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Biomedical subjects

I Drury

Publications and source records attributed to I Drury.

At least 19 recordsLinked to original sources
PubMed1992

Unilateral 14 and 6 Hz positive bursts.

We describe the unilateral occurrence of 14 and 6 Hz positive bursts in successive EEGs in a 25-year-old woman following surgical resection of a left parietal arteriovenous malformation which had caused a left parieto-temporal intracerebral hematoma. This is only the second reported case of unilateral 14 and 6 Hz positive bursts. This could represent either a normal pattern seen unilaterally because of a skull defect or be a manifestation of neuronal damage.

Adult↗
PubMed1991

Myoclonus in adult Huntington's disease.

Two brothers with clinically definite adult Huntington's disease developed disabling myoclonus years after the first signs of the disease. Their electroencephalograms were consistent with a primary generalized epilepsy, although neither man had seizures. The myoclonus was controlled with valproic acid therapy.

Adult↗
PubMed1991

Variance of interburst intervals in burst suppression.

Each EEG performed over a 3 year period at the University of Michigan with a diagnosis of generalized burst-suppression (BS) was reviewed. Ten EEGs from 10 patients with hypoxic-ischemic encephalopathy (HIE-BS) and 21 records from 8 patients with pentobarbital induced burst-suppression for treatment of status epilepticus (SE-BS) were reviewed. For each EEG, the mean duration of 40 interburst intervals (IBIs) as well as their coefficient of variability were calculated. We found that in the SE-BS group the coefficient of variability of IBI duration was highly correlated with the logarithm of mean IBI duration while in the HIE-BS group, there was no significant correlation between these 2 variables. This suggests that the underlying mechanism causing BS is different in the 2 groups and might be related to a uniform and progressive affection of similar brain structures in the SE-BS group and a more patchy and variable pathology in the HIE-BS group.

Adolescent↗
PubMed1991

Triphasic waves in coma from brainstem infarction.

There have been reports on patients in stupor or coma from a variety of disorders that affect the brain diffusely, notably hepatic failure, whose EEGs showed triphasic waves. We describe a patient in coma with neurologic signs localizing to the brainstem who had triphasic waves on EEG. This case further confirms the nonspecific nature of triphasic waves.

Aged↗
PubMed1991

Allele-specific sequencing confirms novel prion gene polymorphism in Creutzfeldt-Jakob disease.

We analyzed the prion protein coding sequence in a familial Creutzfeldt-Jakob disease patient who did not have any of the currently recognized prion protein mutations. Denaturing gradient gel electrophoresis indicated that the prion protein coding sequence was heterozygous at least one location. We isolated each allele by denaturing gradient gel electrophoresis and directly sequenced. We found a DNA polymorphism at codon 178 that predicted the amino acid substitution, aspartate----asparagine. Whether this represents a benign polymorphism or pathogenic mutation will depend on analysis of the functional consequences of this change. Denaturing gradient gel electrophoresis and allele-specific sequencing proved to be efficient means of analyzing sequence polymorphisms in this gene.

Adult↗
PubMed1991

Felbamate for partial seizures: results of a controlled clinical trial.

Felbamate (2-phenyl-1,3-propanediol dicarbamate) has a favorable preclinical profile in animal models of epilepsy. We present the results of a double-blind, randomized, placebo-controlled clinical trial in patients with partial seizures. Criteria for entry included a requirement for four or more partial seizures per month despite concomitant therapeutic blood levels of phenytoin and carbamazepine. Fifty-six patients (mean age, 31.4 years; 32 men, 24 women) completed the trial. The mean seizure frequencies for the 8-week periods analyzed were felbamate = 34.9, placebo = 40.2. Felbamate was statistically superior to placebo in seizure reduction, percent seizure reduction, and truncated percent seizure reduction. The mean felbamate dosage was 2,300 mg/d. Plasma felbamate concentrations ranged from 18.4 to 51.9 mg/l, mean = 32.5 mg/l. Adverse experiences during felbamate therapy were minor and consisted primarily of nausea and CNS effects. This trial indicates that felbamate is safe and effective in the treatment of comedicated patients with severely refractory epilepsy.

Adult↗
PubMed1990

Familial Creutzfeldt-Jakob disease without periodic EEG activity.

Four members of a kindred with Creutzfeldt-Jakob disease are reported, in whom myoclonus did not develop and in whom serial electroencephalograms performed late in their illness failed to show periodic sharp wave complexes. Otherwise, the patients' disease duration, clinical features, and neuropathological findings were similar to those described in sporadic cases of Creutzfeldt-Jakob disease. Our findings and those reported by others suggest that periodic electroencephalographic activity may be rare in familial forms of Creutzfeldt-Jakob disease, as it is in other slow transmissible encephalopathies.

Animals↗
PubMed1990

Epileptiform abnormalities during sleep in Rett syndrome.

We recorded all-night electroencephalograms (EEGs)/polysomnograms on 2 consecutive nights from 4 children (ages 4-11 years) with Rett syndrome. The first 10 sec of each 60 sec epoch were analyzed with counts of left and right hemisphere spikes and correlated with sleep stage. Spike counts were lowest during wakefulness. Spikes were most frequent over parasagittal regions during all sleep stages and varied from 0.28 +/- 0.03 to 40.4 +/- 0.7 (mean +/- S.E.M.) spikes/hemisphere/min. Spike counts were 51-109% higher during NREM sleep than during REM sleep. In 3 of 4 subjects, spikes were most frequent during light NREM sleep. Spikes increased in frequency during the second half of the night. We conclude that in Rett syndrome, epileptiform activity is maximally expressed in stage 1-2 NREM sleep and during the early morning hours. Sleep EEG features may be useful in the diagnosis of Rett syndrome.

Child↗
PubMed1989

14-and-6 Hz positive bursts in childhood encephalopathies.

14-and-6 Hz positive bursts, a benign epileptiform variant, have also been described in comatose children with liver disease, chiefly Reyes syndrome. To determine the incidence of this pattern in children in stupor or coma, 154 portable EEGs in 111 children with mental status changes were reviewed. Seven children showed 14-and-6 Hz bursts in the setting of moderate to marked background slowing. They were similar to positive bursts seen in normals in location, duration, morphology, frequency and repetition rate. They differed in being readily activated by stimulation. The etiology was toxic/metabolic in 4 cases, primary cerebral insult in 2 cases and a combination of the two in 1 case. Amongst an age-matched control population, 5 of 75 showed 14-and-6 Hz positive bursts in stage I or II sleep. There were no statistically significant differences in incidence rates between the 2 groups. 14-and-6 Hz positive bursts may occur in diverse encephalopathies of childhood, not just Reyes syndrome. The similar incidence rate, morphology and topography to normals suggest that the presence of these wave forms in encephalopathies represents persistence of a normal EEG feature rather than an expression of some underlying pathophysiological process.

Acoustic Stimulation↗
PubMed1989

Epileptiform patterns of children.

Infants and children display almost the entire range of interictal and ictal epileptiform patterns, exclusive of those seen in the neonatal period. This paper reviews patterns seen in the idiopathic and secondary forms of epilepsies, both generalized and partial, as well as periodic patterns and benign epileptiform variants as they appear in childhood. The discussion focuses on interictal activities, the abnormalities most commonly seen in the EEG laboratory. Special attention is paid to differential diagnostic features; the distinctions between significant epileptiform patterns and normal background features of the maturing child's EEG can be particularly challenging. A large number of illustrations are provided to demonstrate not only the classic epileptiform patterns but also many of the less typical presentations, since children's EEGs show a greater number of atypical waveforms.

Cerebral Cortex↗
PubMed1987

Fulminant demyelinating polyradiculoneuropathy resembling brain death.

A fulminant polyradiculoneuropathy resulted in a clinical state like brain death. Sequential EEG studies showed normally reactive alpha activity and spontaneous variability between wakefulness, drowsiness and sleep. EEG studies are valuable in such states in suggesting at least partial integrity of cortical neuronal activities, where no clinical measure is available.

Brain Death↗
PubMed1985

Pyknoleptic petit mal.

Pyknoleptic petit mal is a childhood epilepsy syndrome characterized by frequent absence seizures and a specific EEG pattern. The EEG trait is dominantly inherited. It represents the paradigm of primary generalized epilepsy with cortico-reticular participation. The clinical features include disturbances of awareness and/or responsiveness and frequently associated events such as mild clonic components, postural changes and automatisms. Treatment is usually successful in eliminating seizures and the prognosis is favorable for terminal remission though generalized tonic-clonic seizures may ensue.

Adolescent↗
PubMed1985

An acute syndrome with psychiatric symptoms and EEG abnormalities.

Four patients with abrupt onset of psychosis had prominent periodic EEG abnormalities with diffuse sharp waves. Other laboratory studies, including CSF and CT, were normal. The EEG abnormalities disappeared within 1 to 7 days. Clinical improvement was complete and commenced after the EEG showed improvement. The cause remains obscure, but it seems to be a transient organic disturbance of cerebral function that must be distinguished from primary psychiatric disorders.

Acute Disease↗