bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of digitalis on central demyelinative conduction block in vivo
Authors: Kaji Ryuji , Sumner Austin J. 
Published: January 2005

AbstractIn searching for agents effective in treating multiple sclerosis, we studied the effect of a short‐acting digitalis, ouabain, on conduction block in an animal model of central nervous system demyelination. The electrogenic sodium/potassium pump, which digitalis specifically inhibits, is responsible for part of the resting membrane potential and also the activity‐related membrane hyperpolarization following high‐frequency impulses. The latter causes intermittent conduction block in demyelinated fibers. Therefore, digitalis might be expected to reverse demyelinative conduction blocks by reducing the threshold at the blocking node. Somatosensory evoked potentials were monitored in 11 rats with spinal cord demyelination before and after systemic administration of ouabain (0.1–0.6 mg or 0.21–1.58 mg/kg IP). In all rats, slowed conduction velocity of the compound action potential through the lesion was significantly reversed, and failure to transmit high‐frequency impulses was improved upon. The amplitude of the cortical somatosensory evoked potentials also increased significantly. Digitalis is a promising therapeutic agent for trial in patients with multiple sclerosis.
Neocortical propagation in temporal lobe spike foci on magnetoencephalography and electroencephalography
Authors: Sutherling W. W. , Barth D. S. 
Published: January 2005

AbstractPropagation of the neuronal population of the interictal epileptic spike was quantified in 5 patients with complex partial epilepsy arising from temporal lobe using electroencephalography and magnetoencephalography. During the spike complex in each patient there was a spike at the deep sphenoidal electrode and a spike at the superficial scalp electrode on spontaneous electroencephalography. In each patient the sphenoidal spike had a different peak latency than the scalp spike, consistent with spike propagation. Electroencephalography was used to trigger two magnetoencephalographic averages of stereotyped spikes during the sphenoidal peak and the scalp peak. Magnetoencephalography discriminated the centers of two cortical spike populations at different latencies, showing deeper localization with sphenoidal trigger and more superficial localization with scalp trigger in each patient (p < 0.05). Latency differences and propagation distances of spikes were consistent with the conduction velocity of corticocortical fibers. Noninvasive estimates of the cortical surface area of the spikes agreed with estimates obtained by electrocorticography over temporal neocortex. These findings indicate propagation of neuronal populations active during human interictal spikes between deep and superficial cortex of temporal lobe, likely by monosynaptic or oligosynaptic pathways. This interictal system appears to be partly independent of the hippocampal interictal system in complex partial epilepsy.
Infarcts of undetermined cause: The NINCDS stroke data bank
Authors: Sacco R. L. , Ellenberg J. H. , Mohr J. P. , Tatemichi T. K. , Hier D. B. , Price T. R. , Wolf P. A. 
Published: January 2005

AbstractIn a prospective study of 1,805 hospitalized patients in the Stroke Data Bank of the National Institute of Neurological and Communicative Disorders and Stroke, the 1,273 with infarction were classified into diagnostic subtypes. Diagnosis was based on the clinical history, examination, and laboratory tests including computed tomography, noninvasive vascular imaging, and where safe and relevant, angiography. Five hundred and eight cases (fully 40%) were labeled as infarcts of undetermined cause (IUC), of which 138 (27%) were evaluated with both computed tomography and angiography. The clinical syndrome and computed tomographic and angiographic findings in 91 (65.9%) of these 138 IUC cases were clearly not attributable to large‐artery thrombosis and could permit reclassification of the infarct as due to some form of embolism. Failure to define a source of embolus kept them in the category of IUC. Thirty‐one cases (22.5%) could be reclassified as due to stenosis or thrombosis of a large artery, and 16 (11.6%) as lacunar infarction. To determine if those selected for angiography among the IUC patients differed from those with other final diagnoses, a stepwise multiple logistic model was used. The most important characteristics were young age, presence of a superficial infarct, prior transient ischemic attack, low weakness score, and presentation with a nonlacunar syndrome. The results of the model suggest that angiography use was determined by clinical characteristics uniformly across centers and not by final diagnosis. Continued use of the category IUC may help clarify risk factors and stroke subtypes, allow new mechanisms of ischemic stroke to be uncovered, and prevent classification categories of stroke used in clinical trials from becoming too broad.
Results of surgical treatment in patients with bitemporal epileptiform abnormalities
Authors: So Norman , Olivier André , Andermann Frederick , Gloor Pierre , Quesney L. Felipe 
Published: January 2005

AbstractFifty‐three of 57 patients who had evidence of bitemporal epileptiform abnormalities and who required investigation with stereotactic depth electroencephalography (SDEEG) recordings to determine the site of origin of seizures underwent surgical resection for the treatment of their epilepsy. A minimum of 2 years' follow‐up was available in 48 patients who underwent a temporal lobe resection. In this group, 19 patients (40%) were greatly improved, and of these 14 (29%) became seizure free and 5 (10%) had no more than 3 seizures each year. Another 22 patients (46%) showed a worthwhile reduction in seizure frequency of at least 50%. Seven patients (15%) were not significantly improved. An etiological factor of early convulsions before age 3 (usually febrile) was associated with a better outcome. Both the lack of a strong predominance for SDEEG‐recorded seizures to arise in the resected temporal lobe and the presence of residual epileptiform abnormalities in the postexcision electrocorticogram were correlated with poorer results.
Hereditary long Q‐T syndrome presenting as epilepsy: Electroencephalography laboratory diagnosis
Authors: Gospe Sidney M. , Choy Michael 
Published: January 2005

AbstractPatients with hereditary Q‐T interval prolongation can present with seizures, syncope, and sudden death. In 2 siblings with autosomal dominant familial long Q‐T syndrome, electroencephalographic examinations performed 6 and 2 years before diagnosis included electrocardiographic tracings documenting the cardiac abnormality. A timely diagnosis of this condition may have prevented the death of 1 of these patients. Measurement of the corrected Q‐T interval on electrocardiographic tracings obtained in the electroencephalography laboratory should be considered in selected patients.
Xenon computed tomography measuring cerebral blood flow in the determination of brain death in children
Authors: Ashwal Stephen , Schneider Sanford , Thompson Joseph 
Published: January 2005

AbstractLocal cerebral blood flow was measured using stable xenon computed tomography in 21 children, 10 of whom were clinically brain dead and had electrocerebral silence as determined by electroencephalography. Radioisotopic brain scanning in 9 patients showed no visible cerebral activity in all patients and minimal residual sagittal sinus activity in 4. In this population, mean cerebral blood flow as measured by xenon computed tomography was 1.3 ± 1.6 ml/min/100 gm. Respiratory support was discontinued in 8 patients, and 2 patients had cardiac arrest. Eleven profoundly comatose children who did not meet all clinical criteria for brain death and who had markedly suppressed but not isoelectric electroencephalograms had an average cerebral blood flow of 33.5 ± 16.3 ml/min/100 gm as determined by xenon computed tomography. Flows in this group ranged from 11.8 ± 4.1 to 62.3 ± 1.9 ml/min/100 gm. There was no difference in cerebral blood flow in those children who survived (30.4 ± 16.3 ml/min/100 gm; n = 7) compared with those who died acutely (38.3 ± 14.3 ml/min/100 gm; n = 4). Two patients who survived had average total flows of only 11.8 and 12.1 ml/min/100 gm. Our findings suggest that in infants and children older than 1 month, (1) cerebral blood flow below approximately 10 ml/min/100 gm is consistent with clinical brain death, (2) cerebral blood flow of less than 5 ml/min/100 gm is consistent with no flow as demonstrated by radionuclide techniques, and (3) flow of more than 10 to 15 ml/min/100 gm is associated with the potential for survival.
Peripheral pharmacokinetics of apomorphine in humans
Authors: Gancher Stephen T. , Woodward William R. , Boucher Brian , Nutt John G. 
Published: January 2005

AbstractApmorphine, a potent dopamine agonist, has been used in acute and chronic studies of parkinsonism and other neurological disorders. To define its peripheral pharmacokinetics, we administered apomorphine by subcutaneous injection, by subcutaneous infusion, and by intravenous infusion to 15 patients with parkinsonism and measured plasma apomorphine levels by high‐performance liquid chromatography with electrochemical detection. The peak drug levels and area under the curve were closely correlated with the dose administered; time to peak was brief and was independent of dose. The variation in absorption was high between subjects but low within individual subjects. In 11 of 15 subjects, the disappearance of drug could be described by a two‐compartment model, with a distribution half‐life of 5 minutes and an elimination half‐life of 33 minutes. The drug absorption, volume of distribution, plasma clearance, and half‐lives were similar for subcutaneous injection, subcutaneous infusion, and intravenous infusion. We conclude that apomorphine is rapidly and completely absorbed from subcutaneous tissue, correlating with the rapid onset of clinical effects, and that the brief duration of clinical action of the drug is explained by its rapid clearance.
Amyotrophic lateral sclerosis: An unconventional autoimmune disease?
Authors: Drachman Daniel B. , Kuncl Ralph W. 
Published: January 2005

AbstractThe possibility of an autoimmune mechanism of pathogenesis in amyotrophic lateral sclerosis has long been considered, but the evidence to support a conventional autoimmune process, reviewed here, is inconclusive. However, antibodies that react in vitro with gangliosides have recently been found in sera of a large majority of patients with classical amyotrophic lateral sclerosis and other motor neuron syndromes. A working hypothesis is proposed, suggesting how antibodies might be related to the disease process. The hypothesis attempts to account for (1) a pathogenic role of antibodies directed against the carbohydrate components of glycolipids, (2) the selectivity of the process for motor neurons, (3) an antibody‐mediated mechanism that could result in apparently degenerative neuropathological changes without signs of inflammation, and (4) a type of autoimmune response that is extremely difficult to suppress by conventional means. Although the evidence for this hypothesis is by no means complete, its critical features are all testable.
Activated T cells in HTLV‐I–associated myelopathy: Autologous mixed lymphocyte reaction
Authors: Minato Sei‐ichiro , Itoyama Yasuto , Fujii Naoki , Kira Jun‐ichi , Goto Ikuo , Yamamoto Naoki 
Published: January 2005

AbstractWe examined the autologous mixed lymphocyte reaction in human T‐cell lymphotropic virus type I‐associated myelopathy to elucidate the known increase in spontaneous proliferation of peripheral blood lymphocytes. Proliferative responses in the autologous mixed lymphocyte reaction test were significantly increase (34,205 cpm) in cells from 9 patients with the myelopathy, as compared with findings (18,695 cpm) in the control subjects. When non‐T‐cell fractions were depleted from autologous mixed lymphocyte reaction cultures, proliferative responses were completely suppressed in the control subjects, while proliferation of the peripheral blood lymphocytes from the groups with the myelopathy were not affected by depletion of non‐T‐cell fractions. The increase in spontaneous proliferation of peripheral blood lymphocytes from the groups with the myelopathy were not affected by depletion of non‐T‐cell fractions. The increase in spontaneous proliferation of peripheral blood lymphocytes in patients with the myelopathy is probably not related to an increase in autologous mixed lymphocyte reactions.
Protease nexin I immunostaining in alzheimer's disease
Authors: Rosenblatt Dorrie E. , Geula Changiz , Mesulam M‐Marsel 
Published: January 2005

AbstractImmunohistochemical experiments showed that a small subset of neuritic plaques in brains affected by Alzheimer's disease stain positively with an antibody to the protease inhibitor protease nexin I. Nearly all plaques and tangles throughout the brain also showed a heightened avidity for a protease nexin I antibody‐antigen aggregate, suggesting that plaques and tangles may have a particularly high density of protease nexin I–binding sites. These observations provide further evidence for a potential disruption of protein processing in the brains of patients with Alzheimer's disease.
Isoelectric focusing studies of serum and cerebrospinal fluid in patients with antecedent poliomyelitis
Authors: Salazar‐Grueso Edgar F. , Grimaldi Luigi M. E. , Roos Raymond P. , Variakojis Renata , Jubelt Burk , Cashman Neil R. 
Published: January 2005

AbstractThe post‐poliomyelitis syndrome (PPS) refers to symptoms of new weakness, fatigue, and pain years after recovery from acute poliomyelitis. Oligoclonal IgG bands have been reported in the cerebrospinal fluid (CSF) from PPS patients, suggesting that the syndrome is immune mediated or caused by persistent viral infection. We studied 15 paired serum and CSF samples and 6 unpaired CSF samples from a total of 21 patients with a prior history of poliomyelitis. Quantitative immune studies failed to show evidence for increased intrathecal IgG production relative to patients with noninflammatory central nervous system (CNS) disease. We found definite oligoclonal IgG bands in the CSF from only 1 patient, who also carried a diagnosis of multiple sclerosis. An isoelectric focusing poliovirus antigen overlay study showed evidence that suggested a CNS‐specific antipoliovirus immune response in only 1 patient. Our results fail to support a dysimmune or persistent viral cause for post‐poliomyelitis progressive muscular atrophy or PPS.
Bilateral somatosensory evoked potentials in four patients with long‐standing surgical hemispherectomy
Authors: Mauguière François , Desmedt John E. 
Published: January 2005

AbstractFour patients were studied electrophysiologically 8 to 24 years after surgical removal of one cerebral hemisphere without damage to the striatum or diencephalon. Somatosensory evoked potentials(SEPs)to electrical stimulation of the median nerve on the left or right side were averaged and mapped out over the scalp. Stimulation on the side opposite to the missing hemisphere evoked brief P9 and P14 farfields and a slow N18 negative potential of 15‐to 25‐msec duration bilaterally. No additional focal response was detected over the remaining (ipsilateral) hemisphere for 60 msec after the stimulus. Because long‐standing hemispherectomy entails massive retrograde degeneration of thalamocortical neurons, the preserved P14 and N18 responses must reflect neural activities generated below the thalamus that are volume conducted to the scalp bilaterally. The data clarify several current issues in the evaluation of SEP components.
Complex partial status epilepticus provoked by “crack” cocaine
Authors: Ogunyemi Abayomi O. , Locke George E. , Kramer Lynn D. , Nelson Lowell 
Published: January 2005

AbstractA 53‐year‐old woman with a history of chronic abuse of “crack” cocaine developed isolated complex partial status epilepticus after 3 days of frequent cocaine use. The electroencephalogram demonstrated focal epileptiform activity. Follow‐up for 1 year during which she reported continuous abstinence from cocaine and anticonvulsants revealed no recurrence of seizures.
Alteration in extracellular amino acids after traumatic spinal cord injury
Authors: Panter S. Scott , Yum Sabrina W. , Faden Alan I. 
Published: January 2005

AbstractIt has recently been demonstrated that N‐methyl‐D‐aspartate antagonists limit tissue damage after spinal cord trauma, implicating excitatory amino acids in the secondary injury response. To determine whether spinal cord trauma alters the concentrations of extracellular amino acids, microdialysis was conducted in spinal cord during and after administration of impact trauma. Extracellular concentrations of excitatory, inhibitory, and nontransmitter amino acids were elevated after trauma, with the degree of increase related to severity of injury. Moderate trauma resulted in an immediate but transient increase (200‐400%) in the extracellular levels of all amino acids measured. Severe trauma produced a more prolonged and significant increase (400‐630%) in the concentrations of extracellular amino acids, including aspartate and glutamate. These results are consistent with the hypothesis that excitatory amino acids may contribute to delayed tissue injury after central nervous system trauma.
Neuronal intranuclear inclusion disease in a child: Diagnosis by rectal biopsy
Authors: Goutières F. , Mikol J. , Aicardi J. 
Published: January 2005

AbstractA 15‐year‐old boy presented with progressive pyramidal and extrapyramidal signs, anterior horn cell dysfunction, and behavioral disturbances suggesting a diagnosis of neuronal intranuclear inclusion disease. The diagnosis was confirmed by examination of a rectal biopsy specimen that showed typical intranuclear inclusions in the neurons of the myenteric plexus. Diagnosis of neuronal intranuclear inclusion disease during life appears to be possible.
Prenatal and perinatal antecedents of febrile seizures
Authors: Nelson Karin B. , Ellenberg Jonas H. 
Published: January 2005

AbstractWe examined prenatal and perinatal characteristics as possible risk factors for febrile seizures in a large pediatric population. Family history was among the few identified factors that made an important contribution to vulnerablility to febrile seizures; however, no more than 6% of febrile seizures could be attributed to a characteristic of family history. Maternal illness, smoking history, and a few rare neonatal characteristics were associated with increases in risk. No complication of labor or delivery was an important risk factor for febrile seizures.
A survey of epileptic disorders in Southwest France: Seizures in elderly patients
Authors: Loiseau Jérǒme , Loiseau Pierre , Duché Bernard , Guyot Martine , Dartigues Jean‐François , Aublet Bruno 
Published: January 2005

AbstractAn underestimation of epileptic seizures occurring in aged patients is likely. In an epidemiological survey undertaken in Southwest France, the annual incidence rate per 100,000 persons 60 years or older was 127.2 for all seizures (101.3 in persons aged 60 to 69, 150.4 in those aged 70 to 79, and 139.9 in persons 80 years or older). It was 34.1 for symptomatic localization‐related and undetermined epilepsies, 16.1 for isolated seizures, and 77.0 for seizures related to an acute situation, such as metabolic derangements, stroke, or head trauma. In this survey, seizures with an onset age of 60 or older represented 28.0% of the confirmed epilepsies, 17.5% of the isolated seizures, and 52.6% of the acute symptomatic seizures. These figures differ dramatically from those in most previous reports concluding that age‐specific incidence declined through adult life. They are closer to the data from more recent reports. The main reason for such a high incidence of epileptic seizures in elderly patients is the number of acute symptomatic (or situation‐related) seizures. However, even chronic epilepsies increase in frequency in aging persons. Cerebrovascular disease was the most frequently recognized origin (53.9% of the patients with confirmed epilepsies) and brain tumor was found in 32.9% of the patients.
Neuropathology of immunohistochemically identified brainstem neurons in Parkinson's disease
Authors: Halliday G. M. , Li Y. W. , Blumbergs P. C. , Joh T. H. , Cotton R. G. H. , Howe P. R. C. , Blessing W. W. , Geffen L. B. 
Published: January 2005

AbstractRegional loss of immunohistochemically identified neurons in serial sections through the brainstem of 4 patients with idiopathic Parkinson's disease was compared with equivalent sections from 4 age‐matched control subjects. In the Parkinson brains, the catecholamine cell groups of the midbrain, pons, and medulla showed variable neuropathological changes. All dopaminergic nuclei were variably affected, but were most severely affected in the caudal, central substantia nigra. The pontine noradrenergic locus ceruleus showed variable degrees of degeneration. There was also a substantial loss of substance P–containing neurons in the pedunculopontine tegmental nucleus. However, the most severely affected cell group in the pons was the serotonin‐synthesizing neurons in the median raphe. In the medulla, substantial neuronal loss was found in several diverse cell groups including the adrenaline‐synthesizing and neuropeptide Y–containing neurons in the rostral ventrolateral medulla, the serotonin‐synthesizing neurons in the raphe obscurus nucleus, the substance P–containing neurons in the lateral reticular formation, as well as the substance P–containing neurons in the dorsal motor vagal nucleus. Lewy bodies were present in immunohistochemically identified neurons in many of these regions, indicating that they were affected directly by the disease process. These widespread but region‐ and transmitter‐specific changes help account for the diversity of motor, cognitive, and autonomic manifestations of Parkinson''s disease.