bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of prolactin in autoimmune demyelination: Suppression of experimental allergic encephalomyelitis by bromocriptine
Authors: Riskind Peter N. , Massacesi Luca , Doolittle Teresa H. , Hauser Stephen L. 
Published: January 2005

AbstractSeveral lines of evidence suggest that the anterior pituitary hormone prolactin has a stimulatory role on immune function and that pharmacological suppression of prolactin secretion with the dopamine‐agonist bromocriptine suppresses both humoral and cellular immunity. Here, we describe the effects of prolactin‐suppression on the course of experimental allergic encephalomyelitis in female Lewis rats. Initiation of continuous bromocriptine treatment before immunization reduced both the severity and incidence of clinical signs of acute experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis–immunized rats experienced a threefold rise in basal prolactin levels on day 4 after immunization and maintained elevated prolactin levels on day 10, before the onset of neurological signs of experimental allergic encephalomyelitis. Bromocriptine treatment reduced prolactin levels to those of shamimmunized rats. In vivo bromocriptine pretreatment inhibited splenic lymphocyte proliferative responses in vitro to the immunizing antigen and to concanavalin A. Moreover, bromocriptine therapy was protective when initiated 1 week after the initial immunization and was also effective in suppression of late disease. These results indicate that (1) prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, (2) bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and (3) inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolaction on the effector limb of the immune response during experimental allergic encephalomyelitis.
Mitochondrial dysfunction in multiple symmetrical lipomatosis
Authors: Berkovic Samuel F. , Andermann Frederick , Shoubridge Eric A. , Carpenter Stirling , Robitaille Yvon , Andermann Eva , Melmed Calvin , Karpati George 
Published: January 2005

AbstractMultiple symmetrical lipomatosis is a striking clinical finding associated with a variety of peripheral and central nervous system abnormalities. We describe 4 unrelated patients with evidence of mitochondrial dysfunction in skeletal muscle. Multiple symmetrical lipomatosis is an additional, albeit unusual, manifestation of the expanding clinical spectrum of mitochondrial diseases.
Fatal varicella‐zoster virus meningoradiculitis without skin involvement
Authors: Dueland Aud N. , Devlin Mary , Martin John R. , Mahalingam Ravi , Cohrs Randall , Manz Herbert , Trombley Irene , Gilden Donald 
Published: January 2005

AbstractA 77‐year‐old man with T‐cell lymphoma developed an acute fatal meningoradiculitis of cranial nerve roots and cauda equina, pathologically and virologically confirmed to be caused by varicella‐zoster virus. This is the first report of fatal varicella‐zoster virus‐induced neurological disease in the absence of skin lesions. Varicellazoster virus should be included in the differential diagnosis of acute radiculoneuropathy in the immunocompromised patient, particularly because antiviral treatment for varicella‐zoster virus exists.
Cerebrovascular abnormalities in pediatric stroke: Assessment using parenchymal and angiographic magnetic resonance imaging
Authors: Wiznitzer Max , Masaryk Thomas J. 
Published: January 2005

AbstractThree‐dimensional (volume) magnetic resonance angiography is a noninvasive technique the images the intracranial and cervical arterial vasculature without contrast agents. Twenty‐four children with strokes had combined parenchymal magnetic resonance imaging and magnetic resonance angiography 1 day to 4 years after acute presentation. Eight had had prior intra‐arterial angiography. Eighteen magnetic resonance angiographic studies showed arterial stenosis or occlusion in the vascular distribution of magnetic resonance image‐defined brain infarction and, in 7 children, in the same location as previously defined abnormalities on intra‐arterial angiography. One child had a normal intra‐arterial angiogram and magnetic resonance angiogram. The other 5 children with normal magnetic resonance angiographic studies included 3 with presumed embolic disease, 1 with meningitis, and 1 with Crohn's disease‐related vasculitis. Collateral flow patterns could be determined in 4 children. Artifact presenting as filling defects in vessels was present in 10 studies, but did not interfere with interpretation of 8 studies. Combined magnetic resonance imaging/magnetic resonance angiography provides a screening technique to evaluate noninvasively brain parenchyma and vasculature in children with suspected large‐vessel abnormalities, allowing selection for intra‐arterial angiography and vasculature in children with suspected large‐vessel abnormalities, allowing selection for intra‐arterial angiography and serial monitoring of vascular abnormalities over time and during therapeutic intervention.
The acetylcholine‐induced flare response in evaluation of small fiber dysfunction
Authors: Benarroch Eduardo E. , Low Phillip A. 
Published: January 2005

AbstractWe inotophoresed acetylcholine on the dorsum of the foot and simultaneously measured flare and sweat responses using laser Doppler and sudorometric techniques, respectively. We compared these responses with those induced by histamine. Both acetylcholine and histamine produced dosedependent flare, but only acetylcholine produced sweat responses. Responses to acetylcholine and histamine were blocked by hexamethonium chloride and pyrilamine maleate, respectively (p < 0.01). We compared flare and sweat responses in 26 control subjects, 21 asymptomatic diabetic patients and 41 patients (17 diabetic, 24 nondiabetic) with pain symptoms suggestive of small fiber neuropathy and normal sensation (n = 15) or mild to moderate (n = 19) or severe (n = 7) sensory loss. No patient had trophic foot lesions. Basal skin blood flow and maximal flare responses were not significantly different among the various subgroups (Control subjects, 49 ± 7.4; asymptomatic diabetic patients, 29 ± 4; patients with small fiber neuropathy and normal sensation, 34 ± 6; with neuropathy and mild to moderate sensory loss, 29 ± 4.8; and with neuropathy and severe sensory loss, 35 ± 5 ml/100 gm, for flare response, respectively). Flare responses lower than the lowest found in control subjects occurred in 5 of 21 asymptomatic diabetic patients, 4 of 15 patients with small fiber neuropathy and normal sensation, 5 of 19 with neuropathy and mild to moderate sensory loss, and 1 of 7 with neuropathy and severe sensory loss. Abnormal (persistent or decreased) sweat responses occurred in 10 of 21 asymptomatic diabetic patients, 12 of 15 patients with small fiber neuropathy and normal sensation, 13 of 19 with neuropathy and mild to moderate sensory loss, and 7 of 7 with neuropathy and severe sensory loss. Acetylcholine and histamine stimulate the afferent branch of the flare axon reflex by nicotinic and H1 receptors, respectively. Concurrent measurement of flare and sweat responses, but not the flare alone, may identify patients with small fiber neuropathy, in the absence of trophic foot lesions.
Quantification of mu and non–mu opiate receptors in temporal lobe epilepsy using positron emission tomography
Authors: Mayberg Helen S. , Sadzot Bernard , Meltzer Carolyn Cidis , Fisher Robert S. , Lesser Ronald P. , Dannals Robert F. , Lever John R. , Wilson Alan A. , Ravert Hayden T. , Wagner Henry N. , Bryan R. Nick , Cromwell Christina C. , Frost J. James 
Published: January 2005

AbstractAlterations in a variety of neurotransmitter systems have been identified in experimental models of epilepsy and in brain tissue from patients with intractable temporal lobe seizures. The availability of new high‐affinity radioligands permits the study of some neuroreceptors in vivo with positron emission tomography (PET). We previously characterized the in vivo binding of 11C‐carfentanil, a potent and selective mu opiate receptor agonist, and described increases in 11C‐carfentanil binding in the temporal neocortex of patients with unilateral temporal lobe epilepsy. These studies have been extended to 11C‐diprenorphine, which labels mu, kappa, and delta opiate receptor subtypes. Paired measurements of opiate receptor binding were performed with PET using 11C‐carfentanil and 11C‐diprenorphine in patients with unilateral temporal lobe seizures. Carfentanil binding, reflecting changes in mu opiate receptors, was increased in the temporal neocortex and decreased in the amygdala on the side of the epileptic focus. Diprenorphine binding, reflecting mu as well as non–mu opiate subtypes, was not significantly different among regions in the focus and nonfocus temporal lobes. Regional glucose metabolism, measured using 18F‐2‐fluoro‐2‐deoxyglucose, was decreased in the mesial and lateral aspects of the temporal lobe ipsilateral to the epileptogenic focus. The variation in pattern of carfentanil and diprenorphine binding supports a differential regulation of opiate subtypes in unilateral temporal lobe epilepsy.
Evaluation of a competitive NMDA antagonist (D‐CPPene) in feline focal cerebral ischemia
Authors: Chen M. , Bullock R. , Graham D. I. , Frey P. , Lowe D. , McCulloch J. 
Published: January 2005

AbstractThe effects of a competitive, N‐methyl‐D‐aspartate (NMDA) receptor antagonist, D(‐)E‐4‐(3‐phosphonoprop‐2‐enyl)‐piperazine‐2‐carboxylic acid (D‐CPPene), on the volume of ischemic brain damage was assessed by quantitative histological study in 35 chloralose‐anesthetized cats. Focal cerebral ischemia was produced by permanent occulsion of one middle cerebral artery and the animals were killed by transcardiac perfusion fixation 6 hours later. Pretreatment with D‐CPPene (1.5, 4.5, or 15 mg/kg, administered intravenously 15 minutes prior to occlusion, with subsequent drug infusions to maintain a plateau in the plasma drug concentrations) effected dose‐dependent reductions in the volume of ischemic brain damage. At the highest dose studied (15 mg/kg, plus an infusion of 170 m̈g/kg/min), D‐CPPene reduced the volume of ischemic damage in the cerebral cortex by more than 75% compared to vehicle‐treated control animals. The plasma concentration of D‐CPPene, which is associated with a half maximal reduction in the volume of ischemic damage, was estimated to be 24 m̈g/ml during the initial 120 minutes after the middle cerebral artery occlusion. Treatment with D‐CPPene (15 mg/kg, plus an infusion of 170 m̈g/kg/min) initiated 1 hour after occlusion reduced the volume of ischemic brain damage in the cerebral cortex by 30%, but this response did not achieve statistical significance. Precise definition of dose dependency for the anti‐ischemic effects of NMDA antagonists and the therapeutic time window are influenced greatly by brain pharmacokinetics of the agents. Such data are crucial if the potent anti‐ischemic effects of NMDA antagonists observed in animals are to be translated into meaningful clinical evaluation of such agents in stroke and head trauma.
Short‐latency autogenic inhibition in patients with parkinsonian rigidity
Authors: Delwaide P. J. , Pepin J. L. , De Noordhout A. Maertens 
Published: January 2005

AbstractThe spinal Ib interneuron efficacy has been compared in 11 control subjects and 19 patients with parkinsonian rigidity. In normal subjects, gastrocnemius medialis nerve stimulation induces an inhibition of the soleus H reflex for 3 to 8 msec with a peak at 5 msec of 83.72 ± 7.28% of the control value of H reflex. In parkinsonian patients, inhibition is reduced or even replaced by facilitation, which also peaks at 5 msec. The departures from normal values correlate with rigidity intensity assessed by the Webster scale. Increase in rigidity is associated, first, with a reduction of inhibition and, from a score of 2 or more, with facilitation replacing the normal inhibition. In addition to providing an electrophysiological index of rigidity, reduction in autogenic inhibition might be one of the neurophysiological mechanisms underlying rigidity. In association with the known hyperactivity of the Ia inhibitory interneuron in Parkinson's disease, reduction of activity of Ib interneuron could be explained by an increased activity in the reticularis gigantocellularis nucleus; its efferent tracts both inhibit Ib interneurons and activate Ia interneurons.
Uhthoff's symptom in optic neuritis: Relationship to magnetic resonance imaging and development of multiple sclerosis
Authors: Scholl Georgina Bates , Song Hu‐Shien , Wray Shirley H. 
Published: January 2005

AbstractEighty‐one patients with a first attack of isolated optic neuritis, 40 with Uhthoff's symptom (Group 1) and 41 without (Group 2), were studied. All had a neurovisual examination, 74 of 81 patients had the pattern visual evoked potential recorded at rest, and 43 had magnetic resonance imaging brain scans. The pattern visual evoked potential P100 latency was prolonged, Group 1 with a mean of 136 ± 19 msec, Group 2 with a mean of 131 ± 19 msec (control subjects, 102 ± 5 msec; n = 84), and the P100 amplitude was reduced, without significant difference between the groups. Abnormal magnetic resonance imaging scans were present in significantly more patients in Group 1 (P < 0.025). Treatment of optic neuritis with corticosteroids had no effect on the evolution or duration of Uhthoff's symptom. Overall, 35 of 81 (43%) patients, followed for a mean of 3.5 years, developed multiple sclerosis. The incidence was significantly greater in Group 1 (p < 0.01). Uhthoff's symptom also correlated with a higher incidence of recurrent optic neuritis. We conclude that Uhthoff's symptom is a prognostic indicator for the early development of multiple sclerosis.
Reduced D2 dopamine and muscarinic cholinergic receptor densities in caudate specimens from fluctuating parkinsonian patients
Authors: Ahlskog J. Eric , Richelson Elliott , Nelson Albert , Kelly Patrick J. , Okazaki Haruo , Tyce Gertrude M. , van Heerden Jon A. , Stoddard Susan L. , Carmichael Stephen W. 
Published: January 2005

AbstractBinding of spiperone and 3‐quinuclidinyl benzilate (QNB), both labeled with hydrogen 3 (3H), were measured in caudate tissue obtained from 8 living parkinsonian patients at the time of cerebral transplantation. This was a clinically homogeneous group of patients: All remained predominantly responsive to levodopa, although with Marchked disability secondary to clinical fluctuations (short‐duration responses) and medication‐induced dyskinesias; all were receiving substantial doses of levodopa and 6 of the 8 patients were additionally receiving bromocriptine or pergolide. Binding densities of dopamine D2 receptors, as measured by [3H]spiperone binding, were reduced in this group of patients, compared to caudate specimens from autopsy control subjects. This finding may reflect medication‐induced receptor downregulation. Parallel changes occurred with muscarinic cholinergic receptors; [3H]QNB binding was significantly reduced, compared to autopsy control values. This reduction of muscarinic receptors might be due to loss of nigrostriatal terminals that are known to contain muscarinic receptors. Alternatively, muscarinic receptors may have been downregulated by increased corticostriatal glutamatergic input to cholinergick cells, inferred to be present based on the prominent levodopa‐induced dyskinesias. Finally, receptor deficits could have also been a reflection of more widespread degenerative cerebral disease, although levodopa‐refractory symptoms were generally not pronounced in these patients.
Paravermal infarct and isolated cerebellar dysarthria
Authors: Amarenco Pierre , Chevrie‐Muller Claude , Roullet Etienne , Bousser Marchie‐Germaine 
Published: January 2005

AbstractA patient with isolated cerebellar dysarthria is reported. Computed tomography showed a small infarct in the left paravermal zone of the rostal cerebellum (lobulus simplex and semilunaris superior) in the territory of the medial branch of the superior cerebellar artery. This patient demonstrates the important role of this area of cerebellum in the control of voice.
Alterations of dopaminergic and noradrenergic innervations in motor cortex in parkinson's disease
Authors: Gaspar Patricia , Duyckaerts Charles , Alvarez Chantal , Javoy‐Agid France , Berger Brigitte 
Published: January 2005

AbstractThe motor areas of the cerebral cortex contain dense dopaminergic and noradrenergic innervation in humans. We looked for changes of these innervations in cases with Parkinson's disease (PD). The density of fibers immunolabeled with tyrosine hydroxylase or dopamine‐beta‐hydroxylase was evaluated in the primary motor, premotor, and prefrontal cortical regions in 6 cases with PD and 7 control cases. Reductions of both noradrenergic and dopaminergic cortical innervations were observed, with similar magnitudes of reduction found in the motor and prefrontal regions of the cortex. Depletion of noradrenergic innervation was diffuse, involving all cortical laminae. Depletion of dopaminergic innervation was laminar specific, with the most significant reductions in layers I and II; reductions in layers V and VI were either less marked (prefrontal cortex) or not detectable (primary motor). The results suggest the existence of two separate mesocortical dopaminergic systems in humans, with the one distributing to upper cortical layers being preferentially involved in PD.
Frequency and distribution of Alzheimer's disease in Europe: A collaborative study of 1980–1990 prevalence findings
Authors: Rocca Walter A. , Hofman Albert , Brayne Carol , Breteler Monique M. B. , Clarke Michael , Copeland John R. M. , Dartigues Jean‐Francois , Engedal Knut , Hagnell Olle , Heeren Thea J. , Jonker Cees , Lindesay James , Lobo Antonio , Mann Anthony H. , Mölsä Pekka K. , Morgan Kevin , O'Connor Daniel W. , Droux Arnaldo da Silva , Sulkava Raimo , Kay David W. K. , Amaducci Luigi 
Published: January 2005

AbstractWe reanalyzed and compared current prevalence estimates of Alzheimer's disease in Europe. Studies characterized as follows qualified for comparison: dementia defined by the Diagnostic and Statistical Manual for Mental Disorders, 3rd edition, or equivalent criteria; Alzheimer's disease diagnosed by the National Institute of Neurological and Communicative Disorders and Stroke‐Alzheimer's Disease and Related Disorders Association or equivalent criteria; case‐finding through direct individual examination; appropriate sample size; and inclusion of institutionalized persons. Of the 23 European surveys of dementia considered, six fulfilled the inclusion criteria. When age and sex were considered, there were no major geographic differences in the prevalence of Alzheimer's disease across Europe. Overall European prevalence (per 100 population) for the age groups 30 to 59, 60 to 69, 70 to 79, and 80 to 89 years was, respectively, 0.02, 0.3, 3.2, and 10.8. Prevalence increased exponentially with advancing age and, in some populations, was consistently higher in women. Prevalence remained stable over 15 years in one study.
Etiology of motor or sensory stroke: A prospective study of the predictive value of clinical and radiological features
Authors: Chimowitz M. I. , Furlan A. J. , Sila C. A. , Paranandi L. , Beck G. J. 
Published: January 2005

AbstractThe diagnostic utility of clinical and radiological features for distinguishing penetrating artery disease from other causes of stroke has been questioned. To address this issue, we prospectively evaluated more than 40 features in 85 patients with pure motor, sensorimotor, or pure sensory syndromes. Nonischemic causes were present in 4 patients. The causes of ischemic stroke in the other 81 patients were penetrating artery disease (32 patients), large artery occlusive disease (17), cardioembolism (12), other causes (8), and undetermined (12). Of the features evaluated, frequent transient ischemic attacks (≥ 1/day), transient ischemic attacks occurring only within 1 week of stroke, pure motor hemiparesis (similar involvement of face, arm, and leg), pure sensory stroke, and round or oval infarction were associated (p< 0.05) with penetrating artery disease. However, only pure sensory stroke involving two or more regions of the body and pure motor hemiparesis associated with subcortical infarction of less than 1.5 cm had positive predictive values exceeding 90% for penetrating artery disease. Carotid bruit ipsilateral to an anterior circulation in farction, monoparesis, and striatocapsular infarction had positive predictive values exceeding 90% for causes other than penetrating artery disease; however, half of the striatocapsular infarctions were of undetermined cause. These data suggest that certain clinical and radiological features are useful for distinguishing penetrating artery disease from other causes of stroke.
Preproenkephalin messenger RNA—containing neurons in striatum of patients with symptomatic and presymptomatic huntington's disease: An in situ hybridization study
Authors: Albin Roger L. , Qin Ying , Young Anne B. , Penney John B. , Chesselet Marie‐Francoise 
Published: January 2005

AbstractPrevious studies have revealed a loss of enkephalin immunoreactivity in the terminals of striatal neurons projecting to the external globus pallidus in patients with early grades of Huntington's disease (HD). To assess the status of the perikarya of striatal enkephalinergic neurons, we performed in situ hybridization histochemistry with a radiolabeled RNA probe complementary to preproenkephalin messenger RNA. We studied postmortem brain tissue of 6 patients with symptomatic HD, 7 control subjects, and 2 presymptomatic carriers of the HD allele. There was a significant reduction in the areal density of striatal neurons expressing preproenkephalin messenger RNA in the patients with symptomatic HD, but the level of labeling in the remaining cells was not altered compared with the control subjects. In the specimens from presymptomatic individuals, there was no reduction of areal density of preproenkephalin messenger RNA‐containing neurons in the striatum, despite the fact that loss of enkephalin immunoreactivity in the external globus pallidus had been previously demonstrated in the same brains. The results correlate with the previous demonstration of depleted enkephalin immunoreactive terminals in the external globus pallidus in patients with symptomatic HD. They also suggest that the early loss of enkephalin immunoreactivity observed in the external globus pallidus of presymptomatic carriers of the HD allele is not related to a generalized death of striatal enkephalinergic neurons early in the course of the disease.