bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of cerebral hemodynamics on stroke risk: One‐year follow‐up of 30 medically treated patients
Authors: Powers William J. , Tempel Lee W. , Grubb Robert L 
Published: January 2005

AbstractThe importance of hemodynamic factors in the pathogenesis and treatment of ischemic cerebrovascular disease is not clear. We have investigated the relationship between cerebral hemodynamics and the subsequent risk of stroke in 30 medically treated patients with symptomatic occlusion or greater than 75% intracranial stenosis of the carotid arterial system. Positron emission tomography (PET) was used to evaluate the regional hemodynamic status of the cerebral circulation. Clinical follow‐up to 1 year post‐PET was available for all patients. The incidence at 1 year of all strokes was 1/9 for patients with normal hemodynamics and 1/21 for patients with abnormal hemodynamics. The 1‐year incidence of ipsilateral ischemic stroke was 1/9 for hemodynamically normal patients and 0/21 in the abnormal group. The 21 patients in the abnormal group fulfilled entry criteria for the Extracranial‐Intracranial Bypass Trial. The 0/21 incidence of ipsilateral ischemic stroke at 1 year was compared with the 1‐year rate of 0.109 for the 714 medically treated patients from the Bypass Trial. We were able to reject with better than 90% certainty (p = 0.089) the hypothesis that our sample of patients came from a population with an ipsilateral ischemic stroke rate of 0.109 or greater. Thus, in this small sample, we found no evidence that PET evidence of abnormal cerebral hemodynamics identifies a subgroup of patients at higher risk for early stroke if treated medically with antithrombotic drugs.
Controlled release of dopamine from a polymeric brain implant: In vivo characterization
Authors: During Matthew J. , Freese Andrew , Sabel Bernhard A. , Saltzman W. Mark , Deutch Ariel , Roth Robert H. , Langer Robert 
Published: January 2005

AbstractIntracerebral microdialysis was used to evaluate the long‐term in vivo release of dopamine from ethylene‐vinyl acetate (EV Ac)‐dopamine copolymer matrix discs for up to 65 days following striatal implantation. Dopamine release occurred through a single cavity present on one side of the disc, which was otherwise fully coated with an additional, impermeable layer of EV Ac. At 20 days following implantation of the device, extracellular concentrations of dopamine within the striatum reached micromolar levels, over 200‐fold greater than control values. Release of dopamine was shown to be stable and maintained for the 2‐month duration of the experiment. Histological examination confirmed the biocompatible nature of the implant. There are potential applications of this technology to the treatment of Parkinson's disease and other neurological and psychiatric disorders.
Human choroid plexus cells can be latently infected with human immunodeficiency virus
Authors: Harouse Janet M. , Wroblewska Zofia , Laughlin Mark A. , Hickey William F. , Schonwetter Barry S. , Gonzalez‐Scarano Francisco 
Published: January 2005

AbstractThe human immunodeficiency virus (HIV) penetrates the central nervous system, particularly the cerebrospinal fluid, early in the course of HIV infection, and may cause a progressive encephalopathy in patients prior to the development of the acquired immunodeficiency syndrome. Neither the specific mechanism for penetration of the virus into the central nervous system nor the pathophysiological basis for these abnormalities is well understood. We cultured cells from the choroid plexus of 3 individuals who died of causes unrelated to the acquired immunodeficiency syndrome and demonstrated that these cells can be infected with type 1 HIV. Infection of cells of the choroid plexus may provide an initial route of entry of HIV into the cerebrospinal fluid and, together with the macrophage, a route of entry into the brain.
Simple and choice reaction time in patients with human immunodeficiency virus infection
Authors: Perdices Michael , Cooper David A. 
Published: January 2005

AbstractThe performance of 56 homosexual men infected with human immunodeficiency virus (HIV) was compared to that of 23 HIV antibody‐seronegative controls on simple (SRT) and choice (CRT) reaction time tasks. Patients were classified into 3 groups according to Centers for Disease Control clinical criteria. There were 18 patients who had acquired immunodeficiency syndrome (AIDS), 18 who had AIDS‐related complex (ARC), and 20 who were HIV antibody‐seropositive but otherwise asymptomatic (HIV‐Ab+). The SRT task consisted of 5 trials, each containing 10 target stimuli. The CRT task consisted of 10 trials, each containing 5 target stimuli randomly interspersed with 5 nontarget stimuli. The mean response latency of each of the patient groups on the SRT task was not significantly different from that of controls. However, the performance of patients with AIDS or ARC on the CRT task was significantly lower than that of controls, whereas that of HIV‐Ab+ patients was not. Analysis of the quality of RT task performance also indicated that the impairment of processing efficiency at higher levels of task difficulty reflected a disruption of processing prior to the response selection stage.
Continuous and intermittent levodopa differentially affect basal ganglia function
Authors: Juncos Jorge L. , Engber Thomas M. , Raisman Rita , Susel Zvi , Thibaur Florence , Ploska Alain , Agid Yves , Chase Thomas N. 
Published: January 2005

AbstractThe effects of continuous and intermittent levodopa treatment on behavioral and biochemical indexes of basal ganglia function were compared in rats with unilateral 6‐hydroxydopamine lesions of the nigrostriatal dopamine pathway. Animals treated for 30 days with intermittent levodopa exhibited behavioral sensitization manifested by an enhanced rotational response to apomorphine; the rotational response of rats treated with an equivalent dose of levodopa by continuous infusion did not differ from that of saline‐treated controls. Dopamine receptor up‐regulation in the denervated striatum relative to the intact striatum was statistically significant for D1 but not D2 receptors: This asymmetry in dopamine receptor levels was diminished following intermittent levodopa treatment. Glutamic acid decarboxylase activity, modestly elevated in all groups in the denervated striatum relative to the intact striatum, increased substantially over control values bilaterally as a result of intermittent, but not continuous, levodopa treatment. These findings suggest a relation between the schedule of chronic levodopa administration and the development of behavioral sensitization, possibly as a consequence of alterations in neuronal systems located downstream from striatal dopamine receptors. The behavioral sensitization induced by chronic, intermittent dopaminomimetic treatment may serve as a model for motor fluctuations in Parkinson's disease.
Swellings of proximal axons in a case of motor neuron disease
Authors: Sasaki Shoichi , Maruyama Shoichi , Yamane Kiyomi , Sakuma Hideo , Takeishi Makoto 
Published: January 2005

AbstractSerial semithin sections of lumbar anterior horn cells from a patient with rapidly progressive sporadic motor neuron disease were searched for direct connections between swellings of neuronal processes and perikarya. Focal swellings of the proximal axons were not uncommonly seen to be connected directly to perikarya. These swellings varied in shape and size and some were identified as spheroids. Most of the cell bodies connected with swellings showed otherwise normal architecture. These observations suggest that the focal swellings of proximal axons, particularly the distal portion of the initial segment and the first internode of the myelinated axon, indicate an early pathological change, and may represent functionally and morphologically vulnerable sites.
Stroke risk and age do not predict behavioral activation of brain blood flow
Authors: Ewing James R. , Brown Gregory C. , Gdowski James W. , Do Robert Simkins , Levine Steven R. , Welch K. M. A. 
Published: January 2005

AbstractTwenty‐four neurologically normal subjects, 12 in their twenties and 12 in their sixties, were included in a protocol that studied the relationship of resting cerebral blood flow and cerebral blood flow activation by neuropsychological testing to age and stroke risk factors. Both age and a stroke risk index were predictive of a reduced resting cerebral blood flow. Despite this, cerebral blood flow activation relative to resting flow was preserved. Subclinical lesions of deep white matter are proposed to explain the apparently paradoxical result that resting cerebral blood flow is decreased by factors that damage cerebral vessels, while cerebral vascular reactivity is unimpaired.
Postmortem detection of measles virus in non‐neural tissues in subacute sclerosing panencephalitis
Authors: Brown Hannah R. , Goller Nancy L. , Rudelli Raoul D. , Dymecki Jerzy , Wisniewski Henryk M. 
Published: January 2005

AbstractSubacute sclerosing panencephalitis, a rare, progressive, fatal central nervous system disease of children, is caused by measles virus. Clinical signs occur months to several years after recovery from acute measles infection. It is not known where the virus persists while the disease is inapparent. Involvement of organs outside the central nervous system has rarely been documented. To search for possible peripheral reservoirs of measles virus we used in situ hybridization to probe for measles virus RNA and immunocytochemical studies to localize measles virus antigens in a variety of organs taken at autopsy from confirmed cases of subacute sclerosing panencephalitis. Seven of 9 cadavers were found to contain measles virus RNA or antigens, or both, in at least one location outside the central nervous system. These sites included lymphoid organs such as thymus, spleen, lymph nodes, and tonsil, suggesting a role for lymphocytes in disease pathogenesis. Virus was also detected in kidney, lung, and glandular tissues such as pancreas, adrenal, and pituitary. These reservoirs may provide the antigenic stimulus leading to the elevated humoral response characteristic for subacute sclerosing panencephalitis.
Localization of immunoreactive thymosin α1 in astrocytes of normal human brain
Authors: Su Yuan‐liang , Loon Ho Kang , Dalakas Marinos C. , Mutchnick Milton G. 
Published: January 2005

AbstractWe employed an immunocytochemical method to examine human brain for the presence of immunoreactive thymosin α1 (Tα1), a peptide derivative of thymic tissue, using a well‐characterized antiserum. For cell identification, serial sections were stained with antisera to thymosin β4(Tβ4), another thymic peptide that identifies oligodendrocytes, and with anti‐glial fibrillary acidic protein (GFAP) antiserum that stains astrocytes in a double‐staining technique using avidin‐biotinylated horseradish peroxidase or avidin‐biotinylated alkaline phosphatase complex. Antiserum to Tα1 stained the cell body, but not the processes, of GFAP‐positive astrocytes, suggesting that Tα1 is a common antigen shared between thymus and astrocytes. Because Tα1 and its precursor molecule play a role in cell proliferation and immunomodulation, our findings could explain the role of astrocytes in certain central nervous system diseases.
Direct evidence for calcium‐induced ischemic and reperfusion injury
Authors: Uematsu Daisuke , Greenberg Joel H. , Reivich Martin , Hickey William F. 
Published: January 2005

AbstractChanges in cytosolic free calcium ([Ca2+]i) in the cat cortex were measured in vivo by indo‐1 fluorometry during cerebral ischemia and reperfusion and were correlated to the histopathological ischemic changes. These changes were most pronounced in stroke cases with an increase in [Ca2+]i throughout the ischemic and reperfusion periods. Cases without a [Ca2+]i increase showed no histopathological change in the cortical gyrus in which [Ca2+]i was measured. The data support the hypothesis that an increase in [Ca 2+]i during cerebral ischemia and reperfusion leads to neuronal damage.
Neuropathological distinction between Parkinson's dementia and Parkinson's plus Alzheimer's disease
Authors: de la Monte Suzanne M. , Wells Sarah E. , Hedley‐Whyte E. Tessa , Growdon John H. 
Published: January 2005

AbstractThe distinctive clinical features of dementia in Parkinson's disease (PDD) and Parkinson's plus Alzheimer's disease (PD + AD) suggest different patterns of cerebral atrophy in these conditions. To determine the pathoanatomical substrates of dementia in PDD and PD + AD, morphometric analysis of 5 standardized coronal slices was used to identify volumetric changes in cerebral tissue. In PDD (n = 4) there were 9 to 23% reductions in cross‐sectional area of cerebral cortex, a 38% loss of tissue in the globus pallidus + putamen, and an 18% reduction in area of the amygdala, whereas in PD + AD (n = 6) there was severe global atrophy of the cerebral cortex (27–29% reductions) moderate atrophy of white matter (10–19% reductions), and 40% reductions in areas of globus pallidus + putamen and the amygdale relative to neuropathologically intact controls (n = 14). Immunostaining with anti‐glial fibrillary acidic protein disclosed significant gliosis of all four major subdivisions of neocortex in PD + AD and gray matter of the caudate, putamen, globus pallidus, and thalamus in both PDD and PD + AD relative to controls. The findings suggest that dementia in PDD is mainly subcortical in origin and due to neuronal degeneration in basal ganglia, the amygdale, and thalamus. In PD + AD the same pattern and degree of subcortical degeneration is evident, but there are clearly superimposed lesions involving cortical neurons and long projection fibers coursing through cerebral white matter that most likely account for the distinctive manifestations of dementia in this condition compared with PDD.
Limbic P3 potentials, seizure localization, and surgical pathology in temporal lobe epilepsy
Authors: Puce Aina , Kalnins Renate M. , Berkovic Samuel F. , Bladin Peter F. 
Published: January 2005

AbstractLimbic P3 event‐related potentials were recorded from mesial temporal electrodes implanted for presurgical investigation in 70 patients with intractable focal seizures. IN 46 (81%) of 57 patients with unilateral temporal lobe epilepsy, the limbic P3 potential was absent or rudimentary ipsilateral to the seizure focus and a robust P3 potential was always elicite from the nonepileptogenic temporal lobe. Bilateral P3 potentials were recorded in 6 patients (10%) with unilateral temporal lobe epilepsy. In the remaining 5 patients in the group with unilateral temporal lobe epilepsy, results showed P3 bilaterally absent (2 patients), P3 present in a unilateral investigation (1 patient), P3 absent contralateral to the seizure focus (1 patient), and technically unsatisfactory recordings (1 patient). Bilaterally absent P3 potentials were noted in 2 patients with bilateral temporal lobe epilepsy. In 6 patients with technically adequate P3 studies and extratemporal seizures, bilaterally present P3 potentials were noted. Sensitivity and specificity of P3 absence as a predictor of an epileptoghenic temporal lobe were 87% and 95%, respectively. Tissue specimens of the hippocampus were available in 22 patients (43%). Thirteen hippocampi showed sclerosis, all of which were associated with unilaterally absent P3 potentials. Nine hippocampi were normal (5 patients with the P3 absent, 4 with P3 present). Sensitivity and specificity of an absent limbic P3 as a function of hippocampal pathological findings were 100% and 44%, respectively. Absent limbic P3 potentials in temporal lobe epilepsy thus indicate strucutal or functional hippocambal abnormality and may add important information in presurgical evaluation with depth electrodes of patients who have temporal lobe epilepsy.
Galactosylceramide: A reliable serum index of demyelination in multiple sclerosis
Authors: Lubetzki C. , PharmD Y. Thuillier , PharmD A. Galli , Lyon‐Caen O. , Lhermitte F. , Zalc B. 
Published: January 2005

AbstractEight patients with multiple sclerosis were followed for several months to determine if serum levels of galactosylceramide, a major lipid component of myelin, correlate with the clinical evolution of the disease. In the patients with the chronic progressive form of multiple sclerosis, galactosycleramide remained undetectable. In the patients with relapsing‐remitting multiple sclerosis, there was a good correlation between the elevation of serum galactosylcermide levels and clinical relapses. This serum assay should prove of value in the follow‐up of patients with multiple sclerosis.
Midbrain dopaminergic cell loss in parkinson's disease: Computer visualization
Authors: German Dwight C. , Manaye Kebreten , Smith Wade K. , Woodward Donald J. , Saper Clifford B. 
Published: January 2005

AbstractComputer visualization techniques were used to map the distribution of dopaminergic neurons within midbrain tissue sections from 5 parkinsonian patients and 3 age‐matched control subjects. The Parkinsonian brains had over 50% fewer dopaminergic neurons within the midbrain than age‐matched normal brains. The cell loss occurred within the combined substantia nigra (dopaminergic nucleus A9) and retrorubral (dopaminergic nucleus A8) areas (> 61%) and the ventral tegmental area (dopaminergic nucleus A10) (> 42%). The cell loss was greatest within the ventral portion of the substantia nigra zona compacta. The specific pattern of cell loss is very similar to the pattern of cells that project to the striatum (as opposed to cortical and limbic sites) in animal neuroanatomical tracing experiments. These data suggest that Parkinson's disease preferentially destroys midbrain dopaminergic neurons in nuclei A8, A9, and A10, which project to the striatum.
Low prevalence of neurological and neuropsychological abnormalities in otherwise healthy HIV‐1–infected individuals: Results from the multicenter AIDS cohort study
Authors: McArthur Justin C. , Cohen Bruce A. , Selnes Ola A. , Kumar Ashok J. , Cooper Kay , McArthur Julie H. , Soucy Gerry , Cornblath David R. , Chmiel Joan S. , Wang Mei‐Cheng , Starkey Danna L. , Ginzburg Harold , Ostrow David G. , Johnson Richard T. , Phair John P. , Polk B. Frank 
Published: January 2005

AbstractAccurate description of the prevalence of neurological impairment in healthy individuals who are infected with human immunodeficiency virus type 1 (HIV‐1) has relevance for public health policy, for employment issues, and for planning future health needs. Within the Multicenter AIDS Cohort Study, we determined the cross‐sectional prevalence of neurological abnormalities in 270 HIV‐1 seropositive homosexual and bisexual men in Centers for Disease Control Groups II and III, using a control group of 193 HIV‐1 seronegative homosexual men. Utilizing a neurological and neuropsychological screening battery, we found no differences in the prevalence of neuropsychiatric symptoms or in neuropsychological performance. One hundred nineteen subjects with abnormalities on screening tests completed additional neuropsychological testing and had neurological examinations. The majority had normal results and the frequency of neurological abnormalities and impaired neuropsychological performance was not significantly increased among HIV‐1 seropositive subjects. Most of the abnormalities could be attributed to causes other than HIV‐1. One subject had mild HIV‐1–related dementia, yielding a prevalence of 3.7:1,000 (95% confidence interval: 0.19–23.7:1,000). Magnetic resonance imaging demonstrated sulcal prominence and focal areas of high signal intensity in white matter in 63% of HIV‐1 seropositive subjects and 48% of uninfected control subjects. Abnormalities in cerebrospinal fluid were noted in 23 (85%) of 27 HIV‐1–infected individuals. Our studies indicate that the prevalence of dementia and other HIV‐1–related neurological disorders is very low among healthy HIV‐1 seropositive homosexual men. The confounding effects of factors such a substance abuse or preexisting medical conditions must be considered in the neurological evaluation of such patients.
Vestibular responses in wernicke's encephalopathy
Authors: Furman Joseph M. R. , Becker James T. 
Published: January 2005

AbstractTwo patients with Wernicke's encephalopathy were evaluated with quantitative vestibulo‐ocular reflex and ocular motor testing. Vestibulo‐ocular reflex testing included caloric irrigation, earth vertical axis rotational sinusoids, and rotational impulses. Both patients demonstrated hypoactive vestibular responses to both caloric and rotational stimuli at the time of presentation. One patient had upbeating nystagmus that diminished with upgaze, downgaze, or convergence. Following treatment with thiamine, both patients' vestibular responses improved but remained abnormal, with a short vestibulo‐ocular reflex time constant and increased low‐frequency rotational phase lead. Impairment of the velocity storage element attributable to damage to the vestibular nucleus and nucleus prepositus hypoglossi may account for this permanent effect on the vestibulo‐ocular reflex.
AIDS‐related vacuolar myelopathy is not associated with coinfection by human T‐lymphotropic virus Type I
Authors: Brew Bruce J. , Hardy William , Zuckerman Evelyn , Chien Nancy , Paul Morris , Rosenblum Marc , Gadler Hakan , Vahlne Anders , Gold Jonathan , Armstrong Donald A. , Price Richard W. 
Published: January 2005

AbstractAssessment of antibodies against human T‐lymphotropic virus type I (HTLV‐I) by enzyme‐linked immunoassay, immunofluorescence, and Western blot was undertaken in patients with pathologically or clinically diagnosed acquired immunodeficiency syndrome‐related vacuolar myelopathy to determine whether this retrovirus could be etiologically implicated in this disorder. No serological evidence for HTLV‐I was found in the patients with vacuolar myelopathy, though 1 patient with an atypical myelopathy did have antibodies against HTLV‐I.
A case of adult‐onset dementia with argyrophilic grains
Authors: Itagaki S. , McGeer P. L. , Akiyama H. , Beattie B. L. , Walker D. G. , Moore G. R. W. , McGeer E. G. 
Published: January 2005

AbstractA case of progressive dementia in a 68‐year‐old woman was characterized by the postmortem finding of widespread argyrophilic grains in the cerebral cortex. The grains consisted of 10‐ to 13‐nm filaments in deposits ranging up to 9 μm in length and 3 μm in diameter. The grains stained positive with Alz‐50 monoclonal antibody. Cortical brain tissue levels were minimally elevated for acetylcholinesterase, moderately reduced for choline acetyltransferase, and sharply reduced for glutaminase. Although the case was clinically indistinguishable from Alzheimer's disease, plaque and tangle pathological findings were absent. We confirm cortical changes of the type described by Braak and Braak and provide additional data on subcortical changes in this case.
Abnormalities of the electron transport chain in idiopathic parkinson's disease
Authors: Parker William Davis , Boyson Sally J. , Parks Janice K. 
Published: January 2005

AbstractIdiopathic Parkinson's disease may have a low‐level familial association but does not follow mendelian patterns of inheritance. Since inheritance of some components of the electron transport chain is nonmendelian and since inhibition of the electron transport chain with the toxin 1‐methy1‐4‐phenyl‐1,2,3,6‐tetrahydropyridine models Parkinson's disease in humans and animals, we evaluated catalytic activities of the electron transport chain in platelet mitochondria purified from patients with idiopathic Parkinson's disease. All 10 patients studied had significant reductions of complex I (NADH:ubiquinone oxidoreductase) activity. Succinate:cytochrome c oxidoreductase activity was less strikingly reduced. We hypothesize that the complex I abnormality may have an etiological role in the pathogenesis of Parkinson's disease and that this defect may be derived via the mitochondrial genome.