bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebral hemodynamics in ischemic cerebrovascular disease
Authors: Powers William J. 
Published: January 2005

AbstractDuring the past decade, technological advances have made it possible to measure regional cerebral hemodynamics in individual patients. Studies performed with these techniques have demonstrated that the degree of carotid stenosis correlates poorly with the hemodynamic status of the ipsilateral cerebral circulation. The primary determinant of cerebral perfusion pressure and blood flow under these circumstances is the adequacy of collateral circulatory pathways. Since collateral circulation varies from patient to patient, there is no critical degree of carotid stenosis that consistently produces hemodynamic compromise of the cerebral circulation. It is, thus, time to abandon the concept of the hemodynamically significant carotid stenosis as it relates to the pathogenesis and treatment of cerebrovascular disease. Measurement of regional cerebral hemodynamics have provided new insight into the pathogenesis of tranisent ischemic attacks and generated some preliminary data on the prognostic and therapeutic importance of chronic reductions in regional cerebral perfusion pressure. Further investigations into the importance of hemodynamic factors in ischemic stroke can now be based on accurate assessment of cerebral (not carotid or vertebrobasilar) hemodynamics in the context of other coexisting epidemiological, clinical, hematological, and angiographic risk factors.
Analysis of retroviral sequences in the spinal form of multiple sclerosis
Authors: Rozenberg Flore , Lefebvre Suize , Lubetzki Catherine , Lebon Pierre , Lyon‐Caen Olivier , Brahic Michel , Bureau Jean‐François 
Published: January 2005

AbstractThe polymerase chain reaction was used, in a blind study, to look for retroviral sequences in DNA extracted from the peripheral blood mononuclear cells of 11 patients with the spinal form of multiple sclerosis (MS). Control subjects consisted of 7 patients with other neurological diseases and 5 healthy blood donors. Three sets of oligonucleotides were used. They could detect all known human oncoretroviruses, lentiviruses, or spumaretroviruses. The primers recognized conserved sequences in the long terminal repeats of the proviral DNA. Control experiments showed that the primers crossreacted within the human immunodeficiency virus or human T‐cell lymphotropic virus group and that they provided the expected level of sensitivity. Therefore the assay could have detected not only known human retroviruses but also new related members. In spite of this, no retroviral sequences were detected in either the MS or the control specimen.
Epidemiology of encephalitis in children: A 20‐Year survey
Authors: Koskiniemi Marjaleena , Rautonen Jukka , Lehtokoski‐Lehtiniemi Eeva , Vaheri Antti 
Published: January 2005

AbstractFour hundred five children from the Helsinki area who were 1 month to 16 years old were treated for acute encephalitis at the Children's Hospital, University of Helsinki, from January 1968 through December 1987. Encephalitis occurred most commonly in children 1 to 1.9 years of age, among whom the incidence was 16.7 per 100,000 child‐years. The incidence remained quite high until the age of 10 years, and then gradually declined to 1.0 per 100,000 child‐years at the age of 15 years. Since 1983, when mumps, measles, and rubella vaccination eradicated the encephalitides associated with these microbes, the major associated agents have been varicella‐zoster, Mycoplasma pneumoniae, and respiratory and enteroviruses. In infants younger than 1 year of age, the major agents were enteroviruses, herpes simplex virus, and the group of “others,” whereas in older children, respiratory viruses and Mycoplasma Pneumoniae as well as varicella‐zoster virus, dominated. In children aged 1 to 11 months, the causal agent could not be identified in one‐half of all cases, whereas in children who were at least 10 years old, the etiology remained unknown in only one‐fourth of cases. Male dominance was most evident in the 4‐ to 9‐year age group. The difference in etiology between males and females was significant (p = 0.02); mumps and varicella were more common in boys, and adenovirus and Mycoplasma pneumoniae were more common in girls. The overall male‐to‐female ratio was 1.4:1. Characteristic seasonal variation occurred in encephalitides associated with mumps, measles, and entero‐ and respiratory viruses. In the whole series, some accumulation appeared in February and March. Less than one‐half of this number appeared in July and August.
Serial gadolinium‐enhanced magnetic resonance imaging scans in patients with early, relapsing‐remitting multiple sclerosis: Implications for clinical trials and natural history
Authors: Harris Jonathan O. , Frank Joseph A. , Patronas Nicholas , McFarlin Dale E. , McFarland Henry F. 
Published: January 2005

AbstractSix patients with early, mild, relapsing‐remitting multiple sclerosis were studied with monthly gadolinium‐enhanced magnetic resonance imaging scans for 8 to 11 months. Numerous enhancing lesions were observed irrespective of clinical activity. Four of the 6 patients had one or more enhancing lesions present on each examination. The other 2 patients had enhancing lesions noted in 7 and 9 of 11 months. In contrast, only two clinical exacerbations were observed during the study period. Neither the exacerbations nor other changes in symptoms or signs correlated with occurrence of the enhancing lesions. Enhancement generally persisted for less than 1 month. The opening of the blood‐brain barrier as reflected by gadolinium enhancement on magnetic resonance imaging may represent ongoing disease activity in patients with mild, relapsing‐remitting multiple sclerosis who are clinically stable. The frequency of these lesions appears to be sufficient to use as an outcome measure in clinical trials testing clinical efficacy in patients with early, relapsing‐remitting multiple sclerosis.
Central sleep apnea and arterial compression of the medulla
Authors: Miyazaki Masahito , Hashimoto Toshiaki , Sakurama Noriko , Yoshimoto Tsutomu , Tayama Masanobu , Kuroda Yasuhiro 
Published: January 2005

AbstractWe report a 5‐year‐old with central sleep apnea associated with compression of the medulla oblongata by abnormal looping of the left vertebral artery. The magnetic resonance imaging findings raise the possibility that compression of the respiratory center by an aberrant vertebral artery might cause central sleep apnea.
Epileptiform electroencephalographic abnormalities in liver transplant recipients
Authors: Wszolek Z. K. , Aksamit A. J. , Ellingson R. J. , Sharbrough F. W. , Westmoreland B. F. , Pfeiffer R. F. , Steg R. E. , De Groen P. C. 
Published: January 2005

AbstractWe retrospectively studied patients who had undergone orthotopic liver transplantation and who also had electroencephalography to determine whether epileptiform changes were associated with a poor neurological outcome. Study groups were 36 patients who died after transplantation (141 electroencephalograms) and underwent neuropathological examination, 11 who died (18 electroencephalograms) but did not have autopsy, and a third group of 34 (62 electroencephalograms) who remained alive. Epileptiform activity was seen in electroencephalograms of 14 of the patients who died (11 from the autopsy group) and in 2 of those who remained alive. All had multiple epileptiform abnormalities and clinical or subclinical seizures. The incidence of epileptiform activity after orthotopic liver transplantation was fivefold higher in the nonsurvivors. Serious cerebral structural changes were found in 10 of the 11 patients who underwent autopsy. Epileptiform activity in the electroencephalograms of patients who had undergone orthotopic liver transplantation indicates a poor prognosis. It should alert the clinician to investigate further for potentially treatable causes.
Calcium channel antagonists and human immunodeficiency virus coat protein–mediated neuronal injury
Authors: Lipton Stuart A. 
Published: January 2005

AbstractRecent evidence in vitro has suggested that neuronal injury observed in the acquired immunodeficiency syndrome dementia complex may depend, at least in part, on toxic effects of the human immunodeficiency virus type 1 envelope protein, gp120. This laboratory previously reported that members of the dihydropyridine class of calcium channel antagonists, nimodipine and nifedipine, greatly attenuate the rise in intracellular calcium engendered by gp120 and prevent subsequent neuronal injury. The relatively low (nanomolar) concentrations of dihydropyridines that were effective suggested that their action might be exerted at the level of the L‐type of voltage‐dependent calcium channels. In the present study, I tested members of the three other major classes of Ca2+ channel antagonist drugs to determine if they too could prevent neurotoxicity induced by gp120. At the maximal dose that did not cause neuronal damage in and of itself, a diphenylalkylamine piperazine derivative (flunarizine, 10 μM) was the most effective, a phenylalkylamine (verapamil, 100 μM) was possibly effective, whereas a benzothiazepine (diltiazem, 1 μM) was ineffectual in protecting rat retinal ganglion cells from gp120‐induced toxicity in vitro. To explain these results, previous work has shown that the various classes of Ca2+ channel antagonists may exhibit differential potency in blocking voltage‐dependent Ca2+ current in neurons, with dihydropyridines and flunarizine being the most potent at neuronal calcium channels. Moreover, these channels on mammalian central neurons are relatively insensitive to agents such as verapamil and diltiazem compared with other cell types like muscle. The low micromolar concentrations necessary for potency of flunarizine is in keeping with that predicted by binding and electrophysiological studies for block of voltage‐dependent calcium channels. Other mechanisms of neuroprotection by flunarizine from gp120, however, cannot be totally excluded.
Ocular motor abnormalities in human immunodeficiency virus infection
Authors: Merrill Pauline T. , Paige Gary D. , Abrams Richard A. , Jacoby Robert G. , Clifford David B. 
Published: January 2005

AbstractWe studied ocular motor performance in 47 subjects with human immunodeficiency virus (HIV) infection and 25 normal control subjects. Saccade accuracy was the most sensitive measure, being significantly poorer for all four HIV‐positive groups (asymptomatic, acquired immunodeficiency syndrome [AIDS] without dementia, and AIDS with dementia, and AIDS‐related complex) than for control subjects. While saccade duration and peak velocity were not significantly different across groups, the scatter of saccade duration was increased in all HIV‐positive groups. Saccade latency was not significantly affected. In both simple and complex antisaccade tasks, the asymptomatic, AIDS, and AIDS dementia groups made significantly fewer correct‐way antisaccades than did control subjects. Latencies of correct‐way antisaccades were increased for the AIDS and AIDS dementia groups in the simple antisaccade trials, and for all HIV‐positive groups in the complex trials. Fixation stability was significantly worse in the AIDS dementia group than in control subjects. Smooth pursuit gain was Decemberreased in the asymptomatic, AIDS, and AIDS dementia groups for the least demanding trial. One or more ocular motor abnormalities were present in 15 (88%) asymptomatic subjects, 11 (69%) with AIDS‐related complex, and 14 (100%) AIDS patients without or with dementia.
Focal neuronal migration disorders and intractable partial epilepsy: A study of 30 patients
Authors: Palmini André , Andermann Frederick , Olivier André , Tampieri Donatella , Robitaille Yvon , Andermann Eva , Wright Geoffrey 
Published: January 2005

AbstractWe studied 30, patients with partial epilepsy and a radiological or pathological diagnosis of localized neuronal migration disorders, with a view to surgical treatment. Eight patients had identifiable prenatal etiological factors. The frequency of complex partial, partial motor, and secondarily generalized seizures was approximately 70° each. Drop attacks were present in 27°: Their presence usually correlated with a lesion involving the central region. Partial motor or generalized convulsive status epilepticus occurred in 30°, and was most frequently associated with extensive structural abnormalities involving two or more lobes. A full‐scale intelligence quotient of less than 80 was found in 44°. Magnetic resonance imaging (MRI) was superior to computed tomography for identification of the dysplastic cortical lesions. In one third, MRI showed only subcortical abnormalities. It did not allow distinction between true pachygyria, focal cortical dysplasia, or the forme fruste of tuberous sclerosis. The epileptogenic area was usually more extensive than the lesion; it was multilobar in more than 70° of patients. Of 26 surgically treated patients, a histological diagnosis of the type of neuronal migration disorder was possible in 22:12 had focal cortical dysplasia and 10 the forme fruste of tuberous sclerosis. In the remaining 4, no definite histological diagnosis was made, since the maximally abnormal tissue could not be examined. In the latter, and in the 4 nonoperated patients, the diagnosis of neuronal migration disorder was based on imaging findings. The presence of the forme fruste of tuberous sclerosis correlated with delayed psychomotor development and more extensive epileptogenic areas.
Peripheral blood γ‐δ T cells lyse fresh human brain—Derived oligodendrocytes
Authors: Freedman Mark S. , Ruijs Theodora C. G. , Selin Liisa K. , Antel Jack P. 
Published: January 2005

AbstractT cells are postulated to contribute to the injury of the oligodendrocyte‐myelin complex underlying the demyelinating disease multiple sclerosis (MS). The apparent lack of class I or II major histocompatibility complex (MHC) expression in situ on human oligodendrocytes and the consistent failure to identify a universal myelin antigen in MS suggest that the immune damage might be mediated by effector T cells that are capable of reacting in an antigen‐nonspecific and possibly MHC‐unrestricted manner, such as T cells expressing the γ‐δ T‐cell receptor. Since γ‐δ T cells are reported to be present in MS plaques and an increased number are found in the cerebrospinal fluid of patients with MS, we directly examined whether γ‐δ T cells are capable of inducing injury to human oligodendrocytes. We found, using a 6‐hour 51Cr release assay, that oligodendrocytes cultured from surgically resected human brain specimens were effectively lysed in a dose‐dependent manner by human γ‐δ T Cells (28 ± 5% mean specific lysis, n = 6, at an effector‐target ratio of 20:1). Although heat shock protein HSP72, a putative γ‐δ T‐cell recognition molecule, could be induced in vitro in our oligodendrocytes, an antibody to HSP72 did not inhibit γ‐δ T cell‐mediated lysis of oligodendrocytes. These results suggest that γ‐δ T cells gaining entry into the central nervous system may be deleterious to oligodendrocytes and thus may contribute to the pathogenesis of MS.
Focal conduction block in the dorsal root ganglion in experimental allergic neuritis
Authors: Stanley Glenn P. , McCombe Pamela A. , Pender Michael P. 
Published: January 2005

AbstractAcute experimental allergic neuritis was induced in Lewis rats by inoculation with bovine intradural root myelin and adjuvants. In terminal experiments, sensory conduction was assessed in rats with hindlimb ataxia and weakness by stimulating the exposed sciatic nerve and recording directly from the exposed L‐4 spinal nerve, dorsal root ganglion, dorsal root, and dorsal root entry zone. Focal conduction block was present in a high proportion of large‐diameter fibers in the dorsal root ganglion. In contrast, nerve conduction in the peripheral nerve and spinal nerve was essentially normal apart from probable conduction block in some fibers in the proximal spinal nerve in a minority of rats. The afferent volley arriving at the dorsal root entry zone of the spinal cord was greatly reduced, as a consequence of the conduction block in the dorsal root ganglion and probable conduction block in the dorsal root. The M wave recorded from the fourth dorsal interosseus muscle of the hindfoot was normal in amplitude but slightly prolonged in latency and the H reflex was absent. These electrophysiological findings correlated well with the histological findings of inflammation and prominent demyelination in the dorsal root ganglia and dorsal roots with minimal involvement of the proximal spinal nerve and no involvement of the sciatic nerve. It is concluded that the hindlimb ataxia in rats with this form of acute experimental allergic neuritis is due to demyelination‐induced nerve conduction block in the dorsal root ganglia and probably in the dorsal roots.
Cytochrome C oxidase deficiency and Long‐Chain acyl coenzyme A dehydrogenase deficiency with Leigh's subacute necrotizing encephalomyelopathy
Authors: Reichmann Heinz , Scheel Helmut , Bier Bert , Ketelsen Uwe‐Peter , Zabransky Siegfried 
Published: January 2005

AbstractA female infant was seen at the age of 2 months because of hypotonia, delayed motor development, and lactic acidosis, and she died at age 13 months due to respiratory failure. In a muscle specimen taken at 11 months and in a liver specimen obtained 1.5 hours postmortem, we found decreased activities of cytochrome c oxidase and longchain acyl coenzyme A dehydrogenase. Neuropathological changes were typical for Leigh's subacute necrotizing encephalomyelopathy. To our knowledge, this is the first report of a combined defect of complex IV of the respiratory chain and of the long‐chain specific acyl coenzyme A dehydrogenase of β‐oxidation in muscle and liver.
Striatal D2 receptor status in patients with Parkinson's disease, striatonigral degeneration, and progressive supranuclear palsy, measured with 11C‐raclopride and positron emission tomography
Authors: Brooks D. J. , Ibanez V. , Sawle G. V. , Playford E. D. , Quinn N. , Mathias C. J. , Lees A. J. , Marsden C. D. , Bannister R. , Frackowiak R. S. J. 
Published: January 2005

AbstractEquilibrium striatal: cerebellar 11C‐raclopride (RAC) uptake ratios reflect the density of striatal dopamine D2 binding sites. Using positron emission tomographic scanning we have measured striatal RAC uptake in 6 untreated patients with Parkinson's disease (PD), 5 chronically treated patients with PD and a fluctuating response to L‐dopa, 10 patients with striatonigral degeneration (SND), and 9 patients with progressive supranuclear palsy (PSP). Regional cerebral blood flow was determined also, with C15O2. Mean strital: cerebellar RAC uptake was not significantly different from normal in untreated patients with PD, though 2 of these 6 patients showed significantly increased putamen tracer binding. Mean caudate and putamen: cerebellar RAC uptake ratios of the group with PD and fluctuating response to L‐dopa were significantly reduced by 30% and 18%, respectively. The patients with SND had lesser, but significant, 10% and 11% decreases in mean caudate and putamen: cerebellar RAC uptake ratios, respectively, whereas patients with PSP showed 24% and 9% reductions in caudate and putamen: cerebellar RAC binding. Striatal and frontal blood flow were significantly reduced in patients with PSP, but not in patients with PD or SND. In conclusion, striatal D2 binding potential is normal or raised in untreated patients with PD, but reduced in patients with PD and a fluctuating response to L‐dopa. Patients with SND and PSP show a decrease in striatal RAC binding, but to a lesser extent than patients with PD and a fluctuating response to treatment. Failure of patients with SND and PSP to respond well to L‐dopa cannot therefore be due to losss of striatal D2 sites alone, but must reflect loss of other basal ganglia connections.
Congenital hypomyelination neuropathy with arthrogryposis multiplex congenita
Authors: Boylan Kevin B. , Ferriero Donna M. , Greco Claudia M. , Sheldon R. Ann , Dew Michael 
Published: January 2005

AbstractA term male infant is described with an isolated disorder of peripheral myelination. At necropsy, the great majority of medium‐to‐large axons were unmyelinated. Electron microscopy showed normal axons and redundant lamination of basement membrane, suggestive of early onion bulb pathology. Immunohistochemistry of peripheral nerve showed deficiency of the myelin proteins P2 and Po, myelin basic protein, and myelin‐associated glycoprotein. Arrest of peripheral myelination at the promyelin stage appears to be the origin of myelin deficiency.
Distribution of cisternal blood in patients with acute hydrocephalus after subarachnoid hemorrhage
Authors: Hasan Djo , Tanghe Hervé L. J. 
Published: January 2005

AbstractThe distribution of cisternal blood in relation to the development of acute hydrocephalus was studied in 246 consecutive patients with aneurysmal subarachnoid hemorrhage who were admitted within 72 hours. Patients with evidence on the initial computed tomograph (CT) of subarachnoid hemorrhage caused by other than a ruptured aneurysm and patients with a negative angiography were excluded. Acute hydrocephalus (defined as a bicaudate index, measured on the initial CT or on a repeat CT within 1 week after subarachnoid hemorrhage, exceeding the 95th percentile for age) was found on the initial CT in 50 (20%) of the 246 patients and on a repeat CT in 9 other patients. Ventricular blood was found significantly more often in patients with acute hydrocephalus than in those in whom acute hydrocephalus did not develop (28 of 59 {47%} versus 58 of 187 {31%}; χ2 = 4.634, p = 0.031). When the analysis was restricted to the 86 patients with ventricular blood, no significant differences were found in the total amount of cisternal blood and in the distribution of cisternal blood between patients with and without hydrocephalus. In contrast, among the 160 patients with ventricular blood, hydrocephalus was associated with a slightly higher total amount of cisternal blood (Wilcoxon's rank sum test, p = 0.023), and significantly more patients with acute hydrocephalus had a higher score in both ambient cisterns than patients without acute hydrocephalus (20 of 31 {65%} versus 41 of 129 {32%}; χ2 = 10.007, p = 0.002). We conclude that the risk of acute hydrocephalus developing in patients without ventricular blood following rupured aneurysm is significantly increased in those with a high cisternal score for blood in both ambient cisterns.