bluuebunny/crossref_metadata_2025_split huggingface dataset:
Imaging of human brain lesions with an ω3 site radioligand
Authors: Benavides JesùS , Cornu Philippe , Dennis Trevor , Dubois Alain , Hauw Jean‐Jacques , Mackenzie Eric T. , Sazdovitch Véronique , Scatton Bernard 
Published: January 2005

AbstractThe topography and magnitude of increase in peripheral type benzodiazepine binding sites (ω3 sites) was investigated autoradiographically in the brains of patients with ischemic cerebrovascular disease, with multiple sclerosis, and withj malignant glioma.3H‐PK 11195, a selective ω3 site ligand, was employed. A manyfold increase in ω3 site density was observed in all these disease states; this increase reflects macrophage invasion or glial proliferation or both as demonstrated by neuropathological studies carried out in parallel. There was an excellent spatial correlation between increased ω3 site densities and extent of the lesion histologically. Specifically, an elevated density of ω3 sites was observed in the plaques of demyelination in multiple sclerosis patients, in the periphery of infarcted zones in stroke patients, and throughout tumor in patients with grade IV astrocytomas. As our approach is applicable to both tomographic (in vivo) and autoradiographic investigations, imaging of ω3 sites may be considered for the detection and monitoring of the natural evolution of many disorders of the human central nervous system.
Stretch reflex dynamics in spastic elbow flexor muscles
Authors: Powers R. K. , Campbell D. L. , Rymer W. Z. 
Published: January 2005

AbstractPrevious studies of stretch reflexes in patients with spastic hypertonia have emphasized the dynamic character of stretch reflex output. In contrast, our own studies of stretch reflex dynamics in spastic elbow flexor muscles of 14 hemiparetic human subjects have shown that stretch‐evoked torque displays a relatively weak dependence on stretch velocity, and there is generally no preferential enhancement of dynamic as compared with static reflex output. Moreover, stretch reflex dynamics are broadly similar in voluntarily activated spastic and normal elbow flexor muscles. These findings support our hypothesis that spastic hypertonia results primarily from a decrease in stretch reflex threshold. The strong velocity dependence of stretch‐evoked electromyographic activity in initially inactive spastic muscles could be due to a decrease in reflex threshold with increasing stretch velocity, rather than an abnormal velocity‐dependent increase in stretch reflex responsiveness.
Patterns of serum IgM antibodies to GM1 and GD1a gangliosides in amyotrophic lateral sclerosis
Authors: Pestronk Alan , Adams Robert N. , Cornblath David , Kuncl Ralph W. , Drachman Daniel B. , Rn Lora Clawson 
Published: January 2005

AbstractWe studied the incidence and clinical correlates of serum antibodies to GM1 and GD1a gangliosides in patients with classical amyotrophic lateral sclerosis (ALS) and other “motor nerve” syndromes. Serum antibodies to GM1 and GD1a gangliosides were measured using enzyme‐linked immunosorbent assays. Our results showed that polyclonal immunoglobulin M (IgM) antibodies to the GM1 or GD1a ganglioside or both were present at serum dilutions of 1:25 to 1:4,000 in 78% (57/73) of patients with ALS. Only 8% of normal controls had similar antibodies. The pattern of serum antibody reactivity correlated with the pattern of clinical involvement in our patients. Selective reactivity to GDla ganglioside was common when upper motor neuron signs were prominent. IgM reactivity to GM1 ganglioside was common in ALS patients with prominent lower motor neuron signs. Most patients with motor neuropathies had serum reactivity to both GM1 and GDla gangliosides. These results provide further evidence of ongoing autoimmune processes in ALS patients. There is a strong relationship between serum antiganglioside antibodies and patterns of clinical involvement in ALS.
Central effects of drugs used in migraine prophylaxis evaluated by visual evoked potentials
Authors: Diener Hans‐Christoph , Scholz Erich , Dichgans Johannes , Gerber Wolf‐Dieter , Jäck Agnes , Bille Artur , Niederberger Uwe 
Published: January 2005

AbstractThe present study used recordings of visual potentials evoked by pattern reversal (VEPs) to investigate the central effects of three drugs used in migraine prophylaxis: the calcium channel blocker nifedipine, the beta‐1‐selective blocker metoprolol, and the nonselective beta adrenoreceptor blocker propranolol. The study involved 58 patients with common or classical migraine who were treated in a double‐blind randomized study over a period of 7 months, while the effectiveness of prophylactic treatment was recorded in headache diaries that were subjected to time series analysis. VEPs were recorded at the beginning of a 2‐month baseline period without treatment, after 4 months of treatment, and at the end of a 3‐month washout period. At baseline, migraine patients had significantly higher VEP amplitudes and longer latencies than did a group of 87 healthy control subjects. Patients were separated by statistical analysis into responders and nonresponders to each prophylactic treatment. Nifedipine had no effects on the frequency, intensity, and duration of migraine attacks, nor on amplitude and latency of the VEPs. In contrast, the use of beta blockers resulted in a significant decrease in VEP amplitude, both in responders and nonresponders, whereas VEP latency remained unchanged. VEP amplitudes returned to the initial values at follow‐up in the nonresponders, but stayed at lower levels in responders. Beta blockers thus appear to have a significant effect on the increased excitability of the visual system in patients with migraine, although their action is not directly related to their reduction of migraine frequency.
Positron tomography demonstrates frontal lobe hypometabolism in progressive supranuclear palsy
Authors: Goffinet A. M. , De Voider A. G. , Gillain C. , Rectem D. , Bol A. , Michel C. , Cogneau M. , Labar D. , Laterre C. 
Published: January 2005

AbstractA regional analysis of cerebral glucose metabolism was carried out in 9 patients with progressive supranuclear palsy by using positron emission tomography with fluorodeoxyglucose as the tracer. A consistent metabolic map of frontal hypometabolism was found in 7 patients. Brain metabolism was normal in 1 subject and diffusely decreased in another. In the 7 patients with selective hypofrontality, motor and premotor areas were severely hypometabolic, while heteromodal association cortex and paralimbic regions were comparatively less affected. Although this pattern of frontal alterations, probably due to disconnection, appeared consistent with the clinical features of the disease, it proved difficult to correlate the metabolic maps with neuropsychological disturbances.
Hypoxic‐ischemic spinal cord injury following perinatal asphyxia
Authors: Clancy Robert R. , Sladky John T. , Rorke Lucy B. 
Published: January 2005

AbstractThe role of spinal cord injury in the pathogenesis of abnormal motor signs (depressed tone and reflexes) following severe perinatal hypoxia‐ischemia was prospectively evaluated by clinical, electrophysiological, and neuropathological examinations in 18 asphyxiated neonates. All infants had an abnormal mental status (lethargy or coma), and seizures were present in 12. Neuromuscular examinations revealed hypotonia or flaccidity and hyporeflexia or areflexia in all infants. Neuropathological examinations of the cerebrum and spinal cord were conducted in the 12 neonates who expired. Cerebral pathological findings included cortical neuronal necrosis in 10 of 12 and subcortical white matter injury in 5 of 12. All infants with coma or seizures displayed diffuse cortical injury, but no injury conformed to a parasagittal “watershed” distribution. Spinal cord gray matter displayed prominent ischemic necrosis in 5 patients who were typically flaccid and areflexic. Electromyographic examinations of all 6 survivors were abnormal, consistent with recent injury to the lower motor neuron above the level of the dorsal root ganglion. We conclude that ischemic injury to anterior horn cells within spinal cord gray matter is relatively common among hypotonic‐hyporeflexic neonates following severe perinatal hypoxia‐ischemia. Although the acute neurological syndrome of neonatal asphyxia is often overshadowed by prominent cerebral signs such as coma and seizures, the motor abnormalities may be partially attributed to concurrent spinal cord injury.
Altered expression of genes for amyloid and cytoskeletal proteins in alzheimer cortex
Authors: Clark Arthur W. , Krekoski Craig A. , Parhad Irma M. , Liston Dane , Julien Jean‐Pierre , Hoar David I. 
Published: January 2005

AbstractRecent studies have indicated a normal gene dose for the amyloid precursor protein (APP) in Alzheimer's disease (AD). These findings leave open the possibility that elevated levels of messenger RNA (mRNA) for this protein may contribute to the pathogenesis of AD. Using Northern analysis, we compared the levels of mRNA for the APP and 3 cytoskeletal proteins in parietal cortex of 6 brains having marked AD‐type degeneration with the levels of these mRNAs in 6 control samples. The cytoskeletal mRNAs studied were those for the human neurofilament 68‐kDa subunit (HNFL), for α‐tubulin, and for glial fibrillary acidic protein (GFAP). A ribonuclease (RNase) protection assay was also used to compare AD and control HNFL mRNA levels. The mRNAs for APP, HNFL, and α‐tubulin were diminished in AD cortex. The decrement for APP mRNA was less than that for HNFL or α‐tubulin. The message for GFAP in AD cortex showed no loss. The findings support a general deficit in neuronal mRNAs, including that for APP. They do not exclude the possibility of elevated levels of the message for the APP in small neuronal subsets, in subcortical neurons projecting to cortex, or as a generalized phenomenon in earlier stages of the disease.
Early cerebellar degeneration in twins with infantile neuroaxonal dystrophy
Authors: Barlow John K. , Sims Katherine B. , Kolodny Edwin H. 
Published: January 2005

AbstractDizygotic twin girls with typical infantile neuroaxonal dystrophy (INAD) were studied at age 19 months with computed tomography and magnetic resonance imaging (MRI). Both methods showed distinct atrophy confined to the cerebellum and MRI revealed diffuse signal abnormality of the cerebellar parenchyma. This neuroimaging evidence for selective early involvement of the cerebellum is consistent with both the typical presenting symptoms and the gross pathological findings in the disorder. Neuroimaging may aid in differentiation of INAD from other neurodegenerative disorders with onset in late infancy, providing impetus for diagnostic biopsy and early genetic counseling.
Pathogenesis of dyskinesias in parkinson's disease
Authors: Mouradian M. M. , Heuser I. J. E. , Baronti F. , Fabbrini G. , Juncos J. L. , Chase T. N. 
Published: January 2005

AbstractAbnormal involuntary movements complicate the management of a majority of patients with advanced Parkinson's disease. The ability of levodopa to induce dyskinesias and alleviate parkinsonism has generally been considered a continuous dose‐dependent pharmacological spectrum. In this study, the acute dose‐response profile of intravenously administered levodopa for both inducing dyskinesia and alleviating parkinsonism, and its duration of action on these motor manifestations were evaluated in 52 parkinsonian patients. The minimum dose of levodopa required to produce mild dyskinetic movements was significantly lower in patients with fluctuations in motor response compared with those who had a stable response to standard oral therapy; the minimum dose for antiparkinsonian benefit, however, failed to show significant differences. The rate of disappearance of dyskinetic movements was faster than the rate of reappearance of parkinsonian signs following withdrawal of a steady‐state infusion of levodopa. The dissociation of the pharmacodynamic profile of the two major motor effects of levodopa suggests their mediation through two different central pharmacological mechanisms, perhaps involving the two classes of dopamine receptors or other transmitter systems, and could have important implications for the design of future antiparkinsonian agents.
Spinal cord and peripheral nerve pathology in AIDS: The roles of cytomegalovirus and human immunodeficiency virus
Authors: Grafe Marjorie R. , Wiley Clayton A. 
Published: January 2005

AbstractWe examined spinal cords, nerve roots, or peripheral nerves of 27 patients who died with acquired immunodeficiency syndrome (AIDS) for the presence of cytomegalovirus (CMV) and human immunodeficiency virus (HIV) by immunoperoxidase techniques in paraffin‐embedded tissue. Vacuolar myelopathy was seen in 8 of 26 spinal cords (31%) and microglial nodules were seen in 13 (50%). All of the patients with lateral column vacuolar myelopathy showed severe brain pathology. HIV antigens had been detected in the brains of 15 (55%) of the 27 patients but were detected in only 3 (11%) of 26 spinal cords and were not localized to regions of vacuolar myelopathy. This suggests that the vacuolar myelopathy may be due to a remote or indirect effect of HIV or other infectious agent. CMV antigens were detected in none of the patients who showed vacuolar myelopathy but were detected in 2 of the 13 with microglial nodules. Focal nerve root or peripheral nerve inflammation was seen in 7 patients; 4 had CMV antigens and none had HIV antigens. CMV appears to be an important cause of inflammatory peripheral neuropathy in AIDS patients.
Neuropathological abnormalities in developmental dysphasia
Authors: Cohen Morris , Campbell Rebecca , Yaghmai Farviar 
Published: January 2005

AbstractThe brain of a 7‐year‐old girl with developmental dysphasia who died of complications of infectious mononucleosis was examined grossly and histologically. The neuropathological studies revealed atypical symmetry of the plana temporale and a dysplastic gyrus on the inferior surface of the left frontal cortex along the inferior surface of the sylvian fissure. These anomalies are likely related to midgestation, the period of neuronal migration from the germinal matrix to the cerebral cortex, and are consistent with a neurodevelopmental cause of developmental dysphasia.
Postmortem analysis of adrenal–medulla–to–caudate autograft in a patient with parkinson's disease
Authors: Hurtig Howard , Joyce Jeffrey , Sladek John R. , Trojanowski John Q. 
Published: January 2005

AbstractA 53‐year‐old physician who had a 10‐year history of progressive idiopathic parkinsonism survived for 4 months after autologous adrenal‐medulla‐to‐right‐caudate autograft but he received little clinical benefit. A small number of chromaffin cells in the graft site survived; they expressed neurofilament proteins and chromogranin A, but scant tyrosine hydroxylase. The striatum on both sides showed almost complete loss of [3H]mazindol binding to dopamine‐uptake sites; the density of dopamine receptors was decreased adjacent to the transplant but increased rostral to the transplant. These results demonstrate that autografted chromaffin cells can survive for 4 months after transplantation and that related changes in dopamine receptors can be quantified.
Atherosclerosis: Current concepts on pathogenesis and interventional therapies
Authors: Yatsu Frank M. , Fisher Marc 
Published: January 2005

AbstractAtherosclerosis, the primary pathological condition accounting for most stroke syndromes, has been the intense focus of epidemiological, basic, and clinical investigations. Since these studies have direct bearing on the prevention of atherothrombotic brain infarction, this review emphasizes those advances in treatment resulting from their findings. The two most prominent theories on the pathogenesis of atherosclerosis relate to aberrations in lipoprotein metabolism and to enhanced proliferation of smooth muscle cells; likely, the theories are complementary. As a practical guideline for preventive therapy, the importance of using the total cholesterol level is stressed, although finer distinctions must rely on the low‐density and high‐density lipoprotein concentrations and their normalization. Since prevention of stroke may ultimately be its most effective therapy, consideration of cholesterol level, akin to strategies for preventing coronary heart disease, and efforts to avert platelet adhesion or aggregation and coagulation are warranted.
Cerebrospinal fluid content of diazepam binding inhibitor in chronic hepatic encephalopathy
Authors: Rothstein Jeffrey D. , McKhann Guy , Guarneri Patrizia , Barbaccia Maria Luisa , Guidotti Alessandro , Costa Erminio 
Published: January 2005

AbstractThe neuropeptide diazepam binding inhibitor (DBI) is an endogeneous allosteric modulator of gamma‐aminobutyric acid (GABA) receptors at the benzodiazepine recognition site. Recent theories on the neurochemical cause for hepatic encephalopathy have implicated activation of inhibitory neurotransmitter GABA systems. In 20 patients with hepatic disease, blood and cerebrospinal fluid (CSF) levels of ammonia and amino acids were measured. As in previous studies there was a selective elevation of CSF amino acids as well as a correlation between CSF glutamine levels and encephalopathy. CSF DBI levels were maximally elevated 5‐fold in patients with hepatic encephalopathy, but they were normal in those patients with liver disease not associated with changes in mental status and in patients with nonhepatic encephalopathy. Levels of DBI correlated with the clinical staging of hepatic encephalopathy. These data suggest that DBI may participate in the modulation of cerebral function in hepatic encephalopathy.
Residual ethylene oxide in hollow fiber hemodialysis units is neurotoxic in vitro
Authors: Windebank Anthony J. , Blexrud Marceil D. 
Published: January 2005

AbstractEthylene oxide gas is used to sterilize plastic medical equipment including capillary flow dialysis membranes. To test whether ethylene oxide ratained in the dialyzers might be neurotoxic, tissue culture medium was incubated in the blood compartment of dialyzers. Embryonic rat dorsal root ganglion neurons were then incubated in this medium for up to 5 days. During the first 24 hours axonal growth was normal. During the next 24‐hour period varicosities appeared on axons, and after 4 days neuron cell bodies died. The pattern of degeneration was identical to that observed when cultures were exposed to an atmosphere containing 1 ppm ethylene oxide gas. Culture medium introduced into dialyzers after routine prerinsing still caused degeneration, which was not completely abolished even by a 10‐liter rinse. When medium was exposed to identical dialyzers sterilized by gamma irradiation, no changes were seen in culture. Identical morphological changes were produced by using dialysis patient serum in the culture medium in place of the usual calf bovine serum. Such changes were never seen with control human serum. Since ethylene oxide is toxic to the human peripheral nervous system, it is proposed that ethylene oxide in dialyzers may contribute to the progressive neuropathy observed in patients on long‐term hemodialysis.
Evidence for a novel picornavirus in human dermatomyositis
Authors: Rosenberg Neil L. , Rotbart Harley A. , Abzug Mark J. , Ringel Steven P. , Levin Myron J. 
Published: January 2005

AbstractWe prepared RNA probes from cloned segments of human and murine enteroviruses (EVs) for in situ hybridization of skeletal muscle biopsies from patients with dermatomyositis (DM), polymyositis, other inflammatory myopathies, and noninflammatory muscle diseases, and from normal control subjects. A probe derived form Theiler's murine encephalomyelitis virus (TMEV) detected viral RNA within mononuclear cells of the interstitial connective tissue in 3 of 5 patients with adult‐onset DM. None of these patients showed positive hybridization to probes derived from human EVs (poliovirus type 1 and Coxsackei virus B3) applied to subjacent sections of the same biopsies. The remaining 2 adult DM patients, 4 patients with childhood‐onset DM, and 24 and non‐DM patients did not react with either TMEV or human entervirus probes. Histochemical stains for esterase and immunoperoxidase stains for Mac‐1 antigen in the 3 DM patients who reacted positively revelaed positive cells in the same distribution as, but in far greater number than, those positive by in situ hybridization. Immunoperoxides staining for HLA‐DR antigens revealed positive cells in the same distribution and number as were seen with the TMEV probe. We conclude that an EV‐like agent, more closely related to TMEV than to human EVs, may be associated with DM and that this agent is probably localized within muscle macrophages that express class II major histocompatibility complex antigens.
Abnormal pattern electroretinogram in Alzheimer's disease: Evidence for retinal ganglion cell degeneration?
Authors: Katz Barrett , Rimmer Steve , Iragui Vicente , Katzman Robert 
Published: January 2005

AbstractWe recorded pattern‐reversal electroretinograms, flash electroretinograms, pattern‐reversal visual evoked potentials, and flash visual evoked potentials in 6 patients with clinically diagnosed Alzheimer's disease and 6 age and sex matched control subjects. The mean amplitude of the pattern‐reversal electroretinogram in the Alzheimer patients was significantly less than that of the control group (p = 0.004). This anomaly of the pattern‐reversal electroretinogram may be a reflection of documented axonal depletion within the optic nerve and the degeneration of retinal ganglion cells seen in Alzheimer's disease. We found Alzheimer patients to have normal pattern‐reversal visual evoked potentials and flash electroretinograms, but a delayed second positive component of the flash visual evoked potential. This combination of findings may be of diagnostic import in Alzheimers disease.
Decreased glucose utilization in the striatum and frontal lobe in probable striatonigral degeneration
Authors: de Volder A. G. , Francart J. , Laterre C. , Dooms G. , Bol A. , Michel C. , Goffinet A. M. 
Published: January 2005

AbstractNine positron emission tomography studies of regional cerebral glucose metabolism were performed in 7 patients with probable striatonigral degeneration, a disorder characterized by parkinsonian features and absent or poor response to L‐dopa. When compared with values obtained in normal volunteers, mean cerebral glucose metabolism was slightly reduced in subjects with striatonigral degeneration who, in addition, had a marked (20.5%, ± 3 SD) relative hypometabolism in putaminal and caudate nuclei. Significant hypometabolism was also found in motor/premotor as well as in prefrontal cortex. In 2 subjects who were studied twice a deterioration of relative striatal metabolism paralleled clinical evolution. Magnetic resonance imaging disclosed the presence of abnormal iron deposits in the putamen in all cases but showed no cortical anomalies. These results suggest that positron emission tomography with [18F] fluorodeoxyglucose may provide an index of cell and processes degeneration in the striatum in striatonigral degeneration and is able to detect functional deficits in frontal cortex. The presence of striatal hypometabolism might be a predictor of a poor reponse to L‐dopa.
Antiphospholipid antibodies
Authors: Levine Steven R. , Welch K. M. A. 
Published: January 2005

AbstractLupus anticoagulants and anticardiolipin antibodies, known collectively as antiphospholipid antibodies, are becoming established as markers for increased risk of thrombosis, including ischemic cerebrovascular disease. In this brief review, we highlight evidence for an against a pathogenetic role of these antibodies in ischemic brain disease and comment on currently available laboratory studies to detect them. Future research on the association of antiphopholipid antibodies with nerological disease should focus on establishing the pathogenicity of these antibodies, identifying groups at high risk for recurrent ischemic cerebrovascular events, and initiating prospective multicenter natural history and treatment protocols.