bluuebunny/crossref_metadata_2025_split huggingface dataset:
Absence of postoperative hyponatremia syndrome in young, healthy females
Authors: Wijdicks Eelco F. M. , Larson Timothy S. 
Published: January 2005

AbstractYoung and previously healthy females have been reported to develop severe postoperative hyponatremia with a fatal outcome. The clinical presentation is dramatic, with seizures, respiratory arrest, and permanent, often catastrophic, brain damage. The true incidence is unknown. We report a survey of 290,815 surgical procedures on females at the Mayo Clinic from 1976 to 1992. Postoperatively 1,498 females had cardiopulmonary arrest, 255 had a metabolic encephalopathy, 32 had new‐onset seizures, and 6 had central pontine myelinolysis. We failed to identify any association of respiratory arrest with postoperative hyponatremia. Our findings indicate that the postoperative hyponatremia syndrome in young, healthy females with respiratory arrest is extremely uncommon.
Neurological complications from fat emulsion therapy
Authors: Schulz Paul E. , Weiner Susan P. , Haber Leslie M. , Armstrong Dawna D. , Fishman Marvin A. 
Published: January 2005

AbstractFat emulsion therapy is convenient for parenterally administering calories and essential fats. We report 2 children with neurological complications of fat emulsion therapy that arose before any systemic findings. The complications included focal and generalized seizures, weakness, and altered mental status. Biopsy and autopsy findings included cerebral endothelial and intravascular lipid deposition. Early recognition of fat emulsion therapy complications is essential as the neurological complications are potentially reversible with alteration of the parenteral diet.
Diagnosis of Epstein‐Barr virus–induced central nervous system infections by DNA amplification from cerebrospinal fluid
Authors: Landgren Magnus , Kyllerman Mårten , Bergström Tomas , Dotevall Leif , Ljungström Lars , Ricksten Anne 
Published: January 2005

AbstractA nested polymerase chain reaction was used for the detection of Epstein‐Barr virus DNA in 1 patient with encephalitis, and in 1 patient with myelitis. Epstein‐Barr virus DNA was detected in cerebrospinal fluid samples obtained at the onset of neurological symptoms in both patients, and serological findings indicated ongoing Epstein‐Barr virus infection. In the patient with encephalitis, herpes simplex virus type 1 DNA was transiently detected in the cerebrospinal fluid, while Epstein‐Barr virus DNA was still present on day 44 after admittance. Single‐photon emission computed tomography in this patient indicated a frontal bilateral hypoperfusion. The diagnostic value of polymerase chain reaction on cerebrospinal fluid and serum samples for Epstein‐Barr virus infections of the central nervous system is emphasized.
Course and outcome of acute cerebellar ataxia
Authors: Connolly Anne M. , Dodson W. Edwin , Prensky Arthur L. , Rust Robert S. 
Published: January 2005

AbstractWe report a study of 73 consecutive children with acute cerebellar ataxia, representing all of the children evaluated at St. Louis Children's Hospital during a 23‐year‐period to whom this diagnosis could appropriately be assigned. Twenty‐six percent had chickenpox, 52% had other illnesses that were presumed to be viral, and in 3% the ataxia was related to immunization. Nineteen percent had no definite prodrome. Sixty children were followed for 4 months or longer after onset of their ataxia (mean, 7.4 ± 6.0 years). Ninety‐one percent (55/60) of these, including all children with chickenpox, recovered completely from ataxia. Eighty‐nine percent (39/44) of the children with non‐varicella‐related ataxia recovered completely from the ataxia, a much better rate of recovery than what was found in prior large studies. One fifth of the children followed for more than 4 months experienced transient behavioral or intellectual difficulties, but only 5 of the 60 children demonstrated sustained learning problems. This study represents the largest reported series of acute cerebellar ataxia and the most complete characterization of the clinical features and outcome of this illness.
Monoclonal IgM antibodies to GM1 and asialo‐GM1 in chronic neuropathies cross‐react with Compylobacter jejuni lipopolysaccharides
Authors: Wirguin I. , Suturkova‐Milosevic Lj. , Della‐Latta P. , Fisher T. , Brown R. H. , Latov N. 
Published: January 2005

AbstractWe tested monoclonal IgM anti‐GM1 and asialo‐GM1 antibodies from 6 patients with chronic motor neuropathies for binding to lipopolysccharides (LPS) from three strains of Campylobacter jejuni. Four of the 6 patients showed strong reactivity with LPS from at least one of the three C. jejuni strains tested as shown by enzyme‐linked immunosorbent assay or western blot. Preabsorption with GM1 or asialo‐GM1, or blocking with cholera toxin, prevented antibody binding to LPS. These studies indicate that human anti‐GM1 or anti–asialo‐GM1 antibodies cross‐react with LPS from certain strains of C. jejuni, and that bacterial LPS might provide antigenic stimuli for the activation of B cells expressing anti‐GM1 antibodies.
Deletion in the CMT1A locus on chromosome 17p11.2 in hereditary neuropathy with liability to pressure palsies
Authors: Verhalle D. , Löfgren A. , Nelis E. , Dehaene I. , Theys P. , Lammens M. , Dom R. , Van Broeckhoven C. , Robberecht W. 
Published: January 2005

AbstractHereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disease of peripheral nerves, characterized by recurrent focal neuropathies often with an underlying asymptomatic polynuropathy. We report the clinical, electrophysiological, and histopathological findings in three families with HNPP and confirm the presence of a deletion on chromosome 17p11.2, including all the markers known to be duplicated in Charcot‐Marie‐Tooth disease type 1A. This deletion appears to be the underlying molecular deficit in this disease and provides additional evidence for the importance of this locus for peripheral nerve function.
Brain morphology in normal and dyslexic children: The influence of sex and age
Authors: Schultz Robert T. , Cho Nam K. , Staib Lawrence H. , Kier Leon E. , Fletcher Jack M. , Shaywitz Sally E. , Shankweiler Donald P. , Katz Len , Gore John C. , Duncan James S. , Shaywitz Bennett A. 
Published: January 2005

AbstractMorphometric magnetic resonance imaging techniques were used to compare the convolutional surface area of the planum temporale, temporal lobe volume and superior surface area, and an estimate of overall brain volume in a homogeneous sample of 17 dyslexic children (7 girls) and 14 nonimpaired children (7 girls). Substantial sex differences were apparent for all measured regions, with all the measurements in boys being significantly larger. Age, even within the narrow range employed here (7.5–9.7 years), was positively correlated with the size of each brain region. While initial analyses suggested smaller left hemisphere structures in dyslexics compared to control subjects, subsequent analyses controlling for age and overall brain size revealed no significant differences between dyslexics and nonimpaired children on a variety of measures, in particular surface area and symmetry of the planum temporale. We suggest that differences in subject characteristics (i.e., sex, age, handedness, and definition of dyslexia) as well as procedural variations in the methods used to acquire images and to define and measure anatomical regions of interest such as the planum temporale all may play an important role in explaining apparent discrepant results in the neuroimaging literature on dyslexia.
Seizure exacerbation and status epileptics related to carbamazepine‐10,11‐epoxide
Authors: So Elson L. , Ruggles Kevin H. , Cascino Gregory D. , Ahmann Peter A. , Weatherford Karen W. 
Published: January 2005

AbstractOver a 3‐year period, we encountered 6 adults whose seizure control unexpectedly deteriorated with the occurrence of partial status epilepticus and daily multiple seizures. Analysis of the case histories and subsequent clinical follow‐up for 1 1/2 to 3 years disclosed the following evidence that demonstrates the role of carbamazepine‐epoxide in the development of the seizure exacerbation: (1) There were high serum carbamazepine‐epoxide concentrations while serum carbamazepine concentrations were lower than or the same as baseline levels; (2) all patients were taking drugs that are known to increase serum carbamazepine‐epoxide concentrations; (3) status epilepticus failed to respond to intravenous phenytoin loading; (4) seizure exacerbation in all patients was corrected by withholding carbamazepine dose; (5) seizure exacerbation recurred in 1 patient who resumed the same dose of carbamazepine; and (6) there were no prior status epilepticus or daily multiple seizures despite previous toxicities with other antiepileptic drugs in 3 patients. Our experience shows that inconspicuous elevation of carbamazepine‐epoxide levels during polytherapy may precipitate a distinct state of drug toxicity characterized by severe exacerbation of seizures. Mental retardation may be a predisposition to this condition.
Parceling of mesial frontal motor areas during ideation and movement using functional magnetic resonance imaging at 1.5 tesla
Authors: Tyszka J. M. , Grafton S. T. , Chew W. , Woods R. P. , Colletti P. M. 
Published: January 2005

AbstractFinger movement–related responses were identified in there discrete sites of mesial frontal cortex in 7 normal subjects using high resolution functional magnetic resonance imaging. During imagination of the same movements there was a differential response with rostral areas more active than caudal areas. Humans have multiple motor areas in mesial frontal cortex that subserve different functions in motor planning and execution.
Treatment of Guillain‐Barré syndrome with high‐dose immune globulins combined with methylprednisolone: A pilot study
Authors:   The Dutch Guillain‐Barré Study Group
Published: January 2005

AbstractIn an open study 25 patients with Guillain‐Barré syndrome were treated for 5 days with intravenous immune globulins in a dose of 0.4 gm/kg of body weight/day and 0.5 gm of methylprednisolone intravenously per day. The results of this combined treatment were compared with the results from a group of 74 patients who were treated with immune globulins only in a recent Dutch Guillain‐Barré trial. In the methylprednisolone–immune globulin treatment group, 19 of 25 patients (76%) improved by one or more functional grades after 4 weeks, as compared with 39 (53%) of 74 patients treated with immune globulin alone (p = 0.04). Also the median time required to the stage of walking independently was reduced in the methylprednisolone–immune globulin treatment group. This pilot study suggests that combined treatment with methylprednisolone and immune globulins in patients with the Guillain‐Barré syndrome is more effective than treatment with immune globulins alone; a randomized clinical trial might confirm this.
Cerebrospinal fluid human immunodeficiency virus type 1 (HIV‐1) p24 antigen levels in HIV‐1–related dementia
Authors: Royal W. , Selnes O. A. , Concha M. , Nance‐Sproson T. E. , McArthur J. C. 
Published: January 2005

AbstractHuman immunodeficiency virus type 1 (HIV‐1) p24 antigen, a putative marker of virus load, was assayed in 79 blood and 83 cerebrospinal fluid (CSF) samples from 90 HIV‐1–seropositive individuals with or without demetia. Twenty‐eight subjects had no evidence of neuropsychological impairment, 17 had mild impairment without objective evidence of dementia, and 45 were demented. HIV‐1 p24 antigen was detected more frequently in CSF samples from demented (19/40) than normal (1/26) or mildly impaired (1/17) subjects and in 67% of individuals with significant dementia (MSK stages 2–4). p24 Antigen was detected less frequently in CSF from demented subjects on antiretroviral drugs than untreated demented individuals. Overall, the sensitivity of the antigen capture assay in CSF among demented individuals was 47.5%; the specificity, 95.0%; positive predictive value, 90.4%; negative predictive value, 66.1%; and the efficieny, 72.2%. A direct relationship was also noted between the degree of congnitive impairment and blood p24 antigen detection frequency and antigen concentration. CD4+ blood lymphocyte counts were lower for demented individuals, and HIV‐1 p24 antigen was detected more frequently and p24 antigen concentration was higher in blood and CSF from individuals with low CD4+ blood lymphocyte counts. β2‐Microglobulin levels were higher in CSF from demented subjects and correlated directly with CSF p24 antigen concentration. However, in contrast to CD4+ blood lymphocyte counts and β2‐microglobulin levels, only p24 antigen concentration correlated with dementia severity. Therefore, p24 antigen can be a useful marker for dementia related to HIV‐1 infection.
Cognitive functions and quality of life in patients with low‐grade gliomas: The impact of radiotherapy
Authors: Taphoorn M. J. B. , Schiphorst A. Klein , Snoek F. J. , Lindeboom J. , Wolbers J. G. , Karim A. B. M. F. , Huijgens P. C. , Heimans J. J. 
Published: January 2005

AbstractThe role of early radiotherapy in the treatment of low‐grade gliomas is controversial. For this reason the impact of radiotherapy on quality of life was studied in long‐term survivors of biopsy‐proved low‐grade gliomas without signs of tumor recurrence. Twenty patients (age range, 18–66 years) had been treated with early radiotherapy; the other 21 patients (age range, 19–65 years) had undergone surgery or biopsy only. The interval from diagnosis to testing ranged from 1 to 12 years (mean, 3.5 years). Nineteen patients with low‐grade hematological malignancies, surviving 1 to 15 years without central nervous system involvement, served as control subjects. Apart from the neurological and functional status, the patients' cognitive, affective, and psychological status was determined. None of the survivors had significant neurological impairment and the Karnofsky index for them was at least 70. However, more specific examinations of cognitive functions and the affective status (Profile of Mood States) indicated that, compared to the control subjects, the patients with low‐grade gliomas had significantly more cognitive disturbances and suffered more frequently from fatigue and depressed moods. The two groups with low‐grade gliomas, on the other hand, did not differ significantly on any of these measures. It is concluded that radiotherapy did not cause these disturbances and had no negative impact on quality of life in these patients.
Pharmacological evaluation of the cholinergic system in progressive supranuclear palsy
Authors: Litvan I. , Blesa R. , Clark K. , Nichelli P. , Atack J. R. , Mouradian M. M. , Grafman J. , Chase T. N. 
Published: January 2005

AbstractSevere cholinergic loss occurs in the brains of patients with progressive supranuclear palsy. To evaluate the functional implications of this neuronal deficit, dose‐response curves were obtained in patients with progressive supranuclear palsy and normal control subjects undergoing intravenous cholinergic blockade (scopolamine) and stimulation (physo‐stigmine). Physostigmine had no significant neurobehavioral effects at any does in patients with progressive supranuclear palsy. Scopolamine, at low and medium doses, significantly impaired memory performance of both groups, but worsened the gait of only the patients. High‐dose scopolamine, which could not be tolerated by the patients, resulted in gait deterioration among control subjects. Thus, patients with progressive supranuclear palsy have increased sensitivity to cholinergic blockade compared to control subjects. Since loss of cholinergic neurons appears to contribute to the pathogenesis of certain cognitive and motor deficits found in progressive supranuclear palsy, the use of oral anticholinergics should ordinarily be avoided in this disorder. On the other hand, physostigmine at clinically tolerated dose levels seems to be terapeutically ineffective.
Use of proton magnetic resonance spectroscopy for monitoring disease progression in multiple sclerosis
Authors: Arnold Douglas L. , Riess Gerald T. , Matthews Paul M. , Francis Gordon S. , Collins D. Louis , Wolfson Christina , Antel Jack P. 
Published: January 2005

AbstractDecreases in brain N‐acetylasparatate are associated with neuronal loss or dysfunction. We report a longitudinal study in which changes in the N‐acetylaspartate to creatine resonance intensity ratio measured by brain proton magnetic resonance spectroscopy were used to follow the progression of brain pathology in 7 patients with multiple sclerosis over an 18‐month period. Four of the patients had a history of recurrent relapses and 3 had a secondary progressive course. All had clinical and magnetic resonance imaging evidence of persistent neurological abnormalaties. At 6‐month intervals proton magnetic resonance spectra were obtained and the N‐acetylaspartate–creatine ratio was determined for each patient. The volumes of hyperintense signal from lesions on conventional magnetic resonance images and the Kurtzke Expanded Disability Status Scale scores were determined concurrently. At the onset of the study, the N‐acetylaspartate–creatine ratio was significantly (p < 0.05) lower in the central brain volumes from the patients than in 13 normal control subjects. At 12 and 18 months of follow‐up, the ratio had decreased further in all patients (p < 0.05), consistent with progressive accumulation of neuronal damage. In contrast to magnetic resonance spectra data, changes in lesion volume on magnetic resonance images or disability status did not reach significance over this period. Subgroup analysis showed that changes (increases or decreases) in the N‐acetylaspartate–creatine ratio between consecutive 6‐month examinations correlated significantly (r = –0.74, p < 0.005) with changes in lesion volume on magnetic resonance images in patients with a history of relapses. This pilot study suggests that proton magnetic resonance spectroscopy may be useful in evaluating the progression of cerebral damage in multiple sclerosis using a novel quantitative index based on neuronal damage or dysfunction.
Leber's hereditary optic neuropathy mitochondrial DNA mutations in multiple sclerosis
Authors: Kellar‐Wood H. , Robertson N. , Govan G. G. , Compston D. A. S. , Harding A. E. 
Published: January 2005

AbstractThe observation of a multiple sclerosis (MS)–like illness in patients, particularly women, who carry the most common Lber's hereditary optic neuropathy mitochondrial DNA (mtDNA) mutation may indicate a contributory role for mitochondrial genes in genetic susceptibility to MS. We screened 307 unrelated MS patients, ascertained from population surveys, for the pathogenic Leber's hereditary optic neuropathy mutations at positions 11778 and 3460 of mt DNA, and also studied 20 patients with prominent and early optic nerve involvement. In addition, these 307 patients and 129 control subjects were investigated for the base change at position 13708, which has been suggested to paly a role in the pathogenesis of Leber's hereditary optic neuropathy. Neither of the pathogenic mtDNA mutations occured in the unselected MS patients. The 13708 base change was present in MS patients at a frequency similar to that in healthy control subjects. Three of the patients selected on the basis of severe optic nerve involvement had either the 11778 (one) or 3460 (two) mutations associated with Leber's herediatary optic neuropathy. All were women and none had affected relatives. We conclude that these mutations do not contribute to genetically determined susceptibility in typical MS patients, although a mitochondrial genetic component in the etiology of MS remains possible. A subgroup of MS patients, particularly females with severe bilateral visual failure due to optic neuropathy, may harbor a Leber's hereditary optic neuropathy mutation and we suggest that mtDNA analysis is appropriate in these patients.
Patterns of cerebral glucose metabolism detected with positron emission tomography differ in multiple system atrophy and olivopontocerebellar atrophy
Authors: Gilman Sid , Koeppe Robert A. , Junck Larry , Kluin Karen J. , Lohman Mary , St. Laurent Roy T. 
Published: January 2005

AbstractWe used positron emission tomography with [18F] fluorodeoxyglucose to study local cerebral metabolic rates for glucose (ICMRglc) in patients with multiple system atrophy (MSA), sporadic olivopontocerebellar atrophy (sOPCA), and dominantly inherited olivopontocerebellar atrophy (dOPCA) in comparison with normal control subjects. In MSA, absolute lCMRglc was significantly decreased in the brainstem, cerebellum, putamen, thalamus, and cerebral cortex. In sOPCA, absolute lCMRglc was significantly decreased in the brainstem, cerebellum, putamen, thalamus, and cerebral cortex. In dOPCA, absolute lCMRglc was significantly decreased in the brainstem and cerebellum but not in the other structures. Examination of lCMRglc normalized to the cerebral cortex in comparison with normal controls revealed in MSA significant decreases in the brainstem, cerebellum, and putamen but, in both sOPCA and dOPCA, significant decreases only in the brainstem and cerebellum. The findings indicate that these three disorders all show a marked decrease of lCMRglc in the brainstem and cerebellum but differ in the degree of hypometabolism in forebrain and cerebral cortical structures. The results are consistent with the possibility that, in many cases, sOPCA will evolve into MSA. Moreover, positron emission tomography may provide helpful diagnostic information in these neurodegenerative diseases.
Decreased tyrosine hydroxylase content in the dopaminergic neurons of MPTP–intoxicated monkeys: Effect of levodopa and GM1 ganglioside therapy
Authors: Kastner A. , Herrero M. T. , Hirsch E. C. , Guillen J. , Luquin M. R. , Javoy‐Agid F. , Obeso J. A. , Agid Y. 
Published: January 2005

AbstractParkinson's disease is characterized by the degeneration of melanized dopaminergic neurons of the substantia nigra. The functional capacity of the surviving dopaminergic neurons is affected, as suggested by the subnormal levels of tyrosine hydroxylase messenger RNA and protein found in the remaining cells. The reduced expression of tyrosine hydroxylase may be due to either the evolving neurodegenerative process or its downregulation, possibly secondary to chronic levodopa treatment. The cellular content of tyrosine hydroxylase was determined in the mesencephalon from 16 Macaca fascicularis monkeys, using a semiquantitative immunocytochemical method. Thirteen monkeys were rendered parkinsonian by weekly intravenous injections of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) for 2 (subacute treatment) or 20 (chronic treatment) weeks. Three of the monkeys received levodopa and 3 others received GM1 ganglioside. The loss of dopaminergic neurons in the mesencephalon of the MPTP‐intoxicated monkeys was severe in the substantia nigra, intermediate in cell groups A8 and A10, and almost undetectable in the central gray substance. After both subacute and chronic treatment, the cellular content of tyrosine hydroxylase was reduced by 40% in the surviving neurons of the lesioned substantia nigra, but by less in the other mesencephalic dopaminergic regions. Neuronal survival and tyrosine hydroxylase content in monkeys that had received levodopa were not significantly different. The cellular content of tyrosine hydroxylase was increased in the substantia nigra of the monkeys that received GM1 ganglioside injections. The results show that the decreased expression of tyrosine hydroxylase found in nigral dopaminergic neurons after partial degeneration of the mesostriatal dopaminergic system is not influenced by levodopa treatment and is partially reversed by GM1 ganglioside administration.