bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ontogeny of seizures induced by leucine‐enkephalin and β‐endorphin
Authors: Snead O. Carter , Stephens Helen 
Published: January 2005

AbstractRats ranging in postnatal age from 6 hours to 28 days were implanted with cortical and depth electrodes as well as an indwelling cannula in the lateral ventricle. We then administered varying amounts of the opiate peptides leucine‐enkephalin and β‐endorphin intracerebroventricularly with continous electroencephalographic monitoring.Leucine‐enkephalin produced electrical seizure activity in rats as young as 2 days. β‐Endorphin administration was associated with seizures at the fifth postnatal day, with a high incidence of apnea resulting in death in animals as young as 6 hours. An adult seizure response to β‐endorphin and leucine‐enkephalin was seen at 15 and 28 days of age, respectively. Naloxone blocked the seizure produced by these opiate peptides in all age groups. The data indicate that the opiate peptides are potent epileptogenic compounds in developing brain, that seizures induced by leucine enkephalin differ from those caused by β‐endorphin, and that petit mal–like seizure activity can be an adult response in the rodent.
Acquired perinatal leukoencephalopathy
Authors: Leviton Alan , Gilles Floyd H. 
Published: January 2005

AbstractBetween 36 and 44 weeks after conception, telencephalic white matter in the newborn appears to be particularly vulnerable to insults that result in morphological disturbances. Available evidence indicates that this disorder (or group of disorders), named acquired perinatal leukoencephalopathy, reflects a decrease in blood flow through the distal vessels supplying paraventricular white matter and/or a metabolic disturbance produced by, or in response to, an infectious agent. Major advances in our understanding of the causes, mechanisms, and sequelae of acquired perinatal leukoencephalopathy may be made in the next decade because of improvement in brain imaging techniques, improved survival of high‐risk babies, and relatively routine follow‐up of these high‐risk babies.
Congenital hydrocephalus and eye abnormalities with severe developmental brain defects: Warburg's syndrome
Authors: Bordarier C. , Aicardi J. , Goutieres F. 
Published: January 2005

AbstractFive patients are reported with Warburg's syndrome, characterized by: (1) congenital hydrocephalus, (2) severe neonatal neurological dysfunction, (3) abnormalities of the anterior and posterior chambers of the eyes, (4) absence of known cause, and (5) severe developmental abnormalities of cortical gyration and architectonics. Fourteen similar published cases are reviewed. The syndrome can be diagnosed during life on the conjunction of the first four features listed. Evidence is adduced that this syndrome is a genetically determined condition with an autosomal recessive mode of inheritance and with a 25% recurrence risk for offspring of the parents of an affected infant.
Iron uptake by mammalian cortical neurons
Authors: Swaiman Kenneth F. , Machen Valynda L. 
Published: January 2005

AbstractAlthough iron accumulates in the brain in a number of pathological conditions, including Hallervorden‐Spatz syndrome, Parkinson's disease, and neurosyphilis, studies of brain iron metabolism have been performed only rarely. Neuronal‐enriched cultures were prepared from fetal mouse brain. After 18 days the cells were exposed to radiolabeled iron. Total iron uptake and incorporation into ferritin were rapid and linear over four hours. The addition of either methylamine or ammonium chloride, both known blockers of transferrin‐iron release through their lysosomotropic properties, inhibited total iron uptake. Methylamine also inhibited the rate of ferritin‐iron incorporation, most likely by interfering with transferrin‐iron release. The data suggest that neuronal iron transport, much like that in other mammalian tissues, is transferrin mediated and that blockers of transferrin‐iron release may be of value in conditions in which there is brain iron overload.
The neurobiology of vascular head pain
Authors: Moskowitz Michael A. 
Published: January 2005

AbstractNervous connections between the trigeminal ganglia and cerebral blood vessels have recently been identified in experimental animals and have been termed the trigeminovascular system. Existence of this system in humans is inferential. Trigeminovascular neurons and their peripheral unmyelinated nerve fibers contain the neurotransmitter peptide substance P. Most newly synthesized substance P is transported from ganglion cell bodies to afferent nerve fibers, where depolarization‐induced release of neurotransmitter into the wall of the cerebral blood vessel occurs. Substance P dilates pial arteries, increases vascular permeability, and activates cells that participate in the inflammatory response. The relationship of trigeminovascular fibers to the pathogenesis of vascular head pain sheds light on possible mechanisms of migraine and other central nervous system conditions associated with headache and inflammation.
In vivo phosphorus nuclear magnetic resonance spectroscopy in status epilepticus
Authors: Petroff Ognen A. C. , Prichard James W. , Behar Kevin L. , Alger Jeffrey R. , Shulman Robert G. 
Published: January 2005

AbstractBicuculline‐induced status epilepticus was studied in paralyzed rabbits ventilated with an oxygen and nitrous oxide mixture. An Oxford Instruments TMR 32–200 spectrometer was used to record phosphorus 31 nuclear magnetic resonance spectra of the in vivo brain. An array of conventional physiological variables including the electroencephalogram was simultaneously recorded. Several features were consistently observed during status epilepticus: (1) Phosphocreatine levels fell to about two‐thirds of their control values and remained at that level despite a gradual decline in seizure activity: (2) intracellular pH declined and then remained constant, whereas seizure discharges declined; (3) adenosine triphosphate levels remained constant at their control values. These new, lower levels of brain phosphocreatine and intracellular pH were largely unaffected by increases in seizure activity brought about by elevation of blood pressure from levels too low to support adequate cerebral perfusion, by waning of anticonvulsant drug effect, or by repeated doses of bicuculline.
Peripheral nerve function and metabolic control in diabetes mellitus
Authors: Troni Walter , Carta Quirico , Cantello Roberto , Caselle Maria Teresa , Rainero Innocenzo 
Published: January 2005

AbstractMeasurement of conduction velocity along the H reflex arc was used to study sensorimotor peripheral nerve function in diabetic patients during short‐ and long‐term improvement of hyperglycemia. In ten type I diabetics a slight (p < 0.05) conduction increase occurred after 6 hours of normal glycemia induced by an artificial endocrine pancreas. Similar but more prominent improvement occurred in twelve type I diabetics treated with continuous subcutaneous insulin injection for 6 months. The results suggest that nerve conduction slowing in diabetic patients stems partly from reversible, nonstructural abnormalities and partly from more slowly reversible morphological or chemical changes in peripheral nerve.
Changes in the human vestibulo‐ocular reflex after loss of peripheral sensitivity
Authors: Baloh R. W. , Honrubia V. , Yee R. D. , Hess K. 
Published: January 2005

AbstractQuantitative rotational testing was used to study changes in the vestibulo‐ocular reflex of patients with unilateral and bilateral peripheral vestibular lesions. Compared with normal subjects, the patients exhibited a characteristic pattern of decreased gain and increased phase lead at low frequencies of sinusoidal stimulation and decreased time constants on impulsive stimulation. By contrast, gain and phase measurements on high‐frequency–low‐amplitude sinusoidal stimulation were often normal. In the patients with bilateral lesions, the results of caloric testing correlated with the results of low‐frequency rotational testing but not with the results of high‐frequency testing. There are two main clinical implications of these findings. First, patients with absent response to caloric stimulation (unilateral or bilateral) may have a normal response to high‐frequency sinusoidal rotation (i.e., the frequencies that constitute most natural head movements). This probably explains why such patients do not report oscillopsia. Second, low‐frequency sinusoidal rotational testing and caloric testing are more sensitive than high‐frequency sinusoidal or impulsive rotational testing for detecting early loss of vestibular sensitivity due, for example, to ototoxic drugs.
Cerebellar atrophy following phenytoin intoxication
Authors: Lindvall Olle , Nilsson Bengt 
Published: January 2005

AbstractCerebellar degeneration has been demonstrated in several patients receiving phenytoin therapy. In most cases it has been unclear, however, whether the degeneration was caused by the drug per se or by other mechanisms known to lead to cerebellar damage. We describe a patient who developed a marked cerebellar atrophy, demonstrated on computed tomographic scan, following an episode of acute, severe phenytoin intoxication. The patient received phenytoin prophylactically for 21/2 months after an uncomplicated subarachnoid hemorrhage and was in good health when the treatment was started. He has never had seizures, and no other possible cause of chronic cerebellar changes is known. The initially severe clinical signs of cerebellar dysfunction have subsided slowly. We conclude that phenytoin can directly cause cerebellar degeneration.
Age‐related differences in brain electrical activity of healthy subjects
Authors: Duffy Frank H. , Albert Marilyn S. , McAnulty Gloria , Garvey Arthur J. 
Published: January 2005

AbstractA combined neurophysiological (electroencephalographic [EEG] and sensory evoked potential) and neuropsychological investigation was performed on 63 healthy men ranging in age from 30 to 80 years. Although alpha frequency diminished slightly with age, neither amplitude nor frequency demonstrated a high age correlation. Alpha blocking, in contrast, did correlate with age, in the direction of reduced alpha reactivity. EEG background activity underwent significant age‐correlated change, consisting of reductions in slow activity and augmentation of fast activity i.e., EEG desynchronization. Previously reported age‐related EEG slowing may be related to the presence of disease in the populations studied. Topographic analysis revealed that the greatest change occurred in the temporal lobes. More change was noted either early or late in the age span, suggesting that aging is a nonlinear process. More features were derived from the right hemisphere than from the left, suggesting that the aging process is not completely symmetrical.
Effect of aging on the accuracy of visually guided saccadic eye movement
Authors: Warabi Tateo , Kase Manabu , Kato Takamasa 
Published: January 2005

AbstractChanges in oculomotor behaviors with aging were studied in normal young and elderly subjects. Saccadic eye movments induced by presentation of a visual target were analyzed. Elderly subjects commonly showed an elongation of the time to locate the target, accompanied by an increase in reaction times (mean increase, 100 ms) and a decrease in saccadic velocities. The decrease in the velocity was particularly notable when a large‐amplitude saccade was executed. In spite of the slowed motor responses, most elderly subjects preserved the function necessary to execute a correct saccade toward the visual target. The saccadic slowing was accompanied by an increase in saccade duration. Although a longer time was necessary for elderly subjects to locate the target, the accuracy of the initial saccades was not different from that of young subjects. One group of elderly subjects showed extremely long reaction times. These subjects, displaying no abnormal neurological symptoms, were not able to locate the visual target with initial saccades. They had to execute multistep saccades typically seen in patients with degenerative neurological diseases.
Conjugate eye deviation after acute hemispheric stroke: Delayed recovery after previous contralateral frontal lobe damage
Authors: Steiner Israel , Melamed Eldad 
Published: January 2005

AbstractIn 42 patients with acute unilateral ischemic or hemorrhagic hemispheric stroke, conjugate eye deviation toward the lesioned side was usually of brief duration. It subsided within 48 hours in 24 patients (57%) and lasted no longer than 5 days in 38 patients (90%). Early disappearance of conjugate eye deviation was an isolated phenomenon and preceded any improvement in the other focal neurological deficits, which persisted in their initial severity. In 6 additional patients with stroke, conjugate eye deviation was remarkably prolonged, lasting from 13 to more than 43 days. In all 6 there was evidence for preexisting damage to the contralateral frontal region. Our study suggests that early recovery of conjugate eye deviation in patients with acute hemispheric stroke may be mediated by the contralateral unaffected frontal eye field.
Neurological complications of bone marrow transplantation in childhood
Authors: Wiznitzer Max , Packer Roger J. , August Charles S. , Burkey Pa Edith D. 
Published: January 2005

AbstractBone marrow transplantation, used in the treatment of cancer, aplastic anemia, and metabolic diseases, involves the use of potentially neurotoxic agents to suppress immunity and eradicate malignancy. Fifty‐seven patients with a median age of 11 years (age range, 6 months to 24 years) underwent bone marrow transplantation at the Children's Hospital of Philadelphia. Fifty‐nine percent developed neurological abnormalities. Twenty‐six patients (46%) had central nervous system (CNS) dysfunction, including infection (8), cerebrovascular accident (5), CNS leukemia (7), metabolic encephalopathy (5), and paraparesis with CNS toxoplasmosis (1). Neuropsychological dysfunction was present in 4 of 5 longterm survivors who were tested. Fourteen of 19 patients (74%) on whom postmortem examination was performed were found to have CNS abnormalities, including cerebral atrophy (10), focal cerebral injury (6), leukemia (5), and infection (3). Fourteen patients (24%) had peripheral nervous system dysfunction. CNS dysfunction was more common in patients with lymphoreticular malignancies. Cerebrovascular accidents (in patients with lymphoreticular malignancies) and infections (in our general population and in patients with lymphoreticular malignancies) occurred more often in our patients than in patients with similar illnesses who did not undergo bone marrow transplantation. The combination of prior treatment and preparative therapy for bone marrow transplantation predisposes patients to neurological and neuropsychological sequelae.
Hippocampal dendritic abnormalities in a rat model of phenylketonuria
Authors: Lacey Daniel J. 
Published: January 2005

AbstractAn increased concentration of dendritic spines was present in one region of the hippocampus in rats made hyperphenylalaninemic (phenylketonuria model). It is uncertain whether this finding resulted from an actual hyperplasia or a failure of maturational spine reduction. The result is unusual in that Golgi studies of most mental retardation syndromes and relevant animal models have shown loss of dendritic spines.
Phenytoin interacts with calcium channels in brain membrances
Authors: Greenberg David A. , Cooper Edward C. , Carpenter Celia L. 
Published: January 2005

AbstractPhenytoin at concentrations of between 30 and 300 μM inhibited binding of the calcium antagonist {3H} nitrendipine to voltage‐dependent calcium channels in brain membranes. Other anticonvulsants (phenobarbital, carbamazepine, valproic acid, and clonazepam) failed to inhibit binding or did so only at concentration much higher than occur clinically. Calcium channel blockade may be important in the clinical actions of phenytoin, including certain of the adverse effects of the drug.
The role of myelin P2 protein in the production of experimental allergic neuritis
Authors: Rostami Abdolmohammad , Brown Mark J. , Lisak Robert P. , Summer Austin J. , Zweiman Burton , Pleasure David E. 
Published: January 2005

AbstractMyelin P2 protein has been proposed as the primary antigen in whole myelin‐induced experimental allergic neuritis (EAN). We investigated the neuritogenic properties of P2 by sensitizing Lewis rats with complete Freund's adjuvant (CFA) containing P2, P2 plus phosphatidyl serine, or whole myelin containing an equivalent amount of P2. Animals were examined using a battery of clinical, electrophysiological, immunological, and morphological methods. Myelinimmunized rats developed the characteristic features of EAN. P2‐sensitized rats developed a similar but much less intense disorder. When rats were sensitized with P2 in the presence of phosphatidyl serine, however, they developed radiculoneuropathy that was indistinguishable from myelin‐induced EAN. Inoculation with phosphatidyl serine plus complete Freund's adjuvant or complete Freund's adjuvant alone had no detectable effect on peripheral nerves. These studies demonstrate that sensitization of rats with a single myelin antigen, P2 protein, is sufficient to induce the clinical, electrophysiological, and neuropathological features of EAN.
The aging human brain
Authors: Creasey Helen , Rapoport Stanley I. 
Published: January 2005

AbstractPostmortem and computed tomographic studies demonstrate many anatomical, morphological, and neurochemical differences between brains of old and young human beings. The variability of the results is great, however, and brains of some old subjects have characteristics of brains of younger controls. Furthermore, important aspects of brain functional activity are not reduced in the elderly. These include resting cerebral oxidative metabolism and “crestallized” intelligence as represented by verbal subtests on the Wechsler Adult Intelligence Scale. In the absence of superimposed disease (which frequently limits aging studies), overall functions can be maintained at high and effective levels because of the plasticity and redundancy capabilities of the human brain.
IgG production within the central nervous system: A critical review of proposed formulae
Authors: Lefvert Ann Kari , Link Hans 
Published: January 2005

AbstractDemonstration of intrathecal IgG production is employed in the diagnosis of various neurological disorders. This pathological IgG fraction in cerebrospinal fluid (CSF) can be visualized directly as oligoclonal bands by electrophoresis or isoelectric focusing or can be calculated as “excess” or “synthesized” IgG according to different formulae. A comparison of the results obtained with isoelectric focusing and with five formulae showed that even though three of the formulae discriminated well between a reference population and patients with multiple sclerosis, all five gave wrong and misleading results in the presence of blood‐brain barrier damage, as defined by an abnormally raised CSF/serum albumin ratio. A mathematical and statistical evaluation of the different formulae showed only those based on covariance between CSF/serum IgG and CSF/serum albumin to be valid, and these only when values of CSF/serum albumin were normal. Among the five formulae the IgG index (equal to CSF/serum IgG:CSF/serum albumin) is unique in having a comparitively small and constant maximal relative error resulting from the variation coefficients of the IgG and albumin assays. In the case of blood‐brain barrier damage, there exists currently no valid procedure to calculate intrathecally produced IgG; in such instances sensitive electrophoretic or isoelectric focusing methods demonstrating oligoclonal IgG bands are most appropriate to demonstrate intrathecal IgG production.
Cerebrospinal fluid acetylcholinesterase activity in senile dementia of the Alzheimer type
Authors: Tune Larry , Gucker Stephen , Folstein Marshal , Oshida Leslie , Coyle Joseph T. 
Published: January 2005

AbstractAcetylcholinesterase (AChE) activity was measured in cerebrospinal fluid (CSF) samples from 36 individuals, including 12 persons with Alzheimer's disease, 12 normal controls, and 12 patients with other dementias. AChE activity also was measured in 47 normal subjects whose ages ranged from 20 to 84 to evaluate the effect of age on AChE activity than in age‐matched controls and patients with other dementia syndromes. No correlation was found between duration of illness, age, or severity of illness (as measured by the Mini‐Mental State Examination score) and CSF AChE activity in Alzheimer's disease. AChE increased significantly over the age range of 20 to 84. CSF AChE activity may prove to be a useful diagnostic test to confirm the clinical diagnosis of moderate to severe Alzheimer's disease.
In vivo estimation of muscle protein synthesis in myotonic dystrophy
Authors: Halliday David , Ford G. C. , Edwards Richard H. T. , Rennie Michael J. , Griggs Robert C. 
Published: January 2005

AbstractThe rate of muscle protein synthesis in patients with myotonic dystronic has been studies, and result correlated with total muscle mass. Whole body and skeletal muscle protein synthesis were estimated by stable isotope methodology with a primed, continuous infusion of 1‐[13C]leucine with measurement of incorporation of [13C] leucine into muscle into muscle protein in biospy samples. Whole body leucine flux, protein synthesis, and protein breakdown were only slightly depressed, but muscle protein synthesis was markedly decreased, in myotonic dystrophy. This depression of muscle protein synthesis in myotonic dystrophy correlates with previous observations of impaired insulin‐induced muscle uptake of amino acids and support the suggestion that muscle wasting in this disease is the consequence of defective anabolism in muscle.
Atypical presentations of pyridoxine‐dependent seizures: A treatable cause of intractable epilepsy in infants
Authors: Goutières Françoise , Aicardi Jean 
Published: January 2005

AbstractWe repport on 3 patients with atypical pyridoxine‐dependent seizures. Each had either late onset of convulsions(2 cases)or seizure‐free intervals of up to several months' duration in the absence of pyridoxine supplementation. The findings, taken together with those in 9 previously reported cases, indicate that a trial of pyridoxine shoul be performed in all seizure disorders with onset before 18 months of age, regardless of type.
Local cerebral metabolic rate for glucose during petit mal absences
Authors: Engel Jerome , Lubens Perry , Kuhl David E. , Phelps Michael E. 
Published: January 2005

AbstractFour patients with primary generalized or true petit mal epilepsy were studied with positron emission tomography using f'{18} fluorodeoxyglucose (FDG). FDG studies were carried out during 10 minutes of hyperventilation before and again after medical control of spontaneous absences. Before seizures were controlled all 4 patients demonstrated frequent bilaterally synchronous three‐per‐second spike‐and‐wave discharges associated with altered consciousness. After spontaneous seizures were controlled, hyperventilation produced only electroencephalographic slowing without clinical symptoms in 3; the fourth patient had absences less frequently. Patterns of local cerebral metabolic rate for glucose (CMRGlc) were normal and identical for ictal and interictal scans; there was, however, a 2.5‐ to 3.5‐fold diffuse ictal increase in global CMRGlc evident when ictal studies were compared with hyperventilation control studies in which no seizures occurred. The CMRGlc was similar in the two scans obtained from the patient who had absences during both studies. No anatomical substrate of petit mal epilepsy was identified. The CMRGlc in these patients during petit mal absences was higher than that recorded in other patients during partial or generalized convulsive seizures. This difference may reflect the fact that petit mal absences are not associated with postictal depression.