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pubmedabstracts_2025

meta_pmid int64	meta_language string	meta_mesh_ids list	meta_mesh_terms list	meta_pubdate_year string	meta_pubdate_month string	text string
9,633,662	eng	[ "D000818", "D001419", "Q000302", "D015169", "D018857", "D006358", "D006863", "D008460", "Q000382", "D013552", "Q000382", "D013997" ]	[ "Animals", "Bacteria", "Colony Count, Microbial", "Food Packaging", "Hot Temperature", "Hydrogen-Ion Concentration", "Meat", "Swine", "Time Factors" ]	1998	Apr	Evaluation of the extent and type of bacterial contamination at different stages of processing of cooked ham. In an attempt to determine the composition and origin of the spoilage flora of refrigerated vacuum-packed cooked ham, the changes in microbial numbers and types were followed along the processing line. Results revealed Lactobacillus sake and Leuconostoc mesenteroides ssp. mesenteroides as the major causative agents of spoilage of sliced ham stored at 4 degrees C and 12 degrees C, due to recontamination in the cutting room. On the contrary, the progressive deterioration of whole ham under the same storage conditions was associated with a non-identifiable group of leuconostoc-like bacteria. Except for lactic acid bacteria, no other organism grew in vacuum packs of either sliced or whole ham. Although atypical leuconostocs could not be detected among isolates recovered from freshly produced whole ham, they appeared to survive cooking and proliferate during storage. Neither these organisms however, nor Lact. sake and Leuc. mesenteroides were important in curing and tumbling as carnobacteria, mainly Carnobacterium divergens, and Brochothrix thermosphacta dominated at this stage. A progressive inversion of the ham microflora from mostly Gram-negative at the beginning of processing to highly Gram-positive prior to cooking was noted. Listeria monocytogenes cross-contaminated ham during tumbling. However, the pathogen was always absent from the vacuum-packed product provided that heating to a core temperature of 70 degrees C occurred and recontamination during slicing and packing was prevented. The percentage distribution of different species of lactic acid bacteria as well as the uncommon phenotypic characteristics of some strains were discussed.
9,633,663	eng	[ "D000263", "Q000378", "D001426", "Q000378", "D001431", "D001433", "D001435", "D004926", "Q000201", "Q000302", "Q000821", "D008163", "D012475", "Q000201", "Q000302", "Q000821", "D012680", "D013997" ]	[ "Adenylate Kinase", "Bacterial Proteins", "Bacteriological Techniques", "Bacteriolysis", "Bacteriophages", "Escherichia coli", "Luminescent Measurements", "Salmonella", "Sensitivity and Specificity", "Time Factors" ]	1998	Apr	Specific assays for bacteria using phage mediated release of adenylate kinase. A sensitive and rapid assay method for the specific detection of bacteria was developed using Escherichia coli and Salmonella newport as the test organisms. Bacteriophages were used to provide specific lysis of the bacteria and then the release of cell contents was measured by ATP bioluminescence. Increased sensitivity was obtained by focusing on the bacteria's adenylate kinase (AK) as the cell marker instead of ATP as conventionally used. Fewer than 10(3) E. coli cells could be readily detected in less than 1 h. Salmonella newport assays, although as sensitive, were slower and took up to 2 h. The effects of the culture medium, the phage, and the presence of non-specific bacteria were examined.
9,633,664	eng	[ "D000391", "D000818", "D000881", "Q000382", "D001408", "Q000302", "D001431", "D018397", "Q000382", "D008855", "D009276", "D012988", "D013171", "Q000302" ]	[ "Air Microbiology", "Animals", "Anthrax", "Bacillus anthracis", "Bacteriological Techniques", "Equidae", "Microscopy, Electron, Scanning", "Namibia", "Soil Microbiology", "Spores, Bacterial" ]	1998	Apr	Airborne movement of anthrax spores from carcass sites in the Etosha National Park, Namibia. Tests for airborne movement of anthrax spores downwind from three heavily contaminated carcass sites were carried out under a range of wind conditions. Anthrax spores were detected in just three of 43 cyclone or gelatin filter air samples taken at distances of 6, 12 and 18 m from the sites. In addition, nine positives resulted during sampling sessions in which the site was mechanically disturbed, with a further five positives being found in sessions subsequent to those in which the site had been disturbed. The three positive samples not related to man-made disturbance were associated with the highest winds experienced during the study. Despite colony counts exceeding 100 on the culture plates in three instances, calculations showed that these represented very low worst case probable spore inhalation rates for animals or humans exposed to such levels. The low number of positives, the clear pattern of rapidly declining numbers of anthrax spores with distance downwind from the centres of the sites apparent on settle plates, and the persisting levels of contamination despite wind and rain, collectively suggest that the anthrax spores were associated with fairly heavy particles, although this was not seen by electron microscopy on soil samples from the sites. Overall, the findings are interpreted as indicating that it is very unlikely that Etosha animals contract anthrax by the inhalation route while simply in transit near or across a carcass site. The significance of the observations in relation to weather conditions in the Etosha, other studies on particulate aerosols in the region, and reports of long-distance airborne movement of microbes, is discussed.
9,633,665	eng	[ "D000818", "D001426", "Q000032", "D002417", "D015169", "D004591", "D019453", "Q000737", "Q000254", "Q000302", "Q000502", "D006360", "Q000032", "D018869", "D015151", "D008460", "Q000382", "D013696", "D013997" ]	[ "Animals", "Bacterial Proteins", "Cattle", "Colony Count, Microbial", "Electrophoresis, Polyacrylamide Gel", "Escherichia coli O157", "Heat-Shock Proteins", "Heat-Shock Response", "Immunoblotting", "Meat", "Temperature", "Time Factors" ]	1998	Apr	Heat shock and thermotolerance of Escherichia coli O157:H7 in a model beef gravy system and ground beef. Duplicate beef gravy or ground beef samples inoculated with a suspension of a four-strain cocktail of Escherichia coli O157:H7 were subjected to sublethal heating at 46 degrees C for 15-30 min, and then heated to a final internal temperature of 60 degrees C. Survivor curves were fitted using a linear model that incorporated a lag period (TL), and D-values and 'time to a 4D inactivation' (T4D) were calculated. Heat-shocking allowed the organism to survive longer than non-heat-shocked cells; the T4D values at 60 degrees C increased 1.56- and 1.50-fold in beef gravy and ground beef, respectively. In ground beef stored at 4 degrees C, thermotolerance was lost after storage for 14 h. However, heat-shocked cells appeared to maintain their thermotolerance for at least 24 h in ground beef held to 15 or 28 degrees C. A 25 min heat shock at 46 degrees C in beef gravy resulted in an increase in the levels of two proteins with apparent molecular masses of 60 and 69 kDa. These two proteins were shown to be immunologically related to GroEL and DnaK, respectively. Increased heat resistance due to heat shock must be considered while designing thermal processes to assure the microbiological safety of thermally processed foods.
9,633,666	eng	[ "D000293", "D000328", "D017668", "D001714", "Q000145", "Q000175", "Q000453", "D003866", "Q000145", "Q000175", "Q000453", "D005163", "D005190", "D005260", "D006801", "D007494", "Q000453", "D008297", "D008875", "D016017", "D011618", "Q000145", "Q000175", "Q000453", "D012042", "D015203", "D012307", "D012559", "Q000145", "Q000175", "Q000453", "D012562", "Q000145", "Q000175", "Q000453" ]	[ "Adolescent", "Adult", "Age of Onset", "Bipolar Disorder", "Depressive Disorder", "Factor Analysis, Statistical", "Family", "Female", "Humans", "Ireland", "Male", "Middle Aged", "Odds Ratio", "Psychotic Disorders", "Registries", "Reproducibility of Results", "Risk Factors", "Schizophrenia", "Schizophrenia, Disorganized" ]	1998	Jun	The structure of psychosis: latent class analysis of probands from the Roscommon Family Study. The nosologic structure of psychotic illness, still influenced as much by historical as empirical perspectives, remains controversial. Latent class analysis was applied to detailed symptomatic and outcome assessments of probands (n=343) with broadly defined schizophrenia and affective illness ascertained from a population-based psychiatric registry in Roscommon County, Ireland. First-degree relatives (n=942) were assessed by personal interview and/or review of hospital record. Six classes were found, all of which bore substantial resemblance to current or historical nosologic constructs. In order of decreasing frequency, they were (1) classic schizophrenia, (2) major depression, (3) schizophreniform disorder, (4) bipolar-schizomania, (5) schizodepression, and (6) hebephrenia. These classes differed on many historical and clinical variables not used in the latent class analysis. Compared with relatives of controls, significantly increased rates of major depression were seen in relatives of depressed and schizodepressed probands. Significantly increased rates of bipolar illness were restricted to relatives of bipolar-schizomanic probands. The risks for schizophrenia and schizophrenia spectrum disorders were significantly increased in relatives of all proband classes except major depression. This increase was moderate for bipolar-schizomanic probands, substantial for schizophrenic, schizophreniform, and schizodepressed probands, and marked for hebephrenic probands. These results suggest a relatively complex typology of psychotic syndromes consistent neither with a unitary model nor with a Kraepelinian dichotomy. The familial vulnerability to psychosis extends across several syndromes, being most pronounced in those with schizophrenialike symptoms. The familial vulnerability to depressive and manic affective illness is somewhat more specific.
9,633,669	eng	[ "D000313", "Q000294", "Q000502", "D000328", "D000368", "D001794", "Q000502", "D004837", "Q000097", "Q000502", "D005260", "D006321", "Q000294", "Q000503", "D006339", "Q000502", "D006801", "D008297", "D008875", "D009132", "Q000737", "Q000294", "D009206", "Q000737", "D009638", "Q000097", "Q000502", "D016584", "Q000097", "Q000175", "Q000503", "D010555", "D011865", "D013315", "Q000097", "Q000175", "Q000503", "D013564", "Q000502" ]	[ "Adrenal Medulla", "Adult", "Aged", "Blood Pressure", "Epinephrine", "Female", "Heart", "Heart Rate", "Humans", "Male", "Middle Aged", "Muscles", "Myocardium", "Norepinephrine", "Panic Disorder", "Personality Inventory", "Radioisotope Dilution Technique", "Stress, Psychological", "Sympathetic Nervous System" ]	1998	Jun	Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks. The sympathetic nervous system has long been believed to be involved in the pathogenesis of panic disorder, but studies to date, most using peripheral venous catecholamine measurements, have yielded conflicting and equivocal results. We tested sympathetic nervous function in patients with panic disorder by using more sensitive methods. Sympathetic nervous and adrenal medullary function was measured by using direct nerve recording (clinical microneurography) and whole-body and cardiac catecholamine kinetics in 13 patients with panic disorder as defined by the DSM-IV, and 14 healthy control subjects. Measurements were made at rest, during laboratory stress (forced mental arithmetic), and, for 4 patients, during panic attacks occurring spontaneously in the laboratory setting. Muscle sympathetic activity, arterial plasma concentration of norepinephrine, and the total and cardiac norepinephrine spillover rates to plasma were similar in patients and control subjects at rest, as was whole-body epinephrine secretion. Epinephrine spillover from the heart was elevated in patients with panic disorder (P=.01). Responses to laboratory mental stress were almost identical in patient and control groups. During panic attacks, there were marked increases in epinephrine secretion and large increases in the sympathetic activity in muscle in 2 patients but smaller changes in the total norepinephrine spillover to plasma. Whole-body and regional sympathetic nervous activity are not elevated at rest in patients with panic disorder. Epinephrine is released from the heart at rest in patients with panic disorder, possibly due to loading of cardiac neuronal stores by uptake from plasma during surges of epinephrine secretion in panic attacks. Contrary to popular belief, the sympathetic nervous system is not globally activated during panic attacks.
9,633,671	eng	[ "D000328", "D000553", "D000596", "Q000008", "D002395", "Q000097", "Q000502", "D018592", "D004311", "D005260", "D006719", "Q000097", "D006801", "D008297", "D008734", "Q000097", "D008875", "D009638", "Q000097", "Q000502", "D010789", "D010919", "D016574", "Q000097", "Q000503", "Q000628", "D012701", "Q000097", "Q000502", "D014364", "Q000097", "D019805", "Q000494" ]	[ "Adult", "Ambulatory Care", "Amino Acids", "Catecholamines", "Cross-Over Studies", "Double-Blind Method", "Female", "Homovanillic Acid", "Humans", "Male", "Methoxyhydroxyphenylglycol", "Middle Aged", "Norepinephrine", "Phototherapy", "Placebos", "Seasonal Affective Disorder", "Serotonin", "Tryptophan", "alpha-Methyltyrosine" ]	1998	Jun	Effects of tryptophan depletion vs catecholamine depletion in patients with seasonal affective disorder in remission with light therapy. Although hypotheses about the therapeutic mechanism of action of light therapy have focused on serotonergic mechanisms, the potential role, if any, of catecholaminergic pathways has not been fully explored. Sixteen patients with seasonal affective disorder who had responded to a standard regimen of daily 10000-lux light therapy were enrolled in a double-blind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor alpha-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites. Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P<.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version. The beneficial effects of light therapy in the treatment of seasonal affective disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.
9,633,672	eng	[ "D000596", "Q000008", "D003866", "Q000097", "Q000188", "Q000503", "D004569", "D005526", "D006801", "D008297", "D012701", "Q000502", "D017367", "Q000627", "D012890", "Q000502", "D014364", "Q000097" ]	[ "Amino Acids", "Depressive Disorder", "Electroencephalography", "Food, Formulated", "Humans", "Male", "Serotonin", "Selective Serotonin Reuptake Inhibitors", "Sleep", "Tryptophan" ]	1998	Jun	Rapid tryptophan depletion, sleep electroencephalogram, and mood in men with remitted depression on serotonin reuptake inhibitors. In previous studies, depletion of brain serotonin by administration of a tryptophan-free amino acid drink (TFD) (1) temporarily reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) in euthymic patients who had a history of major depression, and (2) enhanced rapid eye movement (REM) sleep in normal volunteers. In this study, we hypothesized that the TFD would not only increase depressive symptoms but also the propensity for REM sleep in euthymic patients treated with SSRIs. Ten fully remitted, medicated male patients who had a history of major depressive episode ingested a 100-g TFD (the experimental dose) or a 25-g TFD (designed to be the control drink) in double-blind, random order on separate days. The effects were assessed with mood ratings, plasma tryptophan concentrations, and an all-night sleep electroencephalogram. The TFDs produced a dose-dependent reduction in plasma tryptophan concentrations, sleep latency, and REM latency, as well as increased REM percentage, REM minutes, REM density, and total sleep time. Neither strength of TFD altered mood to a clinically significant degree. Although the TFD affected plasma tryptophan concentrations and various sleep measures, our study did not confirm previous reports that TFD temporarily reversed the antidepressant effects of SSRIs in euthymic patients. Our patients, however, had been treated for a longer period with SSRIs and were more fully remitted at the time of the study. Our results suggest that TFD-induced relapse in SSRI-treated patients in remission decreases as a function of treatment duration, degree of remission, or both.
9,633,673	eng	[ "D000293", "D000328", "D001921", "Q000033", "D002552", "Q000033", "D002555", "Q000502", "D005260", "D006801", "D008279", "D008297", "D008875", "D011618", "Q000175", "D012559", "Q000175" ]	[ "Adolescent", "Adult", "Brain", "Cerebral Ventricles", "Cerebrospinal Fluid", "Female", "Humans", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Psychotic Disorders", "Schizophrenia" ]	1998	Jun	Cerebral gray matter volume deficits in first episode psychosis. Structural brain differences including decreased gray matter and increased cerebrospinal fluid volumes have been observed in the brains of chronically ill patients with schizophrenia. We hypothesized that deficits in gray matter volume would be present in patients presenting with a first episode of nonaffective psychosis. We used magnetic resonance imaging to compare the brains of 77 patients assessed as having a first episode of psychosis (meeting DSM-III-R criteria for schizophrenia, schizophreniform disorder, schizoaffective disorder, delusional disorder, or psychotic disorder not otherwise specified) with those of 61 healthy controls matched for age, sex, race, and parental socioeconomic status. Axial, dual-echo scans of the whole brain were segmented into gray matter, white matter, and cerebrospinal fluid compartments using a computerized volumetric approach. These measures were corrected for the significant effects of intracranial volume and age prior to performing between-group comparisons. The first episode psychosis group had significantly smaller gray matter volume (t[136] = -2.2; P = .03) and greater cerebrospinal fluid volume (t[136] = 2.5; P = .02) than normal controls. In the patient group, gray matter volumes were positively correlated with estimates of IQ but not with age of onset, duration of illness, or measures of premorbid functioning. Deficits in gray matter volume are present in patients experiencing first episode nonaffective psychosis. The magnitude of these differences is smaller than has been described in more chronically ill patients.
9,633,674	eng	[ "D019260", "D005192", "D006801", "D012008", "D015203", "D012559", "Q000175", "Q000453", "D012565" ]	[ "Expressed Emotion", "Family Health", "Humans", "Recurrence", "Reproducibility of Results", "Schizophrenia", "Schizophrenic Psychology" ]	1998	Jun	Expressed emotion and psychiatric relapse: a meta-analysis. Expressed emotion (EE) is a measure of the family environment that has been demonstrated to be a reliable psychosocial predictor of relapse in schizophrenia. However, in recent years some prominent nonreplications of the EE-relapse relationship have been published. To more fully address the question of the predictive validity of EE, we conducted a meta-analysis of all available EE and outcome studies in schizophrenia. We also examined the predictive validity of the EE construct for mood disorders and eating disorders. An extensive literature search revealed 27 studies of the EE-outcome relationship in schizophrenia. Using meta-analytic procedures, we combined the findings of these investigations to provide an estimate of the effect size associated with the EE-relapse relationship. We also used meta-analysis to provide estimates of the effect sizes associated with EE for mood and eating disorders. The results confirmed that EE is a significant and robust predictor of relapse in schizophrenia. Additional analyses demonstrated that the EE-relapse relationship was strongest for patients with more chronic schizophrenic illness. Interestingly, although the EE construct is most closely associated with research in schizophrenia, the mean effect sizes for EE for both mood disorders and eating disorders were significantly higher than the mean effect size for schizophrenia. These findings highlight the importance of EE in the understanding and prevention of relapse in a broad range of psychopathological conditions.
9,633,675	eng	[ "D000328", "D000704", "D001143", "Q000502", "D001794", "Q000502", "D004636", "Q000706", "D005260", "D006339", "Q000502", "D006801", "D007557", "Q000453", "D008016", "D016014", "D008297", "D011336", "D011569", "Q000706", "D013313", "Q000175", "Q000453", "D017741", "Q000523", "D014947", "Q000453" ]	[ "Adult", "Analysis of Variance", "Arousal", "Blood Pressure", "Emergency Service, Hospital", "Female", "Heart Rate", "Humans", "Israel", "Life Change Events", "Linear Models", "Male", "Probability", "Psychiatric Status Rating Scales", "Stress Disorders, Post-Traumatic", "Survivors", "Wounds and Injuries" ]	1998	Jun	A prospective study of heart rate response following trauma and the subsequent development of posttraumatic stress disorder. Physiological arousal during traumatic events may trigger the neurobiological processes that lead to posttraumatic stress disorder (PTSD). This study prospectively examined the relationship between heart rate and blood pressure recorded immediately following a traumatic event and the subsequent development of PTSD. Eighty-six trauma survivors who presented at the emergency department of a general hospital were followed up for 4 months. Heart rate and blood pressure were recorded on arrival at the emergency department. Heart rate, anxiety, depression, and PTSD symptoms were assessed 1 week, 1 month, and 4 months later. The clinician-administered PTSD scale defined PTSD status at 4 months. twenty subjects (23%) met PTSD diagnostic criteria at the 4-month assessment (PTSD group), and 66 (77%) did not (non-PTSD group). Subjects who developed PTSD had higher heart rates at the emergency department (95.5+/-13.9 vs 83.3+/-10.9 beats per minute, t=4.4, P<.001) and 1 week later (77.8+/-11.9 vs 72.0+/-9.5 beats per minute, t=2.25, P<.03), but not after 1 and 4 months. The groups did not differ in initial blood pressure measurement. Repeated-measures analysis of variance (ANOVA) for heart rate showed a significant group effect (P<.02), time effect (P<.001), and group x time interaction (P<.001). The time effect and group x time interaction remained significant when adjusted for sex, age, trauma severity, immediate response, and dissociation during the traumatic event. Elevated heart rate shortly after trauma is associated with the later development of PTSD.
9,633,679	eng	[ "D000978", "Q000266", "Q000627", "D018491", "Q000266", "Q000627", "D004359", "D049672", "D049673", "D006801", "D007980", "Q000266", "Q000627", "D010300", "Q000188", "Q000266" ]	[ "Antiparkinson Agents", "Dopamine Agonists", "Drug Therapy, Combination", "History, 19th Century", "History, 20th Century", "Humans", "Levodopa", "Parkinson Disease" ]	1998	Jun	History of levodopa and dopamine agonists in Parkinson's disease treatment. Striatal dopamine deficiency in Parkinson's disease (PD), first described in 1960, was a key event that led to the era of levodopa therapy. In 1961, levodopa was first tried in PD patients, but throughout most of the 1960s the results were inconsistent. In 1967, questions about the effectiveness of levodopa in PD were finally set aside when Cotzias and colleagues reported dramatic improvement in PD patients with oral administration of levodopa in increasing amounts over long periods. The major side effects of levodopa administration, i.e., dyskinesias and motor fluctuations, also became apparent at this time. In the early 1970s, the advantages of adding a dopa decarboxylase inhibitor to treatment were discovered--reducing side effects and gaining better symptom control--and the first levodopa combination, carbidopa/levodopa, became commercially available in 1975. Since then, PD researchers have attempted to overcome complications with such techniques as continuous levodopa infusion and, most recently, long-acting levodopa combinations. A dopamine agonist, apomorphine, was used in 1970 as a means to overcome side effects and loss of levodopa efficacy. However, side effects and difficulty of administration limited its use. Dopamine agonists began to find a place in routine treatment of PD after the discovery of bromocriptine's benefits in PD in 1974. Since then, new approaches have been tried, such as dopamine agonist monotherapy and early therapy in combination with levodopa. The development of new dopamine agonists has led to characterization of dopamine receptor subtypes and agonists targeted to stimulation of specific receptors.
9,633,681	eng	[ "D000203", "Q000145", "D000368", "D000978", "Q000009", "Q000627", "D002230", "Q000009", "Q000627", "D003692", "D004305", "D004338", "D004409", "Q000209", "D005260", "D006801", "D007980", "Q000009", "Q000627", "D008297", "D008875", "D009460", "Q000187", "D010300", "Q000175", "Q000188" ]	[ "Activities of Daily Living", "Aged", "Antiparkinson Agents", "Carbidopa", "Delayed-Action Preparations", "Dose-Response Relationship, Drug", "Drug Combinations", "Dyskinesia, Drug-Induced", "Female", "Humans", "Levodopa", "Male", "Middle Aged", "Neurologic Examination", "Parkinson Disease" ]	1998	Jun	Implications of the 5-year CR FIRST trial. Sinemet CR Five-Year International Response Fluctuation Study. Almost since the introduction of levodopa for Parkinson's disease (PD), its side effects have concerned clinicians. One strategy to avoid side effects has been to delay levodopa therapy; an alternative has been to use early therapy but to avoid fluctuations in plasma levodopa levels. This latter strategy led to the development of sustained-release carbidopa-levodopa, which was compared with immediate-release carbidopa-levodopa in the CR Five-Year International Response Fluctuation Study (FIRST), a 5-year multicenter study of early, levodopa-naive PD patients. The incidence of motor fluctuations was lower than expected for both groups, and patients receiving sustained-release carbidopa-levodopa fared better on the activities of daily living portion of the Unified Parkinson's Disease Rating Scale and on portions of the Nottingham Health Profile. The trial demonstrated the value of low-dose therapy, the lack of toxicity of this low-dose approach over 5 years in early PD.
9,633,680	eng	[ "D000978", "Q000009", "Q000493", "Q000627", "D003342", "Q000187", "Q000503", "D004298", "Q000378", "D015259", "Q000009", "Q000493", "Q000627", "D006801", "D009434", "Q000187", "Q000503", "D010300", "Q000188", "Q000503", "D011954", "Q000187", "Q000502", "D013378", "Q000187", "Q000503" ]	[ "Antiparkinson Agents", "Corpus Striatum", "Dopamine", "Dopamine Agents", "Humans", "Neural Pathways", "Parkinson Disease", "Receptors, Dopamine", "Substantia Nigra" ]	1998	Jun	Mechanism of action of dopaminergic agents in Parkinson's disease. As the substantia nigra degenerates in Parkinson's disease (PD), the nigrostriatal pathway is disrupted, reducing striatal dopamine and producing PD symptoms. Although dopamine does not readily cross the blood-brain barrier, its precursor, levodopa, does. Levodopa is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and catechol-O-methyltransferase (COMT). Because gastric AADC and COMT degrade levodopa, the drug is given with inhibitors of AADC (carbidopa or benserazide), and inhibitors of COMT will also enter clinical use. Although the exact site of decarboxylation of exogenous levodopa to dopamine in the brain is unknown, most striatal AADC is located in nigrostriatal dopaminergic nerve terminals. Newly synthesized dopamine is stored in the terminals and then released, stimulating postsynaptic dopamine receptors and mediating the antiparkinsonian action of levodopa. Dopamine agonists act directly on postsynaptic dopamine receptors, thus obviating the need for metabolic conversion, storage, and release. How the actions of dopaminergic drugs produce side effects and how these side effects should be managed are discussed.
9,633,682	eng	[ "D000203", "Q000145", "D000328", "D000368", "D000547", "Q000008", "Q000009", "D000978", "Q000008", "Q000009", "D002230", "Q000008", "Q000009", "D018680", "Q000008", "Q000009", "D003692", "D018491", "Q000008", "Q000009", "D004338", "D004359", "D005260", "D006801", "D007980", "Q000008", "Q000009", "D008297", "D008875", "D009460", "Q000187", "D010300", "Q000175", "Q000188", "D012642", "Q000008", "Q000009" ]	[ "Activities of Daily Living", "Adult", "Aged", "Amantadine", "Antiparkinson Agents", "Carbidopa", "Cholinergic Antagonists", "Delayed-Action Preparations", "Dopamine Agonists", "Drug Combinations", "Drug Therapy, Combination", "Female", "Humans", "Levodopa", "Male", "Middle Aged", "Neurologic Examination", "Parkinson Disease", "Selegiline" ]	1998	Jun	Initiating therapy for Parkinson's disease. Accurate diagnosis and individualized assessment of the risks and benefits of available antiparkinsonian medications should guide initiation of treatment for patients with early Parkinson's disease (PD). In general, the goals of treatment for younger patients (less than age 60 years) are control of impairing symptoms, sparing of levodopa to minimize long-term complications, and consideration of neuroprotection. The primary initial medication choices for patients under age 50 years include selegiline, amantadine, and anticholinergic agents. Patients in their fifties may require a dopamine agonist in addition to or instead of selegiline to achieve adequate symptom control. If the desired response is still not achieved, sustained-release carbidopa-levodopa should be added, followed by adjunctive amantadine or anticholinergic therapy. For older patients (60 years and over), improvement of functional impairment is the primary goal. For these patients, a special concern is to avoid inducing or exacerbating cognitive impairment. Sustained-release carbidopa-levodopa is considered first-line treatment for these patients. Inadequate response can be handled by a trial of immediate-release carbidopa-levodopa and then addition of a dopamine agonist when maximum levodopa doses are reached. Anticholinergic agents, amantadine, and selegiline should be avoided because of their CNS effects.
9,633,683	eng	[ "D000978", "Q000008", "Q000009", "D018491", "Q000008", "Q000009", "D004305", "D004334", "D004359", "D006801", "D007980", "Q000008", "Q000009", "D009460", "Q000187", "D010300", "Q000175", "Q000188", "D016896" ]	[ "Antiparkinson Agents", "Dopamine Agonists", "Dose-Response Relationship, Drug", "Drug Administration Schedule", "Drug Therapy, Combination", "Humans", "Levodopa", "Neurologic Examination", "Parkinson Disease", "Treatment Outcome" ]	1998	Jun	Adjuncts to levodopa therapy: dopamine agonists. The classical role of dopamine agonists in Parkinson's disease (PD) therapy is adjunctive treatment to levodopa once "wearing-off" fluctuations or more malignant types of "on-off" swings have developed. Dopamine agonists reduce the frequency, severity, and duration of "off" periods while allowing the levodopa dose to be reduced. Interest is growing in the role of dopamine agonists as primary monotherapy in PD. Studies of early monotherapy have shown that, even with sustained treatment, drug-induced dyskinesias rarely develop. However, this approach is successful for more than 3 years in only about 30% of all PD patients. Continuous dopaminergic stimulation via subcutaneous dopamine agonist infusions is being investigated as a way to control levodopa-associated peak-dose dyskinesias. Early combined treatment with levodopa has been suggested as effective while avoiding long-term complications, but the therapy remains controversial. Despite the entry of several new dopamine agonists into clinical practice, the ideal agonist, with long duration of action and efficacy equal to that of levodopa, is still lacking. The clinical pharmacology of dopamine agonists is reviewed.
9,633,684	eng	[ "D000978", "Q000008", "Q000009", "D001577", "Q000008", "Q000009", "D002394", "Q000502", "D065098", "D002396", "Q000008", "Q000009", "D004305", "D004347", "D004359", "D004791", "Q000008", "Q000009", "D006801", "D007980", "Q000008", "Q000009", "Q000493", "D009570", "D009596", "D010300", "Q000175", "Q000188", "Q000201", "D010422", "Q000008", "Q000009", "D000077867" ]	[ "Antiparkinson Agents", "Benzophenones", "Catechol O-Methyltransferase", "Catechol O-Methyltransferase Inhibitors", "Catechols", "Dose-Response Relationship, Drug", "Drug Interactions", "Drug Therapy, Combination", "Enzyme Inhibitors", "Humans", "Levodopa", "Nitriles", "Nitrophenols", "Parkinson Disease", "Pentanones", "Tolcapone" ]	1998	Jun	Extending levodopa action: COMT inhibition. Degradation of levodopa in the periphery is known to be associated with motor fluctuations and dyskinesia in Parkinson's disease (PD) patients. The enzyme catechol-O-methyltransferase (COMT) is responsible for much of this degradation. Therefore, inhibiting COMT activity is one method of extending the action of levodopa. The new nitrocatechol-type COMT inhibitors entacapone, nitecapone, and tolcapone inhibit COMT in the periphery; tolcapone also inhibits COMT activity centrally. COMT inhibitors increase patients' duration of response to levodopa and reduce response fluctuations. Administration may prolong levodopa-induced dyskinesia, but peak-dose dyskinesia does not appear to increase. To reduce dyskinesia, the total daily dose of levodopa can be reduced.
9,633,685	eng	[ "D000978", "Q000008", "Q000009", "D003704", "Q000175", "Q000188", "D003937", "D004359", "D006801", "D009483", "D010300", "Q000175", "Q000188", "D011379", "D011619", "Q000008", "Q000009" ]	[ "Antiparkinson Agents", "Dementia", "Diagnosis, Differential", "Drug Therapy, Combination", "Humans", "Neuropsychological Tests", "Parkinson Disease", "Prognosis", "Psychotropic Drugs" ]	1998	Jun	Managing the neuropsychiatric symptoms of Parkinson's disease. Neuropsychiatric symptoms frequently complicate the treatment of Parkinson's disease (PD). Approximately 27% of PD patients are demented, and approximately 19% are cognitively impaired without being demented. These 46% of patients are prone to development of delirium when they take antiparkinsonian drugs. Approximately 40% of PD patients are depressed. The depression may be endogenous or exogenous, apathetic or agitated. Approximately 40% of PD patients are anxious or have panic attacks. The attacks may or may not be associated with depression. This article reviews the diagnosis of these symptoms and discusses their management.
9,633,686	eng	[ "D000818", "D000978", "Q000493", "Q000633", "D017209", "Q000187", "D002470", "Q000187", "D004298", "Q000378", "D006801", "D007980", "Q000493", "Q000633", "D009410", "Q000139", "D009474", "Q000187", "D010300", "Q000188", "Q000209", "D051381", "D017382", "Q000378", "D013378", "Q000187" ]	[ "Animals", "Antiparkinson Agents", "Apoptosis", "Cell Survival", "Dopamine", "Humans", "Levodopa", "Nerve Degeneration", "Neurons", "Parkinson Disease", "Rats", "Reactive Oxygen Species", "Substantia Nigra" ]	1998	Jun	Levodopa neurotoxicity: experimental studies versus clinical relevance. Levodopa therapy remains the major form of treatment for the symptoms of Parkinson's disease (PD). However, there has been a suspicion that its use may hasten the progression of nigral cell degeneration. This concept is based on the ability of levodopa to generate reactive oxygen species and the apparent involvement of oxidative stress as a component of the degenerative process that occurs in PD. Indeed, in vitro autoxidation of levodopa causes oxidative stress, leading to neuronal destruction by necrosis or apoptosis. However, its chronic administration to normal rats or primates has not been associated with clear evidence for destruction of the nigrostriatal pathway. In contrast, in situations in which the nigrostriatal tract is already damaged, there is some evidence to suggest that levodopa treatment can produce further cell destruction associated with oxidative processes. However, levodopa does not appear to be toxic to the development of fetal nigral neurons or to the survival of fetal cell transplants. There is no clinical evidence to suggest that levodopa has adverse effects on dopamine cells in normal humans or on the viability of remaining dopaminergic cells in patients with PD. However, it is only now that specific clinical trials designed to examine the potential neurotoxicity of levodopa are being undertaken.
9,633,690	eng	[ "D001327", "Q000382", "D002648", "D006801", "D001523", "Q000382", "D009422", "Q000382", "D009771", "Q000382", "D013290", "Q000150", "D005879", "Q000382" ]	[ "Autoimmune Diseases", "Child", "Humans", "Mental Disorders", "Nervous System Diseases", "Obsessive-Compulsive Disorder", "Streptococcal Infections", "Tourette Syndrome" ]	1998	Jun	Tourette's syndrome and 'PANDAS': will the relation bear out? Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. Despite strong evidence of the importance of hereditary factors in the etiology of Tourette's syndrome (TS), research findings have consistently pointed to a role of environmental influences. A recent line of research has suggested that tic disorders and associated behavioral disturbances, such as obsessive-compulsive disorder, might develop following streptococcal infection by the process of molecular mimicry, whereby antibodies directed against bacterial antigens cross-react with brain targets. Such investigations have given rise to the notion that there is a spectrum of childhood neurobehavioral disorders (termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection [PANDAS]) that arise by postinfectious autoimmune mechanisms. This article reviews research results supporting the concept of PANDAS and discusses their limitations. Well-designed and adequately controlled studies are needed to determine whether there is a true etiologic relation between streptococcal infection and the onset or exacerbation of childhood neuropsychiatric disorders and whether the use of immune-modifying therapies for these conditions is rational.
9,633,691	eng	[ "D001519", "Q000502", "D001927", "Q000175", "Q000503", "Q000523", "D002540", "Q000502", "D006801", "D008279", "D012016" ]	[ "Behavior", "Brain Diseases", "Cerebral Cortex", "Humans", "Magnetic Resonance Imaging", "Reference Values" ]	1998	Jun	The behavioral neurology of cerebral white matter. Behavioral neurology has primarily focused on brain-behavior relations as revealed by disorders of the cerebral cortex and subcortical gray matter. Disorders of cerebral white matter have received less attention. This article considers the contribution of cerebral white matter to normal behavioral function and the effects of white matter disorders on behavior. Diffuse dysfunction is more common than focal impairment, and the term white matter dementia has been proposed as a clinical entity. Conventional neuroimaging has enabled more accurate identification of white matter regions participating in neurobehavioral operations, and newer imaging techniques may define white matter connectivity within and between the hemispheres. As an essential component of neural networks, cerebral white matter contributes to cognitive and emotional functions, and lesions of white matter disconnect these networks to produce neurobehavioral syndromes.
9,633,692	eng	[ "D000328", "D017668", "D000368", "D000369", "D001057", "Q000235", "D002886", "Q000235", "D003704", "Q000453", "Q000235", "Q000503", "D005260", "D005625", "Q000503", "D005838", "D006801", "D008297", "D008875", "D016016", "D013702", "Q000503" ]	[ "Adult", "Age of Onset", "Aged", "Aged, 80 and over", "Apolipoproteins E", "Chromosomes, Human, Pair 17", "Dementia", "Female", "Frontal Lobe", "Genotype", "Humans", "Male", "Middle Aged", "Proportional Hazards Models", "Temporal Lobe" ]	1998	Jun	Familial aggregation in frontotemporal dementia. Frontotemporal dementia (FTD) is a common, non-Alzheimer's dementia. Its familial occurrence has been reported, but the frequency of positive family history is unknown. We carried out a nationwide genetic-epidemiologic study of FTD in the Dutch population of 15 million people. The family history of dementia was analyzed in 74 FTD patients and 561 age- and gender-matched control subjects. We found one or more first-degree relatives with dementia before age 80 in 38% (28 of 74) of FTD patients, but only in 15% (84 of 561) of control subjects. Ten percent of FTD patients had two or more first-degree relatives with dementia compared with 0.9% of the control subjects. Seven percent of FTD patients showed the ApoE4E4 genotype versus 2.3% of the control subjects. The first-degree relatives of FTD had a risk of 22% for dementia before age 80 compared with 11% in relatives of control subjects. The age of onset of dementia in affected first-degree relatives of FTD patients (60.9+/-10.6 years) was significantly lower than among affected relatives of control subjects (72.3+/-8.5 years). The first-degree relatives of FTD patients were 3.5 times (95% CI, 2.4 to 5.2) more at risk for developing dementia before age 80 than relatives of control subjects. The hazard ratio in the subgroup with unknown linkage to chromosome 17 was 2.4 (95% CI, 1.5 to 3.7). This study documents the importance of genetic factors in a proportion of FTD patients with the age at onset of dementia in first-degree relatives being 11 years earlier than in the general population.
9,633,693	eng	[ "D000328", "D000368", "D000369", "D000544", "Q000235", "D002102", "D002874", "D002886", "Q000235", "D002893", "Q000235", "D003704", "Q000175", "Q000235", "D005625", "Q000473", "Q000503", "D008040", "Q000235", "D006239", "D006801", "D008297", "D008875", "D010375", "D011328", "Q000235", "D013702", "Q000473", "Q000503" ]	[ "Adult", "Aged", "Aged, 80 and over", "Alzheimer Disease", "Cadaver", "Chromosome Mapping", "Chromosomes, Human, Pair 17", "Chromosomes, Human, Pair 3", "Dementia", "Frontal Lobe", "Genetic Linkage", "Haplotypes", "Humans", "Male", "Middle Aged", "Pedigree", "Prions", "Temporal Lobe" ]	1998	Jun	Hereditary dysphasic disinhibition dementia: a frontotemporal dementia linked to 17q21-22. The clinical and pathologic features of hereditary dysphasic disinhibition dementia (HDDD) are described to determine whether it is a variant of known dementias. Several dementing disorders have clinical and pathologic similarities with AD, Pick's disease, and the "nonspecific" dementias. A detailed description of clinical and pathologic presentation will aid classification, but ultimately the discovery of causative gene(s) will define these disorders. The authors performed a clinical assessment: gross and microscopic pathologic evaluation of brain tissue, genetic linkage studies, and sequence analyses. HDDD is an autosomal-dominant frontotemporal dementia with many similarities to Pick's disease. Salient clinical features are global dementia with disproportionate dysphasia and "frontotemporal" symptoms. A linkage between HDDD and 17q21-22 was shown, with a maximum lod score of 3.68 at zero recombination. Several dementias have been linked to the same region and have been termed frontotemporal dementia with parkinsonism linked to chromosome 17. These disorders may represent phenotypic variants arising from mutations within a common gene.
9,633,694	eng	[ "D000368", "D000483", "D000544", "Q000235", "D019389", "Q000235", "D005838", "D006801", "D018895", "Q000235", "D009154", "Q000235", "D010300", "Q000235", "D011110", "Q000235" ]	[ "Aged", "Alleles", "Alzheimer Disease", "Cytochrome P-450 CYP2D6", "Genotype", "Humans", "Microsatellite Repeats", "Mutation", "Parkinson Disease", "Polymorphism, Genetic" ]	1998	Jun	Association of CYP2D microsatellite polymorphism with Lewy body variant of Alzheimer's disease. To examine the genetic association of CYP2D6 locus with Lewy body variant (LBV) and Parkinson's disease (PD). Allelic association was studied in patients with pure AD, LBV, and PD by using the CYP2D microsatellite, the (dG-dT)n dinucleotide repeat (n=16 to 27) located between CYP2D8P and CYP2D7 genes, and the CYP2D6 B and D mutations. We found overrepresentation of the alleles longer than 21 repeat (the long-type alleles) in LBV (allele frequency, 0.313) (odds ratio=1.99, p=0.019 by chi2 test) and in PD (0.298) (odds ratio=1.86, p=0.037), but not in pure AD (0.196), compared with the age-matched control (0.186). Strong association was noted of the long-type alleles with the CYP2D6 B mutation (odds ratio=88.50, p < 0.001 by Fisher's exact test), but not with the D mutation or the deletion of CYP2D6 gene. The CYP2D locus is closely associated with LBV and PD. The CYP2D6 B mutation may be involved in pathogenesis of LBV and PD in a dominant-negative manner, or in the linkage disequilibrium of the CYP2D microsatellite to another pathogenic gene locus.
9,633,695	eng	[ "D000368", "D000544", "Q000175", "Q000503", "Q000523", "D001921", "Q000000981", "Q000473", "D002560", "Q000502", "D016002", "D018450", "D005260", "D005544", "D006801", "D008279", "D008297", "D009483", "D015899" ]	[ "Aged", "Alzheimer Disease", "Brain", "Cerebrovascular Circulation", "Discriminant Analysis", "Disease Progression", "Female", "Forecasting", "Humans", "Magnetic Resonance Imaging", "Male", "Neuropsychological Tests", "Tomography, Emission-Computed, Single-Photon" ]	1998	Jun	Preclinical prediction of Alzheimer's disease using SPECT. Regional cerebral perfusion measured by single photon emission computed tomography (SPECT) was examined as a preclinical predictor of the development of Alzheimer's disease (AD). Singular value decomposition was used to produce 20 SPECT factors (known as vectors) (n=152). Vector scores were then computed for four groups (n=136), differing in cognitive status: Group 1--normal controls at both baseline and follow-up; Group 2--subjects with "questionable" AD at both baseline and follow-up; Group 3--subjects with questionable AD at baseline who converted to AD on follow-up (Converters); Group 4--subjects with AD at baseline. All SPECT data in the analyses were gathered at baseline. The four groups could be distinguished on the basis of their baseline SPECT data (p < or = 0.00005; hit rate=83%). Regional decreases in perfusion were most prominent among Converters in the hippocampal-amygdaloid complex, the posterior cingulate, the anterior thalamus, and the anterior cingulate. Inclusion of apolipoprotein E status did not significantly improve the discrimination. SPECT data gathered and analyzed in this manner may be useful as one aspect of the preclinical prediction of AD. Three of the four brain regions important for discriminating Converters from normal controls involve a distributed brain network pertaining to memory, suggesting that this network may be selectively affected in the earliest stages of AD.
9,633,696	eng	[ "D017677", "D000368", "D000369", "D000544", "Q000453", "Q000401", "D015140", "Q000453", "Q000401", "D005260", "D006801", "D015994", "D008297", "D017678", "D012959", "D013624" ]	[ "Age Distribution", "Aged", "Aged, 80 and over", "Alzheimer Disease", "Dementia, Vascular", "Female", "Humans", "Incidence", "Male", "Sex Distribution", "Socioeconomic Factors", "Taiwan" ]	1998	Jun	Incidence and subtypes of dementia in southern Taiwan: impact of socio-demographic factors. To determine the incidence rate (IR) and subtypes of dementia in southern Taiwan. From a cohort of 2,915 community inhabitants aged 65 years and over, 2,507 and 2,175 subjects participated in the first- and second-year follow-up surveys, respectively. A two-phase study used the Mini-Mental State Examination in phase I and the Consortium to Establish a Registry of Alzheimer's Disease (CERAD) neuropsychological battery and the neurobehavioral examination in phase II. We applied International Classification of Diseases (ICD)-10NA criteria for dementia, National Institute of Neurological and Communication Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) guidelines for Alzheimer's disease (AD), and National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria for vascular dementia (VaD). The annual IR for total dementia was 1.28%, which increased with age from 0.77% for 65- to 74-year-olds to 6.19% for persons aged 85 years or older. AD (25 cases, 41.7%, IR=0.54%) was the most common cause of dementia, followed by VaD (19 cases, 31.7%, IR=0.41%) and mixed dementia (9 cases, 15.0%). After adjusting for sex, increasing age was significantly associated with total dementia and AD (p < 0.01). Illiteracy was associated with a marginally increased risk for total dementia (aRR=1.59, p < 0.1) as was being female for AD (aRR = 1.92, p < 0.1). The 2-year mortality rate was high among the demented (48% in total dementia, 38% in AD, and 60% in VaD). The age-specific incidence of dementia in Taiwan is approaching that of developed countries and the low prevalence of dementia (especially VaD) may be mainly due to the high mortality. Age was the major risk factor for total dementia and AD. Being female was probably a risk factor for AD, as was illiteracy for total dementia.
9,633,698	eng	[ "D000368", "D000544", "Q000175", "Q000000981", "Q000378", "D001284", "D001921", "Q000000981", "Q000378", "D005260", "D005947", "Q000378", "D006801", "D007091", "D008279", "D008297", "D008875", "D012016", "D014018", "D014055" ]	[ "Aged", "Alzheimer Disease", "Atrophy", "Brain", "Female", "Glucose", "Humans", "Image Processing, Computer-Assisted", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Reference Values", "Tissue Distribution", "Tomography, Emission-Computed" ]	1998	Jun	Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer's disease. To determine whether the hypometabolism observed in PET images of patients with Alzheimer's disease (AD) is due entirely to brain atrophy. Reduced brain glucose metabolism in AD patients measured using PET has been reported by numerous authors. Actual glucose metabolic values in AD may be reduced artificially because of brain atrophy, which accentuates the partial volume effect (PVE) on data collected by PET. Using segmented MR images, we corrected regional cerebral metabolic rates for glucose for PVEs to evaluate the effect of atrophy on uncorrected values for brain metabolism in AD patients and healthy control subjects. Global glucose metabolism was reduced significantly before and after correction in AD patients compared with controls. Before PVE correction, glucose metabolic values in patients were lower than in control subjects in the inferior parietal, frontal, and lateral temporal cortex; in the posterior cingulate; and in the precuneus. These reductions remained significantly lower after PVE correction, although in the posterior cingulate the difference in metabolism between AD patients and control subjects lessened. Regional glucose metabolism of these areas with PVE correction was lower in moderately-severely demented patients than in mildly demented patients. Reduced glucose metabolism measured by PET in AD is not simply an artifact due to an increase in CSF space induced by atrophy, but reflects a true metabolic reduction per gram of tissue.
9,633,697	eng	[ "D000368", "D000375", "Q000502", "D053327", "D001057", "Q000097", "Q000235", "D002318", "Q000209", "D003072", "Q000150", "Q000235", "Q000523", "D005838", "D006579", "D006801", "D006943", "Q000150", "D006973", "Q000150", "D008137", "D008297", "D009483", "D011446", "D012307", "D014728" ]	[ "Aged", "Aging", "Apolipoprotein E4", "Apolipoproteins E", "Cardiovascular Diseases", "Cognition Disorders", "Genotype", "Heterozygote", "Humans", "Hyperglycemia", "Hypertension", "Longitudinal Studies", "Male", "Neuropsychological Tests", "Prospective Studies", "Risk Factors", "Veterans" ]	1998	Jun	Midlife cardiovascular risk factors, ApoE, and cognitive decline in elderly male twins. To investigate the combined effect of the apolipoprotein E epsilon4 (ApoE4) allele and midlife cardiovascular risk factors on cognitive decline. Data are from the National Heart, Lung, and Blood Institute Twin Study-a longitudinal cardiovascular epidemiologic study of World War II male veteran twins currently in its 27th year of follow-up. Subjects were assessed for cardiovascular risk factors, including BP and glucose levels, at mean ages 48, 58, and 63 years. Participants in the current study are 410 individual twin subjects for whom cognitive function was measured twice, at ages 63 and 73 years. Ten-year change scores in performance on neuropsychological test examinations were adjusted for age, education, baseline score, and incident cardiovascular disease. For the sample as a whole, we observed a significant decline (p < 0.01) in cognitive performance over the 10 years of follow-up. ApoE4 carriers with midlife hyperglycemia experienced the greatest decline in performance, which was also greater than expected from the separate effects combined. Midlife hypertension and ApoE4, were each associated with excess decline in performance on tests of psychomotor speed. Their joint effect, however, was not greater than expected from the separate effects combined. ApoE4 and midlife cardiovascular risk factors may have a synergistic effect on decline in cognitive function. This effect may be due to greater vascular or degenerative damage among subjects with ApoE*4.
9,633,699	eng	[ "D015331", "D004185", "D005260", "D017048", "D006296", "Q000706", "D006801", "D007297", "D008297", "D008875", "D008910", "D009103", "Q000503", "Q000628", "D010045" ]	[ "Cohort Studies", "Disability Evaluation", "Female", "Health Care Costs", "Health Services", "Humans", "Inpatients", "Male", "Middle Aged", "Minnesota", "Multiple Sclerosis", "Outpatients" ]	1998	Jun	Health care utilization in multiple sclerosis: a population-based study in Olmsted County, MN. The authors sought to determine acute ambulatory- and hospital-billed charges for the Olmsted County, Minnesota Multiple Sclerosis (MS) Disability Prevalence Cohort and compare them to those incurred by the general population. Billed charges for 155 people with clinically definite or laboratory-supported MS were compared with those of age- and gender-matched non-MS controls. Billing data, including all inpatient and outpatient acute and rehabilitative medical care charges over a 5-year period surrounding a December 1, 1991 prevalence date, were analyzed. Data were correlated with level of disability using the Minimal Record of Disability for MS. Median total annual billed charges for most individuals with MS, including those with less severe ($1,277) and relapsing-remitting illness ($1,348), did not differ from those for controls ($1,327, p=0.075). Only those with severe MS (22.6%) had median annual medical charges higher than controls ($5,440, p < 0.001). Male patients with MS had higher median annual total charges ($2,353) than male controls ($762, p=0.003). Total charges for female patients with MS ($1,440) were not different from those for female controls ($1469). Median annual outpatient charges were 15% more for the MS group ($1,418) than for controls ($1,231). Patients with MS had a mean of 0.2 hospital admissions annually compared with 0.1 annual admissions per control patient. Among variables collected on persons with MS, the Expanded Disability Status Scale was the strongest predictor of level of charges (p < 0.001). Acute ambulatory- and hospital-billed charges for most patients with MS do not differ from those of the general population.
9,633,700	eng	[ "D000328", "D001921", "Q000473", "Q000503", "D003072", "Q000175", "Q000523", "D005260", "D005625", "Q000473", "Q000503", "D006801", "D008279", "Q000379", "D008297", "D008875", "D009103", "Q000175", "Q000503", "Q000523", "D009483" ]	[ "Adult", "Brain", "Cognition Disorders", "Female", "Frontal Lobe", "Humans", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Multiple Sclerosis", "Neuropsychological Tests" ]	1998	Jun	Relation between MR abnormalities and patterns of cognitive impairment in multiple sclerosis. This study correlated the extent of abnormalities detected by different magnetic resonance imaging (MRI) techniques [proton density (PD)-weighted, T1-weighted, and magnetization transfer imaging (MTI)] with the overall cognitive, frontal lobe, and memory impairments in patients with MS. There were 30 clinically definite MS patients, with different disease courses. psychoactive/steroid treatments, mood disorders, acute relapse phase. Neuropsychological test results. Total (TLL) and frontal (FLL) lesion loads assessed from PD-weighted, T1-weighted (22 patients), and MTI (22 patients) MRI scans. Average lesion MT ratios (MTR) and analysis of the MTR histograms from brain tissue axial slabs on MTI scans. Patients with frontal lobe deficits (n=15) or memory impairment (n-17) had a higher TLL on PD scans (p=0.04 and p=0.01, respectively). Patients with frontal lobe deficits had higher FLL on PD scans (p=0.01) and TLL on MTI (p=0.03) scans. No significant relationships between the extent of T1-weighted lesion loads and the presence of any neuropsychological impairment. Mean MTR of both MS lesions and whole brain tissue was lower in patients with frontal lobe impairment (p=0.04). MRI lesion loads correlated significantly with some neuropsychological test scores. Lesion loads on PD-weighted MRI and MTI-derived measures are associated with cognitive decline in MS patients. Overall macroscopic and microscopic brain damage is more important than the corresponding regional brain disease in determining deficits of selective cognitive domains.
9,633,701	eng	[ "D000328", "D001921", "Q000473", "D004185", "D005260", "D006801", "D008279", "D008297", "D008875", "D009103", "Q000175", "Q000503", "Q000523", "D009420", "Q000503", "D009483", "D012016" ]	[ "Adult", "Brain", "Disability Evaluation", "Female", "Humans", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Multiple Sclerosis", "Nervous System", "Neuropsychological Tests", "Reference Values" ]	1998	Jun	Correlation of volumetric magnetization transfer imaging with clinical data in MS. We examined the relations between quantitative volumetric estimates of cerebral lesion load based on magnetization transfer imaging (MTI), clinical data, and measures of neuropsychological function in 44 patients with clinically diagnosed MS. In this population we assessed the correlation between several volumetric MTI measures, measures of neurologic function (Kurtzke Expanded Disability Status Scale and Ambulation Index), and disease duration using Spearman's correlation coefficient. Patients were classified on the basis of neuropsychological test performance as severely impaired, moderately impaired, and normal. We assessed differences between these groups with respect to MTI results using the Kruskal-Wallis test. MTI measures corrected for brain volume were found to correlate with disease duration (p < 0.01) and showed suggestive correlations with measures of neurologic impairment (p < 0.05). Individual neuropsychological tests correlated with MTI measures corrected and not corrected for brain volume (p < 0.001). An MTI measure not corrected for brain volume differed (p < 0.05) between severely impaired, moderately impaired, and normal patients. These preliminary results suggest that volumetric MTI analysis provides new measures that reflect more accurately the global lesion load in the brain of MS patients, and they may serve as a method to study the natural course of the disease and as an outcome measure to evaluate the effect of drugs.
9,633,702	eng	[ "D000293", "D000906", "Q000032", "D000907", "Q000032", "D015153", "D002648", "D004797", "D005260", "D006801", "D008297", "D009474", "Q000276", "D011699", "Q000276", "Q000473", "D013291", "Q000276", "D005879", "Q000276", "Q000503" ]	[ "Adolescent", "Antibodies", "Antibodies, Bacterial", "Blotting, Western", "Child", "Enzyme-Linked Immunosorbent Assay", "Female", "Humans", "Male", "Neurons", "Putamen", "Streptococcus", "Tourette Syndrome" ]	1998	Jun	Antibodies against human putamen in children with Tourette syndrome. Similar to the model for Sydenham's chorea, antineuronal antibodies, which develop in response to a preceding streptococcal infection, have been speculated to have a role in the development of Tourette syndrome (TS). Serum antibodies against human caudate, putamen, and globus pallidus (interna and externa) were assayed by enzyme-linked immunosorbent assay (ELISA) and Western blot techniques and results were correlated with clinical characteristics and markers of streptococcal infection. A total of 41 children with TS (mean age, 11.3 years) and 39 controls (mean age, 12.1 years) were included. Compared with controls, TS subjects had a significant increase in the mean (p=0.006) and median (p=0.002) ELISA optical density (OD) levels of serum antibodies against putamen, but not caudate or globus pallidus. Western blots on 20 control and 20 TS serum samples showed that specific antibodies to caudate/putamen occurred more frequently in TS subjects at 83, 67, and 60 kDa; antigens were present in a synaptosomal fraction. TS subjects with a positive family history of tics had higher OD values (p < or = 0.04), but no association was shown with age of tic onset, tic severity, sudden onset of tics, or presence of attention-deficit hyperactivity disorder or obsessive-compulsive disorder. Risk ratio calculations in TS and control groups and in study subjects dichotomized for high and low putamen OD values were similar for titers of antistreptolysin O > or = 166 or antideoxyribonuclease B > or = 170. A subgroup analysis limited to subjects with elevated streptococcal titers, however, showed a significantly (p < or = 0.004) larger number of TS subjects with elevated OD levels. Children and adolescents with TS had significantly higher serum levels of antineuronal antibodies against putamen than did controls, but their relation to clinical characteristics and markers for streptococcal infection remains equivocal.
9,633,703	eng	[ "D000328", "D000368", "D000369", "D000818", "D000906", "Q000032", "D001681", "Q000592", "D015153", "Q000592", "D001905", "Q000008", "Q000276", "Q000627", "D004421", "Q000188", "Q000276", "D005138", "D005152", "D005260", "D006801", "D007267", "D008297", "D051379", "D008875", "D009334", "D012680", "D016896" ]	[ "Adult", "Aged", "Aged, 80 and over", "Animals", "Antibodies", "Biological Assay", "Blotting, Western", "Botulinum Toxins", "Dystonia", "Eyebrows", "Facial Muscles", "Female", "Humans", "Injections", "Male", "Mice", "Middle Aged", "Neck Muscles", "Sensitivity and Specificity", "Treatment Outcome" ]	1998	Jun	Mouse bioassay versus Western blot assay for botulinum toxin antibodies: correlation with clinical response. To compare the mouse protection bioassay (MPB) to the Western blot assay (WBA) in detecting antibodies against botulinum toxin A (BTX-A) and to correlate the assay results with clinical responses to BTX-A injections. MPB and WBA assay results were compared in 51 patients (34 nonresponders and 17 responders) who received BTX-A injections, most commonly for cervical dystonia. A subset of patients received a "test" injection into either the right eyebrow (14) or right frontalis (12). Twelve patients with antibodies against BTX-A (Ab+) detected by WBA did not demonstrate antibodies (Ab-) by MPB. Conversely, five patients were Ab+ by MPB but Ab- by WBA. Specificity of the MPB was 100% on all three parameters (clinical, eyebrow, and frontalis injections), whereas WBA specificity was only 71% for clinical response but 100% for both eyebrow and frontalis responses. Sensitivities for both assays were low (33 to 53%). Of the 16 patients previously Ab+ by MPB, seven became negative on retesting after a mean interval of 33 months (range, 6 to 93 months). The lower specificity of the WBA compared to the MPB suggests that the WBA detects nonblocking antibodies. Eyebrow and frontalis "test" injections correlated well with MPB and WBA results and with clinical responses and may be useful in the evaluation of BTX nonresponders.
9,633,704	eng	[ "D000203", "D000328", "D000368", "D004311", "D005260", "D005677", "Q000627", "D006801", "D007262", "D008297", "D008875", "D009068", "Q000502", "D010300", "Q000188", "Q000503", "D010919", "D011446", "D011597", "Q000502", "D012720", "D016138", "Q000502" ]	[ "Activities of Daily Living", "Adult", "Aged", "Double-Blind Method", "Female", "G(M1) Ganglioside", "Humans", "Infusions, Intravenous", "Male", "Middle Aged", "Movement", "Parkinson Disease", "Placebos", "Prospective Studies", "Psychomotor Performance", "Severity of Illness Index", "Walking" ]	1998	Jun	Parkinson's disease: improved function with GM1 ganglioside treatment in a randomized placebo-controlled study. Studies in animal models of Parkinson's disease (PD) suggest that GM1 ganglioside treatment can restore neurologic and dopaminergic function. In view of positive preclinical findings and the results of a previous open-label study demonstrating efficacy of GM1 in PD patients, this study compared effects of GM1 ganglioside and placebo on motor functions in PD patients. Forty-five patients with mild to moderate PD were studied. The primary efficacy measure was change in the Unified Parkinson's Disease Rating Scale (UPDRS) motor score. After three independent baseline assessments, patients received IV infusion of the test drug (1,000 mg GM1 or placebo) and then self-administered either GM1 or placebo twice daily (200 mg/day, subcutaneously) for 16 weeks. Patients were examined during monthly follow-up visits. There was a significant difference between groups in UPDRS motor scores at 16 weeks (p=0.0001). The activities of daily living portion of the UPDRS (off-period assessment) also showed a significant effect in favor of the GM1-treated patients (p=0.04). GM1-treated patients also had significantly greater mean improvements than placebo-treated patients in performance of timed motor tests including tests of arm, hand, and foot movements, and walking. GM1 was well tolerated and no serious adverse events were reported. This study demonstrates that GM1 ganglioside treatment enhances neurologic function significantly in PD patients. Further study is warranted to evaluate long-term effects of GM1 in PD patients and to elucidate further the mechanisms underlying patient improvements.
9,633,705	eng	[ "D000342", "Q000209", "D000368", "D000369", "D003072", "Q000209", "D003951", "D018450", "D005260", "D006306", "D006801", "D008297", "D008875", "D009026", "D009069", "Q000209", "D017678", "D012893", "Q000209", "D013494", "Q000175", "Q000503", "Q000523", "D011795", "D016019", "D014786", "Q000209" ]	[ "Affective Symptoms", "Aged", "Aged, 80 and over", "Cognition Disorders", "Diagnostic Errors", "Disease Progression", "Female", "Health Surveys", "Humans", "Male", "Middle Aged", "Mortality", "Movement Disorders", "Sex Distribution", "Sleep Wake Disorders", "Supranuclear Palsy, Progressive", "Surveys and Questionnaires", "Survival Analysis", "Vision Disorders" ]	1998	Jun	Progressive supranuclear palsy: a survey of the disease course. The most accurate knowledge about progressive supranuclear palsy (PSP) comes from small sample studies that preclude precise estimation of the proportion of PSP patients affected with various symptoms and the examination of factors predicting survival time. To describe the course of PSP in a large clinically diagnosed sample of PSP patients and to identify factors predicting survival time. We surveyed the caregivers of 318 living and 119 deceased patients with progressive supranuclear palsy. The main outcome measures were a principal symptom severity questionnaire and a signs and symptoms questionnaire. The estimated age of PSP symptom onset depends critically on how symptom onset is defined, with estimates differing by as much as 1.5 years. Men and women were represented equally (51.6% versus 48.4%) in the living sample, but men formed 61.8% of the deceased sample. Men were diagnosed later than women following symptom onset (33.4 versus 24.1 months) and died earlier following the diagnosis (37.0 versus 47.6 months). Motor and visual symptoms appeared first, followed by emotional and personality problems, cognitive impairment, and sleep changes. Whereas motor symptoms eventually affected almost every patient, emotional/personality and cognitive symptoms did not. The early onset, presence of falls, slowness, and inability to move eyes downward early in the development of the disease predicted survival time. PSP is a rapidly progressive disease dominated by motor symptoms, and it affects men more frequently than women.
9,633,706	eng	[ "D000368", "D007839", "D006225", "Q000503", "D006801", "D008875", "D010300", "Q000503", "D011597", "Q000502", "D011698", "Q000502", "D012016" ]	[ "Aged", "Functional Laterality", "Hand", "Humans", "Middle Aged", "Parkinson Disease", "Psychomotor Performance", "Pursuit, Smooth", "Reference Values" ]	1998	Jun	Visuomotor control abnormalities in patients with unilateral parkinsonism. Visuomotor performance is known to be disturbed in patients who have advanced Parkinson's disease (PD). The degree of impairment in the early stages of PD was investigated in both the symptomatic and asymptomatic hand of patients with unilateral disease. We examined the visuomotor performance of 10 early unilateral parkinsonian patients and 15 control subjects by using several tracing and tracking tasks that were performed with unseen hands, in which feedback was given through a screen cursor. Significant impairment in control of movement direction was found in tracing of screen paths but not in tracking. Significant slowing of movement was found in target tracking, whereas tracing velocity was normal. Although all patients were judged by standard clinical criteria to be unilaterally affected, visuomotor functions were found to be impaired equally in both hands. Visuomotor control of movement direction and movement velocity is performed independently. Performance along both control dimensions is impaired in the mild stages of parkinsonism, even before the appearance of motor symptoms.
9,633,707	eng	[ "D000328", "D004558", "D005073", "Q000502", "D005260", "D006801", "D015640", "Q000502", "D008297", "D009119", "Q000502", "D018482", "Q000502", "D013003", "Q000502", "D013979", "Q000502" ]	[ "Adult", "Electric Stimulation", "Evoked Potentials, Somatosensory", "Female", "Humans", "Ion Channel Gating", "Male", "Muscle Contraction", "Muscle, Skeletal", "Somatosensory Cortex", "Tibial Nerve" ]	1998	Jun	Effects of voluntary contraction on tibial nerve somatosensory evoked potentials: gating of specific cortical responses. We evaluated vertex-parietal P37, N50, and contralateral N37 somatosensory evoked potentials (SEPs) to posterior tibial nerve stimulation during weak (20 to 30%) and strong (80 to 90%) ipsilateral gastrocnemius-soleus contraction. The results were compared with data obtained during full relaxation. P37 and N50 were attenuated significantly during weak contraction and then abolished during strong contraction, whereas the contralateral N37 was not. The N37 potential spreads over the vertex and over the ipsilateral parietal region during strong contraction. The Cz'-F3 montage was not appropriate for detecting these SEP patterns. These findings suggest that thalamic or cortical gating mechanisms affect specific cortical responses. P37 and N50 could reflect the arrival of the afferent volley into the motor areas from thalamic and cortical (subareas 1 and 2 of S1) projections. N37 could be generated in subarea 3b. Differential analysis of N37 and P37 is required in clinical practice, mainly in those conditions that involve the motor system and in those conditions in which tonic muscular activity is increased.
9,633,708	eng	[ "D001291", "D003955", "Q000706", "D007600", "D015999", "D009422", "Q000175", "Q000628", "D009462", "Q000379", "D010818", "D006113", "D014481" ]	[ "Attitude of Health Personnel", "Diagnostic Tests, Routine", "Judgment", "Multivariate Analysis", "Nervous System Diseases", "Neurology", "Practice Patterns, Physicians'", "United Kingdom", "United States" ]	1998	Jun	Practice styles of US compared to UK neurologists. This study assessed variation between neurologists in the United States and United Kingdom in their diagnostic and treatment decisions for commonly encountered neurologic presentations, and identified explanatory factors for any observed variation. All 210 consultant neurologists in the United Kingdom and a nationally representative sample of 595 US neurologists received mailed surveys containing three detailed clinical scenarios depicting patients with (1) a single unprovoked seizure occurring 3 days previously, (2) early Parkinson's disease, and (3) dementia. The main study outcome measures were self-reported decisions regarding diagnostic test ordering and treatment, which were assessed after each scenario. Neurologists' practice characteristics, certainty about the diagnosis, and attitudes toward uncertainty were also measured. Survey response rates were 92% of US and 63% of UK neurologists. A higher proportion of US than UK neurologists indicated they would order additional diagnostic tests for all three scenarios (all p < 0.05); 77% of UK compared with 26% of US neurologists would manage a single unprovoked seizure without antiepileptic medication (p < 0.0001), but treatment of early Parkinson's disease was not different. Nearly all US and UK neurologists would obtain a neuroimaging study in the evaluation of dementia. International differences persisted after adjustment for differences in demographic and practice characteristics and for attitudes toward test use and clinical uncertainty. We identified large international variation in clinical decisions across three common neurologic conditions. Cross-country collaboration should explore these differences to develop consensus on standards of care.
9,633,709	eng	[ "D000328", "D000368", "D000369", "D001281", "Q000150", "D002545", "Q000150", "Q000628", "D002561", "Q000150", "Q000628", "D005194", "Q000379", "D005260", "D006333", "Q000150", "D006801", "D007297", "D008297", "D008875", "D009462", "Q000379", "D010818", "D016016", "D012008", "D012044", "D016019", "D016896" ]	[ "Adult", "Aged", "Aged, 80 and over", "Atrial Fibrillation", "Brain Ischemia", "Cerebrovascular Disorders", "Family Practice", "Female", "Heart Failure", "Humans", "Inpatients", "Male", "Middle Aged", "Neurology", "Practice Patterns, Physicians'", "Proportional Hazards Models", "Recurrence", "Regression Analysis", "Survival Analysis", "Treatment Outcome" ]	1998	Jun	Ischemic stroke: outcomes, patient mix, and practice variation for neurologists and generalists in a community. A variety of methods was used to compare patient mix, practice variation, survival, and recurrence after first ischemic stroke among Rochester, MN residents. The significance of the results for neurologists and generalists was examined. Age, stroke severity, congestive heart failure (CHF), and the interaction between atrial fibrillation and patient groups were determinants of survival. Without atrial fibrillation, patients on neurology services and patients on general services with neurology consultation had better survival than those without neurology consultation, adjusting for age, stroke severity, and CHF. With atrial fibrillation, patients on general services with neurology consultation had no better survival compared with those without neurology consultation; patients on neurology services had worse survival (p=0.002). There was no difference in stroke recurrence. Evaluation by a neurologist is associated with better survival for most patients with ischemic stroke but not those with atrial fibrillation. Only a randomized trial can determine whether this association is causal.
9,633,710	eng	[ "D000293", "D000328", "D000755", "Q000150", "D001288", "Q000502", "D002544", "Q000175", "Q000209", "Q000523", "D002648", "D003071", "Q000502", "D006801", "D009483", "D012680" ]	[ "Adolescent", "Adult", "Anemia, Sickle Cell", "Attention", "Cerebral Infarction", "Child", "Cognition", "Humans", "Neuropsychological Tests", "Sensitivity and Specificity" ]	1998	Jun	Cognitive screening examinations for silent cerebral infarcts in sickle cell disease. In children with sickle cell disease (SCD), silent cerebral infarcts are the most frequent cause of neurologic injury. We determined the sensitivity and specificity of selective neurocognitive measures when separating children with silent cerebral infarcts and SCD from sibling controls. Additionally, we tested the validity of the same cognitive measures to identify patients with overt strokes. We examined performance on a neuropsychologic battery containing measures of attention/executive, spatial, language, memory, and motor functioning for seven children with SCD and silent cerebral infarct, 21 children with SCD and overt stroke, and 17 normal siblings. Diagnosis of cerebral infarct was based on results of MRI. Measures from the attention and executive domains were the most useful for identifying children with silent cerebral infarct. The Test of Variables of Attention was the most robust measure and yielded a sensitivity rate of 86% and a specificity rate of 81%. This measure also showed a sensitivity rate of 95% in identifying overt stroke. Brief cognitive screening measures, if properly constructed, may be an effective means of identifying children with silent cerebral infarct. Future prospective studies should be pursued to assess the utility of cognitive screening for silent cerebral infarcts in SCD.
9,633,711	eng	[ "D000368", "D000925", "Q000627", "D001458", "D002561", "Q000150", "Q000628", "D005260", "D005676", "D006493", "Q000627", "D006801", "D008297", "D011446", "D011655", "Q000453", "Q000401", "D012307", "D013923", "Q000453", "Q000209", "D013924", "Q000453", "Q000517" ]	[ "Aged", "Anticoagulants", "Bandages", "Cerebrovascular Disorders", "Female", "Gravity Suits", "Heparin", "Humans", "Male", "Prospective Studies", "Pulmonary Embolism", "Risk Factors", "Thromboembolism", "Thrombophlebitis" ]	1998	Jun	Pneumatic sequential compression reduces the risk of deep vein thrombosis in stroke patients. To determine if pneumatic sequential compression devices (SCDs) combined with subcutaneous heparin and antiembolic hose reduce the risk of deep vein thrombosis (DVT) and pulmonary embolism (PE) in stroke patients. DVTs and PEs are serious complications among hospitalized stroke patients. Subcutaneous heparin and SCDs have both been used to prevent DVT. It is not known if SCDs combined with subcutaneous heparin can improve the protection afforded by heparin alone. The study group was comprised of nonhemorrhagic stroke patients admitted to the neurology service from October 1988 through June 1996. From October 1988 through April 1991 (233 patients), and during February 1993 (16 patients), patients received 5,000 U subcutaneous heparin twice daily and antiembolic hose. From June 1991 through January 1993 and from March 1993 through June 1996 (432 patients) all nonambulatory stroke patients had SCDs applied to both legs in addition to subcutaneous heparin and antiembolic hose. Twenty-three of 249 patients (9.2%; 21 of 233 and two of 16 patients) treated with heparin alone developed DVT and six patients (2.4%) developed PE (six of 233 and zero of 16). Half the PE cases (three of six) were fatal and all PEs were in patients with DVT. Eighty-three of the 249 patients were nonambulatory. Twenty-two of the 23 DVTs and all the PEs developed in nonambulatory patients. Only one DVT (0.23%) and no PEs occurred among the 432 patients (148 nonambulatory) treated with SCDs as well as heparin. The addition of SCDs resulted in more than a 40-fold reduction in the risk of DVT. Nonambulatory stroke patients have an increased risk for DVT and PE. Adding SCDs to treatment with subcutaneous heparin and antiembolic hose reduced the risks of DVTs and PEs. SCDs should be considered for adjunctive DVT prophylaxis in nonambulatory stroke patients.
9,633,712	eng	[ "D000293", "D000328", "D001741", "Q000706", "D002545", "Q000139", "Q000453", "Q000209", "D002561", "Q000139", "Q000453", "Q000209", "D005260", "D006801", "D013287", "Q000009", "D015994", "D008297", "D012307", "D019966", "Q000208", "D014505", "D044465", "Q000706" ]	[ "Adolescent", "Adult", "Black or African American", "Brain Ischemia", "Cerebrovascular Disorders", "Female", "Humans", "Illicit Drugs", "Incidence", "Male", "Risk Factors", "Substance-Related Disorders", "Urban Population", "White People" ]	1998	Jun	Illicit drug-associated ischemic stroke in the Baltimore-Washington Young Stroke Study. Limited information exists on the frequency, trends in occurrence, risk factors, mechanisms, and outcome of ischemic stroke associated with illicit drug use among young adults in a geographically defined population. We reviewed ischemic stroke in young adults (aged 15 to 44 years) in 46 regional hospitals for 1988 and 1991. We examined stroke mechanisms and outcome in patients with recent drug use. Recent illicit drug use was noted in 51/422 (12.1%) stroke patients. Patients with drug use were more likely than other stroke patients to be black (p=0.01), aged 25 to 39 years (p=0.004), and smokers (p=0.006), and were less likely to have hypertension (p=0.004) or diabetes mellitus (p=0.004). Drug use was the probable cause of stroke in 20 (4.7%) patients. Among 31 (7.3%) patients with drug use as a possible stroke mechanism, more likely diagnoses included cardioembolic stroke in 18, hematologic/collagen vascular in 6, nonatherosclerotic vasculopathy in 5, and atherosclerosis in 3. There was no difference in outcome between drug-associated and non-drug associated stroke. Recent illicit drug use occurs in 12.1% of young adult stroke patients. Drug-associated young adult stroke seems to relate to vascular mechanisms other than those related to hypertension or diabetes. Case-control studies are needed.
9,633,713	eng	[ "D000368", "D000369", "D001488", "Q000000981", "Q000473", "D002545", "Q000150", "Q000175", "D002343", "Q000000981", "Q000473", "D002533", "D002539", "Q000150", "Q000175", "D002561", "Q000150", "Q000175", "D005260", "D006801", "D008279", "D008297", "D008875", "D012008", "D016019", "D014057", "D014711", "Q000000981", "Q000473" ]	[ "Aged", "Aged, 80 and over", "Basilar Artery", "Brain Ischemia", "Carotid Artery, Internal", "Cerebral Angiography", "Cerebral Arterial Diseases", "Cerebrovascular Disorders", "Female", "Humans", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Recurrence", "Survival Analysis", "Tomography, X-Ray Computed", "Vertebral Artery" ]	1998	Jun	Dolichoectasia of the intracranial arteries in patients with first ischemic stroke: a population-based study. The objective of this study was to estimate the frequency of intracranial arterial dolichoectasia among patients with first ischemic stroke and to compare clinical characteristics, survival, and recurrence in those with and without the abnormality. Dolichoectasia may cause cerebral infarction by thrombosis, embolism, stenosis, or occlusion of deep penetrating arteries. The chi-square, Fisher's exact, and logrank tests were used to compare clinical characteristics, survival, and recurrence for patients with and without dolichoectasia among the 387 residents of Rochester, MN, who had brain CT or MRI for first cerebral infarction from 1985 through 1989. Twelve patients (3.1%) had dolichoectasia. Patients with dolichoectasia were more likely to have had stroke fitting a clinical and radiographic pattern of lacunar infarction than those without (42% and 17% respectively; p=0.04). Dolichoectasia was detected in the vertebrobasilar system in eight patients (66.7%), in the carotid system in two patients (16.7%), and in both circulatory systems in two patients (16.7%). There were no significant differences in the following characteristics among those with and without dolichoectasia: age, sex, hypertension, diabetes, smoking, and preceding transient ischemic attack. Patients with dolichoectasia had better survival (relative risk [RR] for death, 0.26; p=0.04) after first cerebral infarction but higher rates of stroke recurrence (RR, 2.4; p=0.02). Dolichoectasia is detected in 38 of patients with first cerebral infarction and is associated with better survival but higher rates of stroke recurrence.
9,633,714	eng	[ "D000716", "D002536", "Q000033", "D006801", "D008488" ]	[ "Anatomy, Artistic", "Cerebral Arteries", "Humans", "Medical Illustration" ]	1998	Jun	Arterial territories of the human brain: cerebral hemispheres. The development of neuroimaging has allowed clinicians to improve clinicoanatomic correlations in patients with stroke. Anatomic structures are well delineated on MRI, but there is a lack of standardization in their arterial supply. As in our previous study depicting the arterial supply of the brainstem and cerebellum, we present a system of 12 axial sections of the hemispheres depicting the dominant arterial territories, the most important anatomic structures, and Brodmann's areas. The area of variation of the cortical territory of the anterior, middle, and posterior cerebral arteries is also represented. These sections may be used as a practical tool to determine arterial territories on CT or MRI, and may help establish consistent clinicoanatomic correlations in patients with supratentorial stroke.
9,633,715	eng	[ "D000293", "D000328", "D000368", "D000369", "D002543", "Q000209", "D002550", "Q000002", "Q000000981", "Q000473", "D002648", "D002675", "D005260", "D006261", "Q000209", "D006801", "D008137", "D008279", "D008297", "D008875", "D009422", "Q000209", "D011446", "D012189", "D012307", "D012640", "Q000209", "D014057" ]	[ "Adolescent", "Adult", "Aged", "Aged, 80 and over", "Cerebral Hemorrhage", "Cerebral Veins", "Child", "Child, Preschool", "Female", "Headache", "Humans", "Longitudinal Studies", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Nervous System Diseases", "Prospective Studies", "Retrospective Studies", "Risk Factors", "Seizures", "Tomography, X-Ray Computed" ]	1998	Jun	A longitudinal study of patients with venous malformations: documentation of a negligible hemorrhage risk and benign natural history. The natural history of cerebral venous malformations has not been well documented, and the clinical significance of these common lesions remains controversial. The objective of this study was to follow longitudinally the clinical course of patients with cerebral venous malformations to document the natural history of the lesion. Ninety-two patients with radiographically confirmed venous malformations were entered into the study between 1987 and 1996. Annual follow-up was maintained by clinic visits and/or phone interviews. Sixty-three patients (25 men and 38 women) with more than 1 year of follow-up were analyzed. McNemar's test and logistic regression analysis was applied to prevalence of presenting symptoms over time. An average per patient follow-up of 4.2 years yielded 2,721 retrospective and 301 prospective lesion-years for analysis. Average age at diagnosis was 39.1 years (SD, 18.7 years; range, 2 to 73 years). The most frequent lesion locations included the frontal lobe (55.6%, n=35) and the cerebellum (27%, n=17). The most frequent presentations included headache (50.8%, n=32), focal neurologic deficits (39.7%, n=25), and seizure (30.2%, n=19). Prevalence of headache (p=0.048) and seizure (p=0.016) decreased over time without treatment of the lesion. A second cerebrovascular lesion was identified in 12 patients (19%). Two patients had a symptomatic intracerebral hemorrhage attributable to their venous malformation. Risk of hemorrhage was 0.15% per lesion-year (95% CI, 0.06 to 0.38%). This study establishes that the natural history of venous malformations is benign, that the risk of hemorrhage from these lesions is negligible, and that conservative therapy is warranted.
9,633,716	eng	[ "D000293", "D000328", "D001927", "Q000175", "Q000235", "Q000503", "D002539", "Q000175", "Q000235", "Q000503", "D002544", "Q000175", "Q000235", "Q000503", "D002560", "Q000502", "D003704", "Q000235", "Q000473", "Q000523", "D018450", "D005260", "D005799", "D006801", "D008279", "D008297", "D008875", "D008881", "Q000235", "D009483", "D010375", "D010641", "D012867", "Q000473", "D015899" ]	[ "Adolescent", "Adult", "Brain Diseases", "Cerebral Arterial Diseases", "Cerebral Infarction", "Cerebrovascular Circulation", "Dementia", "Disease Progression", "Female", "Genes, Dominant", "Humans", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Migraine Disorders", "Neuropsychological Tests", "Pedigree", "Phenotype", "Skin", "Tomography, Emission-Computed, Single-Photon" ]	1998	Jun	SPECT study of a German CADASIL family: a phenotype with migraine and progressive dementia only. We describe the clinical, molecular, genetic, MRI, and SPECT features of a German family with autosomal dominant migraine and dementia, mapping to the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) locus. We studied the correlation of cerebral blood flow, MRI, and cognitive function. CADASIL is a small-vessel disease of the brain mapped to chromosome 19p13.1. Mutations of the Notch3 gene cause this disorder. Most phenotypes are characterized by transient ischemic attacks (TIAs) and lacunar strokes leading to dementia. Migraine is frequent. A single photon emission computed tomographic (SPECT) study of this disorder has not yet been published. We studied 13 individuals clinically and performed neuroimaging studies with MRI and SPECT. Genetic analysis strongly supported linkage to the CADASIL locus, and the disease haplotype was found in six individuals. Analysis by single-strand confirmation polymorphism did not identify Notch3 mutations. All affected individuals had MRI white matter hyperintensities and four individuals had additional basal ganglial signal abnormalities. Four affected individuals had migraine, two of whom had slowly progressive dementia. TIAs, stroke, and focal neurologic signs were absent. Cerebral blood flow reduction in SPECT studies of affected individuals matched with MRI signal abnormalities. Cognitive impairment was linked to signal abnormalities and hypoperfusion in the basal ganglia. Demented patients had a pattern of frontal, temporal, and basal ganglial hypoperfusion. We describe a CADASIL phenotype that is characterized by the absence of focal neurologic symptoms and present the first SPECT study of this disorder.
9,633,718	eng	[ "D002012", "Q000150", "Q000453", "D002648", "D005152", "Q000503", "D005260", "D006261", "Q000150", "Q000453", "Q000628", "D006801", "D008297", "D008881", "Q000503", "D009041", "Q000150", "Q000453", "D010146", "Q000150", "Q000453", "D015995", "D012016", "D013334", "D011795", "D013704", "Q000503", "D018781", "Q000209", "Q000503" ]	[ "Bruxism", "Child", "Facial Muscles", "Female", "Headache", "Humans", "Male", "Migraine Disorders", "Motion Sickness", "Pain", "Prevalence", "Reference Values", "Students", "Surveys and Questionnaires", "Temporomandibular Joint", "Tension-Type Headache" ]	1998	Jun	Childhood headache at school entry: a controlled clinical study. Our objective was to study the prevalence of different headache types, characterizations, and triggers of headache in Finnish children starting school. Questionnaires were sent to 1,132 families with 6-year-old children. Children with headache disturbing their daily activities (n=96) and an asymptomatic control group of children (n=96) participated in a clinical interview and examination. Children with headache had significantly more bruxism (odds ratio [OR], 1.9; 95% CI, 1.0 to 3.4), tenderness in the occipital muscle insertion areas (OR, 4.8; 95% CI, 1.8 to 12.7), and tenderness in the temporomandibular joint areas (OR, 2.8; 95% CI, 1.3 to 6.0). They also had more travel sickness (OR, 3.4; 95% CI, 1.7 to 6.7) than control children. Eating ice cream (OR, 5.3; 95% CI, 1.4 to 20.3), fear (OR, 3.7; 95% CI, 1.2 to 11.2), and anxiety (OR, 3.2; 95% CI, 1.0 to 10.8) triggered headache more often in migraineurs than in children with tension-type headache. Children with migraine also reported more frequently abdominal (OR, 5.6; 95% CI, 1.7 to 18.1) and other (OR, 3.5; 95% CI, 1.2 to 9.8) pain concurrently with headache, and they used medication for pain relief more often (OR, 3.1; 95% CI, 1.0 to 9.5). Headache classification in children may be improved by palpation of occipital muscle insertions and temporomandibular joint areas, and by discerning a history of triggering events and concurrent symptoms.
9,633,717	eng	[ "D000209", "Q000378", "D000210", "Q000503", "D000368", "D002561", "Q000150", "Q000378", "D005260", "D005340", "Q000032", "D006801", "D007249", "Q000209", "D008137", "D008297", "D008875", "D012008", "D012016", "D012307" ]	[ "Acute-Phase Proteins", "Acute-Phase Reaction", "Aged", "Cerebrovascular Disorders", "Female", "Fibrinogen", "Humans", "Inflammation", "Longitudinal Studies", "Male", "Middle Aged", "Recurrence", "Reference Values", "Risk Factors" ]	1998	Jun	Persistent inflammatory response in stroke survivors. Goals were to determine how long acute-phase markers remain elevated after ischemic stroke and how marker levels relate to stroke risk factors, stroke mechanism, and subsequent vascular events. Fibrinogen (FIB), C-reactive protein (CRP), leukocytes (WBC), neutrophils (PMN), interleukin-6, and interleukin-1 receptor antagonist were measured at stroke onset and at 6 weeks, 6 months, and 1 year after enrollment, or until a vascular event occurred in 136 acute ischemic stroke patients, 76 patients with comparable risk factors for stroke, and 48 age-balanced healthy subjects. Multivariate logistic analysis showed that prior stroke and FIB level predicted new events in stroke patients (p < 0.04 for both), whereas congestive heart failure (p < 0.02) and creatinine level (p < 0.006) were predictive in at-risk patients. After controlling for infection, FIB, CRP, and PMN levels at baseline were higher in at-risk but not in stroke patients with recurrent events (p < 0.05 for all). At 1 year, FIB levels remained elevated in event-free stroke survivors compared with levels in the risk and control groups (p < 0.001 for both). FIB also remained higher in stroke survivors who had atheroembolism (AE) compared with non-AE stroke survivors (381+/-72 versus 342+/-78 mg/dL, p < 0.02). Peripheral vascular disease was an independent predictor (p < 0.0001) of longitudinal FIB in stroke survivors. Of note, both WBC and PMN levels were chronically elevated in patients with stroke risk factors and in stroke survivors (p < 0.0001 for both) compared with healthy elderly subjects. Most acute-phase markers decline gradually after stroke, but FIB remains significantly elevated and is associated with increased risk for recurrent vascular events.
9,633,719	eng	[ "D000293", "D000328", "D000368", "D000369", "D001810", "Q000502", "D002560", "Q000502", "D005260", "D006801", "D008297", "D008875", "D008881", "Q000000981", "Q000503", "D010101", "Q000502", "D014055" ]	[ "Adolescent", "Adult", "Aged", "Aged, 80 and over", "Blood Volume", "Cerebrovascular Circulation", "Female", "Humans", "Male", "Middle Aged", "Migraine Disorders", "Oxygen Consumption", "Tomography, Emission-Computed" ]	1998	Jun	Global cerebral blood flow, blood volume, and oxygen metabolism in patients with migraine headache. Migraine headaches with and without aura are representative of vascular headache states traditionally thought to be mediated by alterations in vascular tone. Validation of this theory has been hampered in part by technical difficulties inherent in the measurement of cerebral blood flow (CBF). The purpose of this study was to compare CBF measured during migraine and migraine-free states using PET. Patients with a minimum of one migraine headache without aura per month (International Headache Society [IHS] criteria) underwent measurement of CBF, cerebral blood volume (CBV), oxygen extraction, and metabolism during an episode of spontaneous migraine headache. Imaging was repeated during a migraine-free period of at least 48 hours. PET radiotracers used were: CBF, H(2)15O; CBV, C15O; oxygen metabolism, 15O2. In nine patients (seven female and two male), global CBF (mL/min/100 g [SD]) was measured as 52.70 (6.9) during migraine and 59.65 (10.6) in the migraine-free state; p=0.028. CBV (mL/100 g [SD]) was 3.6 (0.43) during the symptomatic state and 3.8 (0.55) after the migraine; p=0.047. Oxygen metabolism (mL/min/100 g [SD]) was 3.68 (0.9) during migraine and 3.38 (1.02) without headache; p=0.211. The oxygen extraction ratio was 0.48 (0.15) and 0.41 (0.12) during migraine and migraine-free states, respectively; p=0.132. In patients experiencing migraine without aura, CBF and CBV are reduced during the headache phase. Cerebral oxygen metabolism and oxygen extraction are not significantly affected.
9,633,720	eng	[ "D000041", "D000293", "D000368", "D005260", "D006261", "Q000453", "Q000503", "D006801", "D015994", "D008297", "D008499", "D008875", "D008881", "Q000453", "Q000503", "D013647", "D014937" ]	[ "Absenteeism", "Adolescent", "Aged", "Female", "Headache", "Humans", "Incidence", "Male", "Medical Records", "Middle Aged", "Migraine Disorders", "Task Performance and Analysis", "Work" ]	1998	Jun	Migraine and reduced work performance: a population-based diary study. This article estimates lost work days and lost work day equivalents in a population sample of migraineurs, differentiating work loss due to headache episodes that met criteria for migraine from migrainous headaches not meeting full criteria and nonmigrainous headaches. A random digit dialing survey of 5,071 adults identified 800 subjects with migraine headaches. By clinical examination, a subsample of 225 met migraine diagnostic criteria; 174 of these patients completed at least 11 weeks of daily diaries. This report concerns the subgroup of 122 individuals with regular paid employment. Subjects completed a daily diary over a 3-month period to assess the occurrence of headaches and International Headache Society (IHS) criteria for each headache occurrence. We report estimates of lost work days and lost work day equivalents by type of headache. Participants reported headaches on 8.1 work days, of which 2.2 headache days met criteria for migraine (IHS 1.1, 1.2), and an additional 2.1 headache days were migrainous without meeting full migraine criteria (IHS 1.7). On average, migraineurs missed 1.1 days of work due to headache in 3 months, of which 0.7 lost work days were due to migraine and 0.3 were due to migrainous headaches. When at work with headache, work effectiveness was reduced 41% for migraine headaches, 28% for migrainous headaches, and 24% for other headaches. Over 3 months, migraineurs experienced an average of 3.0 lost work day equivalents, of which 1.4 were due to migraine and an additional 0.7 were due to migrainous headaches. The most disabled 20% of the participants accounted for 77% of the lost work days; 40% of subjects accounted for 75% of the lost work day equivalents. Employed migraine sufferers experienced considerable work loss and reduced work performance due to headache. The most severely affected migraineurs accounted for most of the reduced work performance. Targeting the most severely affected persons may be necessary to reduce work loss among migraineurs substantially.
9,633,721	eng	[ "D000293", "D000328", "D000375", "Q000502", "D000704", "D001921", "Q000473", "D002561", "Q000175", "Q000209", "D002648", "D018450", "D000795", "Q000150", "D006801", "D008137", "D008279", "D008875" ]	[ "Adolescent", "Adult", "Aging", "Analysis of Variance", "Brain", "Cerebrovascular Disorders", "Child", "Disease Progression", "Fabry Disease", "Humans", "Longitudinal Studies", "Magnetic Resonance Imaging", "Middle Aged" ]	1998	Jun	Quantitative analysis of cerebral vasculopathy in patients with Fabry disease. This study's purpose was to obtain a quantitative natural history of the cerebrovascular involvement in Fabry disease. Fabry disease is an X-linked recessive disorder due to alpha-galactosidase A deficiency. Progressive accumulation of ceramidetrihexoside within the intima and media of cerebral blood vessels causes ischemic lesions in the majority of affected patients. Determination of the natural history of the cerebral vasculopathy in Fabry disease is important to assess the effects of therapeutic intervention in this disorder. A longitudinal MRI study of 50 patients who had a total of 129 MRI scans was performed. The burden of cerebrovascular disease was determined using direct linear measurement. On T2-weighted MRI scans, 32% of the patients had no lesions (mean age, 33 years), 16% had gray matter lesions only (mean age, 36 years), 26% had lesions in white matter only (mean age, 43 years), and 26% had lesions in white and gray matter (mean age, 47 years). Disease burden increased with age, but no patient younger than 26 had lesions on MRI. All patients older than 54 had cerebrovascular involvement. The distribution of MRI-detectable lesions was typical of a small-vessel disease. Only 37.5% of patients with cerebral lesions had neurologic symptoms. These findings provide a predictable outcome measure to assess the effect of molecular interventions on the cerebrovascular circulation in Fabry disease.
9,633,722	eng	[ "D001483", "D015139", "D002549", "Q000235", "D005260", "D005838", "D006239", "D006801", "D008297", "D005810", "Q000502", "D009154", "Q000235", "D018991", "Q000235", "D010375", "D010641", "D016133" ]	[ "Base Sequence", "Blotting, Southern", "Diffuse Cerebral Sclerosis of Schilder", "Female", "Genotype", "Haplotypes", "Humans", "Male", "Multigene Family", "Mutation", "Myelin Proteolipid Protein", "Pedigree", "Phenotype", "Polymerase Chain Reaction" ]	1998	Jun	Duplication of the proteolipid protein gene is the major cause of Pelizaeus-Merzbacher disease. Pelizaeus-Merzbacher disease (PMD), an X-linked recessive dysmyelination disorder, is caused by mutations in the proteolipid protein (PLP) gene. However, missense mutations were only found in a fraction of PMD patients, even in families that showed linkage with the PLP locus on Xq22. Here we describe the use of an extended protocol that includes screening for both missense mutations and duplications. Two groups of patients were analyzed, one group with 10 independent PMD families and one group with 24 sporadic patients suspected of PMD. Missense mutations in the PLP gene were identified by sequencing. PLP gene duplications were detected by quantitative polymerase chain reaction and/or Southern blot analysis. Sequencing of the PLP gene revealed four mutations in group 1 and one mutation in group 2. However, inclusion of duplication analysis in the screening protocol raised the amount of mutations found in group 1 from 40 to 90%, and in group 2 from 4 to 25%. These results demonstrate that duplications of the PLP gene are the major cause of PMD. Furthermore, it appears that the phenotype resulting from PLP duplications is relatively mild, and that many probands are nontypical PMD patients.
9,633,723	eng	[ "D000008", "Q000000981", "Q000453", "D000328", "D015331", "D006801", "D015994", "D008875", "D009378", "Q000000981", "D018317", "Q000000981", "Q000453", "D009456", "Q000000981", "Q000453", "D010386", "Q000000981", "Q000453", "D013902", "D013899", "Q000000981", "Q000453", "D014057" ]	[ "Abdominal Neoplasms", "Adult", "Cohort Studies", "Humans", "Incidence", "Middle Aged", "Neoplasms, Multiple Primary", "Nerve Sheath Neoplasms", "Neurofibromatosis 1", "Pelvic Neoplasms", "Radiography, Thoracic", "Thoracic Neoplasms", "Tomography, X-Ray Computed" ]	1998	Jun	CT imaging in adults with neurofibromatosis-1: frequent asymptomatic plexiform lesions. The authors examined the incidence and radiologic characteristics of plexiform neurofibromas in neurofibromatosis-1 (NF-1) to define a cohort at greatest risk for malignant nerve-sheath tumors. Plexiform neurofibromas are a frequent complication of NF-1. They can impair function, produce disfigurement, and be the site for the development of malignant nerve-sheath tumors. The incidence and natural history of plexiform neurofibromas is unknown. CT imaging of the chest, abdomen, and pelvis was performed in 91 of 125 consecutive adults (age, > or = 16 years) with NF-1. Twenty percent of patients had plexiform neurofibromas of the chest in the paraspinal, mediastinal, or supraclavicular area. Approximately 40% of patients had abnormal abdominal/pelvic scans. The paraspinal, sacral plexus, sciatic notch, and perirectal regions were the most common sites. Most plexiform neurofibromas were asymptomatic. Imaging also revealed a number of tumors, including malignant nerve-sheath tumors, adrenal tumors, carcinoids, and schwannomas. The frequency of plexiform lesions and other tumors in NF-1 indicates that clinicians should monitor young adults carefully; however, imaging characteristics alone cannot reliably distinguish benign from malignant lesions.
9,633,724	eng	[ "D002675", "D005260", "D006801", "D007223", "D007231", "D008297", "D016472", "Q000209", "Q000517", "Q000601", "D011446", "D016136", "Q000150", "Q000503", "Q000601", "D013116", "Q000601", "D013997", "D016896", "D001750", "Q000209", "Q000517", "Q000628", "D014563", "Q000502" ]	[ "Child, Preschool", "Female", "Humans", "Infant", "Infant, Newborn", "Male", "Motor Neuron Disease", "Prospective Studies", "Spina Bifida Occulta", "Spinal Cord", "Time Factors", "Treatment Outcome", "Urinary Bladder, Neurogenic", "Urodynamics" ]	1998	Jun	Tethered cord syndrome in occult spinal dysraphism: timing and outcome of surgical release. To investigate the influence of neurosurgical intervention on the appearance of upper motor neuron (UMN) signs in newborns diagnosed with occult spinal dysraphism and tethered cord (TC) during the first month of life. A prospective study (1990 to 1996) of 22 consecutive newborns with occult spinal dysraphism monitored for the appearance of UMN signs. Untethering was performed when neurologic or urodynamic investigation indicated the presence of UMN dysfunction. Of 22 patients, 10 remained free of UMN symptoms during follow-up (mean, 67+/-22 months). Untethering was performed in 12 of 22 patients because of the presence of UMN symptoms. In 7 of these 12 patients, there was a documented asymptomatic period of 13+/-11 months before the onset of UMN symptoms. Untethering at a mean age of 18+/-17 months restored normal neurologic and urinary function in all patients (mean postoperative follow-up, 25+/-16 months). Of the 12 children, 5 presented with UMN signs at birth. In these children, untethering was performed at a mean age of 9+/-5 months. In two of these five patients, UMN symptoms did not resolve after surgery, and ongoing conservative bladder treatment was required (mean follow-up, 37+/-14 months). In none of the 12 operated children did signs of retethering occur. A significant number (10/22) of children born with occult spinal dysraphism and TC did not develop UMN symptoms during follow-up; neurosurgical correction after the appearance of an UMN sign restored normal neurologic and urinary function in all children; and untethering in children presenting at birth with UMN symptoms resulted in poorer outcome.
9,633,725	eng	[ "D000293", "D000328", "D004569", "D004827", "Q000503", "Q000601", "D005260", "D005625", "Q000503", "Q000601", "D006801", "D008297", "D008875", "D016896" ]	[ "Adolescent", "Adult", "Electroencephalography", "Epilepsy", "Female", "Frontal Lobe", "Humans", "Male", "Middle Aged", "Treatment Outcome" ]	1998	Jun	EEG findings in frontal lobe epilepsies. As a group, epilepsies of frontal lobe origin are thought to be poorly localized using surface EEG recordings. This finding may depend on the specific areas of frontal lobe from which the seizures originate or the pathologic substrate. We reviewed the presurgical surface EEGs of patients with frontal lobe epilepsy who underwent epilepsy surgery. The specific area of the frontal lobe where seizures originated was determined by 1) intracranial ictal EEG recordings, or 2) the presence of a structural lesion, identified by imaging studies in patients who achieved complete seizure control following surgery. We differentiated patients whose seizures began in the dorsolateral frontal convexity from those whose seizures began in the medial frontal region, and we correlated EEG findings in the interictal, postictal, and ictal states with seizure semiology, pathologic substrate, and surgical outcome. Four of nine patients had seizures originating in the dorsolateral frontal convexity and five had medial frontal onset seizures. Patients whose seizures originated from the dorsolateral convexity had focal interictal epileptiform abnormalities that localized to the region of seizure onset. Patients whose seizures began in the medial frontal region had either no interictal epileptiform abnormality or had multifocal epileptiform discharges. Patients whose seizures began in the dorsolateral convexity showed focal electrographic seizure activity that was localizing. This rhythmic fast activity did not appear to be substrate-specific. Patients whose seizure onset localized to the medial frontal region did not show focal electrographic seizure at clinical onset. We conclude that the scalp EEG recordings of frontal lobe epilepsies contain features that enable differentiation of seizures originating from two different regions of the frontal lobe.
9,633,727	eng	[ "D000293", "D000328", "D000368", "D000369", "D000906", "Q000032", "D001379", "Q000009", "Q000627", "D004311", "D004359", "D005260", "D005938", "Q000008", "Q000009", "Q000627", "D006801", "D007166", "Q000009", "Q000627", "D008297", "D008875", "D009157", "Q000188", "D011239", "Q000008", "Q000009", "Q000627", "D011950", "Q000276", "D017211" ]	[ "Adolescent", "Adult", "Aged", "Aged, 80 and over", "Antibodies", "Azathioprine", "Double-Blind Method", "Drug Therapy, Combination", "Female", "Glucocorticoids", "Humans", "Immunosuppressive Agents", "Male", "Middle Aged", "Myasthenia Gravis", "Prednisolone", "Receptors, Cholinergic", "Treatment Failure" ]	1998	Jun	A randomized double-blind trial of prednisolone alone or with azathioprine in myasthenia gravis. Myasthenia Gravis Study Group. We compared prednisolone (PRED) and azathioprine (AZA) versus prednisolone alone in the treatment of MG. Prednisolone alone or combined with azathioprine is widely used in the treatment of MG, but no randomized placebo-controlled comparative trial data are available. The prednisolone dose and clinical outcome were compared in a multicenter randomized double-blind study of 34 MG patients who were followed up for 3 years. One group (PRED + AZA) received prednisolone (on alternate days) plus azathioprine (2.5 mg/kg); the other group received prednisolone on alternate days plus placebo (PRED + PLAC). Initial high-dose prednisolone (1.5 mg/kg on alternate days) was tapered at remission to the minimal dose required to maintain remission. The prednisolone dose did not differ significantly between the two groups at 1 year (median values: PRED + AZA, 37.5 mg on alternate days; PRED + PLAC, 45 mg on alternate days) but was reduced at 2 and 3 years in the PRED + AZA group (median value at 3 years: PRED + AZA, 0 mg on alternate days; PRED + PLAC, 40 mg on alternate days; p=0.02). Relapses and failures to remit over the 3 years were more frequent in the PRED + PLAC group. There was a sharp rise in the anti-acetylcholine receptor (AChR) titers in the PRED + PLAC group at 2 years. Incidence of side effects was slightly less in the PRED + AZA group. Azathioprine as an adjunct to alternate day prednisolone in the treatment of antibody-positive generalized MG reduces the maintenance dose of prednisolone and is associated with fewer treatment failures, longer remissions, and fewer side effects.
9,633,726	eng	[ "D000328", "D002940", "Q000502", "D004569", "D004833", "Q000175", "Q000503", "Q000601", "D005260", "D006801", "D015994", "D008279", "D008297", "D008875", "D015995", "D003294", "Q000453", "D016896" ]	[ "Adult", "Circadian Rhythm", "Electroencephalography", "Epilepsy, Temporal Lobe", "Female", "Humans", "Incidence", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Prevalence", "Seizures, Febrile", "Treatment Outcome" ]	1998	Jun	Nocturnal temporal lobe epilepsy. To analyze clinical, electrophysiologic, and neuroradiologic characteristics and prognostic factors in a group of patients with temporal lobe epilepsy (TLE) and complex partial seizures (CPS) occurring exclusively or predominantly after they fall asleep or before they awaken. CPS arising during sleep are classically identified with frontal lobe epilepsy. TLE associated with seizures occurring only or predominantly during sleep (nocturnal TLE) is less common. From a series of patients with refractory TLE studied between 1980 and 1996, the authors identified 26 patients (15 men) with nonlesional nocturnal TLE (mean age, 40 years). Clinical and laboratory characteristics of these individuals were studied and compared with a group of 72 age-matched, randomly selected patients with nonlesional TLE and predominantly diurnal seizures (diurnal TLE). Mean age at seizure onset was similar for both groups (16.3 versus 18.7 years). In the nocturnal TLE group, 2 of 26 patients had a positive family history of epilepsy, 18 reported an aura, 4 presented with CPS in clusters, 11 had unilateral and 15 bilateral temporal EEG abnormalities, and 14 of 21 studied had unilateral mesial temporal atrophy. None of these factors differed significantly in the two groups except for higher frequency of the following in the diurnal TLE group compared with the nocturnal TLE group: positive family history for epilepsy (33% versus 8%, p=0.01), estimated frequency of seizures (median, 14 versus 2 per month; p < 0.01), and presence of antecedent febrile convulsions (33% versus 11%, p=0.04). In the nocturnal TLE group, eight patients underwent surgical therapy and became seizure free (follow-up, > 12 months). Only two were seizure free on medication. Infrequent and nonclustered seizures, rare family history of epilepsy, and low prevalence of childhood febrile convulsions characterize nocturnal TLE. Within the TLEs, the nocturnal TLE form seems to have a better surgical prognosis.
9,633,729	eng	[ "D000293", "D000328", "D017668", "D002648", "D002675", "D002895", "Q000235", "D015246", "Q000235", "D004827", "Q000235", "D005260", "D017353", "D005838", "D006801", "D008607", "Q000235", "D008297", "D009136", "Q000453", "Q000235", "D010641", "D012091", "Q000235" ]	[ "Adolescent", "Adult", "Age of Onset", "Child", "Child, Preschool", "Chromosomes, Human, Pair 5", "Deoxyribonuclease EcoRI", "Epilepsy", "Female", "Gene Deletion", "Genotype", "Humans", "Intellectual Disability", "Male", "Muscular Dystrophies", "Phenotype", "Repetitive Sequences, Nucleic Acid" ]	1998	Jun	Epilepsy and mental retardation in a subset of early onset 4q35-facioscapulohumeral muscular dystrophy. The gene for facioscapulohumeral muscular dystrophy (FSHD) has been mapped to chromosome 4q35. In most patients with FSHD, a deletion of 3.3 kb tandemly repeated units within the EcoRI fragment that can be detected by probe p13E-11 is associated with the disease. To elucidate the relation between the phenotype and the genotype in FSHD, we examined 91 Japanese unrelated families with a clinical diagnosis of FSHD (140 patients, 205 healthy individuals). Of these, 78 families (86%) had 4q35-FSHD (127 patients), in which 20 patients (20/127, 16%) were classified as early onset FSHD. We found that all nine patients with the smallest EcoRI fragments (10 to 11 kb) were classified among the early onset group (9/20, 45%), and these patients showed a high frequency of both epilepsy (4/9, 44%) and mental retardation (8/9, 89%). In contrast, none of the remaining patients with 4q35-FSHD had epilepsy or mental retardation. We conclude that FSHD patients with a large gene deletion in the FSHD gene region tend to have a higher chance of showing severe clinical phenotypes with CNS abnormalities. This finding may have practical implications for genetic counseling, although the molecular genetic background remains unclear.
9,633,728	eng	[ "D015139", "D002675", "D004247", "Q000032", "D004272", "Q000235", "Q000378", "D003576", "Q000378", "D006651", "D006801", "D007150", "D007223", "D008297", "D018485", "Q000473", "D009132", "Q000201", "Q000473", "D010375", "D016133" ]	[ "Blotting, Southern", "Child, Preschool", "DNA", "DNA, Mitochondrial", "Electron Transport Complex IV", "Histocytochemistry", "Humans", "Immunohistochemistry", "Infant", "Male", "Muscle Fibers, Skeletal", "Muscles", "Pedigree", "Polymerase Chain Reaction" ]	1998	Jun	Clinical manifestations of mitochondrial DNA depletion. We studied five new patients with mitochondrial DNA (mtDNA) depletion to better define the clinical spectrum of this disorder. mtDNA depletion has been associated with myopathy or hepatopathy, or both, in infants and young children. Involvement of the CNS and peripheral nervous system has not been clearly established. We reviewed the clinical course and performed morphologic, biochemical, and genetic analyses of muscle samples from five patients. Age at onset ranged from 3 months to 5 years, and one patient survived until age 10 1/2 years. Two patients had laboratory and clinical features reminiscent of dystrophinopathy, two had evidence of brain involvement, and two had peripheral neuropathy. Muscle biopsy specimens in all patients showed abundant ragged-red fibers. Biochemistry showed cytochrome c oxidase deficiency in all patients tested and decreased activities of other respiratory chain complexes in some. Inheritance appeared to be autosomal recessive, suggesting that mutations in nuclear DNA are responsible for mtDNA depletion. mtDNA depletion should be considered in children with mitochondrial disorders of uncertain etiology, and criteria for diagnosis are proposed.
9,633,730	eng	[ "D000236", "Q000097", "Q000150", "Q000601", "D000368", "D000690", "Q000150", "Q000503", "D002118", "Q000097", "D018450", "D017809", "D005260", "D006801", "D006961", "Q000150", "D008297", "D008875", "D018908", "Q000503", "D010281", "Q000097", "D010282", "Q000097", "Q000150", "Q000601", "D016105" ]	[ "Adenoma", "Aged", "Amyotrophic Lateral Sclerosis", "Calcium", "Disease Progression", "Fatal Outcome", "Female", "Humans", "Hyperparathyroidism", "Male", "Middle Aged", "Muscle Weakness", "Parathyroid Hormone", "Parathyroid Neoplasms", "Parathyroidectomy" ]	1998	Jun	Primary hyperparathyroidism and ALS: is there a relation? An association between primary hyperparathyroidism (PHP) and amyotrophic lateral sclerosis (ALS) has been noted; however, a causal relation between these disorders has not been confirmed. We report five patients (three men, two women) meeting El Escorial criteria for ALS who also had PHP. In three patients, the diagnosis of PHP was made during the laboratory evaluation for motor neuron disease, and in one patient, the diagnosis of PHP preceded the onset of weakness by 5 months and in another by 2 years. Serum calcium levels in all five patients were elevated, ranging from 11.2 to 12.8 mg/dL (normal, <10.4 mg/dL), as were levels of parathyroid hormone (PTH). All five patients underwent parathyroid adenoma resection with subsequent normalization of serum calcium and PTH levels. Each patient had progressive weakness resulting in death 1 to 3 years following parathyroidectomy. Resection of parathyroid adenomas in patients meeting El Escorial criteria for ALS did not alter the course of ALS. PHP and ALS appear to be coexisting but unrelated disorders.
9,633,731	eng	[ "D000328", "D000368", "D000690", "Q000175", "Q000378", "D001224", "Q000031", "Q000378", "D005260", "D006801", "D008279", "D009682", "D008297", "D008875", "D009044", "Q000378", "D011712", "Q000378", "D012016", "D014018" ]	[ "Adult", "Aged", "Amyotrophic Lateral Sclerosis", "Aspartic Acid", "Female", "Humans", "Magnetic Resonance Imaging", "Magnetic Resonance Spectroscopy", "Male", "Middle Aged", "Motor Cortex", "Pyramidal Tracts", "Reference Values", "Tissue Distribution" ]	1998	Jun	Decreased N-acetylaspartate in motor cortex and corticospinal tract in ALS. The primary objectives of this study were to test whether 1) N-acetylaspartate (NAA), a neuronal marker, is reduced in motor cortex and corticospinal-tract (CST) brain regions of ALS patients; and 2) motor cortex NAA correlates to a clinical measurement of upper motor neuron function in ALS patients. Ten probable or definite ALS patients and nine neurologically normal control subjects were studied. Three axial planes of two-dimensional 1H MRSI data were collected, using a single spin-echo multislice sequence (TE140/TR2000). Two of the 1H MRSI planes were positioned superior to the lateral ventricles, and one plane was positioned at the level of the internal capsule. Spectroscopy voxels were selected from motor cortex, frontal cortex, parietal cortex, medial gray matter, centrum semiovale white matter, anterior internal capsule, and posterior internal capsule. Peak integrals were obtained for the three major 1H MRSI singlet resonances, NAA, creatine and phosphocreatine (Cr), and cholines (Cho). Maximum finger-tap rate was used as a clinical measurement of upper motor neuron function. In ALS, brain NAA/(Cho+Cr) was reduced 19% (p=0.024) in the motor cortex and 16% (p=0.021) in the CST (centrum semiovale and posterior internal capsule) regions. NAA/ (Cho+Cr) was not reduced in frontal cortex, parietal cortex, medial gray matter, or anterior internal capsule. There was a significant relation between ALS motor cortex NAA/(Cho+Cr) and maximum finger-tap rate (r=0.80; p=0.014). NAA/(Cho+Cr) was reduced in motor cortex and CST regions and unchanged in other brain regions of ALS patients when compared with controls. These findings are consistent with the known distribution of neuronal loss in ALS. The positive correlation between motor cortex NAA/(Cho+Cr) and maximum finger-tap rate suggests that reduced NAA/(Cho+Cr) is a surrogate marker of motor cortex neuron loss in ALS. These findings support the study of 1H MRSI NAA measurement as an objective and quantitative measurement of upper motor neuron dysfunction in ALS.
9,633,732	eng	[ "D000208", "D000328", "D000368", "D000818", "D001323", "Q000032", "D001327", "Q000276", "D001342", "Q000150", "Q000276", "D005260", "D006801", "D008297", "D008875", "D009369", "Q000150", "D009422", "Q000276", "D009474", "Q000276", "D011233", "D011863", "Q000379", "D051381", "D011978", "Q000276" ]	[ "Acute Disease", "Adult", "Aged", "Animals", "Autoantibodies", "Autoimmune Diseases", "Autonomic Nervous System Diseases", "Female", "Humans", "Male", "Middle Aged", "Neoplasms", "Nervous System Diseases", "Neurons", "Precipitin Tests", "Radioimmunoassay", "Rats", "Receptors, Nicotinic" ]	1998	Jun	Neuronal nicotinic ACh receptor antibody in subacute autonomic neuropathy and cancer-related syndromes. Autoantibodies specific for the acetylcholine receptor (AChR) of skeletal muscle (containing the alpha1 subunit) impair neuromuscular transmission in myasthenia gravis (MG). AChRs mediating fast synaptic transmission through autonomic ganglia are structurally similar to muscle AChR, but contain the alpha3 subunit. We propose that ganglionic AChR autoimmunity may cause dysautonomia. To test serum of patients with autonomic neuropathy for autoantibodies of neuronal ganglionic AChR specificity. We developed an immunoprecipitation radioassay by complexing epibatidine (125I-labeled high affinity agonist) to a Triton X-100-solubilized AChR antigen from peripheral neuroblastoma membranes. Monoclonal rat immunoglobulins (IgG) specific for muscle or neuronal AChRs validated the assay's specificity. We tested serum from 52 healthy subjects, 12 patients with subacute autonomic neuropathy, and 248 patients with other neurologic disorders. Twelve patients had antibodies that bound unequivocally to ganglionic AChR. Five had subacute autonomic neuropathy, and three (of six tested) had Isaacs' syndrome; four of these eight had a carcinoma (lung, bladder, rectum, thyroid). The remaining four seropositive patients (two Lambert-Eaton syndrome, one dementia, one sensory neuronopathy) all had Ca2+ channel antibodies and three had small cell lung carcinoma. No healthy subject had ganglionic AChR antibodies, nor did 62 patients with MG and muscle AChR antibodies. Neuronal AChR antibodies are a novel serologic marker of neurologic autoimmunity. The pathogenicity of neuronal AChR autoantibodies in autonomic neuropathy, Isaacs' syndrome, or other neurologic disorders remains to be shown, as has been demonstrated for muscle AChR antibodies in MG. An autoimmune and potentially paraneoplastic etiology is implicated in seropositive patients.
9,633,733	eng	[ "D015526", "Q000145", "Q000503", "Q000523", "D000328", "D003071", "Q000502", "D018450", "D005260", "D015658", "Q000209", "D006801", "D008297", "D008875", "D011597", "Q000502", "D012307", "D015819", "Q000150", "D016019" ]	[ "AIDS Dementia Complex", "Adult", "Cognition", "Disease Progression", "Female", "HIV Infections", "Humans", "Male", "Middle Aged", "Psychomotor Performance", "Risk Factors", "Substance Abuse, Intravenous", "Survival Analysis" ]	1998	Jun	Variable progression of HIV-associated dementia. A consecutive series of 71 patients diagnosed with HIV-associated dementia (HAD) (1984-1994) were studied to characterize the clinical course of HAD, and to identify predictive markers of rapid neurologic progression. Neurologic progression rate was determined from the change in the Memorial Sloan Kettering (MSK) dementia severity score from diagnosis to death. Those with the most rapid progression in neurologic disability were compared with those with slow or no progression. Autopsy material was immunostained for macrophage activation markers and gp41 in 30 individuals. Median survival was 3.3 months and 6.1 months for rapid-progression and no-progression patients, respectively. Rapid progression was associated with injection drug use but not with race, gender, or age. CD4+ cell counts were lower at diagnosis among rapid-progression than no-progression patients but no differences in AIDS-defining illnesses or patterns of antiretroviral therapy were found. At presentation, rapid-progression patients had more prominent symptoms of mental slowing than those with no progression; however, no other clinical features, CSF, or imaging features distinguished the groups. Less abundant macrophage activation in both basal ganglia and midfrontal gyrus regions, as judged by HAM56 immunostaining, was noted in 9 no-progression patients, compared with 12 rapid-progression patients. Neurologic progression and survival with HAD is highly variable. A significant proportion of individuals with dementia have prolonged survival of more than 12 months and remain cognitively stable. A history of injection drug use and presentation with prominent psychomotor slowing is associated with more rapid neurologic progression, and these patients tend to show more abundant macrophage activation within the CNS.
9,633,734	eng	[ "D000328", "D019380", "Q000627", "D001810", "Q000502", "D002560", "Q000502", "D003072", "Q000150", "D006679", "Q000150", "Q000175", "Q000188", "Q000503", "D006801", "D008279", "D008875", "D010487", "Q000098", "D012016", "D015215", "Q000627" ]	[ "Adult", "Anti-HIV Agents", "Blood Volume", "Cerebrovascular Circulation", "Cognition Disorders", "HIV Seropositivity", "Humans", "Magnetic Resonance Imaging", "Middle Aged", "Periaqueductal Gray", "Reference Values", "Zidovudine" ]	1998	Jun	Increased cerebral blood volume in HIV-positive patients detected by functional MRI. To study changes in cerebral hemodynamics related to HIV infection. Cerebral injury is a well-known manifestation of HIV infection. Physiologic changes in the HIV brain may precede structural changes and may be detected by functional MRI (fMRI). Dynamic contrast fMRI was used to measure the cerebral blood volume (CBV) in 13 patients infected with HIV and in 7 healthy control subjects. Significant increases in dynamic CBV were found in the deep (p < 0.001) and cortical gray matter (p < 0.05) of HIV-positive (HIV+) patients. Patients with definite cognitive impairment showed significantly greater increases in CBV in the deep gray matter (DGM) compared with those without impairment. In one patient with rapidly progressive cognitive impairment, these abnormalities reversed and paralleled clinical improvement after initiation of zidovudine monotherapy. This study supports the hypothesis that HIV infection is associated with significant cerebral hemodynamic changes, particularly in the DGM, that may contribute to cognitive dysfunction in AIDS. Functional MRI may be useful for early detection of cerebral injury and for the assessment of novel therapies.
9,633,735	eng	[ "D000328", "D044467", "Q000235", "D000995", "Q000627", "D002170", "D002494", "Q000382", "D015331", "D016172", "D005260", "D014644", "Q000235", "D006801", "D008297", "D008581", "Q000382", "D009169", "Q000235", "Q000302", "Q000472", "D012150", "D013045", "D014376", "Q000382" ]	[ "Adult", "American Indian or Alaska Native", "Antitubercular Agents", "Canada", "Central Nervous System Infections", "Cohort Studies", "DNA Fingerprinting", "Female", "Genetic Variation", "Humans", "Male", "Meningitis", "Mycobacterium tuberculosis", "Polymorphism, Restriction Fragment Length", "Species Specificity", "Tuberculosis" ]	1998	Jun	M. tuberculosis molecular variation in CNS infection: evidence for strain-dependent neurovirulence. To determine the molecular diversity among Mycobacterium tuberculosis isolates associated with central nervous system tuberculosis (CNS TB) in a defined cohort of HIV uninfected patients. A retrospective analysis was performed of clinical and laboratory data for all patients with CNS TB diagnosed in Manitoba, Canada, between 1979 and 1996. Restriction fragment-length polymorphisms (RFLP) of archival isolates of M. tuberculosis from CNS TB patients were determined and interpreted against the frequency of different isolates from all TB patients in the years 1992 to 1996. Among 2,334 patients with active TB, CNS TB was diagnosed in 42 (1.8%); meningitis with or without tuberculoma in 76%; and tuberculoma alone in 24%. CNS TB patients were significantly more likely to be young (<40 years old), female, and of Aboriginal origin. Morbidity (fixed/recurrent CNS deficit) rate was 29% and mortality rate was 26%. An adverse outcome, either morbidity or mortality, was significantly more common in those with meningitis. RFLP analysis of isolates (n=19) from CNS TB patients revealed 13 distinct restriction patterns with a predominance of the type 1 pattern (n=6). The frequency of type 1 restriction pattern was significantly greater in patients with CNS TB compared to all TB patients in Manitoba. CNS TB continues to have a high morbidity and mortality despite modern methods of detection and treatment. Although several strains of M. tuberculosis cause CNS TB, the current study suggests that the occurrence of CNS TB may be strain-dependent.
9,633,736	eng	[ "D000328", "D001921", "Q000473", "D004185", "D004305", "D004311", "D005260", "D006801", "D008279", "D008297", "D008775", "Q000008", "Q000009", "Q000627", "D009103", "Q000175", "Q000188", "Q000503", "D009333", "D018696", "Q000008", "Q000009", "Q000627", "D012008", "D013116", "Q000473" ]	[ "Adult", "Brain", "Disability Evaluation", "Dose-Response Relationship, Drug", "Double-Blind Method", "Female", "Humans", "Magnetic Resonance Imaging", "Male", "Methylprednisolone", "Multiple Sclerosis", "Neck", "Neuroprotective Agents", "Recurrence", "Spinal Cord" ]	1998	Jun	Randomized trial comparing two different high doses of methylprednisolone in MS: a clinical and MRI study. To assess the efficacy of two different high doses of intravenous methylprednisolone (IVMP) for the treatment of relapses in MS. IVMP is the treatment of choice for MS relapses, but it is unknown whether its effects are dose related. We conducted a double-blind, randomized study. Follow-up included serial clinical and MRI recordings at baseline and at 7, 15, 30, and 60 days after the beginning of treatment. Outcome measures were the number of brain and cervical spinal cord MRI contrast-enhancing lesions, and the Expanded Disability Status Scale score. Both treatment regimens improved clinical scores and reduced the number of MRI enhancing lesions during the follow-up period. The higher dose of IVMP was significantly more effective than the lower dose in reducing the number of MRI contrast-enhanced lesions at 30 and 60 days, mainly by decreasing the rate of new lesion formation. The higher dosage of IVMP has a more powerful and prolonged action in maintaining blood-brain barrier integrity after a clinical relapse.
9,633,738	eng	[ "D000203", "D000328", "D000368", "D000369", "D000701", "Q000009", "Q000627", "D003929", "Q000188", "Q000503", "D004311", "D005260", "D005500", "D006801", "D008297", "D008875", "D010146", "Q000503", "D010166", "D011788", "D012890", "Q000502", "D014147", "Q000009", "Q000627" ]	[ "Activities of Daily Living", "Adult", "Aged", "Aged, 80 and over", "Analgesics, Opioid", "Diabetic Neuropathies", "Double-Blind Method", "Female", "Follow-Up Studies", "Humans", "Male", "Middle Aged", "Pain", "Palliative Care", "Quality of Life", "Sleep", "Tramadol" ]	1998	Jun	Double-blind randomized trial of tramadol for the treatment of the pain of diabetic neuropathy. The objective of this study was to evaluate the efficacy and safety of tramadol in treating the pain of diabetic neuropathy. The pain of diabetic neuropathy is a major cause of morbidity among these patients and treatment, as with other small-fiber neuropathies, is often unsatisfactory. Tramadol is a centrally acting analgesic for use in treating moderate to moderately severe pain. This multicenter, outpatient, randomized, double-blind, placebo-controlled, parallel-group study consisted of a washout/screening phase, during which all analgesics were discontinued, and a 42-day double-blind treatment phase. A total of 131 patients with painful diabetic neuropathy were treated with tramadol (n=65) or placebo (n=66) tramadol, which were administered as identical capsules in divided doses four times daily. The primary efficacy analysis compared the mean pain intensity scores in the tramadol and placebo groups obtained at day 42 of the study or at the time of discontinuation. Secondary efficacy assessments were the pain relief rating scores and a quality of life evaluation based on daily activities and sleep characteristics. Tramadol, at an average dosage of 210 mg/day, was significantly (p < 0.001) more effective than placebo for treating the pain of diabetic neuropathy. Patients in the tramadol group scored significantly better in physical (p=0.02) and social functioning (p=0.04) ratings than patients in the placebo group. No statistically significant treatment effects on sleep were identified. The most frequently occurring adverse events with tramadol were nausea, constipation, headache, and somnolence. The results of this placebo-controlled trial showed that tramadol was effective and safe in treating the pain of diabetic neuropathy.
9,633,740	eng	[ "D001921", "Q000000981", "Q000473", "D002555", "Q000502", "D003560", "Q000150", "Q000503", "Q000601", "D004027", "Q000503", "D006801", "D019585", "Q000175", "Q000209", "D008279", "D008297", "D008875", "D010523", "Q000150", "Q000503", "Q000601", "D011312", "D012422", "D012894", "Q000502", "D013126", "D014057" ]	[ "Brain", "Cerebrospinal Fluid", "Cysts", "Diencephalon", "Humans", "Intracranial Hypotension", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Peripheral Nervous System Diseases", "Pressure", "Rupture, Spontaneous", "Sleep Stages", "Spinal Nerve Roots", "Tomography, X-Ray Computed" ]	1998	Jun	Spontaneous intracranial hypotension resulting in stupor caused by diencephalic compression. A 51-year-old man had a 4-month history of progressive headache and gradual onset of somnolence. MRI suggested spontaneous intracranial hypotension (SIH) with diencephalic compression, but he did not improve after three epidural blood patches. He became alert following intrathecal saline infusion that normalized his CSF pressure. A CSF leak was noted on spinal MRI and confirmed with CT contrast myelography. Surgical ligation of a torn dural root sleeve isolating a ruptured Tarlov's cyst resulted in permanent cure.
9,633,739	eng	[ "D049672", "D049673", "D006782", "Q000266", "Q000458", "D006801", "D009422", "Q000266", "Q000628", "D009462", "Q000266", "D015143" ]	[ "History, 19th Century", "History, 20th Century", "Hospitals, Special", "Humans", "Nervous System Diseases", "Neurology", "Philadelphia" ]	1998	Jun	Philadelphia Infirmary for Nervous Diseases: America's original model of institutional neurology. The role and contributions of the Philadelphia Orthopedic Hospital and Infirmary for Nervous Diseases in the development of neurology in 19th-century America are described. American neurology was largely born during the Civil War through the work of S.W. Mitchell at Turner's Lane Hospital. With the closing of this military facility, the United States was left without an institution dedicated to neurologic research and the treatment of nervous system diseases. Nineteenth century archival data, including original Trustees' minutes, annual board of managers reports, patient case books, and published research from the Philadelphia Orthopedic Hospital and Infirmary for Nervous Diseases were studied. The Philadelphia Orthopedic Hospital and Infirmary for Nervous Diseases promoted the development of neurology in the United States through three main activities. First, it offered patients with primary nervous system diseases, arthritis, and orthopedic disorders specialized care that was unavailable at medical universities. Second, its medical staff, especially Mitchell, provided opportunities for advanced neurologic education. Postgraduate physicians interested in neurologic disease attended formal lectures and directly participated in the operation of outpatient clinics and inpatient rounds. Finally, its formalized record system in the form of case books facilitated neurologic research. These records formed the basis of landmark publications by Mitchell, Sinkler, Osler, and others on rest therapy, spastic palsies, chorea, and other topics. As America's first and comprehensive peacetime neurologic facility, the Philadelphia Orthopedic Hospital and Infirmary for Nervous Diseases fostered the evolution of neurology as a separate, viable specialty in the post-Civil War period and provided a particular focus for the study of interactions among orthopedic, nutritional, and neurologic disorders.
9,633,737	eng	[ "D000368", "D000701", "Q000008", "Q000009", "Q000627", "D018592", "D003692", "D004311", "D005260", "D006562", "Q000150", "D006801", "D008297", "D008875", "D009437", "Q000188", "Q000503", "Q000821", "D010098", "Q000008", "Q000009", "Q000627", "D010146", "Q000503", "D016896" ]	[ "Aged", "Analgesics, Opioid", "Cross-Over Studies", "Delayed-Action Preparations", "Double-Blind Method", "Female", "Herpes Zoster", "Humans", "Male", "Middle Aged", "Neuralgia", "Oxycodone", "Pain", "Treatment Outcome" ]	1998	Jun	Efficacy of oxycodone in neuropathic pain: a randomized trial in postherpetic neuralgia. Although opioid analgesics are used in the management of neuropathic pain syndromes, evidence of their efficacy remains to be established. We evaluated the clinical efficacy and safety of oxycodone in neuropathic pain using postherpetic neuralgia as a model. Patients with postherpetic neuralgia of at least moderate intensity were randomized to controlled-release oxycodone 10 mg or placebo every 12 hours, each for 4 weeks, using a double-blind, crossover design. The dose was increased weekly up to a possible maximum of 30 mg every 12 hours. Pain intensity and pain relief were assessed daily, and steady (ongoing) pain, brief (paroxysmal) pain, skin pain (allodynia), and pain relief were recorded at weekly visits. Clinical effectiveness, disability, and treatment preference were also assessed. Fifty patients were enrolled and 38 completed the study (16 men, 22 women, age 70+/-11 years, onset of postherpetic neuralgia 31+/-29 months, duration of pain 18+/-5 hours per day). The oxycodone dose during the final week was 45+/-17 mg per day. Compared with placebo, oxycodone resulted in pain relief (2.9+/-1.2 versus 1.8+/-1.1, p=0.0001) and reductions in steady pain (34+/-26 versus 55+/-27 mm, p=0.0001), allodynia (32+/-26 versus 50+/-30 mm, p=0.0004), and paroxysmal spontaneous pain (22+/-24 versus 42+/-32 mm, p=0.0001). Global effectiveness, disability, and masked patient preference all showed superior scores with oxycodone relative to placebo (1.8+/-1.1 versus 0.7+/-1.0, p=0.0001; 0.3+/-0.8 versus 0.7+/-1.0, p=0.041; 67% versus 11%, p=0.001, respectively). Controlled-release oxycodone is an effective analgesic for the management of steady pain, paroxysmal spontaneous pain, and allodynia, which frequently characterize postherpetic neuralgia.
9,633,741	eng	[ "D000368", "D002545", "Q000188", "D002305", "Q000139", "Q000000981", "D002561", "Q000188", "D017809", "D005260", "D006801", "D008875", "D010490", "Q000139", "Q000000981", "D010960", "Q000009", "Q000627", "D011994", "D015912", "Q000009", "D010959", "Q000009", "Q000627", "D014463" ]	[ "Aged", "Brain Ischemia", "Cardiac Tamponade", "Cerebrovascular Disorders", "Fatal Outcome", "Female", "Humans", "Middle Aged", "Pericardial Effusion", "Plasminogen Activators", "Recombinant Proteins", "Thrombolytic Therapy", "Tissue Plasminogen Activator", "Ultrasonography" ]	1998	Jun	Hemopericardium and cardiac tamponade after thrombolysis for acute ischemic stroke. Hemorrhage is the major complication of IV recombinant tissue plasminogen activator (rt-PA) treatment for stroke. We report three patients with mild or indistinct cardiac symptoms prior to thrombolysis in whom hemodynamically significant cardiac tamponade occurred after treatment with rt-PA. Acute ischemic stroke patients may have undetected myocardial or pericardial disease that may pose a risk for hemopericardium and life-threatening tamponade after treatment with rt-PA.
9,633,742	eng	[ "D000368", "D002545", "Q000150", "Q000175", "D005158", "Q000209", "Q000503", "D006801", "D008279", "D008280", "D008297", "D010812", "D011149", "Q000098", "Q000473", "D014836" ]	[ "Aged", "Brain Ischemia", "Facial Paralysis", "Humans", "Magnetic Resonance Imaging", "Magnetics", "Male", "Physical Stimulation", "Pons", "Volition" ]	1998	Jun	Isolated voluntary facial paresis due to pontine ischemia. We describe a patient with isolated voluntary facial paresis due to a unilateral lacunar lesion in the contralateral mediodorsal middle base of the pons. Transcranial magnetic stimulation confirmed the involvement of supranuclear corticofacial tract fibers and sparing of the corticolingual and corticospinal connections. This observation demonstrates that the fibers conveying voluntary orofacial activation descend mediodorsally at the level of the middle pons and that the fibers conveying emotional activation may be assumed to converge below this level.
9,633,744	eng	[ "D014695", "D015170", "Q000502", "D006801", "D008026", "D008279", "D008297", "D008875", "D009333", "D013116", "Q000473", "Q000601", "D013118", "Q000175", "Q000209", "Q000503", "D014057", "D017287", "Q000009" ]	[ "Cerebral Ventriculography", "Cerebrospinal Fluid Pressure", "Humans", "Ligation", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Neck", "Spinal Cord", "Spinal Cord Diseases", "Tomography, X-Ray Computed", "Ventriculoperitoneal Shunt" ]	1998	Jun	Upper cervical myelopathy associated with low CSF pressure: a complication of ventriculoperitoneal shunt. A patient who had undergone ventriculoperitoneal shunting developed upper cervical myelopathy. His CSF pressure was markedly low, and deformation of the spinal cord and shrinkage of the subarachnoid space at the upper cervical level were found in radiologic examinations. Ligation of the shunt tube resulted in almost complete recovery. The effect of excessive drainage may have caused the abnormalities.
9,633,745	eng	[ "D002535", "Q000002", "D002675", "D003937", "D005260", "D006429", "Q000151", "Q000175", "Q000209", "D006801", "D007223", "D008279", "D014057" ]	[ "Cerebral Aqueduct", "Child, Preschool", "Diagnosis, Differential", "Female", "Hemiplegia", "Humans", "Infant", "Magnetic Resonance Imaging", "Tomography, X-Ray Computed" ]	1998	Jun	Congenital bilateral perisylvian polymicrogyria presenting as congenital hemiplegia. We report three children with pure congenital hemiplegia found to have congenital bilateral perisylvian polymicrogyria (CBPP). None of our patients had the seizures, oromotor dysfunction, or cognitive impairment usually associated with CBPP. CBPP may be more common and heterogeneous than previously thought, is easily recognized by MRI, and should be included in the differential diagnosis of the young child presenting with congenital hemiplegia.
9,633,746	eng	[ "D000293", "D002331", "Q000097", "Q000134", "Q000652", "D002648", "D002675", "D005260", "D005334", "Q000097", "Q000134", "Q000652", "D005759", "Q000097", "Q000134", "Q000652", "D006801", "D007223", "D007231", "D008297", "D016920", "Q000097", "Q000134", "Q000652", "D009422", "Q000097", "Q000134", "Q000652", "D009994", "D012016", "D012640", "Q000097", "Q000134", "Q000652" ]	[ "Adolescent", "Carnitine", "Child", "Child, Preschool", "Female", "Fever", "Gastroenteritis", "Humans", "Infant", "Infant, Newborn", "Male", "Meningitis, Bacterial", "Nervous System Diseases", "Osmolar Concentration", "Reference Values", "Seizures" ]	1998	Jun	CSF levels of carnitine in children with meningitis, neurologic disorders, acute gastroenteritis, and seizure. Carnitine concentrations in CSF, serum, and urine in normal febrile children and children with meningitis, neurologic disorders, and dehydration were studied. Carnitine levels in CSF were 1/10 compared with serum in normal febrile children. These levels increased two- to three-fold in the pathologic conditions studied. Since damage to the blood-brain barrier occurs in these conditions, higher blood-brain barrier permeability might explain CNS carnitine accumulation.
9,633,747	eng	[ "D000368", "D016913", "D001026", "D007562", "Q000209", "D006801", "D007430", "D008297", "D011183", "D012709", "Q000627" ]	[ "Aged", "Blood Component Transfusion", "Coronary Artery Bypass", "Creutzfeldt-Jakob Syndrome", "Humans", "Intraoperative Care", "Male", "Postoperative Complications", "Serum Albumin" ]	1998	Jun	Creutzfeldt-Jakob disease (CJD) after blood product transfusion from a donor with CJD. We report a second case of an association between an albumin transfusion and Creutzfeldt-Jakob disease. On balance, we believe our case represents a chance and not a causal relation.
9,633,748	eng	[ "D001927", "Q000139", "Q000503", "D002444", "Q000008", "Q000009", "D002511", "Q000008", "Q000009", "D062787", "D004409", "Q000503", "D005260", "D006801", "D008297", "D008875", "D009207", "Q000139", "D012894", "Q000502" ]	[ "Brain Diseases", "Cefuroxime", "Cephalosporins", "Drug Overdose", "Dyskinesia, Drug-Induced", "Female", "Humans", "Male", "Middle Aged", "Myoclonus", "Sleep Stages" ]	1998	Jun	Cefuroxime-induced encephalopathy. We describe four patients who developed an encephalopathic syndrome characterized by obtundation or stupor, myoclonic jerks, and asterixis in association with cefuroxime therapy. Three patients had renal failure. These cases suggest that cefuroxime in overdose or in conventional doses in patients with renal failure can cause a reversible encephalopathy. This syndrome may have been unrecognized because it usually occurs in severely ill patients with additional causes for encephalopathy.
9,633,749	eng	[ "D000328", "D001483", "D002319", "Q000503", "D004272", "Q000235", "D017079", "Q000502", "D005260", "D006801", "D008969", "D015394", "D009132", "Q000473", "D009136", "Q000235", "Q000473", "Q000503", "D009154", "Q000235", "D009420", "Q000503", "D016133", "D012150", "D012313", "Q000235", "D000077278", "D012358", "Q000235" ]	[ "Adult", "Base Sequence", "Cardiovascular System", "DNA, Mitochondrial", "Exercise Tolerance", "Female", "Humans", "Molecular Sequence Data", "Molecular Structure", "Muscles", "Muscular Dystrophies", "Mutation", "Nervous System", "Polymerase Chain Reaction", "Polymorphism, Restriction Fragment Length", "RNA", "RNA, Mitochondrial", "RNA, Transfer, Met" ]	1998	Jun	A new mitochondrial tRNA(Met) gene mutation in a patient with dystrophic muscle and exercise intolerance. A 30-year-old woman with a novel heteroplasmic U4409C mtDNA mutation in the tRNA(Met) gene presented with growth retardation, muscle weakness, severe exercise intolerance, and lactic acidosis. Muscle biopsy showed unusually severe dystrophic features. The mutation was not present in maternal relatives or 25 healthy subjects. Single-fiber PCR-RFLP analysis of mtDNA showed higher proportion of the mutation in COX-negative than in COX-positive muscle fibers.
9,633,750	eng	[ "D000293", "D000690", "Q000175", "D001921", "Q000473", "D006801", "D008279", "D008297", "D011712", "Q000473", "D012016" ]	[ "Adolescent", "Amyotrophic Lateral Sclerosis", "Brain", "Humans", "Magnetic Resonance Imaging", "Male", "Pyramidal Tracts", "Reference Values" ]	1998	Jun	MRI in juvenile ALS: a patient report. We describe the MR images of a patient with juvenile ALS. MRI of the brain showed bilateral hyperintensities along the corticospinal tracts extending from the corona radiata to the brainstem on T2-weighted images. These findings should be differentiated from the slight hyperintensities seen in the posterior limbs of the internal capsules in normal subjects.
9,633,751	eng	[ "D000368", "D001921", "Q000473", "D003937", "D004568", "D004576", "D005260", "D006801", "D008279", "D011602", "Q000175", "D014202", "Q000175" ]	[ "Aged", "Brain", "Diagnosis, Differential", "Electrodiagnosis", "Electromyography", "Female", "Humans", "Magnetic Resonance Imaging", "Psychophysiologic Disorders", "Tremor" ]	1998	Jun	Electrophysiological aids in distinguishing organic from psychogenic tremor. The clinical differentiation of tremors of organic and psychogenic origin can be difficult. We describe a patient with unilateral upper limb tremor that was initially considered to have a psychogenic cause, but subsequent frequency analysis of EMG signals and accelerometer recordings indicated that the tremor was organic in nature. An ischemic lesion in the contralateral lentiform nucleus found on MRI supported this conclusion. Quantitative electrophysiologic studies may thus be useful in distinguishing organic from psychogenic tremor.
9,633,752	eng	[ "D000978", "Q000627", "D004581", "D006801", "D007854", "Q000009", "D008297", "D008875", "D016273", "D010300", "Q000188", "Q000453", "D011177", "D015995" ]	[ "Antiparkinson Agents", "Electronics", "Humans", "Lead", "Male", "Middle Aged", "Occupational Exposure", "Parkinson Disease", "Postal Service", "Prevalence" ]	1998	Jun	High prevalence of parkinsonism after occupational exposure to lead-sulfate batteries. Seven of nine postal workers exposed to lead-sulfate batteries over a period of up to 30 years developed parkinsonian symptoms. One of the remaining two showed left-hand bradykinesia and one was not available for examination. The high prevalence and cause of parkinsonism in these patients remains unexplained. Lead intoxication may play a role in the occurrence of parkinsonian symptoms, but involvement of sulfate and other sulfur compounds must also be considered.
9,633,753	eng	[ "D000328", "D001483", "D001921", "Q000473", "D001933", "Q000473", "D005260", "D006801", "D008279", "D008297", "D008875", "D012091", "D013132", "Q000175", "Q000235", "D013788", "Q000473" ]	[ "Adult", "Base Sequence", "Brain", "Brain Stem", "Female", "Humans", "Magnetic Resonance Imaging", "Male", "Middle Aged", "Repetitive Sequences, Nucleic Acid", "Spinocerebellar Degenerations", "Thalamus" ]	1998	Jun	The brainstem and thalamic lesions in dentatorubral-pallidoluysian atrophy: an MRI study. We studied the frequency and characteristics of brainstem and thalamic lesions in dentatorubral-pallidoluysian atrophy using MRI. Of 15 subjects diagnosed by DNA analysis, 13 had lesions in the pontine base, nine in the midbrain, and five in the thalamus. Lesions were correlated positively with the patient's age, but not with neurologic features or numbers of CAG repeats. Patients with Machado-Joseph disease or spinocerebellar ataxia 1 did not show these characteristic lesions.
9,633,754	eng	[ "D000339", "Q000187", "D000978", "Q000627", "D004305", "D005260", "D006801", "D007262", "D007980", "Q000627", "D008297", "D008875", "D010300", "Q000188", "Q000523", "D012647" ]	[ "Affect", "Antiparkinson Agents", "Dose-Response Relationship, Drug", "Female", "Humans", "Infusions, Intravenous", "Levodopa", "Male", "Middle Aged", "Parkinson Disease", "Self-Assessment" ]	1998	Jun	Mood response to levodopa infusion in early Parkinson's disease. Mood response to levodopa infusion was studied in 18 Parkinson's disease (PD) patients during the first year of levodopa therapy before and after 2-hour (1.0 mg/kg/h) levodopa infusions at baseline and 6- and 12-month follow-up. Mood elevation was greatest after a 2-day levodopa holiday at the 6- and 12-month assessments. Age, sex, duration and severity of PD, and ongoing oral levodopa dose did not correlate with mood response. Mood response in these patients differs from that seen in advanced patients, possibly because of sensitization to levodopa's mood effects.
9,633,755	eng	[ "D000293", "D000328", "D002648", "D005133", "Q000502", "D005260", "D006801", "D019586", "Q000150", "D008279", "D008297", "D015835", "Q000209", "Q000503", "D012851", "Q000150", "Q000175" ]	[ "Adolescent", "Adult", "Child", "Eye Movements", "Female", "Humans", "Intracranial Hypertension", "Magnetic Resonance Imaging", "Male", "Ocular Motility Disorders", "Sinus Thrombosis, Intracranial" ]	1998	Jun	Unusual ocular motility disturbances with increased intracranial pressure. We evaluated nine patients with external ophthalmoparesis and increased intracranial pressure. The eye movements normalized when the intracranial pressure was controlled. Investigations for an underlying cause of elevated cerebrospinal fluid pressure are warranted when ocular motility disorders are present.
9,633,756	eng	[ "D000328", "D005240", "D005260", "D006801", "D008279", "D008297", "D009902", "Q000175", "Q000503", "D010775", "D010865", "D015349", "Q000502", "D014785", "Q000502" ]	[ "Adult", "Feasibility Studies", "Female", "Humans", "Magnetic Resonance Imaging", "Male", "Optic Neuritis", "Photic Stimulation", "Pilot Projects", "Vision, Monocular", "Vision, Ocular" ]	1998	Jun	Visual activation patterns in patients with optic neuritis: an fMRI pilot study. We studied the use of functional MRI (fMRI) with visual stimulation in nine patients with unilateral optic neuritis. Eight healthy subjects served as controls. Patients showed reduced activation upon stimulation of the affected eye, on average 33% (range 0 to 156%) of the average monocular activation in the control group. Decreased activation was also seen for the unaffected eye (61% of control values, range 3 to 133%). We conclude that fMRI with visual stimulation is feasible in patients with optic neuritis and deserves future study.
9,633,757	eng	[ "D000975", "Q000627", "D000978", "Q000627", "D004305", "D004311", "D006801", "D010300", "Q000188", "D012642", "Q000627", "D014810", "Q000008", "Q000134", "Q000627" ]	[ "Antioxidants", "Antiparkinson Agents", "Dose-Response Relationship, Drug", "Double-Blind Method", "Humans", "Parkinson Disease", "Selegiline", "Vitamin E" ]	1998	Jun	Alpha tocopherol in CSF of subjects taking high-dose vitamin E in the DATATOP study. Parkinson Study Group. Alpha-Tocopherol concentrations were determined in the CSF of patients with early untreated Parkinson's disease receiving 2,000 IU vitamin E orally per day. After treatment the concentrations increased significantly (p < 0.001) by 76+/-10 (SE)%. The net increases in CSF alpha-tocopherol concentrations after treatment showed a significant positive correlation with the number of days of vitamin E ingestion (p < 0.001). Thus, high-dose vitamin E treatment results in elevating CSF vitamin E levels and possibly brain vitamin E levels.
9,633,758	eng	[ "D000368", "D001288", "Q000502", "D002561", "Q000503", "D007839", "Q000502", "D006801", "D013577" ]	[ "Aged", "Attention", "Cerebrovascular Disorders", "Functional Laterality", "Humans", "Syndrome" ]	1998	Jun	Unilateral neglect: a common but heterogeneous syndrome. The neglect syndrome is a cluster of neurologic symptoms commonly found after right hemisphere damage. This study investigates the degree of association between the main components in a representative sample of 69 patients at 2 to 3 days poststroke. Despite evidence of statistically significant associations between components, many dissociations were found, indicating that neglect is a highly heterogeneous condition.
9,633,760	eng	[ "D000328", "D000368", "D000690", "Q000175", "Q000503", "D004558", "D004568", "D005260", "D006801", "D008297", "D008875", "D016472", "Q000175", "Q000503", "D009431", "Q000502", "D013126", "Q000503" ]	[ "Adult", "Aged", "Amyotrophic Lateral Sclerosis", "Electric Stimulation", "Electrodiagnosis", "Female", "Humans", "Male", "Middle Aged", "Motor Neuron Disease", "Neural Conduction", "Spinal Nerve Roots" ]	1998	Jun	Root stimulation studies in the evaluation of patients with motor neuron disease. Nerve root stimulation may be employed in patients with motor neuron disease (MND) to rule out motor neuropathy with conduction block. The diagnostic utility of these studies is unknown, in part because the range of amplitude changes across nerve root segments in patients with active neuronal degeneration has not been well studied. We reviewed root stimulation studies in 32 patients (59 nerves) with MND and found segmental amplitude reduction from 0 to 45%, a range similar to values reported for normal subjects; there was no suggestion of conduction block based on our usual criteria.
9,633,759	eng	[ "D000293", "D000328", "D000368", "D000369", "D000375", "Q000502", "D000483", "D000544", "Q000235", "D001057", "Q000235", "D002648", "D005091", "Q000235", "D005787", "D005838", "D006801", "D026503", "D008875", "D011110", "Q000235", "D011971", "Q000235" ]	[ "Adolescent", "Adult", "Aged", "Aged, 80 and over", "Aging", "Alleles", "Alzheimer Disease", "Apolipoproteins E", "Child", "Exons", "Gene Frequency", "Genotype", "Humans", "Low Density Lipoprotein Receptor-Related Protein-1", "Middle Aged", "Polymorphism, Genetic", "Receptors, Immunologic" ]	1998	Jun	Confirmation of an association between a polymorphism in exon 3 of the low-density lipoprotein receptor-related protein gene and Alzheimer's disease. C766T, a polymorphism in exon 3 of the gene for the low-density lipoprotein receptor-related protein (LRP), was found to be associated with late-onset Alzheimer's disease (AD). We developed a PCR-restriction enzyme-based assay to analyze this allele in 234 AD patients and 103 controls. We confirmed that the LRP C766T polymorphism was in disequilibrium with AD--the C/C genotype was present in 76% of AD patients and 60% of controls (p < 0.01); however, the LRP polymorphism did not influence age at onset of AD.
9,633,761	eng	[ "D000082", "Q000627", "D000276", "Q000627", "D000328", "D018712", "Q000627", "D004305", "D004359", "D005260", "D005938", "Q000008", "Q000627", "D006801", "D007251", "Q000188", "Q000503", "D000068556", "D000068576", "D016899", "Q000627", "D008297", "D009103", "Q000188", "Q000503", "D011241", "Q000008", "Q000627", "D012008" ]	[ "Acetaminophen", "Adjuvants, Immunologic", "Adult", "Analgesics, Non-Narcotic", "Dose-Response Relationship, Drug", "Drug Therapy, Combination", "Female", "Glucocorticoids", "Humans", "Influenza, Human", "Interferon beta-1a", "Interferon beta-1b", "Interferon-beta", "Male", "Multiple Sclerosis", "Prednisone", "Recurrence" ]	1998	Jun	Low-dose steroids reduce flu-like symptoms at the initiation of IFNbeta-1b in relapsing-remitting MS. To determine whether low-dose prednisone reduces flu-like symptoms at the initiation of interferon beta 1-b (IFNbeta-1b), we studied 71 patients with clinically definite, relapsing-remitting multiple sclerosis who were started on IFNbeta-1b. Patients were randomized to receive prednisone plus paracetamol or only paracetamol and were monitored for side effects. Systemic side effects were minimal in the steroid group compared with the nonsteroid group during the first 15 days of treatment (p=0.005). At 3 months, both groups showed a similar frequency of flu-like symptoms. No differences in local reaction between the two groups were observed throughout the study.
9,633,762	eng	[ "D000050", "Q000473", "D000328", "D001055", "Q000097", "D002819", "Q000097", "Q000150", "Q000175", "D005260", "D019788", "D006402", "Q000150", "D006801", "D008279", "D019275", "D014055" ]	[ "Acanthocytes", "Adult", "Apolipoproteins B", "Chorea", "Female", "Fluorodeoxyglucose F18", "Hematologic Diseases", "Humans", "Magnetic Resonance Imaging", "Radiopharmaceuticals", "Tomography, Emission-Computed" ]	1998	Jun	Neuroacanthocytosis and aprebetalipoproteinemia. A 30-year-old woman presented with a progressive neurologic disorder characterized by seizures, buccolingual dyskinesias, orofacial tics, choreiform movements, atrophy, and areflexia. Investigations revealed normal lipid profile except for aprebetalipoproteinemia. Phase-contrast and electron microscopy showed 35 to 40% acanthocytes. MRI and 18fluorodeoxyglucose-PET studies showed caudate atrophy and hypometabolism. The phenotype of this patient is neuroacanthocytosis and its association with aprebetalipoproteinemia may represent a new subentity of the disorder.
9,633,763	eng	[ "D000328", "D002533", "D002560", "Q000502", "D018450", "D005150", "Q000150", "Q000175", "Q000503", "D006429", "Q000209", "D006801", "D008279", "D008297", "D008881", "Q000209", "D014666", "Q000503" ]	[ "Adult", "Cerebral Angiography", "Cerebrovascular Circulation", "Disease Progression", "Facial Hemiatrophy", "Hemiplegia", "Humans", "Magnetic Resonance Imaging", "Male", "Migraine Disorders", "Vasomotor System" ]	1998	Jun	Progressive facial hemiatrophy: abnormality of intracranial vasculature. Progressive facial hemiatrophy (PFH) or Parry-Romberg syndrome is associated with ipsilateral brain lesions and neurologic symptoms. We describe a 35-year-old man with PFH and frequent hemiplegic migraine. On cerebral angiography, reversible vessel caliber changes were seen within the symptomatic hemisphere. An abnormality of the intracranial vasculature may be present in some patients with PFH and neurologic manifestations.
9,633,786	eng	[ "D000375", "Q000502", "D001794", "Q000502", "D018660", "D006332", "Q000473", "Q000503", "D002940", "Q000502", "D005260", "D006352", "D006801", "D006973", "Q000473", "Q000503", "D008297", "D008875", "D009206", "Q000473", "D012727" ]	[ "Aging", "Blood Pressure", "Blood Pressure Monitoring, Ambulatory", "Cardiomegaly", "Circadian Rhythm", "Female", "Heart Ventricles", "Humans", "Hypertension", "Male", "Middle Aged", "Myocardium", "Sex Characteristics" ]	1998	May	Lack of association between blood pressure variability and left ventricular mass in essential hypertension. Blood pressure (BP) variability could induce detrimental effects on left ventricular (LV) structure in hypertension. We investigated the association between short-term BP variability, assessed with 24-h noninvasive ambulatory BP monitoring, and LV mass at echocardiography in 1822 untreated subjects (953 men, 869 women) with essential hypertension (EH). The standard deviation (SD) of daytime and night-time systolic BP (SBP, r = 0.13/0.10; both P < .001), but not of diastolic BP, showed a weak correlation with LV mass. Because the SD of daytime SBP showed a direct association with average 24-h SBP (r = 0.27), subjects were ranked into quartiles of the distribution of 24-h SBP. For each quartile, the subjects with SD of daytime (and night-time) SBP below or above the median were classified at low or high BP variability. In both genders, subjects with high daytime SBP variability were older than those at low variability (both P < .01). Within each quartile, LV mass did not differ between the groups at low v those at high SBP variability. Overall, age-adjusted LV mass index was 115 and 115 g/m2 in men at low and high daytime SBP variability (P = .84), and 116 and 114 g/m2 in men at low and high nighttime SBP variability (P = .31). The corresponding values in women were 98 and 99 g/m2 (P = .53) and 98 and 99 g/m2 (P = .64). In conclusion, when the effects of age, gender, and average 24-h BP are taken into account, short-term BP variability assessed with noninvasive monitoring is unrelated to LV mass in subjects with EH.
9,633,787	eng	[ "D000328", "D017704", "Q000502", "D005260", "D006339", "Q000502", "D006801", "D006973", "Q000503", "D007333", "D008297", "D008875", "D012016", "D012044", "D013577" ]	[ "Adult", "Baroreflex", "Female", "Heart Rate", "Humans", "Hypertension", "Insulin Resistance", "Male", "Middle Aged", "Reference Values", "Regression Analysis", "Syndrome" ]	1998	May	Heart rate variability and baroreflex sensitivity in hypertensive subjects with and without metabolic features of insulin resistance syndrome. Both abnormal autonomic control of heart rate, assessed by heart rate variability (HRV) and baroreflex sensitivity (BRS), and insulin resistance syndrome are common in hypertensive patients. It is not known, however, whether abnormalities in HRV and BRS in hypertension are related to the insulin-resistance syndrome. Therefore, we compared HRV and BRS in hypertensive subjects with and without metabolic features of the insulin-resistance syndrome. HRV was analyzed using the autoregressive method from a 45-min electrocardiographic recording (15 min lying, sitting, and standing) and BRS using the Valsalva maneuver. The groups were matched for age, sex, and antihypertensive medication, and age- and sex-matched normotensive subjects served as a control group (n = 69 in each group). The insulin-resistance syndrome was defined using the criteria of 1) hypertension (blood pressure >160/90 mm Hg), 2) hypertriglyceridemia (fasting serum triglycerides > or =2.0 mmol/L), and 3) hyperinsulinemia (fasting serum insulin > or =12 mU/L). Standard deviation of RR intervals, total, very-low-, and low-frequency power of HRV were significantly lower in hypertensive subjects with insulin-resistance syndrome compared to hypertensive subjects without the syndrome and to normotensive controls (P < .001 for all), but the hypertensive group without the syndrome did not differ from the normotensive group. High-frequency power of HRV (P < .01) and BRS (P < .05) were reduced in both hypertensive groups compared to the normotensive group. In multiple regression analysis, systolic blood pressure (P < .01) and serum triglyceride level (P < .001) were independent predictors of reduced total power of HRV, but BRS was related only to systolic blood pressure (P < .01). Thus, most of the abnormalities in overall HRV seem to be confined to the subgroup of hypertensive subjects with insulin-resistance syndrome, but baroreflex and respiratory modulation of heart rate are impaired also in hypertensive subjects without metabolic features of insulin-resistance syndrome.
9,633,788	eng	[ "D000328", "D000375", "Q000502", "D001794", "Q000502", "D002940", "Q000502", "D019314", "Q000097", "D005260", "D006801", "D006973", "Q000097", "Q000503", "Q000628", "D008297", "D008875", "D012016", "D012727" ]	[ "Adult", "Aging", "Blood Pressure", "Circadian Rhythm", "Dehydroepiandrosterone Sulfate", "Female", "Humans", "Hypertension", "Male", "Middle Aged", "Reference Values", "Sex Characteristics" ]	1998	May	Relationship between blood pressure variability and serum dehydroepiandrosterone sulfate levels. Decreased diurnal blood pressure variability and low dehydroepiandrosterone sulfate (DHEAS) levels are important predictors of cardiovascular morbidity and mortality. The aim of the study was to determine the relationship between DHEAS levels and diurnal blood pressure variability in normotensive subjects and in patients with essential hypertension of both genders. An ambulatory blood pressure monitor (ABPM), Meditech O2 device and radioimmunoassay were used for ambulatory blood pressure monitoring and the determination of DHEAS levels, respectively. A close correlation (P < .001) was found between the diurnal indices and plasma DHEAS levels of the 387 subjects (86 normotensive and 301 hypertensive patients) participating in the study. Decreased plasma DHEAS levels were associated in both genders, and in both normotensive and hypertensive patients with significantly (P < .001) lower diurnal indices. There was a close correlation (P < .001) between the age-related decrease in plasma DHEAS levels and diurnal indices in both genders. Systolic and diastolic blood pressure variability changed parallel to plasma DHEAS levels in both genders, whether hypertension was present or not. Additional investigations are needed to find out whether reduced DHEAS levels play a role in decreased diurnal indices or whether both can be traced back to one and the same cause.
9,633,789	eng	[ "D000293", "D000328", "D000375", "Q000502", "D017704", "Q000502", "D001794", "Q000502", "D002940", "Q000502", "D003971", "D005260", "D006339", "Q000502", "D006728", "Q000097", "D006801", "D008297", "D008991", "D013599", "D013997", "D017086", "Q000097", "Q000503" ]	[ "Adolescent", "Adult", "Aging", "Baroreflex", "Blood Pressure", "Circadian Rhythm", "Diastole", "Female", "Heart Rate", "Hormones", "Humans", "Male", "Monitoring, Physiologic", "Systole", "Time Factors", "beta-Thalassemia" ]	1998	May	Blood pressure and heart rate in young thalassemia major patients. The analysis of blood pressure (BP) and heart rate (HR) variability is currently used to investigate the mechanisms responsible for cardiovascular control; therefore, we assessed whether an impairment of 24-h BP and HR profiles and sympathovagal interaction modulating cardiovascular function was present in patients with thalassemia major (TM) in preclinical phase of heart disease. Nine beta-thalassemic patients 18 years old without clinical signs of cardiac failure and 9 age- and sex-matched controls were studied. Twenty-four-hour-ambulatory BP and HR were measured using the SpaceLabs 90207 device. A truncated Fourier series with four harmonics was used to describe the diurnal blood pressure profile. Mean 24-h ambulatory systolic BP, diastolic BP, and mean arterial pressure were significantly lower in TM patients than in normal subjects (P < .05). A significantly higher nighttime HR value was found in TM patients (P < .05). More than 40% of the TM patients did not show a significant diurnal BP and HR rhythm. In TM patients, the overall amplitude of systolic BP, diastolic BP, and HR was significantly lower than in controls (P < .01). The night/day differences of systolic BP, diastolic BP, and HR were significantly lower in TM patients than in normals (P < .01). Furthermore, we performed power spectral analysis on short-term continuous finger BP and HR data in supine position and during passive head-up tilt. Total spectral power of systolic BP was significantly lower in patients than controls (P < .05). Low-frequency (LF) power of systolic BP and diastolic BP and LF/high-frequency (HF) ratio of HR were significantly lower during tilt in TM patients compared to controls (P < .05). High-frequency power of HR was significantly higher in patients than controls (P < .05). The baroreflex gain assessed by alpha-index was the same in supine position but was higher in TM patients during passive tilt (P < .05). An inverse relationship between LF/HF ratio of HR and hemoglobin levels in TM patients was found. Finally, plasma norepinephrine levels were significantly lower in thalassemics (P < .005). In young TM patients in a preclinical stage of heart disease, these findings demonstrated abnormal 24-h BP and HR rhythms and a decreased short-term variability of BP and HR, in particular in the LF range, showing a diminished sympathetic activity.
9,633,790	eng	[ "D000328", "D057911", "D000959", "Q000627", "D002908", "D016232", "Q000097", "D005260", "D006133", "Q000097", "D006352", "D006801", "D006973", "Q000188", "D019808", "Q000627", "D008297", "D009206", "Q000473" ]	[ "Adult", "Angiotensin Receptor Antagonists", "Antihypertensive Agents", "Chronic Disease", "Endothelins", "Female", "Growth Substances", "Heart Ventricles", "Humans", "Hypertension", "Losartan", "Male", "Myocardium" ]	1998	May	Changes of plasma endothelin and growth factor levels, and of left ventricular mass, after chronic AT1-receptor blockade in human hypertension. The stimulation of autocrine and paracrine factors such as basic fibroblast- (bFGF) and platelet-derived (PDGF) growth factors mediates many of the growth-promoting actions of angiotensin II. The aim of this study was to evaluate the effect of chronic AT1-receptor blockade on plasma endothelin-1 (ET-1) and growth factors levels, and on left ventricular mass, in essential hypertension (EH). The study population consisted of 16 patients with mild-moderate EH, and 25 normotensive controls. In the EH patients under basal conditions, and after 3 and 6 months of chronic therapy with Losartan 50 mg/day, we measured serum levels of ET-1, bFGF and PDGF, and tumor necrosis factor (TNF). At the same time, all patients underwent 24-h ambulatory blood pressure monitoring and an echocardiographic evaluation to measure the thickness of the posterior wall (PWT) of the left ventricle and of the interventricular septum (IVS). The healthy controls underwent the same analyses, under basal conditions, at baseline and after 3 and 6 months of observation. In the EH patients, after 3 months of AT1-receptor blockade bFGF was reduced from 13.6 +/- 0.7 to 10.9 +/- 0.7 pg/mL (P < .004), and both TNF and PDGF were significantly decreased (P < .006 and P < .007, respectively). After 6 months of therapy, ET-1 was significantly diminished in comparison with baseline (6.9 +/- 0.8 v 5.5 +/- 0.1 fmol/mL; P < .05), and the reduction in the levels of growth factors were even more significant than at 3 months of treatment. Both PWT and IVS were significantly changed after 6 months of therapy with losartan after basal evaluation (P < .05, respectively). Systolic and diastolic 24-h blood pressures declined significantly after 3 and 6 months of therapy with losartan (P < .01, respectively). It seems likely that the inhibition of the action of angiotensin II by the specific AT1-receptor blockade, by reducing circulating levels of ET-1 and those of some growth factors, may offer an advantage regarding the effect on hypertensive cardiovascular changes in human hypertension.
9,633,792	eng	[ "D000818", "D001835", "Q000502", "D002199", "Q000502", "D004396", "D005070", "D005632", "D006973", "Q000139", "Q000503", "D007333", "D008297", "D008833", "Q000502", "D051381", "D017207", "D012709", "Q000493" ]	[ "Animals", "Body Weight", "Capillary Permeability", "Coloring Agents", "Evans Blue", "Fructose", "Hypertension", "Insulin Resistance", "Male", "Microcirculation", "Rats", "Rats, Sprague-Dawley", "Serum Albumin" ]	1998	May	Reduction of capillary permeability in the fructose-induced hypertensive rat. Impaired insulin transcapillary transport and the subsequent decrease in insulin delivery to target organs have been suggested to play a role in insulin resistance. These defects were studied in fructose-fed rats, an animal model with insulin resistance. For this study, male Sprague-Dawley rats were fed with either a 60% fructose enriched (F) or a standard chow diet (N) for a total of 2, 4, or 8 weeks. Capillary permeability to albumin was assessed at the end of each dietary period by quantifying the extravasation of albumin-bound Evans blue (EB) dye in different organs. Unanesthetized animals were injected with Evans blue dye (20 mg/kg) in the caudal vein 10 min before being killed and EB dye was extracted by formamide from selected organs collected after exsanguination. As expected, rats had an increase in blood pressure upon feeding with fructose at 4 and 8 weeks (F, 149 +/- 3 mm Hg; N, 139 +/- 3 mm Hg; P < .05). Using this technique, we showed a 56% and a 51% reduction in capillary permeability in skeletal muscles at 4 and 8 weeks of fructose feeding, respectively (4 weeks: N, 44.5 +/- 5.0 microg/g of dry tissue; F, 19.8 +/- 4.2 microg/g of dry tissue; P < .01 and 8 weeks: N, 23.3 +/- 3.7 microg/g of dry tissue; F, 11.3 +/- 4.0 microg/g of dry tissue; P < .05). Similar changes were observed at 4 weeks in the thoracic aorta (N, 82.8 +/- 8.8 microg/g of dry tissue; F, 53.0 +/- 5.1 microg/g of dry tissue; P < .02) and skin (N, 36.0 +/- 5.3 microg of dry tissue; F, 15.0 +/- 2.3 microg/g of dry tissue; P < .02) and at 8 weeks in the liver (N, 107.5 +/- 4.3 microg/g of dry tissue; F, 80.9 +/- 3.2 microg/g of dry tissue; P < .01). In conclusion, fructose feeding is accompanied by a significant and selective reduction of Evans blue leakage primarily in skeletal muscle and liver, and transiently in the skin and aorta, consistent with a role for decreased tissue insulin delivery in insulin resistance.
9,633,791	eng	[ "D000818", "D001158", "Q000187", "Q000473", "D000077868", "D001794", "Q000187", "D003900", "D065128", "D006973", "Q000139", "Q000378", "Q000473", "D010666", "Q000494", "D011743", "Q000494", "D011759", "Q000494", "D051381", "D017207", "D044022", "D012965", "D013997" ]	[ "Animals", "Arteries", "Atrasentan", "Blood Pressure", "Desoxycorticosterone", "Endothelin Receptor Antagonists", "Hypertension", "Phenylpropionates", "Pyrimidines", "Pyrrolidines", "Rats", "Rats, Sprague-Dawley", "Receptor, Endothelin A", "Sodium Chloride", "Time Factors" ]	1998	May	Effect of chronic treatment with two different ET(A) selective endothelin receptor antagonists on blood pressure and small artery structure of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Chronic treatment with a combined ET(A) and ET(B) endothelin receptor antagonist blunts hypertension development and small artery hypertrophy in deoxycorticosterone acetate (DOCA)-salt treated rats, in which endothelin-1 is overexpressed in endothelial cells of blood vessels. To determine whether ET(A) receptor antagonism played a predominant role in these findings, in this study the effects of two orally active ET(A) selective endothelin receptor antagonists, A-127722.5 and LU 135252, were evaluated on blood pressure and small artery structure in DOCA-salt hypertensive rats. Rats received A-127722.5 (30 mg/kg/day) or LU 135252 (50 mg/kg/day) in their drinking water since induction of hypertension. Whereas three of 10 untreated DOCA-salt hypertensive rats died, in the two treated groups none died and all appeared healthier. Systolic blood pressure of treated DOCA-salt hypertensive rats, measured with the tail cuff method, was lower than that of untreated DOCA-salt hypertensive rats by a mean of 20 mm Hg (P < .01) after 4 weeks of treatment with A-127722.5 and by 14 mm Hg (P < .01) with LU 135252. Cardiac and aortic relative weights were unaffected by treatment with either agent. Small arteries of the mesenteric, coronary, renal, and femoral vasculature, examined under standardized conditions after mounting on a wire myograph, were found to exhibit significant inward hypertrophic remodeling in DOCA-salt hypertensive rats. DOCA-salt hypertensive rats treated with A-127722.5 had a significantly smaller media width and media-to-lumen ratio in the four vascular beds examined, and rats treated with LU 135252 showed these findings in mesenteric and renal small arteries. These results demonstrate that chronic ET(A) selective antagonism induces similar effects to those of combined ET(A)/ET(B) receptor antagonists in DOCA-salt hypertensive rats; namely, mild reduction in development of hypertension and blunting of small artery morphological changes, and also appears to improve survival. These results suggest a role of ET(A) receptors in the endothelin dependent component of blood pressure elevation in DOCA-salt hypertensive rats, and in the small artery morphological changes present in this model of experimental hypertension.
9,633,793	eng	[ "D000803", "Q000097", "Q000378", "D000804", "Q000031", "Q000097", "Q000493", "Q000494", "D000818", "D000959", "Q000494", "D001794", "Q000187", "D007668", "Q000378", "D019808", "Q000494", "D008297", "D051381", "D017207", "D011945", "Q000502", "D012083", "Q000097" ]	[ "Angiotensin I", "Angiotensin II", "Animals", "Antihypertensive Agents", "Blood Pressure", "Kidney", "Losartan", "Male", "Rats", "Rats, Sprague-Dawley", "Receptors, Angiotensin", "Renin" ]	1998	May	Renal uptake of circulating angiotensin II in Val5-angiotensin II infused rats is mediated by AT1 receptor. Previous studies have demonstrated that augmentation of intrarenal angiotensin II (ANG II) levels during ANG II induced hypertension involves both endogenous formation and accumulation of circulating ANG II. The present work extends these findings and determines whether accumulation of infused ANG II in the kidney requires AT1 receptor activation by using Val5-ANG II as the infused peptide. Male Sprague-Dawley rats were uninephrectomized and divided into three groups: control (n = 6), Val5-ANG II (exogenous form) infused (n = 8), and Val5-ANG II infused rats treated with losartan (n = 8). Val5-ANG II, which has the same biological and immunoreactive properties as endogenous ANG II, was infused at 40 ng/min via an osmotic minipump implanted subcutaneously. By day 12, systolic blood pressure (SBP) increased significantly in Val5-ANG II infused rats (197 +/- 7 mm Hg). As previously shown, the development of hypertension in ANG II infused rats was prevented by losartan treatment. Blood and kidney samples were harvested, subjected to HPLC to separate Val5-ANG II (exogenous) from Ile5-ANG II (endogenous) and the fractions were measured by radioimmunoassay. In the Val5-ANG II infused rats treated with losartan, total plasma ANG II levels were elevated to a greater extent than in rats not treated with losartan (289 +/- 20 v 119 +/- 14 fmol/mL). However, losartan markedly decreased by 88% the enhancement of intrarenal Val5-ANG II content that occurred in the rats infused with Val5-ANG II alone. These results demonstrate that AT1 receptor blockade markedly reduces the intrarenal uptake of circulating ANG II that occurs in ANG II induced hypertension.

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