bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of silent cerebellar lesions by increasing the inertial load of the moving hand
Authors: Manto M. , Godaux E. , Jacquy J. 
Published: January 2005

AbstractIn a previous study, we analyzed the hypermetria of wrist flexion movements in patients with a cerebellar syndrome. We found that hypermetria augmented when the inertial load of the moving hand was artificially increased. In the present study, we applied the same protocol to patients with an apparently normal neurological examination, in spite of a cerebellar lesion documented by magnetic resonance imaging. In all of these patients, the addition of a mass to the moving hand caused the appearance of a hypermetria. This lack of adaptation of fast and accurate movements to an increased inertia thus appears as a new diagnostic tool enabling the detection of silent cerebellar lesions.
Cerebral oxygen supply and utilization during infant cardiac surgery
Authors: Plessis Adre J. Du , Newburger Jane , Jonas Richard A. , Hickey Paul , Naruse Hiroo , Tsuji Miles , Walsh Amy , Walter Gene , Wypij David , Volpe Joseph J. 
Published: January 2005

AbstractThe survival of infants with congenital heart disease has improved dramatically. However, the incidence of neurological injury in infants surviving cardiac surgery remains considerable. These neurological sequelae are attributable at least in part to hypoxia‐ischemia/reperfusion, which inevitably accompanies infant heart surgery with deep hypothermia, cardiopulmonary bypass, and circulatory arrest. To begin to identify mechanisms of brain injury during infant cardiac surgery, we used near‐infrared spectroscopy to study the relationship between cerebral intravascular (hemoglobin) and mitochondrial (cytochrome aa3) oxygenation in 63 infants (aged 1 day to 9 months) undergoing deep hypothermic repair of congenital heart defects, throughout the intraoperative period. Moreover, we assessed the effect of postnatal age on these changes. The cerebral concentration of oxidized cytochrome aa3 decreased from the onset of deep hypothermic cardiopulmonary bypass, despite apparent abundant intravascular oxygenation manifested by a simultaneous increase in the cerebral concentration of oxyhemoglobin. During this interval infants older than 2 weeks had a greater decrease in oxidized cytochrome aa3 than did infants 2 weeks old or younger. During deep hypothermic circulatory arrest, cerebral levels of oxidized cytochrome aa3 remained depressed while those of oxyhemoglobin declined. With reperfusion following circulatory arrest, the recovery of oxidized cytochrome aa3 was delayed, despite a rapid recovery of intravascular oxygenation (HbO2). After rewarming and 60 minutes of reperfusion, only 46% of infants recovered to the baseline level of cerebral oxidized cytochrome aa3. These findings demonstrate a paradoxical dissociation of changes in intravascular and mitochondrial oxygenation during hypothermic cardiopulmonary bypass; a pronounced decrease of mitochondrial oxygenation is established during induction of hypothermia and a delay in recovery of mitochondrial oxygenation occurs following circulatory arrest. These effects were more pronounced in infants older than 2 weeks than in younger infants. The data suggest potentially deleterious impairments of intrinsic mitochondrial function or of delivery of intravascular oxygen to the mitochondrion or both, effects previously undetected and apparently influenced by cerebral maturation.
Active and passively induced experimental autoimmune encephalomyelitis in common marmosets: A new model for multiple sclerosis
Authors: Massacesi Luca , Genain Claude P. , Lee‐Parritz David , Letvin Norman L. , Canfield Donald , Hauser Stephen L. 
Published: January 2005

AbstractA chronic relapsing‐remitting form of experimental autoimmune encephalomyelitis was induced in the common marmoset Callithrix jacchus following a single immunization with human white matter. Individual animals in this species are born as natural bone marrow chimeras, allowing transfer of functional T‐cell populations between genetically distinct siblings. The acute disease was characterized clinically by mild neurological signs. Pathologically, the disease was characterized by perivascular mononuclear cell infiltrates, large foci of primary demyelination, and reactive astrogliosis. No animal displayed hemorrhagic‐necrotic lesions or polymorphonuclear cell infiltrates characteristic of other acute forms of primate experimental autoimmune encephalomyelitis. A late spontaneous relapse occurred in each of 2 animals followed for 3 to 12 months subsequent to recovery from the acute attack. In these animals, chronic lesions consisted of mononuclear cell infiltrates within large sharply defined areas of demyelination and astrogliosis, and resembled active plaques of chronic multiple sclerosis. Proliferative responses to myelin basic protein but not to myelin proteolipid protein were present in peripheral blood lymphocytes of immunized animals. Furthermore, myelin basic protein–reactive T‐cell lines derived from immunized donors induced clinical signs of experimental autoimmune encephalomyelitis when adoptively transferred into a sibling, indicating that myelin basic protein–reactive T cells can induce disease in this species. Because of its clinical and pathological similarity to human multiple sclerosis and the ability to adoptively transfer experimental autoimmune encephalomyelitis, this model system should prove useful in the analysis of the immunological mechanisms responsible for autoimmune demyelination in outbred primates.
The role of hypoventilation in a sheep model of epileptic sudden death
Authors: Johnston S. Claiborne , Horn Jan K. , Valente John , Simon Roger P. 
Published: January 2005

AbstractUnexpected sudden death is a common event in otherwise healthy epileptics, though its etiology has remained unclear. Many authors have suggested cardiac arrhythmias as the cause, and limited data in humans and animal studies have supported this. However, autopsy series in humans have shown pulmonary edema, a phenomenon not compatible with a sudden arrhythmic death, as a possible cause. We developed a model of status epilepticus in unanesthetized, chronically instrumented sheep in which sudden death and pulmonary edema occur. Catecholamine levels and seizure type and duration did not differ between animals dying suddenly and those surviving. Benign arrhythmias were generated in all animals; in no case did an arrhythmia account for the death of an animal. Striking hypoventilation was demonstrated in the sudden death group but not in the surviving animals. Differences in peak left atrial and pulmonary artery pressures, and in extravascular lung water were also demonstrated; pulmonary edema did not account for the demise of the sudden death animals. Thus, our model of epileptic sudden death supports a role of central hypoventilation in the etiology of sudden unexpected death and confirms the association with pulmonary edema. The importance of arrhythmia in its pathogenesis is not confirmed.
The effect of interferon‐β on blood—brain barrier disruptions demonstrated by constrast‐enhanced magnetic resonance imaging in relapsing—remitting multiple sclerosis
Authors: Stone Lael A. , Frank Joseph A. , Albert Paul S. , Bash Craig , Smith Mary E. , Maloni Heidi , McFarland Henry F. 
Published: January 2005

AbstractMagnetic resonance imaging (MRI) has been a valuable tool to understand the pathophysiology and natural history of multiple sclerosis (MS), and increasing attention is focusing on the use of MRI findings as outcome measures in treatment trials in MS. The recently completed trial of interferon‐β‐1b (IFN‐β1b) demonstrated a decrease in accumulation of diseased tissue on T2‐weighted images and a reduction in new lsions on T2‐weighted images. To examine the effect of IFN‐β1b on blood‐brain barrier (BBB) breakdown, and to provide additional insights into the usefulness of MRI in the evolution of effectiveness of experimental treatments in MS, we used the contrast‐enhanced lesion frequency of 7‐month baseline MRIs compared with the enhanced lesion frequency for 6‐month treatment period MRIs in 14 relapsing‐remitting (RR) MS patients. Longer baselines were also available for analysis in a subset of 8 patients, as these patients had been followed by monthly MRI in a natural history study for up to 4 years prior to the current study. A significant reduction in the total or new enhancing lesion frequency was detected in the patients analyzed as a whole, and 13 of 14 of the patients demonstrated a reduction in enhancing lesion frequency on treatment over the 6 months studied. These findings suggest that IFN‐β has a mechanism of action that at least temporarily inhibits the opening of the BBB in RRMS patients. This trial also illustrates the usefulness of a baseline versus treatment trial design to evaluate the effect of drug therapy in MS.
Recovery from wernicke's aphasia: A positron emission tomographic study
Authors: Weiller Cornelius , Isensee Christian , Rijntjes Michel , Huber Walter , Müller Stefan , Bier Dirk , Dutschka Klaus , Woods Roger P. , Noth Johannes , Diener Hans Christoph 
Published: January 2005

AbstractChanges in the organization of the brain after recovery from aphasia were investigated by measuring increases in regional cerebral blood flow (rCBF) during repetition of pseudowords and during verb generation. Six right‐handed patients who had recovered from Wernicke's aphasia caused by an infarction destroying the left posterior perisylvian language zone were compared with 6 healthy, right‐handed volunteers. In the control subjects, strong rCBF increases were found in the left hemisphere in the posterior part of the superior and middle temporal gyrus (Wernicke's area), and during the generation task in lateral prefrontal cortex (LPFC) and in inferior frontal gyrus (Broca's area). There were some weak right hemisphere increases in superior temporal gyrus and inferior premotor cortex. In the patients, rCBF increases were preserved in the frontal areas. There was clear right hemisphere activation in superior temporal gyrus and inferior premotor and lateral prefrontal cortices, homotopic to the left hemisphere language zones. Increased left frontal and right perisylvian activity in patients with persisting destruction of Wernicke's area emphasizes redistribution of activity within the framework of a preexisting, parallel processing and bilateral network as the central mechanism in functional reorganization of the language system after stroke.
Motor reorganization in acquired hemidystonia
Authors: Ceballos‐Baumann A. O. , Passingham R. E. , Marsden C. D. , Brooks D. J. 
Published: January 2005

AbstractRegional cerebral blood flow (rCBF) was measured with H215O positron emission tomography in 5 patients with acquired hemidystonia (AHD) due to structural lesions of the basal ganglia or posterior thalamus contralateral to the dystonic limb. Patients were scanned at rest and when performing paced joystick movements in freely chosen directions with the dystonic and then the unaffected arm. Findings were compared with those of 5 age‐matched controls performing joystick movements with the right arm. At rest, there was decreased activity in ventroanterior thalamus, posterior thalamus, angular gyrus ipsilateral to the lesion, and bilateral frontoorbital cortex. At a similar level of significance, increased resting activity was found in lentiform nucleus, hippocampus, and anterior insula contralateral to the lesion. Using the affected arm, AHD cases showed significant overactivity of contralateral prefrontal, lateral premotor cortex, rostral supplementary motor area, anterior cingulate area 32, bilateral sensorimotor cortex (SMC) and insula, mesial parietal cortex, and ipsilateral cerebellum. There was similar frontal overactivity when the unaffected arm performed the joystick movements, though SMC and insula overactivity was contralateral rather than bilateral. The associated frontal overactivity on movement is consistent with acquired dystonia being a syndrome of thalamofrontal disinhibition due to structural disruption of basal ganglia inhibitory control. Our findings also suggest that cortical activation during movement of the unaffected limb is abnormal in acquired hemidystonia.
Circulating adhesion molecules and tumor necrosis factor receptor in multiple sclerosis: Correlation with magnetic resonance imaging
Authors: Hartung Hans‐Peter , Reiners Karlheinz , Archelos Juan J. , Michels Marco , Seeldrayers Pierrette , Heidenreich Fedor , Pflughaupt Karl W. , Toyka Klaus V. 
Published: January 2005

AbstractAdhesion molecules are important in T‐cell trafficking to sites of inflammation. We determined levels of circulating vascular cell adhesion molecule‐1 (VCAM‐1), L‐selectin, and E‐selectin in the serum of 147 patients with definite multiple sclerosis of the remitting‐relapsing or secondary progressive type. Soluble VCAM‐1 and L‐selectin concentrations were increased compared to levels in a large group of control subjects. Levels were highest in patients with gadolinium‐enhancing lesions on magnetic resonance imaging (VCAM‐1: 1,011 ± 276 vs 626 ± 87 ng/ml; L‐selectin: 1,130 ± 272 vs 793 ± 207 ng/ml [mean ± standard deviation]; p > 0.0001 vs patients without enchancing lesions). Serum levels of soluble tumor necrosis factor receptor (60 kd) were also raised (2.64 ± 1.23 vs 2.17 ± 0.69 ng/ml in subjects with other neurological diseases and 2.1 ± 0.77 ng/ml in healthy control subject; p < 0.05). Soluble VCAM‐1 and L‐selectin levels were correlated to concentrations of soluble tumor necrosis factor receptor. In 13 patients with viral encephalitis, similar observations were made. Raised levels of soluble VCAM‐1 and L‐selectin probably reflect cytokine‐induced endothelial cell and T‐lymphocyte/monocyte activation occurring in the process of T‐cell migration into the central nervous system. Tumor necrosis factor‐alpha may be critically involved.
Striatal 3,4‐dihydroxyphenylalanine decarboxylase in aging: Disparity between postmortem and positron emission tomography studies?
Authors: Kish Stephen J. , Zhong Xiaohui H. , Hornykiewicz Oleh , Haycock John W. 
Published: January 2005

AbstractRecent positron emission tomography (PET) studies using 3,4‐[18F]fluorodihydroxyphenylalanine ([18F]fluorodopa) have reported little or no Decemberrement in dopaminergic function in human striatum (caudate and putamen) during aging. In contrast, previous postmortem studies have reported Marchked age‐dependent Decemberreases in the activity of dopa Decemberarboxylase (DDC), a variable upon which the PET determinations depend. Using quantitative blot immunolabeling techniques, we measured DDC protein concentrations in postmortem striata of 28 neurologically normal subjects ranging in age from 17 to 103 years. We found a significant, albeit modest, age‐dependent Decemberrease in the concentration of DDC protein in caudate (r = −0.50, p < 0.05) but not in putamen (r = −0.16, p > 0.05), with mean values of the 87‐year‐old group being 27% (caudate) and 12% (putamen) lower than those of the 30‐year‐old group. The absence of a robust effect of aging upon striatal DDC protein is consistent with the [18F]fluorodopa‐PET studies that report either no change or only a relatively small Decemberrease in striatal 18F accumulation during aging. To the extent that aging is associated with a substantial loss of striatal dopaminergic nerve terminals, the present results also suggest that DDC protein synthesis may be upregulated in those dopaminergic neurons that survive the aging process and, therefore, that striatal [18F]fluorodopa uptake indices may provide an overestimate of the number of dopaminergic nerve terminals during physiological aging.
Decreased single‐photon emission computed tomographic {123I}β‐CIT striatal uptake correlates with symptom severity in parkinson's disease
Authors: Seibyl J. P. , Marchek K. L. , Quinlan D. , Sheff K. , Zoghbi S. , Zea‐Ponce Y. , Baldwin R. M. , Fussell B. , Smith E. O. , Charney D. S. , Hoffer P. B. , Innis R. B. 
Published: January 2005

AbstractPrevious studies have utilized single‐photon emission computed tomography (SPECT) to demonstrate decreased {123I}β‐CIT striatal uptake in idiopathic Parkinson disease (PD) patients. The present study extendss this work by examining SPECT outcome measures in a larger group of PD patients with varying disease severity. Twenty‐eight l‐dopa‐responsive PD patients (Hoehn‐Yahr stages 1–4) and 27 healthy controls had SPECT scans at 18 to 24 hours after injection of {123I}β‐CIT. Specific to nondisplaceable striatal uptake ratios (designated V3″) were correlated with Hoehn‐Yahr stage and Unified Parkinson's Disease Rating Scale (UPDRS) subscores. Linear discriminant function analyses utilizing striatal uptakes, putamen‐to‐caudate ratios, and ipsilateral‐contralateral asymmetry indices were performed. Decreased striatal tracer uptake (V3″) was correlated with total UPDRS score for both contralateral and ipsilateral striatum. Putamen uptake was relatively more reduced than caudate with mean putamen:caudate ratios of 0.50 ± 0.17 and 0.82 ± 0.09 for PD patients and controls, respectively. Ipsilateral:contralateral asymmetry was significantly greater in PD patients than controls. Discriminant function analysis utilizing V3″ for ipsilateral and contralateral caudate and putamen correctly classified all 55 cases. These data demonstrate Marchked differences in {123I}β‐CIT SPECT measures in healthy controls and PD patients. The significant correlation of SPECT measures with motor severity suggests {123I}β‐CIT may be a useful Marchker of disease severity in PD.
Reduction of β‐amyloid peptide42 in the cerebrospinal fluid of patients with Alzheimer's disease
Authors: Motter R. , Vigo‐Pelfrey C. , Kholodenko D. , Barbour R. , Johnson‐Wood K. , Galasko D. , Chang L. , Miller B. , Clark C. , Green R. , Olson D. , Southwick P. , Wolfert R. , Munroe B. , Lieberburg I. , Seubert P. , Schenk D. 
Published: January 2005

AbstractIn this clinical study, the cerebrospinal fluid (CSF) level of a Novemberel form of the β‐amyloid peptide (Aβ) extending to position 42 (Aβ42) was determined in patients with Alzheimer's disease (AD) as well as controls. In addition to measurement of CSF Aβ42 levels, total Aβ peptides, microtubule‐associated protein τ, and apolipoprotein E (ApoE) genotype were also assessed. It is interesting that CSF Aβ42 levels were found to be significantly lower in AD patients relative to controls, whereas total Aβ levels were not. Aβ42 has recently been shown to preferentially deposit in the brain tissue of patients with AD, suggesting that diminished clearance may account for its reduction in CSF. As previously reported, τ levels were increased in AD patients; however, neither Aβ42 nor τ levels were apparently influenced by the ApoE genotype.
Oxidative damage to protein in sporadic motor neuron disease spinal cord
Authors: Shaw Pamela J. , Ince Paul G. , Falkous Gavin , Mantle David 
Published: January 2005

AbstractThe recent discovery that defects in the gene encoding copper‐zinc superoxide dismutase (SOD1) are associated with some cases of familial motor neuron disease has heightened interest in the possibility that free radical mechanisms may contribute to selective motor neuron injury. Sporadic and familial motor neuron diseases are clinically and pathologically very similar and may share common pathophysiological mechanisms. Thus the role of free radical mechanisms as a contributory factor to motor neuron injury in the common sporadic form of motor neuron disease requires urgent exploration, particularly as this may provide an avenue for therapy aimed at retarding pathological progression. We investigated oxidative damage to proteins in the lumbar spinal cord by quantifying the protein carbonyl level from 19 patients with sporadic motor neuron disease, 8 neurologically normal control subjects, and 11 neurological disease control subjects, most of whom had slowly progressive neurodegenerative disease. In sporadic motor neuron disease the mean protein carbonyl level in the spinal cord was increased by 119% (p < 0.02) compared to normal control subjects and by 88% (p < 0.04) compared to the neurological disease control subjects. These data contribute to the emerging evidence that oxidative damage may play a contributory role in the neuronal death in sporadic motor neuron disease. This mechanism may be particularly important in a subset of patients with motor neuron disease.
Genetic control of multiple sclerosis: Increased production of lymphotoxin and tumor necrosis factor‐α by HLA‐DR2+ T cells
Authors: Zipp Frauke , Weber Frank , Huber Susanne , Sotgiu Stefano , Czlonkowska Anna , Holler Ernst , Albert Ekkehard , Weiss Elisabeth H. , Wekerle Hartmut , Hohlfeld Reinhard 
Published: January 2005

AbstractLymphotoxin (LT) and tumor necrosis factor‐α (TNF‐α) play an important role in the pathogenesis of multiple sclerosis (MS). MS is associated with the HLA‐DR2, Dw2, DQ6 HLA class II haplotype. Because both LT and TNF‐α are encoded in the HLA region, the HLA association of MS may be related to the production of these cytokines. To test this hypothesis, we investigated the production of LT, TNF‐α, and interferon‐γ (IFN‐γ) by CD4+ T‐cell lines (TCLs) specific for myelin basic protein (MBP) or tetanus toxoid (TT) isolated from MS patients and normal controls. After stimulation with specific antigen but not mitogen, TCLs from HLA‐DR2+ donors produced significantly more LT and TNF‐α, than TCLs from DR2− donors. In contrast, HLA‐DR2+ and DR2− TCLs did not differ in the production of IFN‐γ, a cytokine also produced by T cells but not encoded in the HLA region. Increased secretion of LT and TNF‐α was unrelated to the specificity (MBP vs TT), MHC restriction (HLA‐DR2 vs other DR molecules), or source (MS vs normal) of the TCLs. There was no significant association of the cytokine production with individual LT or TNF‐α alleles, indicating that the increased production of these cytokines may be linked to other polymorphic genes in this region. The results suggest that the association of MS with HLA‐DR2 implies a genetically determined propensity of T cells to produce increased amounts of LT and TNF‐α.
Significance of spikes recorded on electrocorticography in nonlesional medial temporal lobe epilepsy
Authors: Tran T. A. , Spencer S. S. , Marks D. , Javidan M. , Pacia S. , Spencer D. D. 
Published: January 2005

AbstractWhether spikes recorded by intraoperative electrocorticography imply active epileptogenicity has not been adequately addressed. We performed preresection and postresection electrocorticography on 47 patients with nonlesional medial temporal lobe epilepsy who were undergoing surgery for the treatment of medically refractory epilepsy. A standard anteromedial temporal lobectomy was performed on all patients, with no additional resection, regardless of electrocorticographic findings. Patients were divided into two groups: Group I (no seizures or rare seizures) and Group II (recurrent seizures). Recorded spikes were analyzed for distribution and spike discharge rate. On preresection electrocorticography, 83% of Group I and 82% of Group II had spikes in the anterior temporal lobe. The spike discharge rate was equally distributed between high frequency and low frequency for both groups (not significant). Although spikes localized to the posterior temporal neocortex were seen more in Group II (64%) than Group I (39%), this was not a significant difference (p > 0.1). Most of these patients had a low‐frequency spike discharge rate. On postresection electrocorticography, 80% of Group I and 75% of Group II had residual spikes. The majority of these had a lowfrequency spike discharge rate and were localized to the Marchgin of resection. We found no correlation between residual spikes on preresection and postresection electrocorticography and outcome. These findings do not support the role of intraoperative electrocorticography in guiding mesial temporal lobe resection.