Sudden death in epileptic rats exposed to nocturnal magnetic fields that simulate the shape and the intensity of sudden changes in geomagnetic activity: an experiment in response to Schnabel, Beblo and May.

To test the hypothesis that sudden unexplained death (SUD) in some epileptic patients is related to geomagnetic activity we exposed rats in which limbic epilepsy had been induced to experimentally produced magnetic fields designed to simulate sudden storm commencements (SSCs). Prior studies with rats had shown that sudden death in groups of rats in which epilepsy had been induced months earlier was associated with the occurrence of SSCs and increased geomagnetic activity during the previous night. Schnabel et al. [(2000) Neurology 54:903-908] found no relationship between SUD in human patients and geomagnetic activity. A total of 96 rats were exposed to either 500, 50, 10-40 nT or sham (less than 10 nT) magnetic fields for 6 min every hour between midnight and 0800 hours (local time) for three successive nights. The shape of the complex, amplitude-modulated magnetic fields simulated the shape and structure of an average SSC. The rats were then seized with lithium and pilocarpine and the mortality was monitored. Whereas 10% of the rats that had been exposed to the sham field died within 24 h, 60% of the rats that had been exposed to the experimental magnetic fields simulating natural geomagnetic activity died (P<.001) during this period. These results suggest that correlational analyses between SUD in epileptic patients and increased geomagnetic activity can be simulated experimentally in epileptic rats and that potential mechanisms might be testable directly.

New-onset mesial temporal lobe epilepsy in a 90-year-old: clinical and EEG features.

Although there is a peak in the incidence of epilepsy in the elderly compared with the general population, complex partial seizures represent less than 15% of the seizure types reported. We report on a 92-year-old woman with a 2-year history of daily complex partial seizures. Prolonged video/EEG recording showed bilateral anterior mesial temporal interictal spikes, which predominated on the left, and two typical seizures arising from the left temporal area. Cranial MRI scanning showed multiple lacunar infarcts without temporal lobe involvement or mesial temporal atrophy. Our case appears to be oldest patient in the literature with newly diagnosed mesial temporal lobe epilepsy confirmed by video/EEG recording.

Neuronal hypertrophy in the neocortex of patients with temporal lobe epilepsy.

The underlying cause of neocortical involvement in temporal lobe epilepsy (TLE) remains a fundamental and unanswered question. Magnetic resonance imaging has shown a significant loss in temporal lobe volume, and it has been proposed that neocortical circuits are disturbed functionally because neurons are lost. The present study used design-based stereology to estimate the volume and cell number of Brodmann's area 38, a region commonly resected in anterior temporal lobectomy. Studies were conducted on the neocortex of patients with or without hippocampal sclerosis (HS). Results provide the surprising finding that TLE patients have significant atrophy of neocortical gray matter but no loss of neurons. Neurons are also significantly larger, dendritic trees appear sparser, and spine density is noticeably reduced in TLE specimens compared with controls. The increase in neuronal density we found in TLE patients is therefore attributable to large neurons occupying a much smaller volume than in normal brain. Neurons in the underlying white matter are also increased in size but, in contrast to other reports, are not significantly elevated in number or density. Neuronal hypertrophy affects HS and non-HS brains similarly. The reduction in neuropil and its associated elements therefore appears to be a primary feature of TLE, which is not secondary to cell loss. In both gray and white matter, neuronal hypertrophy means more perikaryal surface area is exposed for synaptic contacts and emerges as a hallmark of this disease.

Hyperglycemia associated with protease inhibitors in an urban HIV-infected minority patient population.

BACKGROUND: Hyperglycemia and new-onset diabetes mellitus have been reported to occur in HIV-infected patients treated with protease inhibitors. OBJECTIVE: To determine the effect of protease inhibitor therapy on serum glucose in a predominantly minority patient population. DESIGN: Retrospective record review. SETTING: Clinical HIV program of an urban Veterans Affairs medical center. PATIENTS: All HIV-infected patients receiving a protease inhibitor over a one-year period from September 1996 through August 1997. RESULTS: One hundred seventeen patients not previously known to be diabetic received protease inhibitors; seven (6%) developed symptomatic diabetes mellitus. Eight other patients had one or more serum glucose values >150 mg/dL. Mean random glucose values for patients who did not develop diabetes were higher during therapy than prior to initiation of protease inhibitors. CONCLUSIONS: Urban minority HIV-infected patients receiving combination antiretroviral therapy including a protease inhibitor may be at increased risk for the development of hyperglycemia and diabetes mellitus. Risk factors for diabetes mellitus should be identified and blood glucose monitored in all patients receiving protease inhibitors.

Vagus nerve stimulation therapy for epilepsy in older adults.

The authors assessed the efficacy, safety, and tolerability of vagus nerve stimulation (VNS) for refractory epilepsy in 45 adults 50 years of age and older. They determined seizure frequency, adverse effects, and quality of life. At 3 months, 12 patients had a >50% decrease in seizure frequency; at 1 year, 21 of 31 studied individuals had a >50% seizure decrease. Side effects were mild and transient. Quality of life scores improved significantly with time.

Evidence for a novel gene for familial febrile convulsions, FEB2, linked to chromosome 19p in an extended family from the Midwest.

Febrile convulsions are a common form of childhood seizure. It is estimated that between 2 and 5% of children will have a febrile convulsion before the age of 5. It has long been recognized that there is a significant genetic component for susceptibility to this type of seizure. Wallace, Berkovic and co-workers recently reported linkage of a putative autosomal dominant febrile convulsion gene to chromosome 8q13-21. We report here another autosomal dominant febrile convulsion locus on chromosome 19p. Linkage analysis in this large multi-generational family gave a maximum pairwise lod score of 4.52 with marker Mfd120 at locus D19S177. Linkage to the chromosome 8 locus was excluded in this family. Haplotype analysis using both affected and unaffected family members indicates that this febrile convulsion gene, which we call FEB2 , can be localized to an 11.7 cM, 1-2 Mb section of chromosome 19p13.3, between loci D19S591 and D19S395.

Postictal neurogenic pulmonary edema: experience from an ECT model.

Neurogenic pulmonary edema (NPE) is thought to rarely occur after seizures. Paradoxically, NPE is frequently found (>80%) at autopsy in epileptic patients who die unexpectedly. The reason for the discrepancy between the frequency of NPE found at autopsy and that after uncomplicated seizures is unclear. The literature suggests that subclinical NPE occurs rarely after uncomplicated seizures and resolves within a few hours, but is undetected because of infrequent use of routine chest radiographs early after a seizure occurs. This pilot study examined the frequency of subclinical, radiographically confirmed NPE after electroconvulsive therapy (ECT)-induced seizures. If shown to occur, ECT-induced subclinical NPE would provide an easily reproducible model to study NPE after seizures in patients with epilepsy. Given that sudden unexplained death syndrome accounts for approximately 10% of the deaths in patients with epilepsy, an easily reproducible model for NPE would have heuristic value. We examined 12 patients undergoing ECT for depression with chest radiographs before and after ECT. In this group, only 1 of the 12 patients had subclinical NPE in their post-ECT radiograph. We conclude that subclinical NPE does not significantly occur after seizures in patients undergoing ECT and therefore, would not serve as an application for research.

Electrocerebral inactivity associated with obstructive sleep apnea.

We report a child who demonstrates near electrocerebral silence secondary to obstructive apnea during polysomnography. The mechanism of this suppression of cortical activity appears to be related to hypoxemia in the absence of a malignant arrhythmia.

Enteric eradication of vancomycin-resistant Enterococcus faecium with oral bacitracin.

The emergence of vancomycin-resistant Enterococcus faecium (VREF) has produced a therapeutic dilemma. The colonization of the intestinal tract with VREF may predispose patients to infections by this organism and may contribute to its nosocomial spread. It is reasonable to attempt to eradicate VREF from colonized patients. The optimal regimen, however, is unknown and this study was designed to evaluate the efficacy of oral regimens of vancomycin and bacitracin for the elimination of VREF from the enteric tract. Enterococcal isolates were tested for susceptibilities to vancomycin, bacitracin, and ampicillin with median minimum inhibitory concentrations of > 512 micrograms/ml, 10 units/ml, and 128 micrograms/ml, respectively. All patients were given an initial trial of oral vancomycin 125 mg every 6 h for 10 days. Those who failed oral vancomycin were then given oral bacitracin 25,000 units every 6 h for 10 days due to its favorable in vitro activity. VREF was eradicated from the stools of 42% of patients (eight of 19) receiving oral vancomycin as compared with all eight patients receiving oral bacitracin (P < 0.01). The organism recurred in two bacitracin patients (25%) 8 and 20 days after completion of therapy. Whether prior vancomycin therapy predisposed patients to colonization by VREF was also examined. Ten (53%) of 19 patients had received prior vancomycin therapy before isolation of VREF from the stool. Our data suggest that oral bacitracin may be an effective alternative to commercially available oral vancomycin for the eradication of VREF from the enteric tract.

Varicella in pediatric patients.

OBJECTIVE: To summarize the literature describing the epidemiology, transmission, clinical manifestations, diagnosis, treatment, and prevention of varicella in the pediatric population. DATA SOURCES: A literature search of English-language articles from 1982 to 1992 using MEDLINE and bibliographies of relevant articles. The search term used was varicella. STUDY SELECTION: All review articles and original studies addressing the epidemiology, transmission, clinical manifestations, complications, diagnosis, treatment, and prevention of varicella in pediatric patients were reviewed. Emphasis was placed on controlled studies done in the US. DATA EXTRACTION: Data from human studies were extracted by the authors and evaluated according to patient population, sample size, dosing regimen, efficacy, and safety. DATA SYNTHESIS: Varicella-zoster virus is a highly contagious virus that produces a common and costly disease in the pediatric population. The primary manifestation of varicella is the eruption of vesicular lesions. In most cases varicella is benign, but it can be associated with serious complications. Diagnosis is based primarily on clinical findings. Otherwise healthy children have traditionally received only symptomatic treatment for varicella, but recent literature suggests that antiviral therapy may be useful in these patients. Immunocompromised patients benefit from both symptomatic and antiviral therapy. Isolation and varicella-zoster immune globulin are used to prevent varicella. In the future, varicella vaccine will play an important role in preventing the disease. Varicella vaccine has been shown to be immunogenic and clinically effective in both healthy and immunocompromised children. Adverse reactions associated with the vaccine include fever, injection-site reactions, and rash. Although zoster can follow vaccination, the incidence appears to be lower in vaccinated individuals. Preliminary studies have shown that the vaccine provides protection from varicella-zoster virus for an extended period of time. CONCLUSIONS: Varicella is a common, usually benign disease of childhood. All patients may benefit from symptomatic therapy. Current literature does not support the use of antiviral therapy in all pediatric patients with varicella. When commercially available, varicella vaccine will play an important role in prevention. Long-term studies are needed to fully assess the risk of developing varicella and zoster following vaccination.

Latency of brainstem response in children.

Brainstem electric responses were obtained on a group of 70 normal hearing children, aged 5-11 years, matched by age and sex. The recordings were examined for differences in latencies between the sexes at each age. The results showed that males have a longer latency than females, but when broken down into age groups, the latency of children aged 5-7 years was the same, and the latency of children aged 8-11 years differed. The results for latency of wave V of the whole group showed the greatest difference. The reason why such a sex difference should occur in middle childhood is discussed, but no physical cause found.