bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postvaccinal parkinsonism
Authors: Alves Rosana S. C. , Barbosa Egberto R. , Scaff Milberto 
Published: December 2004

AbstractA 5‐year‐old boy, with a history of fever beginning 15 days after a vaccination for measles, developed a rigid‐akinetic syndrome 3 days after the fever began. A spinal tap obtained 1 week after the onset of fever showed pleocytosis with a monocellular pattern. A CT scan of the head and EEG did not disclose any abnormality. An MRI performed 3 months after the event, however, showed clear‐cut evidence of bilateral substantia nigra lesions, suggesting secondary gliosis. The response to levodopa was good, but adverse reactions appeared early. The child is now 7 years old. Bromocriptine, deprenyl, and levodopa have produced a remarkable improvement of the parkinsonian features.
Hemifacial spasm due to peripheral injury of facial nerve: A neuclear syndrome?
Authors: Martinelli P. , Giuliani S. , Ippoliti M. 
Published: December 2004

AbstractFour cases of hemifacial spasm (HFS) are reported. The spasm followed a few months after injury to a peripheral branch of the seventh nerve. An EMG examination of facial muscles disclosed the typical finding of HFS: spontaneous activity, paradoxical cocontraction, and diffusion of spontaneous or provoked blinking. A nuclear involvement, secondary to the nerve lesion, is the most likely pathophysiological explanation for similar cases of HFS.
Hemiballism and tremor due to ependymal cyst
Authors: Bejar Jose M. , Kepes John , Koller William C. 
Published: December 2004

AbstractA 21‐year‐old woman was admitted with right hemiballism and tremor. She had tremor since the age of 6 years. At age 12, an intracerebral, left paraventricular space‐occupying lesion was found and treated with 4,500 rads. Increasing tremor was associated with mass enlargement. By age 20, there was insidious presentation of right hemiballism. At age 21, she had craniotomy and a large septate cyst was opened and drained. Biopsy of the cyst wall revealed that it was consistent with ependymal cyst. Postoperatively the hemiballism resolved and the tremor improved. This case is unusual due to the presentation of hemiballism caused by ependymal cyst.
The possible role of iron in the etiopathology of parkinson's disease
Authors: Youdim M. B. H. , Ben‐Shachar D. , Riederer P. 
Published: December 2004

AbstractThe identification of 6‐ hydroxydopamine (6‐ OHDA) and N‐ methyl‐ 4‐ phenyl‐ 1, 2, 3, 6‐ tetrahydropyridine (MPTP) as dopaminergic neurotoxins that can induce parkinsonism in humans and animals has contributed to a better understanding of Parkinson's disease (PD). Although the involvement of similar neurotoxins has been implicated in PD, the etiology of the disease remains obscure. However, the recently described pathology of PD supports the view for a state of oxidative stress in the substantia nigra (SN), resulting as a consequence of the selective accumulation of iron in SN zone compacta and within the melanized dopamine neurons. Whether iron is directly involved cannot be ascertained. Nevertheless, the biochemical changes due to oxidative stress resulting from tisue iron overload (siderosis) are similar to those now being identified in parkinsonian SN. These include the reduction of mitochondrial electron transport, complex I and III activities, glutathione peroxidase activity, glutathione (GSH) ascorbate, calcium‐ binding protein, and superoxide dismutase and increase of basal lipid peroxidation and deposition of iron. The participation of iron‐ induced oxygen free radicals in the process of nigrostriatal dopamine neuron degeneration is strengthened by recent studies in which the neurotoxicity of 6‐ OHDA has been linked to the release of iron from its binding sites in ferritin. This is further supported by experiments with the prototypeiron chelator, desferrioxamine (Desferal), a free‐ radical inhibitor, which protects against 6‐ OHDA‐ induced lesions in the rat. Indeed, intranigral iron injection in rats produces a selective lesioning of dopamine neurons, resulting in a behavioral and biochemical parkinsonism.
Cocaine‐related movement disorders
Authors: Cardoso Francisco E. C. , Jankovic Joseph 
Published: December 2004

AbstractWe describe four patients, two with Tourette's syndrome, one with the combination of idiopathic dystonia and essential‐like tremor, and one with tardive dystonia, who noted marked exacerbation of their movement disorders after exposure to cocaine. These patients provide support for the hypothesis that dopaminergic preponderance plays an important role in the pathogenesis of certain hyperkinetic movement disorders. Cocaine should be regarded as an important cause or precipitant of hyperkinetic movement disorders.
Treatment of parkinson's disease with the partial dopamine agonist EMD 49980
Authors: Bravi Daniele , Davis Thomas L. , Mouradian M. Maral , Chase Thomas N. 
Published: December 2004

AbstractThe motor effects of the partial dopamine agonist EMD 49980 were evaluated in parkinsonian patients under controlled conditions. EMD 49980 monotherapy resulted in a mild improvement in parkinsonian symptoms, but when co‐administered with levodopa, had no significant effect on dyskinesias or on the antiparkinsonian effect of the dopamine precursor. These results suggest that EMD 49980 exerts a net weak dopamine agonist effect but fails to ameliorate levodopa‐induced dyskinesias.
Reflex blepharospasm associated with bilateral basal ganglia lesion
Authors: Larumbe R. , Vaamonde J. , Artieda J. , Zubieta J. L. , Obeso J. A. 
Published: December 2004

AbstractA patient with a bilateral striatal lesion secondary to anoxia presented reflex blepharospasm associated with parkinsonism and dystonia in the limbs. The blink reflex excitability curve was enhanced and the R‐2 response prolonged as in patients with essential blepharospasm. The findings in this patient support the notion that blepharospasm may be secondary to basal ganglia dysfunction through abnormal facilitation of reticular formation neurons controlling facial nucleus motoneuron excitability.
Stereotyped hand clasping: An unusual tardive movement disorder
Authors: Kaneko Kiyotoshi , Yuasa Tatsuhiko , Miyatake Tadashi , Tsuji Shoji 
Published: December 2004

AbstractWe report an 83‐year‐old woman with vascular parkinsonism who presented with stereotyped rhythmical hand‐clasping movements after 18 months exposure to neuroleptics. Although stereotypical rhythmical orolinguomasticatory and limb movements are the most common tardive dyskinesia in the elderly, we feel this woman's hand clasping represents another unusual expression of a tardive movement disorder.
Primary progressive freezing gait
Authors: Achiron A. , Ziv I. , Goren M. , Goldberg H. , Zoldan Y. , Sroka H. , Melamed E. 
Published: December 2004

AbstractFreezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi‐infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60−82 years; 74 ± 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 ± 1.9 years (range, 0.5−6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the “walking‐over‐lines” maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow‐up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings. We therefore conclude that primary progressive freezing gait should be recognized as a distinct neurological entity, unique in its clinical presentation and natural course. The lack of response to levodopa raises the possibility that nondopaminergic pathways might be involved.
Quantification of postural sway patterns in tardive dyskinesia
Authors: van Emmerik R. E. A. , Sprague R. L. , Newell K. M. 
Published: December 2004

AbstractAn assessment was made of the orientation and variability in postural center of pressure patterns in individuals with tardive dyskinesia (TD) and/or developmental disability during quiet standing. Postural patterns were compared and contrasted between four groups of individuals: those with (a) TD and developmentally disabled (severely and profoundly retarded); (b) developmental disability only; (c) TD but of normal intelligence; and (d) a healthy control group. The center of pressure displacements were derived from the lateral, vertical, and anterior‐posterior force and moment components of force platform measurements. Analyses demonstrated that individuals with TD in combination with developmental disability had a different center of pressure orientation and variability compared to healthy individuals and individuals suffering only from developmental disability or TD. The center of pressure pattern in the developmentally disabled TD group was characterized by a more prominent lateral orientation, whereas in the other three groups, it had a more predominant anterior‐posterior orientation. In addition, the variability in these orientation components was much smaller in the developmentally disabled TD group, indicating a more regular pattern of sway in the center of pressure during quiet standing in these individuals. These findings show that assessments of postural center of pressure profile orientation and variability may be useful indicators for investigating TD, especially in distinguishing between developmental disability and TD.
Persistent movement disorders induced by buspirone
Authors: Lewitt Peter A. , Walters Arthur , Hening Wayne , McHale Denise 
Published: December 2004

AbstractBuspirone, an azospirone compound, is a nonsedative anxiolytic that has achieved wide usage since its introduction in 1987. Although relatively free of side‐effects, there have been several instances of dyskinesia and dystonia associated with the use of buspirone. We report two patients with persistent movement disorders that developed after prolonged treatment with the drug. One patient developed a lasting problem of cervical–cranial dystonia and tremors after treatment with buspirone at a dosage of 40 mg/day for several weeks. Another, receiving 30 mg/day for 6 weeks, experinced an exacerbation of preexisting spasmodic torticollis and tardive dyskinesia as well as the onset of involuntary phonations. As shown by these and other examples, buspirone poses the risk for inducing or exacerbating several types of movement disorders.
Reversible striatal hypermetabolism in a case of sydenham's chorea
Authors: Goldman Serge , Amrom Dina , Szliwowski Henri B. , Detemmerman Dominique , Goldman Sylvie , Bidaut Luc M. , Stanus Etienne , Luxen André 
Published: December 2004

AbstractWe studied a 10‐year‐old girl with Sydenham's chorea (SC) using positron emission tomography (PET) with fluorodeoxyglucose (FDG). Choreic movements involved the head and the left side of her body. PET showed increased glucose metabolism in the right caudate nucleus and putamen. Three months after complete recovery, striatal glucose metabolism had returned to normal in the caudate nucleus. In the right putamen, glucose metabolism had decreased compared to that in the first study but remained elevated compared to that of normal young adults. We propose that the transient striatal hypermetabolism may have been due to increased afferent inputs to the striatum as a consequence of striatal or subthalamic nucleus dysfunction.
Cerebellar ataxia in ataxic hemiparesis? A kinematic and EMG analysis
Authors: Wild Barbara , Dichgans Johannes 
Published: December 2004

AbstractIt has recently been proposed that the ataxia in ataxic hemiparesis is a clumsiness common to all patients with hemiparesis and not indicative of any involvement of corticopontocerebellar or cerebellocortical pathways. In disagreement with this view, we report here that a patient with ataxic hemiparesis, following a lesion of the corona radiata, showed the disorders in kinematic and electromyographic (EMG) parameters of goal‐directed movements that have recently been demonstrated to be characteristic of patients with cerebellar lesions. This suggests involvement of corticopontocerebellar or cerebellocortical pathways in ataxic hemiparesis.
Proximal and distal reaction times (RTs) are not differentially affected in parkinson's disease
Authors: Schugens M. M. , Daum I. , Richter S. , Scholz E. , Canavan A. G. M. 
Published: December 2004

AbstractThe hypothesis was tested that proximal and distal reaction times (RTs) might be differentially affected in Parkinson's disease (PD). Twelve patients with PD were compared with 12 age‐matched healthy controls on tests of finger‐, hand‐, leg‐, and torso‐RTs. Patients were significantly slower in initiating all movements and were slower in executing all movements except for the leg (stepping) task. Choice‐ versus simple‐RTs were also not differentially affected in the PD group. In the healthy subjects, age was significantly positively correlated with response initiation times (RITs) but not with movement times (MTs).
Orobuccal dyskinesia associated with trihexyphenidyl therapy in a patient with parkinson's disease
Authors: Hauser Robert A. , Olanow C. W. 
Published: December 2004

AbstractDyskinesia is a common adverse effect complicating chronic dopaminergic therapy for Parkinson's disease. Movements are frequently choreic in nature and have been ascribed to overstimulation of “supersensitive” striatal postsynaptic dopamine receptors. Anticholinergic medications, despite some clinical efficacy in Parkinson's disease, have rarely been reported to cause dyskinesia. We report a patient with Parkinson's disease who developed orobuccal dyskinesia while being treated with trihexyphenidyl (Artane). Dyskinesia was observed following the introduction of trihexyphenidyl, resolved with its discontinuation, and reappeared with its reinstitution. Carbidopa‐levodopa (Sinemet) alone did not cause dyskinesia but augmented dyskinesia associated with trihexyphenidyl.
Levodopa‐induced dyskinesias in Parkinson's disease phenomenology and pathophysiology
Authors: Marconi Roberto , Lefebvre‐Caparros Dominique , Bonnet Anne‐Marie , Vidailhet Marie , Dubois Bruno , Agid Yves 
Published: December 2004

AbstractThe aim of this study was to provide further insight into the phenomenology and pathophysiology of monophasic and biphasic dyskinesias induced by levodopa in Parkinson's disease. For this purpose, the type, localization, severity, and timing of dyskinesias were evaluated in 15 parkinsonian patients in relation to motor disability after administration of levodopa using a video‐electromyographic recording device. Foot‐dystonia, myoclonus, and akathisia were observed in most patients. The dyskinesias started in the foot, usually on the side most affected by the disease, and spread in an “ascending wave” to the contralateral side, the trunk, and upper extremities. In a few patients, onset was axial, spreading almost instantaneously to all limbs. The dyskinesias were dystonic and ballistic at the start, and became increasingly choreic as they attained the upper limbs. Their intensity was maximal in the lower limbs, then progressively decreased, while increasing in upper limbs and head. The results indicate that there is no strict dichotomy between biphasic and monophasic dyskinesias. In other words, there is a “continuum” between the first dyskinesias and those observed during the period of maximal clinical improvement. These dyskinesias can also appear in reverse order, as if there were an “oscillator” determining a sequence of alternating patterns.
A multicenter double‐blind placebo‐controlled trial of pergolide as an adjunct to sinemet® in Parkinson's disease
Authors: Olanow C. W. , Fahn S. , Muenter M. , Klawans H. , Hurtig H. , Stern M. , Shoulson I. , Kurlan R. , Grimes J. D. , Jankovic J. , Hoehn M. , Markham C. H. , Duvisin R. , Reinmuth O. , Leonard H. A. , Ahlskog E. , Feldman R. , Hershey L. , Yahr M. D. 
Published: December 2004

AbstractThree hundred and seventy‐six subjects with advanced Parkinson's disease participated in a prospective, double‐blind placebo‐controlled study of the dopamine agonist pergolide mesylate as an adjunct to Sinemet®. At 6 months, patients randomized to pergolide had a statistically singnificant improvement in total Parkinson's score, scores of activities of daily living, motor function, number of “off” hours, Hoehn and Yahr stage, and numerous parameters of parkinsonian function including bradykinesia, rigidity, gait, and dexterity. This benefit was obtained with the addition of a mean dose of 2.94 mg of pergolide, which permitted a 24.7% reduction in dose of levodopa. Adverse reactions were, for the most part, mild, reversible, and not of major clinical significance. No significant cardiac or electrocardiographic abnormalities were detected. This study demonstrates that pergolide mesylate, as an adjunct to levodopa, is an effective antiparkinsonian agent that provides clinical improvement while permitting a reduction in levodopa dose.
Visual control of arm movement in Parkinson's disease
Authors: Klockgether Thomas , Dichgans Johannes 
Published: December 2004

AbstractPatients with Parkinson's disease (PD) are more dependent on visual information during movements than normals. To investigate the mechanisms underlying deterioration of movement under nonvisual conditions, we studied two‐dimensional pointing movements to randomly occurring targets. The experimental design allowed us to systematically manipulate visual feedback during the movement by removing vision of the target, of the moving hand, or of both. Execution of pointing movements in PD deviated most severely from that of normals when PD patients moved without vision of their own moving hand. Under this condition, undershooting of the target appeared, and movements were particularly slow. In contrast, with complete vision or when only vision of the target was occluded, pointing movements of PD patients were accurate and faster. PD patients had no difficulties selecting the correct movement direction. Reaction times were longer in PD patients irrespective of the availability of visual feedback. Our findings suggest that the ability of PD patients to use nonvisual feedback during execution of arm movements is impaired.
Variable onset of adult inherited focal dystonia: A problem for genetic studies
Authors: Micheli S. , Fernández‐Pardal M. , Quesada P. , Brannan T. , Obeso J. A. 
Published: December 2004

AbstractWe present two families with adult‐onset focal dystonias with marked variability in disease expression, discuss the clinical findings in relation to the literature, and comment on the difficulties in determining the pattern of inheritance.
N‐0923, a selective dopamine D2 receptor agonist, is efficacious in rat and monkey models of Parkinson's disease
Authors: Belluzzi J. D. , Domino E. F. , May J. M. , Bankiewicz K. S. , McAfee D. A. 
Published: December 2004

AbstractCertain aminotetralins are known to be potent dopamine D2 receptor agonists. N‐0923, [‐]2‐(N‐propyl‐N‐2‐thienylethylamino)‐5‐hydroxytetralin HCl, recognizes the high and low affinity states of the D2 receptor in membranes from bovine caudate with a Klow of 79 nM. The selectivity ratio is D2/D1 = 15 and D2/α2 = 1.4. N‐0923 also inhibits dopamine uptake and prolactin secretion, and it is an antagonist at the α2 receptor. N‐0923 (3–300 nmol/kg, s.c.) induced dose‐dependent contralateral turning behavior in rats with unilateral 6‐hydroxydopamine lesions of the substantia nigra. The ED50 of 30 nmol/kg was effective for 1 h. The positive enantiomer (N‐0924; 300 nmol/kg, s. c.) was without effect. A hemiparkinsonian syndrome was induced in four Macaca nemestrina monkeys by unilateral infusion of the neurotoxin MPTP into the right carotid artery. Video recordings of free‐moving behavior revealed bradykinesia, disuse of the contralateral upper limb and turning in a direction ipsilateral to the lesion. N‐0923 (3–300 nmol/kg, i.m.) induced contralateral turning behavior, exploratory activity, and contralateral limb usage. The ED50 for turning (30 nmol/kg) was effective for 0.5 h. The potency order for induction of contralateral rotations was (+)‐PHNON‐0923 > bromocriptine. N‐0924 (300 nmol/kg, i. m.) was ineffective. We conclude that N‐0923 may be useful as a therapeutic agent in the treatment of Parkinson's disease.
Withdrawal akathisia: Case reports and a proposed classification of chronic akathisia
Authors: Lang Anthony E. 
Published: December 2004

AbstractTwo patients with akathisia developing only after neuroleptic dosage reduction or withdrawal are described. The literature dealing with tardive or chronic akathisia is reviewed with an emphasis on the existence of variants including the occurrence of symptoms upon withdrawal of the causative drug. A classification of tardive or chronic akathisia syndrome is proposed.
Gait abnormality in essential tremor
Authors: Singer Carlos , Sanchez‐Ramos Juan , Weiner William J. 
Published: December 2004

AbstractEssential tremor (ET) has been described as a monosymptomatic disorder. In reports describing large series of patients with ET, there are rare patients who exhibit a noticeable gait disorder. However, we have observed that patients with ET and normal gait often exhibit an abnormality of tandem gait. To investigate this observation, we examined whether a gait disorder was present in 36 consecutive patients (mean age 69) with ET. We employed a tremor rating scale that scored tremor amplitude, location, and disability. In all patients, gait and tandem gait were separately evaluated. Eighteen of 36 patients (50%) exhibited tandem gait abnormalities in the presence of a normal narrow‐based gait compared to 11 of 40 age‐matched controls (28%) (p < 0.05). Abnormality of tandem gait was more frequently present in older ET patients and those with 5 years of disease duration. No relationship was found between presence of tandem gait abnormality and gender, tremor severity, head involvement, or positive family history. The finding of a tandem gait abnormality in 50% of ET patients suggests that cerebellar dysfunction may be important in its pathophysiology.