bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oligoclonai IgG bands in cerebrospinal fluid and serum during asymptomatic human immunodeficiency virus infection
Authors: Grimaldi L. M. E. , Castagna A. , Lazzarin A. , Pristerá R. , Bianchi G. , Moroni M. , Roos R. P. 
Published: January 2005

AbstractSerum and cerebrospinal fluid (CSF) samples from asymptomatic patients seropositive for human immunodeficiency virus (HIV) showed frequent evidence of intrathecal IgG synthesis and oligoclonai IgG bands, with different isoelectric focusing patterns in serum and CSF; 2 of 7 had a CSF pleocytosis. The results suggest frequent, early, chronic central nervous system infection following HIV infection.
Motor fluctuations in Parkinson's disease: Central pathophysiological mechanisms, Part I
Authors: Fabbnni G. , Mouradian M. M. , Junecos J. L. , Schlegel J. , Mohr E. , Chase T. N. 
Published: January 2005

AbstractThe duration of the antiparkinsonian action of levodopa was studied in 48 patients with various response patterns to the oral administration of the dopamine precursor. Deterioration in motor scores after abrupt cessation of a steady‐state intravenous levodopa infusion occurred at two successive rates: an initial rapid phase followed by a terminal slower phase. Efficacy half‐time Decemberreased and initial efficacy Decemberay slope increased with progression of levodopa response groups from never treated to stable responders, and then to fluctuating responders of the wearing‐off type and finally of the on‐off type. Efficacy half‐time exceeded plasma levodopa half‐life in the 2 nonfluctuating groups, approximated it in those patients with wearing‐off responses, and was significantly shorter in patients with fluctuations of the on‐off type. The half‐times for the Decemberline in antiparkinsonian efficacy and dyskinesia severity differed significantly, suggesting different pharmacological mechanisms. Motor fluctuation severity correlated best with initial efficacy Decemberay slope, and both were best predicted by parkinsonian symptom severity. The dyskinesia Decemberay rate correlated most closely with levodopa dose. These results support the view that progressive dopamine neuron degeneration reduces the brain's ability to buffer shifts in levodopa availability attending its periodic oral administration; the clinical result is wearing‐off phenomenon. The on‐off phenomenon as well as dyskinesia apparently reflects additional secondary changes related to levodopa therapy and occurring postsynaptically.
Motor fluctuations in Parkinson's disease: Central pathophysiological mechanisms, part II
Authors: Mouradian M. M. , Junecos J. L. , Fabbrini G. , Schlegel J. , Bartko J. J. , Chase T. N. 
Published: January 2005

AbstractThe contribution of central pharmacodynamic mechanisms to the pathogenesis of motor fluctuations in advanced Parkinson's disease was studied in 29 patients by evaluating their acute response to intravenously injected. levodopa. While the threshold dose for an antiparkinsonian effect did not change, that for induction of dyskinesia showed a progressive reduction in 4 groups: (1) levodopa‐naive patients, (2) those with a stable response to oral administration, and (3) those with wearing‐off or (4) on‐off fluctuations. Concomitantly, the therapeutic window for levodopa narrowed and the levodopa dose—antiparkinsonian response slope increased. The antiparkinsonian threshold dose correlated best with duration of symptoms; the dyskinesia threshold dose, therapeutic window, and dose‐response slope related most closely with the duration of levodopa treatment. The differing dose‐response profiles for the antiparkinosonian and dyskinetic effects suggest involvement of Septemberarate pharmacological mechanisms. The present results, taken together with previous observations that the wearing‐off phenomenon responds promptly to plasma levodopa stabilization while on‐off fluctuations tend to diminish over several days, suggest that postsynaptic modifications, presumably at the receptor level, serve as the major determinant for the increasing difficulty with optimal dose adjustment and motor fluctuations, especially of the on‐off type, which complicate levodopa therapy of patients with advance Parkinson's disease.
In vivo measurement of cytosolic free calcium during cerebral ischemia and reperfusion
Authors: Uematsu Daisuke , Greenberg Joel H. , Reivich Marchtin , Karp Andrea 
Published: January 2005

AbstractAn increase in cytosolic free calcium concentration ([Ca2 +]i) may trigger irreversible cell injury following cerebral ischemia. We have measured changes in [Ca2 +]i in cat cortex in vivo during ischemia produced by 1 hour of middle cerebral artery occlusion and during 30 minutes of reperfusion. Indo‐1, a fluorescent Ca2+ indicator, was loaded into the exposed cortex by superfusion, and changes in the [Ca2+]i signal (400/506 nm ratio)were measured microfluorometrically during ultraviolet excitation (340 nm). The nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide (NAD/NADH) redox state and hemodynamic changes were measured simultaneously. The animals showing severe deterioration in their electroencephalograms (EEG) showed a progressive increase in the [Ca2+]i signal during ischemia (baseline: 1.46 0.05; 60 minutes after occlusion: 2.99 0.37; n = 7). At 30 minutes following reperfusion, the animals showing little recovery in their EEG exhibited a further increase in [Ca2+}i (4.71 0.87,n = 3), whereas animals showing significant recovery in their EEG also showed recovery of {Ca2+]i(1.55 0.09, n = 4). By contrast, the moderate or mild stroke animals with less deterioration in their EEGs showed no increase in [Ca2+]i during either ischemia or reperfusion. These data suggest that the increase in [Ca2+]i might be closely related not only to deterioration of brain function during ischemia but also to poor recovery during the reperfusion period.
Recording of movement‐related potentials from the human cortex
Authors: Neshige Ryuji , Lüders Hans , Friedman Lee , Shibasaki Hiroshi 
Published: January 2005

AbstractA patient with intractable epilepsy secondary to a brain tumor was evaluated with a chronically implanted array of 64 stainless‐steel subdural electrodes covering the perirolandic area. Cortical potentials associated with voluntary, selfpaced middle‐finger extension were recorded simultaneously from subdural and scalp electrodes using a computerassisted method for averaging movement‐related potential (MRP) in relation to electromyographic (EMG) onset. A high‐amplitude negative potential, Bereitschaftspotential/negative slope (BP/NS′), preceding the onset of the EMG activity by more than 1 sec was recorded in an extremely localized fashion exclusively from electrodes placed in the precentral hand motor area as well as in the more medial part of the somatosensory hand area. These results suggest that the hand motor and sensory areas have an essential participation in the generation of MRPs and, therefore, also in the preparation of voluntary finger movements.
A double‐blind randomized crossover trial of bromocriptine and placebo in restless legs syndrome
Authors: Walters Arthur S. , Hening Wayne A. , Kavey Neil , Chokroverty Sudhansu , Gidro‐Frank Steve 
Published: January 2005

AbstractA double‐blind randomized crossover study of 7.5 mg bromocriptine at bedtime versus placebo was conducted in 30‐day phases (with a 2‐week washout period between phases) in 6 patients with idiopathic restless legs syndrome. Five patients experienced partial subjective improvement in restlessness and paresthesias on bromocriptine as opposed to placebo and expressed a desire to continue on the medication. On bromocriptine, the patients showed polysomnographically a mean Decemberrease of 43% from control and a mean Decemberrease of 57% from placebo in the number of periodic movements of sleep per hour of sleep (p < 0.025). Two of 3 patients with abnormally Decemberreased total sleep time and sleep efficiency showed an improvement in these measures on therapy. The dopamine agonist bromocriptine may be a useful therapy in some patients with restless legs syndrome.
Leukoencephalopathy among native indian infants in northern Quebec and Manitoba
Authors: Black Deborah N. , Booth Fran , Watters Gordon V. , Andermann Eva , Dumont Charles , Halliday William C. , Hoogstraten J. , Kabay Michel E. , Kaplan Paige , Meagher‐Villemure Kathleen , Michaud Jean , O'gorman Gus 
Published: January 2005

AbstractWe report 14 cases of a severe familial leukoencephalopathy among native North American Indian infants in northern Quebec and Manitoba. Affected infants have hypotonia and mild motor delay, followed by seizures, hypotonia or spasticity, eye deviation, and abnormal posture during a Februaryrile illness around 6 months of age. Death follows a rigid, vegetative state that manifests days to months after disease onset and is Marchked in some cases by prominent autonomic disturbances, blindness, and cessation of head growth. Symmetrical hemispheric white matter lucencies and diffuse hypomyelination of the cerebral hemispheres and brainstem are the radiological and pathological hallMarchks. This disease differs from the known diseases of cerebral myelin. An autosomal recessive pattern of inheritance awaits statistical confirmation. The proposed cause is a delay in development or abnormal turNovemberer of central nervous system myelin.
Cerebrospinal fluid levels of quinolinic acid in Huntington's disease and schizophrenia
Authors: Schwarcz Robert , Tamminga Carol A. , Kurlan Roger , Shoulson Ira 
Published: January 2005

AbstractThe concentration of the endogenous excitotoxin quinolinic acid was determined in the cerebrospinal fluid of drug‐free patients suffering from Huntington's disease or schizophrenia (control group). In both diseases, quinolinic acid concentrations were highly variable (< 4–48 nM) but the mean levels for each disease group were not significantly different from each other or from the quinolinic acid concentration of normal cerebrospinal fluid. Analysis of steady‐state cerebrospinal fluid quinolinic acid concentration is unlikely to be of value as a diagnostic tool in Huntington's disease.
Cerebrospinal fluid neurochemistry in the myoclonic subtype of Alzheimer's disease
Authors: Kaye Jeffrey A. , May Conrad , Atack John R. , Daly Eileen , Sweeney Daniel L. , Flint Beal M. , Kaufman Seymour , Milstien Sheldon , Friedland Robert P. , Rapoport Stanley I. 
Published: January 2005

AbstractMonoamine metabolites, biopterin, acetylcholinesterase (AChE) activity, and somatostatin‐like immunoreactivity (SLI) were determined in the lumbar cerebrospinal fluid (CSF) of 24 patients with dementia of the Alzheimer type (DAT) without myoclonus or extrapyramidal signs, in 8 patients with DAT and myoclonus, and in 14 age‐matched healthy control subjects. In patients with DAT with myoclonus as compared with both DAT patients without myoclonus and control subjects, the concentrations of homovanillic acid and biopterin were significantly Decemberreased. 5‐Hydroxyindole‐acetic acid was significantly lower in patients with myoclonic DAT as compared to patients with nonmyoclonic DAT, but not significantly lower than in control subjects. CSF AChE and SLI were significantly reduced in patients with DAT with or without myoclonus, as compared with control subjects, but AChE and SLI were not significantly different between dementia groups. These results, suggest that DAT patients with myoclonus represent a distinct clinical and neurochemical DAT subtype.
Neurological abnormalities associated with remote occupational elemental mercury exposure
Authors: Albers James W. , Kallenbach Lee R. , Fine Lawrence J. , Langolf Gary D. , Wolfe Robert A. , Donofrio Peter D. , Alessi Anthony G. , Stolp‐Smith Kathryn A. , Bromberg Marchk B. ,   Mercury Workers Study Group
Published: January 2005

AbstractWe examined 502 subjects, 247 of whom had occupational elemental mercury exposures 20 to 35 years previously, to identify potential exposure‐related neurological abnormalities. Few significant (p < 0.05) differences existed between exposed and unexposed subjects. However, multiple linear regression analysis demonstrated several significant correlations between Decemberlining neurological function and increasing exposure as determined by urine mercury measurements from the exposure interval. Subjects with urine mercury peak levels above 0.6 mg/L demonstrated significantly Decemberreased strength, Decemberreased coordination, increased tremor, Decemberreased sensation, and increased prevalence of Babin‐ski and snout reflexes when compared with the remaining subjects. Furthermore, subjects with clinical polyneuropathy had significantly higher peak levels than normal subjects (0.85 vs 0.61 mg/L; p = 0.04), but not increased exposure duration (20.1 vs 20.8 quarters; p = 0.34), and 28% of subjects with peak levels above 0.85 mg/L had clinical evidence of polyneuropathy, compared with 10% of remaining subjects (p = 0.005). Although exposure was not age dependent, several neurological measures showed significant age‐mercury interaction, suggesting that natural neuronal attrition may unmask prior exposure‐related subclinical abnormalities.
HTLV‐I‐associated myelopathy: Oligoclonal immunoglobulin G bands contain anti‐HTLV‐I p24 antibody
Authors: Grimaldi Luigi M. E. , Roos Raymond P. , Devare Sushilkumar G. , Casey James M. , Marchuo Yasunori , Hamada Takeshi , Tashiro Kunio 
Published: January 2005

AbstractHuman T‐cell lymphotropic virus type I (HTLV‐I)‐associated myelopathy (HAM) and tropical spastic paraparesis belong to a new group of neurological diseases associated with retroviral infection. An HTLV‐I‐like virus has recently been implicated in multiple sclerosis as well. We studied paired cerebrospinal fluid and serum specimens from HAM and multiple sclerosis patients by isoelectric focusing and an isoelectric focusing HTLV‐I p24 overlay technique to clarify the role of HTLV‐I in these diseases. We detected oligoclonal bands by isoelectric focusing with silver‐staining in cerebrospinal fluid, but not serum, from all 5 HAM and all 9 multiple sclerosis patients. An isoelectric focusing HTLV‐I p24 overlay technique demonstrated anti‐p24 antibody in HAM cerebrospinal fluid at a different pI distribution than that seen in paired serum, indicating local synthesis of anti‐p24 antibody within the central nervous system. Oligoclonal bands in HAM cerebrospinal fluid corresponded in pI distribution to anti‐p24 antibody activity, suggesting the presence of an ongoing HTLV‐I infection in the central nervous system. Multiple sclerosis patients had no evidence of anti‐HTLV‐I activity by p24 radioimmunoprecipitation assay, Western immunoblots, or isoelectric focusing HTLV‐I p24 overlay analysis. Our data support a role for HTLV‐I as an etiological agent in HAM, but not in multiple sclerosis.
McArdle's disease: Biochemical and molecular genetic studies
Authors: Servidei Serenella , Shanske Sara , Zeviani Massimo , Lebo Roger , Fletterick Robert , DiMauro Salvatore 
Published: January 2005

AbstractWe have analyzed muscle biopsy specimens from 48 patients with biochemically proven phosphorylase deficiency (McArdle's disease) by sodium doDecemberylsulphate polyacrylamide gel electrophoresis (SDS‐PAGE), immunoblotting, and immunotitration (enzyme‐linked immunosorbent assay [ELISA]). Thirty‐five of the 42 patients studied by SDS‐PAGE and immunoblot, and 41 of the 48 patients studied by ELISA had no detectable enzyme protein. Six patients had Marchkedly Decemberreased phosphorylase protein by all three assays, and only 1 patient had a normal amount of protein. No apparent correlation existed between the presence or absence of enzyme protein and the clinical presentation or muscle glycogen concentration. Northern analysis was performed on muscle RNA in 4 patients: messenger RNA was normal in 2, abnormally short in 1, and absent in the fourth, indicating heterogeneity 0of the molecular lesion in McArdle's disease.
Intraventricular hemorrhage in the premature infant—current concepts. Part I
Authors: Volpe Joseph J. 
Published: January 2005

AbstractAlthough the incidence of periventricular‐intraventricular hemorrhage (IVH) has decreased in recent years, the increasing survival rates for the smallest premature infants indicate that the lesion will continue to be a major problem in neonatal intensive care facilities. The neuropathology is characterized by an elemental lesion, bleeding into the subependymal germinal matrix, with subsequent rupture into the lateral ventricle. Important neuropathological consequences are germinal matrix destruction, posthemorrhagic hydrocephalus, and periventricular hemorrhagic infarction. The last of these appears to be a venous infarction and is a critical determinant of neurological outcome. Neuropathological accompaniments, not caused by the IVH, include periventricular leukomalacia and pontine neuronal necrosis. The pathogenesis of IVHs is related to intravascular, vascular, and extravascular factors. Intravascular factors involve primarily control of blood flow and pressure in the microcirculation of the germinal matrix. Particular pathogenetic importance can be attached to fluctuations in cerebral blood flow, abrupt increases in flow, decreases in flow with injury to matrix vessels, increases in cerebral venous pressure, and, in selected infants, disturbances of platelet function and coagulation. Vascular factors relate to the microcirculation of the matrix, the site of the initial bleeding. A maturation‐dependent alteration in vascular integrity and a vulnerability of matrix vessels to ischemic injury appear important. Extravascular factors include those relevant to mesenchymal and glial support for matrix vessels and to local fibrinolytic activity in the germinal matrix. The latter may be a manifestation of the proteolytic activity now recognized to be of general importance in developmental remodeling of the mammalian central nervous system.
Benign versus chronic progressive multiple sclerosis: Magnetic resonance imaging features
Authors: Koopmans R. A. , Li D. K. B. , Grochowski E. , Cutler P. J. , Paty D. W. 
Published: January 2005

AbstractThe extent of disease as detected by magnetic resonance imaging was compared between 32 patients with benign multiple sclerosis (MS) and 32 patients with the chronic progressive form matched for age, sex, and disease duration. Computer‐assisted quantitation of magnetic resonance images revealed a higher mean lesion load in chronic progressive multiple sclerosis (CPMS); however, in approximately 20% of benign MS patients the lesion load was higher than that in the CPMS patients. CPMS patients had a higher number of infratentorial lesions, yet similar numbers of supratentorial lesions, when compared with benign MS patients. The degree of confluency of lesions and the clinical expression of infratentorial lesions were typically higher in the CPMS patients. Benign MS was characterized by a lower degree of confluency and a higher number of asymptomatic infratentorial lesions. Thus, magnetic resonance imaging shows characteristic differences in magnetic resonance‐detected changes between MS patients with different clinical courses.
Dominantly inherited dementia and parkinsonism, with non‐alzheimer amyloid plaques: A new neurogenetic disorder
Authors: Rosenberg Roger N. , Green Joseph B. , White Charles L. , Sparkman Dennis R. , Dearmond Stephen J. , Kepes John J. 
Published: January 2005

AbstractA family is described in which a dominant form of inheritance, probably autosomal dominant, expresses severe dementia and parkinsonism as the major clinical features. Neuropathological correlates in two autopsied members of this family consisted of extracellular hyaline eosinophilic, congophilic amyloid plaques in decreasing order of frequency in the cerebral cortex, basal ganglia, thalamus, and substantia nigra, and atrophy and gliosis of the basal ganglia and substantia nigra. The extracellular plaques did not stain with antibody raised against the prion protein nor with two separate anti‐amyloid A4 antibodies. The combination of dominantly inherited dementia with parkinsonism and extracellular plaques in this distribution that are amyloid and prion protein antibody negative has not been previously reported and thus may represent a new neurological genetic disorder.
The olfactory and cognitive deficits of parkinson's disease: Evidence for independence
Authors: Doty Richard L. , Riklan Manuel , Deems Daniel A. , Reynolds Constance , Stellar Stanley 
Published: January 2005

AbstractIn the present study we sought to determine whether the olfactory deficits of parkinsonism are related to the cognitive and perceptual‐motor manifestations of the disease. Pearson correlation coefficients were computed among a number of olfactory, neurological, and neuropsychological measures obtained from 58 Parkinson's disease patients, including the University of Pennsylvania Smell Identification Test, a modified Randt memory test, a reaction time test, a finger‐tapping test, ratings of motor and neurological function, and selected verbal and performance subtests of the Wechsler Adult Intelligence Scale–Revised. Data from 38 patients with Parkinson's disease who received odor detection threshold testing were also evaluated. The intercorrelation matrix was subjected to a principal components factor analysis which yielded six clear‐cut factors: cognitive/memory, gross motor, oral motor, fine motor, olfactory, and tremor. The olfactory factor received strong and nearly exclusive loadings from the olfactory measures (which did not evidence meaningful loadings on any of the other factors). A ten‐trial jackknife procedure revealed the factor structure to be stable. Further support of the independence of the olfactory variables from the other measures was provided by multiple regression and canonical correlation analyses. Overall, these findings lend support to the hypothesis that the olfactory disorder of parkinsonism is independent of the cognitive, perceptual‐motor, and memory manifestations of the disease.
Correlation of immunological studies and disease progression in chronic progressive multiple sclerosis
Authors: Trotter John L. , Clifford David B. , McLnnis Jane E. , Griffeth Rogers C. , Bruns Kathy A. , Perlmutter Monica S. , Anderson Charles B. , Collins Kelly G. , Banks Geneva , Hicks Byron C. 
Published: January 2005

AbstractThirty untreated patients with clinically definite chronic progressive multiple sclerosis were matched with 10 patients with clinically stable definite multiple sclerosis and 16 patients with other neurological diseases. A group of 12 normal control (NC) volunteers was matched to these groups. All patients with chronic progressive multiple sclerosis and normal control subjects were analyzed for the concanavalin A suppressor assay, mitogen stimulation, and phenotyping of peripheral blood mononuclear cells. In addition, serum was analyzed for interleukin‐2 levels. Results of mitogen stimulation studies did not distinguish the groups. Concanavalin A–induced suppression was significantly decreased in the patients with chronic progressive multiple sclerosis (p < 0.01). Phenotyping of fresh cells showed an elevated CD4 : CD8 ratio in the patients with chronic progressive multiple sclerosis. Neither phenotyping nor concanavalin A–induced suppression correlated with or predicted the degree of disability, but the serum levels of interleukin‐2 correlated inversely with disability (p < 0.01) and directly with a poor prognosis after 18 months of observation (p < 0.05). Serum levels of interleukin‐2 decreased as the disease progressed.