bluuebunny/crossref_metadata_2025_split huggingface dataset:
GABA‐mimetic drugs enhance apomorphine‐induced contralateral turning in rats with unilateral nigrostriatal dopamine denervation: Implications for the therapy of Parkinson's disease
Authors: Bennett James P. , Ferrari Marina B. , Cruz C. Joseph 
Published: January 2005

AbstractThe underlying mechanisms responsible for advanced Parkinson's disease's becoming refractory to dopamimetic therapies are unclear. Postmortem brain studies indicate that patients with Parkinson's disease have decreased basal ganglia γ‐aminobutyric acid (GABA) function in addition to profound striatal dopamine (DA) deficiencies. In experimental animals, GABA‐utilizing striatal and nigral projection neurons appear to mediate motor behaviors arising from the stimulation of striatal DA receptors by agonists. We have examined the ability of directly and indirectly acting GABA‐mimetic drugs to alter turning behavior elicited by administering apomorphine, a DA agonist, to rats with unilateral lesions of dopaminergic nigrostriatal neurons. Low doses of directly acting postsynaptic GABA agonists (progabide, 4,5,6,7‐tetrahydroisoxazolo[5,4‐c]pyridin—3‐01) or a neuronal GABA transport inhibitor (SKF 100330‐A) potentiate apomorphine‐induced turning. Higher doses of these agents or acute inhibition of GABA catabolism inhibits turning. Our results suggest that low doses of certain GABA‐mimetics will improve the responses of patients with Parkinson's disease to concurrent DA receptor agonist therapy.
Tabacco‐induced primary‐position upbeat nystagmus
Authors: Sibony Patrick A. , Evinger Craig , Manning Karen A. 
Published: January 2005

AbstractThe effects of tobacco smoking on the eye movements of normal human subjects were studied using direct current electrooculography and the magnetic search coil technique. Tobacco induced a transient primary‐position upbeat nystagmus in the dark, which was suppressed by visual fixation. It obeyed Alexander's law and was associated with oblique upward fast phases that alternated from side to side. Tobacco‐induced nystagmus exhibited a latency of onset at 40 to 90 seconds, a duration of 10 to 20 minutes, and maximum slow‐phase velocities at 2 to 3 minutes. We suggest that tobacco induces primary‐position upbeat nystagmus through the excitatory effects of nicotine on the central vestibular pathways.
Type 1 human poliovirus binds to human synaptosomes
Authors: Brown Robert H. , Johnson David , Ogonowski Mark , Weiner Howard L. 
Published: January 2005

AbstractPoliovirus is a neurotropic virus that selectively infects human motoneurons in vivo. The basis for the specificity of this infection is not fully understood. It has been suggested that this tropism occurs because motoneurons are the only neurons to express poliovirus receptors. We have examined this hypothesis by measuring the binding of 125I‐labeled poliovirus type 1 to neural tissues. With this assay we have detected highly specific binding sites in human but not rodent neural tissue. Regional assays of binding in human central nervous system homogenates demonstrate that binding sites are not confined to motoneurons. Rather, they are widely distributed throughout the human neuraxis. Particularly in the forebrain, binding is more abundant in gray than white matter. For this reason, we performed tissue fractionation studies which indicate that poliovirus binding sites are enriched in synaptosomes, the subfraction of central nervous system gray matter tissue rich in synaptic endings. The preferential expression of poliovirus binding sites in synaptic endings may be an important factor in the motor tropism of this virus, inasmuch as the major category of neurons with synaptic endings outside the central nervous system are motoneurons; thus, particles of virus may preferentially bind to this cell type during poliovirus viremia.
Electrophysiological dfierences between demented and nondemented patients with Parkinson's disease
Authors: Goodin Douglas S. , Aminoff Michael J. 
Published: January 2005

AbstractLong‐latency auditory evoked potentials were studied in demented and nondemented patients with Parkinson's disease who were matched for age, stage of disease, duration of illness, and amount and nature of antiparkinsonian medication. We found clear electrophysiological differences between the two groups of patients in that the N1, N2, and P3 peak latencies were prolonged in the demented group compared both to the nondemented group and to normal controls. Moreover, the N1 latency but not the N2 and P3 latency prolongation distinguished the demented parkinsonian patients from demented patients with Alzheimer's disease. These results provide strong evidence for the existence of different subtypes of dementia and suggest that electrophysiological recordings may be helpful in establishing the underlying pathogenesis of a dementia syndrome when there is clinical uncertainty.
Deficiency of a cholinergic differentiating factor in fibroblasts of patients with Alzheimer's disease
Authors: Kessler John A. 
Published: January 2005

AbstractSkin fibroblasts from patients with Alzheimer's disease and from apparently normal control subjects were compared for their production of a cholinergic differentiating factor. The factor's activity was assayed by measuring the induction of choline acetltransferase (CAT) activity in cultured sympathetic neurons. Culture medium conditioned by exposure to normal human fibroblasts induced substantial levles of CAT activity in sympathetic neurons, indicating that human fibroblasts produce a soluble factor that promotes cholinergic expression. In contrast, medium conditioned by Alzheimer fibroblasts induced only about one‐third as much CAT activity, a highly significant reduction (p < 0.01). These observations suggest that Alzheimer fibroblasts may be deficient in their secretion of a cholinergic factor and raise the possibility that the pathophysiology of the disease is related to a defect in the release of this factor. The fibroblast abnormalities suggest that Alzheimer's disease may be a systemic disease involving nonneuronal cells that are outside as well as within the brain.
Caloric‐induced nystagmus with isoelectric electroencephalogram
Authors: Nayyar Manmohan , Strobos Robert J. , Singh Brij M. , Brown‐Wagner Marie , Pucillo Anthony 
Published: January 2005

AbstractCaloric vestibular testing induced nystagmus in a patient with an isoelectric electroencephalogram after cardiopulmonary arrest. This has been demonstrated previously in patients in a chronic persistent vegetative state with intact brainstem reflexes, but never in a patient with an isoelectric electroencephalogram. Animal studies indicate that the quick phase of nystagmus and horizontal saccades are generated in the paramedian pontine reticular formation. The present case supports the conclusion that caloric‐induced nystagmus originates in the brainstem in rudimentary form.
Chronic inflammatory demyelinating polyradiculoneuropathy associated with pregnancy
Authors: McCombe P. A. , McManis P. G. , Frith J. A. , Pollard J. D. , McLeod J. G. 
Published: January 2005

AbstractIn a series of 61 patients with the relapsing variety of chronic inflammatory demyelinating polyneuropathy, there were 16 women of childbearing age, 9 of whom became pregnant. In 4 of these women, the onset of neuropathy occurred in pregnancy and in the other 5 relapses occurred during pregnancy. These was a significant increase in the number of relapses during the year of pregnancy, and a tendency for symptoms to worsen during the third trimester or immediate postpartum period. It is concluded that there is an increased risk of relapse of chronic inflammatory demyelinating polyneuropathy in pregnancy.
Whipple's disease confined to the central nervous system
Authors: Adams Melanie , Rhyner Patricia A. , Day John , DeArmond Stephen , Smuckler Edward A. 
Published: January 2005

AbstractProgressive hypersomnia, memory disturbance, and vertical ophthalmoplegia developed in a 63‐year‐old woman. The diagnosis of Whipple's disease of the central nervous system was suggested by her presentation and results of studies using magnetic resonance imaging. Despite a one‐month course of antibiotics, active Whipple's disease, localized to the central nervous system, was found at autopsy.
Chronic progressive myelopathy associated with elevated antibodies to human T‐lymphotropic virus type I and adult T‐cell leukemialike cells
Authors: Osame Mitsuhiro , Matsumoto Makoto , Usuku Koichiro , Izumo Shuji , Ijichi Naomi , Amitani Hiroyoko , Tara Mitsutoshi , Igata Akihiro 
Published: January 2005

AbstractSix adult patients had a chronic progressive myelopathy that possessed the following features: (1) high antibody titers to human T‐lymphotropic virus type I (HTLV‐I) in serum and cerebrospinal fluid (CSF); (2) predominantly upper motor neuron disorder, symmetrical, with mild sensory and bladder disturbances; and (3) presence of adult T‐cell leukemia–like cells in both peripheral blood and CSF. We refer to this entity as HTLV‐I–associated myelopathy (HAM). Electrophoretic studies of immunoglobulin G in CSF using Western blot analysis characteristically demonstrated p24 and p32 bands. Rates of intra‐blood–brain barrier synthesis were determined and found increased in the patients with HAM. Corticosteroid treatment produced clinical improvement in all of 4 patients. A retrospective survey of CSF samples was carried out in 287 patients with neurological disorders, and 6 additional patients with HAM were identified.
Sardinia, a high‐risk area for multiple sclerosis: A prevalence and incidence study in the district of alghero
Authors: Rosati Giulio , Aiello Isidoro , Pirastru Maria I. , Mannu Luisella , Demontis Giuseppe , Becciu Sebastiano , Sau Gianfranco , Zoccheddu Alberto 
Published: January 2005

AbstractFindings from small descriptive studies carried out in the last few years in Sardinia suggest that this region is now of high rather than medium risk for multiple sclerosis. It is uncertain whether this high prevalence reflects a different approach in case finding over time or a true change in disease occurrence. We report the results of a prevalence and incidence survey conducted in the district of Alghero, a community of 78,000 people in northwest Sardinia. Based on data from 31 patients, the average annual incidence for the period 1971 through 1980 was 4.1 per 100,000. On December 31, 1980, the prevalence rate was 59 per 100,000. The results support the view that Sardinia is now a high‐risk area for multiple sclerosis, and further suggest a rise in the occurrence of the disease in recent years.
Generation of human B‐cell hybridomas secreting monoclonal anti–myelin‐associated glycoprotein antibodies from a patient with neuropathy
Authors: Spatz Linda , Lieberson Becky , Abraham Judith , Miller Orlando J. , Miller Dorothy A. , Latov Norman 
Published: January 2005

AbstractHuman hybridomas that secrete monoclonal IgM anti–myelin‐associated glycoprotein antibodies were generated by fusion with cells from a patient with peripheral neuropathy and IgM monoclonal gammopathy. Karyotypic analysis of the hybridoma cells revealed no chromosomal abnormalities. The cells were positive for cell‐surface idiotype HLA‐DR and the plasma cell antigen PCA‐1, and negative for the B‐cell determinant B4 and for Leu‐1, which has been postulated to distinguish a subpopulation of B cells that secrete IgM with autoantibody activity.
The effect of spontaneous reperfusion on metabolic function in early human cerebral infarcts
Authors: Hakim A. M. , Pokrupa R. P. , Villanueva J. , Diksic M. , Evans A. C. , Thompson C. J. , Meyer E. , Yamamoto Y. L. , Feindel W. H. 
Published: January 2005

AbstractTwelve patients were studied within 48 hours of stroke using positron emission tomography to determine cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), oxygen extraction fraction, cerebral blood volume, cerebral pH (CpH), and cerebral metabolic rate for glucose (CMRGlc), the last calculated using published normal rate constants (CMRGlc[N]) and those for severe ischemia. In these studies, a cortical region of severe ischemia (I) was outlined, its metabolic and perfusion properties evaluated, and its length measured. The contralateral uninvolved cortical rim (C) in these patients and the cortical rim in 5 older normal patients were used for comparison. The length of region I correlated with the neurological deficit measured independently by a clinical scoring method. The 12 patients fell into two groups: Group I (8 patients), whose CBF in I was 9.3 ± 2.5 ml/100 gm/min (mean ± SEM) and was in every patient lower than that in C (33.1 ± 2.2), and Group 2 (4 patients), whose CBF in I was 42.1 ± 8.5 ml/100 gm/min and was in every case higher than that in C (28.2 ± 1.5). In Group I, region I showed a CMRGlc(N)/CMRo2 ratio of 0.22 ± 0.06 and a CpH of 6.83 ± 0.06. In Group 2, the same ratio in the region I was 0.58 ± 0.09 and the CpH was 7.12 ± 0.05. The CMRGlc (N)/CMRo2 ratio for the contralateral hemisphere was comparable in the two groups. Our data suggest that, within 48 hours of the clinical onset of stroke, the ischemic cortex is already reperfused in one third of patients. Those ischemic regions with persistent hypoperfusion appear acidotic, whereas in the reperfused regions, despite evidence of an increased CMRGlc/CMRo2 ratio, acidosis is not evident. The implications of these findings for therapies proposed in acute human cerebral ischemia are discussed.
Multiple sclerosis disease activity correlates with gadolinium‐enhanced magnetic resonance imaging
Authors: Gonzalez‐Scarano F. , Grossman Robert I. , Galetta Steve , Atlas Scott W. , Silberberg Donald H. 
Published: January 2005

AbstractMagnetic resonance imaging provides a method of visualizing multiple sclerosis plaques, but the age and activity of these plaques cannot be determined with routine magnetic resonance images. Gadolinium DTPA is a paramagnetic contrast agent that does not cross an intact blood–brain barrier. We studied 16 patients with multiple sclerosis, using magnetic resonance imaging, gadolinium‐enhanced magnetic resonance imaging, and computed tomographic scans. Gadolinium enhancement of multiple sclerosis plaques correlated with the clinical activity of the disease and corresponded anatomically with the symptoms and signs. We conclude that gadolinium enhancement of magnetic resonance images is a promising tool in the investigation of multiple sclerosis lesions and that it may provide a method for objective follow‐up in clinical trials.
Calcium channels and calcium channel antagonists
Authors: Greenberg David A. 
Published: January 2005

AbstractChanges in free intracellular Ca2+ levels provide signals that allow nerve and muscle cells to respond to a host of external stimuli. A major mechanism for elevating the level of intracellular Ca2+ is the influx of extracellular Ca2+ through voltage‐dependent channels in the cell membrane. Recent research has yielded new insights into the physiological properties, molecular structure, biochemical regulation, and functional heterogeneity of voltage‐dependent Ca2+ channels. In addition, Ca2+ channel antagonist drugs have been developed that are valuable both as probes of channel structure and function and as therapeutic agents. Preliminary evidence suggests that these drugs may be useful in the treatment of diverse neurological disorders, including headache, subarachnoid hemorrhage, stroke, and epilepsy.
Levodopa pharmacokinetic mechanisms and motor fluctuations in Parkinson's disease
Authors: Fabbrini G. , Juncos J. , Mouradian M. M. , Serrati C. , Chase T. N. 
Published: January 2005

AbstractThe contribution of the peripheral and central pharmacokinetic mechanisms of levodopa to the pathogenesis of the motor fluctuations that complicate its long‐term administration was studied in 28 parkinsonian patients. The rate of levodopa clearance from the general circulation, its plasma half‐life, and apparent volume of distribution were indistinguishable between patients with the on‐off or the wearing‐off phenomenon and those with a stable response to levodopa or those who had not been previously treated with levodopa. Peripheral pharmacokinetic factors are thus unlikely to account for the development of these response fluctuations. Conversely, the efficacy half‐time of levodopa differed markedly among the four response groups studied and may provide a quantitative index of central mechanisms that favor the development of the wearing‐off and on‐off phemonena. Although symptom duration was the best predictor of the severity of untreated parkinsonism, levodopa dose correlated best with response half‐time. The wearing‐off phenomenon may primarily reflect the loss of buffering capacity caused by degeneration of the dopamine neurons, while the development of the on‐off phenomenon appears to require additional postsynaptic changes, possibly at the receptor level.
Rett's syndrome: Characterization of respiratory patterns and sleep
Authors: Glaze Daniel G. , Frost James D. , Zoghbi Huda Y. , Percy Alan K. 
Published: January 2005

AbstractRett's syndrome is a progressive disorder that occurs in females and is characterized by autistic behavior, dementia, ataxia, loss of purposeful use of the hands, and seizures. Patients with Rett's syndrome have been observed to have stereotyped hand movements (hand‐washing) and to exhibit intermittent hyperventilation. To characterize more precisely the sleep and respiratory patterns associated with this disorder, polygraphic studies were made during sleep and wakefulness in 11 patients with this syndrome. These studies showed abnormal respiratory patterns during wakefulness, and abnormal sleep and electroencephalographic characteristics. The patients had decreased percentages of rapid‐eye‐movement sleep, and during wakefulness, a pattern of disorganized breathing was observed in all 11 patients and consisted of hypoxia followed by a period of increased respiratory rate and effort. The occurrence of disorganized breathing and compensatory hyperpnea during wakefulness with regular, continuous breathing during sleep is characteristic of Rett's syndrome and suggests an altered or impaired voluntary/behavioral respiratory control system.
Cerebral ptosis with contralateral arteriovenous malformation: A report of two cases
Authors: Lowenstein Daniel H. , Koch Thomas K. , Edwards Michael S. 
Published: January 2005

AbstractWe describe two patients with chronic unilateral ptosis and contralateral hemispheric arteriovenous malformations. Both patients were brought to our attention after a subacute or acute neurological deterioration. Analysis of prior photographs showed the ptosis progressed up to the time of presentation and significantly resolved following surgical removal of the arteriovenous malformation. The partially reversible and chronic nature of the ptosis in these two patients represents a particularly unusual form of cerebral ptosis.
Peptide‐containing nerve fibers in human cerebral arteries: Immunocytochemistry, radioimmunoassay and in vitro pharmacology
Authors: Edvinsson Lars , Ekman Rolf , Jansen Inger , Ottosson Anders , Uddman Rolf 
Published: January 2005

AbstractNerve fibers containing neuropeptide Y, vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin generelated peptide (CGRP) were seen in the adventitia or at the adventitia–media border of human cerebral arteries obtained during neurosurgical procedures Radioimmunoassay of human cerebral arteries, removed at autopsy, revealed that the levels of the four peptides did not differ among the major cerebral arteries. There was, however, a gradual decline in peptide concentrations with increasing age of the patients, as measured in the proximal part of the middle cerebral artery. Pharmacological experiments on fresh segments of cerebral (pial) arteries in vitro revealed that neuropeptide Y caused vasoconstriction per se but did not potentiate the contractile response of noradrenaline. VIP, peptide histidine methionine‐27 (PHM‐27), SP, neurokinin A (NKA), and human CGRP potently relaxed vessels precontracted by prostaglandin F2α, the relative potency being human CGRP ≥ SP ≥ VIP ≥ NKA ≥ PHM‐27. The amount of relaxation varied between 55% (SP) and 96% (human CGRP) of the prostaglandin F2α–induced contraction. The peptide effects were not antagonized by propranolol, atropine, or cimetidine, suggesting an action that does not involve adrenergic, cholinergic, or histaminergic receptors.
Neural cell adhesion molecule in normal, denervated, and myopathic human muscle
Authors: Cashman Neil R. , Covault Jonathan , Wollman Robert L. , Sanes Joshua R. 
Published: January 2005

AbstractThe neural cell adhesion molecule (N‐CAM) is a cell‐surface glycoprotein that may mediate some intercellular adhesive interactions in the nervous system. In adult rat muscle, N‐CAM is concentrated near neuromuscular junctions and on satellite cells, but is nearly undetectable in nonsynaptic portions of myofibers. However, N‐CAM is abundant throughout myofibers in denervated and regenerating muscles. Using affinity‐purified antibodies to N‐CAM, we were able to demonstrate a similar distribution and regulation of N‐CAM in human muscle. Myofiber N‐CAM was not detectable immunohistochemically in any of 10 normal biopsies or in 4 biopsies that were abnormal but showed no evidence of fiber denervation or regeneration. N‐CAM was present, however, at end plates, nerves, and satellite cells in normal human muscle. In contrast, myofiber N‐CAM was detected in 16 of 16 patients with histological evidence of denervation and in 10 of 10 patients who had myopathy with degenerating/regenerating myofibers. In addition, 2 of 2 histologically nondiagnostic biopsies from patients with amyotrophic lateral sclerosis contained N‐CAM–positive myofibers. Immunoblot analysis also detected N‐CAM in denervated and myopathic, but not normal, human muscle. These results suggest that N‐CAM may play a role in muscle reinnervation or regeneration and that N‐CAM immunohistochemistry may complement conventional techniques in the diagnosis of neuromuscular disease.
β‐Endorphin, ACTH, and catecholamine responses in chronic autonomic failure
Authors: Polinsky Ronald J. , Brown Robert T. , Lee Grace K. , Timmers Kim , Culman Juraj , Foldes Ondrej , Kopin Irwin J. , Recant Lillian 
Published: January 2005

AbstractPlasma epinephrine (EPI), norepinephrine (NE), β‐endrophin, and corticotropin (ACTH) responses were measured during insulin‐induced hypoglycemia in normal subjects and in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). In normal subjects, there was a striking rise in EPI, NE, β‐endorphin, and ACTH following the nadir of hypoglycemia. Both β‐endorphin and ACTH responses were significantly lower than normal in patients with MSA, in contrast to normal levels in IOH patients. No correlation was observed between the degree of adrenergic insufficiency and the β‐endorphin and ACTH responses. The normal peptide responses in IOH are consistent with involvement limited to the peripheral sympathetic nervous system, whereas lesions in the central nervous system in MSA interfere with release of β‐endorphin and ACTH in response to hypoglycemia. The strong correlation between β‐endorphin and ACTH levels is consistent with their common origin. Peripheral adrenergic activity is not essential for β‐endorphin and ACTH release in humans.