bluuebunny/crossref_metadata_2025_split huggingface dataset:
Memory disturbances following anterior communicating artery rupture
Authors: Irle Eva , Wowra Berndt , Kunert Hanns J. , Hampl Jürgen , Kunze Stefan 
Published: January 2005

AbstractThirty patients with lesions due to the rupture and repair of an aneurysm of the anterior communicating artery were compared neuropsychologically with 27 patients with ruptures but no lesions and 30 normal control subjects. Patients with combined lesions in the basal forebrain and striatum (n = 5), or basal forebrain, striatum, and ventral frontal cortex (n = 7), had severe memory deficits, whereas patients with lesions in the basal forebrain (n = 7) or the striatum (n = 5) alone showed virtually no deficits. Patients with lesions of the basal forebrain and ventral frontal cortex together (n = 6) showed mild memory deficits. In contrast to the memory effects, emotional changes were most pronounced in patients with striate lesions alone. Basal forebrain or ventral frontal lesions ameliorated rather than aggravated the emotional effects of striate lesions. It is suggested that the basal forebrain and the striatum form links of different pathways related to mnemonic information processing. Both systems may be able to compensate for a dysfunction of the other, but lesions of both systems together may lead to strong and unrecoverable memory deficits.
Corticotropin‐releasing hormone–induced seizures in infant rats originate in the amygdala
Authors: Baram Tallie Z. , Hirsch Edouard , Snead O. Carter , Schultz Linda 
Published: January 2005

AbstractThe neuroanatomical substrate of seizures induced by picomolar amounts of corticotropin‐releasing hormone in infant rats was investigated. Electrographic and behavioral phenomena were monitored in 42 rat pups aged 5 to 22 days. Rat pups carried bipolar electrodes implanted in subcortical limbic structures, as well as cortical electrodes and intracerebroventricular cannulae. The administration of corticotropin‐releasing hormone produced age‐specific seizures within minutes, which correlated with rhythmic amygdala discharges. Paroxysmal hippocampal and cortical discharges developed subsequently in some rats. Corticotropin‐releasing hormone–induced electrographic and behavioral seizures originate in the amygdala.
Oxidative metabolism in muscle mitochondria from patients with chronic alcoholism
Authors: Cardellach F. , Galofré J. , Grau J. M. , Casademont J. , Hoek J. B. , Rubin E. , Urbano‐Márquez A. 
Published: January 2005

AbstractWe investigated the effect of long‐term ethanol intake on the function of skeletal muscle mitochondria from 30 human alcoholics. Mitochondrial studies included (1) oxidative phosphorylation, (2) the activity of the individual complexes of the respiratory chain, and (3) the cytochrome content. State 3 and state 4 oxidation rates with glutamate‐malate, succinate, tetramethyl‐p‐phenylenediamine–ascorbate, and acetylcarnitine‐malate, the activity of the individual complexes of the respiratory chain, and the concentration of mitochondrial cytochromes were comparable in control subjects and alcoholic patients, and also in myopathic and nonmyopathic alcoholic patients. These results demonstrate that alcoholic myopathy is not associated with a deficiency in mitochondrial energy supply.
Shared T‐cell receptor gene usage in experimental allergic neuritis and encephalomyelitis
Authors: Clark Lise , Heber‐Katz Ellen , Rostami Abdolmohamad 
Published: January 2005

AbstractExperimental allergic neuritis, an autoimmune disease of the peripheral nervous system, is a model for human Guillain‐Barré syndrome. Experimental allergic neuritis is mediated by CD4+ T cells reactive with myelin P2 protein. We demonstrate that these T cells use the same members of T‐cell receptor V gene families for both their alpha (Vα2) and beta (Vβ8) chains as T cells that cause experimental allergic encephalomyelitis, an autoimmune disease of the central nervous system. Furthermore, these T cells appear to be idiotypically related. Therefore, completely different T‐cell lines with different antigen specificities, producing entirely different diseases, share common T‐cell receptors.
3‐O‐methyldopa administration does not alter fluorodopa transport into the brain
Authors: Guttman Mark , Léger Gabriel , Cedarbaum Jesse M. , Reches Avinoam , Woodward William , Evans Alan , Diksic Mirko , Gjedde Albert 
Published: January 2005

AbstractTo determine if 3‐O‐methyldopa (3OMd) significantly inhibits the transport of 6‐{18F} fluorodopa (6‐FD) into the brain at the concentration normally encountered during L‐dopa administration, we performed 6‐FD studies with positron emission tomography in cynomolgus monkeys in the presence and absence of 3OMd. Infusion of 3OMd was designed to produce plasma concentrations equivalent to those seen in patients on chronic L‐dopa therapy. Plasma 3OMd levels of 39 ± μM did not alter the blood–brain transfer rate of 6‐FD. 6‐FD positron emission tomographic studies in parkinsonian patients will therefore not be altered by 3OMd present in the blood in those patients taking L‐dopa preparations. These results do not support the hypothesis that transport of L‐dopa into the brain is inhibited by 3OMd to cause the declining response seen in patients with advanced Parkinson's disease.
Serum IgG antibody to ganglioside GQ1b is a possible marker of Miller Fisher syndrome
Authors: Chiba Atsuro , Kusunoki Susumu , Shimizu Teruo , Kanazawa Ichiro 
Published: January 2005

AbstractWe studied serum anti‐glycolipid antibodies by enzymelinked immunosorbent assay and thin‐layer chromatography–enzyme immunoassay in six consecutive patients with typical Miller Fisher syndrome. In all six, increased activity of IgG antibody against ganglioside GQ1b was present in the early phase and reduced with time, whereas such activity was not detected in normal control subjects and disease control subjects including those with Guillain‐Barrë syndrome. Anti‐GQ1b IgG antibody is a new possible diagnostic marker of Miller Fisher syndrome and could well be related to the disease process itself.
Sensory neuropathy associated with monoclonal immunoglobulin M to GD1b ganglioside
Authors: Daune Geneviè C. , Farrer Robert G. , Dalakas Marinos C. , Quarles Richard H. 
Published: January 2005

AbstractA 67‐year‐old woman with a sensory polyneuropathy was shown to have a serum monoclonal immunoglobulin M λ antibody with a titer of 1:10,000 toward GD1b ganglioside. The immunoglobulin M also reacted with some other gangliosides containing disialosyl groups such as GD2, GD3, and GQ1b, but it did not react with GM1, LM1, or GD1a. The principal reactive ganglioside in human cauda equina was GD1b.
Human immunodeficiency virus type 1–infected monocytic cells can destroy human neural cells after cell‐to‐cell adhesion
Authors: Tardieu Marc , Héry Christiane , Peudenier Sylviane , Boespflug Odile , Montagnier Luc 
Published: January 2005

AbstractPrimary cultures of human embryonic neurons and astrocytes have been used to test the interactions between neural cells and either human immunodeficiency virus type 1 (HIV‐1) or HIV‐1–infected monocytes. After direct infection with HIV‐1, neither morphological alteration of neurons and astrocytes nor signs of viral replication were observed. Similarly, cultured human neurons and astrocytes were resistant to incubation with the supernatant of HIV‐1–infected U937 cells, a human monoblastoid cell line. In contrast, HIV‐1–infected U937 monocytic cells adhered to neural cells and induced large plaques of necrosis surrounding them. This cytopathic effect began at the time of viral replication (day 16 after infection). Its intensity depended on that of viral replication, and its range was identical to the region of diffusion of viral antigens, as judged by immunocytochemistry. The cytopathic effect was not dependent on the release of free radicals. It could not be induced by cytokines or cytokine‐stimulated U937 cells. It is likely that this cytopathic effect depends on the release of viral antigens either within the site of adherence itself or within close range of the astrocyte membrane.
Ganglioside GD1b is the target antigen for a biclonal IgM in a case of sensory‐motor axonal polyneuropathy: Involvement of N‐acetylneuraminic acid in the epitope
Authors: Younes‐Chennoufi Amena Ben , Léger Jean‐Marc , Hauw Jean‐Jacques , Preud'Homme Jean‐Louis , Bouche Pierre , Aucouturier Pierre , Ratinahirana Heri , Lubetzki Catherine , Lyon‐Caen Olivier , Baumann Nicole 
Published: January 2005

AbstractWe report on a 54‐year‐old man with a sensory‐motor polyneuropathy associated with a biclonal IgM‐k gammopathy, which reacted with the ganglioside GD1b. Examination of nerve biopsy specimens showed some reduction in the density of myelinated fibers and axonal degeneration with a loss of large fibers and a relative increase in the density of small fibers. Immunodetection on thin‐layer chromatography of the glycolipid antigens showed strong reactivity of the patient's serum IgM‐k with GD1b ganglioside and weak binding to GD1a. The biclonal IgM antibodies did not react with GM1, asialo‐GM1, GT1b, GD2, or GD3. Indirect immunofluorescence staining showed binding of IgM‐k mainly in a crescent‐like pattern on the internal side of myelin sheaths, which could correspond either to an enlarged periaxonal (adaxonal) space or to the internal mesaxon or to both. The immunostaining was abolished after absorption of the serum with GD1b.
Physiological abnormalities in hereditary hyperekplexia
Authors: Matsumoto Joseph , Fuh Peter , Nigro Michael , Hallett Mark 
Published: January 2005

AbstractFive patients from a kindred with hereditary hyperekplexia had physiological testing. The surface‐recorded electromyographic pattern of audiogenic muscle jerks was identical to that of the normal acoustic startle reflex. Testing at graded stimulus intensities indicated an increase in the gain of the acoustic startle reflex. Nose‐tap stimuli resulted in short‐latency generalized electromyographic bursts that were similar to the R1 component of the blink reflex. Electrical stimulation of peripheral nerves elicited a pattern of generalized muscle jerks that was similar to that of the acoustic startle reflex. Somatosensory evoked potentials, brainstem auditory evoked potentials, and cortical auditory evoked potentials were normal. The primary physiological abnormality in hereditary hyperekplexia is widespread elevated gain of vestigial withdrawal reflexes in the brainstem and possibly the spinal cord, most likely resulting from increased excitability of reticular neurons.
Dystonia induced by combined treatment with L‐dopa and MK‐801 in parkinsonian monkeys
Authors: Rupniak N. M. J. , Boyce S. , Steventon M. J. , Iversen S. D. , Marsden C. D. 
Published: January 2005

AbstractWe examined whether the N‐methyl‐D‐aspartate antagonist MK‐801 (dizocilpine) would reverse parkinsonism or potentiate the effects of L‐dopa in primates treated with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP). In contrast to its effect in rodent models, treatment with MK‐801 (0.1 mg/kg) caused bradykinesia and ataxia in parkinsonian primates, but no locomotor stimulation. Coadministration of MK‐801 (0.1 mg/kg) with L‐dopa (20 mg/kg) induced marked dystonia accompanied by bradykinesia and ataxia. Dystonia was not induced by either treatment given alone. These findings indicate that MK‐801 should not be advocated as an adjunct to dopamine agonist therapy in Parkinson's disease.
Parkinsonism‐inducing neurotoxin MPP+: Uptake and toxicity in nonneuronal COS cells expressing dopamine transporter cDNA
Authors: Kitayama S. , Shimada S. , Uhl G. R. 
Published: January 2005

AbstractExpression of a cloned dopamine transporter complementary DNA in COS cells allows these primate kidney cells to accumulate the parkinsonism‐inducing neurotoxin metabolite MPP+ (1‐methyl‐4‐phenylpyridinium) avidly, and MPP+ toxicity results. By documenting that the dopamine transporter can confer MPP+ sensitivity to nonneural cells, these results highlight the key role that this transporter could play in mechanisms underlying parkinsonism.
New magnetic resonance techniques for evaluating cerebrovascular disease
Authors: Fisher Marc , Sotak Christopher H. , Minematsu Kazuo , Li Limin 
Published: January 2005

AbstractMagnetic resonance (MR) imaging of acute stroke has made important contributions to diagnosis. Several novel MR technologies, now in preclinical and clinical development, will contribute to stroke diagnosis and perhaps help to guide therapy. MR angiography is the most clinically advanced new MR technology and offers the clinician a method to image noninvasively the extra‐ and intracranial vasculature. Diffusion‐weighted MR imaging can demonstrate ischemic lesions quantitatively within minutes of onset in experimental stroke models, and human application is proceeding. Perfusion MR studies can reveal the presence or absence of cerebral perfusion in specific arterial territories. MR spectroscopy can assess tissue metabolites in vivo and reveal changes in these metabolites associated with ischemic injury. The combination of these new MR techniques should provide a plethora of information about the extent of ischemic lesions, associated vascular and perfusion deficits, and metabolic consequences. This information will afford the clinician the opportunity to assess and subtype ischemic stroke patients more rapidly and could be used to monitor therapeutic responses.
Impaired mesial frontal and putamen activation in Parkinson's disease: A positron emission tomography study
Authors: Playford E. D. , Jenkins I. H. , Passingham R. E. , Nutt J. , Frackowiak R. S. J. , Brooks D. J. 
Published: January 2005

AbstractSelection of movement in normal subjects has been shown to involve the premotor, supplementary motor, anterior cingulate, posterior parietal, and dorsolateral prefrontal areas. In Parkinson's disease (PD), the primary pathological change is degeneration of the nigrostriatal dopaminergic projections, and this is associated with difficulty in initiating actions. We wished to investigate the effect of the nigral abnormality in PD on cortical activation during movement. Using C15O2 and positron emission tomography (PET), we studied regional cerebral blood flow in 6 patients with PD and 6 control subjects while they performed motor tasks. Subjects were scanned while at rest, while repeatedly moving a joystick forward, and while freely choosing which of four possible directions to move the joystick. Significant increases in regional cerebral blood flow were determined with covariance analysis. In normal subjects, compared to the rest condition, the free‐choice task activated the left primary sensorimotor cortex, left premotor cortex, left putamen, right dorsolateral prefrontal cortex and supplementary motor area, anterior cingulate area, and parietal association areas bilaterally. In the patients with PD, for the free‐choice task, compared with the rest condition, there was significant activation in the left sensorimotor and premotor cortices but there was impaired activation of the contralateraputamen, the anterior cingulate, supplementary motor area, and dorsolateral prefrontal cortex. Impaired activation of the medial frontal areas may account for the difficulties PD patients have in initiating movements.
Absence of persistent infection with enteroviruses in muscles of patients with inflammatory myopathies
Authors: Leon‐Monzon Marta , Dalakas Marines C. 
Published: January 2005

AbstractWe searched for enteroviral nucleic acid sequences using the polymerase chain reaction and slot–blot hybridization in coded muscle biopsy specimens from 39 patients with active inflammatory myopathies (polymyositis, dermatomyositis, and inclusion–body myositis) and from 16 patients with other neuromuscular diseases, including patients with postpolio syndrome. For primers, we used sequences of the noncoding region at the 5′ end of the viral RNA. We failed to detect specific enteroviral nucleic acid sequences in the muscle biopsy specimens. Because this sensitive technique can amplify even low copy numbers of the viral genome, it appears unlikely that a persistent enteroviral infection is the cause of inflammatory myopathies.
Patterns of reactivity of human anti‐GM1 antibodies with spinal cord and motor neurons
Authors: Corbo Massimo , Quattrini Angelo , Lugaresi Alessandra , Santoro Maria , Latov Norman , Hays Arthur P. 
Published: January 2005

AbstractHuman anti‐GM1 antibodies from patients with lower motor neuron disease or predominantly motor neuropathy recognize carbohydrate determinants shared by GM1 and related glycolipids and glycoproteins, but the identity of the antigens to which they bind in tissue is unknown. We examined the binding of anit‐GM1 antibodies with differing fine specificities to spinal cord, isolated motor neurons, and dorsal root ganglia neurons in order to characterize the tissue antigens. All anti‐GM1 antibodies tested bound to the surface of bovine spinal motor neurons and immunostained the gray matter of unfixed sections of spinal cord. The staining was blocked by cholera toxin, which is specific for GM1, indicating that GM1 itself was the target antigen. Binding to white matter was more variable and depended on fixation and the fine specificities of the antibodies. The anti‐GM1 antibodies did not bind to dorsal root ganglia neurons in tissue sections or in culture. These studies suggest that the autoantibodies migh exert their effect, in part, by binding to GM1 on the surface of motor neurons, and that the absence of binding to dorsal root ganglia neurons might explain the lack of sensory abnormalities in affected patients.
Ipsilateral fast corticospinal pathways do not account for recovery in stroke
Authors: Palmer E. , Ashby P. , Hajek V. E. 
Published: January 2005

AbstractWe tested the hypothesis that in adult humans, recovery from stroke results from the emergence of ipsilateral, fastconducting corticospinal pathways. In 10 patients recovering from stroke, the unaffected hemisphere was stimulated with an electromagnet and changes in the firing probability of single biceps motor units were used to derive postsynaptic potentials in single biceps motoneurons. Stimuli sufficient to excite the neurons of the fast‐conducting corticospinal pathway (as shown by short‐latency facilitation of contralateral biceps motoneurons) did not produce short‐latency depolarization of ipsilateral biceps motoneurons. The hypothesis is therefore not supported.
The cortical lesion of Huntington's disease: Further neurochemical characterization, and reproduction of some of the histological and neurochemical features by N‐methyl‐D‐aspartate lesions of rat cortex
Authors: Storey Elsdon , Kowall Neil W. , Finn Stephen F. , Mazurek Michael F. , Beal M. Flint 
Published: January 2005

AbstractHuntingtons's disease is a progressive neurodegenerative disease in which the basal ganglia are preferentially affected. Recent evidence, however, suggests involvement of the cerebral cortex as well, with sparing of neurochemically defined subsets of gamma‐aminobutyric acid (GABA)‐ergic interneurons. In the present study, we examined changes in concentrations of the amino acid neurotransmitters GABA, glutamate, and aspartate in nine cortical regions from 23 patients with advanced Huntington's disease and 12 control brains. GABA concentrations were significantly increased in eight of the nine regions, consistent with a sparing of GABAergic local circuit neurons in the context of progressive cortical atrophy. Small but significant increases in glutamate were found in six of the nine regions, while aspartate levels were generally unaffected. Striate cortex (Brodmann's area 17) showed the most profound increases in GABA and glutamate. We also investigated the effects of powdering the excitotoxins N‐methyl‐D‐aspartate (NMDA) or kainic acid onto the dura of rats. The resulting lesions were examined at 1 week and 6 months. The NMDA‐induced lesions showed striking sparing of parvalbumin‐positive neurons (a subset of GABAergic interneurons), and this sparing was reflected in neurochemical measurements of GABA; kainic acid lesions failed to display this selectivity. Somatostatin, cholecystokinin, and vasoactive intestinal polypeptide concentrations were spared by the NMDA‐induced lesions, and substance P levels were significantly increased. These results provide evidence that NMDA excitotoxic lesions of cerebral cortex can produce a selective pattern of neuronal damage similar to that which occurs in Huntington's disease.
Calbindin‐D28K in the basal ganglia of patients with parkinsonism
Authors: Ito Hidefumi , Goto Satoshi , Sakamoto Shizuki , Hirano Asao 
Published: January 2005

AbstractAn immunohistochemical study was carried out to investigate the topographic distribution of calbindin‐D28K in the human basal ganglia and substantia nigra and its alterations in patients with idiopathic Parkinson's disease (PD), parkinsonism‐dementia complex on Guam, progressive supranuclear palsy, and striatonigral degeneration. In normal control subjects, calbindin‐D28K immunoreactivity was identified in the medium‐sized neurons and neuropil of the matrix compartment of the striatum, the woolly fiber arrangements of the globus pallidus, and the fiber structures of the pars reticulata of the substantia nigra. Calbindin‐D28k expression in the basal ganglia of patients with PD and parkinsonism‐dementia on Guam was not different from that of control subjects, suggesting that the matrical output pathway is spared in these disorders. In contrast, its disruption is inferred from the observed disorganization of woolly fibers in the globus pallidus of patients with progressive supranuclear palsy and the reduced calbindin‐D28k reactivity in the putaminal matrix and the pars reticulata of the substantia nigra of subjects with striatal degeneration. Thus, our results indicate that calbindin‐D28k is a useful marker for the projection system from the matrix compartment and that its expression is modified in patients with progressive supranuclear palsy and striatal degeneration.
Adenosine: A potential mediator of seizure arrest and postictal refractoriness
Authors: During Matthew J. , Spencer Dennis D. 
Published: January 2005

AbstractAdenosine is a potent inhibitory neuromodulator and has been proposed as an endogenous anticonvulsant. Depth electrodes modified to include a microdialysis probe were implanted for 10 to 16 days in the hippocampi of 4 patients with intractable complex partial epilepsy to test the hypothesis that during seizures extracellular adenosine reaches levels that may depress epileptiform activity. Samples were collected bilaterally at 3‐minute intervals before, during, and after a single, spontaneous‐onset seizure in each patient. All seizures commenced in one hippocampus and propagated to the contralateral hippocampus. Extracellular adenosine levels increased by 6‐ to 31‐fold with the increase significantly greater in the epileptogenic hippocampus. During seizures, levels of adenosine in the dialysate reached concentrations as high as 2.5 μM, reflecting extracellular concentrations of approximately 65 μM. Adenosine at concentrations of 40 to 50 μM depresses epileptiform activity in vitro, so the levels we report may suppress seizure activity in vivo. Moreover, adenosine levels remain elevated above basal values for the entire 18‐minute postical period. These data support the role of adenosine in mediating seizure arrest and postictal refractoriness and suggest that treatments which facilitate adenosine may be effective in preventing seizures.