bluuebunny/crossref_metadata_2025_split huggingface dataset:
Galanin immunoreactivity is increased in the nucleus basalis of meynert in Alzheimer's disease
Authors: Beal M. Flint , MacGarvey Usha , Swartz Kenton J. 
Published: January 2005

AbstractA depletion of large cholinergic neurons in the nucleus basalis of Meynert is a consistent finding in Alzheimer's disease (AD). The nucleus basalis of Meynert also contains interneurons and afferents that may modulate its functioning. In the present study we examined neurochemical markers for neuropeptides, amino acid neurotransmitters, and monoaminergic neurotransmitters in postmortem samples of the nucleus basalis in 16 control subjects and 30 patients with AD. There were no significant changes in glutamate, aspartate, taurine, gamma‐aminobutyric acid (GABA), and catecholamines; however, concentrations of serotonin, 5‐hydroxyindoleacetic acid, and 5‐hydroxytryptophol were significantly reduced. Choline acetyltransferase activity was significantly reduced, consistent with previous reports. Galanin immunoreactivity was significantly increased twofold in the patients with AD, but there were no significant changes in substance P, somatostatin, or neuropeptide Y immunoreactivity. Since galanin inhibits acetylcholine release, and produces cognitive deficits in animals, increased galanin immunoreactivity in the nucleus basalis of Meynert in AD may contribute to the cognitive deficits that characterize the illness.
Methods for estimating the number of motor units in human muscles
Authors: Stein Richard B. , Yang Jaynie F. 
Published: January 2005

AbstractThe number of motor units in the thenar muscle group was calculated by dividing the surface electromyogram and twitch force, in maximal stimulation of the median nerve, by estimates of the average electromyogram and twitch force from single units. The following three techniques were used to estimate the average electromyogram from single units: spike‐triggered averaging from units recorded with a needle electrode, intramuscular microstimulation of motor nerve branches, and graded whole nerve stimulation at the wrist. The first two techniques also provided independent estimates of motor unit numbers based on the average force generated by single units. The five estimates (three based on the electromyogram and two on force) ranged from 116 to 170 motor units in the thenar group. Correcting for cancellation when unit responses sum to form the compound action potential or twitch increased the estimated number of units, which ranged from 130 to 179. The estimates were not statistically different from one another but were substantially lower than some previous electrophysiological estimates based on graded whole nerve stimulation. The recruitment pattern of single units during whole nerve stimulation was recorded and simulated mathematically. The most likely reason for the higher estimates in previous studies using graded whole nerve stimulation is shown to be alternation of motor units. Potential errors in all the techniques are discussed and compared.
Motor unit numbers and contractile properties after spinal cord injury
Authors: Yang Jaynie F. , Stein Richard B. , Jhamandas Jack , Gordon Tessa 
Published: January 2005

AbstractThe number of motor units in the thenar muscle group was estimated in 11 patients with cervical spinal cord injuries. The surface electromyogram and twitch force, in response to maximal stimulation of the median nerve was divided by the average surface electromyogram and twitch of single units. The average single unit size was obtained by intramuscular microstimulation of motor nerve branches and by graded whole nerve stimulation, which provided three independent estimates, two based on the electromyogram and one based on force. The motor unit estimates from the patients covered a wide range, some had essentially normal motor units both in numbers and contracatile properties, while others had varying reductions in numbers of units. Those patients who showed a large reduction in motor unit numbers also had greatly enlarged units, which produced an average of up to sixfold the normal force. These enlarged units summed to produce maximal compound action potentials and twitches that were sometimes indistinguishable from normal. Magnetic resonance imaging scans of the cervical spine obtained from some patients provided independent evidence that patients with low motor unit counts had sustained direct injury to the anterior aspect of the spinal cord at the relevant segmental levels. Some patients showed a normal number of motor units long after the injury. No evidence of transneuronal degeneration could be demonstrated in the thenar group in these patients with the current techniques.
Failure of nine‐month phenobarbital administration to reverse amygdaloid‐kindled seizure susceptibility in cats
Authors: Hiyoshi Toshio , Wada Juhn A. 
Published: January 2005

AbstractUpon completion of left amygdaloid kindling, 4 cats underwent long‐term phenobarbital administration during the subsequent 5‐ to 9‐month rest period. Plasma phenobarbital levels were maintained above 15 to 20 μg/ml and were restimulated following plasma phenobarbital washout. Three cats served as nonmedicated controls. All 7 cats were subjected to repeated 6‐hour sleep monitoring for observation of interictal discharges, which were observed most often in the immediate postictal period. Their frequency decreased gradually throughout the experiment in both the medicated and control animals, but they never completely disappeared except from the contralateral amygdala in 1 medicated animal. Upon primary site restimulation, all of the medicated animals responded with a generalized convulsion once the afterdischarge was induced. When these animals underwent secondary‐site amygdaloid kindling, 3 showed a positive transfer effect. The findings suggest that although phenobarbital is a potent anticonvulsant, it has little effect on the acquired seizure susceptibility of previously amygdaloid kindled cats.
A comparison of neurological, metabolic, structural, and genetic evaluations in persons at risk for Huntington's disease
Authors: Grafton Scott T. , Mazziotta John C. , Pahl Jorg J. , George‐Hyslop Peter St. , Haines Jonathan L. , Gusella James , Hoffman John M. , Baxter Lewis R. , Phelps Michael E. 
Published: January 2005

AbstractWe compared four diagnostic data sets for the assessment of individuals at risk for Huntington's disease. Fifty‐four chorea‐free persons were evaluated by neurological examination, positron emission tomography measurement of glucose metabolism, radiographic computerized tomographic measurement of caudate size, and genetic testing at the polymorphic DNA loci D4S10, D4S43, and D4S125. Twelve (22%) persons had abnormal caudate metabolism, 6(11%) had subtle abnormalities of motor control, and 7(13%) had computed tomographic evidence of caudate atrophy, compared with an expected gene frequency of 34% for this population. In 20 persons with unambiguous genetic test results or the subsequent phenotypic expression of Huntington's disease (chorea), there was a greater sensitivity of the positron emission tomographic measurement of caudate metabolism (75%) relative to computed tomography (33%) or the clinical examination (17%) for the determination of a subpopulation of probable Huntington's disease gene carriers. Hypometabolism of the putamen and globus pallidus, and hypermetabolism of the precentral gyrus were also associated with a high probability of carrying the Huntington's disease gene. The findings support the hypothesis that abnormalities of cerebral metabolism precede clinical or structural (computed tomographic) abnormalities in gene‐postive individuals at risk for Huntington's disease.
Impairment of sequences of memory‐guided saccades after supplementary motor area lesions
Authors: Gaymard B. , Pierrot‐Deseilligny Ch. , Rivaud S. 
Published: January 2005

AbstractDifferent paradigms of saccades were recorded electro‐oculographically in 2 patients with infraction affecting the left supplementary motor area. Saccades made toward visual targets (visually‐guided saccades) or away from them (antisaccades) were normal in both patients. Memory‐guided saccades, made to the remembered position of a flash occurring 2 seconds before, were preserved in 1 patient and only slightly impaired in the other. However, sequences of two or three memory‐guided saccades were severely impaired in both patients. It has previously been reported that the supplementary motor area plays an important role in programming sequential limb movements. Our data suggest that this area plays a similar role in the control of sequential eye movements.
Guanidino compounds that are increased in cerebrospinal fluid and brain of uremic patients inhibit GABA and glycine responses on mouse neurons in cell culture
Authors: De Deyn Peter P. , Macdonald Robert L. 
Published: January 2005

AbstractFour guanidino compounds that have been found to be markedly increased in cerebrospinal fluid and brain tissue of uremic patients, namely, guanidine, methylguanidine, creatinine, and guanidinosuccinic acid, were applied to mouse spinal cord neurons in primary dissociated cell culture to evaluate their effects on postsynaptic responses to gammaaminobutyric acid (GABA) and glycine. Intracellular microelectrode recording techniques were used. Guanidine, methylguanidine, creatinine, and guanidinosuccinic acid reversibly and in a dose‐dependent manner inhibited both GABA and glycine responses. Guanidinosuccinic acid was the most potent inhibitor of the amino acid responses, followed in decreasing potency by methylguanidine, guanidine, and creatinine. Guanidinosuccinic acid inhibited responses to GABA and glycine, at concentrations similar to those found in cerebrospinal fluid and brain tissue of patients with terminal renal insufficiency. The other guanidino compounds tested exerted their effects only at concentrations higher than those found in uremic biological fluids and tissues. The inhibitory effect of guanidine and methylguanidine on responses to GABA was additive. The effect of the guanidino compounds on GABA responses was not antagonized by coapplication of the benzodiazepine‐receptor antagonist CGS 9896. The results suggest that guanidine, methylguanidine, creatinine, and guanidinosuccinic acid inhibited responses to the inhibitory neurotransmitters GABA and glycine by blocking the chloride channel. The observed action of the studied guanidino compounds might contribute to the pathogenesis of the complex neurological symptomatology encountered in uremia.
Eyelid movements before and after botulinum therapy in patients with lid spasm
Authors: Manning Karen A. , Evinger Craig , Sibony Patrick A. 
Published: January 2005

AbstractQuantitative analysis of lid motility is presented for 4 individuals with hemifacial spasm and 1 with Meige's syndrome. The data were obtained, by means of a magnetic search coil technique, prior to and 1 week after injection of botulinum toxin into the orbicularis oculi muscle. Before treatment, the peak velocity of blink‐related lid lowering and lid raising was slower than normal, yet lid saccades were normal. After botulinum treatment, significant decreases occurred in (1) the amplitude of blinks and lid saccades, and (2) the peak velocity of the blink down‐phase. Botulinum treatment significantly alters blink lid‐lowering kinematics, while saccadic lid‐lowering kinematics are normal, providing further evidence that the orbicularis oculi muscle does not play a primary role in downward lid saccades.
Magnetic motor‐evoked potentials in epilepsy: Effects of the disease and of anticonvulsant medication
Authors: Hufnagel Andreas , Elger Christian E. , Marx Werner , Ising Anton 
Published: January 2005

AbstractMagnetic motor‐evoked potentials were recorded in 53 patients with medically intractable, mainly temporal lobe epilepsy and compared with potentials of 110 healthy volunteers. The motor‐evoked potentials were reevaluated in 16 of the 53 patients after substantial reduction of antiepileptic drug doses. The objective was to assess the effect of epilepsy and of anticonvulsant medication on the central motor system. In subjects receiving antiepileptic treatment, cortical threshold intensities were markedly elevated and peripheral latencies were prolonged. Cortical threshold intensities and peripheral latencies decreased to approach control values after anticonvulsant medication was reduced but were increased in patients treated with 2 or 3 anticonvulsant agents instead of 1. Additionally, high levels of interictal epileptiform activity and a high frequency of seizures significantly decreased the central motor conduction time and, in part, threshold intensities. The central motor conduction time was further diminished after reduction of anticonvulsant treatment and increased when several drugs were administered. The duration of epilepsy, the location of the epileptic focus, and the type of the epileptic seizure did not affect motor‐evoked potentials. Conclusively, central motor pathways are endogenously facilitated by epileptiform activity even if clinical signs of their involvement are absent. Anticonvulsant medication exerts major reversible effects on magnetic motor‐evoked potentials.
MEG versus EEG localization test using implanted sources in the human brain
Authors: Cohen David , Cuffin B. Neil , Yunokuchi Kazutomo , Maniewski Roman , Purcell Christopher , Cosgrove G. Rees , Ives John , Kennedy John G. , Schomer Donald L. 
Published: January 2005

AbstractIt is believed that the magnetoencephalogram (MEG) localizes an electrical source in the brain to within several millimeters and is therefore more accurate than electroencephalogram (EEG) localization, reported as 20 mm. To test this belief, the localization accuracy of the MEG and EEG were directly compared. The signal source was a dipole at a known location in the brain; this was made by passing a weak current pulse simulating a neural signal through depth electrodes already implanted in patients for seizure monitoring. First, MEGs and EEGs from this dipole were measured at 16 places on the head. Then, computations were performed on the MEG and EEG data separately to determine the apparent MEG and EEG source locations. Finally, these were compared with the actual source location to determine the MEG and EEG localization errors. Measurements were made of four dipoles in each of three patients. After MEGs with weak signals were discounted, the MEG average error of localization was found to be 8 mm, which was worse than expected. The average EEG error was 10 mm, which was better than expected. These results suggest that the MEG offers no significant advantage over the EEG in localizing a focal source. However, this does not diminish other uses of the MEG.
Cytomegalovirus neuropathy in acquired immunodeficiency syndrome: A clinical and pathological study
Authors: Said G. , Lacroix C. , Chemouilli P. , Goulon‐Goeau C. , Roullet E. , Penaud D. , De Broucker T. , Meduri G. , Vincent D. , Torchet M. , Vittcoq D. , Leport C. , Vildé J. L. 
Published: January 2005

AbstractWe have observed typical cytomegalovirus cytopathology associated with multifocal inflammatory and necrotic lesions of peripheral nerve in biopsy specimens from 4 patients who developed a rapidly progressive, multifocal neuropathy late in the course of human immunodeficiency virus infection. The inflammatory infiltrates, which contained numerous polymorphonuclear cells, were associated with mixed, axonal, and demyelinative lesions of nerve fibers. One of these patients improved on treatment with DHPG (9‐[2‐hydroxy‐1(hydroxymethyl) ethoxymethyl] guanine) and remains stable after 18 months. The other 3 died soon after the onset of the neuropathy. In another patient with acquired immunodeficiency syndrome, who developed a severe, predominantly motor neuropathy of the lower limbs, the nerve biopsy did not reveal cytomegalovirus inclusions, but the neurological deficit improved on treatment with DHPG. The patient died from cachexia 2 months later; numerous cytomegalovirus lesions were found in the spinal cord at the time of postmortem examination. The multifocal necrotic endoneurial nerve lesions with polymorphonuclear cell infiltration we describe may help identify cytomegalovirus neuropathy when characteristic inclusions are not present in the biopsy specimen.
Quinolinic acid in cerebrospinal fluid and serum in HIV‐1 Infection: Relationship to clinical and neurological status
Authors: Heyes Melvyn P. , Brew Bruce J. , Martin Alex , Price Richard W. , Salazar Andres M. , Sidtis John J. , Yergey James A. , Mouradian M. Maral , Sadler Abigail E. , Keilp John , Rubinow David , Markey Sanford P. 
Published: January 2005

AbstractQuinolinic acid is an “excitotoxic” metabolite and an agonist of N‐methyl‐D‐aspartate receptors. Of patients infected with human immunodeficiency virus type 1 (HIV‐1) who were neurologically normal or exhibited only equivocal and subclinical signs of the acquired immunodeficiency syndrome (AIDS) dementia complex, concentrations of quinolinic acid in cerebrospinal fluid (CSF) were increased twofold in patients in the early stages of disease (Walter Reed stages 1 and 2) and averaged 3.8 times above normal in later‐stage patients (Walter Reed stages 4 through 6). However, in patients with either clinically overt AIDS dementia complex, aseptic meningitis, opportunistic infections, or neoplasms, CSF levels were elevated over 20‐fold and generally paralleled the severity of cognitive and motor dysfunction. CSF concentrations of quinolinic acid were significantly correlated to the severity of the neuropsychological deficits. After treatment of AIDS dementia complex with zidovudine and treatment of the opportunistic infections with specific antimicrobial therapies, CSF levels of quinolinic acid decreased in parallel with clinical neurological improvement. By analysis of the relationship between levels of quinolinic acid in the CSF and serum and integrity of the blood‐brain barrier, as measured by the CSF: serum albumin ratio, it appears that CSF levels of quinolinic acid may be derived predominantly from intracerebral sources and perhaps from the serum. While quinolinic acid may be another “marker” of host‐ and virus‐mediated events in the brain, the established excitotoxic effects of quinolinic acid and the magnitude of the increases in CSF levels of the acid raise the possibility that quinolinic acid plays a direct role in the pathogenesis of brain dysfunction associated with HIV‐1 infection.
Myoclonus in adult Huntington's disease
Authors: Vogel Caryn M. , Drury Ivo , Terry L. Cass , Young Anne B. 
Published: January 2005

AbstractTwo brothers with clinically definite adult Huntington's disease developed disabling myoclonus years after the first signs of the disease. Their electroencephalograms were consistent with a primary generalized epilipsy, although neither man had seizures. The myoclonus was controlled with valproic acid therapy.
Early loss of astrocytes in herpes simplex virus–induced central nervous system demyelination
Authors: Itoyama Yasuto , Sekizawa Tsuyoshi , Openshaw Harry , Kogure Kyuya , Goto Ikuo 
Published: January 2005

AbstractImmunohistochemistry was used to study herpes simplex virus type 1–induced central nervous system demyelination in the trigminal root entry zone of mice inoculated with herpes simplex virus type 1 by the corneal route. There was no change in peripheral nervous system myelin as shown by immunostaining for Po glycoprotein. Double immunoperoxidase staining for herpes simplex virus type 1 antigens and glial fibrillary acidic protein showed that most of the infected cells were astrocytes. Glial fibrillary acidic protein immunostaining was completely lost in the inferior medial portion of the trigeminal root entry zone at 6 days after herpes simplex virus type 1 inoculation, a time when central nervous system myelin was preserved as indicated by immunostaining for myelin basic protein. The pattern of glial fibrillary acidic protein staining did not change and herpes simplex virus type 1 antigens were no longer detected after day 8. There was a progressive loss of myelin basic protein staining within the area unstained by glial fibrillary acidic protein antisera on days 8 to 14. This pattern of astrocyte loss before central nervous system demyelination is strikingly different from the reactive astrocytosis seen in other demyelinating lesions, such as acute experimental allergic encephalomyelitis, progressive multifocal leukoencephalopathy, or acute multiple sclerosis. Herpes simplex virus type 1 infection in mice provides an unusual model of acute central nervous system demyelination preceded by a loss of astrocytes.
In vitro demyelination by serum antibody from patients with guillain‐barré syndrome requires terminal complement complexes
Authors: Sawant‐Mane S. , Clark M. B. , Koski C. L. 
Published: January 2005

AbstractSerum from 7 patients who had acute‐phase Guillain‐Barré syndrome with high anti‐peripheral nerve myelin antibody activity (54 to 210 units/ml) was compared with serum from 3 patients in the recovery phase (0 to 17 units/ml) and serum from 7 disease control subjects (0 to 24 units/ml) and 7 normal control subjects (0 to 7 units/ml) for its ability to demyelinate rodent dorsal root ganglion cultures. The demyelinating capacity of each serum was quantitated by counting the percent of damaged internodal segments in each of four cultures. All sera from patients in the acute phase GBS caused 50 to 78% demyelination, in contrast with 6 to 19% by the sera from all 3 patients in the recovery phase and all other control subjects. The degree of demyelination correlated with anti‐peripheral nerve myelin antibody activity of the sera and demyelination was complement‐dependent. Further, cultures were treated with an immunoglobulin M (IgM) fraction of an acute‐phase Guillain‐Barré syndrome plasma plus normal human serum depleted of complement component C7. Only those cultures treated with IgM and C7‐depleted human serum reconstituted with purified C7 resulted in 50.8% demyelination, which was significantly greater than the 14.2 to 16.2% demyelination observed in the presence of heat‐inactivated, C7‐depleted human serum plus purified C7 or in the absence of C7 or antibody. In summary, our work suggests that anti‐peripheral nerve myelin antibody in Guillain‐Barré syndrome mediated complement dependent‐demyelination of rodent dorsal root ganglion cultures. Further, this in vitro demyelination required generation of activation complexes of the terminal complement cascade.