience more deleterious outcomes either because of having a more severe TBI or because of the cumulative effects of repetitive TBI. MethodsWe conducted a case–control study of all emergency department visits and hospital discharges for TBI from 1998 through 2011 in a statewide population. The severity of TBI, repetitive TBI, and other demographic and clinical characteristics were compared between persons with TBI with preexisting ESD (cases) and those without (controls). Significant differences in proportions were evaluated with confidence intervals. Logistic regression was used to examine the association of the independent variables with ESD. ResultsDuring the study period, 236,164 individuals sustained TBI, 5646 (2.4%) of which had preexisting ESD. After adjustment for demographic and clinical characteristics, cases were more likely to have sustained a severe TBI (OR=1.49; 95% CI=1.38–1.60) and have had repetitive TBI (OR=1.54; 95% CI=1.41–1.69). ConclusionThe consequences of TBI may be greater in individuals with ESD owing to the potential for a more severe or repetitive TBI. Seizure control is paramount, and aggressive management of comorbid conditions among persons with ESD and increased awareness of the hazard of repetitive TBI is warranted. Furthermore, future studies are needed to examine the long-term outcomes of cases in comparison with controls to determine if the higher risk of severe or repetitive TBI translates into permanent deficits.

Sensitivity testing of the Seizure Severity Questionnaire (SSQ)

The sensitivity of the Seizure Severity Questionnaire (SSQ) was evaluated using pooled data from open-label extensions of two clinical trials in patients with partial-onset seizures. The SSQ includes questions relating to frequency and helpfulness of warning signs as well as frequency, severity, and bothersomeness of ictal and postictal effects. Differences between mean change from baseline for each SSQ item for responders and nonresponders were described and compared between patients solely with complex partial seizures (CPSs: responders, n=166; nonresponders, n=127) and those solely with secondarily generalized partial seizures (SGPSs: responders, n=26; nonresponders, n=24) at baseline. Seizure Severity Questionnaire total score and individual SSQ items related to ictal movement, consciousness, bothersomeness of postictal effects, and frequency of postictal emotional effects showed differentiation between seizure type responders. These data provide further validation of the SSQ by demonstrating its sensitivity in describing treatment effects.

What is the cause of post-traumatic stress disorder following subarachnoid haemorrhage? Post-ictal events are key

Post-traumatic stress disorder (PTSD) is common after subarachnoid haemorrhage (SAH) and causes poor outcome. Knowing which SAH events cause the stress leading to PTSD development could allow for their severity, and so the chances of PTSD, to be reduced. The dramatic nature of SAH onset has meant ictal events have been the presumed cause. Frequent loss of consciousness (LOC) at ictus, and presumed resultant amnesia, however, means this might not be correct. We examined two hypotheses for how SAH patients develop PTSD despite frequent LOC. Firstly, has the frequency of amnesia for ictal events subsequent to LOC been overestimated? Secondly, is it the stress of post-ictal events, rather than ictal events, which causes PTSD? Sixty SAH patients, 18 months post-ictus, were assessed for PTSD, LOC at ictus, memory for ictal events, as well as which aspects of their SAH, ictal and post-ictal, were psychologically stressful. Patients also underwent neuropsychological examination. Of patients, 36.7% had PTSD. Memory overall for ictal events was more common than expected: 50% reported LOC, and only 18% reported no memory. However, memory was not associated with PTSD development. Rather, the key predictor of PTSD was the stress of post-ictal events. The stress of ictal events, cognitive impairment and clinical characteristics were unrelated to PTSD development. Post-ictal events included realizing that their life could have/had changed, that they may have been left with long-term problems, that they could have died and that they had little memory for some SAH events and regaining consciousness. The traumatic quality of an SAH lies in post-ictal events, rather than ictal events. These events are related to the patients' adjustment to the experience of having had an SAH. Reducing the traumatic severity of these events could potentially reduce the likelihood of PTSD in SAH patients and so improve their outcome.

Introduction

Several observations make it worthwhile to take a closer look at postictal events, which are defined as manifestations of seizure-induced reversible alterations in neuronal function. The postictal period may adversely affect the quality of life, considering the duration and severity of postictal events. The postictal period is often longer than the seizure itself. Postictal events such as psychosis, confusion, aphasia, and paresis can be incapacitating. On a more positive side, the increased seizure threshold seen during the postictal period may offer clues for development of more effective seizure treatment. In this issue, experts in the field elucidate the postictal period from different viewpoints, including the mechanism of the postictal period, its diagnostic challenges, and its management.

Cerebrospinal fluid and serum NT-proBNP concentrations in children with epilepsy

The cardio-neuro-endocrine axis seems to be involved in the cascade of postictal events in children. The aim of this study was to assess the relationship between childhood epilepsy and cerebrospinal fluid (CSF) or serum concentrations of the N-terminal pro B-type natriuretic peptide (NT-proBNP) interictally. A total of seventy-four children agreed to participate in the study. Twenty-two children with epilepsy and mild developmental delay (mean+/-SD [median] age 5.8+/-4.9 [4.3] years), 15 children with newly diagnosed multiple sclerosis (MS) (15.1+/-1.4 [15.3] years) and 37 children with cryptogenic mild developmental delay (8.0+/-4.6 [7.4] years), serving as controls, were eligible. In children with epilepsy, interictal CSF NT-proBNP concentrations were greater when compared to the MS group and to controls (mean+/-SD [median] 193.0+/-78.1 [176.0]ng/L vs. 147.8+/-60.2 [138.0]ng/L vs. 140.4+/-36.5 [134.0]ng/L; p=0.014 and p=0.009). In contrast, serum NT-proBNP concentrations and the CSF/serum NT-proBNP ratio did not differ between groups. Greater CSF NT-proBNP concentrations in children with epilepsy may reflect an unspecific activation of the cardio-neuro-endocrine system involving endocrinological stress-response mechanisms interictally. The relationship between epilepsy and the cardio-neuro-endocrine axis may further the understanding of seizure susceptibility in children as well as influences of epilepsy on central modulation of autonomic cardiovascular control.

Sleep apnea as a transient, post-ictal event: Report of a case

A 53-year-old epileptic man had two seizures during polysomnography. Significant sleep apnea followed each (apnea-hypopnea indices (AHIs) of 22 and 20.4 for the 2 h following seizure one and 47.7 for the 53 min following seizure two). Lower hourly AHIs (range: 6.0-14.1) occurred for the remainder of the study. Results were not position-dependent. This suggests that epilepsy can transiently worsen sleep apnea, with implications for treatment.

Effect of epilepsy, seizures and epileptiform EEG discharges on cognitive function.

Patients with an established diagnosis of epilepsy were included in three groups on the basis of the absence (Group 2) or presence (Group 3) of epileptiform EEG discharges or subtle seizures (Group 4) during the cognitive assessment procedure. A separate age-matched non-epileptic control group (Group 1) was formed. Twenty-five patients were included in each of the four groups. Thus, a total of 100 patients were investigated. The patients were assessed with continuous 21-channel EEG and video-monitoring, combined with cognitive testing. The results show consistently lower performance on cognitive tests for Group 4, the group with subtle seizures. The difference with the control group was significant for the intelligence subtests and for the complex information processing test (p < 0.05). No transient cognitive impairment was found. The results are discussed in the light of possible factors that may be responsible for the lower test-scores in the patients of Group 4: both the ictal effects of the seizures themselves, postictal effects and the effects of the epileptiform EEG discharges may have had an impact on cognitive performance. Finally the absence of evidence for transient cognitive impairment in a group with frequent epileptiform EEG discharges is discussed in detail.

Palinacousis—Auditory Perseveration: Two Cases and a Review of the Literature

Palinacousis is an auditory illusion rarely reported in cases of temporal lobe dysfunction. Detailed observations where made by Jacobs et al. in 1973. Since that time, only a few other cases have been described in the literature. After reviewing the literature and comparing our clinical experience, we believe that palinacousis can occur as an aura, a simple partial seizure, a complex partial seizure, and/or a postictal event. Within one academic year, we observed two patients who experienced palinacousis. Palinacousis maybe more common than recognized in patients with receptive aphasias or diffuse cerebral dysfunction, whose language deficits preclude adequate description. It is important to differentiate palinacousis from auditory hallucinations seen in psychotic and psychiatric patients. Identification of palinacousis as an aura, simple partial seizure, complex partial seizure, and/or postictal phenomenon can help localize potential lesions and improve patient care.

Post-ictal antinociception effects of audiogenic seizures in metaphit-treated rats

Post-ictal antinociception effects of audiogenic seizures in metaphit-treated rats

Interictal and Postictal Circadian and Ultradian Luteinizing Hormone Secretion in Men with Temporal Lobe Epilepsy

Hypothalamic regulation of the reproductive axis in temporal lobe epilepsy (TLE), represented by the ultradian pulsatile secretion of luteinizing hormone (LH), has been shown to be altered interictally and postictally. Our objective is to determine if epilepsy or seizures disrupt normal circadian fluctuations of LH as well as circadian organization of ultradian bursts of LH. We characterized LH secretion in 10 men with TLE during two 24-h blocks: an interictal epoch and a postictal epoch initiated by a seizure. Serum LH was measured every 10 min and characterized by circadian and ultradian patterns with cosinor and deconvolution analysis. Mean peak serum concentrations of LH occurred at approximately 0400 in controls, were significantly delayed approximately 5 h interictally, and were randomly distributed postictally. Burst amplitudes differed significantly by phase among controls, with the largest amplitudes between 0101 and 0700 and the smallest between 1301 and 1900. No phase differences were present in interictal or postictal epochs. Burst frequency weakly but significantly was slowest between 0101 and 0700 in controls, but did not differ significantly by phase in either interictal or postictal epochs. Postictal LH burst frequencies, but not amplitudes, were significantly decreased immediately postictally. The pulsatile secretion of LH in TLE is abnormal both in the circadian as well as the ultradian domain. Interictal effects consist mainly in loss of circadian fluctuations in LH burst amplitude, whereas postictal effects consist of altered burst timing. Altered daily patterns of neuroendocrine signals may underlie other disorders of homeostasis in TLE.

Unilateral cortical spreading depression is an early marker of audiogenic kindling in awake rats

Spreading depression (SD), a self-propagating wave of reversible cellular depolarization, is thought to play an important role in brain pathophysiology. SD and seizures are closely related events but little is known about involvement of SD in chronic epileptogenesis. Here we show that cortical SD is the first and highly reproducible manifestation of audiogenic kindling induced by repeated sound stimulation of WAG/Rij rats with genetic audiogenic and absence epilepsy. Repetition of sound-induced running seizures in freely moving rats led to an appearance and gradual intensification of post-running facial and forelimb clonic convulsions coupled with afterdischarge in the fronto-parietal cortex. Before the development of these traditional manifestations of audiogenic kindling, an unilateral cortical SD wave began to be triggered by audiogenic seizures. Once cortical SD appeared, it became a permanent component of subsequent seizures. SD was always recorded in the hemisphere ipsilateral to the running direction. Only at the late stages of audiogenic kindling SD developed bilaterally. To estimate the contribution of SD in postictal effects of audiogenic seizures, we compared cortical activity after seizures induced SD or not. It was found that only seizures with cortical SD were followed by postictal suppression of spontaneous spike-wave discharges displayed by WAG/Rij rats. The results show that (1) cortical SD is readily triggered by brief sensory-induced seizures in awake animals; (2) SD may be responsible for postictal changes in cortical activity; (3) unilateral initiation of SD suggests asymmetrical recruitment of the cortex into seizure network during audiogenic kindling.

Temporal lobe epileptic activity mimicking dementia: a case report

Epileptic activity is an underdiagnosed cause that can determine a disruption of memory and cognitive performance, leading an incorrect diagnosis of dementia. We report a 68-year-old man, referred with a 5-year history of subtle behavioral changes and a subjective memory impairment, who was admitted to our department because of recurrent episodes of confusional state lasting from 1 week. Neuropsychological evaluation demonstrated a marked impairment of all cognitive domains examined. Electroencephalogram (EEG) recording showed frequent almost continuous sharp waves localized on the bilateral posterior temporal regions with mild right side predominance. Treatment with phenytoin reversed his cognitive dysfunction and behavioral disturbances. We presume that ictal temporal lobe epileptiform activity is the cause of his confusional episodes and cognitive dysfunction, showing an electroclinical picture of complex partial status epilepticus. However, we hypothesize that the interictal discharges and ictal and postictal effects of subclinical seizures could be involved in the behavioral changes and memory impairment complained by our patient in the last years.

Effects of epileptiform EEG discharges on cognitive function: Is the concept of “transient cognitive impairment” still valid?

In this article we review the existing evidence on the cognitive impact of interictal epileptiform EEG discharges. Such cognitive impairment occurs exclusively in direct relation to episodes of epileptiform EEG discharges and must be distinguished from (post) ictal seizure effects and from the nonperiodic long-term “stable” interictal effects caused by the clinical syndrome or the underlying etiology. Especially in patients with short nonconvulsive seizures, characterized often by difficult-to-detect symptoms, the ictal or postictal effects may be overlooked and the resulting cognitive effects may be erroneously related to the epileptiform EEG discharges. The existing epidemiological data show that the prevalence of cognitive impairment during epileptiform EEG discharges is low. In one study 2.2% of the patients referred to a specialized epilepsy center for EEG recording showed a definite relationship between epileptiform EEG discharges and cognitive impairments (“transient cognitive impairment”). Several studies have sought to analyze to what extent cognitive impairment can be attributed to epileptiform EEG discharges among the other epilepsy factors (such as the effect of the clinical syndrome). These studies show that epileptiform EEG discharges have an additional and independent effect, but this effect is mild and limited to transient mechanistic cognitive processes (alertness, mental speed). This finding concurs with clinical studies that also reported only mild effects. In only exceptional cases are epileptiform EEG discharges the dominant factor explaining cognitive impairment. In addition, some studies have indicated that such mild effects may accumulate over time (when frequent epileptiform EEG discharges persist over years) and consequently result in effects on stable aspects of cognitive function such as educational achievement and intelligence. Hence, the clinical relevance is that early detection of cognitive effects of epileptiform EEG discharges and subsequent treatment may prevent a definite impact on cognitive and educational development. The disruptive effects of epileptiform EEG discharges on long-term potentiation, as established in animal experiments, may be one of the neurophysiological mechanisms underlying this accumulation. In conclusion the concept of “transient cognitive impairment” is still valid, but refinement of methodology has shown that a large proportion of presumed transient cognitive impairment can be attributed to subtle seizures, while interictal epileptic activity accounts for a much smaller part of the cognitive effects than previously thought. In particular cryptogenic partial epilepsies are associated with the risk of cognitive impairment. We hope that increased clinical awareness of this need for early detection will stimulate longitudinal and prospective research that eventually also will provide an answer to the questions of when and how epileptiform discharges that are not part of a seizure need to be treated.

Quantitative assessment of seizure severity for clinical trials: a review of approaches to seizure components.

Quantitative assessment of seizure severity has been approached using a variety of systems. This review describes currently available methods and possible new approaches to seizure assessment for clinical trials. A review of the literature on methods of seizure assessments resulted in tabulation of the seizure rating scales known as VA, Chalfont-National Hospital, Liverpool, Hague, and the Occupational Hazard Scale. Seizures have been evaluated by simply counting all events, counting events by type, by clinician ratings, patient ratings, and combinations. Each of the scales has advantages and disadvantages. Most scales share core components: seizure frequency, seizure type, seizure duration, postictal events, postictal duration, automatisms, seizure clusters, known patterns, warnings, tongue biting, incontinence, injuries, and functional impairment. This review revealed a partial consensus about aspects of seizures that are important markers for severity. However, usefulness of the existing scales is limited by lack of data on responsiveness. New approaches are needed to assess changes in seizure severity as a result of an intervention in a clinical trial.