bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuropathy and anti‐myelin‐associated glycoprotein IgM M proteins: T cell regulation of M protein secretion in vitro
Authors: Latov Norman , Godfrey Maurice , Thomas Yoland , Nobile‐Orazio Eduardo , Spatz Linda , Abraham Judith , Perman Gayle , Freddo Lorenza , Chess Leonard 
Published: January 2005

AbstractIn patients with plasma cell dyscrasia, individual clones of antibody‐producing cells proliferate abnormally and secrete monoclonal antibodies or M proteins in excess. The cause of the monoclonal proliferation of lymphocytes and M protein secretion is unknown and it is not known whether the M protein–secreting B cells are autonomous or capable of responding to regulatory T cells. We carried out experiments using lymphocytes from a patient with neuropathy and plasma cell dyscrasia whose IgM M protein bound to the myelin‐associated glycoprotein (MAG) to determine whether secretion of the M protein in vitro was responsive to T cell help or suppression. M protein secretion was measured by an enzyme‐linked immunosorbent assay system for measuring anti‐MAG IgM, and the number of M protein–secreting lymphocytes was enumerated by a reverse hemolytic plaque assay specific for the M protein idiotype. The patient's B cells were maximally stimulated by pokeweed mitogen–activated autologous OKT4+T‐helper cells and the helper effect was inhibited by OKT8+suppressor/cytotoxic T cells. Low levels of M protein secretion in the absence of T cells were also observed and there was partial stimulation of M protein secretion by T cells in the absence of pokeweed mitogen.
Left ear suppression on verbal dichotic tests in patients with multiple sclerosis
Authors: Rubens Alan B. , Froehling Brian , Slater Gerald , Anderson David 
Published: January 2005

AbstractVerbal dichotic listening tests employing nonsense consonant‐vowel stimulus pairs were administered to 11 right‐handed patients with chronic multiple sclerosis and to 10 right‐handed normal controls. A highly significant reduction of left‐ear scores was found in the multiple sclerosis group. We propose that the basis for this finding is a disconnection of the auditory callosal pathway and that dichotic listening tests may be of value in detecting the presence of lesions of the deep white matter of the cerebral hemispheres in multiple sclerosis.
Preservation of hypothalamic dopaminergic neurons in Parkinson's disease
Authors: Matzuk Martin M. , Saper Clifford B. 
Published: January 2005

AbstractThe integrity of the hypothalamic neuroendocrine dopaminergic neurons in Parkinson's disease was assessed by comparing the numbers and distribution of melanin‐pigmented neurons in the arcuate and periventricular nuclei in 7 parkinsonian and 5 normal brains. No significant differences were observed. In contrast to theories suggesting that Parkinson's disease involves a universal degeneration of central catecholaminergic neurons, the hypothalamic neuroendocrine dopaminergic neurons do not appear to be involved by the disease.
Corticospinal tract conduction time in multiple sclerosis
Authors: Mills Kerry R. , Murray Nicholas M. F. 
Published: January 2005

AbstractAnodal shocks of 400 to 700 V from a low‐output impedance stimulator applied percutaneously over the motor cortex evoke muscle action potentials in partially voluntarily activated contralateral muscles. Cathodal shocks from the same device applied to the cervical spinal cord produce maximal ipsilateral muscle action potentials in a relaxed limb. This technique was used to study the central motor pathway in 15 healthy subjects and 8 patients with clinically definite multiple sclerosis. As stimuli were applied in the axilla, over the C7 vertebral level, and over the arm area of the motor cortex, recordings were made of muscle action potentials of forearm flexor muscles. In controls, cord‐to‐axilla conduction time was 4.1 ± 0.61 ms, and cortex‐to‐cord time was 4.4 ± 0.75 ms. In patients, cord‐to‐axilla conduction times were normal, while central conduction times were either markedly prolonged (6.4 to 31 ms) or absent. This technique is a potentially powerful tool for the investigation of central motor pathways in healthy subjects and patients with neurological disease.
Postoperative neurological deficits may occur despite unchanged intraoperative somatosensory evoked potentials
Authors: Lesser R. P. , Raudzens P. , Lüders H. , Nuwer M. R. , Goldie W. D. , Morris H. H. , Dinner D. S. , Klem G. , Hahn J. F. , Shetter A. G. , Ginsburg H. H. , Gurd A. R. 
Published: January 2005

AbstractWe describe 6 patients who demonstrated postoperative neurological deficits despite unchanged somatosensory evoked potentials during intraoperative monitoring. Although there is both experimental and clinical evidence that somatosensory evoked potentials are sensitive to some types of intraoperative mishap, the technique should be empolyed with an awareness of its possible limitations.
α‐1 Adrenoceptors are decreased in human epileptic foci
Authors: Brière Richard , Sherwin Allan L. , Robitaille Yvon , Olivier André , Quesney Luis F. , Reader Tomas A. 
Published: January 2005

AbstractCortical α‐1 adrenoceptors were measured in tissues obtained from 10 patients immediately following temporal lobectomy for intractable partial epilepsy. At operation each patient exhibited spontaneous spiking restricted to either the anterior (n = 5) or posterior (n = 5) portion of the first two temporal gyri. Control samples were obtained from the nonspiking half of the same gyrus. Receptor‐binding assays were performed on isolated cortical membranes using [3H]prazosin. There was a reduction (p < 0.01) in the receptor density (βmax) of the sites in the epileptic foci without any change in affinity (mean ± SEM): spiking—βmax, 160.5 ± 11.3 fmol/mg protein; affinity, 0.17 ± 0.04 nM; nonspiking—βmax, 218.8 ± 15.6 fmol/mg protein; affinity 0.17 ± 0.04 nM. This relative decrease in α‐1 adrenoceptor density may be the substratum of a noradrenergic hyposensitivity that could contribute to a localized diminution in inhibitory mechanisms in epileptic foci.
Contingent negative variation in headache
Authors: de Nordhout Alain Maertens , Timsit‐Berthier Martine , Timsit Meyer , Schoenen Jean 
Published: January 2005

AbstractContingent negative variation (CNV), an event‐related slow cerebral potential, was analyzed in 79 consecutive headache patients. Compared to normal controls (n = 33), CNV did not differ in tension headache (n = 21) or in combined headaches with a predominant tension component (n = 13). The mean amplitude of CNV was significantly (p < 0.001) increased in migraine (n = 29) as well as in combined headache with predominant migraine (n = 16). All migraineurs were studied between attacks and without prophylactic treatment. CNV may be a useful diagnostic test in headache. Its increased amplitude in migraine might reflect central catechol‐aminergic hyperactivity.
Atrial size, atrial fibrillation, and stroke
Authors: Caplan L. R. , D'Cruz I. , Hier D. B. , Reddy H. , Shah S. 
Published: January 2005

AbstractM‐mode and two‐dimensional echocardiographic images were reviewed retrospectively in 20 patients with atrial fibrillation and ischemic stroke with no known valvular disease and in 20 patients with atrial fibrillation without known stroke. Left atrial size was measured and analyzed without knowledge of patient grouping. Two‐dimensional echocardiography showed that 90% of the stroke patients had left atrial enlargement compared with only 20% in the nonstroke group. This finding suggests that left atrial enlargement may convey additional stroke risk in patients with atrial fibrillation.
Cytoskeletal protein abnormalities in neurodegenerative diseases
Authors: Goldman James E. , Yen Shu‐Hui 
Published: January 2005

AbstractThe nervous system is a rich source of filamentous proteins that assume critical roles in determining and maintaining neuronal form and function. Neurons contain three major classes of these cytoskeletal organelles: microtubules, intermediate filaments, and microfilaments. They also contain a variety of proteins that organize them and serve to connect them with each other. Such major neurodegenerative diseases as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as a variety of toxic neuropathies, are characterized pathologically by intraneuronal filamentous inclusions. Recent studies using biochemical and immunocytochemical techniques have established that these abnormalities represent disorganized states of the neuronal cytoskeleton and have determined some of the specific molecular constituents of these inclusions. This knowledge has led to new ways of thinking about their origins.
Deficits in orofacial sensorimotor function in Parkinson's disease
Authors: Schneider Jay S. , Diamond Shirley G. , Markham Charles H. 
Published: January 2005

AbstractOrofacial sensorimotor function was assessed in patients with Parkinson's disease and in age‐matched controls. Tests were designed to assess sensory function, motor abilities, and the integration of sensory information for the performance of specific movements. Patients with Parkinson's disease and normal subjects both made more errors with increasing age; however, overall, patients with Parkinson's disease made significantly more errors in our tests than did normal subjects. Interestingly, patients with Parkinson's disease showed greater deficits in tests of sensory function and sensorimotor integration than in tests of motor function. These results suggest that one aspect of Parkinson's disease consists of complex deficits in the utilization of specific sensory inputs to organize and guide movements. The results are further discussed in relation to a proposed sensory gating or filtering schema of basal ganglia motor functioning.
Thymosin β4 is a shared antigen between lymphoid cells and oligodendrocytes of normal human brain
Authors: Dalakas Marinos C. , Trapp Bruce D. 
Published: January 2005

AbstractIn the normal human brain, immunoreactive thymosin β4, a well‐characterized thymic extract, was demonstrated specifically in the cell bodies and processes of a subset of interfascicular and satellite oligodendrocytes with their stained processes terminating around myelin sheaths. Antisera directed against two other thymic polypeptides, thymosin α1 and α7, did not react. In lymphoid tissues, thymosin β4 was present in macrophages, Langerhans' cells of the skin, and the interdigitating cells of the thymus. Thus, a subset of oligodendrocytes shares a common antigen of thymic origin with the reticular–dendritic and phagocytic lymphoid cells—all Ia+ immunocompetent cells that participate in the presentation of antigens to T cells. The subset of thymosin β4‐positive oligodendrocytes is antigenically distinct and may play a role in the immune surveillance of the central nervous system or the demyelinating processes induced by antigen‐presenting activated macrophages.
Epidemiology of clinically diagnosed Alzheimer's disease
Authors: Rocca Walter A. , Amaducci Luigi A. , Schoenberg Bruce S. 
Published: January 2005

AbstractThis report reviews the current status of descriptive and analytic epidemiology of clinically diagnosed Alzheimer's disease (AD). Since AD can be diagnosed with certainty only at autopsy, currently available epidemiological data are based on a presumed clinical diagnosis. Current data indicate that AD represents a major health problem, at least in the developed countries. The prevalence ratio for AD ranges between 1.9 and 5.8 cases per 100 population aged 65 and over. Moreover, its prevalence is likely to increase in the next twenty years as a consequence of current demographic trends. The prevalence ratio for AD increases steeply with age and is higher in females. Incidence rates show a similar pattern, suggesting that AD should not be subdivided in a presenile and a senile form based on age of onset alone. Annual incidence rates of 2.4 cases per 100,000 population between ages 40 and 60, and 127 cases per 100,000 population after age 60 have been reported. Several case‐control studies show that the occurrence of either dementia or Down's syndrome in other family members, advanced age of the mother at subject's birth, and head injury are possible risk factors.
Edrophonium: An aid in the diagnosis of acute organophosphate poisoning
Authors: Maselli Ricardo , Jacobsen John H. , Spire Jean‐Paul 
Published: January 2005

AbstractUnsuspected accidental cutaneous exposure to an organophosphate insecticide caused flaccid paralysis in a 10‐year‐old girl. Electromyogram demonstrated repetitive compound muscle action potentials in response to a single stimulus of nerve; decremental response, more prominent at higher rates of stimulation; worsening of decremental response after edrophonium injection; and normal nerve conduction velocities. Electromyogram with repetitive nerve stimulation and an edrophonium test may provide a simple and rapid method for diagnosis of acute organophosphate poisoning.
Neurophysiological techniques as an aid to surgical treatment of primary brain tumors
Authors: Morris Harold H. , Lüders Hans , Hahn Joseph F. , Lesser Ronald P. , Dinner Dudley S. , Estes Melinda L. 
Published: January 2005

AbstractWe describe a method of cortical stimulation for localizing functional area of brain before operation for primary brain tumors that was carried out in 14 patients. The method is unique in that the stimulation is done over several days using chronically indwelling subdural electrode arrays. In addition to cortical stimulation findings, somatosensory evoked potentials were helpful in locating the sensorimotor strip. The neurophysiological data have allowed an aggressive neurosurgical attack without producing a functional deficit.
Focal cerebral vasculitis associated with circulating immune complexes and brain irradiation
Authors: Groothuis Dennis R. , Mikhael Michael A. 
Published: January 2005

AbstractIn this report we describe a patient with a benign glioma treated with surgery and radiation. After a period of stability he developed subacute bacterial endocarditis, and deteriorated neurologically. Computed tomographic scans did not show recurrent tumor. An angiogram showed vasculitis restricted to the previously irradiated area. Secondary to subacute bacterial endocarditis was the presence of high levels of circulating immune complexes. His neurological status was unchanged after antibiotics, but improved after treatment with dexamethasone. We interpret the clinical course as an immune‐complex–mediated vasculitis superimposed on a subclinical radiation vasculitis. This case supports the hypothesis that immune mechanisms may be involved in delayed radiation injury to the nervous system.
Cerebrospinal fluid pharmacokinetics of intrathecal morphine sulfate and D‐Ala2‐D‐Leu5‐enkephalin
Authors: Moulin Dwight E. , Inturrisi Charles E. , Foley Kathleen M. 
Published: January 2005

AbstractUsing an implantable pump system to deliver drugs and sample cerebrospinal fluid (CSF), we assessed rostral redistribution and systemic uptake after intrathecal bolus injection and steady‐state infusion of morphine sulfate and the opioid peptide D‐Ala2‐D‐Leu5‐enkephalin (DADL) in two patients. Following bolus injection, the mean CSF elimination half‐lives for morphine sulfate and DADL were 94 and 115 minutes, respectively. With the catheter tip at L2, the ratio of lumbar to cisternal (L/C) concentrations of morphine sulfate was about 7:1, and with the catheter tip at T10, the L/C ratios of morphine sulfate and DADL were approximately 2:1, indicating that this ratio is dependent in part on the level of intrathecal drug administration. CSF levels of morphine sulfate at steady state were three orders of magnitude higher than those in plasma. The CSF pharmacokinetics of morphine sulfate and DADL are similar, with supraspinal redistribution of these opioids via the CSF likely playing an important role in the generation of analgesia and central nervous system side effects.
Type 2 and type 3 Gaucher disease: A morphological and biochemical study
Authors: Kaye Edward M. , Ullman M. David , Wilson Edward R. , Barranger John A. 
Published: January 2005

AbstractGlucocerebroside levels were measured in the brains of patients with neuronopathic forms (types 2 and 3) of Gaucher disease and compared to those obtained from control brain. Nine separate brain regions (frontal, temporal, occipital, and cerebellar cortices; thalamus; corpus striatum; pons; medulla; and dentate nuclei) were analyzed. In all the Gaucher brains studied, the greatest glucocerebroside accumulation occurred within the occipital cortex, with lesser amounts in the temporal and frontal areas. The cerebellar cortex, corpus striatum, and thalamus in Gaucher brains had mildly increased levels of glucocerebroside, especially when the values were expressed as a percentage of total nonhydroxy fatty‐acid cerebroside. Brainstem structures (pons and medulla) and dentate nuclei did not have increased glucocerebroside levels when compared to levels from similar control areas. However, when glucocerebroside concentration was expressed as a percentage of total non‐hydroxy fatty‐acid cerebroside, the type 2 Gaucher brainstem structures did show a slight increase in glucocerebroside levels over control levels. Neuropathological studies demonstrated the presence of Gaucher cells, gliosis, and microglial nodules within the type 2 brains. The neuropathological findings correlated with the glucocerebroside accumulation in the type 2 brains. Despite the similar pattern of glucocerebroside accumulation in the type 3 brain, no neuropathological abnormalities were seen. Thus, this study demonstrated that within several brain regions, both neuronopathic forms of Gaucher disease have elevated glucocerebroside levels, and that in the type 2 brains, the glucocerebroside accumulation correlated positively with the neuropathological findings.
Glial bundle formation in spinal roots following experimental neuronopathy
Authors: Yamamoto Teiji , Iwasaki Yuzo , Konno Hidehiko , Kudo Hiroko 
Published: January 2005

AbstractSpinal motor neurons and dorsal root ganglion cells were caused to degenerate by axoplasmic transport of toxic lectins via the sciatic nerve. Within a few months, loss of axons and glial bundle formation were seen in the proximal portions of the L4–6 ventral and dorsal roots. The glial bundles observed were structurally the same as those described in humans, but they were occasionally also invested with Schwann cell cytoplasmic processes, the cell membrane of which was directly apposed to that of astrocytes. Basal lamina surrounding the outer surface of the bundles was shared by these two as a continuous sheet. This unique complex of astroglial and Schwann cell processes, completely covered by basal lamina, may be a newly formed interface between the central and peripheral nervous systems and thus may serve as a guide and potential pathway for regenerating neurites.
Nerve growth factor and Alzheimer's disease
Authors: Hefti Franz , Weiner William J. 
Published: January 2005

AbstractAlzheimer's disease is associated with a pronounced loss of the cholinergic neurons that form the ascending cholinergic projections of the basal forebrain. Even though the disease is also characterized by changes in other neuronal systems and by a high frequency of neuronal plaques and tangles, the cholinergic deficit seems to be a principal element responsible for the memory loss typical of Alzheimer's disease. This review summarizes findings in experimental animals which indicate that nerve growth factor (NGF), a well‐characterized protein, acts as a neurotrophic factor for cholinergic neurons of the basal forebrain. NGF is present in the target areas of these cholinergic neurons and affects their survival, fiber growth, and expression of transmitter‐specific enzymes. Furthermore, NGF is able to prevent the degeneration of cholineric neurons in adult rats with experimental lesions mimicking the cholinergic deficit in Alzheimer's disease. These findings suggest that increasing the availability of NGF to human cholinergic cells might promote their survival in certain disease processes. Additional steps are discussed for establishing the possible involvement of NGF in the pathogenesis of Alzheimer's disease and the development of an effective therapy.
Contrapulsion of saccades and ipsilateral ataxia: A unilateral disorder of the rostral cerebellum
Authors: Ranalli Paul J. , Sharpe James A. 
Published: January 2005

AbstractContralateral pulsion of saccades and ipsilateral limb ataxia were manifestations of unilateral damage to the rostral cerebellum studied in a patient with occlusion of one superior cerebellar artery. The saccadic disorder consisted of three elements: (1) horizontal saccades away from the lesion during attempted vertical saccades, resulting in oblique trajectories; (2) hypermetria of contralateral saccades; and (3) hypometria of ipsilateral saccades. Magnetic search coil oculography showed that durations of the horizontal components of oblique contrapulsive saccades were lengthened toward the durations of the vertical components. Lengthening of horizontal vectors indicated temporal coupling of the orthogonal components, as occurs in normal oblique saccades. The bias of saccades arose proximal to brainstem loci that decompose commands for oblique saccades into their horizontal and vertical vectors. Contrapulsion of saccades may be explained by imbalanced cerebellar outflow.
Electrographic status epilepticus in fatal anoxic coma
Authors: Simon Roger P. , Aminoff Michael J. 
Published: January 2005

AbstractElectrographic status epilepticus in the absence of conspicuous somatic motor manifestations is described in 10 patients who were comatose following anoxic–ischemic brain damage. The outcome was unfavorable and the response to anticonvulsant drugs was poor. We describe a clinical sign predictive of the electroencephalographic findings, namely brisk, small‐amplitude, mainly vertical eye movements readily detectable by passively elevating the lids. However, similar eye movements may infrequently be found in patients whose electroencephalograms show abnormal spike discharges without the occurrence of electrographic status epilepticus following cerebral anoxia, as in 2 other patients we describe.
Locus ceruleus lesions and eosinophilic inclusions in MPTP‐treated monkeys
Authors: Forno Lysia S. , Langston J. William , DeLanney Louis E. , Irwin Ian , Ricaurte George A. 
Published: January 2005

AbstractSystemic administration of the recently discovered neurotoxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) produces severe clinical parkinsonism and degeneration of the substantia nigra in humans and monkeys. In previous studies, no convincing structural damage to nerve cells outside the substantia nigra could be demonstrated in subhuman primates. Using a protracted MPTP regimen and older animals, we now report locus ceruleus lesions and eosinophilic inclusion bodies in squirrel monkeys. The inclusions were seen only in areas where Lewy bodies are found in human Parkinson's disease. No such abnormalities were seen in control animals. These findings suggest that similarities between the neuropathology of MPTP‐induced parkinsonism in the monkey and human Parkinson's disease are greater than first thought and increase the usefulness of the MPTP monkey model for research in Parkinson's disease.