bluuebunny/crossref_metadata_2025_split huggingface dataset:
The relationship of serotonin to depression in Parkinson's disease
Authors: Mayeux Richard , Stern Yaakov , Sano Mary , Williams Janet B. W. , Cote Lucien J. 
Published: January 2005

AbstractWe have previously reported a correlation between depression in patients with idiopathic Parkinson's disease and decreased concentrations of the cerebrospinal fluid content of the serotonin metabolite, 5‐HIAA. To further examine this relationship, we repeated the study in a new cohort of patients while they remained on dopaminergic medications, conducted follow‐up interviews and examinations in our original cohort, and conducted an open trial of the serotonin precursor, 5‐hydroxytryptophan in a group of new patients with depression. We were again able to demonstrate a significant reduction in cerebrospinal 5‐HIAA in depressed patients in comparison to controls and patients without depression. Demented patients with Parkinson's disease, particularly those with concurrent depression, had the lowest values of 5‐HIAA. No new cases of depression occurred in our orignial cohort after 21/2 years of follow‐up, and depression remitted following conventional or experimental treatment in four patients. Depression improved in six of the seven new patients following oral 5‐hydroxytryptophan. Three of these patients allowed a repeat lumbar puncture, and the concentration of 5‐HIAA increased following 5‐hydroxytryptophan. These three studies support our hypothesis that depression in idiopathic Parkinson's disease is associated with a reduction in brain serotonin. However, it also suggests that other factors, biological or environmental, may be causal factors.
Tardive dystonia in patients with Tourette's syndrome
Authors: Singh Sanjay K. , Jankovic Joseph 
Published: January 2005

AbstractWe describe two patients with Gilles de la Tourette's syndrome (TS) who developed tardive dystonia after treatment with neuroleptics. The dystonic movements persisted after the offending drugs were stopped and improved with tetrabenazine. Tardive dystonia in TS has not been documented previously.
Tardive akathisia: An analysis of clinical features and response to open therapeutic trials
Authors: Burke Robert E. , Kang Un Jung , Jankovic Joseph , Miller Lucinda G. , Fahn Stanley 
Published: January 2005

AbstractIn recent years, there has been increasing recognition that akathisia occurs not only as an acute, self‐limited complication of dopamine (DA) antagonist treatment, but also as a persistent form, called tardive akathisia. We present a retrospective analysis of clinical features and therapeutic trials in 52 cases of this disorder. Although most patients developed this disorder after years of DA antagonist treatment (mean = 4.5 years), a significant proportion (34%) developed it within 1 year. The characteristic motor features included frequent, complex stereotyped movements. The legs were most frequently involved, showing marching in place and crossing/uncrossing. Trunk rocking, respiratory grunting and moaning, and complex hand movements such as face rubbing or scratching also occurred. In the 26 patients who were able to discontinue DA antagonists, akathisia persisted for years (mean = 2.7 years, range of 0.3–7 years) until abatement of symptoms or last follow‐up. Younger patients were more likely to have remission or therapeutic suppression of akathisia at follow‐up. In our experience, the catecholamine‐depleting drugs reserpine and tetrabenazine were the most effective agents for suppressing symptoms, producing improvement in 87 and 58% of patients treated, respectively. However, improvement was limited in many patients, and at last follow‐up only 33% of patients had complete abatement of their symptoms. In conclusion, tardive akathisia is a particularly disabling form of tardive dyskinesia, frequently persistent for years and often resistant to therapy.
Hemiballismus: Study of a case using positron emission tomography with 18f1uoro‐2‐deoxyg1ucose
Authors: Dubinsky Richard M. , Baker Michael , Hallett Mark , Greenberg Michael , di Chiro Giovanni 
Published: January 2005

AbstractA 64‐year‐old man had right‐sided persistent hemiballismus. Cerebral computed tomography (CT) and 0.5‐T magnetic resonance imaging (MRI) showed no abnormalities, but 1.5‐T MRI showed decreased signal intensity of the putamina, greater on the left than on the right. The subthalamic area was normal on CT and MRI. Positron emission tomography with 18fluoro‐ 2‐deoxyglucose showed marked hypometabolism of the left putamen (60% of the right) and hypermetabolism of the left parietal lobe (138% of the right). The decreased metabolism of the left putamen may indicate a reduction in neuronal firing. The pathophysiology of the hemiballismus in this case may be loss of tonic inhibition of the lateral globus pallidus from the putamen, leading in turn to greater inhibition of the subthalamic nucleus, less excitation of the medial globus pallidus, and less inhibition of the thalamus and motor cortex, and thus allowing expression of the ballistic movements. allowing expression of the ballistic movements.
Ataxia telangiectasia: A reappraisal of the ocular motor features and their value in the diagnosis of atypical cases
Authors: Stell R. , Bronstein A. M. , Plant G. T. , Harding A. E. 
Published: January 2005

AbstractThe eye movements of four patients with ataxia telangiectasia (AT), three of whom had an unusual neurological presentation, were studied. All had striking abnormalities of saccadic generation with markedly hypometric saccades, increased saccadic latency, but normal saccadic velocity. Three patients used head thrusts to aid refixation. In addition, there was absence of smooth pursuit and optokinetic nystagmus, and hyperactive vestibular responses. Two of the four patients had, in addition, periodic alternating nystagmus. This combination of an ocular motor apraxia with superadded cerebellar ocular motor abnormalities, and possibly periodic alternating nystagmus, should strongly suggest the diagnosis of AT, even if the clinical syndrome is otherwise atypical.
Betel nut‐induced extrapyramidal syndrome: An unusual drug interaction
Authors: Deahl Martin 
Published: January 2005

AbstractTwo cases are described of chronic schizophrenic patients maintained on depot neuroleptics, who developed severe extrapyramidal symptoms following a period of heavy betel nut consumption. A mechanism for this effect is proposed based on the pharmacological antagonism of the anticholinergic agent, procyclidine, by the active alkaloid ingredient of the betel, arecoline.
The effect of nocturnal physiological sleep on various movement disorders
Authors: Silvestri Rosalia , De Domenico Pietro , Di Rosa Antonio E. , Bramanti Placido , Serra Salvatore , Di Perri Raoul 
Published: January 2005

AbstractThirty‐one subjects affected by different movement disorders underwent polygraphic and videotape monitoring during nocturnal sleep, to assess movement patterns during the night. It was possible to distinguish two categories of disorders according to their pattern of movements. In the largest group (Meige's syndrome, blepharospasm, amyotrophic choreoacanthocytosis, Tourette syndrome, tonic foot, hemiballism) abnormal movements were still present during sleep, but decreased in frequency and amplitude in all stages. The second group presented three syndromes (nocturnal paroxysmal dystonia, nocturnal myoclonus, restless legs syndrome), in which light nonrapid‐eye‐movement sleep induced a strong activation of abnormal movements, whereas rapid‐eye‐movement sleep suppressed them.
Paralysis agitans and levodopa in “Ayurveda”: Ancient Indian medical treatise
Authors: Manyam Bala V. 
Published: January 2005

AbstractNeurologic diseases (Vata rogas, Sanskrit) and the pharmacologic treatment of them were described in the ancient Indian medical system—Ayurveda. This article explores paralysis agitans, which was described under the name Kampavata. Mucuna pruriens (Atmagupta, Sanskrit), which contains levodopa, was used in the treatment of Kampavata. Existence of paralysis agitans prior to the industrial revolution is not just of historical interest, but would also suggest that under the hypothesis of exposure to environmental toxins as a possible cause of paralysis agitans, natural organic compounds with worldwide distribution should also be considered.
A clinical and genetic study of familial Parkinson's disease
Authors: Maraganore D. M. , Harding A. E. , Marsden C. D. 
Published: January 2005

AbstractThe clinical features of familial Parkinson's disease (PD) were investigated by examining the families of 20 British probands who were selected on the basis of having clinically typical PD and at least one affected relative. Forty‐nine secondary cases were identified. These subjects were clinically indistinguishable from sporadic cases of idiopathic PD. If it is assumed that familial PD has a genetic basis, pedigree and segregation analysis suggested autosomal dominant inheritance of a gene or genes with reduced penetrance as the most likely explanation. The data did not support the possibilities of either mitochondrial or polygenic inheritance, although the latter cannot be excluded. The role of genetic factors in sporadic cases of PD remains unclear.
Combined resting–postural tremor of the head with a changing axis
Authors: Rapoport Abraham , Braun Hava , Aviv Alex , Sarova Ida 
Published: January 2005

AbstractWhen essential tremor involves the head, it produces a rhythmic, periodic movement with a certain fixed frequency and a variable amplitude. The axis of the tremor has been described as either horizontal (no‐no) or vertical (yes‐yes) and is present when the head is in an action or postural position. Seven patients who differ in symptoms are described; one subgroup exhibited a combined resting‐postural head tremor with a changing axis.
Machado‐Joseph disease: An autosomal dominant motor system degeneration
Authors: Rosenberg Roger N. 
Published: January 2005

AbstractMachado‐Joseph disease is an autosomal dominant spinocerebellar degeneration. It expresses itself clinically with variable expression. Type one patients have early onset with a rapid progression of symptoms including spasticity, rigidity and myokymia. Type two patients are the most common phenotype with ataxia and spasticity. Type three patients develop progressive ataxia with variable amyotrophy. All patients have ophthalmoparesis and normal mental status. The neuropathology consists of neuronal loss and gliosis in the substantia nigra, motor cranial nuclei, dentate nucleus of the cerebellum, and variable neuronal loss with gliosis in the cerebellar cortex and neostriatum. The cerebral cortex is normal histologically. The inferior olivary nuclei are normal, thus separating this disease from olivopontocerebellar atrophy (OPCA). The disease has a worldwide distribution including families described in Portugal, the Azores, Spain, Italy, United States, Canada, Brazil, China, Taiwan, and Japan. The gene has not been mapped for this disease but the locus on chromosome 6p mapped for most families with OPCA has been excluded for this disorder.
Effect of aging and dopaminomimetic therapy on mitochondrial respiratory function in Parkinson's disease
Authors: Bravi Daniele , Anderson Jeffrey J. , Dagani Fiorenzo , Davis Thomas L. , Ferrari Rosaria , Gillespie Marge , Chase Thomas N. 
Published: January 2005

AbstractOxygen consumption and enzyme activity were evaluted in platelet mitochondria from 17 patients with Parkinson's disease. In comparison with age‐matched controls, no consistent abnormality could be discerned in complex I, complex II‐III, or complex IV oxygen consumption, or in the enzyme activity of these respiratory chain complexes. Neither chronic therapy with levodopa/carbidopa alone nor in combination with deprenyl significantly affected any measure of mitochondrial respiratory function. There was no discernible relationship between patient age or disease severity and any parameter of mitochondrial respiration. Moreover, blood lactate levels following glucose loading were not different in patients and controls. These results fail to support the occurrence of a generalized defect in any mitochondrial respiratory function in Parkinson's disease.
Muscle trophic factor: I. Assay of a muscle trophic factor by measurement of muscle cell nuclei
Authors: Ozawa Eijiro , Kohama Kazuhiro 
Published: January 2005

AbstractA method for assaying a skeletal muscle cell trophic factor in chicken serum is described. The number of myoblast and myotube nuclei was considered to reflect the rate of myoblast multiplication and was thus adopted as an index for the activity of the trophic factor. In a 35‐mm Falcon plastic Petri dish, 2.5 × 104 to 105 myoblasts were cultured. The culture medium consisted of 85% Eagle's minimum essential medium and 15% horse serum. The assay medium was composed of 2.4 ml of this culture medium and 0.1 ml of partially purified trophic factor of appropriately diluted chicken serum. Four dishes were prepared for each sample under identical conditions. On day 4 of incubation, cells were fixed, stained, and observed under a microscope, and the number of nuclei in 20 fields was counted. The mean number of nuclei obtained from the four dishes was used to denote a single point. A three‐point common‐zero method of slope‐ratio assay was used to calculate activity. The activity of the trophic factor was expressed with reference to the effect of the control serum on myoblast multiplication.
Muscle trophic factor: III. Effect of hormones and tissue extracts on muscle trophic‐factor activity
Authors: Ozawa Eijiro , Kohama Kazuhiro 
Published: January 2005

AbstractThe ability of classical hormones or extract from adult chicken tissues to replace or influence the activity of chicken skeletal muscle cell trophic factor was investigated. Pituitary gland extract did not replace the trophic factor in a range equivalent to the serum concentrations of somatotropin, although high concentrations of such extract showed a significant ability to mimic trophic‐factor activity. Insulin, triiodothyronine, testosterone, dihydrotestosterone (Stanolone), and estradiol did not show any ability to mimic trophic‐factor activity. Both pituitary extract and insulin showed a potentiating effect on the trophic factor when added to the medium; however, the concentrations necessary for this effect were too high to be considered physiologic. Triiodothyronine, testosterone, Stanolone, and estradiol did not potentiate the trophic factor; indeed, at higher concentrations, these hormones actually suppressed the activity of the trophic factor. Every tissue extract examined showed, to a greater or lesser extent, the ability to potentiate the trophic factor.
Peripheral nerve responses during ischemia in the evaluation of diabetic neuropathy
Authors: Horowitz Steven H. , Ginsberg‐Fellner Fredda 
Published: January 2005

AbstractThe stability of sensory conduction and evoked potentials during ischemia has been used in the evaluation of diabetic neuropathy and diabetic control (Hgb A1C). Six newly diagnosed juvenile diabetics were studied at diagnosis and 3 to 12 months later. In three patients in good control, ischemic “resistance” became normal. In three patients in poor control, resistance remained increased; two of these three experienced a 10%–20% slowing in conduction velocity. Similar relationships between control and ischemic resistance are found in long‐term diabetics. These data suggest that abnormal ischemic resistance may herald the onset of an electrical and clinical neuropathic state.
Myopathies with abnormal mitochondria: A clinicopathologic classification
Authors: Kamieniecka Zofia , Schmalbruch Henning 
Published: January 2005

AbstractOf 185 patients with myopathy, 22 showed abnormal muscle mitochondria. In 12 of the 22 patients, all of whom had ocular myopathy or the ophthalmoplegia‐plus syndrome, muscle biopsies contained 5%–25% “ragged red” fibers. In 4 patients with a facioscapulohumeral distribution of weakness, ragged red fibers were less numerous (3%–8%). In both groups, routine histology showed almost normal muscle. The remaining 6 patients were clinically heterogeneous, all without ptosis or ophthalmoplegia. The biopsies of three of these patients showed severely affected muscle. It is possible that mitochondrial changes in these muscles were nonspecific. Electromyography indicated or suggested a myogenic lesion in 21 of the 22 patients; in 10, the serum creatine kinase was increased.
The regional curare test and electrophysiologic diagnosis of myasthenia gravis: Further studies
Authors: Horowitz Steven H. , Sivak Mark 
Published: January 2005

AbstractFive hundred consecutive patients were evaluated for myasthenia gravis with repetitive stimulation of the median and ulnar nerves. Axillary nerve stimulation and repeated stimulation of wrist nerves following regional curare administration to the hand were performed when necessary. Abnormal responses were seen in 95% of 297 patients with generalized disease and in 35% of 54 patients with ocular disease, all of whom were clinically responsive to anticholinesterases. Identical responses were also seen in 32% of 124 patients with possible generalized disease, all of whom lacked clinical responsiveness to anticholinesterases. Abnormalities occurred following regional curare administration in 29% of 224 patients with normal responses during repetitive stimulation alone. This program for evaluating patients with suspected myasthenia gravis continues to be successful, safe, and practical.
A clinical review
Authors: Siegel Irwin M. 
Published: January 2005

AbstractThe optimal management of muscular dystrophy is multidisciplinary and aggressive in nature. Serial assessment aids in determining the functional stage of the disease and in indicating specific therapies. Physical therapy can augment strength through exercise and relieve contracture through passive stretching. Occupational therapy is employed to help the patient manage his activities of daily living within the restrictions imposed on him by his disease. Progressive disability can be delayed through a variety of physiatric and orthopedic techniques, including surgical release of lower‐extremity contracture, repair of foot and ankle deformity, and correction of scoliosis. Appropriate orthoses are available, as are a variety of special devices to facilitate ongoing care for postambulatory patients. Physicians treating the muscular dystrophies should be aware of the complications of these diseases, particularly cardiomyopathy, pulmonary failure, and psychological and social problems.
Morphology and physiology of skeletal muscle in aging rodents
Authors: Caccia Mario R. , Harris John B. , Johnson Margaret A. 
Published: January 2005

AbstractAging in the rodent is accompanied by a progressive loss of skeletal muscle fibers. The muscle twitch also becomes slower, probably as a result of fibertype conversion from “fast‐twitch” to “slow‐twitch.” The loss of muscle fibers precedes signs of obvious weakness and appears to involve the loss of entire functioning motor units. In the mouse, this loss of motor units correlates with a loss of axons from the innervating nerve trunks.
Protein synthesis in skeletal muscle following acute exhaustive exercise
Authors: Rogers Peter A. , Jones George H. , Faulkner John A. 
Published: January 2005

AbstractCell‐free and whole‐tissue protein synthesis was studied in skeletal muscle of untrained male guinea pigs that had undergone a treadmill run to exhaustion. Experiments using explants from the gastrocnemius muscle maintained in organ culture demonstrated that the ability of the acutely exercised muscle to incorporate amino acids into protein had increased. Compared to polyribosomes prepared from several lower hind limb muscles of nonexercised guinea pigs, polyribosomes from the same muscle in exhausted guinea pigs had incorporated almost 50% more radioactive leucine into protein. However, the polysome profiles of control and exercised muscle were identical, and no difference in the total polysome RNA content could be detected. The efficiency of in‐vitro protein synthesis using washed membrane‐bound polyribosomes (microsomes) isolated from acutely exercised skeletal muscle was 50% greater than with microsomes from rested control muscle.
Application of lectin cytochemistry to the study of human neuromuscular disease
Authors: Bonilla Eduardo , Schotland Donald L. , Wakayama Yoshihiro 
Published: January 2005

AbstractThis is a review of the application of cell surface cytochemistry to the study of human neuromuscular disease. The advantages and limitations of the use of lectins coupled to peroxidase are discussed, and the application of this technique is illustrated by a study of the surface of muscle cells in Duchenne muscular dystrophy and polymyositis.
Red blood cell alterations in muscular dystrophy: The role of lipids
Authors: Plishker Gordon A. , Appel Stanley H. 
Published: January 2005

AbstractBiochemical, morphologic, and biophysical studies support the concept that the red blood cell (RBC) membrane is altered in both myotonic muscular dystrophy (MyD) and Duchenne muscular dystrophy (DMD). These studies have not identified a primary metabolic defect that would explain the various alterations of membrane properties. Since the lipid milieu of the membrane affects most membrane properties, it has been extensively investigated in MyD and DMD. Although some studies have suggested specific lipid abnormalities, no reproducible alterations have been reported in the major lipid constituents of the RBC membrane in these disorders. These findings suggest that major alterations of the predominant membrane lipids are not involved in these diseases. Furthermore, studies of the RBC membrane do not provide definitive statements as to the inborn error of metabolism, whether proteins or lipid constituents are primarily affected, or even whether the described alterations are intrinsic to the membrane or are secondary to some circulating factors. Nevertheless, RBCs have proved useful in demonstrating the involvement of the plasma membrane in muscle disorders and should be important in defining how such membrane perturbations affect transport mechanisms.
Some factors affecting spontaneous transmitter release in dystrophic mice
Authors: Shalton Penny M. , Wareham Anthony C. 
Published: January 2005

AbstractNeuromuscular junctions of slow‐ and fast‐twitch skeletal muscles from dystrophic (dy2J/dy2J) and control mice of the C57BL/6J strain were used to investigate the effect of muscular dystrophy on nerve‐terminal regulation of their intracellular concentration of free calcium ions. The frequency of spontaneous miniature endplate potentials (MEPPs) was taken as an indicator of the intraterminal free calcium ion concentration. Dicoumarol, 2,4‐dinitrophenol, ruthenium red, and the calcium ionophore A‐23187 all potentiated the MEPP frequency in dystrophic muscles at concentrations which had negligible effects on normal muscles. Dystrophic muscle preparations were also more sensitive to an increased extracellular calcium concentration. Usually, these manipulations had more effect on the nerve terminals of dystrophic slow muscle than on those of dystrophic fast muscle. We conclude that muscular dystrophy alters the nerve terminal's ability to regulate the concentration of intracellular free calcium ions.