bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuropsychological Effect of Temporal Lobe Resection in Preadolescent Children with Epilepsy
Authors: Szabó C. Akos , Wyllie Elaine , Stanford Lisa D. , Geckler Cheri , Kotagal Prakash , Comair Youssef G. , Thornton Allen E. 
Published: August 2005

Summary: Purpose: Numerous studies have demonstrated changes in cognitive, memory, and language functioning in adults and adolescents after temporal lobectomy, yet little information is available regarding neuropsychological outcome in preadolescent children. Methods: We studied pre‐and postoperative neuropsychological test results from 14 children who underwent temporal lobe resection for intractable epilepsy at age 7–12 years (mean 9.4 years). Results: Thirteen patients (93%) had no seizures or less than one seizure a year at follow‐up 23‐48 months (mean 34 months) after operation. Postoperative neuropsychological testing was performed 6–9 months (mean 7 months) after surgery in 13 patients and 36 months after the first operation in 1 patient who underwent two‐stage resection of a tumor. Verbal, Performance, and Full Scale IQ were initially in the low‐average range, with no significant change across the pre‐and postoperative evaluations. Immediate verbal memory performance decreased significantly in children who initially performed above the median preoperatively and tended to decrease in children who had left rather than right temporal lobe resection. Significant postoperative decreases in delayed memory scores were independent of preoperative ability or side of resection. Conclusions: Our small study suggests vulnerability to postoperative decline in immediate verbal memory scores in preadolescent children who have higher baseline immediate memory function or undergo left rather than right temporal lobe resection, similar to that observed in adolescents in adults. The entire group exhibited a statistically significant decrease in delayed verbal memory. Study of larger series of patients will be important to clarify further the short‐and long‐term risks and benefits of temporal lobe resection in childhood.
When Should Induction Protocols Be Used in the Diagnostic Evaluation of Patients with Paroxysmal Events?
Authors: Parra Jaime , Kanner Andrés M. , Iriarte Jorge , Gil‐Nagel Antonio 
Published: August 2005

Summary: Purpose: To determine the timing of spontaneous psychogenic nonepileptic events (PNEE) during video‐EEG telemetry (VEEG), and the need to use induction protocols (IP). Methods: We studied 100 consecutive patients (75 females, 25 males) admitted to our inpatient VEEG unit from July 1994 to June 1996 for differential diagnosis of paroxysmal events. We recorded the time to the first diagnostic spontaneous event, identified by the patient or a family member as typical. Episodes were classified as PNEE, physiologic nonepileptic events (PhysNEE), and epileptic seizures (ES). Results: The mean duration of VEEG was 74 ± SD 54.1 h. In 82 patients, a diagnostic event occurred spontaneously. The first event was an ES in 22 patients, a PNEE in 53, and a PhysNEE in 7. The time to first diagnostic event was significantly shorter for PNEE than for ES [15.0 ± SD 16.3 h (range 5 min to 58 h) vs. 28.6 ± SD 34.0 h (range 1–110 h) F= 15.621, p <0.00011. In the first 24 h, 77.4% of the patients with PNEE had an event. By 48 h, all but 2 (96.2%) had had diagnostic events. After the first 58 h of monitoring, all patients with PNEE experienced a spontaneous diagnostic event. Conclusion: Spontaneous events can be expected to occur within 48 h in most patients with PNEE. Therefore, if IP are to be used as a diagnostic tool, we suggest that they be withheld during the initial 48 h of VEEG monitoring.
Positive and Negative Psychotropic Effects of Lamotrigine in Patients with Epilepsy and Mental Retardation
Authors: Ettinger Alan B. , Weisbrot Deborah M. , Saracco Jennifer , Dhoon Aliasgar , Kanner Andres , Devinsky Yorrin 
Published: August 2005

Summary: Purpose: To describe significant positive or negative psychotropic effects of lamotrigine (LTG) observed in epilepsy patients with mental retardation (MR). Methods: Seven mentally retarded epilepsy patients, [5 with Lennox‐Gastaut syndrome (LGS)] who experienced significant behavioral improvements or worsening after addition of LTG to their medication regimen were studied. Results: LTG produced behavioral improvements in 4 patients. Patient 1, a 14‐year‐old girl, had LTG added to valproate (VPA) and thioridazine, resulting in diminished lethargy, less hyperactivity, and more appropriate speech. In a 17‐year‐old boy (patient 2) LTG added to VPA, phenytoin (PHT), and gabapentin (GBP) lessened irritability and hyperactivity. In patient 3, a 41‐year‐old woman, LTG added to PHT, VPA, and carbamazepine (CBZ) diminished lethargy and enhanced her social interactions. In patient 4, a 27‐year‐old man, LTG monotherapy diminished irritability and hyperactivity. Adverse behavioral effects were noted in 3 patients. In patient 5, a 43‐ year‐old man, LTG added to PHT, phenobarbital (PB), lorazepam, sertraline, and thioridazine produced irritability, hyperactivity, and poor cooperation. In patient 6, a 29‐year‐old woman, LTG added to VPA produced frequent screaming, temper tantrums, increased rocking movements, and hyperactivity. In patient 7, a 29‐year‐old man, LTG added to VPA and PHT resulted in severe exacerbation of baseline behaviors, including self‐injurious activity, temper tantrums, and failure to obey simple instructions. Conclusions: In some patients with epilepsy and MR, LTG has significant positive or negative effects on behavior.
Brain Thyrotropin‐Releasing Hormone Content Varies Through Amygdaloid Kindling Development According to Afterdischarge Frequency and Propagation
Authors: de Gortari P. , Joseph‐Bravo P. , Monroy‐Ruiz J. , Martínez A. , Cisneros M. , Guardiola A. Fernández 
Published: August 2005

Summary: Purpose: Thyrotropin‐releasing hormone (TRH), present in extra hypothalamic brain areas, has been proposed to have neuromodulatory functions and to be susceptible to change by electrical stimulation paradigms. We measured TRH concentrations of several brain areas during kindling development before its establishment and determined whether the changes detected in TRH levels were related to the behavioral stages of kindling, the number of stimulations required to reach these stages and, with the electrophysiological parameters characteristic of this paradigm (amygdaloid afterdischarge (AD) frequency, duration, and propagation). Methods: Male Wistar rats were implanted stereotaxically with indwelling bipolar electrodes in the basolateral nucleus of the amygdala and with two stainless‐steel electrodes epidurally in frontal cortex. Amygdaloid kindling was induced by daily electrical stimulation; AD frequency and duration were recorded and analyzed throughout the development of kindling. TRH was extracted from several regions and quantified by radioimmunoassay (RIA). Results: Modifications in TRH concentrations were detected, depending on the region assayed, from stage II of kindling. A positive correlation was noted between the levels of TRH and the frequency and propagation of AD, but not with the number of stimulations. The rate of change in TRH concentration in relation to AD frequency or duration was highest in frontal cortex followed by hippocampus and amygdala. Conclusions: A graded response was noted in the increase in TRH concentration dependent on the increase of AD frequency and propagation. The rate of response correlated with the region's epileptogenic susceptibility.
Antiepileptic Drugs as a Cause of Worsening Seizures
Authors: Perucca E. , Gram L. , Avanzini G. , Dulac O. 
Published: August 2005

Summary: Purpose: Although the paradoxical ability of anti‐epileptic drugs (AEDs) to increase seizure activity has been recognized for decades, the underlying mechanisms are poorly understood and few systematic studies have addressed this problem. This article is intended to provide a critical review of available literature on this topic. Methods: Information was collected by means of computerized literature searches, screening of journals and textbooks, and consultation with colleagues. Mechanisms which potentially might precipitate underlying drug‐induced exacerbation of seizures were considered based on available pharmacologic and clinical knowledge. Results: The reviewed information suggests that a paradoxical increase in seizure frequency may occur as a result of at least two separate mechanisms. The first appears to involve a nonspecific manifestation of drug intoxication; seizure‐worsening in this context is usually reversible by dosage reduction or elimination of unnecessary polypharmacy. Conversely, the other mechanism may involve a distinct adverse primary action of the drug in specific seizure types or in syndromic forms. Carabamazepine, in particular, has been reported to precipitate or exacerbate a variety of seizures, most notably absence, atonic, or myoclonic seizures in patients with generalized epilepsies characterized by bursts of diffuse and bilaterally synchronous spike‐and‐wave EEG activity. Phenytoin and vigabatrin also have been implicated in worsening of seizures, particularly generalized seizures, whereas gabapentin has been associated repeatedly with precipitation of myoclonic jerks. Benzodiazepines occasionally have been reported to precipitate tonic seizures, especially when given intravenously to control other seizure types in patients with Lennox‐Gastaut syndrome. Seizure deterioration has been reported also with other drugs; though in most cases evidence is still insufficient for meaningful conclusions to be drawn. Conclusions: Drug‐induced exacerbation of seizures is a serious and common clinical problem that is often unrecognized or overlooked by the treating physician. Its occurrence appears to be related to three possible causes: an incorrect diagnosis of seizure type or syndromic form, lack of knowledge about certain drugs that are contraindicated in specific types of epilepsies, or to prescription of excessive drug dosages and drug combinations. Further studies are required to evaluate the prevalence of this phenomenon of drug‐induced exacerbation of seizures, to investigate its mechanisms in greater detail and to characterize additional prognostic factors that may be used for early identification of patients at risk.
Treatment of Refractory Status Epilepticus with Propofol: Clinical and Pharmacokinetic Findings
Authors: Stecker Mark M. , Kramer Thomas H. , Raps Eric C. , O'Meeghan Rosemary , Dulaney Eugene , Skaar Debra J. 
Published: August 2005

Summary: Purpose: We compared propofol with high‐dose barbiturates in the treatment of refractory status epilepticus (RSE) and propose a protocol for the administration of propofol in RSE in adults, correlating propofol's effect with plasma levels. Methods: Sixteen patients with RSE were included; 8 were treated primarily with high‐dose barbiturates and 8 were treated primarily with propofol. Results: Both groups of patients had multiple medical problems and a subsequent high mortality. A smaller but not statistically significant fraction of patients had their seizures controlled with propofol (63%) than with high‐dose barbiturate therapy (82%). The time from initiation of high‐dose barbiturate therapy to attainment of control of RSE was longer (123 min) than the time to attainment of seizure control in the group receiving propofol (2.6 min, p = 0.002). Plasma concentrations of propofol associated with control of SE were 14 μM ± 4 (2.5 μg/ml). Recurrent seizures were common when propofol infusions were suddenly discontinued but not when the infusions were gradually tapered. Conclusions: If used appropriately, propofol infusions can effectively and quickly terminate many but not all episodes of RSE. Propofol is a promising agent for use in treating RSE, but more studies are required to determine its true value in comparison with other agents.
Reversible Pseudoatrophy of the Brain and Mental Deterioration Associated with Valproate Treatment
Authors: Guerrini Renzo , Belmonte Anna , Canapicchi Raffaello , Casalini Claudia , Perucca Emilio 
Published: August 2005

Summary: Purpose: To describe an 11‐year‐old girl with symptomatic localization‐related epilepsy and normal intelligence who developed reversible mental deterioration and pseudoatrophic brain changes while receiving valproate (VPA). Methods: Assessment of mental function using Wechsler Intelligence Scale for Children‐III (WISC) and Raven's Progressive Matrices (PM), EEG recordings while awake and asleep, and brain magnetic resonance imaging (MRI), were performed at the beginning of VPA therapy, after 2 years and 8 months of treatment and following VPA discontinuation. Results: After 2 years and 6 months on VPA (≤26 mg/kg/day) the girl insidiously developed mental deterioration (loss of 18 IQ points and drop in age‐adjusted PM score from the 95th to the 50th percentile) associated with MRI‐documented pseudoatrophy of the brain. Onset of severe cognitive impairment coincided with serum VPA concentrations near 100 μg/ml. There were no other manifestations of drug toxicity or hyperammonemia. Background EEG activity was normal. Reduction of VPA dosage and subsequent discontinuation 4 months later resulted in disappearance of clinical symptoms with a 20‐point improvement at IQ testing and recovery of previous PM score. Repeat MRI showed disappearance of pseudoatrophic changes. Conclusions: The striking cognitive improvement and reversal of pseudoatrophic brain changes following VPA discontinuation strongly suggest a drug‐induced condition. Based on this and previous reports, the syndrome of VPA‐associated mental deterioration and pseudoatrophy of the brain appears to encompass different but possibly related clinical entities, which include parkinsonism with cognitive deterioration, mental deterioration with signs of VPA‐toxicity, and isolated mental deterioration, as seen in our patient. A drug‐induced effect should be considered whenever cognitive deterioration and imaging findings of brain atrophy occur in VPA‐treated patients.
The Syndromic Classification of the International League Against Epilepsy: A Hospital‐Based Study from South India
Authors: Murthy J. M. K. , Yangala Ravi , Srinivas Mantha 
Published: August 2005

Summary: Purpose: To determine the distribution of various epilepsies and epileptic syndromes in the epileptic population treated in a university hospital in a developing country. Methods: Data concerning 2,531 patients with epilepsy seen between January 1989 and June 1994 were analyzed using the international League Against Epilepsy (ILAE) classification. Results: Of 2,531 cases, 48% fell into ILAE categories 1.3, 3.2, or 4.1 (cryptogenic, without unequivocal generalized or focal seizures; or situation‐related seizures, respectively). Localization‐related epilepsies (LREs) and epileptic syndromes (1.1, 1.2, 1.3) were found in 1,591 (62.9%) patients; of these patients, symptomatic localization‐related epilepsies totaled 62.7%, and idiopathic localization‐related epilepsies accounted for only 0.7%. Juvenile myoclonic epilepsy was the most common type of idiopathic generalized epilepsy (IGE), comprising 4.9% of the total study population and 7.7% of patients registered in the epilepsy clinic. A combination of childhood and juvenile absence epilepsies were found in only 0.4% of the total study population.Single computed tomography (CT) enhancing lesion (SCTEL) and focal cerebral calcification (FCC) accounted for 22% of the etiologic factors for localization‐related epilepsies. Neurologic deficits were found in 9.5% of patients with SCTEL; none were found with FCC. None of the patients with these lesions had any history of antecedent events that suggested CNS involvement. In patients with localization‐related epilepsies with unremarkable clinical data, the proportion of CT scans showing SCTELs was 39 (95% confidence interval [CI], 0.35–0.43) and 0.18 (95% CI, 15–0.21) for FCCs. The proportion for both lesions together was 0.57 (95% CI, 0.53–0.61). Seizures did not recur once the lesion resolved in patients with SCTELs. In patients with FCCs, seizure remission was 71.5% (95% CI, 53.7–85.4) at 3 years. Conclusions: This study illustrates the rarity in one patient population of some of the syndromes and categories described in the ILAE classification. Childhood and juvenile absence epilepsies together formed a small proportion. SCTEL and FCC were important etiologic factors for localization related epilepsies. The epilepsy associated with SCTEL was a form of benign epilepsy; epilepsy associated with FCC had remission rates similar to other remote symptomatic epilepsies. Without neuroimaging evidence, these 2 lesions would have been missed and the patients might have been grouped under cryptogenic localization related epilepsy. For this reason, we emphasize the need for neuroimaging in patients with localization related epilepsies with unremarkable clinical findings, before classification into the cryptogenic category. In the absence of neuroimaging, such patients should be classified as “probably cryptogenic.”
Seizures with Fever After Unprovoked Seizures: An Analysis in Children Followed from the Time of a First Febrile Seizure
Authors: Berg Anne T. , Darefsky Amy S. , Holford Theodore R. , Shinnar Shlomo 
Published: August 2005

Summary: Purpose: To determine how the onset of unprovoked seizures influences recurrence of seizures with fever in children followed from the time of a first febrile seizure. Methods: In a prospective cohort of children (n = 428) identified at the time of a first febrile seizure, predictors of a second seizure with fever were identified. The occurrence of a first unprovoked seizure was treated as a time‐dependent covariate in a Cox regression model rather than as a censoring point as it traditionally has been in the past. Results: One hundred forty‐three (33.4%) children had further seizures. Seven had further seizures with fever only after onset of unprovoked seizures. After adjustment was made for the four previously described predictors of recurrent febrile seizures (age at onset, family history, height of fever, and duration of fever), the onset of unprovoked seizures was associated with a rate ratio of 3.47 (p = 0.0015), indicating a large increase in the risk of further seizures with fever after onset of unprovoked seizures. Conclusions: Young children who develop unprovoked seizures after a febrile seizure are at substantial risk for further seizures with fever. This may represent part of the spectrum of benign febrile seizures or it may represent the so‐called “epilepsy triggered by fever” spectrum. It affects only a small proportion of children with febrile seizures; however, in some children, it may be useful information to consider when making treatment decisions.
Selection of Phenytoin Responders and Nonresponders in Male and Female Amygdala‐Kindled Sprague–Dawley Rats
Authors: Löscher Wolfgang , Cramer Sybille , Ebert Ulrich 
Published: August 2005

Summary: Purpose: We recently described that, by repeated testing of the anticonvulsant phenytoin (PHT), it is possible to select responders and nonresponders from large populations of amygdala‐kindled Wistar rats. Whereas responders show marked and reproducible increases of focal seizure threshold (afterdischarge threshold; ADT) on repeated testing of PHT, 75 mg/kg i.p., nonresponders do not show any significant ADT increase after this dose, thus allowing use of these subgroups in the search for mechanisms of pharmacoresistance in temporal lobe epilepsy. In this study, we examined whether PHT responders and nonresponders can also be selected from large groups of kindled rats of the Sprague‐Dawley strain. Methods: Male and female Sprague‐Dawley rats were amygdala kindled, followed by once weekly i.p. testing of PHT. Results: In contrast to recent experiments in Wistar rats, 75 mg/kg PHT did not induce significant ADT increases in Sprague‐Dawley rats, indicating strain differences in response to this drug after kindling. When the dose was lowered to 50 or 25 mg/kg, significant and reproducible ADT increases were obtained in Sprague‐Dawley rats of both genders. Therefore these doses were used for selection of responders and nonresponders in a total of 42 rats. Almost 50% of the rats were PHT responders, responders, whereas no rat was a nonresponder when tested in up to six subsequent drug trials. Many rats were variable responders (i.e., showed ADT increases in some but not all trials), which was not due to low or variable drug absorption after i.p. injection. Conclusions: The data indicate that, in contrast to Wistar rats, Sprague‐Dawley rats are not suited for selection of PHT nonresponders, but rather are quite responsive to this drug. A further difference to the Wistar strain is the truncated dose‐response with loss of anticonvulsant efficacy at 75 mg/kg in kindled Sprague‐Dawley rats, which may, at least in part, explain the inconsistent results reported on the anticonvulsant efficacy of PHT in this strain in the literature. The lack of anticonvulsant activity after administration of 75 mg/kg may be a result of kindling, because administration of this dose before kindling causes a significant ADT increase in this strain. This kindling‐induced alteration of the anticonvulsant activity of PHT is a phenomenon that contrasts Sprague‐Dawley with Wistar rats and deserves further investigation.
Hemicranial Volume Deficits in Patients with Temporal Lobe Epilepsy With and Without Hippocampal Sclerosis
Authors: Briellmann Regula S. , Jackson Graeme D. , Kalnins Renate , Berkovic Samuel F. 
Published: August 2005

Summary: Purpose: In patients with refractory temporal lobe epilepsy, studies have suggested volume deficits measured by MRI of brain structures outside the epileptogenic hippocampus. Hippocampal sclerosis (HS) is a frequent, but not obligate, finding in such patients. The present study examines the influence of the presence of HS on quantitative magnetic resonance imaging (MRI) measurements. Methods: We analyzed 47 patients and 30 controls by quantitative MRI, including intracranial volume (ICV), hemicranial volume, hippocampal volume (HCV), and T2relaxometry. MRI results were compared with histological findings in the resected temporal lobe. Results: Histology documented HS in 35 patients (HS group) and other findings in 12 patients (no‐HS group). In both groups, the hemicranial volume ipsilateral to the epileptogenic focus was significantly smaller than on the contralateral side (p <0.004). The HCV on both sides was smaller in the HS group compared with patients without HS (p ≥ 0.004). Unilateral hippocampal atrophy and increased T, value were found in 71% of patients with HS, and bilaterally normal HCV and T, value were found in 67% of patients without HS. Conclusions: The smaller hemicranial volume on the focus side, irrespective of the presence or absence of HS suggests a different pathogenic mechanism for the additional hemicranial volume deficit, compared to HS itself. The contralateral HCV deficit depends on the presence of HS, indicating a pathogenic connection between damage to both hippocampi.