bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison between lergotrile and bromocriptine in parkinsonism
Authors: Teychenne P. F. , Pfeiffer R. F. , Bern S. M. , McInturff D. , Calne D. B. 
Published: January 2005

AbstractThe therapeutic and adverse effects of two ergot derivatives, bromocriptine and lergotrile, were compared in idiopathic parkinsonism. At both low (50 mg daily) and high (150 mg daily) dosage there was a similar but not identical profile of response. Initially, lergotrile tended to induce more severe but always transient hypotension. At higher doses, bromocriptine caused more dyskinesia.Neurological deficits improved with increasing doses up to an average daily level of 80 to 150 mg of ergot derivatives combined with levodopa, 450 to 1,150 mg, and carbidopa, 45 to 115 mg. However, efficacy often declined at the highest doses of antiparkinsonian agents.Adverse effects caused by ergot derivatives are more common with dosages greater than 100 mg per day. In general, the best overall therapeutic results with bromocriptine and lergotrile were obtained in the dose range of 50 to 100 mg daily for each.It is concluded that bromocriptine and lergotrile are similar in their therapeutic properties and that both are comparable in efficacy to levodopa plus carbidopa (though optimal results are commonly obtained by combining submaximal doses of levodopa with ergot derivatives). The role for each drug in the treatment of parkinsonism is likely to be determined by factors such as cost (bromocriptine) and hepatotoxicity (lergotrile).
Ectopic generation of impulses and cross‐talk in spinal nerve roots of “dystrophic” mice
Authors: Rasminsky Michael 
Published: January 2005

AbstractIn “dystrophic” mice, many spinal root axons are bare and closely apposed to one another in midroot. The direction of nerve impulse traffic in lumbosacral spinal nerve roots was determined by biphasic recording of spontaneous activity. In normal mice, impulse traffic in dorsal and ventral roots is directed toward and away from the spinal cord, respectively. However, in spinal root fibers of dystrophic mice, impulses also originate in midroot and are propagated toward both the spinal cord and the periphery. Impulses originate in midroot as single isolated events, in bursts at frequencies of up to 100 Hz, or as continuous activity persisting for several minutes in single fibers. Ectopically arising activity in some single fibers is consistently associated with transmission of an impulse in another fiber past the site of origin of the ectopically arising impulse. Thus impulses arise in the spinal root axons of dystrophic mice both spontaneously and as a result of cross‐talk between single fibers.
Papulosis atrophicans maligna (Köhlmeier‐Degos disease): A disseminated occlusive vasculopathy
Authors: McFarland H. Richard , Wood William G. , Drowns Bruce V. , Meneses Antonio C. O. 
Published: January 2005

AbstractMalignant atrophic papulosis usually presents as pathognomonic skin lesions followed by acute abdominal pain, bowel perforation, peritonitis, and death. Rare patients who may lack gastrointestinal symptoms present with central nervous system manifestations, including headache, paresthesias, weakness, and rapid deterioration to death. The patient reported here was a 47‐year‐old man whose neurological symptoms apparently preceded his cutaneous lesions. His course consisted of a disseminated neurological disease and exacerbated following a herpes zoster infection. His condition rapidly deteriorated despite corticotropin, glucocorticoids, and low‐molecular‐weight dextran. Necropsy revealed a disseminated occlusive vasculopathy and diffuse encephalomyelomalacia of the brain and spinal cord. A review of autopsied patients with central nervous system involvement is provided.
A technique for the elution of cell‐surface antibody from human brain tissue
Authors: Gilden Donald , Devlin Mary , Wroblewska Zofia 
Published: January 2005

AbstractAn artifical system is described in which anti‐dinitrophenyl (DNP) antibody attaches to hapten‐conjugated human brain tissue. Treatment of this material with acetic acid at pH 2.5 to 3.0 for 90 seconds followed by immediate neutralization results in dissociation of antibody from the hapten‐conjugated brain. Less than 1 ng of specific antibody can be detected, as determined by the ability of eluted material to combine with DNP in an established radioimmunoassay system. Similar methods may be applied to neurological disorders in which immunoglobulins are thought to be produced in the central nervous system.
Infantile spasms in down syndrome: A report of 5 cases and review of the literature
Authors: Pollack Michael A. , Golden Gerald S. , Schmidt Rina , Davis Jessica A. , Leeds Norman 
Published: January 2005

AbstractFive patients with Down syndrome (DS) and infantile spasms were examined in a four‐year interval. Previous reports of this association have been infrequent except during experimental treatment with 5‐hydroxytryptophan, a precursor of serotonin. Malformations of the brain in DS are associated with an increased incidence of epilepsy, and both gross and cytoarchitectural anomalies have been described. The severity and distribution of these central nervous system anomalies presumably predispose to the infantile spasms. The contribution of altered serotonin metabolism is uncertain.
Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation
Authors: Ginsberg Myron D. , Budd William W. , Welsh Frank A. 
Published: January 2005

AbstractThe effects of severe cerebral ischemia on postischemic brain perfusion were examined in a series of pentobarbital‐anesthetized cats. Ischemia of 15 or 30 minutes' duration was produced by occlusion of both common carotid arteries and the basilar artery and was coupled with mild systemic hypotension. A 90‐minute period of normotensive postischemic recirculation was permitted in some animals. In 9 of 10 animals studied at the end of the ischemic insult and not allowed to recover, blood flow in the cerebral hemispheres was greatly reduced, with minimal flow (0.01 to 0.11 ml gm−1 min−1) persisting only in scattered perisulcal regions in 4 animals. Following 15 minutes of ischemia, blood flow was restored uniformly during recirculation, though at subnormal levels (31 to 35% of control). In contrast, 30 minutes of prior ischemia led to marked heterogeneities of local cerebral perfusion during recirculation, with multiple zones of persistent severe ischemia. Thus, while recirculation was suboptimal following both 15 and 30 minutes of ischemia, the 30‐minute insult led to focal postischemic perfusion abnormalities that were sufficiently severe to make the possibility of functional recovery appear unlikely.
Diffuse cerebral ischemia in the cat: II. Regional metabolites during severe ischemia and recirculation
Authors: Welsh Frank A. , Ginsberg Myron D. , Rieder Wendy , Budd William W. 
Published: January 2005

AbstractMetabolite levels were measured in seven brain regions in cats after 15 or 30 minutes of a severe ischemic insult and after a 90‐minute period of recirculation following 15 or 30 minutes of ischemia. Brain levels of phosphocreatine were depleted after a 15‐ or 30‐minute insult, and lactate levels were extremely high at both times. The adenosine triphosphate (ATP) content in many brain areas and the presence of microregions of low reduced nicotinamineadenine dinucleotide in the brains of the animals that had 15 minutes of ischemia suggested that the ischemia, though severe, was not complete.Recirculation following a 15‐minute insult restored brain levels of ATP and phosphocreatine to 70 to 100% of control values in all regions analyzed. In contrast, metabolic recovery from a 30‐minute insult was regionally heterogeneous. Thus, there was persistent depression of ATP and phosphocreatine and elevation of lactate, which was localized in discrete cortical foci near the longitudinal midline. The factors governing the localization of metabolic failure must have become manifest during the recirculation period since the ischemic insult itself caused similar metabolic perturbations in all cortical regions.
Differences in reaction times and average evoked potentials as a function of direct and indirect neural pathways
Authors: Ledlow Alexa , Swanson James M. , Kinsbourne Marcel 
Published: January 2005

AbstractAverage evoked potentials and manual response latencies were collected during a simple detection task in which brief visual stimuli were presented to the left and right visual fields. Latencies generated by the ipsilateral stimulushand combinations were shorter than contralateral combinations only under certain conditions, impugning the hypothesis that the reaction time difference reflects interhemispheric transfer time. Certain evoked potential components recorded contralateral to the stimulus occurred earlier than their ipsilateral counterparts, but whether this difference can be interpreted as representing interhemispheric transfer time is also questioned.
Cerebral carbohydrate metabolism during hypoglycemia and anoxia in newborn rats
Authors: Vannucci Robert C. , Vannucci Susan J. 
Published: January 2005

AbstractThe cerebral metabolic responses to perinatal hypoglycemia and anoxia were studied in newborn rats given regular insulin (30 units per kilogram of body weight). Animals were observed for up to 2 hours with no apparent ill effects in spite of blood glucose concentrations of 0.75 mmol per liter. When exposed to 100% nitrogen at 37°C, hypoglycemic animal survived only one‐tenth as long as littermate controls with normal blood glucose levels (4.7 mmol/L). Pretreatment of hypoglycemic rats with glucose (10 mmol/kg) 10 and 30 minutes prior to nitrogen exposure nearly completely reversed the anoxic vulnerability. Hypoglycemia led to progressive reductions in crebral glycogen and glucose; however, only glucose reverted to normal levels 20 minutes after systemic glucose administration. The glycolytic intermediates glucose 6‐phosphate and lactate were also lower during hypoglycemia. Brain glucose levels below 0.1 mmol per kilogram were associated with a disrupted cerebral energy state, reflected by declines in phosphocreatine (33%) and adenosine triphosphate (ATP) (10%). Cerebral energy utilization (metabolic rate) was minimally reduced (−7.2%) by hypoglycemia and returned to the control value (2.36 mmol ∼ P/kg/min) with glucose treatment. The cerebral energy reserves ATP, adenosine diphosphate, and phosphocreatine delined more rapidly and to a lower level in hypoglycemic rats subjected to 2 1/2 minutes of anoxia than in normoglycemic animals rendered similarly hypoxic. The findings suggest that decreased anoxic resistance of hypoglycemic newborn rats is not primarily a function of reduced brain glycogen or altered cerebral metabolic rate. The presence of endogenous cerebral glucose stores combined with continued circulating glucose (cerebrovascular perfusion) appear to be critical factors for maintaining perinatal hypoxic survival.
Hemifacial spasm and the facial nucleus
Authors: Ferguson John H. 
Published: January 2005

AbstractSpontaneous and associated hyperkinetic facial movements and contracture which follow injury to the seventh cranial nerve (postparalytic hemifacial spasm) or arise without known previous injury (cryptogenic hemifacial spasm) are pathological motor phenomena not found in the distribution of other cranial or somatic motor nerves. The commonly expressed hypotheses of pathogenesis—aberrant regeneration and fiber excitation by false synapse formation (ephapses) at the site of injury—cannot account for all aspects of these phenomena or for the uniqueness of such movements to the distribution of the seventh nerve.The suggestion is made that the existing diversity of facial motor behavior, which encompasses voluntary, emotional, and especially automatic, associated, and reflexive movements, is based on a unique central organization that sets it apart from other motor groups. I hypothesize that because of this organization, the changes following axonal injury—which include selective deafferentation, glial response, axonal sprouting, functional reconnection, and hyperexcitability from dendritic spike generation—can unmask and augment automatic, associated, and reflexive movements already present in the facial neuronal network to result in facial hyperkinesia.
Paroxysmal beta activity in the pediatric electroencephalogram
Authors: Nealis James G. T. , Duffy Frank Hopkins 
Published: January 2005

AbstractA total of 5,401 electroencephalograms performed in the Seizure Unit at Children's Hospital Medical Center over a 12‐month period were analyzed for the presence of paroxysmal beta activity. Nine examples were found in patients under the age of 10 years, each of whom had a clinical seizure disorder. Seven patients showed abnormalities such as tumor, cerebral dysgenesis, or hydrocephalus on CAT scans or skull roentgenograms. Paroxysmal beta activity should be considered a manifestation of a seizure disorder. Furthermore, the finding of paroxysmal beta activity on an electroencephalogram in the young child should lead to further evaluation for a possible structural lesion.
Alteration in erythrocyte membrane structure in duchenne muscular dystrophy
Authors: Wakayama Y. , Hodson A. , Pleasure D. , Bonilla E. , Schotland D. L. 
Published: January 2005

AbstractFreeze‐fracture studies of erythrocytes from patients with Duchenne muscular dystrophy revealed depletion of particles on both fracture faces of the plasma membrane. This study indicates that the structure of the erythrocyte plasma membrane is abnormal in Duchenne dystrophy and supports the concept that a generalized membrane abnormality is present in this disease.
Paired helical filaments in neurovisceral lipidosis (juvenile dystonic lipidosis)
Authors: Horoupian Dikran S. , Yang S. Samuel 
Published: January 2005

AbstractPaired helical filaments, the ultrastructural substrate of Alzheimer neurofibrillary change, were found in great number in a 29‐year‐old patient with neurovisceral lipidosis. The abnormal filaments were frequently present in the distended neurons and axons. The clinical, pathological, and ultrastructural findings were consistent with juvenile dystonic lipidosis, which is considered to be a variant of type C Niemann‐Pick disease. The association of Alzheimer neurofibrillary change and central nervous system lipidosis is reviewed.
Characterization of antioligodendrocyte serum
Authors: Traugott Ute , Snyder D. Stephen , Norton William T. , Raine Cedric S. 
Published: January 2005

AbstractAn antioligodendrocyte serum (AOS) has been raised in rabbits against preparations of isolated bovine oligodendrocytes. The antibody was assayed by two techniques. By complement fixation with isolated oligodendrocytes, the titer of the antibody was 1:64 to 1 : 128. By indirect immunofluorescence testing of oligodendrocyte suspensions and frozen brain sections, the titer of the AOS was 1 : 256 to 1 : 512. When unabsorbed AOS was used, immunofluorescent staining proved it specific for bovine oligodendrocytes in suspension and in sections, and for human oligodendrocytes in sections. In cell suspensions, the staining was membrane related and in sections, cytoplasmic. The oligodendrocyte staining could be totally removed by absorption of AOS against oligodendrocyte suspensions, whereas absorption against bovine myelin, bovine myelin basic protein, and bovine neurons did not affect the staining reaction. AOS also stained Schwann cells, a property possibly related to antigens shared with oligodendrocytes. It is concluded that AOS is specific for oligodendrocytes and can now be applied to fundamental and disease‐related problems in the central nervous system.
Remyelination in multiple sclerosis
Authors: Prineas J. W. , Connell F. 
Published: January 2005

AbstractChronic plaques in central nervous system tissue fixed by in situe perfusion for electron microscopy were examined for evidence of remyelination in 2 patients with multiple sclerosis (MS). Fibers with abnormal central myelin sheaths of several types were found at the margins of most of the plaques studied. The most common of these were: (1) the presence of bare stretches of axon between contiguous internodes, (2) the presence of thin paranodes, (3) internodes which changed markedly in thickness along their length due to premature termination of superficial or deep myelin lamellae that ended as hypertrophic lateral loops, and (4) abnormally thin internodes which were of uniform thickness along their length, which were shorter than normal, and which terminated in the form of normal nodal complexes. The finding of internodes of the last type at the edges of many plaques indicates that remyelination by oligodendrocytes can occur in the adult human CNS and that it is common in some cases of MS, although limited in its extent.
Computerized tomography in the diagnostic evaluation of multiple sclerosis
Authors: Hershey Linda A. , Gado Mokhtar H. , Trotter John L. 
Published: January 2005

AbstractSixty‐six patients with a tentative or certain diagnosis of multiple sclerosis (MS) were examined with cranial computerized tomography (CT). Abnormalities found in 19 (29%) included discrete areas of decreased white matter density, enlarged ventricles, cortical atrophy, and focal areas of contrast enhancement. The presence of white matter lucencies and ventricular dilatation correlated with an increased incidence of diffuse hyperreflexia and mental impairment. Since half the patients with contrast‐enhancing lesions were clinically stable, their lesions may represent acute asymptomatic plaques. Abnormalities on CT scan were observed more often in older patients whose disease had lasted longer and was clinically more definite. Since findings were sparse in early, less definite disease, the use of CT as a purely diagnostic tool is limited.
Visual evoked potentials and the visuogram in multiple sclerosis
Authors: Bodis‐Wollner Ivan , Hendley Charles D. , Mylin Leland H. , Thornton John 
Published: January 2005

AbstractVisual evoked potential (VEP) latency to a sinusoidal grating pattern was measured in each eye of 103 patients with multiple sclerosis (MS) and compared with results in a control group of 56 patients hospitalized for other neurological conditions. Of the 50 patients classified as having definite MS, 90% showed prolonged latency (over 131 msec) in one or both eyes. In each eye of 24 of the MS patients, psychophysical measurement of the detectability of grating patterns was obtained. This test was abnormal in 11 of 13 patients with definite MS, 3 of 4 with probable MS, and 5 of 7 with possible MS. There was no concordance between prolonged VEP latency and visual impairment as revealed by the psychophysical test. Apparently pathways determining VEP latency and spatial contrast detection may be unequally affected in MS.
Central vestibular involvement in peroneal muscle atrophy: A preliminary report
Authors: Melgaard B. , Zilstorff K. 
Published: January 2005

AbstractA family is presented in which 6 out of 8 members were found to have peroneal muscle atrophy. Neurophysiological and histopathological evidence for the hypertrophic form of this disease was obtained in 3 patients. Three patients with peroneal muscle atrophy and 1 unaffected family member had abnormal differential caloric tests. This is the first report of an apparently hereditary dysfunction of the central vestibular system associated with a hereditary neuropathy.
Selective chromatolysis of neurons in the gerbil brain: A possible consequence of “epileptic” activity produced by common carotid artery occlusion
Authors: Brown A. W. , Levy D. E. , Kublik M. , Harrow J. , Plum F. , Brierley J. B. 
Published: January 2005

AbstractUnilateral (50 to 118 minutes) and bilateral (2 to 33 minutes) carotid artery occlusion in gerbils resulted in two distinct types of neuronal alteration: ischemic cell change (ICC) in selectively vulnerable brain regions, and selective chromatolysis (SC) confined to the deeper layers of the cortex, the Sommer sector of zone h1, and the paramedian region (PM) of the hippocampus.In typical SC the nucleus was eccentric and the Nissl Substance was lost in the central eosinophilic cytoplasm. In electron micrographs this area of cytoplasm showed disruption of smooth and rough endoplasmic reticulum with disaggregation of polyribosomes and accumulation of mitochrondria and various dense bodies. SC was identified at 2 to 3 hours and was still recognizable at five days. When bilateral carotid artery occlusion lasted 5 to 6 minutes, SC was seen in the hippocampal Sommer sector and cerebral cortex, while ICC was restricted to the endfolium (h3–5). Unlike ICC, the frequency of SC was not related to the duration of ischemia but probably to the epileptic seizures (overt and subclinical) initiated by ischemia in the gerbil. These changes must be considered when the gerbil is employed as a model of experimental stroke.
Effects of bicuculline‐induced seizures on cerebral metabolism and circulation of rats rendered hypoglycemic by starvation
Authors: Blennow G. , Folbergrová J. , Nilsson B. , Siesjö B. K. 
Published: January 2005

AbstractTo evaluate the effects of substrate deficiency on cerebral function, metabolism, and blood flow during seizures, rats were injected intravenously with bicuculline (1.2 mg · kg−1) following a 24‐hour period of starvation. During the course of seizures, blood glucose concentrations fell, and when they were reduced to below about 3 μmol · gm−1, cerebral function, metablism, and blood flow altered. Changes in function involved the transition of an electroencephalographic pattern of bursts and suppression into one of frequent or sparse single spikes. Oxygen consumption, which initially increased at least twofold, fell toward normal or subnormal values in the single‐spike period. Cortical blood flow was markedly reduced, and there was an attenuated response to carbon dioxide administration. Simultaneously, a small but clear fall was detected in the cerebral phosphorylation potential, and concentrations of glycolytic metabolites (including lactate) and citric acid cycle intermediates were reduced. Changes in amino acids and ammonia were somewhat similar to those observed in insulin‐induced hypoglycemia, but since the amino acid pool did not fall, the experiments failed to give evidence that amino acids serve as oxidative substrates.The perturbation of cerebral energy state (and of levels of carbohydrate substrates and amino acids) was reversed by glucose administration; but since neither this procedure nor additional bicuculline injections could cause resumption of continuous seizure activity, the results suggest that cellular substrate depletion may have given rise to a sustained disturbance of synaptic transmission.
Position and vibration sensations: Functions of the dorsal spinocerebellar tracts?
Authors: Ross Elliott D. , Kirkpatrick Joel B. , Lastimosa Augusto C. B. 
Published: January 2005

AbstractClinical evidence is presented which establishes for the first time that position and vibration sensations may be carried in the dorsal spinocerebellar tracts. We present a patient who incurred a spinal cord infarction eight months prior to death that caused a Brown‐Séquard syndrome with loss of position and vibration senses in the right lower extremity. The infarction spared the right fasciculus gracilus and thus supports the recent observations in human beings (and animals) that conscious proprioception is not a function of the dorsal columns. The vibratory and position losses were best correlated with the portion of the lesion involving the right dorsal spinocerebellar tract. Arguments are furnished based on physiological experiments in animals that conscious proprioception may be carried by Morin's spinocervicothalamic pathway, which forms part of the dorsal spinocerebellar tract in the spinal cord.