Epileptogenic Discharges Research Articles

BDNF, proBDNF and proBDNF/BDNF ratio with electroencephalographic abnormalities in children with attention deficit hyperactivity disorder: Possible relations to cognition and severity.

Attention deficit hyperactivity disorder (ADHD) with and without subclinical epileptogenic discharges (SED) have been suggested to negatively affect cognitive abilities of children with ADHD. The role of brain-derived neurotrophic factor (BDNF) and its precursor proBDNF in ADHD is in need of being investigated. The aims were to evaluate the levels of serum BDNF, proBDNF and the proBDNF/BDNF ratio in addition to the potential impacts of SED on the children's cognitive abilities and the severity of ADHD. The included participants with ADHD were 30 children with normal electroencephalogram (EEG) (G1) and 30 children with SED (G2), together with 30 healthy children (G3). The cognitive abilities and severity of the disorder were evaluated. The biochemical measures were determined by ELISA. The presence of coexisting SED and nocturnal enuresis has led to a deleterious effect on cognitive processes but not on the severity. The focal epileptogenic discharge was the most common among children in G2. The levels of BDNF in Groups 1 and 2 were less than those in G3. The higher proBDNF/BDNF ratio could be related to the low BDNF levels rather than high proBDNF levels. The findings of this study highlight the importance of investigating the presence of SED and nocturnal enuresis in children with ADHD. Targeting strengthening of cognitive abilities in children with coexisting ADHD and SED is advised. The role of proBDNF in the pathophysiology of ADHD needs further investigation.

SLC4A10 mutation causes a neurological disorder associated with impaired GABAergic transmission.

SLC4A10 is a plasma-membrane bound transporter that utilizes the Na+ gradient to drive cellular HCO3- uptake, thus mediating acid extrusion. In the mammalian brain, SLC4A10 is expressed in principal neurons and interneurons, as well as in epithelial cells of the choroid plexus, the organ regulating the production of CSF. Using next generation sequencing on samples from five unrelated families encompassing nine affected individuals, we show that biallelic SLC4A10 loss-of-function variants cause a clinically recognizable neurodevelopmental disorder in humans. The cardinal clinical features of the condition include hypotonia in infancy, delayed psychomotor development across all domains and intellectual impairment. Affected individuals commonly display traits associated with autistic spectrum disorder including anxiety, hyperactivity and stereotyped movements. In two cases isolated episodes of seizures were reported in the first few years of life, and a further affected child displayed bitemporal epileptogenic discharges on EEG without overt clinical seizures. While occipitofrontal circumference was reported to be normal at birth, progressive postnatal microcephaly evolved in 7 out of 10 affected individuals. Neuroradiological features included a relative preservation of brain volume compared to occipitofrontal circumference, characteristic narrow sometimes 'slit-like' lateral ventricles and corpus callosum abnormalities. Slc4a10 -/- mice, deficient for SLC4A10, also display small lateral brain ventricles and mild behavioural abnormalities including delayed habituation and alterations in the two-object novel object recognition task. Collapsed brain ventricles in both Slc4a10-/- mice and affected individuals suggest an important role of SLC4A10 in the production of the CSF. However, it is notable that despite diverse roles of the CSF in the developing and adult brain, the cortex of Slc4a10-/- mice appears grossly intact. Co-staining with synaptic markers revealed that in neurons, SLC4A10 localizes to inhibitory, but not excitatory, presynapses. These findings are supported by our functional studies, which show the release of the inhibitory neurotransmitter GABA is compromised in Slc4a10-/- mice, while the release of the excitatory neurotransmitter glutamate is preserved. Manipulation of intracellular pH partially rescues GABA release. Together our studies define a novel neurodevelopmental disorder associated with biallelic pathogenic variants in SLC4A10 and highlight the importance of further analyses of the consequences of SLC4A10 loss-of-function for brain development, synaptic transmission and network properties.

Spike-microstates correlate with interictal epileptogenic discharges: a marker for hidden epileptic activity.

Objectively estimating disease severity and treatment success is a main problem in outpatient managing of epilepsy. Self-reported seizures diaries are well-known to underestimate the actual seizure count, and repeated EEGs might not show interictal epileptiform discharges (IEDs), although patients suffer from seizures. In this prospective study, we investigate the potential of microstate analysis to monitor epilepsy patients independently of their IED count. From our databank of candidates for epilepsy surgery, we included 18 patients who underwent controlled resting EEG sessions (with eyes closed, 30 min), at around the same time of the day, during at least four days (range: 4-8 days; mean: 5). Nine patients with temporal foci, six with extratemporal foci, and three with generalized epilepsy were included. Each patient's IEDs were marked and the topographic voltage maps of the IED peaks were averaged, and an individual average spike topography (AST) was created. The AST was then backfitted to each timepoint of the whole EEG resulting in the Spike-Microstate (SMS). The presence of the SMS in the residual EEG outside of the short IEDs epochs was determined for each recording session in each patient and correlated with the occurrence of the IEDs across all recording session, as well as with the drug charge of each day. Overall, SMS was much more represented in the routine EEG than the IEDs: they were identified 262 times more often than IEDs. The SMS time coverage correlated significantly with the IED occurrence rate (rho = 0.56; P < 0.001). If only patients with focal epilepsy were considered, this correlation was even higher rho = 0.69 (P < 0.001). Drug charge per day did not correlate with SMS. In this proof-of-concept study, the time coverage of SMS correlated strongly with the occurrence rate of the IEDs, they can be retrieved in the scalp EEG at a much higher occurrence rate. We conclude that SMS, once obtained for a given patient, are a more abundant marker of hidden epileptic activity than IEDs, in particular in focal epilepsy, and can be used also in absence of IEDs. Future larger studies are needed to verify its potential as monitoring tool and to determine cut-off values when drug protection becomes imperfect.

Changes of interictal epileptiform discharges during medication withdrawal and seizures: A scalp EEG marker of epileptogenicity

ObjectiveTo determine the influence of antiseizure medication (ASM) withdrawal on interictal epileptogenic discharges (IEDs) in scalp-EEG and seizure propensity. MethodsWe included 35 adult unifocal epilepsy patients admitted for presurgical evaluation in the EEG and Epilepsy Unit of Geneva between 2016 and 2020, monitored for at least 5 days. ASM was individually tapered down, and automated IED detection was performed using Epilog PreOp (Epilog NV, Belgium, Ghent). We compared spike rate per hour (SR) at day 1 when patients were on full medication (baseline) with SR at the day with the lowest dose of medication. To determine possible peri-ictal changes of SR, we compared SR 8 h before and after a seizure with the SR at the same time of the baseline day. ResultsOur results showed a significant increase in spiking activity in the day of lowest drug load if compared to spike rate at day on full medication (p < 0.001). The total amount of spikes during 24 h correlated significantly with seizure occurrence (p < 0.0001). We also revealed significant increase in peri-ictal SR, in particular 2–4 h preceding a seizure (p = 0.05) extending up to 3 h after the seizure (p = 0.03) with a short decrease just before seizure occurrence. ConclusionsOur results suggest that SR increases with medication withdrawal and particularly before and after seizures. There is a complex pattern of increase and decrease around seizure onset which explains divergent results in previous studies. SignificancePrecise spike counting at similar circadian periods for a patient could help to determine the risk of seizure occurrence in a personalized fashion.

Factors Associated with Short-Term Seizure Recurrence in Extratemporal Epilepsy Surgery

Introduction: Drug-resistant extratemporal epilepsy is the second cause of referral to epilepsy surgery. Objectives: To identify factors associated with short-term seizure recurrence following extratemporal epilepsy surgery. Materials and Methods: We performed a retrospective study of 19 consecutive patients who underwent surgery for drug-resistant extratemporal epilepsy at the National Institute of Neurology and Neurosurgery of Havana, Cuba, from September 2014 to October 2019. All patients had at least one year of postoperative follow-up. Fisher's exact test was used to search for an association between dichotomous variables. A value of p≤0.05 was considered significant. Results: After one year of follow-up, seizure freedom reached 31.6% (Engel I) and 36.8% showed significant improvement in the number of seizures (Engel II). The frontal location (p=0.046) and incomplete resection of the epileptogenic zone (p=0.017), bilateral interictal discharges on the preoperative electroencephalogram (EEG) (p=0.017), the presence of epileptiform discharges on the postsurgical EEG (p=0.001), and the occurrence of seizures after the sixth month of surgery (p=0.001), were associated with seizures recurrence. Conclusions: After one year, 31.6% of patients operated on for extratemporal epilepsy were seizure-free. The incomplete resection of the epileptogenic zone and the presence of epileptogenic discharges in the postsurgical EEG, and the presence of seizures after the sixth month of surgery were the most significant factors of seizure recurrence.

Combined markers for predicting cognitive deficit in patients with Alzheimer\u2019s disease

BackgroundAlzheimer’s disease (AD) is the most widely recognized type of dementia. It is associated with cell cycle abnormalities including genomic instability and increased micronuclei (MNi) which usually evolve many years before the appearance of the clinical manifestations. Digital electroencephalogram (EEG) has a role in perceiving brain changes in dementia and in early detection of cognitive decline. This study aimed to assess the competency of using neurophysiological markers including absolute power of alpha waves and a cytogenetic marker which comprises scoring of MNi as a step toward early and preclinical diagnosis of AD. The study was conducted on 27 subjects; they were 15 patients diagnosed as sporadic AD and a group of 12 age and sex-matched controls. All subjects were subjected to Mini-Mental State Examination (MMSE), conventional EEG, digital EEG, and cytokinesis-block micronucleus assay (CBMN) in peripheral blood lymphocytes.ResultsConventional EEG showed a normal background activity with no abnormal epileptogenic discharges in both groups. Digital EEG showed significant reduction of the absolute power of alpha waves for AD patients as compared to the control group (P < 0.0001). Score of MNi showed statistical significant difference between the two groups (P < 0.0001). By linking scores of both cognitive state using MMSE and MNi among the group of patients, a significant negative correlation was detected (r = −0.6066). The correlations between cognitive state and the absolute power of alpha wave among the patients revealed a positive correlation (r = 0.2235).ConclusionsThe combination of both cytogenetic and neurophysiological markers can be beneficial for early detection of cognitive decline and may lead to preclinical identification of individuals at increased risk for AD, where at this stage treatment is constructive. The negative correlation between the scores of MNi and MMSE is suggestive for the impact of genomic instability on the cognitive state.

Epileptic discharges in acutely ill patients investigated for SARS-CoV-2/COVID-19 and the absence of evidence.

Galanopoulou and coauthors reported that epileptogenic discharges (ED) were frequent in COVID-19 patients with encephalopathy or possible seizures.1 They found that ED were more prevalent in COVID-19 patients (9/22, 41%) than in patients whose COVID-19 test was negative (1/6, 17%; P = .37; Fisher's exact t-test). They rightly concluded that more information was necessary to test whether COVID-19 infection increases the risk of epileptiform abnormalities. We can learn from small observations and two groups not prespecified but generated during data collection. Is this nonsignificant result evidence of no difference, or only absence of evidence (we need more data)? The Bayes rule can give more insight since it can quantify the uncertainty of a nonsignificant P-value. We have no prior information of EEG abnormalities in COVID-19, but we know that encephalopathic patients in general can have ED because of other confounders (hypoxemia, organ failure). Therefore, the probability of no difference between both groups (null hypothesis) is at least 50%. If there is a difference, each group shares the same chance (25%, H1, the alternative hypothesis). Based on the summary data in the article, we ran a binomial test in JASP, a powerful yet easy-to-use open-source software with classical and Bayesian capabilities.2 The Bayes factor for the COVID-19 + group was 1.35 (Table 1), a posterior median of 0.50 (from a prior median of zero), 95% credible interval (95% CrI): −0.89 to 1.88). The low BF10 and the wide 95% CrI show that the nonsignificant p-value is due to the need for more information, not to a lack of effect or association (Figure 1). This example showcases what is happening with the COVID-19 pandemic at all levels. It is a Bayesian paradigm: We learn more as we collect more data. Our knowledge evolves from complete ignorance to a full understanding of biologic phenomena by processing incoming information. No conflict of interest by any of the authors. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

Detection of epileptic activity in presumably normal EEG.

Monitoring epileptic activity in the absence of interictal discharges is a major need given the well-established lack of reliability of patients’ reports of their seizures. Up to now, there are no other tools than reviewing the seizure diary; however, seizures may not be remembered or dismissed voluntarily. In the present study, we set out to determine if EEG voltage maps of epileptogenic activity in individual patients can help to identify disease activity, even if their scalp EEG appears normal. Twenty-five patients with pharmacoresistant focal epilepsy were included. For each patient, 6 min of EEG with spikes (yes-spike) and without visually detectable epileptogenic discharges (no-spike) were selected from long-term monitoring recordings (EEG 31–37 channels). For each patient, we identified typical discharges, calculated their average and the corresponding scalp voltage map (‘spike-map’). We then fitted the spike-map for each patient on their (i) EEG epochs with visible spikes, (ii) epochs without any visible spike and (iii) EEGs of 48 controls. The global explained variance was used to estimate the presence of the spike-maps. The individual spike-map occurred more often in the spike-free EEGs of patients compared to EEGs of healthy controls (P = 0.001). Not surprisingly, this difference was higher if the EEGs contained spikes (P < 0.001). In patients, spike-maps were more frequent per second (P < 0.001) but with a shorter mean duration (P < 0.001) than in controls, for both no-spike and yes-spike EEGs. The amount of spike-maps was unrelated to clinical variables, like epilepsy severity, drug load or vigilance state. Voltage maps of spike activity are present very frequently in the scalp EEG of patients, even in presumably normal EEG. We conclude that spike-maps are a robust and potentially powerful marker to monitor subtle epileptogenic activity.

EEG efficiency of detecting sub-clinical seizures in critical ill patients: Retrospective study

Introduction Continuous electroencephalography (cEEG) monitoring in the critical care setting demonstrates a linear increase in seizure incidence with declining mental status. Delayed diagnosis and treatment of non-convulsive status epilepticus (NCSE) may lead to increased mortality. No clinical or paraclinical parameter can reliably distinguish elderly patients with delirium with or without patterns compatible with NCSE in the absence of cEEG monitoring. EEG may be over-utilized in our hospital ICUs & usually ordered for most of the patient with altered mental status. We aimed to evaluate the efficiency of EEG to detect subclinical seizures in patients with altered level of consciousness. Methods Single-center retrospective study comprised 24 patients who were hospitalized in King Fahad Specialist Hospital in Dammam between January2017-December2018 due to change of their level of consciousness. Descriptive analysis was used to study the factors involved in the patient findings. Findings/prognosis Only 1 of the 4 patients with subclinical seizures had periodic lateralizing epileptogenic discharges. Only one of the patients with the subclinical seizures was known to have seizure. Last 2 patients were post cardiac arrest & one had brain metastasis. 2 of the patients with the subclinical seizure died few days later because of the seizure or drug side effects. Conclusion Patient with decrease level of consciousness after clinical seizure increase suspicion of subclinical seizure, therefore, early diagnosis of the subclinical seizure allows early management and most likely better outcome. However, there was an over utilization of EEG found in through the study.

F178. Epilepsy and temporal encephaloceles: Presurgical evaluation and surgical outcomes

Introduction Temporal encephalocele (TE) is an under-recognized surgically-remediable cause of medically refractory temporal lobe epilepsy. This study assessed preoperative evaluations [MRI, FDG-PET, routine and prolonged video scalp EEG, intraoperative and extraoperative electrocorticography (ECog)] and short-term surgical outcomes in patients with medically refractory temporal lobe epilepsy due to TE. Methods Patients with medically refractory temporal lobe epilepsy who underwent surgical intervention for known TE at the Mayo Clinic Rochester between January 2008 and July 2017 were identified. Additional patients who underwent surgery for temporal lobe epilepsy were found retrospectively on review of PET-CT or PET-MRI by an experienced neuroradiologist. Minimum required follow-up was 3 months. Results Fifteen patients were identified (female 80%, median age 42.1 years, interquartile range (IQR) 19.3–54.9 years). TE was identified in 7 patients prior to surgery (left 3, right 2, bilateral 2), from radiology re-review in 7 (left 1, right 1, bilateral 5), and intraoperatively in 1 (right). Temporal hypometabolism was present on FDG-PET in 7 of 10 patients, including 5 initial MRI reviews not suggestive of TE. Routine EEG was normal in 7 patients (47%). Prolonged video EEG showed interictal discharges and ictal onset ipsilateral to the TE in all unilateral cases. In bilateral TE, temporal interictal discharges were lateralized in 4 patients and focal ictal onset present in 5 patients. Intraoperative or extraoperative ECog showed widespread mesial and neocortical temporal discharges in 12 of 14 patients. Three patients (20%) underwent focal TE resection, 11 patients (73.3%) anterior temporal lobectomy (ATL), and 1 patient amygdalohippocampal laser ablation. Eight patients (53.3%) were seizure-free at last follow-up (median follow-up duration 7.1 months, IQR 4.2–41.9, 1 focal TE resection, 7 ATL). Focal TE resection was performed only in recent years (median duration of follow-up in focal TE resection 7.2 months, IQR 7–13.8, versus ATL 18.7 months, IQR 4.1–48.8), and comparison of surgical outcome between surgical groups was limited to short-term follow-up. At 6 months, seizure-freedom was achieved in 2 of 3 patient with focal TE resection and 4 of 6 patients with ATL (p > 0.05). Conclusion TE is an easily overlooked etiology of medically refractory temporal lobe epilepsy. Normal routine EEG and unrevealing initial MRI review were seen in nearly half of the patients. Although prolonged video scalp EEG provided concordant localizing information consistent with TE, ECog often showed epileptogenic discharges extending beyond regions around the TE and should be interpreted with caution as short-term follow up remained favorable despite focal TE resection. Long-term follow-up is needed to clarify which surgical approach optimizes seizure outcome while minimizing resection.

Locally stable brain states predict suppression of epileptic activity by enhanced cognitive effort.

Cognitive effort is known to play a role in healthy brain state organization, but little is known about its effects on pathological brain dynamics. When cortical stimulation is used to map functional brain areas prior to surgery, a common unwanted side effect is the appearance of afterdischarges (ADs), epileptiform and potentially epileptogenic discharges that can progress to a clinical seizure. It is therefore desirable to suppress this activity. Here, we analyze electrocorticography recordings from 15 patients with epilepsy. We show that a cognitive intervention in the form of asking an arithmetic question can be effective in suppressing ADs, but that its effectiveness is dependent upon the brain state at the time of intervention. By applying novel techniques from network analysis to quantify brain states, we find that the spatial organization of ADs with respect to coherent brain regions relates to the success of the cognitive intervention: if ADs are mainly localized within a single stable brain region, a cognitive intervention is likely to suppress the ADs. These findings show that cognitive effort is a useful tactic to modify unstable pathological activity associated with epilepsy, and suggest that the success of therapeutic interventions to alter activity may depend on an individual's brain state at the time of intervention.

Interictal High Frequency Oscillations Detected with Simultaneous Magnetoencephalography and Electroencephalography as Biomarker of Pediatric Epilepsy.

Crucial to the success of epilepsy surgery is the availability of a robust biomarker that identifies the Epileptogenic Zone (EZ). High Frequency Oscillations (HFOs) have emerged as potential presurgical biomarkers for the identification of the EZ in addition to Interictal Epileptiform Discharges (IEDs) and ictal activity. Although they are promising to localize the EZ, they are not yet suited for the diagnosis or monitoring of epilepsy in clinical practice. Primary barriers remain: the lack of a formal and global definition for HFOs; the consequent heterogeneity of methodological approaches used for their study; and the practical difficulties to detect and localize them noninvasively from scalp recordings. Here, we present a methodology for the recording, detection, and localization of interictal HFOs from pediatric patients with refractory epilepsy. We report representative data of HFOs detected noninvasively from interictal scalp EEG and MEG from two children undergoing surgery.The underlying generators of HFOs were localized by solving the inverse problem and their localization was compared to the Seizure Onset Zone (SOZ) as this was defined by the epileptologists. For both patients, Interictal Epileptogenic Discharges (IEDs) and HFOs were localized with source imaging at concordant locations. For one patient, intracranial EEG (iEEG) data were also available. For this patient, we found that the HFOs localization was concordant between noninvasive and invasive methods. The comparison of iEEG with the results from scalp recordings served to validate these findings. To our best knowledge, this is the first study that presents the source localization of scalp HFOs from simultaneous EEG and MEG recordings comparing the results with invasive recordings. These findings suggest that HFOs can be reliably detected and localized noninvasively with scalp EEG and MEG. We conclude that the noninvasive localization of interictal HFOs could significantly improve the presurgical evaluation for pediatric patients with epilepsy.

Interictal High Frequency Oscillations Detected with Simultaneous Magnetoencephalography and Electroencephalography as Biomarker of Pediatric Epilepsy

Crucial to the success of epilepsy surgery is the availability of a robust biomarker that identifies the Epileptogenic Zone (EZ). High Frequency Oscillations (HFOs) have emerged as potential presurgical biomarkers for the identification of the EZ in addition to Interictal Epileptiform Discharges (IEDs) and ictal activity. Although they are promising to localize the EZ, they are not yet suited for the diagnosis or monitoring of epilepsy in clinical practice. Primary barriers remain: the lack of a formal and global definition for HFOs; the consequent heterogeneity of methodological approaches used for their study; and the practical difficulties to detect and localize them noninvasively from scalp recordings. Here, we present a methodology for the recording, detection, and localization of interictal HFOs from pediatric patients with refractory epilepsy. We report representative data of HFOs detected noninvasively from interictal scalp EEG and MEG from two children undergoing surgery. The underlying generators of HFOs were localized by solving the inverse problem and their localization was compared to the Seizure Onset Zone (SOZ) as this was defined by the epileptologists. For both patients, Interictal Epileptogenic Discharges (IEDs) and HFOs were localized with source imaging at concordant locations. For one patient, intracranial EEG (iEEG) data were also available. For this patient, we found that the HFOs localization was concordant between noninvasive and invasive methods. The comparison of iEEG with the results from scalp recordings served to validate these findings. To our best knowledge, this is the first study that presents the source localization of scalp HFOs from simultaneous EEG and MEG recordings comparing the results with invasive recordings. These findings suggest that HFOs can be reliably detected and localized noninvasively with scalp EEG and MEG. We conclude that the noninvasive localization of interictal HFOs could significantly improve the presurgical evaluation for pediatric patients with epilepsy.

A neuroimaging study in childhood autism

Background: Childhood autism is now widely viewed as being of developmental neurological origin. Abnormality in neuroimaging is reported in autism.Objectives: To delineate the proportion of structural magnetic resonance imaging (MRI) and electro encephalography (EEG) abnormality among the children with Autism and to assess any association of MRI and EEG changes with co morbid mental illness.Methods: It was a cross sectional descriptive study done at a child and adolescent consultation centre, Dhaka. The study was Carried out from January 2009 to December 2009. Both boys and girls were included in the study. A total of 42 children with childhood autism aged between two and 12 years partici­pated in this study. Diagnosis of autism was based on ICD-10(DCR) criteria. Results: Abnormalities were found to be 35.7% in MRI and 42.9% in EEG. EEG abnormalities were found in the form of defuse slow waves activities, generalized faster activities, epileptogenic discharge and mixed discharge. The abnormalities in MRI was found in the form of diffuse cortical atrophic changes, focal cortical atrophy in frontal and temporal cortex with widening of major sulci, prominent ventricles, periventricular degeneration and abnormal basal ganglia. EEG changes were significantly associated with increased number of co-morbid illness (mental retardation, epilepsy and others). Conclusion: A number of abnom1alities that observed in the present study indicative of relations between structural and physiological dysfunctions and childhood autism. Further exploratory and in-depth researches are certainly required in this field. Intervention of autism needs to address co morbidities for better outcome.

EEG in ICU: A monitoring tool for critically ill patient

Electroencephalographic monitoring provides dynamic information about the brain function that permits early detection of changes in neurologic status, which is especially useful when the clinical examination is limited. Identification of ongoing electrographic seizures, non-convulsive status epilepticus (NCSE), periodic epileptogenic discharges (PED), irreversible cerebral dysfunction i.e., isoelectric tracing would help the care providers in appropriate decision making regarding the management. Non-convulsive seizures (NCSz) are more common than previously recognized and are associated with worse outcome if not treated in time. Majority of seizures at the ICU are not clinically identified because of the disease phenomena or as the patient may remain under sedation. Studies revealed the first NCSz within 1 to 24 hours of EEG monitoring; longer period of monitoring is required in comatose patient and those with PED. Factors associated with an increased risk of NCSz and NCSE include coma, prior clinical seizures, CNS infection, trauma, stroke, hypoxic ischemic encephalopathy, brain tumor, recent neurosurgery, and PED.In resource-poor situation, EEG is frequently requested to confirm brain death, particularly where there is limited information on neurological examination or inconclusive apnea test; or when the patient is in prolonged state of coma. Presence of isoelectric tracing for at least 30 minutes in the EEG along with other clinical evidences is helpful in such situations. Extreme care should be taken for recording and reviewing continuous EEG (cEEG) monitoring at the ICU where sources of electrical noise are present. Patients identified with electrographic seizures and mild to moderate degree encephalopathy, with presence of normal background activities had better outcome compared to those with PED, monorrhythmic alpha beta coma and severe generalized encephalopathy. Real-time detection of ischemia at a reversible state is technologically feasible with cEEG and should be developed into a practical form for prevention of in-hospital infarction. Brain function monitoring with EEG is useful and this is in great demand at the ICU of present time. Such monitoring can help to improve neurological outcome in a variety of ICU settings. DOI: http://dx.doi.org/10.3329/bccj.v2i1.19954 Bangladesh Crit Care J March 2014; 2 (1): 28-34

Ambulatory Electroencephalograms in Neuropsychiatric Practice: Opening Pandora’s Jar

Since the advent of imaging studies such as magnetic resonance imaging (MRI), the role of electroencephalograms (EEGs) has diminished. Simultaneously, computerized scanning and miniaturization of the EEG and its components have allowed us to obtain lengthier recordings in an ambulatory setting. We report on 261 ambulatory electroencephalograms performed consecutively in the two year period of 2011 and 2012 in a busy neurology and neuropsychiatry practice with predominantly geriatric patient population. 23% of these patients had abnormal AEEGs demonstrating clear-cut epileptogenic discharges. The role of these findings in clinical practice, especially in geriatric and psychiatric populations is discussed.

Erratum to “Ambulatory Electroencephalograms in Neuropsychiatric Practice: Opening Pandora’s Jar”

Since the advent of imaging studies such as magnetic resonance imaging (MRI), the role of electroencephalograms (EEGs) has diminished. Simultaneously, computerized scanning and miniaturization of the EEG and its components have allowed us to obtain lengthier recordings in an ambulatory setting. We report on 261 ambulatory electroencephalograms performed consecutively in the two year period of 2011 and 2012 in a busy neurology and neuropsychiatry practice with predominantly geriatric patient population. 23% of these patients had abnormal AEEGs demonstrating clear-cut epileptogenic discharges. The role of these findings in clinical practice, especially in geriatric and psychiatric populations is discussed.

Challenges in the surgical treatment of epilepsy: hypothalamic hamartoma in infancy - case report

INTRODUCTION: Hypothalamic hamartoma is a rare congenital malformation, characterized by epilepsy, especially gelastic seizures, psychomotor developmental delay, mental retardation, behavioral disorders and precocious puberty. Epilepsy has early onset and is usually medically refractory. Etiology and pathophysiological mechanisms are unclear. The EEG can present disorganization and slowing of background activity and multifocal and/or generalized epileptogenic discharges. OBJECTIVE: To report the difficulties and challenges of neurosurgical treatment of a hypothalamic hamartoma in an infant. CASE REPORT: Infant with seizures since eight months old of age. The neurological investigation revealed a lesion in tuber cinereum suggestive of hamartoma. The epilepsy evolved with resistance to antiepileptic drugs, requiring neurosurgical procedure. The endoscopic resection could not be performed because the hamartoma was firmly attached to the hypothalamus. Currently, the child remains with tonic, clonic and atonic seizures. DISCUSSION: Lesionectomy performed by microsurgery or radiosurgery seems to be the most effective treatment for seizure control in patients with hypothalamic hamartomas who do not respond to clinical treatment. Callosotomy may be effective in selected cases, and lobectomy/cortical resections are not related to seizure control. In some patients, particularly in infants, lesionectomy and radiosurgery may be technically unfeasible.

A case of occipital epilepsy with anti-GluRε2 antibody in cerebrospinal fluid, presenting as repeated visual disturbance and headache

A 78-year-old man was admitted to our hospital with repeated attacks of headache and visual hallucinations, which had begun 10 days before. He also displayed left hemispatial neglect and left homonymous hemianopsia during attacks. Brain magnetic resonance imaging (MRI) showed an abnormal high-intense area in the right occipital lobe on diffusion weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) weighted imaging; this lesion was demonstrated as an area of hyperperfusion on ECD-single photon emission computed tomography (SPECT) and hypoperfusion on 123I-BZ-SPECT. Electroencephalography during an attack demonstrated epileptogenic discharges in the right occipital region. Acute urinary retention due to meningoencephalitis appeared 2 weeks after onset of the first attack. Autoantibodies against glutamate receptor epsilon2 were detected in cerebrospinal fluid. We diagnosed the patient with occipital epilepsy due to anti-NMDA receptor antibody encephalitis. Epileptic attacks diminished and MRI and SPECT findings improved following two administrations of intravenous bolus steroid therapy.

Diffusion tensor tractography detection of functional pathway for the spread of epileptiform activity between temporal lobe and Rolandic region

The aim of the study was to assess the connectivity between magnetoencephalographic (MEG) dipoles in the temporal lobe and Rolandic region in children with temporal lobe epilepsy using diffusion tensor imaging (DTI) tractography. Six pediatric patients with intractable focal epilepsy had MEG performed, which showed MEG dipoles over both temporal and Rolandic regions in a unilateral hemisphere. DTI tractography was performed on each patient. Six control subjects were studied for comparison. Two volumes of interest (VOIs) that encompassed the MEG dipoles were drawn, one placed in temporal lobe and the other in Rolandic region. Similar VOIs were placed in the contralateral side in the patients and on both sides in controls. Fractional anisotropy (FA) and trace of the external capsules were compared between patients and controls. In all patients, a tractography pathway traversing through the external capsule, connecting the temporal and Rolandic MEG dipoles, was visualized. However, on the contralateral hemisphere in each patient, there was no evidence of a similar fiber tract. There was no corresponding tractography pathway identified in either hemisphere within the controls. There were no significant differences in FA and trace between the seizure focus side and contralateral side in the patients. There was no significant difference in FA, but a difference in trace between patients and controls. We have found aberrant tractography pathway traversing through the external capsule, connecting two distant foci of epileptiform activity. Chronic interictal epileptogenic discharge could play a causal role in the de novo organization of these tracts.