bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tranfer of language dominance
Authors: Lee Henry , Nakada Tsutomu , Deal Jon L. , Lin Stan , Kwee Ingrid L. 
Published: January 2005

AbstractIt has been suggested that recovery from aphasia may depend on the ability of the nondominant hemisphere to subserve language functions. We describe a patient who illustrates a possible “transfer” of language dominance. The patients sustained two infarcts two years apart, one in each hemisphere, involving mirror image territories in the temporoparietal area. The clinical course of each infract was almost identical, consisting of an initial Wernicke's aphasia which evolved into anomic aphasia during recovery.
Alzheimer's disease: A study of epidemiological aspects
Authors: Heyman Albert , Wilkinson William E. , Stafford Judith A. , Helms Michael J. , Sigmon Alverta H. , Weinberg Tina 
Published: January 2005

AbstractA case‐control study was performed to determine the possible roles of various environmental factors, prior illnesses, drug use, and personal habits in the development of Alzheimer's disease. Such information was collected from 40 patients with onset of dementia prior to age 70 and from 80 community control subjects matched for age, sex, and race. No significant differences were found between patients and control subjects in toxic environmental exposures, animal contacts, smoking, drinking, or unusual dietary habits. A significantly higher frequency of prior thyroid disease was found in women patients than in women control subjects (25.0% and 7.1%, respectively). A history of severe head injury was also obtained significantly more often among the patients than among the controls (15.0% and 3.8%, respectively). Aside from these differences, which may prove to be important associative factors in this illness, there appeared to be no major premorbid demographic or clinical factors associated with this form of dementia. There was evidence, however, of a genetic factor that was manifested in an excess of dementia and mental retardation (including Down's syndrome) in families of patients with Alzheimer's disease.
Severe neurological impairment: Legal aspects of decisions to reduce care
Authors: Beresford H. Richard 
Published: January 2005

AbstractDecisions to reduce care for patients with severe neurological impairment may raise legal questions. The laws of most states now authorize physicians to stop care for those who have suffered irreversible cessation of all functions of the brain (“brain death”). Where state law is not explicit, it is nevertheless probably lawful to regard brain death as death for legal purposes so long as currently accepted criteria are satisfied. Several courts have ruled that it is lawful to reduce care for patients in vegetative states, but have prescribed differing standards and procedures for implementing such decisions. The issue of whether parents can authorize physicians to reduce care for neurologically impaired children is the focus of current litigation. Implicit in this litigation is the question of how severe neurological impairment must be before parents and physicians may lawfully agree to reduce care. For severely impaired but not vegetative adults, there is some legal authority to justify certain decisions to reduce care. The issue of whether withholding feeding from a severely demented patient with life‐threatening medical problems constitutes criminal behavior is now being considered by a state supreme court.
Regional blood flow in compression‐induced brain edema in rats: Effect of dietary vitamin E
Authors: Busto Raul , Yoshida Shinichi , Ginsberg Myron D. , Alonso Ofelia , Smith David W. , Goldberg William J. 
Published: January 2005

AbstractRegional cerebral blood flow (rCBF) was studied autoradiographically in a murine model of focal epidural brain compression, and the effect of vitamin E administration was investigated. Mean cortical CBF was reduced to 0.48 to 0.50 ml/gm/min following 2 or 24 hours of compression. Early (2 hours) following subsequent decompression, a mixed pattern of hypoperfusion and hyperperfusion was observed. Twenty‐four hours later, rCBF heterogeneities were less marked. Comparisons among animal groups raised on vitamin E–supplemented, vitamin E–normal, and vitamin E–deficient diets 2 hours after decompression revealed marked reductions in rCBF in the previously compressed cortex of the last two groups and hyperemia of the underlying hippocampus. The vitamin E–supplemented rats showed increased flow in the previously compressed cortex. In addition, vitamin E supplementation tended to eliminate rCBF gradients between subjacent zones. These data may help explain our previous observations of the beneficial effects of vitamin E on compression‐induced brain edema.
Severe neurological disease associated with hyperparathyroidism
Authors: Patten Bernard M. , Pages Michel 
Published: January 2005

AbstractTwo patients, one with ataxia, internuclear ophthalmoplegia, muscle weakness, atrophy, fasciculations, and bilateral Babinski's signs, the other with dysarthria, dysphagia, muscle weakness, atrophy, fasciculations, and hyperreflexia, had elevated serum calcium and parathyroid hormone levels, establishing the diagnosis of primary hyperparathyroidism (HPT). Removal of a parathyroid adenoma in one patient and three hyperplastic parathyroid glands in the other resulted in remission of the hyperparathroidism but left both patients with residual neurological damage. Postmortem examination of the second patient showed typical features of amyotrophic lateral sclerosis. The findings in these patients show that hyperparathyroidism may be associated with signs of severe central nervous system disease and that patients with unexplained neurological signs or symptoms should be checked for hyperparathyroidism.
DA strain of Theiler's murine encephalomyelitis virus induces demyelination in nude mice
Authors: Roos Raymond P. , Wollmann Robert 
Published: January 2005

AbstractDA strain of Theiler's murine encephalomyelitis virus produces a chronic, progressive demyelinating disease in mice that resembles multiple sclerosis. An immunopathological mechanism for demyelination has been postulated, because there is a brisk immune response with low virus titers at the time of demyelination and because immunosuppression lessens the degree of demyelination. We inoculated Nude mice with DA virus to clarify the role of immune‐mediated demyelination. Animals became paralyzed 3 weeks to 2 months after inoculation, usually dying within a week of appearance of signs. Demyelinated foci were present in the spinal cords, with evidence of degenerating myelin around intact axons as well as completely demyelinated, naked axons. Occasional macrophages were present, but none was seen actively stripping intact myelin lamellae. These results suggest that DA virus lytic infection, without a contribution from the T lymphocyte immune system, is sufficient to produce demyelination. It is likely that DA virus demyelination has varying mechanisms that may be active at different times.
Chronicity of hyponatremia as a factor in experimental myelinolysis
Authors: Norenberg Michael D. , Papendick Rebecca E. 
Published: January 2005

AbstractA recent analysis of hyponatremic patients disclosed that those who were chronically hyponatremic prior to rapid correction subsequently developed central pontine myelinolysis. To test the view that chronicity of hyponatremia is a factor in myelinolysis, we studied a group of rats that were hyponatremic for 1 day and compared it with another group of animals maintained in a hyponatremic state for 3 days prior to the administration of hypertonic saline solution. The 3‐day hyponatremic rats developed more numerous and more severe demyelinative lesions than the 1‐day rats. The findings support the view that duration of hyponatremia is a factor in myelinolysis and that the electrolyte disturbance of chronically hyponatremic patients should be corrected cautiously and relatively slowly.
The protective influence of the locus ceruleus on the blood‐brain barrier
Authors: Harik Sami I. , McGunigal Thomas 
Published: January 2005

AbstractThe functions of the putative noradrenergic innervation of cerebral microvessels from the nucleus locus ceruleus remain ambiguous. Although most evidence indicates that such innervation does not have a major role in the control of cerebral blood flow, there are increasing indications that it modulates transport and permeability functions of the blood‐brain barrier. In this study we investigated the effect of unilateral chemical lesioning of the locus ceruleus on the leakage of radioiodinated human serum albumin across the blood‐brain barrier. Experiments were performed in awake and restrained rats under steady‐state conditions and during drug‐induced systemic arterial hypertension, and in anesthetized and paralyzed rats during bicuculline‐induced seizures. Both hypertension and seizures are known to be associated with increased leakage of macromolecules across the blood‐brain barrier. Albumin leakage into norepinephrine‐depleted forebrain structures ipsilateral to the locus ceruleus lesion was compared with that of the contralateral side. There were no side‐to‐side differences in blood‐brain barrier permeability to albumin under steady‐state conditions, the stress of restraint, or angiotensin‐induced hypertension, or after isoproterenol administration. Norepinephrine‐induced hypertension and seizures, however, caused significant increases in albumin leakage into forebrain structures ipsilateral to the lesion. These results suggest that noradrenergic innervation of cerebral microvessels from the locus ceruleus helps preserve the integrity of the blood‐brain barrier during pathophysiological states associated with hypertension and increased circulating catecholamines.
Rapid alterations of the axon membrane in antibody‐mediated demyelination
Authors: Saida Kyoko , Saida Takahiko , Kayama Hisae , Nishitani Hiroshi 
Published: January 2005

AbstractAlterations of nodal and paranodal axolemma of the rat sciatic nerve were investigated in antigalactocerebroside serum–induced demyelination. A ferric ion–ferrocyanide (FeFCN) stain that appears to stain the regions with a high sodium channel density in nerve fibers was applied. When acute conduction block was initiated 20 to 180 minutes after the antiserum injection, myelin terminal loops began to be detached from the paranodal axolemma and reaction product of FeFCN stain originally localized at the nodes decreased in density and extended to the paranodal axolemma. By the time that complete conduction block was established, 5 hours after the injection, FeFCN stain was barely detectable around the nodal area. The loss of staining was associated with detachment and vesiculovacuolar degeneration of the paranodal myelin. This rapid deterioration and disappearance of normal cytochemical characteristics of the axolemma in the presence of only modest paranodal demyelination could be a morphological correlate of the loss of excitability of the axon membrane.
Serum neuronal growth factor levels in von Recklinghausen's neurofibromatosis
Authors: Riopelle Richard J. , Riccardi Vincent M. , Faulkner Shizuye , Martin Mary C. 
Published: January 2005

AbstractA single neuronal cell biological assay was used to quantitate neuronal growth factors in 87 serum samples from 69 patients in 48 families with von Recklinghausen's neurofibromatosis, plus 16 samples from 16 comparison subjects. Mouse nerve growth factor was used as a standard for the bioassay, and results of serum assays were expressed as nerve growth factor equivalents. Antiserum to mouse nerve growth factor inhibited fractionally serum‐induced neurite outgrowth, while kinetics of neurite outgrowth and maximal cellular response to serum differed from those induced by mouse nerve growth factor. The mean values (± SD) of neuronal growth factors for the patients were 20.5 ± 15.7 pg/mg serum protein, while mean values for the comparison group as a whole were 22.3 ± 15.6 pg/mg serum protein. Sex, race/ethnicity, patient age, and date of sample collection did not significantly influence serum levels among patients or comparison subjects. Three to six serial samples taken from women before pregnancy, during the course of pregnancy, during delivery, and in the postpartum period did not show significant differences from one period to another. These data suggest that human serum does contain non‐nerve‐growth‐factor neuronal growth factors, but that levels of the factors do not contribute to the identification of patients with von Recklinghausen's neurofibromatosis.
Acute Kingella kingae endocarditis with recurrent cerebral emboli in a child with mitral prolapse
Authors: Lee Wei Ling , Dooling Elizabeth C. 
Published: January 2005

AbstractAn 11‐year‐old girl had sudden onset of right hemiplegia and dysphasia with fever. Blood cultures grew Kingella kingae. Echocardiography showed a prolapsed mitral valve vegetation, which became larger during a prolonged course of antibiotics. After seven weeks of therapy, when surgery was being planned, the child deteriorated abruptly. A repeat echocardiogram showed that the vegetation had disappeared. Conservative medical management is usually inadequate in treating vegetations associated with bacterial endocarditis; surgery is advised.
A new form of sea‐blue histiocytosis associated with progressive anterior horn cell and axonal degeneration
Authors: Ashwal Stephen , Thrasher Thais V. , Rice David R. , Wenger David A. 
Published: January 2005

AbstractA 15‐year‐old girl evidenced a slowly progressive central nervous system degenerative disorder. The illness had begun and progressed between ages 1 and 12 years, with ataxia, spasticity, choreoathetosis, early‐onset seizures (which later ceased), and mild retardation. At age 13 she had developed rapidly progressive generalized weakness and atrophy, indicating peripheral nervous system involvement. Laboratory investigation revealed the presence of sea‐blue histiocytes in the bone marrow without evidence of a disorder of sphingolipid metabolism or neuronal ceroid lipofuscinosis. Muscle biopsy showed large‐ and small‐group atrophy, and sural nerve biopsy demonstrated axonal degeneration. This patient's illness appears to be a hitherto undescribed form of “sea‐blue histiocytosis” associated with neurological dysfunction in children.
Monoclonal antibody analysis of mononuclear cells in myopathies. II: Phenotypes of autoinvasive cells in polymyositis and inclusion body myositis
Authors: Engel Andrew G. , Arahata Kiichi 
Published: January 2005

AbstractIn 6 cases of polymyositis and 6 of inclusion body myositis, phenotypes of mononuclear cells focally surrounding and invading muscle fibers were analyzed. By localizing the T8, T4, and Ia markers with direct immunofluorescence and acid phosphatase enzyme cytochemically in the same sections, five different phenotypes were simultaneously identified in a given section: T8+ and T4+ cells that were either activated (Ia+) or not activated (Ia−), and acid phosphatase—reactive and Ia+ macrophages. This approach permitted the separate and quantitative assessment of the distributions of the different phenotypes among the invading versus the surrounding cells. In both polymyositis and inclusion body myositis, the invading cells were selectively enriched in the T8+ cells were more abundant among the surrounding than the invading cellsm and only a small proportion of the T4+ cells were activated. These findings are especially significant in view of the cytotoxic capability of the T8+ cells and because histocompatibility factors permit T8+ but not T4+ cells to recognize an antigen on muscle fibers. Macrophages accounted for 21 to 31% of the cells invading or surrounding nonnecrotic fibers. For purposes of comparison, we also analyzed mononuclear cells in necrotic fibers: 80% of these cells were macrophages, and only 20% were T cells. The findings indicate that in polymyositis and inclusion body myositis, nonnecrotic muscle fibers are injured by autoinvasive T8+ cells that act in concert with macrophages. Further, the findings strongly imply previous sensitization of clones of T cells to muscle fiber—associated surface antigen(s).
Cholesterol and phospholipids in cultured skin fibroblasts from patients with dystonia
Authors: Maltese William A. , De Vivo Darryl C. 
Published: January 2005

AbstractCultured skin fibroblasts from patients with hereditary (recessive) torsion dystonia or adult‐onset sporadic dystonia and from healthy volunteers were compared with respect to total cellular cholesterol, total phospholipid, and phospholipid composition. Differences that could be attributed specifically to dystonia were not detected. The data suggest that the reported cell membrane abnormality in recessive torsion dystonia does not involve a generalized defect in cholesterol or phospholipid metabolism.
Descending paralysis resulting from occult wound botulism
Authors: Rapoport Samuel , Watkins Paul B. 
Published: January 2005

AbstractA 30‐year‐old male drug absuser developed ophthalmoplegia, bulbar paralysis, and limb weakness responsive to edrophonium. However, potentiation of a lowamplitude evoked muscle action potential was produced with repetitive nerve stimulation at 10 Hz, and the clinical and electrophysiological dat suggested the diagnosis of botulism. The source of botulism type B toxin was a clinically obscure cyst produced by subcutaneous infiltration of cocaine two weeks prior to the onset of symptoms. The patienat improved with chronic administration of pyridostigmine bromide and plasmapheresis. Wound botulism may be underdiagnosed because of confususion with inflammatory neuropathy or myasthenia gravis. Neuromuscular transmission studies in patients with acute craniosomatic paralysis can prevent such oversights.
Brain electrical activity in patients with presenile and senile dementia of the Alzheimer type
Authors: Duffy Frank H. , Albert Marilyn S. , McAnulty Gloria 
Published: January 2005

AbstractNeurophysiological and behavioral data obtained from 9 patients with presenile dementia and 10 with senile dementia of the Alzheimer type were compared with similar data from 25 age‐ and sex‐equivalent controls. Compared with the healthy controls, both patient groups demonstrated increased background electroencephalographic slowing with a reduction in fast activity (synchronization). Topographic analyses of data from electroencephalographic and evoked potential studie indicate that areas of maximal group differences between the presenile patients and their controls include the right posterior temporal and, to a lesser extent, left midtemporal to anterior temporal areas, whereas the maximal differences between the senile patient group and their controls involve the midfrontal and anterior frontal lobes, bilaterally. Moreover, right‐sided numerical features derived from topographic maps proved most useful in differentiating the presenile patients and their age‐matched controls, whereas bilateral features were more useful in separating senile patients from their controls. These topographic dissimilarities between patient groups suggest that an age‐disease interaction exists between patients with presenile and senile dementia of the Alzheimer type. Correlational analyses between neuropsychological test scores and neurophysiological features indicate that increased slowing and decreased fast activity were associated with poorer test performance.
Hereditary dysphasic dementia and the Pick‐Alzheimer spectrum
Authors: Morris John C. , Cole Monroe , Banker Betty Q. , Wright David 
Published: January 2005

AbstractHereditary dysphasic dementia is described in terms of its clinicopathological, ultrastructural, and transmissibility characteristics. Its mode of inheritance is autosomal dominant, and its clinical manifestations of progressive dementia and severe dysphasic disturbances are expressed in late adulthood. Complete neuropathological examination of four patients reveals findings typical for Pick's disease (asymmetrical focal cerebral atrophy), Alzheimer's disease (profuse neuritic plaques), and paralysis agitans (neuronal depigmentation, depletion, and Lewy body formation in substantia nigra) in addition to a striking but nonspecific spongiform degeneration of superficial cortical layers. This unique combination of gross morphological and histopathological features qualifies hereditary dysphasic dementia as a distinct entity, but its precise relationship to the well‐recognized adult cortical dementias has been difficult to establish by conventional classification methods. This disorder and other unusual dementing illnesses may be best considered as part of a Pick‐Alzheimer spectrum of cortical neuronal degenerations.
Perinatal cerebral infarction
Authors: Ment Laura R. , Duncan Charles C. , Ehrenkranz Richard A. 
Published: January 2005

AbstractThe diagnosis of perinatal cerebral infarction, although frequently suggested clinically, has been made most commonly at postmortem examination; few infants surviving stroke are reported in the literature. We evaluated 18 infants with perinatal cerebral infarction in a recent twelve‐month interval. Seven were preterm neonates, 6 of whom had experienced neonatal intraventricular hemorrhage. Three full‐term infants were thought to have experienced cerebral infarction in utero and had evidence of well‐defined strokes on computed tomographic scans performed shortly after birth. Eight infants developed stroke at term. The most common cause of cerebral infarction in our series was perinatal asphyxia. Fourteen of the infants were seen with neonatal seizures. Fourteen of the 18 have died or are faring poorly at 4 to 12 months of age (corrected).
Infection of neuronal cell cultures with reovirus mimics in vitro patterns of neurotropism
Authors: Dichter Marc A. , Weiner Howard L. 
Published: January 2005

AbstractPrimary neuronal cell cultures of rat fetal cerebral cortex serve as in vitro models for the study of a variety of neuronal membrane receptors. Such studies have focused primarily on receptors for neurotransmitters and drugs. In the present series of experiments, we have employed this model to study the in vitro pattern of infection with reovirus types 1 and 3, two well‐characterized neurotropic viruses that show specificity for neurons (type 3) or ependymal cells (type 1) in vivo and whose specificity has been linked with surface receptors on somatic cells. We have found that in primary neural cell culture, reovirus type 3 maintained its specificity by infecting neurons whereas reovirus type 1 did not infect neurons. Both serotypes infected astrocytes in the cultures, type 1 to a greater extent than type 3. In addition, reovirus type 3 bound to the surface of neurons whereas type 1 did not. Using recombinant viral clones, the in vitro tropism and the neuronal binding were shown to be properties of the viral hemagglutinin, a small outer capsid viral protein, as is the case with the neurotropism in vivo. It is postulated that the neurotropism of reovirus type 3 is related to the interaction of the viral hemagglutinin with an as yet undefined structure on the neuronal surface.