bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trigeminal evoked potentials following brief air puff: Enhanced signal‐to‐noise ratio
Authors: Hashimoto Isao 
Published: January 2005

AbstractTrigeminal somatosensory evoked potentials (TSEPs) were studied by using fast‐rising air puffs generated by a highspeed air control system. Within 100 ms, air puff stimulation of the face elicited three negative and three positive components over the contralateral, as well as the ipsilateral, sensory area. The air puff TSEPs showed a uniform change in peak latencies and amplitudes as a function of stimulus intensity. The bilateral distribution of the TSEPs stands in sharp contrast to the exclusively contralateral distribution of the SEPs to stimulation of the hand. Air puffs evoked a larger response than electrical stimulation, although the latency remained the same. Unlike electrical stimuli, air puff induces neither stimulus nor muscle artifacts. This, combined with the higher amplitude of the recorded response, enhances the signal‐to‐noise ratio.
Tumor necrosis factor mediates myelin and oligodendrocyte damage in vitro
Authors: Selmaj Krzysztof W. , Raine Cedric S. 
Published: January 2005

AbstractRecombinant human tumor necrosis factor (rhTNF) has been tested for its effect on myelinated cultures of mouse spinal cord tissue. As controls, recombinant human interferon gamma (rhIFN) and interleukin‐2 (rhIL‐2) were tested, as well as T‐cell supernatants, antigalactocerebroside serum, and normal culture medium. It was found that rhTNF induced delayed‐onset (18–24 hr) oligodendrocyte necrosis and a type of myelin dilatation peculiar to this system. Some nerve fibers progressed to demyelination by 72 hours. The myelin dilatation was not reversible by return to normal feeding solution for 3 days. In contrast, rhIFN, rhIL‐2, T‐cell supernatants, and normal medium had little or no effect on cultures. This mechanism differs from other immune‐mediated mechanisms in that it appears that a physiological (not structural) demyelination occurs initially without overt destruction of the myelin sheath. These observations are relevant to the evolution of the multiple sclerosis plaque: dysfunction of ionic channels might contribute to the eventual demise of oligodendrocytes and axons in the longstanding lesion.
Changes in benzodiazepine receptors in alzheimer‐type dementia
Authors: Shimohama Shun , Taniguchi Takashi , Fujiwara Motohatsu , Kameyama Masakuni 
Published: January 2005

AbstractWe studied benzodiazepine receptors in brains obtained at autopsy from 7 normal controls and 7 patients with Alzheimer‐type dementia, using 3H‐flunitrazepam as a ligand. Compared with controls, 3H‐flunitrazepam binding sites were significantly reduced in number in frontal and temporal cortex and hippocampus in the Alzheimer‐type dementia brains. These results suggest that there are significant changes in the number of benzodiazepine receptors in selected brain regions of patients with Alzheimer‐type dementia.
Hypothalamic hamartomas and ictal laughter: Evolution of a characteristic epileptic syndrome and diagnostic value of magnetic resonance imaging
Authors: Berkovic S. F. , Andermann F. , Melanson D. , Ethier R. E. , Feindel W. , Gloor P. 
Published: January 2005

AbstractDetailed study of 4 patients and review of the literature allowed us to delineate further the epileptic syndrome associated with hypothalamic hamartomas, which characteristically begins in infancy with laughing seizures. Because early childhood psychomotor development is usually normal, the condition appears benign and may not even be recognized. The episodes of laughter are brief, frequent, and mechanical in nature. These features distinguish it from other forms of epileptic laughter, particularly that which occurs in temporal lobe epilepsy. Subsequently, the seizures become longer, other seizure types appear, and between the ages of 4 and 10 years, the clinical and electroencephalographic features of secondary generalized epilepsy develop. Cognitive deterioration occurs and severe behavior problems are frequent. Prognosis for seizure control and social adjustment is poor. Cortical abnormality occurs in association with the hypothalamic hamartoma. The lesions are best detected by magnetic resonance imaging but may be difficult to identify by computed tomographic scanning.
An antineuronal autoantibody in paraneoplastic opsoclonus
Authors: Budde‐Steffen Corinna , Anderson Neil E. , Rosenblum Mark K. , Graus Francesc , Ford David , Synek Beth J. L. , Wray Shirley H. , Posner Jerome B. 
Published: January 2005

AbstractSera from 7 patients with paraneoplastic opsoclonus were examined for antineuronal autoantibodies. An antibody against neuronal nuclei was found in serum from a patient with breast cancer, opsoclonus, and ataxia. This antibody recognized 53‐ to 61‐kDa and 79‐ to 84‐kDa antigens in immunoblots of neurons. Anti‐neuronal antibodies were not found in other patients with paraneoplastic opsoclonus.
Speech disorders in olivopontocerebellar atrophy correlate with positron emission tomography findings
Authors: Kluin Karen J. , Gilman Sid , Markel Dorene S. , Koeppe Robert A. , Rosenthal Guy , Junck Larry 
Published: January 2005

AbstractWe compared the severity of ataxic and spastic dysarthria with local cerebral metabolic rates for glucose (ICMRGlc) in is patients with olivepenetecerebeilar atrophy (OPCA). Perceptual analysis was used to examine the speech disorders, and rating scales were devised to quantitate the degree of ataxia and spasticity in the speech of each patient. 1CMRGlc was measured with 18F‐2‐fluoro‐2‐deoxy‐D‐glucose and positron emission tomography (PET). PET studies revealed marked hypometabolism in the cerebellar hemispheres, cerebellar vermis, and brainstem of OPCA patients compared with 30 control subjects. With data normalized to the cerebral cortex, a significant inverse correlation was found between the severity of ataxia in speech and the 1CMRG1c within the cerebellar vermis, cerebellar hemispheres, and brainstem, but not within the thalamus. No significant correlation was found between the severity of spasticity in speech and 1CMRG1c in any of these structures. The findings support the view that the severity of ataxia in speech in OPCA is related to the functional activity of the cerebellum and its connections in the brainstem.
Neurofibrillary tangle formation in the nucleus basalis of meynert ipsilateral to a massive cerebral infarct
Authors: Kato Takeo , Hirano Asao , Katagiri Tadashi , Sasaki Hideo , Yamada Shigeru 
Published: January 2005

AbstractTwo cases of massive cerebral infarct in the territory of the middle cerebral artery on one side of the brain are presented, in which many (Patient 1) or several (Patient 2) neurofibrillary tangle‐bearing neurons were observed in the nucleus basalis of Meynert (nbM), ipsilateral to the infarcts. Tangles were absent or rare in the opposite nbM or in other areas of the brain. Considering the widespread projection of nbM axons to the ipsilateral cerebral cortex, this suggests that formation of neurofibrillary tangles can occur as a retrograde reaction of nbM neurons secondary to massive, old cerebral infarction.
Treatment of patients with neuropathy and anti‐MAG IgM M‐proteins
Authors: Nobile‐Orazio E. , Baldini L. , Barbieri S. , Marchmiroli P. , Spagnol G. , Francomano E. , Scarlato G. 
Published: January 2005

AbstractFive patients with neuropathy and IgM M‐proteins that reacted with myelin‐associated glycoprotein (MAG) were treated for 10 to 20 months with cytostatic agents. In 2 patients, a Decemberrease in serum M‐protein and in anti‐MAG IgM levels coincided with a progressive improvement of neuropathy. No clinical improvement and no Decemberrease of anti‐MAG IgM were observed in the other patients. The close relationship between the Decemberrease of anti‐MAG, M‐proteins and clinical improvement in these patients supports the pathogenetic role of the M‐protein in the neuropathy.
Cerebral hypometabolism in progressive supranuclear palsy studied with positron emission tomography
Authors: Foster Norman L. , Gilman Sid , Berent Stanley , Morin Elizabeth M. , Brown Morton B. , Koeppe Robert A. 
Published: January 2005

AbstractProgressive supranuclear palsy (PSP) is characterized by supranuclear palsy of gaze, axial dystonia, bradykinesia, rigidity, and a progressive dementia. Pathological changes in this disorder are generally restricted to subcortical structures, yet the type and range of cognitive deficits suggest the involvement of many cerebral regions. We examined the extent of functional impairment to cerebral cortical and subcortical structures as measured by the level of glucose metabolic activity at rest. Fourteen patients with PSP were compared to 21 normal volunteers of similar age using18F‐2‐fluoro‐2‐deoxy‐D‐glucose and positron emission tomography. Glucose metabolism was reduced in the caudate nucleus, putamen, thalamus, pons, and cerebral cortex, but not in the cerebellum in the patients with PSP as compared to the normal subjects. Analysis of individual brain regions revealed significant Decemberlines in cerebral glucose utilization in most regions throughout the cerebral cortex, particularly those in the superior half of the frontal lobe. Decemberlines in the most affected regions of cerebral cortex were greater than those in any single subcortical structure. Although using conventional neuropathological techniques the cerebral cortex appears to be unaffected in PSP, significant and pervasive functional impairments in both cortical and subcortical structures are present. These observations help to account for the constellation of cognitive symptoms in individual patients with PSP and the difficulty encountered in identifying a characteristic psychometric profile for this group of patients.
Dual‐label immunocytochemistry of the active multiple sclerosis lesion: Major histocompatibility complex and activation antigens
Authors: Hayashi T. , Morimoto C. , Burks J. S. , Kerr C. , Hauser S. L. 
Published: January 2005

AbstractFresh‐frozen autopsy material containing active inflammatory lesions from 9 different patients with multiple sclerosis (MS) was analyzed by immunocytochemistry using a panel of monoclonal antibodies, and a dual‐label immunocytochemical method was developed which permitted the simultaneous detection of two different surface Marchkers on a single cell. We now report the following. (1) The predominant T‐cell phenotype within MS lesions is CD2,3,8. This phenotype Marchks the suppressor‐cytotoxic subset. (2) These cells do not express the natural killer cell Marchker NKH‐1, which is present on a subset of CD8‐positive cells in peripheral blood. (3) The infiltrating cell expresses class I (HLA A, B, C), but not class II (DR and DQ), major histocompatibility complex (MHC) molecules. (4) Other T‐cell surface molecules, including the activation antigens interleukin‐2 receptor, Ta1, and Tll‐3, as well as the Marchker 2H4, are largely not expressed. (5) Endothelial cells express both class I and class II MHC molecules and the 4B4 molecule in both MS and control tissue. (6) Astrocytes within the vicinity of MS lesions are predominantly class II MHC—negative. These results demonstrate that the T‐cell infiltrate present in MS tissue on autopsy has a restricted phenotypic profile, but they also raise the possibility that, within this population, few activated effector cells are present.
Somatosensory potentials evoked by magnetic stimulation of lumbar roots, cauda equina, and leg nerves
Authors: Tsuji Sadatoshi , Murai Yoshiyuki , Yarita Masaru 
Published: January 2005

AbstractCortical somatosensory evoked potentials (Septembers) were studied by noninvasive magnetic stimulation at T‐10, T‐12, and L‐5 vertebral levels and in mid‐gluteus muscle and ankle in 27 normal subjects and 7 patients with neurological diseases. Cortical components P2 and N2 were recorded in all normal subjects. The mean peak latencies of P2 were 20.3 ± 0.9 (standard deviation), 21.1 ± 1.2, 23.5 ± 1.4, 27.9 ± 2.0, and 38.1 ± 1.8 msec at the T‐10, T‐12, L‐5, mid‐gluteal and ankle sites of stimulation, respectively. No substantial difference in morphology of P2 and N2 was seen between magnetic and electrical stimulation at T‐12. Amplitudes of P2 and N2 were maximal after magnetic stimulation at motor threshold. P2 and N2 may originate from the sensory cortex. P2 and N2 evoked by T‐10 and T‐12 stimulation were normal in peak latency and morphology in patients with polyneuropathy or polyradiculoneuropathy. Peak latencies of P2 and N2 evoked by T‐10 and T‐12 stimulation were significantly delayed in patients with myelopathy. The patients with radiculopathy showed a delayed peak latency and conduction time of P2 evoked by L‐5 stimulation. Magnetic stimulation of spinal root is able to detect lesions of spinal cord noninvasively.
Organization, fine structure, and viability of the human adrenal medulla: Considerations for neural transplantation
Authors: Hansen John T. , Notter Marchy F. D. , Okawara Shige‐Hisa , Gash Don M. 
Published: January 2005

AbstractRecent reports of adrenal medullary autografts in patients with Parkinson's disease raise several important questions with respect to the cell types actually being transplanted as well as the potential for chromaffin cell banking prior to neural transplantation. In this study, we determined the general morphological characteristics of the human adrenal medulla and assessed factors important for the maintenance of cultured chromaffin cells for later use as transplants. The human adrenal medulla contained islands of cortical cells scattered throughout the gland as well as Schwann cells, nerve endings, endothelial cells, pericytes, isolated ganglionic neurons, and connective tissue elements such as fibroblasts and smooth muscle cells. Because many of these cell types are mitotically active, transplantation of medullary fragments that contain these cells could have far‐reaching consequences. One approach that could circumvent the problems arising from multiple cell types in the medulla is differential plating of chromaffin cells prior to transplantation. Differential plating yielded relatively pure populations of chromaffin cells that demonstrated excellent viability if processed within 2 hours after cessation of the gland's circulation. Chromaffin cells cultured in the presence of nerve growth factor exhibited a neuronal phenotype, possessed catecholamine histofluorescence, and displayed tyrosine hydroxylase‐ and dopamine β‐hydroxylase—like immunoreactivity. The sex and age of the donor did not affect cell viability or morphological characteristics.
The Go—No‐Go paradigm in attention deficit disorder
Authors: Trommer Barbara L. , Hoeppner Jo‐Ann B. , Lorber Rudy , Armstrong Kevin J. 
Published: January 2005

AbstractWe administered the go—no‐go paradigm to 44 boys with attention deficit disorder (ADD) and 32 control subjects who did not have ADD. This task requires a subject to emit a simple motor response to one cue while inhibiting the response in the presence of another cue. Commission errors suggest impulsivity, and omission errors suggest inattention. ADD subjects made more total errors than did control subjects (p < 0.03), and more ADD subjects made multiple errors (p < 0.001). Within the ADD group, the nonhyperactive (ADDnoH) subjects were characterized by a high number of commission errors early, and significant improvement with practice (p < 0.01). In contrast, the hyperactive ADD subjects (ADD/H) did not differ from control subjects in number of early commission errors, but differed from both control subjects and ADDnoH subjects in their failure to improve with practice. In addition, the incidence of omission errors was highest in the ADD/H group. This paradigm can be easily incorporated into the assessment of children with suspected ADD and provides an objective measure of inattention and impulsivity. Our data provide cognitive support for the empirical distinction between hyperactive and nonhyperactive children with ADD.
Posture in Parkinson's disease: Impairment of reflexes and programming
Authors: Dietz V. , Berger W. , Horstmann G. A. 
Published: January 2005

AbstractThe leg muscle electromyographic responses induced during stance by impulsive displacements of a treadmill belt (directed forward or backward and at different rates) were studied in a group of patients with Parkinson's disease and a group of age‐matched healthy subjects. Young normal subjects were also studied both before and after intake of a dopamine antagonist (haloperidol). Compensatory gastrocnemius electromyographic responses resulting from backward‐directed displacements were significantly smaller in both the patients and the young normal subjects following intake of haloperidol. The reduced sensitivity of the gastrocnemius muscle to stretch correlated with an inability to compensate for the perturbations. In the patients, the gastrocnemius response was followed by enhanced activation of the tibialis anterior muscle. This was not the case in the normal subjects after intake of dopamine antagonist and is probably not, therefore, the consequence of acute dopamine deficiency. In the patients the angular rotation at the ankle joint induced during faster backward‐directed displacements was slower than that in normal subjects, despite identical amounts of gastrocnemius electromyographic activity. This supports earlier findings of changes in intrinsic muscle stiffness in Parkinson's disease. None of these differences were seen when the tibialis anterior muscle was stretched. This differential behavior of the antagonist leg muscles can best be explained by the different function fulfilled by these muscles in regulation of stance and gait.
Thalamic, brainstem, and cerebellar glucose metabolism in the hemiplegic monkey
Authors: Shimoyama Ichiro , Dauth George W. , Gilman Sid , Frey Kirk A. , Penney John B. 
Published: January 2005

AbstractUnilateral ablation of cerebral cortical areas 4 and 6 of Brodmann in the macaque monkey results in a contralateral hemiplegia that resolves partially with time. During the phase of dense hemiplegia, local cerebral metabolic rate for glucose (lCMRGlc) is Decemberreased significantly in most of the thalamic nuclei ipsilateral to the ablation, and there are slight contralateral Decemberreases. The lCMRGlc is reduced bilaterally in most of the brainstem nuclei and bilaterally in the deep cerebellar nuclei, but only in the contralateral cerebellar cortex. During the phase of partial motor recovery, lCMRGlc is incompletely restored in many of the thalamic nuclei ipsilateral to the ablation and completely restored in the contralateral nuclei. In the brainstem and deep cerebellar nuclei, poor to moderate recovery occurs bilaterally. Moderate recovery occurs in the contralateral cerebellar cortex. The findings demonstrate that a unilateral cerebral cortical lesion strongly affects lCMRGlc in the thalamus ipsilaterally and in the cerebellar cortex contralaterally, but in the brainstem bilaterally. Partial recovery of lCMRGlc accompanies the progressive motor recovery. The structures affected include those with direct, and also those with indirect, connections to the areas ablated.
Chronic remitting‐relapsing experimental allergic encephalomyelitis induced in monkeys with homologous myelin basic protein
Authors: Shaw Cheng‐Mei , Alvord Ellsworth C. , Hruby Sarka 
Published: January 2005

AbstractA chronic remitting‐relapsing form of experimental allergic encephalomyelitis (EAE) has been produced in monkeys sensitized to homologous myelin basic protein in Freund's complete adjuvants by the technique of suboptimal treatment after the onset of disease. Not only does the clinical course resemble that of human multiple sclerosis more closely than does the clinical course of acute EAE, but so also does the histological reaction, with more‐nearly pure demyelination, rather than the hyperacute hemorrhagic‐necrotic lesions that occur so commonly in untreated monkeys with ordinary acute EAE.
A comparison of somatosensory evoked and motor evoked potentials in stroke
Authors: Macdonell R. A. L. , Donnan G. A. , Bladin P. F. 
Published: January 2005

AbstractNineteen patients with radiologically confirmed stroke, and varying degrees of hemiparesis, were studied using somatosensory evoked potentials and the recently developed technique of transcutaneous motor cortex stimulation. The functional deficit caused by stroke was assessed at the time of evoked potential testing and again on follow‐up 2 months after stroke. Stroke location and degree of recovery were compared with the evoked potentials elicited an average of 8 days after the acute event. The motor response was better (p < 0.01) than somatosensory response at predicting an outcome in terms of functional recovery, both overall and when comparing patients with similar degrees of weakness. Normal somatosensory evoked potentials also predicted recovery but were not as sensitive as the motor evoked potentials (0.01 < p < 0.05). Motor evoked potentials in conjunction with clinical assessment may offer a means of more accurately predicting functional outcome following stroke than can be achieved with clinical assessment, with or without somatosensory evoked potentials. The additional finding that cortically evoked motor evoked potentials were delayed only by subcortical lesions is of interest and may extend the understanding of the pathophysiological mechanism of this response in humans.
Intraventricular hemorrhage in the premature infant—current concepts. Part II
Authors: Volpe Joseph J. 
Published: January 2005

AbstractDiagnosis of periventricular‐intraventricular hemorrhage (IVH) and its neuropathological consequences and accompaniments in the living infant has been facilitated greatly by the introduction of real‐time cranial ultrasonography. The major advantages of the technique include high‐resolution capability, portable instrumentation, lack of ionizing radiation, and relative affordability. Prognosis in infants with IVH relates to the mechanisms of brain injury, the most important of which are prior hypoxic‐ischemic insults, posthemorrhagic hydrocephalus, and periventricular hemorrhagic infarction. The last of these is most critical and it is now clear that careful quantitative assessment of the ultrasonographic appearance of the periventricular parenchyma in the infant with IVH during the acute period of illness is of major value in estimating outcome. Prevention of IVH remains the most important goal. Prenatal interventions include prevention of premature birth (currently a very elusive goal in the United States), transportation of the premature infant to a tertiary facility in utero rather than after birth (an approach of proven value), prenatal administration of phenobarbital or vitamin K (initially promising data that require confirmation and amplification), and optimal management of labor and delivery. Postnatal interventions include careful resuscitation of newborns, correction of fluctuating cerebral blood flow velocity, correction or prevention of other major hemodynamic disturbances, and correction of abnormalities of coagulation. Of these interventions the use of muscle paralysis to correct fluctuating cerebral blood flow velocity has shown the most striking benefit vis‐à‐vis prevention of IVH. Postnatal pharmacological interventions that have been studied in detail include the use of phenobarbital, indomethacin, ethamsylate, and vitamin E. No single agent among this group has been shown consistently to lead to a decrease in incidence and severity of IVH. The most promising current data relate to the postnatal administration of ethamsylate (which is not available in the United States). Inconsistent results have been obtained in the study of postnatal administration of phenobarbital, indomethacin, and vitamin E. At present, no pharmacological agent is considered to have benefits that are established clearly enough to warrant recommendation for routine use in premature infants.