bluuebunny/crossref_metadata_2025_split huggingface dataset:
Site of penetrating brain lesions causing chronic acquired stuttering
Authors: Ludlow Christy L. , Rosenberg Jeanette , Salazar Andrés , Grafman Jordan , Smutok Mike 
Published: January 2005

AbstractTen subjects exhibited acquired stuttering that had persisted for 10 to 15 years following penetrating missile wounds sustained during the Vietnam War. None had a history of developmental or chronic adult stuttering. In comparison with other head‐injured subjects and normal control subjects, the subjects with acquired stuttering had significant deficits in skilled rapid hand movements and oral and speech movements, suggesting a motor control disorder. The identified brain lesions of the acquired stuttering group were on the right in 5 subjects, on the left in 4, and bilateral in 1. The internal and external capsules, the frontal white matter, and the striatum were more frequently involved in the acquired stuttering group than in other head‐injured subjects (p ≤ 0.05). This speech rhythm and rate disorder was not associated with evident cortical lesions in either hemisphere but with predominantly unilateral lesions of the subcortical pyramidal and extrapyramidal systems.
Fixation‐off—sensitive epilepsy in eyelid myoclonia with absence seizures
Authors: Panayiotopoulos Chrysostomos P. 
Published: January 2005

AbstractFixation‐off—sensitive epilepsy is documented in a patient with eyelid myoclonia with absences. A series of simple electroencephalographic techniques showed that elimination of visual fixation is the actual stimulus for the eyelid myoclonus.
In vivo labeling of blood T cells: Rapid traffic into cerebrospinal fluid in multiple sclerosis
Authors: Hafler David A. , Weiner Howard L. 
Published: January 2005

AbstractMultiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS). In MS patients being treated with anti–T11, a murine monoclonal antibody which recognizes the sheep red blood cell receptor, it was found that peripheral blood T cells were labeled in vivo by the antibody. Furthermore, anti‐T11 did not lyse cells or enter the cerebrospinal fluid (CSF). In CSF specimens obtained by serial lumbar punctures from patients with progressive MS who received five daily infusions of anti‐T11, 70 ± 12% of the T cells had mouse antibody bound to their surface by 72 to 96 hours. No in vivo staining of CSF T cells was observed in patients infused with anti‐T4, a murine monoclonal antibody that was not found to label T cells in vivo. These results demonstrate that there is rapid movement of lymphocytes from the peripheral blood to the CNS in patients with progressive MS. This rapid trafficking of T cells suggests that the ongoing pathological process within the CNS may be closely linked to the peripheral immune system and may have implications for the monitoring and treatment of MS.
Mitochondrial hydroxyapatite deposits in spinocerebellar degeneration
Authors: Munoz D. G. , Emery E. S. , Highland R. A. 
Published: January 2005

AbstractWe report the presence of crystalline deposits of calcium hydroxyapatite in the mitochondria of 2 children with sporadic spinocerebellar degeneration. The deposits, identified by electron microscopy, were found in the mitochondria of neurons and smooth muscle cells in one patient and in only smooth muscle cells in the second child, but not in other cell types. The calcific nature of the deposits was confirmed by laser microprobe mass analysis. The calcium overload may interfere with mitochondrial function, as has been shown in the cardiomyopathic strain of the Syrian hamster, a model of the cardiomyopathy of Friedreich's ataxia.
Detection of varicella‐zoster virus nucleic acid in neurons of normal human thoracic ganglia
Authors: Gilden Donald H. , Rozenman Yaacov , Murray Ronald , Devlin Mary , Vafai Abbas 
Published: January 2005

AbstractTissue sections from four normal human thoracic ganglia were hybridized in situ with a varicella‐zoster virus—RNA probe. Varicella‐zoster virus was detected in two of four ganglia, localized exclusively in neurons. The detection of latent varicella‐zoster virus genetic material in thoracic ganglia provides further evidence of varicella‐zoster virus latency at multiple levels of the human neuraxis and supports the notion that the neuron is the primary site of herpesvirus latency.
Central motor conduction in motor neuron disease
Authors: Hugon J. , Lubeau M. , Tabaraud F. , Chazot F. , Vallat J. M. , Dumas M. 
Published: January 2005

AbstractCentral motor conduction was assessed in 13 patients with motor neuron disease and in 15 control subjects. All patients with motor neuron disease, even those without clinical pyramidal signs, had slowed central motor conduction, and in some the delays were asymmetrical. Evoked motor potentials represent a new and reliable method to detect physiological abnormalities of central motor pathways early in the course of motor neuron disease.
Mamillary body atrophy in Wernicke's encephalopathy: Antemortem identification using magnetic resonance imaging
Authors: Charness Michael E. , DeLaPaz Robert L. 
Published: January 2005

AbstractWe used magnetic resonance imaging to determine the volume of the mamillary bodies in 9 patients with chronic Wernicke's encephalopathy, 7 patients with presumed Alzheimer's disease, and 37 control patients. The mean mamillary body volume (± standard error) was 21.3 ± 5.8 mm3 in Wernicke patients, 40.1 ± 3.7 mm3 in Alzheimer patients, and 51.7 ± 2.5 mm3 in control patients. Seven of nine (78%) patients with chronic Wernicke's encephalopathy had smaller mamillary bodies than 36 of 37 control patients and 7 of 7 Alzheimer patients. The decrease in mamillary body volume was related neither to patient age nor to degree of ventricular enlargement, and most likely reflects the mamillary body atrophy that is grossly apparent at autopsy in up to 81% of Wernicke patients. This technique provides a means of identifying the most specific macroscopic lesion of chronic Wernicke's encephalopathy.
Functional anatomy of pentylenetetrazol and electroshock seizures in the rat brainstem
Authors: Miller John W. , McKeon Ann C. , Ferrendelli James A. 
Published: January 2005

AbstractThe ability of discrete brainstem injection of γ‐vinyl‐γ‐aminobutyric acid (GVG), an irreversible inhibitor of γ aminobutyric acid transaminase, to prevent pentylenetetrazol (PTZ) seizures and maximal electroshock seizures (MES) was studied and compared in rats. PTZ seizures were prevented by GVG injections in the anterior thalamus, the caudal hypothalamus, the superior colliculus, cerebellar nuclei, and in a large area of the medial medullary, pontine, and mesencephalic tegmentum encompassing the vestibular nuclei, the reticular formation, and portions of the central gray. GVG injections in the substantia nigra did not protect against PTZ seizures. In contrast, tonic hindlimb extension in MES was prevented consistently by injections in the substantia nigra. A minority of injections in the vestibular nuclei, cerebellar nuclei, and parts of the reticular formation also protected against tonic hindlimb extension of MES. These results indicate a striking difference in the functional anatomy of PTZ‐induced seizures and MES. PTZ seizures appear to be mediated by an extensive system involving the reticular formation, diencephalic regions in the vicinity of the anterior medial thalamus and caudal hypothalamus, and bulbar regions which give rise to descending motor pathways to the spinal cord. In contrast to PTZ seizures, MES appears to be mediated by a different neuroanatomical substrate with the present data implicating only the substantia nigra definitely in that process.
Alzheimer's disease and other dementing illnesses in a defined united states population: Incidence rates and clinical features
Authors: Schoenberg Bruce S. , Kokmen Emre , Okazaki Haruo 
Published: January 2005

AbstractIn this study, for the first time to our knowledge, all new cases of Alzheimer's disease and other dementing illnesses have been documented in a well‐defined United States community. A total of 178 patients in an average annual at‐risk population of 18,991 persons over age 29 developed dementia during 1960 through 1964 in Rochester, Minnesota, yielding an average annual incidence rate of 187.5 new cases/100,000/year. The corresponding rate for clinically and/or pathologically diagnosed Alzheimer's disease (the most common cause of dementia in this community) was 123.3 new cases/100,000/year, based on 117 cases. The incidence rates for both dementia in general and Alzheimer's disease in particular rise dramatically with age. All patients were followed to death or to 1982, and the median survival was 63 months. These data include only those in the community who came to medical attention, but they yield higher rates than studies in Scandinavia, indicating a relatively high level of case ascertainment.
Neurological syndrome following bilateral damage to the head of the caudate nuclei
Authors: Richfield Eric K. , Twyman Roy , Berent Stanley 
Published: January 2005

AbstractWe describe a persistent behavioral disorder associated with bilateral destruction of the head of the caudate nuclei. The findings in this case support a role for the caudate nuclei in behavioral functions and are interpreted in view of recent anatomical and physiological information on the connections of the caudate nuclei with the prefrontal cortex.
Treatment of chiasmatic/hypothalamic gliomas of childhood with chemotherapy: An update
Authors: Packer Roger J. , Sutton Leslie N. , Bilaniuk Larissa T. , Radcliffe Jerilynn , Rosenstock Jeffrey G. , Siegel Kathy R. , Bunin Greta R. , Savino Peter J. , Bruce Derek A. , Schut Luis 
Published: January 2005

AbstractChiasmatic/hypothalamic gliomas (CHG) of childhood may cause progressive neurological and visual deterioration. Radiotherapy results in at least transient stabilization of tumor growth in most patients but may also have adverse long‐term effects, especially in young children. Since 1977, children with progressive CHG under 5 years of age at diagnosis have been treated with combination chemotherapy (actinomycin D and vincristine) without radiotherapy. Twentyfour patients, a median of 1.6 years of age at diagnosis, have been treated and followed for a median of 4.3 years (range, 0.3–10 years). All patients are alive. Nine have developed radiographic or clinical progression, occurring a median of 3 years (range, 2–6.5 years) after initiation of treatment. Fifteen of 24 (62.5%) have remained free of progressive disease and have received no other therapy. Tumor shrinkage was documented in 9 of 24 patients but did not clearly relate to long‐term outcome. Full‐scale intelligence quotient (IQ) obtained a median of 3.5 years after diagnosis in patients who received only chemotherapy was a mean of 103 (range 84–133). We conclude that chemotherapy can significantly delay the need for radiotherapy in children with CHG and such a delay may be beneficial regarding long‐term outcome.
Selective brainstem injury in an asphyxiated newborn
Authors: Roland Elke H. , Hill Alan , Norman Margaret G. , Flodmark Olof , MacNab Andrew J. 
Published: January 2005

AbstractWe report the clinical, radiological, and neuropathological features of selective brainstem injury in an asphyxiated term infant. Disproportionate injury to thalamus, basal ganglia, and brainstem with relative sparing of cortex and subcortical white matter is observed occasionally after acute total asphyxia. Although this entity has been well documented neuropathologically, the specific computed tomographic findings have not been reported previously to our knowledge, and the clinical correlation is recognized rarely.
Evidence that amphetamine with physical therapy promotes recovery of motor function in stroke patients
Authors: Crisostomo Edgardo A. , Duncan Pamela W. , Propst Martha , Dawson Deborah V. , Davis James N. 
Published: January 2005

AbstractWe conducted a double‐blind pilot study of 8 patients with established cerebral infarction to evaluate the effect of a single dose of amphetamine on recovery of motor function using the Fugl‐Meyer scale. Four patients received amphetamine; the rest were given placebo. All underwent a session of physical therapy. Patients treated with amphetamine obtained greater increments in motor scores than the controls. Along with animal studies, these findings may allow the development of a pharmacological approach to stroke rehabilitation.
Acquired ocular motor apraxia due to bilateral frontopariental infarcts
Authors: Pierrot‐Deseilligny Charles , Gautier Jean‐Claude , Loron Philippe 
Published: January 2005

AbstractA case of acquired ocular motor apraxia in a 78‐year‐old man is reported. Disordered saccades and pursuit movements in the horizontal and vertical planes were recorded electro‐oculographically. Magnetic resonance imaging showed bilateral border‐zone infarcts, involving the frontal lobes and the superior part of the inferior pariental lobules.
Cerebellar and brainstem hypometabolism in olivopontocerebellar atrophy detected with positron emission tomography
Authors: Gilman Sid , Markel Dorene S. , Koeppe Robert A. , Junck Larry , Kluin Karen J. , Gebarski Stephen S. , Hichwa Richard D. 
Published: January 2005

AbstractWe studied local cerebral metabolic rates for glucose (lCMRglc) with 18F‐2‐fluoro‐2‐deoxy‐D‐glucose and positron emission tomography (PET) in 30 patients with olivopontocerebellar atrophy (OPCA) and 30 age‐matched control subjects without neurological disease. The diagnosis of OPCA was based on the history and physical findings and on the exclusion of other causes of cerebellar ataxia by means of laboratory investigations. Computed tomographic scans revealed some degree of atrophy of the cerebellum in most patients with OPCA, and many also had atrophy of the brainstem. PET studies in these patients revealed significant hypometabolism in the cerebellar hemispheres, cerebellar vermis, and brainstem in comparison with the normal control subjects. A significant relationship was found between the degree of atrophy and the level of lCMRglc in the cerebellum and brainstem. Nevertheless, several patients had minimal atrophy and substantially reduced lCMRglc, suggesting that atrophy does not fully account for the finding of hypometabolism, lCMRglc was within normal limits for the thalamus and cerebral cortex. The data suggest that PET/lCMRglc may be useful as a diagnostic test in patients with the adult onset of cerebellar ataxia.
Mu‐opiate receptors measured by positron emission tomography are increased in temporal lobe epilepsy
Authors: Frost J. James , Mayberg Helen S. , Fisher Robert S. , Douglass Kenneth H. , Dannals Robert F. , Links Jonathan M. , Wilson Alan A. , Ravert Hayden T. , Rosenbaum Arthur E. , Snyder Solomon H. , Wagner Henry N. 
Published: January 2005

AbstractNeurochemical studies in animal models of epilepsy have demonstrated the importance of multiple neurotransmitters and their receptors in mediating seizures. The role of opiate receptors and endogenous opioid peptides in seizure mechanisms is well developed and is the basis for measuring opiate receptors in patients with epilepsy. Patients with complex partial seizures due to unilateral temporal seizure foci were studied by positron emission tomography using 11C‐carfentanil to measure mu‐opiate receptors and 18F‐fluoro‐deoxy‐D‐glucose to measure glucose utilization. Opiate receptor binding is greater in the temporal neocortex on the side of the electrical focus than on the opposite side. Modeling studies indicate that the increase in binding is due to an increase in affinity or the number of unoccupied receptors. No significant asymmetry of 11C‐carfentanil binding was detected in the amygdala or hippocampus. Glucose utilization correlated inversely with 11C‐carfentanil binding in the temporal neocortex. Increased opiate receptors in the temporal neocortex may represent a tonic anticonvulsant system that limits the spread of electrical activity from other temporal lobe structures.
Measurement of immunoreactive myelin basic protein peptide (45–89) in cerebrospinal fluid
Authors: Gupta Manjula K. , Whitaker John N. , Johnson Claire , Goren Hershel 
Published: January 2005

AbstractTo measure myelin basic protein (MBP)‐like material in cerebrospinal fluid, we compared two radioimmunoassays, both using the same antiserum to MBP but one using peptide (45‐89) as the radioligand and standard (peptide assay), and the other using purified MBP as the radioligand and standard (MBP assay), with respect to their diagnostic sensitivity. Cerebrospinal fluid specimens from 185 patients with definite multiple sclerosis (MS) (n = 27), possible MS (n = 63), probable MS (n = 24), and other neurological disease (n = 71) were analyzed using both assays. The diagnostic sensitivity of the peptide assay was significantly better than that of the MBP assay in those with definite MS (sensitivity 59% and 30%, respectively); there was no significant difference in specificity. The peptide assay also showed better correlation with disease activity than the MBP assay: 14 patients classified as having active MS showed significantly higher sensitivity (78.6% versus 38%, p < 0.04) when compared to patients with inactive disease. The MBP assay showed no significant difference between these two groups. Besides the increase in sensitivity, the actual molar concentrations of immunoreactive MBP detected using this peptide assay were considerably higher than those found using the MBP assay. These results show that the use of MBP antisera capable of recognizing epitopes present in the carboxyl half of MBP peptide (45–89) results in more sensitive detection of immunoreactive MBP when used with MBP peptide (45–89) as radiolabeled ligand in the assay.
Uveomeningoencephalitis in a human immunodeficiency virus type 2—seropositive patient
Authors: Hormigo Adília , Bravo‐Marques J. M. , Souza‐Ramalho P. , Pimentel J. , Teixeira Carmo , Martins Rui 
Published: January 2005

AbstractA 35‐year‐old woman developed longstanding uveitis and later a uveomeningoencephalitis of unknown origin and died of toxoplasmal brain abscesses. The presence of immunological impairment, human immunodeficiency virus type 2 (HIV‐2) seropositivity, and multinucleated cells in the brain led us to suspect neurotropic properties for HIV‐2 similar to those of HIV‐1.
Fatal adenovirus meningoencephalitis in a bone marrow transplant patient
Authors: Davis Daron , Henslee P. Jean , Markesbery William R. 
Published: January 2005

AbstractWe describe a bone marrow transplant patient with fatal subacute adenovirus meningoencephalitis, the first such patient reported. Neuropathological examination revealed unique, bilaterally symmetrical degeneration in the inferomedial temporal cortex, amygdaloid nuclei, hippocampi, hypothalamus, and some brainstem nuclei. Viral intranuclear inclusions were noted in these areas by light microscopy and confirmed by electron microscopy. Identification was authenticated by viral culture and the isolation of adenovirus from cerebral cortical tissues, and further confirmed by immunofluorescence and serological methods.
Plasmapheresis alleviates neuropathy accompanying IgM anti—Myelin‐Associated glycoprotein paraproteinemia
Authors: Haas David C. , Tatum Arthur H. 
Published: January 2005

AbstractA patient with peripheral neuropathy accompanying a benign IgM anti—myelin‐associated glycoprotein paraproteinemia has been treated successfully by plasmapheresis for over a year, and during this time, fluctuations in the patient's symptoms and signs have correlated with variations in the serum IgM level. These results suggest that plasmapheresis may be more beneficial for such neuropathies than indicated previously, and they add to the evidence implicating the paraprotein as the cause of the neuropathy.
Suppression of experimental autoimmune neuritis by the oxygen radical scavengers superoxide dismutase and catalase
Authors: Hartung Hans‐Peter , Schäfer Bärbel , Heininger Kurt , Toyka Klaus V. 
Published: January 2005

AbstractMacrophages have been implicated in myelin damage in experimental autoimmune neuritis (EAN). We examined a possible pathogenetic role of toxic oxygen species elaborated by macrophages in EAN by administering oxygen radical scavengers. Early treatment of rats with either catalase or superoxide dismutase (10,000 U/kg/day) protected animals from the development of EAN. Treatment delayed until there was clinical manifestation of EAN (day 13) still markedly attenuated the severity of the disease, as evidenced by clinical assessment, electrophysiological studies, and morphological observation. In cell culture, macrophages from sham‐treated controls generated heightened oxidative metabolic responses indicating in vivo macrophage activation. Addition of catalase or superoxide dismutase abrogated or diminished chemiluminescence and production of reactive oxygen intermediates by macrophages ex vivo. Our findings underscore the importance of macrophages in EAN and provide evidence that, in this model, macrophagederived reactive oxygen intermediates contribute to damage of the myelin sheath.
Nervous system involvement in Fabry's disease: Clinicopathological and biochemical correlation
Authors: Kaye Edward M. , Kolodny Edwin H. , Logigian Eric L. , Ullman M. David 
Published: January 2005

AbstractA detailed neuropathological and biochemical study was performed to evaluate the accmulation of ceramide trihexoside within the central and peripheral nervous systems of 2 patients with Fabry's disease. Luxol fast blue–staining lipid was noted in the leptomeninges and in the choroidal stroma; biochemical studies showed increased quantities of ceramide trihexoside in the cerebrospinal fluid. The permeable blood‐brain barrier and blood‐nerve barrier regions of the central and peripheral nervous systems contained increased quantities of ceramide trihexoside. Some central nervous system nuclei associated with autonnomic function were also noted to store lipid. Other areas of increased ceramide trihexoside accumulation included specific cortical and brainstem structures. Possible sources for this selective accumulation of ceramide trihexoside within the central and peripheral nervous systems include transport of glycolipid from the systemic vascular network and retrograde transsynaptic glycolipid transport.
Complications of long‐term anticoagulation
Authors: Petty G. W. , Lennihan L. , Mohr J. P. , Hauser W. A. , Weitz J. , Owen J. , Towey C. 
Published: January 2005

AbstractWe used life‐table techniques to determine risks of morbidity and mortality associated with long‐term warfarin treatment in an anticoagulation clinic. Cumulative risks for life‐threatening complications and warfarin‐related death among all patients were 1% at 6 months, 5% at 1 year, and 7% at 2 and 3 years. Cox regression analysis using age as a continuous variable failed to show an effect of age on cumulative risks of complication. The occurrence of a minor complication during the course of therapy did not place patients at higher risk for developing a major complication that would prompt discontinuation of therapy or cause death. There was no statistically significant difference between the cumulative risks of patients anticoagulated for cerebrovascular disease and the cumulative risks of patients anticoagulated for other indications.