bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long latency event‐related potentials in patients infected with human immunodeficiency virus
Authors: Goodin Duoglas S. , Aminoff Michael J. , Chernoff David N. , Hollander Harry 
Published: January 2005

AbstractLong latency auditory evoked potentials were recorded in 55 homosexual men infected with human immunodeficiency virus (HIV). Forty‐one of these patients were asymptomatic from the infection and 14 had clinical signs of illness. Nine of the symptomatic patients were demented and 8 (6 of whom were demented) met other diagnostic criteria for acquired immunodeficiency syndrome (AIDS). Cerebral responses were recorded from Fz, Cz, and Pz electrode placements referred to linked mastoids and averaged separately to rare (2,000 Hz) and frequent (1,000 Hz) tones presented in a pseudorandom sequence. Electroencephalography (EEG) was performed in 54 of the patients and magnetic resonance imaging (MRI) or computed tomography (CT) was done in 14 (13 of whom were symptomatic from the infection). The latency of N1, P2, N2, and P3 components was delayed in HIV‐positive patients compared to normal and this was particularly so for the N1, N2, and P3 components. These changes were more marked in those patients who were symptomatic from their infection, especially in those who were demented. They were, however, present to a lesser degree even in asymptomatic (Class II) patients. Thus, 78% of the demented patients and 28% of nondemented patients had a delay in latency of at least one of the evoked potential components beyond the upper limit of our normal population. By contrast, the EEG was normal in all patients with asymptomatic HIV infection and most symptomatic patients, although 5 patients in this latter group had mild generalized slowing. MRI and CT findings were similarly nonspecific, particularly in the nondemented group. Our findings suggest that long latency auditory evoked potentials may be particularly useful in the evaluation of HIV‐infected patients, possibly permitting the early recognition of HIV encephalopathy and identifying those patients with a worse prognosis or in need of more aggressive management; perhaps, also, recording these potentials will permit the course of this disorder, and its response to therapy, to be followed.
Preliminary trial of 3,4‐diaminopyridine in patients with multiple sclerosis
Authors: Bever Christopher T. , Leslie James , Camenga David L. , Panitch Hillel S. , Johnson Kenneth P. 
Published: January 2005

AbstractTen patients with multiple sclerosis (MS) were enrolled in a preliminary trial of the potassium channel blocker, 3,4‐diaminopyridine, to evaluate drug toxicity and pharmacokinetics. The patients were treated with oral 3,4‐diaminopyridine, first with increasing single doses up to 100 mg and then with divided dosage for up to 3 weeks. Paresthesias were reported by all patients and abdominal pain was dose limiting in 6 patients. 3,4‐Diaminopyridine levels and half‐life varied widely from patient to patient. Cerebrospinal fluid levels of 3,4‐diaminopyridine were about 10% of those in serum. Neither seizures nor epileptiform changes on electroencephalographic examination occurred. Small reversible improvements in specific neurological deficits were seen on examination in all patients and reversible improvement in visual evoked response latencies were found in 2 patients. These results suggest that further study of 3,4‐diaminopyridine in patients with MS is warranted.
The dysarthria—clumsy hand syndrome: A distinct clinical entity related to pontine infarction
Authors: Glass Jonathan D. , Levey Allan I. , Rothstein Jeffrey D. 
Published: January 2005

AbstractUsing magnetic resonance imaging, we studied 6 patients with the dysarthria–clumsy hand syndrome. All were found to have pontine infarctions contralateral to the symptomatic side. Clinically, these patients exhibited dysarthria; “clumsiness,” characterized by dysmetria, dysrhythmia, dysdiadochokinesia and sometimes truncal and gait ataxia; and mild ipsilateral weakness. Previous clinical‐anatomical correlations for this syndrome are limited by inconsistencies in clinical diagnostic criteria and low‐resolution imaging methods. In our patients, and in a review of the literature, the overwhelming majority of patients with the dysarthria–clumsy hand syndrome had pontine infarcts. We conclude that if rigid clinical criteria are used, the label of the dysarthria–clumsy hand syndrome predicts a lesion in the contralateral basis pontis.
Mania after brain injury: Neuroradiological and metabolic findings
Authors: Starkstein Sergio E. , Mayberg Helen S. , Berthier Marcelo L. , Fedoroff Paul , Price Thomas R. , Dannals Robert F. , Wagner Henry N. , Leiguarda Ramon , Robinson Robert G. 
Published: January 2005

AbstractWe present a consecutive series of 8 patients who developed a manic episode after a brain injury. Five patients had cortical lesions (4 with damage to the right basotemporal region, and 1 with bilateral damage to the orbitofrontal area). while the other 3 patients had subcortical lesions (white matter of the right frontal lobe, right anterior limb of the internal capsule, and right head of the caudate), a 18fluorodeoxyglucose positron emission tomography scan showed hypometabolism in the right lateral basotemporal region in all 3 patients. These findings suggest a major role for the basal region of the right temporal lobe in the modulation of mood.
Does adrenal graft enhance recovery of dopaminergic neurons in Parkinson's disease?
Authors: Hirsch E. C. , Duyckaerts C. , Javoy‐Agid F. , Hauw J.‐J , Agid Y. 
Published: January 2005

AbstractA 54‐year‐old man with a 5‐year history of Parkinson's disease was treated with an autograft of adrenal medulla into the right caudate nucleus and died 4 months after surgery. Postmortem examination revealed that the graft was necrotic. It consisted mainly of reticulin and collagen fibrosis without catecholaminergic cell bodies identified either by immunohistochemistry or by situ hybridization with labeled human tyrosine hydroxylase (TH) cDNA probe. Sparse TH‐immunoreactive fibers, which did not stain for dopamine‐beta‐hydroxylase (DBH), ran through the graft. In contrast, intense staining for these catecholaminergic markers was found in the untransplanted adrenal medulla. Densely packed TH‐positive, DHB‐negative fibers were found in a restricted zone of the host striatum at the periphery of the graft. This effect was selective since the density of other neurons was not modified. The present study describes an additional patient in whom adrenal medulla autotransplantation failed to improve the parkinsonian disability. It suggests, however, that adrenal medulla grafts may stimulate the sprouting of striatal dopaminergic fibers in a limited zone of the grafted striatum.
Immunohistochemical study of cerebral amyloid angiopathy. III. Widespread alzheimer A4 peptide in cerebral microvessel walls colocalizes with gamma trace in patients with leukoencephalopathy
Authors: Vinters Harry V. , Secor Diana Lenard , Pardridge William M. , Gray Françoise 
Published: January 2005

AbstractBrain tissue from 11 patients with cerebral amyloid angiopathy, changes of Alzheimer's disease, and variable degrees of subcortical leukoencephalopathy was examined by immunohistochemical methods, using primary antibodies to peptide segments representing portions of the Alzheimer A4 (beta‐) peptide or gamma‐trace peptide (seen most commonly in Icelandic patients with cerebral hemorrhage hereditary cerebral hemorrhage with amyloidosis {HCHWA‐I}). Variable A4 immunostaining was seen within cortical (and rarely white matter) parenchyma in the form of senile plaques (with or without central cores), and within capillary and arteriolar walls. Within individual patients, A4 deposits were often primarily parenchymal or vascular, and when they were arterior walls. Within individual patients, A4 deposits were often primarily parenchymal or vascular, and when they vascular they tended to be more prominent in arteriolar than in capillary wall segments. Perivascular A4 deposits were often detected around strongly immunoreactive microvessels. Gamma‐trace immunoreactivity was noted in many a4‐positive microvessel walls, but staining was always less intense than with the anti‐A4 antibody. We conclude that patients with severe cerebral amyloid angiopathy may show wide variastion in the severity and topography of A4 deposits within brain parenchyma. A4 may colocalize with gamma‐trace peptide, suggesting that A4 and gamma‐trace forms of cerebral amyloid angiopathy may not be as biochemically distinctive as has been suggested. Other proteases or protease inhibitors may contribute to the pathogenesis of cerebral amyloid angiopathy or cerebral amyloid angiopathy‐related stroke syndromes.
Hereditary motor and sensory neuropathies and hereditary spastic paraplegia: A magnetic stimulation study
Authors: Clays D , Waddy H. M. , Harding A. E. , Murray N. M. F. , Thomas P. K. 
Published: January 2005

AbstractCentral motor conduction to the small hand muscles was investigated in 59 patients with peroneal muscular atrophy and hereditary spastic paraplegia (HSP) by using transcranial magnetic brain stimulation. These comprised 20 patients with type I hereditary motor and sensory neuropathy (HMSN I), 15 with type II (HMSN II), 4 with HMSN I and 10 with HMSN II with associated pyramidal features, and 10 with the “pure” form of HSP. Central motor conduction was usually normal in HMSN I, HMSN II, and HSP. In HMSN I with pyramidal signs, central motor conduction time was greatly prolonged bilaterally. This result may reflect an associated involvement of the central motor pathways in these patients. In HMSN II with accompanying pyramidal features, 6 of the 10 patients had abnormal central motor conduction, although conduction times were only slightly prolonged, suggesting a different pathophysiological pattern.
Selective hypometabolism in the inferior frontal lobe in depressed patients with Parkinson's disease
Authors: Mayberg Helen S. , Starkstein Sergio E. , Sadzot Bernard , Preziosi Thomas , Andrezejewski Paula L. , Dannals Robert F. , Wagner Henry N. , Robinson Robert G. 
Published: January 2005

AbstractDepression is a frequent finding in patients with Parkinson's disease (PD). Regional cerebral glucose metabolism was measured in depressed and nondepressed patients with PD and in age‐comparable normal control subjects using 2‐[18F]‐fluoro‐2‐deoxy‐D‐glucose and positron emission tomography (PET). Relative metabolic activity in the caudate and orbital‐inferior region of the frontal lobe was significantly lower in the depressed patients with PD as compared to both nondepressed patients and control subjects. There was a significant inverse correlation between relative glucose metabolism in the orbital‐inferior area of the frontal lobe and depression scores. This study suggests that depression in PD is associated with dysfunction in the caudate and orbital‐inferior area of the frontal lobe. This metabolic pattern is unlike that seen in patients with PD who have other behavioral deficits such as dementia, and suggests that disruption of basal ganglia circuits involving the inferior region of the frontal lobe may affect the regulation of mood.
Multiple sclerosis is prevalent in the zoroastrians (Parsis) of India
Authors: Wadia Noshir H. , Bhatia Kailash 
Published: January 2005

AbstractUsing Schumacher's classification, we determined the prevalence rate of clinically definite multiple sclerosis (MS) in the distinct but tiny Zoroastrian (largely Parsi) community in the adjacent cities of Bombay (latitude, 18.55 degrees) and Poona (Pune). On prevalence day, 16 clinically definite cases of MS were counted, 14 in Bom‐ bay and 2 in Poona, from a total Zoroastrian population of 50,053 and 3,399, respectively. The crude prevalence ratio was 26 per 100,000 for Bombay and 58 per 100,000 for Poona The age‐adjusted prevalence ratio for Bom‐ bay was 24 per 100,000, with 95% confidence limits of 13.1 to 40.3. These are much higher than the low rates believed to be prevalent in India, and are comparable with those found in parts of Europe and the United States.
Stroke in pediatric acquired immunodeficiency syndrome
Authors: Park Yong D. , Belman Anita L. , Kim Tae‐Seung , Kure Katsuhiro , Llena Josefina F. , Lantos George , Bernstein Larry , Dickson Dennis W. 
Published: January 2005

AbstractIn a 4½‐year period, 4 of 68 children in a longitudinal study of neurological complications of human immunodeficiency virus (HIV) infection had clinical and/or neuroradiological evidence of stroke, yielding a clinical incidence of stroke in this population of 1.3% per year. During this period, 32 subjects died, and permission for autopsy was granted in 18 of the patients, including 3 of 4 who had clinical evidence of stroke. The prevalence of cerebrovascular pathological features in our consecutive autopsy series was higher than the clinical incidence. At autopsy cerebrovascular disease was documented in 6 (24%) of 25 children with HIV infection, including all 3 children who had clinical evidence of stroke. Four patients had intracerebral hemorrhages, 6 patients had nonhemorrhagic infarcts, and 3 had both. Hemorrhage was catastrophic in 1 child and clinically silent in 3 children, all of whom had immune thrombocytopenia. One child had an arteriopathy that affected meningocerebral arteries. In another child, the arteries of the circle of Willis were aneurysmally dilated. Two children had coexisting cardiomyopathy and subacute necrotizing encephalomyelopathy with vascular proliferation. These results suggest that stroke should be considered when children with HIV infection develop focal neurological signs.
Axonal neuropathy with monoclonal IgG kappa that binds to a neurofilament protein
Authors: Nemni Raffaello , Feltri Maria L. , Fazio Raffaella , Quattrini Angelo , Lorenzetti Isabella , Corbo Massimo , Canal Nicholas 
Published: January 2005

AbstractWe report a 74‐year‐old woman with a slowly progressive sensory motor axonal neuropathy and a monoclonal IgG‐κ that bound to a 68‐kd axonal protein identified as the low molecular weight neurofilament protein. The sera of control subjects and disease controls did not bind to neurofilament protein.
Electroencephalography laboratory diagnosis of prolonged QT interval
Authors: Gospe Sidney M. , Gabor Andrew J. 
Published: January 2005

AbstractPatients with prolongation of the QT interval are at risk for significant neurological morbidity and mortality secondary to ventricular tachyarrhythmias. These patients frequently undergo electroencephalographic (EEG) examination to evaluate episodes of loss of consciousness, which may be associated with convulsions. Electrocardiogram recording as a part of the EEG is a simple and common practice, but analysis for possible QT prolongation is not routinely performed by electroencephalographers. This is, in part, due to the fact that while calculation of the corrected QT interval is straight forward, a calculator is generally required. A nomogram that is presented simplifies determination of the corrected QT interval, facilitating diagnosis of prolongation of the QT interval in the EEG laboratory.
Treatment of spasticity with botulinum toxin: A double‐blind study
Authors: Snow Barry J. , Tsui Joseph K. C. , Bhatt Mohit H. , Varelas Michael , Hashimoto Stanley A. , Calne Donald B. 
Published: January 2005

AbstractWe studied the effect of botulinum‐A toxin on spasticity of the leg adductors in 9 patients who were either chair‐bound or bed‐bound with chronic stable multiple sclerosis. We injected botulinum toxin (400 mouse units) or placebo into the adductor muscles in a randomized, crossover, double‐blind design. Two physicians, who were unaware of the treatment order, used an objective rating scale and independently assessed the patients; interobserver correlation was excellent (r = 0.93‐0.81). We found that botulinum toxin produced a significant reduction in spasticity (p = 0.009) and a significant improvement in the ease of nursing care(p = 0.009). There were no adverse effects during this shortterm trial. This is the first demonstration of the beneficial effect of botulinum toxin on focal spastic muscle contractions.
Hypoglycemia alters striatal amino acid efflux in perinatal rats: An in vivo microdialysis study
Authors: Silverstein Faye S. , Simpson Jennifer , Gordon Kevin E. 
Published: January 2005

AbstractIn adult brain, during insulin‐induced hypoglycemia, striatal extracellular fluid concentrations of the excitatory amino acids glutamate and aspartate rise markedly (fourfold to tenfold). In this study, we used in vivo microdialysis to determine if insulin‐induced hypoglycemia altered striatal amino acid efflux in similar fashion in the immature brain. Microdialysis probes were inserted into the right striatum of rats on postnatal day 7. After a 2‐hour recovery period, in each animal a 30‐minute baseline sample was obtained. Then insulin (0.6 μ/Kg, intraperitoneal injection) was administered (n = 6) and dialysate sampling was continued over the next 210 minutes (terminal blood glucose level < 5 mg/dl). Untreated control rats (n = 6) were sampled over the same time interval. After pre‐column derivatization with o‐Phthaldialdehyde, dialysate samples were assayed by high‐pressure liquid chromatography with electrochemical detection to measure their amino acid content; eight amino acids (glutamate, aspartate, taurine, glutamine, alanine, serine glycine, and asparagine) were consistently detected. In controls, amino acid efflux did not change over 4 hours. In hypoglycemic animals, glutamate efflux increased (peak: 238 ± 85% of baseline, p = 0.02, repeated measures analysis of variance [ANOVA]), glutamine efflux declined (to 44 ± 5% of baseline, P = 0.002, ANOVA), and taurine efflux increased (up to 310 ± 120% of baseline; p < 0.06, ANOVA). In contrast with 9‐to 12‐fold increases in aspartate efflux reported in adult striatum, asparate efflux increased only slighty (to 174 ± 69% of baseline; not significant). In immature rodent brain, overall trends in striatal amino acid efflux during hypoglycemia are similar to patterns reported in adult animals; however, there are major differences in the timing, duration, and magnitude of these responses.
HTLV‐I sequences are not detected in peripheral blood genomic DNA or in brain cDNA of multiple sclerosis patients
Authors: Oksenberg Jorge R. , Mantegazza Renato , Sakai Koichiro , Bernard Claude C. A. , Steinman Lawrence 
Published: January 2005

AbstractHuman T‐cell lymphotropic virus (HTLV‐I) was recently reported to be etiologically associated with multiple sclerosis (MS). Genomic DNA from peripheral blood lymphocytes and brain plaques of patients with MS was analyzed for the presence of sequences homologous to the HTLV‐I pol gene using the polymerase chain reaction and dot blot techniques. Comparison of DNA amplification patterns between patients with MS, and with control subjects who have other autoimmune conditions, with those in healthy control subjects and with an HTLV‐I‐infected cell line indicates that HTLV‐I pol sequence is not present in the peripheral blood of patients with MS, and that the virus is not active in MS brain plaques.
Dystrophin analysis in duchenne and becker muscular dystrophy carriers: Correlation with intracellular calcium and albumin
Authors: Morandi L. , Mora M. , Gussoni E. , Tedeschi S. , Cornelio F. 
Published: January 2005

AbstractImmunocytochemical localization and immunoblot analysis of dystrophin in muscle fibers of 11 obligate and probable, and 7 possible carriers of Duchenne and Becker muscular dystrophy revealed an abnormal expression of the protein in 3 of them. Localization of calcium and albumin, as endogenous markers of extracellular fluid penetration, showed the presence of both molecules inside some fibers lacking dystrophin. Our morphological studies show that the initial stages leading to fiber necrosis in Duchenne muscular dystrophy are present in carriers with mosaicism. Comparison of dystrophin studies with restriction fragment length polymorphism analysis and creatine kinase levels showed that neither immunocytochemical nor immunoblot techniques for dystrophin are sensitive enough to provide a basis for genetic counseling.
Elevated soluble interleukin‐2 receptor levels in patients with active multiple sclerosis
Authors: Adachi Keiko , Kumamoto Toshihide , Araki Shukuro 
Published: January 2005

AbstractThe level of soluble interleukin‐2 receptor (sIL‐2R) was quantitated with enzyme‐linked immunosorbent assay in serum and cerebrospinal fluid obtained from 24 patients with multiple sclerosis and 10 patients with other neurological disorders in whom immunological mechanisms are unlikely to participate. The sIL‐2R level in the serum and cerebrospinal fluid of patients with multiple sclerosis in relapse was significantly higher compared with patients with multiple sclerosis in remission and with controls. The sIL‐2R level, especially in the cerebrospinal fluid, showed higher sensitivity and specificity than other clinical parameters including the cerebrospinal fluid IgG ratio, peripheral lymphocyte CD4/CD8 ratio, cerebrospinal fluid myelin basic protein and oligoclonal bands. Our data suggest that measurement of the sIL‐2R level may be useful in evaluating disease activity in patients with multiple sclerosis.
Cerebrospinal fluid immune complexes in patients exposed to Borrelia burgdorferi: Detection of Borrelia‐specific and ‐nonspecific complexes
Authors: Coyle P. K. , Schutzer Steven E. , Belman Anita L. , Krupp Lauren B. , Golightly Marc G. 
Published: January 2005

AbstractWe analyzed cerebrospinal fluid (CSF) from 32 patients with neurological symptoms and evidence of Borrelia burgdorferi infection (29 were seropositive as determined by enzyme‐linked immunosorbent assay, 2 were cell‐mediated immune positive, and 1 had been seropositive as shown by enzyme‐linked immunosorbent assay 9 months previously). CSF immune complexes were found in 22 (69%) of 32 patients; in 18, there was sufficient sample to isolate immune complexes. By enzyme‐linked immunosorbent assay, isolated immune complexes from 10 of these 18 patients contained antibody specific for B. burgdorferi antigens. The isotypes were IgG (n = 8), IgM (n = 3), and IgA (n = 2). By immunoblot, these antibodies were directed against B. burgdorferi 41‐kDa antigen and occasionally against the 33‐ and 17‐kDa antigens. Anti–B. burgdorferi IgM was present in patients with acute neurological symptoms, was predominantly complexed rather than free, and decreased with clinical recovery in the one serial study. Three patients were nonreactive for free CSF antibodies, but had complexed antibodies to the organism. The preliminary finding of specific B. burgdorferi components in immune complexes in CSF suggests an active process triggered by the organism, even in the absence of other CSF abnormalities.
In vivo 1H spectroscopy of the human brain following electroconvulsive therapy
Authors: Woods Bryan T. , Chiu Tak‐Ming 
Published: January 2005

AbstractRecent advances in the methodology of magnetic resonance spectroscopy now permit localized proton (1H) spectroscopy of the human brain in clinical magnetic resonance systems. In this study, localized 1H spectroscopy was used to observe directly the stimulation of brain metabolic activity in patients undergoing electroconvulsive theraphy (ECT) and to compare results obtained before and after treatments. Persistent increases in lactate were expected on the basis of animal data but these increases were small and equivocal 1 hour after ECT. In contrast, a large increase in a lipid signal from before to after ECT was observed in 5 patients when short echo times were used. We postulate that a significant portion of this lipid signal is related to maximal activation of the phosphatidylinositol second messenger system by single seizures, and that the sustained postictal effects of activation of the phosphatidylinositol system (increased levels of diacylglycerol and free fatty acids) have generalized inhibitory effects potentially relevant to both the clinical pathophysiology of seizures and the efficacy of ECT in major affective disorders.