bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of herpes simplex virus mRNA in latently infected trigeminal ganglion neurons by in situ hybridization
Authors: Tenser Richard B. , Dawson Marilyn , Ressel Steven J. , Dunstan Marie E. 
Published: January 2005

AbstractLatent infection of the trigeminal ganglion with herpes simplex virus type 2 (HSV‐2) was studied in guinea pigs by in situ DNA hybridization. Frozen ganglion sections from animals killed during the period of latent virus infection were studied under nondenaturing conditions. Some sections were treated with deoxyribonuclease (DNase) or ribonuclease (RNase) before incubation with HSV DNA probes. HSV probes consisted of viral DNA nick translated and labeled in vitro with tritiated nucleotides. Bacteriophage lambda DNA, similarly prepared, was used as a control probe. The lamba probe was negative in all situations, including HSV‐2‐infected monolayer cells in cell culture. HSV‐2 probes produced heavy label and, therefore, evidence of hybridization with HSV‐2‐infected monolayer cells. When HSV‐2 probes were incubated with latently infected ganglion sections, hybridization was detected in 71% of guinea pigs and 46% of ganglia. Label was seen only in neurons, and in positive ganglia 0.3 to 5% of neurons were labeled. The amount of label was markedly decreased by pretreatment of ganglion sections with RNase but not DNase, indicating that the DNA probes hybridized to HSV messenger RNA in the latently infected ganglia.
Complex partial seizures on closed‐circuit television and EEG: A study of 691 attacks in 79 patients
Authors: Escueta A. V. Delgado , Bacsal Fe Enrile , Treiman David M. 
Published: January 2005

AbstractAutomatisms of 691 complex partial seizures in 79 patients were studied on closed‐circuit television (CCTV) and by electroencephalography. Simple stereotyped perseverative automatisms such as chewing, swallowing, and fumbling with clothes or sheets followed an initial motionless stare and lapse of consciousness in type I attacks. Ambulatory automatisms, bilateral arm and leg perseverative movements, and tonic adversive head or eye movements (or both) characterized type II attacks, in which a motionless stare was not observed. Type III started with a drop attack followed by confusion, amnesia, and gradual recomposure. Some type II and III attacks are suspected to begin in areas outside the temporal lobe, while type I attacks are thought to originate from the temporal lobe. Further studies using CCTV and depth electrode recordings are necessary to verify these suspicions.
Neurons in human epileptic cortex: Correlation between unit and EEG activity
Authors: Wyler Allen R. , Ojemann George A. , Ward Arthur A. 
Published: January 2005

AbstractA total of 90 neurons were recorded extracellularly from 17 awake patients undergoing craniotomy for excision of epileptogenic cortex. Relationships between single‐unit activity and gross epileptiform spikes recorded locally by the microelectrode or from the immediate overlying cortical surface by electrocorticography (ECoG) were examined. Similar relationships were also sought between interictal bursts from nearby cells when action potentials from several neurons had been recorded simultaneously by the tungsten electrodes. Although 40 single units fired action potentials in some relation to ECoG spikes, the relationships were variable between units and, often, for the same unit. For many units, action potentials were more consistently related to one phase of the local field potential recorded through tungsten microelectrodes than to the ECoG recorded from the overlying cortical surface. Synchronous firing between single units recorded simultaneously by the same microelectrode was rarely seen except at the onset of an ictal event. In addition, a high degree of synchrony between unit firing and local ECoG spikes was recorded in a few patients, but these patients had frequent focal spontaneous seizures. The data imply that in human epilepsy, unlike some animal models of the disorder, relationships between surface epileptiform events and single‐unit burst firing are not easily found in interictal recordings. The data also suggest that synchrony between unit and surface events requires a high degree of synchrony among neurons within the epileptogenic focus.
Valproate‐induced hyperammonemia
Authors: Batshaw Mark L. , Brusilow Saul W. 
Published: January 2005

AbstractA patient with carbamyl phosphate synthetase deficiency had four episodes of hyperammonemia, up to 226 μM, associated with valproate (VPA) treatment. These were accompanied by vomiting, lethargy, and coma. A group of epileptic patients receiving VPA remained asymptomatic but had significantly higher mean plasma ammonium levels when compared to epileptic patients receiving other anticonvulsants: 33.6 ± 1.9 (SEM) versus 23.6 ± 1.5 μM. Thus, VPA caused symptomatic hyperammonemia in a patient with an impairment in urea synthesis and resulted in mildly elevated ammonium levels in epileptic patients. These data suggest that ammonium levels should be monitored in patients receiving VPA who exhibit signs of vomiting or lethargy.
Intradentate colchicine retards the development of amygdala kindling
Authors: Dasheiff Richard M. , McNamara James O. 
Published: January 2005

AbstractThe mechanisms underlying the kindling model of epilepsy are unknown. Presumably, an altered network of neural circuits underlie amygdala kindling. Biochemical and radiohistochemical studies have pointed to the dentate granule cells (DGC) of the hippocampal formation as a member of this altered circuit. To test the role of these cells, colchicine, a neurotoxin of DGC, was directly injected into the dentate gyrus. Prior destruction of DGC retarded the development of amygdala kindling. Destruction of DGC after kindling was completed did not reverse the kindling effect. We conclude that DGC play a key role in the development, but not the permanence, of amygdala kindling. We propose a model whereby the greater the input to the hippocampal formation, the faster limbic kindling will proceed.
Long‐term follow‐up of patients with subacute sclerosing panencephalitis treated with inosiplex
Authors: Dyken Paul R. , Swift Andrea , Durant Robert H. 
Published: January 2005

AbstractDuring the past five years, 15 patients with subacute sclerosing panencephalitis (SSPE) were treated with inosiplex. Using a disability index specifically designed for the disease, this study monitored the course of SSPE in each patient before and during inosiplex therapy. Posttreatment follow‐up ranged from 2 to 144 months. Inosiplex had an apparently beneficial effect on morbidity and mortality in 10 of the 15 patients tested. Eight improved immediately after treatment, 2 had a delayed improvement, and 1 patient stabilized. Four patients followed a typical course for SSPE and died a mean of 9 months after onset. Treatment was not associated with adverse reactions. Due to its low risk‐benefit ratio, inosiplex is recommended for continuous use in SSPE even after extended remissions.
Reversal of debrancher deficiency myopathy by the use of high‐protein nutrition
Authors: Slonim Alfred E. , Weisberg Charlene , Benke Paul , Evans Owen B. , Burr Ian M. 
Published: January 2005

AbstractA child with debrancher deficiency presented with myopathy, recurrent hypoglycemia, and growth failure. Evidence for enhanced gluconeogenesis was demonstrated by low postabsorptive gluconeogenic plasma amino acids, a marked fall in alanine during fasting, and a substantial rise in plasma glucose following protein ingestion. The patient was treated with high‐protein nocturnal intragastric therapy, which resulted in marked improvement in exercise tolerance, muscle strength and mass, electromyographic findings, and growth.
Occipitotemporal epilepsy studied with stereotaxically implanted depth electrodes and successfully treated by temporal resection
Authors: Olivier André , Gloor Pierre , Andermann Frederick , Ives John 
Published: January 2005

AbstractA young woman had seizures suggestive of temporal lobe origin with some clinical features indicative of occipital onset. Electroencephalograms recorded through scalp and sphenoidal electrodes showed predominantly right posterior temporooccipital epileptogenic discharges. Stereotaxic depth electrode recordings from the right temporal and occipital lobes demonstrated that some seizures arose independently from either the temporal or occipital lobes. Most arose within the occipital lobe, but to become clinically evident, the seizure discharge had to spread to the temporal lobe. Following temporal lobe resection, including excision of limbic structures, the patient has remained seizure free for four years except for a few generalized seizures before and after delivery of her child.
Neuroimmunology I: Immunoregulation in neurological disease
Authors: Weiner Howard L. , Hauser Stephen L. 
Published: January 2005

AbstractAberrations in immune function that ultimately result in disease states may involve three aspects of immune regulation: (1) regulatory T cells, which both suppress and induce immune responses; (2) idiotype‐antiidiotype networks, which serve as internal regulatory networks during generation of an immune response; and (3) immune response genes, which determine genetic differences in an individual's immune response. Three major diseases of the nervous system, multiple sclerosis, myasthenia gravis, and acute inflammatory polyneuropathy (Guillain‐Barré syndrome), are classified as “autoimmune” in nature and may be due to underlying disorders of immunoregulation. In multiple sclerosis there is a loss of suppressor T cells in the peripheral blood during attacks, in myasthenia gravis there are thymic abnormalities and antibodies against the acetylcholine receptor, and in acute inflammatory polyneuropathy, macrophage‐mediated destruction of peripheral nerve myelin occurs in the context of sensitized T cells and is usually associated with a preceding viral illness. In each of these disease the following central questions must be answered: (1) against what antigen (or antigens) of the nervous system is the autoimmune response directed? (2) what is the mechanism of immune damage? and (3) what initiates, or triggers, the autoimmune response?
Temporal profile of neuronal damage in a model of transient forebrain ischemia
Authors: Pulsinelli William A. , Brierley James B. , Plum Fred 
Published: January 2005

AbstractThis study examined the temporal profile of ischemic neuronal damage following transient bilateral forebrain ischemia in the rat model of four‐vessel occlusion. Wistar rats were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10, 20, or 30 minutes. Carotid artery blood flow was restored and the rats were killed by perfusion‐fixation after 3, 6, 24, and 72 hours. Rats with postischemic convulsions were discarded. Ischemic neuronal damage was graded in accordance with conventional neuropathological criteria. Ten minutes of four‐vessel occlusion produced scattered ischemic cell change in the cerebral hemispheres of most rats. The time to onset of visible neuronal damage varied among brain regions and in some regions progressively worsened with time. After 30 minutes of ischemia, small to medium‐sized striatal neurons were damaged early while the initiation of visible damage to hippocampal neurons in the h1 zone was delayed for 3 to 6 hours. The number of damaged neurons in neocortex (layer 3, layers 5 and 6, or both) and hippocampus (h1, h3–5, paramedian zone) increased significantly (p < 0.01) between 24 and 72 hours. The unique delay in onset of ischemic cell change and the protracte increase in its incidence between 24 and 72 hours could reflect either delayed‐appearance of ischemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.
Ocular tilt reaction due to an upper brainstem lesion: Paroxysmal skew deviation, torsion, and oscillation of the eyes with head tilt
Authors: Hedges Thomas R. , Hoyt William F. 
Published: January 2005

AbstractA patient with a focal brainstem abscess in the region of the zona incerta developed a chronic oculocephalic dyskinesia in which paraoxysmal tonic skew deviation and torsion of the eyes were coupled with ocular oscillations and head tilt.
Slowly progressive aphasia without generalized dementia
Authors: Mesulam M.‐Marsel 
Published: January 2005

AbstractSix right‐handed patients experienced a slowly progressing aphasic disorder without the additional intellectual and behavioral disturbances of dementia. The symptoms almost universally started in the presenium. The initial difficulty was an anomic aphasia in five of the patients and pure word deafness in the sixth. Continuous and gradual deterioration occurred in the five patients who presented with an anomic aphasia. They eventually experienced additional impairment of reading, writing, and comprehension. In four patients, other areas of comportment were not involved within the 5 to 11 years of follow‐up. A more generalized state of dementia may have emerged in the other two patients, but only after 7 years of progressive and debilitating aphasia. Neurodiagnostic procedures were consistent with preferential involvement of the left perisylvian region. In one patient, cortical biopsy did not show any pathognomonic change; specifically, no neurofibrillary tangles, amyloid plaques, neuronal inclusions, or gliosis were seen. This condition may constitute a syndrome of relatively focal cerebral degeneration with a predilection for the left perisylvian region.
Neurological complications of immunization
Authors: Fenichel Gerald M. 
Published: January 2005

AbstractVaccines prepared from whole, killed organisms (pertussis and possible influenza) may cause neurological allergic reactions producing encephalopathy. These reactions are characterized by acute, monophasic demyelinative processes and occur with no greater frequency than 1 per 100,000 vaccine recipients; onset is within 4 days of immunization, and recovery is usually complete. No evidence suggests that these vaccines produce an insidious, progressive encephalopathy. Only with the swine influenza program of 1976 has Guillain‐Barré syndrome appeared to follow immunization.Vaccines prepared from live‐attenuated viruses (measles, mumps, rubella, and trivalent oral poliovirus) can cause symptomatic viral infection of the nervous system, including measles encephalitis, which occurs in 1 of 1,000,000 vaccine recipients; rubella neuritis, in less than 1 of 10,000 recipients; and paralytic poliomyelitis, in 1 of 3,000,000 vaccine recipients or their close contacts. A cause‐and‐effect relationship between immunization and brachial plexus neuritis, acute transverse myelitis, and cranial neuropathies has been suggested by never proved.
Prostaglandin I2, indomethacin, and heparin promote postischemic neuronal recovery in dogs
Authors: Hallenbeck J. M. , Leitch D. R. , Dutka A. J. , Greenbaum L. J. , McKee A. E. 
Published: January 2005

AbstractForty‐five conditioned male mongrel dogs were exposed to multifocal ischemia sufficient to maintain suppression for 60 minutes of the P1–N1 amplitude of the cortical sensory evoked response (CSER), a quantifiable index of neuronal function. Ischemia was induced and regulated by successive embolization of 20 to 50 μl increments of air via the right internal carotid artery. Subsequently, the P1–N1 amplitude recovery of the CSER was followed for an additional 15, 60, or 120 minutes while the dogs were treated or left untreated. The combination of prostaglandin I2 (PGI2), indomethacin, and heparin promoted a statistically significant augmentation of return of CSER amplitude relative to no treatment, PGI2 alone, indomethacin alone, PGI2 and heparin, indomethacin and heparin, or PGI2 and indomethacin. After 60 minutes of recovery, animals receiving combined PGI2, indomethacin, and heparin achieved a 57% recovery of P1–N1 amplitude relative to baseline, while the corresponding recoveries in all other groups clustered around 20%. By 120 minutes of postischemic follow‐up, the CSER recovery induced by PGI2, indomethacin, and heparin was 80% compared to 17% in untreated animals. By 15 minutes into the recovery period, the combination of the three agents had eliminated very low flows in the “neuron‐disabling” range (defined as 0 to 15 ml/100gm/min for gray matter and 0 to 6 ml/100gm/min for white matter) in contrast to the relative inefficacy of no treatment or treatment with other than the triple combination of drugs. The study lends some support to a planned clinical trial of PGI2, indomethacin, and heparin in acute occlusive stroke in humans.
Neurotoxicity of the pyrimidine synthesis inhibitor N‐phosphonoacetyl‐L‐aspartate
Authors: Wiley R. G. , Gralla R. J. , Casper E. S. , Kemeny N. 
Published: January 2005

AbstractPALA (N‐phosphonoacetyl‐L‐aspartate) impairs de novo pyrimidine biosynthesis by inhibiting the enzyme aspartate transcarbamylase. During cancer chemotherapy trials the drug was given by weekly intravenous infusion. Seizures developed in 9 (11%) of the first 80 patients to receive a total dose of 9 gm/m2 or more. Seven of the affected patients had structural brain lesions; they developed seizures at a lower total dose (median of 16.4 gm/m2) than the 2 patients without clinically detectable brain lesions (115 to 130 gm/m2). Reversible encephalopathy was observed in 6 (7.5%) additional patients without clinically detectable cause other than PALA. Both seizures and encephalopathy began after the second dose of PALA or later. Experiments in rats demonstrated similar delayed‐onset seizures after two or three combined systemic and intracerebral doses of PALA at 4‐day intervals. Concurrent administration of uridine or carbamyl aspartate prevented the development of seizures in rats, indicating that pyrimidine starvation of the central nervous system was responsible for PALA neurotoxicity.
Tetrabenazine has properties of a dopamine receptor antagonist
Authors: Login Ivan S. , Cronin Michael J. , MacLeod Robert M. 
Published: January 2005

AbstractTetrabenazine is considered to act in a manner similar to reserpine to reduce the involuntary movements of tardive dyskinesia or Huntington's disease and to improve psychoses. We determined that tetrabenazine also has properties of a dopamine receptor antagonist by testing the ability of tetrabenazine to block the inhibitory effect of dopamine on prolactin secretion from rat anterior pituitary glands in vitro and to displace3H‐spiperone binding to dopamine receptors in the pituitary, corpus striatum, and a rat transplantable prolactin‐secreting tumor. Under in vitro conditions, 0.5 to 10 μM tetrabenazine directly blocked dopaminergic inhibition of prolactin secretion. Furthermore, 1 hour after tetrabenazine injection (30 mg/kg intraperitoneally) in vivo, when the serum prolactin had increased from 22 ± 9 to 450 ± 52 ng/ml (p< 0.01), pituitary glands of the treated rats examined in vitro were refractory to dopaminergic inhibition of prolactin release. Tetrabenazine apparently interacts with the dopamine receptor, because this drug displaced the dopamine antagonist3H‐spiperone from dopamine receptors of the three different tissues with an apparent inhibitory constant of about 5 μM. We conclude that tetrabenazine has biological and pharmacological properties typical of a dopamine receptor antagonist. These observations should stimulate a reevaluation of the mechanisms for the actions of tetrabenzine previously attributed exclusively to a “reserpine‐like” effect.
Complement activation in muscle fiber necrosis: Demonstration of the membrane attack complex of complement in necrotic fibers
Authors: Engel Andrew G. , Biesecker Gregory 
Published: January 2005

AbstractThe membranolytic C5b‐9 complement membrane attack complex (MAC) is assembled after activation of either the classic or the alternative complement pathway. The quaternary configuration of the MAC macromolecule presents neoantigenic determinants not present on precursor molecules. Consequently, antibodies specific for these neoantigen(s) do not detect nonspecifically bound native complement precursors of MAC. By means of antibodies rendered specific for MAC neoantigen(s), MAC was localized by the immunoperoxidase reaction in cryostat sections of human muscle. In 66 biopsy specimens containing necrotic muscle fibers (Duchenne dystrophy, 13; other dystrophies, 15; inflammatory myopathies, 31; miscellaneous myopathies, 7) all of the necrotic fibers reacted for MAC neoantigen(s). C3 and C9 were also consistently localized in necrotic fibers, but localization of C1q, C4, and IgG was variable and often did not exceed background staining. None of the nonnecrotic fibers reacted for immunoglobulin or complement. Detection of MAC neoantigen(s) in necrotic fibers in a wide variety of muscle diseases unambiguously shows that (1) the lytic complement pathway is consistently activated and participates in muscle fiber necrosis in vivo, and (2) complement reaction products are generated that can stimulate cellular infiltration and phagocytosis of the necrotic fiber. The findings also suggest that cell necrosis in general may involve participation of complement.
Immune regulation in myasthenia gravis: Evidence for an increased suppressor T‐cell population
Authors: Miller Andrea E. , Hudson James , Tindall Richard S. A. 
Published: January 2005

AbstractThe production of anti‐acetylcholine receptor antibodies in myasthenia gravis represe‐hyphen;ts a peresents a persistent and unexplained break in self‐tolerance. The studies reported here demonstrate an altered regulatory T‐cell population with an increase in the percentage of circulation T‐suppress cells as defined by two independently developed murine Monoclonal antibody markers. Leu 2a‐ and OKT8a‐positive cells were significantly increased within the T‐cell population in myasthenia gravis (25.0 ± 6.4% versus 20.7 ± 2.9% and 34.9 ± 7.0% versus 26.0 ± 3.2%, respectively) compard to an age‐ and sex‐equivalent group. In addition, the circulating total T‐cell population was reduced in myasthenia gravis. Patients with symptomatically uncontrolled disease (with or without immunosuppression) demonstrated significantly altered ratios of helper to suppressor T‐cells, while patients whose myasthenia symptoms were controlled did not differ from normal subjects.
Reciprocal excitation of antagonistic muscles as a differentiating feature in spasticity
Authors: Myklebust Barbara M. , Gottlieb Gerald L. , Penn Richard D. , Agarwal Gyan C. 
Published: January 2005

AbstractThe electromyographic activity evoked by forced ankle rotation in spastic patients with cerebral palsy differs markedly from that found in normal subject or in patients with adult‐onset injuries to the central nervous system. Rapid dorsiflexion can produce a strong myotatic reflex electromyogram at 30 to 50 msec in the normal adult's stretched soleus muscle, while the antagonist tibialis anterior muscle remains quiet. The same is true of spastic patients whose injury has an adult onset. In patients with cerebral palsy this early response is found in both muscle groups. The pattern of “reciprocal excitation” is in marked contrast to the reciprocal inhibition normally seen. This reflex behavior suggests a fundamental developmental error in neuronal interconnections of the spinal cord in cerebral palsy.