bluuebunny/crossref_metadata_2025_split huggingface dataset:
The localizing value of depth electroencephalography in 32 patients with refractory epilepsy
Authors: Spencer Susan S. , Spencer Dennis D. , Williamson Peter D. , Mattson Richard H. 
Published: January 2005

AbstractClinical seizure manifestations, physical examination, radiological studies, neuropsychological tests, and scalp and depth electroencephalographic (EEG) studies were done to localize seizure foci in 32 patients, 23 of whom have undergone surgery with more than one year of follow‐up. Of 16 patients with unlocalized scalp EEGs, depth EEG detected a consistent focal seizure onset in 3. Of 15 patients with localized scalp EEGs, depth EEG revealed multiple foci in 3 and inaccurate localization of the focus by scalp EEG in 4. Therefore, localization by scalp EEG was inaccurate in 10 of 31 patients. When depth EEG revealed a consistent focal seizure onset and this localization was used to determine the surgical resection site, good to excellent results were obtained in 12 of 13 patients. When depth EEG revealed additional foci of seizure origin, surgical results were fair or poor in all patients. No other localizing criteria predicted depth EEG results or surgical success with such accuracy. Furthermore, some criteria, including neuropsychological tests and radiological abnormalities, were falsely localizing at times. Therefore, of the presently available localizing criteria, depth EEG appears to be the most accurate.
Use of SEPs to localize degeneration in a rare polyneuropathy: Studies on polyneuropathy associated with pigmentation, hypertrichosis, edema, and plasma cell dyscrasia
Authors: Shibasaki Hiroshi , Ohnishi Akio , Kuroiwa Yoshigoro 
Published: January 2005

AbstractPeripheral and central nerve conduction were studied in five patients who had polyneuropathy associated with pigmentation, hypertrichosis, edema, and plasma cell dycrasia by using the short‐latency somatosensory evoked potential (SEP) to electrical stimulation of the median nerve at the wrist. The clavicular component N9 was markedly reduced inamplitude, and its latency was moderately prolonged. The interpeak latency from N9 to the cervical component N13 was significantly prolonged, indicating a conduction delay in the dorsal root. The interpeak latency from N13 to the cortical component N20 was normal, suggesting normal central conduction. These Physiological findings were consistent with the pathological findings, which showed degeneration of axons and segmental demyelination and remyelination in the sural nerve and extensive segmental demyelination and remyelination in the dorsal root but normal posterior columns of the spina cord. SEP is a noninvasive method of localizing the site of axon or myelin disorder in a peripheral neuropathy.
A placebo‐controlled trial shows no effect of vasopressin on recovery from closed head injury
Authors: Reichert Walter H. , Blass John P. 
Published: January 2005

AbstractVasopressin and its analogues have been claimed to benefit patients with posttraumatic amnesia. To test this hypothesis a double‐blind, placebo‐controlled, prospective trial of vasopressin was carried out in the chronic (rehabilitation) phase of recovery from closed head injury. Seven patients who received vasopressin and 6 who received a placbo were comparable in age, sex, and degree of disability upon entry into the study. Both groups inproved at the same rate in mental status, neurological status, and activities of daily living.
Spinocerebellar degeneration secondary to chronic intestinal malabsorption: A vitamin E deficiency syndrome
Authors: Harding A. E. , Muller D. P. R. , Thomas P. K. , Willison H. J. 
Published: January 2005

AbstractTwo adults are described who developed a progressive neurological disorder more than 20 years after the onset of chronic fat malabsorption. The clinical features included dysarthria, cerebellar ataxia, and prominent proprioceptive loss with depressed or absent tendon reflexes. Serum vitamin E was undetectable in both cases. One patient improved clinically and electrophysiologically after oral therapy with vitamin E. The findings in these patients were similar to those in others recently reported with vitamin E deficiency associated with biliary atresia. Electrophysiological observations suggested that the human deficiency state parallels that found neuropathologically in vitamin E‐deficient animals.
Persistent oligemia of rat cerebral cortex in the wake of spreading depression
Authors: Lauritzen Martin , Jøsrgensen Martin Balslev , Diemer Niels Henrik , Gjedde Albert , Hansen Anker Jóan 
Published: January 2005

AbstractCerebral blood flow during and after spreading depression (SD) was studied in rat brain by quantitative autoradiography. The rise of cortical blood flow during SD was followed by 20 to 25% reduction belwo normal after SD, lasting at least an hour. Blood flow in the putamen, thalamus, and hippocampus did not change at any time during or after SD. Previous measurements of cerebral blood flow in humans showed that migraine attacks may be accompanied by wavelike spreading oligemia (Olesen et al, 1981). We speculate that the spreading oligemia of migraine may be a phenomenon physiologically related to the present finding of an oligemia after SD.
Neuroimmunology II: Antigenic specificity of the nervous system
Authors: Weiner Howard L. , Hauser Stephen L. 
Published: January 2005

AbstractAntigenic specificity of the nervous system refers to a property conveyed by unique cell surface that are present on different classes of nervous system tissue. These structures are a major importance for the study of nervous system structure and function, and can play a central role in determining patterns of nervous system injury. Thus, the major classes of nervous system cell are identified by structures that are unique to them: neurons by the presence of tetanus toxin receptors on their surface and oligodendrocytes by the presence of surface galactocerebroside, for example. With the advent of hybridoma technology, a large number of monoclonal antibodies are being identified which have increased by several orders of magnitude the ability to define subclasses of nervous system tissue according to unique antigens. In addition surface nervous system tissue may determine the specificity of nervous system injruy by (1) functioning as receptors for viruses or (2) being the targets of autoimmune responses. Patterns of viral injury to the nervous system are often extraordinarily selective (e.g., poliiviurs tropism for motor neurons), and nervous system viral tropism is due in some instances to the interaction of a virus with a unique surface antigen on neural cells. The specificity of injury in autoimmune disease (such as that against the acetylcholine receptor in myasthenia gravis) likewise must be explained by an immune response against unique system and other tisseus or between nervous system and infectious agents such as bacteria or viruses. The presence of shared antigenic structures between the nervous system and infectious agents creates the possibility that an immune response generated against a virus may concurrently damage normal nervous system tissue.
Interictal cerebral glucose metabolism in partial epilepsy and its relation to EEG changes
Authors: Engel Jerome , Kuhl David E. , Phelps Michael E. , Mazziotta John C. 
Published: January 2005

AbstractInterictal positron computed tomography (PCT) with 18F‐fluorodeoxyglucose was performed on 50 patients with partial seizure disorders. Electroencephalographic (EEG) monitoring was carried out during the metabolic studies using scalp and sphenoidal electrodes in 33 patients and stereotaxically implanted depth electrodes in 17. Four patients in this series had focal abnormalities on x‐ray computed tomographic scans, but these were at the site of the presumed epileptogenic lesion in only 2. One or more discrete zones of hypometabolism were identified in 35 patients, and only 1 patient appeared to show focal interictal hypermetabolism. No quantitative relationship could be demonstrated between the degree of focal hypometabolism and either the frequency of intericatal EEG spikes or the presence of focal nonepileptifor EEg changes. It was concluded that metabolic and electrophysiological techniques measure different aspects of cerebral dysfunction in seizures diorders. Although interictal PCT in patients with partial epilepsy usually demonstrates zones of hypometabolism, this finding, perŕse, does not reveal the epileptic nature of the abnormality.
Comparative localization of foci in partial epilepsy by PCT and EEG
Authors: Engel Jerome , Kuhl David E. , Phelps Michael E. , Crandall Paul H. 
Published: January 2005

AbstractOne or more intericatal positron computed tomograms of 18F‐fluorodeoxyglucose were obtained on 50 patients with partial seizure disorders. Ictal as well as interictal electroencephalographic (EEG) data were available for all 50 patients, with scalp, sphenoidal, and depth electrode recordings done on 27 and scalp and sphenoidal recordings alone on 23. Thirty‐five patients demonstrated one or more abnormal intericatal zones of hypometabolism, while combined EEG studies were localizing for 36. There were considerable disagreements between the location of metabolic deficits and the epileptic focus revealed by individual scalp and depth EEG recorded ictal and intericatal epileptiform activity; however, there was good correlation between the site of focal hypometabolism and the epileptic focus determined by the combined results of all electrophysiological studies. When focal hypometabolism and focal nonepileptiform EEG abnormalites (i.e., slow waves and attenuation of fast rhythms) were both present in the same patient, their localization agreed completely. Metabolic and combined electrophysiological techniques both occasionally produced false positive as well as false negative results. When used together, the EEG can confirm that a hypometabolic zone is epileptogenic, while FDG scans may indicate whether an epileptic EEG focus represents a lesion or propagation from a distant site.
Diffuse axonal injury and traumatic coma in the primate
Authors: Gennarelli Thomas A. , Thibault Lawrence E. , Adams J. Hume , Graham David I. , Thompson Carson J. , Marcincin Robert P. 
Published: January 2005

AbstractTraumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impariment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussed animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in none of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 in the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group; these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in severe head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.
Blink rates in parkinsonism
Authors: Karson Craig N. , Lewitt Peter A. , Calne Donald B. , Wyatt Richard Jed 
Published: January 2005

AbstractSpontaneous eye blink rates were counted in 54 parkinsonian patients, 52 of whom were receiving levodopa. The mean blink rate of the more disabled patients, 7 per minute, was significantly less than the 17 blinks per minute observed in midly disabled (p < 0.02) and 22 blinks per minute (p < 0.001) in moderately disabled patients. Drug‐induced dyskinesia in 21 patients was associated with an elevated blink rate, 32 per minute, as compared with 12 per minute for non‐dyskinetic patients (p < 0.01).
The effects of dexamethasone administration and withdrawal on water permeability across the blood‐brain barrier
Authors: Reid Alison C. , Teasdale G. M. , McCulloch J. 
Published: January 2005

AbstractWe examined the effects of dexamethasone administration and withdrawal on regional cerebral blood flow (CBF) and the permeability surface area (PS) product for water in the central nervous system of conscious rats. There were no significant changes in CBF. Dexamethasone treatment produced a significant decrease in the PS product for water in the cerebral cortex, while withdrawal of dexamethasone resulted in a significant increase. Water content of the cerebral cortex was also increased in rats from which dexamethasone had been withdrawn. These findings may help in understanding the pathogenesis of brain swelling in some patients.
Neuron loss in the nucleus basalis of meynert in parkinsonism‐dementia complex of Guam
Authors: Nakano Imaharu , Hirano Asao 
Published: January 2005

AbstractThe nucleus basalis of Meynert, which supplies diffuse cholinergic fibers to the cerebral neocortex, was investigated in two cases of parkinsonism‐dementia complex of Guam (PDG). The nucleus basalis of the two PDG patients showed extensive neuron loss when compared with age‐matched non‐Guamanian controls, suggesting the necessity of investigating activity of cholinergic enzymes in the brains of patients with PDG.
Immunocytochemical comparison of neurofibrillary tangles in senile dementia of Alzheimer type, progressive supranuclear palsy, and postencephalitic parkinsonism
Authors: Yen Shu‐Hui , Horoupian Dikran S. , Terry Robert D. 
Published: January 2005

AbstractAntiserum raised against a two‐cycle‐purified human brain microtubule fraction that binds specifically to tangles of senile dementia of the Alzheimer type was tested on the subthalamus, basis pontis, and midbrain sections of two patients with progressive supranuclear palsy. Tangles composed of 15 nm straight fibers in these areas showed positive immunolabeling with the antiserum. The labeling tangles appeared as a fibrous meshwork in neuronal cell bodies and occasionally in short segments of axons. Corresponding sections of brains obtained from patients with idiopathic parkinsonism, striatonigral degeneration, and olivopontocerebellar atrophy treated with the same antiserum did not display peroxidase products. Only in the elderly subjects and patients with postencephalitic parkinsonism did the periaqueductal gray and median raphe show occasional cells that reacted positively with the antiserum. Tangles in the substantia nigra of patients with postencephalitic parkinsonism were also recognized by the antiserum. The results suggest that the two morphologically distinct neurofibrillary tangles share their immunological properties with components present in microtubule fractions of normal brain.
Cerebrospinal fluid monoamine metabolites in narcolepsy and hypersomnia
Authors: Faull Kym F. , Guilleminault Christian , Berger Philip A. , Barchas Jack D. 
Published: January 2005

AbstractTwo groups of patients with the common complaint of excessive daytime sleepiness were examined. One group fulfilled the criteria for narcolepsy. The other had the sole symptom of excessive daytime sleepiness, confirmed by sleep latency tests, which was unaccompanied by systemic illness. Spinal fluid examinations for homovanillic acid, 3,4‐dihydroxyphenylacetic acid, 3‐methoxy‐4‐hydroxyphenylethylene glycol, and 5‐hydroxyindoleacetic acid were carried out before and after administration of probenecid on the 20 patients and 40 controls. Probenecid‐corrected accumulation of the dopamine metabolites was significantly increased in each of the patient groups, suggesting an association between pathological sleepiness and elevated dopamine turnover in the central nervous system.
Axonal atrophy in sensory nerves of the diabetic BB‐Wistar rat: A possible early correlate of human diabetic neuropathy
Authors: Sima Anders A. F. , Bouchier Mark , Christensen Hilary 
Published: January 2005

AbstractClinical, morphological, and biochemical findings reported in the spontaneously diabetic BB‐Wistar rat strongly indicate that this animal may be a true model of human insulin‐dependent diabetes mellitus. As such, it may provide a valuable model in which to study the neuropathic conditions of diabetes. We examined somatic peripheral nerves at five levels in a longitudinal fashion using quantitative morphological techniques. Myelinated fiber atrophy occurred earlier in sensory nerves than in motor nerves and showed a distal to proximal progression with duration of diabetes. Axon/myelin ratios revealed disproportionate shrinkage of axons evident already after 4 months of diabetes in the sural nerve and only after 8 months in the peroneal nerve. Endoneurial edema could not be demonstrated by morphometric means in diabetic nerves. We conclude that the distal symmetrical polyneuropathy in diabetes can be characterized as a mainly sensory axonopathy of dying‐back type.
Abnormalities of erythrocytes in duchenne muscular dystrophy
Authors: Yoshida Mizuko , Ando Kazuya , Satoyoshi Eijiro 
Published: January 2005

AbstractErythrocytes from patients with Duchenne muscular dystrophy (DMD) were studied in relation to the extracellular calcium ion concentration. The shape of fresh erythrocytes in DMD was normal and not affected by Ca++. When DMD erythrocytes were stored in buffer solution with Ca++, however, the rate of the shape change over time was enhanced compared with that of cells from normal controls. The calcium content of DMD erythrocytes stored in buffer solution with Ca++ and dextrose was also two and one‐half times that of control cells. In contrast, when DMD erythroytytes were stored in buffer stored in buffer solution with dextrose but without Ca++, no differences from controls were observed. The adenosine triphosphate content of DMD erythrocytes stored in the buffer solution was not affected by Ca++ concentration.
Passive joint position sense after total hip replacement surgery
Authors: Karanjia Percy N. , Ferguson John H. 
Published: January 2005

AbstractPassive joint position sense was tested in 10 subjects after unilateral total hip replacement surgery (which included capsulectomy). Varied initial limb position, amplitude, and velocity of movement were used. The unoperated side was used as a control. Statistically barely significant errors (p < 0.025) on the operated side were detected at 0.6° per second but not at 2° per second. No significant differences were noted among the different hip positions.The results indicate that the ability to detect passive hip joint position sense remains largely, but not completely, intact after hip joint replacement. The joint capsule, ligaments, and joint surfaces, although not essential for kinesthesia, may provide some limb movement and position information, the absence of which is not now clinically apparent.
Na+ ‐ and K+‐dependent adenosine triphosphatase changes in multiple sclerosis plaques
Authors: Hirsch Hilde E. , Parks Mary Ellen 
Published: January 2005

AbstractNa+ and K+ ‐dependent adenosine triphosphatase [(Na+ + K+)‐ATPase] was studied in microdissected samples from sections of histologically active and inactive plaques of multiple sclerosis. In active plaques the enzyme was found to be markedly reduced in activity, whereas in old, chronic plaques ATPase activities were higher than those of unaffected white matter. White matter from control patients and normal‐appearing white matter from MS patients did not differ with regard to ATPase activities. The results suggest that reversible changes in the sodium pump mechanism may be involved in the pathophysiology of multiple sclerosis.
Specific messenger RNA changes in joseph disease cerebella
Authors: Morrison Marcelle R. , Rosenberg Roger N. 
Published: January 2005

AbstractJoseph disease is an autosomal‐dominant, spinocerebellar degeneration characterized at the biochemical level by elevations in the steady‐state levels of several abundant proteins (H, J, and L) in affected brain areas such as the cerebellar cortex. The increased levels of these proteins could either be a consequence of a relative increase in their de novo synthesis or result from altered rates of proteolysis in degenerating brain cells. These alternatives can be distinguished by comparing the in vitro protein‐synthetic capacities of the messenger ribonucleic acid populations isolated from cerebellar cortex of control subjects and patients with Joseph disease. Protein H (glial fibrillary acidic protein) is synthesized at detectable levels by all messenger ribonucleic acid isolates, and the levels of its translatable messenger ribonucleic acid are reproducibly increased in ribonucleic acids isolated from cerebellar cortex of patients with Joseph disease as compared with those isolated from cerebellar cortex of control subjects. Thus, the increased level of protein H in Joseph disease is a consequence of an increase in its de novo synthesis and is correlated with the increased number of cerebellar glial cells. In contrast to these results, there is no detectable synthesis of proteins J and L by messenger ribonucleic acid populations isolated from cerebellar cortex of either Joseph disease patients or control subjects, suggesting that the increased levels of these proteins in affected cerebellar cortex are a consequence of posttranslational protein modifications.
Regional blood‐to‐tissue transport in ethylnitrosourea‐induced brain tumors
Authors: Blasberg Ronald G. , Kobayashi Tomowo , Horowitz Marc , M Jerry M. , Groothuis Dennis , Molnar Peter , D Joseph D. 
Published: January 2005

AbstractRegional blood‐to‐tissue transport, expressed as a unidirectional transfer rate constant (K), was measureed in experimental brain tumors using alpha‐aminoisobutyric acid (AIB) labeled with carbon 14 and quantitative autoradiography. A total of sixteen oligodendrogliomas, four mixed gliomas, three astrocytomas, two diffuse gliomatoses, one anaplastic astrocytoma, one ependymoma and four malignant schwannomas were studied in 9 rats. The mean Ks for all glioma classifications were similar, averaging 2.6 ± 0.4 (standard error of the mean) ml · kg−1 min−1, and were only slightly higher than those for nontumorous parietal cortex (2.1 ml · kg−1 · min−1), corpus callosum (0.9 ml · kg−1 min−1), and a comparable region of brain tissue in the contralateral hemisphere (1.3 ml · kg−1 · min−1). Values of K varied minimally in the intracerebral gliomas and were marginally correlated with tumor cell morphology in only two tumors. In some (but not all) of the larger gliomas, increased vascularity, with or without endothelial proliferation, was associated with a 3‐to 15‐fold increase in K. Regional K values in malignant schwannomas were highly variable (4 to 207 ml · kg−1 · min−1) and generally were not correlated with specific histological features of the tumor, except in some regions with increased vascularity. Estimates of the average fractional extraction of AIB by the intracranial gliomas and malignant schwannomas were 0.01 and 0.2, respectively; average fractional extractions for nontumorous brain were approximately 0.003.