Chronic Epilepsy Patients Research Articles

Evaluation of latent-transforming growth factor beta-binding protein, dopamine and serotonin in patients with chronic epilepsy according to disease type and body mass index

The study aimed to evaluate some biochemical, immunological, physiological and neurotransmitter variables in chronic epilepsy patients. The study comprised 60 patients with epilepsy and a control group of 30 healthy persons, aged between 15 and 60 years. The investigation involved quantifying the amounts of dopamine, serotonin, latent-transforming growth factor beta-binding protein 1 (LTBP1), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). The findings of the present investigation indicated the following: A notable reduction (p≤0.01) in the levels of latent transforming growth factor binding proteins (LTBP1) relative to the control group. A notable elevation (p≤0.01) in the levels of dopamine, alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) was observed in comparison to the control values. A substantial elevation (p≤0.05) in serotonin levels was observed relative to the control data. This study indicated a reduction in the levels of LTBP1. The concentration of dopamine, serotonin, AST, ALT, and ALP is elevated in patients with persistent epilepsy compared to healthy individuals.

Metabolic Adaptation in Epilepsy: From Acute Response to Chronic Impairment.

Epilepsy is characterized by hypersynchronous neuronal discharges, which are associated with an increased cerebral metabolic rate of oxygen and ATP demand. Uncontrolled seizure activity (status epilepticus) results in mitochondrial exhaustion and ATP depletion, which potentially generate energy mismatch and neuronal loss. Many cells can adapt to increased energy demand by increasing metabolic capacities. However, acute metabolic adaptation during epileptic activity and its relationship to chronic epilepsy remains poorly understood. We elicited seizure-like events (SLEs) in an in vitro model of status epilepticus for eight hours. Electrophysiological recording and tissue oxygen partial pressure recordings were performed. After eight hours of ongoing SLEs, we used proteomics-based kinetic modeling to evaluate changes in metabolic capacities. We compared our findings regarding acute metabolic adaptation to published proteomic and transcriptomic data from chronic epilepsy patients. Epileptic tissue acutely responded to uninterrupted SLEs by upregulating ATP production capacity. This was achieved by a coordinated increase in the abundance of proteins from the respiratory chain and oxidative phosphorylation system. In contrast, chronic epileptic tissue shows a 25-40% decrease in ATP production capacity. In summary, our study reveals that epilepsy leads to dynamic metabolic changes. Acute epileptic activity boosts ATP production, while chronic epilepsy reduces it significantly.

Prediction and analysis of chronic epilepsy using electroencephalographic signals on medical internet of things platform

Epilepsy patients who are presently refractory may be monitored using a seizure prediction Brain-Computer Interface (BCI), which uses electrodes strategically implanted in the brain to anticipate and regulate the onset and duration of a seizure. Real-time approaches to these technologies have challenges, as seen by seizures’ instantaneous electrographic activity. Electroencephalographic (EEG) signals are inherently non-stationary, which means that the regular and seizure signals differ significantly among people with epilepsy. Due to the restricted number of contacts on electrodes, dynamically processed and collected characteristics cannot be employed in a prediction function without causing significant processing delays. Big data can guarantee secure storage in these situations, and it has the maximum processing capability to identify, record, and analyze time in real-time to conduct the seizure event on the timetable. Seizure prediction and location for huge Scalp EEG recordings have been the focus of this study, which used wearable sensor data and deep learning to use cloud storage to develop the systems. A novel technique is suggested to avoid an epileptic seizure and discover the seizure origin from the utilized wearable sensors. Secondly, deep learning architectures called Clustered Autoencoder with Convolutional Neural Network (CAE-CNN), an expanded optimization methodology is presented based on the Principal Component Analysis (PCA), the Hierarchical Searching Algorithm (HSA), and the Medical Internet of Things (MIoT) has been established to define the suggested frameworks based on the collection of big data storage of the wearable sensors in real-time, automatic computation and storage. According to clinical trials, CAE-CNN outperforms the current wearable sensor-based treatment for unresolved chronic epilepsy patients.

Recurrent seizures of autoimmune origin: emerging phenotypes.

Recurrent seizures of autoimmune origin (AEp) are one of the most frequent causes of recurrent seizures or suspected epilepsy of unknown cause. The aim of this study was to identify specific phenotypes corresponding to AEp. We retrospectively reviewed features of patients with recurrent seizures of unknown cause and investigated for suspected AEp (January 2015-May 2018). Patients were separated in: (1) AEpAb+: AEp with positive autoantibodies; (2) AEpAb-: suspected AEp (inflammatory central nervous system (CNS) profile) without autoantibodies; (3) NAEp: epilepsy without CNS inflammation. Eighty-nine epileptic patients underwent a CSF antibody detection. From the remaining 57 epileptic patients (32 excluded for a differential diagnosis), 61.4% were considered as AEp. 21% were AEpAb+ (4 NMDAR, 2 GABAbR, 3 GAD-Ab, 2 LGi1, 1 CASPR2), 40.4% AEpAb-, and 38.6% NAE. AE (AEpAb+ and AEpAb-) was significantly associated with antibody prevalence in epilepsy (APE) score ≥ 4 (80%), encephalitic phase (71.4%), psychiatric involvement (64.7%), cognitive impairment (50%), and status epilepticus (41.2%). Within the group of 29 patients without encephalitic phase and with chronic epilepsy (NEPp), 34.5% were defined as AEp. 10.4% were AEpAb+ (2GAD, 1 CASPR2) and 24.1% were AEpAb-. NEP AEp was associated with non-cerebral autoimmune disorders, short epileptic disease duration, and cognitive impairment. Autoimmune cause (AEp) should be assessed in patient suffering from recurrent seizures of unknown cause. Acute encephalitis is clearly the main AEp phenotype. AEp was also defined in more than one-third of chronic epilepsy patients (NEP) of unknown cause. Then, AEp may be combined with other autoimmune comorbidities, a shorter evolution of recurrent seizures, and cognitive impairment.

Extent of Single-Neuron Activity Modulation by Hippocampal Interictal Discharges Predicts Declarative Memory Disruption in Humans.

Memory deficits are common in epilepsy patients. In these patients, the interictal EEG commonly shows interictal epileptiform discharges (IEDs). While IEDs are associated with transient cognitive impairments, it remains poorly understood why this is. We investigated the effects of human (male and female) hippocampal IEDs on single-neuron activity during a memory task in patients with medically refractory epilepsy undergoing depth electrode monitoring. We quantified the effects of hippocampal IEDs on single-neuron activity and the impact of this modulation on subjectively declared memory strength. Across all recorded neurons, the activity of 50 of 728 neurons were significantly modulated by IEDs, with the strongest modulation in the medial temporal lobe (33 of 416) and in particular the right hippocampus (12 of 58). Putative inhibitory neurons, as identified by their extracellular signature, were more likely to be modulated by IEDs than putative excitatory neurons (19 of 157 vs 31 of 571). Behaviorally, the occurrence of hippocampal IEDs was accompanied by a disruption of recognition of familiar images only if they occurred up to 2 s before stimulus onset. In contrast, IEDs did not impair encoding or recognition of novel images, indicating high temporal and task specificity of the effects of IEDs. The degree of modulation of individual neurons by an IED correlated with the declared confidence of a retrieval trial, with higher firing rates indicative of reduced confidence. Together, these data link the transient modulation of individual neurons by IEDs to specific declarative memory deficits in specific cell types, thereby revealing a mechanism by which IEDs disrupt medial temporal lobe-dependent declarative memory retrieval processes.SIGNIFICANCE STATEMENT Interictal epileptiform discharges (IEDs) are thought to be a cause of memory deficits in chronic epilepsy patients, but the underlying mechanisms are not understood. Utilizing single-neuron recordings in epilepsy patients, we found that hippocampal IEDs transiently change firing of hippocampal neurons and disrupted selectively the retrieval, but not encoding, of declarative memories. The extent of the modulation of the individual firing of hippocampal neurons by an IED predicted the extent of reduction of subjective retrieval confidence. Together, these data reveal a specific kind of transient cognitive impairment caused by IEDs and link this impairment to the modulation of the activity of individual neurons. Understanding the mechanisms by which IEDs impact memory is critical for understanding memory impairments in epilepsy patients.

Effects of eslicarbazepine on slow inactivation processes of sodium channels in dentate gyrus granule cells.

Pharmacoresistance is a problem affecting ∼30% of chronic epilepsy patients. An understanding of the mechanisms of pharmacoresistance requires a precise understanding of how antiepileptic drugs interact with their targets in control and epileptic tissue. Although the effects of (S)-licarbazepine (S-Lic) on sodium channel fast inactivation are well understood and have revealed maintained activity in epileptic tissue, it is not known how slow inactivation processes are affected by S-Lic in epilepsy. We have used voltage clamp recordings in isolated dentate granule cells (DGCs) and cortical pyramidal neurons of control versus chronically epileptic rats (pilocarpine model of epilepsy) and in DGCs isolated from hippocampal specimens from temporal lobe epilepsy patients to examine S-Lic effects on sodium channel slow inactivation. S-Lic effects on entry into and recovery from slow inactivation were negligible, even at high concentrations of S-Lic (300 μmol/L). Much more pronounced S-Lic effects were observed on the voltage dependence of slow inactivation, with significant effects at 100 μmol/L S-Lic in DGCs from control and epileptic rats or temporal lobe epilepsy patients. For none of these effects of S-Lic could we observe significant differences either between sham-control and epileptic rats, or between human DGCs and the two animal groups. S-Lic was similarly effective in cortical pyramidal neurons from sham-control and epileptic rats. Finally, we show in expression systems that S-Lic effects on slow inactivation voltage dependence are only observed in Nav 1.2 and Nav 1.6 subunits, but not in Nav 1.1 and Nav 1.3 subunits. From these data, we conclude that a major mechanism of action of S-Lic is an effect on slow inactivation, primarily through effects on slow inactivation voltage dependence of Nav 1.2 and Nav 1.6 channels. Second, we demonstrate that this main effect of S-Lic is maintained in both experimental and human epilepsy and applies to principal neurons of different brain areas.

Neuronal Nitric Oxide Synthase Contributes to PTZ Kindling Epilepsy-Induced Hippocampal Endoplasmic Reticulum Stress and Oxidative Damage.

Epilepsy is one of the most common chronic neurological disorders which provoke progressive neuronal degeneration. Endoplasmic reticulum (ER) stress has recently been recognized as pivotal etiological factors contributing to epilepsy-induced neuronal damage. However, the specific contribution of epilepsy made to ER stress remains largely elusive. Here we use pentylenetetrazole (PTZ) kindling, a chronic epilepsy model, to identify neuronal nitric oxide synthase (nNOS) as a signaling molecule triggering PTZ kindling epilepsy-induced ER stress and oxidative damage. By genetic deletion of nNOS gene, we further demonstrated that nNOS acts through peroxynitrite, an important member of reactive nitrogen species, to trigger hippocampal ER stress and oxidative damage in the PTZ-kindled mice. Our findings thus define a specific mechanism for chronic epilepsy-induced ER stress and oxidative damage, and identify a potential therapeutic target for neuroprotection in chronic epilepsy patients.

Effective clinical classification of chronic epilepsy into focal and generalized: A cross sectional study

PurposeInvestigations such as EEG and brain imaging are often difficult to obtain in primary care settings of resource-limited regions impacting millions of epilepsy patients. We wanted to test the hypothesis that classification of chronic epilepsy into focal and generalized based on clinical history and examination alone would be comparable to making such a classification with additional inputs from EEG and brain imaging. MethodsTwo investigators independently classified consecutive chronic epilepsy patients into focal, generalized and unclassified epilepsy. Investigator 1 made this determination using clinical history and examination alone whereas Investigator II additionally used EEG and brain imaging too. We calculated inter observer agreement between the two investigators and also looked at the predictors of focal and generalized epilepsy. ResultsFive hundred and twelve patients were recruited. Inter observer agreement between the two investigators in making the focal versus generalized classification was 96.8%, kappa 0.91 (p<0.0001). When EEG and neuroimaging findings were added to clinical information, there was a change in classification in 3.2% patients. Several predictors of focal and generalized epilepsy were identified. ConclusionsClassification of chronic epilepsy into focal and generalized can be done reliably in most patients using clinical information alone. Investigating chronic epilepsy patients with EEG and brain imaging may not be necessary in every patient. The results of our study are especially significant for epilepsy patients living in resource-limited regions where such investigations may not always be available.

Neuronal Nitric Oxide Synthase Contributes to PTZ Kindling-Induced Cognitive Impairment and Depressive-Like Behavior.

Epilepsy is a chronic neurological disease which is usually associated with psychiatric comorbidities. Depsression and cognition impairment are considered to be the most common psychiatric comorbidities in epilepsy patients. However, the specific contribution of epilepsy made to these psychiatric comorbidities remains largely unknown. Here we use pentylenetetrazole (PTZ) kindling, a chronic epilepsy model, to identify neuronal nitric oxide synthase (nNOS) as a signaling molecule triggering PTZ kindling-induced cognitive impairment and depressive-like behavior. Furthermore, we identified that both hippocampal MAPK and PI3K/AKT signaling pathways were activated in response to PTZ kindling, and the increased MAPK and PI3K/AKT signaling activation was paralleled by increased level of reactive oxygen species (ROS) in the hippocampus. However, the PTZ kindling-induced MAPK, PI3K/AKT signaling activities and the ROS level were attenuated by nNOS gene deficiency, suggesting that nNOS may act through ROS-mediated MAPK and PI3K/AKT signaling pathways to trigger cognition deficit and depressive-like behavior in PTZ-kindled mice. Our findings thus define a specific mechanism for chronic epilepsy-induced cognitive impairment and depressive-like behavior, and identify a potential therapeutic target for psychiatric comorbidities in chronic epilepsy patients.

Saccadic Eye Movement Abnormalities in Children with Epilepsy.

Childhood onset epilepsy is associated with disrupted developmental integration of sensorimotor and cognitive functions that contribute to persistent neurobehavioural comorbidities. The role of epilepsy and its treatment on the development of functional integration of motor and cognitive domains is unclear. Oculomotor tasks can probe neurophysiological and neurocognitive mechanisms vulnerable to developmental disruptions by epilepsy-related factors. The study involved 26 patients and 48 typically developing children aged 8–18 years old who performed a prosaccade and an antisaccade task. Analyses compared medicated chronic epilepsy patients and unmedicated controlled epilepsy patients to healthy control children on saccade latency, accuracy and dynamics, errors and correction rate, and express saccades. Patients with medicated chronic epilepsy had impaired and more variable processing speed, reduced accuracy, increased peak velocity and a greater number of inhibitory errors, younger unmedicated patients also showed deficits in error monitoring. Deficits were related to reported behavioural problems in patients. Epilepsy factors were significant predictors of oculomotor functions. An earlier age at onset predicted reduced latency of prosaccades and increased express saccades, and the typical relationship between express saccades and inhibitory errors was absent in chronic patients, indicating a persistent reduction in tonic cortical inhibition and aberrant cortical connectivity. In contrast, onset in later childhood predicted altered antisaccade dynamics indicating disrupted neurotransmission in frontoparietal and oculomotor networks with greater demand on inhibitory control. The observed saccadic abnormalities are consistent with a dysmaturation of subcortical-cortical functional connectivity and aberrant neurotransmission. Eye movements could be used to monitor the impact of epilepsy on neurocognitive development and help assess the risk for poor neurobehavioural outcomes.

Neuronal autoantibodies in epilepsy patients with peri-ictal autonomic findings.

Autonomic dysfunction has frequently been reported in autoimmune encephalitis associated with seizures and there is growing evidence that epilepsy patients may display neuronal autoantibodies (NAAb). The aim of this study was to investigate the frequency of NAAb in epilepsy patients with peri-ictal autonomic findings. Fifty-eight patients (37 women/21 men; average age of 34.2 ± 9.9 years and epilepsy duration of 19.1 ± 9.6 years) who had at least one video-EEG recorded focal or secondary generalized seizure with clear-cut documented peri-ictal autonomic findings, or consistently reported seizures with autonomic semiology, were included. NAAb were tested by RIA or cell based assays. NAAb were present in 17 of 58 (29.3%) patients. Among seropositive patients, antibodies were directed against N-methyl-D-aspartate receptor (NMDAR) in 5 (29%), contactin-associated protein-like 2 (CASPR2) in 5 (29%), uncharacterized voltage gated potassium channel (VGKC)-complex antigens in 3 (18%), glutamic acid decarboxylase (GAD) in 2 (12%), glycine receptor (GLYR) in one (6%) and type A gamma aminobutyric acid receptor (GABAAR) in one patient (6%). Peri-ictal gastrointestinal manifestations, piloerection, ictal fever, urinary urge, and cough occurred more commonly in the seropositive group. The prevalences of psychotic attacks and status epilepticus were significantly increased in the seropositive group. Seropositivity prevalence in our patient group with peri-ictal autonomic findings is higher than other previously reported epilepsy cohorts. In our study, ictal fever-VGKC-complex antibody and pilomotor seizure-GABAAR antibody associations were documented for the first time. Chronic epilepsy patients with peri-ictal autonomic semiology, history of status epilepticus and psychotic disorder may benefit from autoantibody screening.

Psychogenic nonepileptic spells in chronic epilepsy patients with moderate cognitive impairment: the need for video EEG monitoring for adequate diagnosis.

The objective of our study was to emphasize the importance of intensive video EEG monitoring in patients with a well-established diagnosis of epilepsy with moderate cognitive impairment. The idea was to diagnose new onset frequent atypical events prompting the need for frequent emergency room and clinic visits and hospital admissions. Retrospective chart reviews were conducted on patients with chronic epilepsy with moderate cognitive impairment who had an increased incidence of new onset episodes different from the baseline seizures. Data were acquired from electronic medical records. The hospital's Institutional Review Board gave approval for this retrospective analysis of patient records. We retrospectively analyzed data from three patients with an established diagnosis of epilepsy. Extensive chart reviews were performed with emphasis on type and duration of epilepsy and description of baseline seizures and description of new events. There were two men and one woman with moderate cognitive impairment. One subject had generalized epilepsy and other two had temporal lobe epilepsy. The patients were on an average of two to three antiepileptic medicines. The duration of follow-up in our neurology clinic ranged from 9 months to 5 years. The occurrence of increased frequency of these atypical events as described by the caregivers, despite therapeutic anticonvulsant levels, prompted the need for 5-day intensive video EEG monitoring. New atypical spells were documented in all three patients and the brain waves were normal during those episodes. The diagnosis of pseudoseizures was made based on the data acquired during the epilepsy monitoring unit stay. Our data analysis showed that intensive video EEG monitoring is an important tool to evaluate change in frequency and description of seizures even in cognitively impaired patients with an established diagnosis of epilepsy for adequate seizure management.

Side-effects of antiepileptic drugs: The economic burden

PurposeAntiepileptic drugs are a potentially effective treatment for epilepsy. Side-effects are, however, common and the negative consequences necessitate treatment ranging from minor interventions to very expensive hospitalization. This analysis has been conducted to provide insight into the costs of side-effects due to antiepileptic drugs in The Netherlands from a societal perspective. MethodResources allocated to care (grouped according to health, patient and family and other) for five different categories of side-effect were measured using a questionnaire. Standard cost prices were derived from the Dutch costing manual. Chronic epilepsy patients were invited to complete the questionnaire if they had experienced side-effects during the previous 12 months. ResultsBased on data from 203 patients, the total societal costs of common side-effects in 2012 are estimated to be €20,751 CI:15,049–27,196 (US$26,675 CI:19,345–34,960) per patient per year. These consist of: health care costs (mean €4458; US$5731), patient and family costs (i.e. informal care, mean €10,526; US$13,531) and other costs (i.e. productivity losses, mean €5761; US$7406). Examining the different categories of side-effects separately, ranging from the most to the least expensive category, the cost estimates per patient per year were as follows: other (mean €13,228; US$17,005), behavioral (mean €9689; US$12,455), general health (mean €7454; US$9582), cognitive (mean €7285; US$9365) and cosmetic side-effects (mean €2845; US$3657). Subgroup analyses showed significant differences in costs between patients using monotherapy and those using polytherapy when looking at cognitive and cosmetic side-effects. ConclusionThese estimates should be considered in the overall assessment of the economic impact of a pharmacotherapy.

The new wave: time to bring EEG to the emergency department

Emergency electroencephalography (EEG) is indicated in the diagnosis and management of non-convulsive status epilepticus (NCSE) underlying an alteration in the level of consciousness. NCSE is a frequent, treatable, and under-diagnosed entity that can result in neurological injury. This justifies the need for EEG availability in the emergency department (ED). There is now emerging evidence for the potential benefits of EEG monitoring in various acute conditions commonly encountered in the ED, including convulsive status after treatment, breakthrough seizures in chronic epilepsy patients who are otherwise controlled, acute head trauma, and pseudo seizures. However, attempts to allow for routine EEG monitoring in the ED face numerous obstacles. The main hurdles to an optimized use of EEG in the ED are lack of space, the high cost of EEG machines, difficulty of finding time, as well as the expertise needed to apply electrodes, use the machines, and interpret the recordings. We reviewed the necessity for EEGs in the ED, and to meet the need, we envision a product that is comprised of an inexpensive single-use kit used to wirelessly collect and send EEG data to a local and/or remote neurologist and obtain an interpretation for managing an ED patient.

Inflammation in epilepsy: Clinical observations

Over the past decade, an increasing number of observations indicate that activation of inflammatory processes occurs in variety of focal epilepsies. Understanding the feature and consequences of neuroinflammation, including the contribution to development and perpetuation of seizures, as well as to mood or cognitive dysfunction, is a major requisite for delineating its role in epilepsy. The present article discusses the most recent observations supporting the involvement of the inflammatory response in human focal epilepsy. It also evaluates emerging evidence concerning the possibility to identify epilepsy-associated inflammatory biomarkers in cerebrospinal fluid and serum, as well as the potential application of neuroimaging approaches to study the inflammatory reactions in chronic epilepsy patients in vivo, aiming to improve the recognition of appropriate patient populations who might benefit from antiinflammatory or immunomodulatory therapies.

Coexistent pathology in chronic epilepsy patients with neoplasms

Neoplasms are a well-established cause of medically intractable or chronic epilepsy. Certain tumors, including gangliogliomas and dysembryoplastic neuroepithelial tumors, are well known to be associated with cortical dysplasia. This study retrospectively examines the incidence of coexistent pathology in patients with tumors and chronic epilepsy. This study is a retrospective review of 270 tumors arising in patients with medically intractable epilepsy encountered during a 20-year period (1989–2009). Coexistent pathology was noted in 50 of 270 (17.8%) patients, including 27 males (54%) with a mean age at surgery of 18 years (range 1–52 years). The vast majority of lesions (n=40) (80%) were located in the temporal lobe and less commonly in the parietal lobe (n=4) and the occipital lobe (n=3). Tumor diagnoses included ganglioglioma (n=29), dysembryoplastic neuroepithelial tumor (n=10), low-grade glial/glioneuronal neoplasm (n=5), low-grade astrocytoma (n=2), angiocentric glioma (n=1), low-grade mixed glioma (n=1), dysembryoplastic neuroepithelial tumor/ganglioglioma mixed tumor (n=1), and meningioangiomatosis (n=1). Forty-one (82%) tumors represented WHO grade-I neoplasms. Concomitant pathology included malformation of cortical development (cortical dysplasia) in 40 patients (80%) (Palmini et al type-I: n=37; Palmini et al type-II: n=3). Hamartias were identified in 10 patients (20%), hippocampal sclerosis in four patients (8%), and nodular heterotopia in one patient (2%). The true incidence of coexistent pathology (17.8% in this study) was likely underrepresented, given the limited extent of adjacent non-tumoral tissue sampling in cases of resected tumor. Coexistent pathology may account for the incidence of recurrent or residual epilepsy in patients who undergo tumor resection.

MR imaging of implanted depth and subdural electrodes: is it safe?

This study evaluates the safety of imaging chronic epilepsy patients with intracranial depth and subdural electrodes by magnetic resonance (MR). To identify an epileptogenic focus, the precise location of the electrode contacts is necessary, and MR can provide this information. However, many neurosurgeons and neuroradiologists are hesitant to scan patients by MR with these implanted, metallic electrodes for fear of electrode displacement, current induction or heating secondary to the strong magnetic field. In the present study, the subdural electrodes were made of stainless steel with either stainless steel or platinum contacts. The depth electrodes were made of either platinum or a nickel-chromium alloy (nichrome). We reviewed 98 cases in which patients with implanted depth electrodes, subdural electrodes, or both underwent MR scanning. A total of 143 depth electrodes, 688 subdural strips, and 38 subdural grids were implanted in the 98 procedures. MR scanning was performed on a 1.5-T unit and consisted of T1, T2, and/or spoiled gradient echo pulse sequences. There were no documented complications related to the MR scans. Based on this study and a review of the literature, we feel that MR imaging can safely localize intracranial electrodes.

Neocortical dendritic pathology in human partial epilepsy: a quantitative Golgi study.

We used a computerized image-analysis system to perform a quantitative analysis of rapid Golgi-impregnated pyramidal neurons of the third cortical layer of histologically normal cerebral cortex surgically removed from patients with partial epilepsy. Various parameters of 51 neurons from 9 patients and 29 neurons from 5 age-matched controls were compared. Dendritic spine density decreased progressively with increasing duration of seizures, and dendritic swellings were most numerous in epilepsy cases of uncertain etiology and in patients with seizures of longer standing. Neurons from seizure cases showed fewer dendritic branching points and fewer proximal dendritic branches than those from controls, suggesting a simplified dendritic architecture. These findings indicate that neurons in cortex distant from the primary site of epileptogenic activity may be undergoing subtle, progressive degeneration, which may explain the propensity of chronic epilepsy patients to have increased seizure activity and interictal behavioral and cognitive aberrations.