Nonconvulsive Seizures Research Articles

An Exploratory Report on Electrographic Changes in the Cerebral Cortex Following Mild Traumatic Brain Injury with Hyperthermia in the Rat.

Traumatic brain injury (TBI) has the potential to perturb perception by disrupting electrical propagation within and between the thalamus and cerebral cortex. Moderate and severe TBI may result in posttraumatic epilepsy, a condition characterized by convulsive tonic-clonic seizures. Spike/wave discharges (SWDs) of generalized nonconvulsive seizures, also called absence seizures, may also occur as a consequence of brain trauma. As mild hyperthermia has been reported to exacerbate histopathological and behavioral outcomes, we used an unbiased algorithm to detect periodic increases in power across different frequency bands following single or double closed head injury (CHI) under normothermia and hyperthermia conditions. We demonstrated that mild TBI did not significantly alter the occurrence of events containing increases in power between the delta (0.5-4 Hz), theta (4-8 Hz), alpha (8-12 Hz), and beta1 (12-20 Hz) frequency bands in the Sprague Dawley rat 12 weeks after injury. However, when hyperthermia (39°C) was induced before and after CHI, electrographic events containing a similar waveform and harmonic frequency to SWDs were observed in a subset of animals. Further experiments utilizing chronic recordings will need to be performed to determine if these trends lead to absence seizures.

Traditional practices and perceptions of epilepsy among people in Roma communities in Bulgaria

PurposeWe attempted to identify cultural aspects of epilepsy among the Roma community in Bulgaria by elucidating cultural beliefs, traditional treatments, and potential markers of stigma. MethodsWe established representative discussion groups among five distinct Roma subgroups (Lom, Kalderas, Thracian Tinsmiths (Tinkers), Kyustendil Xoroxane and Kopanari) from different Bulgarian regions. Data about local beliefs and treatment strategies were gathered. ResultsMost people were familiar with convulsions but non-convulsive focal seizures were seen not as epileptic but mainly as a “mental problem”. Beliefs about putative etiologies for epilepsy were not uniform as some considered environmental and external factors such as high environmental temperatures, electric shocks, loud music, and fever as causes of seizures while others listed bad experiences, stress, trauma, and fear as possible causes. Epilepsy was seen by some as a divine punishment or resulting from black magic. Most considered epilepsy shameful and an obstacle to children attending school. Despite local differences, there was a uniform belief that epilepsy is incurable by Western medicine and people usually resort to traditional healers. A variety of rituals performed by local healers to treat epilepsy were described. DiscussionMisconceptions about epilepsy may contribute to stigmatization in this population; this may in turn contribute to a high treatment gap in this group. As a result, the majority of Roma children with epilepsy are likely to leave school early, are greatly limited in their choice of spouse (particularly girls), and marriages often occur between people with epilepsy or those with a family history of epilepsy.

Electropositive seizures and non‐convulsive status epilepticus in a critically ill patient with prior skull defect

Epileptiform discharges captured on routine scalp EEG typically carry a surface negative dipole. We present a patient whose continuous EEG recording in the intensive care setting captured frequent electropositive non-convulsive seizures. Epileptiform discharges with positive polarity are common in the pediatric population but have rarely been reported in adult patients. When reported in adults, such patients usually have skull defects. As surface positive discharges are scarce, adult electroencephalographers should be prudent to differentiate such discharges from artifact, particularly in an intensive care setting where EEG artifact is common.

Focal and generalized seizure activity after local hippocampal or cortical ablation of NaV 1.1 channels in mice.

Early onset seizures are a hallmark of Dravet syndrome. Previous studies in rodent models have shown that the epileptic phenotype is caused by loss‐of‐function of voltage‐gated NaV1.1 sodium channels, which are chiefly expressed in γ‐aminobutyric acid (GABA)ergic neurons. Recently, a possibly critical role has been attributed to the hippocampus in the seizure phenotype, as local hippocampal ablation of NaV1.1 channels decreased the threshold for hyperthermia‐induced seizures. However, the effect of ablation of NaV1.1 channels restricted to cortical sites has not been tested. Here we studied local field potential (LFP) and behavior in mice following local hippocampal and cortical ablation of Scn1a, a gene encoding the α1 subunit of NaV1.1 channels, and we compared seizure characteristics with those of heterozygous global knockout Scn1‐/+ mice. We found a high incidence of spontaneous seizures following either local hippocampal or cortical ablation, notably during a transient time window, similar to Scn1a‐/+ mice. Nonconvulsive seizure activity in the injected area was common and preceded generalized seizures. Moreover, mice were susceptible to hyperthermia‐induced seizures. In conclusion, local ablation of NaV1.1 channels in the hippocampus and cortex results in focal seizure activity that can generalize. These data indicate that spontaneous epileptic activity may initiate in multiple brain regions in Dravet syndrome.

Efficacy and economic evaluation of delivery of care with tele-continuous EEG in critically ill patients: a multicentre, randomised controlled trial (Tele-cRCT) study protocol

IntroductionSome critically ill patients are confirmed by continuous electroencephalography (cEEG) monitoring that non-convulsive seizure (NCS) and/or non-convulsive status epilepticus (NCSE) are causes of their depressed level of consciousness. Shortage of...

Predictors of Nonconvulsive Seizure and Their Effect on Short-term Outcome.

Nonconvulsive seizures (NCSs) are common in critically ill adult patients with acute neurologic conditions. However, the effect of NCSs on patient outcome remains unclear. In this study, we aimed to determine the effect of NCSs on short-term outcome and to assess the clinical and EEG factors associated with NCSs. We retrospectively identified 219 adult patients from the EEG reporting system who underwent continuous EEG (cEEG) monitoring between January 2018 and June 2018. Patients with anoxic brain injury were excluded from the study. Clinical, laboratory, and EEG data were reviewed to determine potentially predictive factors of NCSs. The impact of NCSs on in-hospital mortality, length of stay, and disability on discharge was measured; an modified Rankin scale of three or greater was considered disabled. Of the 219 patients included in our study, a total of 14% (n = 31) had NCSs on continuous EEG, of which 42% (n = 13) had their first seizure discharge recorded during the first hour of continuous EEG monitoring. The presence of clinical seizures before continuous EEG (odds ratio = 1.787; 95% confidence interval = 1.197-2.667, P = 0.0045), history of epilepsy (odds ratio = 1.508; 95% confidence interval = 1.027-2.215, P = 0.035), and comatose state (29 vs. 16%; P = 0.0006) were associated with NCSs. Among EEG characteristics, the presence of interictal epileptiform discharges (P < 0.0001), lateralized rhythmic delta activity (P = 0.02), and lateralized periodic discharges (P < 0.0001) were associated with NCSs. Nonconvulsive seizures were significantly associated with longer in-hospital stay (23.68 ± 24.84 vs. 17.14 ± 20.52; P = 0.036) and disability on discharge (87% [n = 27] vs. 13% [n = 4], P = 0.02). However, there was no significant association between NCS and in-hospital mortality (9.6% [n = 3] vs. 10.6% [n = 20]; P = 0.1). Nonconvulsive seizures are associated with longer in-hospital stay and disability on discharge but not with in-hospital mortality in adult patients.

Continuous electroencephalography (cEEG) monitoring in critically ill patients

Critically ill patients need to be treated quickly, carefully, precisely and comprehensively. Neurological status should be concerned because of the severe impact that occurs if it is not immediately handled, that is permanent disability or death. The neurologic problem like non convulsive seizures may not distinctly clear. It is difficult to assess non-convulsive seizure only by clinical physical examination. Continuous Electroencephalography (cEEG) is a useful to measure electrical brain activity. It could be used to identify seizure, cerebral ischemic, monitor and evaluate the medication, and prognostic of the diseases. This equipment is noninvasive and could give real-time information about the patient condition. The complex procedure and availability of skilled technician and competent reviewer, is the barrier to optimize this tools. Besides the benefit and challenge, cEEG is recommended to be used in critically ill patients’ management.&#x0D; Abbreviations used: ADR – Alpha to Delta Ratio; CBF – Cerebral Blood Flow; cEEG – continuous Electroencephalography; CNS – Central Nervous System; CT – Computed Tomography; DCI – Delayed Cerebral Ischemia; EEG – electroencephalography; GCS – Glasgow Coma Scale; ICU – Intensive Care Unit; MRI - Magnetic Resonance Imaging; NCS – Non-Convulsive Seizures; NCSE – Non-Convulsive Status Epilepticus; PAV – Percent Alpha Variability; PEDs – Periodic Epileptiform Discharges; RAV – Relative Alpha Variability; TBI – Traumatic Brain Injury; TCD – Transcranial Doppler&#x0D; Received: 19 Oct 2018Reviewed: 28 Oct 2018Accepted: 5 Nov 2018&#x0D; Citation: Purwandhono A, Hidayati HB, Machin A, Islamiyah WR. Continuous electroencephalography (cEEG) monitoring in critically ill patients. Anaesth Pain &amp; Intensive Care 2018;22 Suppl 1:S46-S52

Experimentally Induced Convulsive Seizures Are Modulated in Part by Zinc Ions through the Pharmacoresistant Cav2.3 Calcium Channel.

Still in 1999 the first hints were published for the pharmacoresistant Cav2.3 calcium channel to be involved in the generation of epileptic seizures, as transcripts of alpha1E (Cav2.3) and alpha1G (Cav3.1) are changed in the brain of genetic absence epilepsy rats from Strasbourg (GAERS). Consecutively, the seizure susceptibility of mice lacking Cav2.3 was analyzed in great detail by using 4-aminopyridine, pentylene-tetrazol, N-methyl-D-aspartate and kainic acid to induce experimentally convulsive seizures. Further, γ-hydroxybutyrolactone was used for the induction of non-convulsive absence seizures. For all substances tested, Cav2.3-competent mice differed from their knockout counterparts in the sense that for convulsive seizures the deletion of the pharmacoresistant channel was beneficial for the outcome during experimentally induced seizures [1]. The antiepileptic drug lamotrigine reduces seizure activity in Cav2.3-competent but increases it in Cav2.3-deficient mice. In vivo, Cav2.3 must be under tight control by endogenous trace metal cations (Zn2+ and Cu2+). The dyshomeostasis of either of them, especially of Cu2+, may alter the regulation of Cav2.3 severely and its activity for Ca2+ conductance, and thus may change hippocampal and neocortical signaling to hypo- or hyperexcitation. To investigate by telemetric EEG recordings the mechanism of generating hyperexcitation by kainate, mice were tested for their sensitivity of changes in neuronal (intracerebroventricular) concentrations of the trace metal cation Zn2+. As the blood-brain barrier limits the distribution of bioavailable Zn2+ or Cu2+ into the brain, we administered micromolar Zn2+ ions intracerebroventricularly in the presence of 1 mM histidine as carrier and compared the effects on behavior and EEG activity in both genotypes. Kainate seizures are more severe in Cav2.3-competent mice than in KO mice and histidine lessens seizure severity in competent but not in Cav2.3-deficient mice. Surprisingly, Zn2+ plus histidine resembles the kainate only control with more seizure severity in Cav2.3-competent than in deficient mice. Cav2.3 represents one important Zn2+-sensitive target, which is useful for modulating convulsive seizures.

Inducing Post-Traumatic Epilepsy in a Mouse Model of Repetitive Diffuse Traumatic Brain Injury.

Traumatic brain injury (TBI) is a leading cause of acquired epilepsy. TBI can result in a focal or diffuse brain injury. Focal injury is a result of direct mechanical forces, sometimes penetrating through the cranium, creating a direct lesion in the brain tissue. These are visible during brain imaging as areas with contusion, laceration, and hemorrhage. Focal lesions induce neuronal death and glial scar formation and are present in 20%-25% of all people who incur a TBI. However, in the majority of TBI cases, injury is caused by acceleration-deceleration forces and subsequent tissue shearing, resulting in nonfocal, diffuse damage. A subpopulation of TBI patients continues to develop post-traumatic epilepsy (PTE) after a latency period of months or years. Currently, it is impossible to predict which patients will develop PTE, and seizures in PTE patients are challenging to control, necessitating further research. Until recently, the field was limited to only two animal/rodent models with validated spontaneous post-traumatic seizures, both presenting with large focal lesions with massive tissue loss in the cortex and sometimes subcortical structures. In contrast to these approaches, it was determined that diffuse TBI induced using a modified weight drop model is sufficient to initiate development of spontaneous convulsive and non-convulsive seizures, even in the absence of focal lesions or tissue loss. Similar to human patients with acquired post-traumatic epilepsy, this model presents with a latency period after injury before seizure onset. In this protocol, the community will be provided with a new model of post-traumatic epilepsy, detailing how to induce diffuse non-lesional TBI followed by continuous long-term video-electroencephalographic animal monitoring over the course of several months. This protocol will detail animal handling, the weight drop procedure, the electrode placement for two acquisition systems, and the frequent challenges encountered during each of the steps of surgery, postoperative monitoring, and data acquisition.

Developing and Implementing a Standardized Ictal Examination in the Epilepsy Monitoring Unit.

The ictal examination is crucial for neuroanatomic localization of seizure onset, which informs medical and neurosurgical treatment of epilepsy. Substantial variation exists in ictal examination performance in epilepsy monitoring units (EMUs). We developed and implemented a standardized examination to facilitate rapid, reliable execution of all testing domains and adherence to patient safety maneuvers. Following observation of examination performance, root cause analysis of barriers, and review of consensus guidelines, an ictal examination was developed and disseminated. In accordance with quality improvement methodology, revisions were enacted following the initial intervention, including differentiation between pathways for convulsive and nonconvulsive seizures. We evaluated ictal examination fidelity, efficiency, and EMU staff satisfaction before and after the intervention. We identified barriers to ictal examination performance as confusion regarding ictal examination protocol, inadequate education of the rationale for the examination and its components, and lack of awareness of patient-specific goals. Over an 18-month period, 100 ictal examinations were reviewed, 50 convulsive and 50 nonconvulsive. Ictal examination performance varied during the study period without sustained improvement for convulsive or nonconvulsive seizure examination. The new examination was faster to perform (0.8 vs 1.5 minutes). Postintervention, EMU staff expressed satisfaction with the examination, but many still did not understand why certain components were performed. We identified key barriers to EMU ictal assessment and completed real-world testing of a standardized, streamlined ictal examination. We found it challenging to reliably change ictal examination performance in our EMU; further study of implementation is warranted.

A case of comorbid obstructive sleep apnea syndrome and epilepsy, presenting as repetitive central sleep apnea following nonconvulsive epileptic seizure during CPAP titration polysomnography

A case of comorbid obstructive sleep apnea syndrome and epilepsy, presenting as repetitive central sleep apnea following nonconvulsive epileptic seizure during CPAP titration polysomnography

Experimental Models of Absence Epilepsy.

Introduction:Absence epilepsy is a brief non-convulsive seizure associated with sudden abruptness in consciousness. Because of the unpredictable occurrence of absence seizures and the ethical issues of human investigation on the pathogenesis and drug assessment, researchers tend to study animal models. This paper aims to review the advantages and disadvantages of several animal models of nonconvulsive induced seizure.Methods:The articles that were published since 1990 were assessed. The publications that used genetic animals were analyzed, too. Besides, we reviewed possible application methods of each model, clinical types of seizures induced, purposed mechanism of epileptogenesis, their validity, and relevance to the absence epileptic patients.Results:The number of studies that used genetic models of absence epilepsy from years of 2000 was noticeably more than pharmacological models. Genetic animal models have a close correlation of electroencephalogram features and epileptic behaviors to the human condition.Conclusion:The validity of genetic models of absence epilepsy would motivate the researchers to focus on genetic modes in their studies. As there are some differences in the pathophysiology of absence epilepsy between animal models and humans, the development of new animal models is necessary to understand better the epileptogenic process and, or discover novel therapies for this disorder.

Non-convulsive seizures in the encephalopathic critically ill cancer patient does not necessarily portend a poor prognosis

BackgroundNon-convulsive status epilepticus (NCSE) is present in 10–30% of ICU patients with altered mental status (AMS) and is associated to poor outcomes. To our knowledge, there is no data describing the prevalence and outcomes of critically ill cancer patients with AMS associated to non-convulsive seizures (NCS) or NCSE. We aim to describe the outcomes and risk factors of critically ill cancer patients with encephalopathy associated with non-convulsive seizures (NCS).MethodsThis is a 3-year prospective observational study in a mixed oncological ICU at MD Anderson Cancer Center. Data of ICU patients with moderate to severe encephalopathy (Glasgow Coma Score < 13) that underwent EEG monitoring to rule out NCS were collected. Multivariate logistic regression was performed to identify risk factors and outcomes.ResultsOf the 317 patients with encephalopathy who underwent EEG monitoring, 14.5% had NCS. Known risk factors such as sepsis, CNS infection, antibiotics, and cardiac arrest were not associated with increased risk of NCS. Patients with NCS were more likely to have received recent chemotherapy (41.3% vs 21.4%; p = 0.0036), have a CNS disease (39% vs 24.4%; p = 0.035), and abnormal brain imaging (60.9% vs 44.6%; p = 0.041). Patients with lower SOFA scores, normal renal function, and absence of shock were likely to have NCS as the cause of their encephalopathy (p < 0.03). After multivariate analysis, only abnormal brain imaging and absence of renal failure were associated with NCS. Mortality was significantly lower in patients with non-convulsive seizures when compared to those without seizures (45.7% vs 64%; p = 0.022); however, there was no significant association of seizures and mortality on a multivariable logistic regression analysis.ConclusionsNCS in critically ill cancer patients is associated with abnormalities on brain imaging and lower prevalence of organ failure. Diagnosis and treatment of NCS should be a priority in encephalopathic cancer patients, as they can have lower mortality than non-seizing patients. Opposite to other populations, NCS should not be considered a poor prognostic factor in critically ill encephalopathic cancer patients as they reflect a reversible cause for altered mentation.

De novo Absence Status Epilepticus in a pediatric cohort: Electroclinical pattern in a multicenter Italian patients cohort

PurposeAbsence Status epilepticus (AS) is a form of Non Convulsive Status Epilepticus defined as a prolonged, generalized and non-convulsive seizure, with an altered content of consciousness. We aim to describe a group of healthy children, who presented recurrent and unprovoked de novo AS as the only manifestation of their epilepsy, with an excellent response to antiepileptic drugs. MethodWe retrospectively reviewed the electroclinical and genetic features of 13 pediatric patients, referring to our epilepsy centers from 2005 to 2019, on the following criteria: (1) regular psychomotor development, (2) one or more unprovoked AS as the only epileptic manifestation, (3) normal blood testing, (4) normal neuroimaging, (5) EEG recording, (6) available follow-up (1–14 years). ResultsPatients are 7 females and 6 males, aged 7–22, with a mean age at AS onset of 9,3 years. All of them started an antiepileptic therapy, with an excellent response to Valproic Acid (VPA) or Ethosuximide (ETS). 5 patients did not start the therapy immediately after the first AS and they presented recurrent AS (from 2 to 4 episodes). 10 of them performed aCGH, karyotype, NGS panel or Whole Exome Sequencing. ConclusionsWe suggest that de novo AS may be a well-defined age-related and self-limited epilepsy syndrome, with a good prognosis and excellent response to therapy, but it comes with a high risk of relapsing if not adequately treated with antiepileptic drugs.

Predictors of Seizure Recurrence after Acute Symptomatic Seizures in Ischemic Stroke Patients.

Purpose Seizure is a well-recognized complication of both remote and acute ischemic strokes. Predictors of seizure recurrence and epilepsy in patients with ischemic stroke who develop acute symptomatic seizures (ASyS) on continuous electroencephalography (cEEG) have not been well studied. Methods We present a five-year retrospective study of acute and remote ischemic stroke patients who developed ASyS on cEEG. We then identified risk factors for the development of seizure recurrence. Results Sixty-five patients with ischemic stroke and ASyS were identified and reviewed. All ASyS were noted to be nonconvulsive seizures. Clinical recurrence of seizures was identified in 19 of these patients (29.2%) at follow-up. Rate of seizure recurrence was higher in remote ischemic stroke patients (84.2%), compared to acute ischemic stroke patients (15.8%, p = 0.0116, OR 0.17, 95% CI 0.049–0.65). Sharp waves/spikes on follow-up EEG significantly correlated with seizure recurrence (p = 0.006, OR 0, 95% CI 0–0.3926). Patients discharged on ≥3 antiepileptic drugs (AEDs) were at a higher risk of having seizure recurrence (p = 0.0015, OR 0.05, 95% CI 0.0089–0.37). Conclusion We identified risk factors of seizure recurrence in patients with ASyS as remote ischemic stroke, requiring multiple AEDs, and the presence of sharp waves on follow-up EEG. This study highlights the usefulness of cEEG in evaluating patients with acute or remote strokes.

A Mouse Model of Repetitive Blast Traumatic Brain Injury Reveals Post-Trauma Seizures and Increased Neuronal Excitability.

Repetitive blast traumatic brain injury (TBI) affects numerous soldiers on the battlefield. Mild TBI has been shown to have long-lasting effects with repeated injury. We have investigated effects on neuronal excitability after repetitive, mild TBI in a mouse model of blast-induced brain injury. We exposed mice to mild blast trauma of an average peak overpressure of 14.6 psi, repeated across three consecutive days. While a single exposure did not reveal trauma as indicated by the glial fibrillary acidic protein indicator, three repetitive blasts did show significant increases. As well, mice had an increased indicator of inflammation (Iba-1) and increased tau, tau phosphorylation, and altered cytokine levels in the spleen. Video-electroencephalographic monitoring 48 h after the final blast exposure demonstrated seizures in 50% (12/24) of the mice, most of which were non-convulsive seizures. Long-term monitoring revealed that spontaneous seizures developed in at least 46% (6/13) of the mice. Patch clamp recording of dentate gyrus hippocampus neurons 48 h post-blast TBI demonstrated a shortened latency to the first spike and hyperpolarization of action potential threshold. We also found that evoked excitatory postsynaptic current amplitudes were significantly increased. These findings indicate that mild, repetitive blast exposures cause increases in neuronal excitability and seizures and eventual epilepsy development in some animals. The non-convulsive nature of the seizures suggests that subclinical seizures may occur in individuals experiencing even mild blast events, if repeated.

The yield of continuous EEG monitoring in the intensive care unit at a tertiary care hospital in Saudi Arabia: A retrospective study.

Background: The practice of continuous EEG monitoring (CEEG) in the intensive care unit (ICU) has spread over the past decade. Building an effective ICU CEEG program demands adequate EEG equipment and human resources. This may not be available in developing healthcare systems. This study sought to shed light on the real-life utility of CEEG at a tertiary healthcare center in the developing healthcare system of Saudi Arabia. Methods: This is a retrospective review of CEEG findings, along with mortality and duration of hospitalization of patients who had CEEG during a 12-month period at the adult ICU at the King Abdulaziz University Hospital (KAUH) in Jeddah, Saudi Arabia. Results: A total of 202 CEEG records were identified. A total of 52 records showed non-convulsive seizures (NCS); 10 clearly fulfilled criteria for non-convulsive status epilepticus. There were 120 patients that had clinical seizures upon presentation. Among them, 36 (30%) had NCS on EEG. The proportion of patients who were deceased at 60 days was higher in patients with NCS than those who didn't have NCS (42% vs 27%, χ 2 = 4.4, df=2, p=0.03). There was no statistically significant association between having rhythmic or periodic patterns without NCS and mortality at 60 days or length of hospital stay. Conclusion: This retrospective study demonstrates a real-world experience from a tertiary care center in Saudi Arabia, a developing healthcare system. ICU CEEG was found to be effective in detecting potentially harmful subclinical patterns, supporting the need to develop ICU CEEG programs. However, the incurred excesses in morbidity and mortality associated with CEEG patterns were relatively modest. Further studies are needed to delineate how the practice of CEEG may be developed in similar healthcare systems to provide meaningful data to clinicians with regards to patient outcomes.

Post-Traumatic Epilepsy and Seizure Susceptibility in Rat Models of Penetrating and Closed-Head Brain Injury.

Traumatic brain injury (TBI) carries a risk of developing post-traumatic epilepsy (PTE). Currently, animal models that replicate clinical PTE (delayed spontaneous and recurrent seizures) are limited, which hinders pre-clinical research. In this study, we used two rat models of penetrating ballistic-like brain injury (PBBI) and closed-head injury (CHI) to induce spontaneous seizures and also measure changes in seizure susceptibility. In the PBBI model, two trajectories (frontal and lateral) and two injury severities for each trajectory, were evaluated. In the CHI model, a single projectile impact to the dorsal/lateral region of the head was tested. Continuous video-electroencephalographic (EEG) recordings were collected for 10 days at 1 or 6 month(s) post-injury. After EEG recording, all rats were given a sub-convulsant dose of pentylenetetrazole (PTZ) to challenge the seizure susceptibility. The video-EEG recording did not detect PTE following the PBBI. Only one CHI rat demonstrated persistent and recurrent non-convulsive seizures detected at 6 months post-injury. However, after PTZ challenge, 50-100% of the animals across different TBI groups experienced seizures. Seizure susceptibility increased over time from 1 to 6 months post-injury across the majority of TBI groups. Injury severity effects were not apparent within the PBBI model, but were evident between PBBI and CHI models. These results demonstrated the difficulties in detecting delayed spontaneous post-traumatic seizures even in a high-risk model of penetrating brain injury. The PTZ-induced increase in seizure susceptibility indicated the existence of vulnerable risk of epileptogenesis following TBI, which may be considered as an alternative research tool for pre-clinical studies of PTE.

Nonconvulsive Seizures in Abusive Head Trauma

The article by Oh et al describes the EEG findings in a group of infants diagnosed with abusive head trauma but does not pay attention to the symptoms that triggered admission.

Epileptic activity in neurological deterioration after ischemic stroke, a continuous EEG study

ObjectiveDespite improvement in acute stroke care, almost 40% of patients with ischemic stroke present neurological deterioration. Neurological deterioration is associated with higher death and dependency rates. Neurological deterioration mechanisms are unknown, and half of neurological deterioration remains unexplained. We postulate that a substantial proportion of neurological deterioration in ischemic stroke is associated with periodic discharges/non-convulsive seizures that negatively impact the recovery of ischemic stroke and worsen symptoms. MethodsRetrospective review of 24 h continuous EEG monitoring (cEEG) performed for neurological deterioration in the stroke unit of a tertiary academic centre. ResultsEighty-one patients were included. cEEG detected epileptic activities in 44% of cases (Non-convulsive seizures/non-convulsive status epilepticus: 10/81 (12%), periodic discharges: 17/81 (21%) and sporadic epileptiform discharges in 14/81 (17%)). The proportion of patients who did not receive recanalization therapy was significantly higher in the NCSE/NCSz/PDs group than in the group devoid of NCSE/NCSz/PDs: 17/22 (77%) vs 13/59 (22%); p < 0,001. Treatment of Non-convulsive seizures /non-convulsive status epilepticus and periodic discharges was followed by EEG improvement in respectively 7/8 and 10/16 of treated patients. ConclusionsNon-convulsive seizures /non-convulsive status epilepticus /periodic discharges are associated to neurological deterioration after ischemic stroke. SignificanceTreatment of Non-convulsive seizures /non-convulsive status epilepticus and periodic discharges, if such patterns are detected, could help prevent adverse metabolic consequences of epileptic activities on ischemic brain tissue.