bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow and histopathology after middle cerebral artery occlusion
Authors: Mohamed A. A. , Gotoh O. , Graham D. I. , Osborne K. A. , McCulloch J. , Mendelow A. D. , Teasdale G. M. , Harper A. M. 
Published: January 2005

AbstractWe used the [14C]iodoantipyrine autoradiography technique to study the effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow (1CBF) in rats that underwent middle cerebral artery (MCA) occlusion. In untreated control animals there were profound localized reductions in 1CBF 30 minutes after MCA occlusion. These were most pronounced in neocortical areas and in the caudate nucleus ipsilateral to the MCA occlusion. In animals pretreated with nimodipine (1 μg · kg−1 · min−1 for 30 minutes before and 30 minutes after MCA occlusion), the ipsilateral decrease in 1CBF in cortical regions was significantly less than that in control animals. The drug did not appear to alter 1CBF in the ipsilateral caudate nucleus. Neuropathological quantification of the ischemic damage present 3 hours after occlusion showed thai: nimodipine pretreatment reduced the volume and extent of cellular damage in the periphery but not in the core of the lesion.
Vasoactive drugs produce selective changes in flow to experimental brain tumors
Authors: Panther Lori A. , Baumbach Gary L. , Bigner Darell D. , Piegors Donald , Groothuis Dennis R. , Heistad Donald D. 
Published: January 2005

AbstractMost vasoactive drugs do not readily penetrate the blood‐brain barrier and do not affect cerebral blood flow. We tested the hypothesis that vasoactive drugs may alter blood flow to brain tumors in which the blood‐brain barrier is abnormal. Blood flow was measured with microspheres in dogs with brain tumors induced by avian sarcoma virus. Intravenously administered adenosine increased blood flow to tumor more than twofold but did not alter flow to normal brain. Intravenously administered norepinephrine decreased blood flow to tumor but not to normal brain. Thus, vasoactive drugs, which have little effect on blood flow to normal cerebrum, produce large changes in blood flow to brain tumors. We also examined responses to systemic hypercapnia. Hypercapnia increased blood flow to normal cerebrum more than twofold but failed to increase flow to tumors. Impaired vasodilator responses to hypercapnia in brain tumors, which cannot be explained primarily by an abnormality of the blood‐brain barrier, probably reflect another fundamental difference between vessels in normal brain and brain tumors. The finding that vasoactive drugs have selective effects on blood flow to brain tumors has important implications for delivery of lipid‐soluble chemotherapeutic drugs to the tumors.
Conduction failure and nerve conduction slowing in experimental allergic neuritis induced by P2‐specific T‐cell lines
Authors: Heininger Kurt , Stoll Guido , Linington Christopher , Toyka Klaus V. , Wekerle Hartmut 
Published: January 2005

AbstractP2‐specific T cells (LiP2/A) mediate experimental allergic neuritis (EAN) in the Lewis rat after adoptive transfer to naive recipients. After a latent period of 4 days, injection of 2 × 106 line cells induced fulminant paraplegia and complete conduction failure in the peripheral nerves and roots, resembling acute axonal breakdown. Injection with 106 cells caused milder clinical signs, nerve conduction failure, and conduction slowing. Clinical and electrophysiological recovery from adoptively transferred EAN was nearly complete and its time course was inversely correlated to the initial severity of EAN. These findings suggest that EAN induced by the P2‐specific T‐cell line can lead to a profound and rapidly evolving nerve dysfunction in a dose‐dependent fashion.
Opening the blood–brain and blood–tumor barriers in experimental rat brain tumors: The effect of intracarotid hyperosmolar mannitol on capillary permeability and blood flow
Authors: Hiesiger E. M. , Voorhies R. M. , Basler G. A. , Lipschutz L. E. , Posner J. B. , Shapiro W. R. 
Published: January 2005

AbstractUsing quantitative autoradiography, we investigated the effect of intracarotid infusions of hyperosmolar mannitol solutions on capillary permeability and blood flow. Capillary permeability, expressed in terms of a blood‐to‐tissue transfer constant (K), was determined in two rat brain tumor models by measuring the entry of 14C‐alpha aminoisobutyric acid into brian tumor, into brain tissue adjacent to tumor, and into cortex. Cerebral blood flow was determined by measuring the uptake of 14C‐iodoantipyrine in one rat brain tumor model. Blood flow was examined in the same regions as K, as well as in the corpus callosum. Before mannitol administration, K values in both Walker 256 (W256) carcinosarcoma and C6 gliomas were much higher than those in cortex. C6 gliomas were about three times more permeable than were W256 tumors. There was a direct correlation between tumor size and increased capillary permeability. Mannitol at a concentration of 1.37 M did not increase the K values for either tumor or adjacent tissue. At 1.6 M, mannitol increased the K values for both tumors (1.7‐fold in C6 glioma and 13‐fold in W256) as well as for adjacent tissue. At both concentrations, mannitol markedly increased cortical K values in all groups: by 48‐to 72‐fold at 1.37 M and by 90‐ to 105‐fold at 1.6 M. The net effect of the mannitol was to reverse the tumor‐to‐cortex permeability relationship. Cortical blood flow increased modestly after intracarotid mannitol administration on both sides of the brain. These data provide little justification for using intracarotid mannitol during chemotherapy of human brain tumors.
A white matter disorder in dementia of the Alzheimer type: A pathoanatomical study
Authors: Brun A. , Englund E. 
Published: January 2005

AbstractIn cases of Alzheimer's presenile and senile dementia, Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT), respectively, we have observed, in addition to the gray matter degeneration, a lesion that has the character of an incomplete infarction confined to the white matter. It is encountered in 60% of both groups, with mild changes in two thirds and moderate or severe changes in one third. It involves the deep white matter symmetrically, tapering off toward the cortex. It is characterized by partial loss of myelin, axons, and oligodendroglial cells; mild reactive astrocytic gliosis; and sparsely distributed macrophages as well as stenosis resulting from hyaline fibrosis of arterioles and smaller vessels. No complete or cavitating infarctions and no hypertensive vascular changes were observed. The white matter changes are thought to be due to hypoperfusion of the concerned white matter territories since, in addition to the white matter hyaline vascular stenosis, these cases show signs of cardiovascular disease, usually with hypotension.The white matter disorder also occurs independent of the gray matter process of AD and SDAT and may be seen as the sole brain lesion in non‐AD subjects. Its occurrence is thus neither regularly related to the severity nor to the regional appearance and accentuation of the cortical Alzheimer process and is thus not likely to be just the result of a wallerian degeneration. Histologically it is similar in several respects to Binswanger's disease, although with some distinct differences. It is thus related to the cerebrovascular group of disorders in addition to AD and SDAT. In view of its frequency and severity, this white matter lesion is important to define, to diagnose, and ultimately to prevent or cure.
Swallowing and speech production in Parkinson's disease
Authors: Robbins Jo Anne , Logemann Jerilyn A. , Kirshner Howard S. 
Published: January 2005

AbstractVideofluoroscopy was used to examine movement patterns during swallowing and speech production in 6 parkinsonian subjects and 6 age‐matched controls. Motility patterns for liquid and semisolid swallows were documented. We performed temporospatial analyses of oropharyngeal structures, particularly the velum, which is prominently involved in both motor speech production and swallowing. Differences were found between groups and conditions. All of the parkinsonian subjects exhibited abnormal oropharyngeal movement patterns and timing during the volitional oral as well as the pharyngeal stage of swallowing; only 50% of these subjects admitted to any swallowing difficulty upon questioning. Two of the subjects with Parkinson's disease aspirated liquids. Duration of velar movement during speech production significantly differentiated the groups (p < 0.01), reflecting reduced range of velar motion. Our findings suggest that rigidity and bradykinesia underlie the volitional speech abnormality as well as the disordered oral and pharyngeal stages of swallowing. Findings indicate that parkinsonian patients may be “silent aspirators” with decreased cough reflexes and lack of awareness of aspiration. The clinical value of videofluoroscopic monitoring of swallowing is that aspiration may be detected and managed early.
Human autonomy and the frontal lobes. Part II: Patient behavior in complex and social situations: The “environmental dependency syndrome”
Authors: Lhermitte F. 
Published: January 2005

AbstractImitation and utilization behavior have previously been described in terms of a simple interaction between an examiner and a patient, and were interpreted as an excessive dependence on environmental cues. In this study, patient dependence was observed in complex situations of everyday life. Two patients with focal unilateral frontal lobe lesions were observed while in a doctor's office, a lecture room, a car, and a garden, while visiting an apartment where various activities were possible, and while in a gift shop. The patients' behavior was striking, as though implicit in the environment was an order to respond to the situation in which they found themselves. The term environmental dependency syndrome is proposed for this condition. It implies a disorder in personal autonomy. Individual psychological traits influenced the way in which loss of autonomy was manifested. This study does not offer a physiological model of autonomy, but it does provide clinical and behavioral observations on the loss of autonomy secondary to unilateral lesions of the frontal lobe.
Dopamine denervation does not alter in vivo 3H‐spiperone binding in rat striatum: Implications for external imaging of dopamine receptors in Parkinson's disease
Authors: Bennett James P. , Wooten G. Frederick 
Published: January 2005

AbstractStriatal particulate preparations, both from rats with lesion‐induced striatal dopamine (DA) loss and from some patients with Parkinson's disease, exhibit increased 3H‐neuroleptic binding, which is interpreted to be the mechanism of denervation‐induced behavioral supersensitivity to dopaminergic compounds. After intravenous 3H‐spiperone (3H‐SP) administration to rats with unilateral nigral lesions, we found no differences in accumulation of total or particulate‐bound 3H‐SP in dopamine‐denervated compared with intact striata. 3H‐SP in vivo binds to less than 10% of striatal sites labeled by 3H‐SP incubated with striatal particulate preparations in vitro. Quantitative autoradiography of 3H‐SP binding to striatal sections in vitro also failed to reveal any effects of dopamine denervation. 3H‐SP bound to striatal sites in vivo dissociates more slowly than that bound to striatal particulate preparations labeled in vitro. Striatal binding properties of 3H‐SP administered in vivo are quite different from the same kinetic binding parameters estimated in vitro using crude membrane preparations of striatum. In addition, striatal binding of in vivo–administered 3H‐SP is not affected by prior lesion of the substantia nigra, which results in profound ipsilateral striatal dopamine depletion. Thus, behavioral supersensitivity to dopaminergic compounds may not be associated with altered striatal binding properties for dopamine receptor ligands in vivo.
Giant axonal neuropathy: Central abnormalities demonstrated by evoked potentials
Authors: Majnemer Annette , Rosenblatt Bernard , Watters Gordon , Andermann Frederick 
Published: January 2005

AbstractPrevious studies of giant axonal neuropathy have reported clinical and pathological findings that indicate involvement of the central nervous system. We studied 3 boys with giant axonal neuropathy, who were 14 to 16 years of age, using auditory, visual, and somatosensory evoked potentials. Absence of waveforms and prolongation of peak and interwave latencies were found. Abnormalities were noted in all modalities. The auditory brainstem evoked response in particular indicated a significant increase in brainstem conduction time. These studies add clinical neurophysiological confirmation of the central nervous system involvement in this disorder and may also provide a means of quantitative evaluation of its progression.
The spatial distribution of fiber loss in diabetic polyneuropathy suggests ischemia
Authors: Dyck Peter James , Karnes Jeannine L. , O'Brien Peter , Okazaki Haruo , Lais Alfred , Engelstad JaNean 
Published: January 2005

AbstractCharacterization and quantitation of the spatial distribution of pathological abnormalities along the length of nerves may be helpful in understanding the underlying mechanisms of diabetic polyneuropathy. To this end, by examining transverse sections of nerve roots and proximal‐to‐distal levels of lower limb nerves in 9 controls and 15 diabetic patients with polyneuropathy, we have determined the myelinated fiber (MF) number, size distribution, median diameter, and variability of density (MFs/mm2) among frames and among fascicles. Even in cases with mild polyneuropathy, fiber loss, a decrrease in the median diameter, and an increase in the variability of density among frames and among fascicles began in proximal nerve and extended to distal levels. Multifocal fiber loss along the length of nerves and sprouting provide the best explanation for these findings. The pattern is dissimilar from that observed in diffuse metabolic disease of Schwann cells, neuronal degeneration, and dying‐back neuropathy, but like that found in experimental ischemic neuropathy induced by embolization of nerve capillaries.
Dopamine D2 receptor density remains constant in treated Parkinson's disease
Authors: Guttman Mark , Seeman Philip , Reynolds Gavin P. , Riederer Peter , Jellinger Kurt , Tourtellotte Wallace W. 
Published: January 2005

AbstractD2 dopamine receptor densities were measured in postmortem samples of the caudate nucleus and putamen from 36 parkinsonian patients. The relationship between the age of the patient, duration of the disease, and duration of L‐dopa therapy versus density of brain D2 dopamine receptors was examined using [3H]spiperone. Receptor density in parkinsonian tissues was constant over the age range of 56 to 90 years, as was the case for control tissues. Density did not change with duration of disease up to 24 years. Treatment with L‐dopa did not cause progressive reduction in receptor density. The diminished clinical response in the final stages of Parkinson's disease is not due to receptor dropout, and must depend on other factors.
Traumatic injury alters opiate receptor binding in rat spinal cord
Authors: Krumins Solveig A. , Faden Alan I. 
Published: January 2005

AbstractRecent studies with dynorphin (an endogenous ligand for the κ‐opiate receptor) and receptor‐selective opiate antagonists have indicated a role for the κ‐receptor in the pathophysiology of spinal cord injury. However, no studies have specifically examined opiate receptor binding in relation to spinal injury. In the present experiments, opiate receptor binding was measured in spinal cord after traumatic injury in rats using the selective radioligands [3H][D‐Ala2, D‐Leu5]enkephalin (δ‐receptor agonist); [3H][D‐Ala2, MePhe4, Gly‐(ol)5]enkephalin (μ‐receptor agonist); and [3H]ethylketocyclazocine (κ‐receptor agonist). The specific binding of ethylketocyclazocine, but not the other agonists, showed a significant, time‐dependent, and localized increase at the injury site. Since dynorphin, which has been implicated as an injury factor after spinal trauma, shows similar localized increases after spinal injury, the present data are consistent with the hypothesis that up‐regulation of the κ‐receptor after injury may contribute to the subsequent secondary injury process.
Kinetics of microcirculatory, NAD/NADH, and electrocorticographic changes in cat brain cortex during ischemia and recirculation
Authors: Dora Eors , Tanaka Kartaro , Greenberg Joel H. , Gonatas Nicholas H. , Reivich Martin 
Published: January 2005

AbstractChanges in microcirculation, the NAD/NADH redox state, and electrical activity during 2 hours of ischemia and 4 hours of reperfusion produced by middle cerebral artery occlusion and release were studied in cats. Twelve animals were classified into three groups of ischemia (mild, moderate, and severe) based on the severity of electrocorticographic (ECoG) depression at the end of the recovery period. Four animals were studied as controls. Occlusion of the middle cerebral artery (MCAO) resulted in a marked but similar degree of reduction in cerebral blood flow (CBF) in all three groups. After this initial change, CBF increased continuously during occlusion in the mild group. CBF in the moderate and severe groups remained at the same low level during the entire period of MCAO. Immediately after MCAO, NAD reduction was increased by approximately 50% in all groups. At the end of MCAO, while the NAD/NADH redox state returned to its pre‐ischemic reference level in the severe group, it remained markedly reduced in the mild and moderate groups. Removal of the clip led to slight reactive hyperemia in the mild and severe groups but not in the moderate group. Immediately after recirculation, NAD/NADH redox was shifted toward oxidation in all groups. However, this reoxidation of NADH was only partial in the mild and moderate groups, and a pronounced hyperoxidation occurred in the severe group. In spite of the similar behavior of CBF in the recovery period, a marked secondary NAD reduction occurred in the moderate group during the recirculation period. It is suggested that this represents cessation of mitochondrial electron transport in the dying cells, accompanied by stimulated anaerobic glycolysis in other cells. The spontaneous oxidation of NADH during MCAO and its hyperoxidation during recirculation in the severe group may be due to an insufficient supply of reducing equivalents into the mitochondria and/or the release of oxidizing substances in the brain.
Diagnostic value of cerebrospinal fluid anti–myelin basic protein in patients with multiple sclerosis
Authors: Warren Kenneth G. , Catz Ingrid 
Published: January 2005

AbstractPrevalence and titer of total, free, and bound cerebrospinal fluid anti–myelin basic protein (MBP) antibodies as well as free/bound ratios were determined in four groups of patients with multiple sclerosis (MS) and three groups of controls. All patients with clinically active MS have elevated levels of total anti‐MBP, which may be present in either free or bound form. Patients whose disease is in remission have undetectable anti‐MBP levels, and some patients with clinically stable disease with residual disability may have detectable antibody titers. Chronically progressive MS is usually associated with high levels of antibody in the bound rather than the free form, resulting in a low or normal free/bound ratio. In contrast, MS exacerbations are characterized by relatively high levels of free anti‐MBP in the cerebrospinal fluid, resulting in a high free/bound antibody ratio. Bound anti‐MBP was also detected in elevated levels in 1 patient with subacute sclerosing panencephalitis and 2 of 8 patients with postinfectious encephalomyelitis. Although elevated levels of cerebrospinal fluid anti‐MBP are not specific for MS, they are strongly associated with disease activity and may be involved in the pathogenesis of demyelination in patients with MS.
Membrane defects in duchenne dystrophy: Protease affecting sarcoplasmic reticulum
Authors: Nagy Béla , Samaha Frederick J. 
Published: January 2005

AbstractHuman muscle sarcoplasmic reticulum (SR) yields three major protein bands. The percent distribution of the mean values of the bands from 15 normal human muscles was 55.4, 14.6, and 30.0 for the 100, 55, and 45‐kDa mass proteins, respectively. A mean distribution similar to that in normal muscle SR was found in preparations from 7 patients with polymyositis and from 7 patients with myotonic dystrophy. In 12 preparations from patients with Duchenne dystrophy, the protein distribution differed from that of preparations from normal muscle. The 100‐kDa mass protein band was decreased, whereas the 55‐ and 45‐kDa mass bands were increased. Protease inhibitors pepstatin A, antipain, and leupeptin, as well as ethyleneglycol‐bis(aminoethyl ether)‐N,N,N′,N′‐tetraacetic acid or ethylenediaminetetraacetic acid, significantly reduced this change. However, some of the changes cannot be prevented by the addition of inhibitors and must be expressed in vivo. Neither protease inhibitors nor chelators affected SR preparations from normal muscle. We found a five‐ to ten‐fold increase in calcium‐activated neutral protease activity in Duchenne dystrophic muscles that degraded the calcium‐adenosinetriphosphatase of SR. The active protease was identified as the cytoplasmic calpain II. The increased activity in Duchenne muscles may explain many reported abnormalities.
Free kappa light chains in multiple sclerosis spinal fluid
Authors: Rudick Richard A. , Pallant Adam , Bidlack Jean M. , Herndon Robert M. 
Published: January 2005

AbstractBased on prior reports of free light chains of immunoglobulin G (IgG) in the cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS), we quantitated free kappa and lambda chains and whole IgG concentrations using sensitive and specific radioimmunoassays (RIAs). The RIA for free kappa chains had a sensitivity of 0.25 μg/ml and was capable of specifically measuring free kappa chains in whole CSF or serum even in the presence of a 4‐log excess of whole IgG. By RIA, free kappa chains were detected in CSF samples from 33 (84%) of 39 MS patients but in only 1 (2.4%) of 42 controls. The control patients included 10 with noninfectious inflamatory diseases and 9 with central nervous system infections. The concentration of free kappa chains in the CSF of the MS patients was 1.40 ± 1.21 μg/ml. Free kappa chains were concentrated in the CSF 71‐ to 120‐fold relative to reference proteins. In contrast, increased levels of free lambda chains or of whole IgG were nonspecific; abnormalities were seen in controls with infections or inflammatory diseases as often as in MS patients. These studies suggest that the measurement of free kappa light chains may have important diagnostic usefulness, since the specificity of the finding for MS appears to be high.
Chronic inflammatory demyelinating polyneuropathy of infancy: A corticosteroid‐responsive disorder
Authors: Sladky John T. , Brown Mark J. , Berman Peter H. 
Published: January 2005

AbstractWe present the clinical, electrophysiological, and histopathological findings in 6 children with early‐onset chronic inflammatory demyelinating neuropathy. The clinical features initially suggested a genetically determined disorder in each patient. Sural nerve biopsy showed changes of chronic demyelination with multifocal endoneurial edema and mononuclear cellular infiltrates. All children improved with corticosteroid therapy.