bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gait disorder of subcortical arteriosclerotic encephalopathy: Binswanger's disease
Authors: Thompson P. D. , Marsden C. D. 
Published: January 2005

AbstractThe abnormality of gait that may occur in patients with subcortical arteriosclerotic encephalopathy (Binswanger's disease) is described in 12 patients in whom difficulty walking was the presenting symptom. Their gaits had elements of both Parkinsonism and ataxia, which were most market in 4 patients unable to stand unaided. The difficulty in using their legs to walk was out of proportion to that of other movements of the lower limbs when lying or seated. In contrast, upper limb mobility and facial expression were relatively preserved. Attention is drawn to the similarity of this gait pattern to that of some patients with hydrocephalus, frontal lobe lesions, and “senile” disorders of gait. A possible mechanism for this Parkinsonian‐ataxia in these various conditions may be their propensity to damage the afferent and efferent interconnections of the leg areas of the motor and supplementary motor areas of the cerebral cortex with, the cerebellum and basal ganglia.
Antiparkinsonian activity of (+)‐PHNO in the MPTP‐treated common marmoset
Authors: Nomoto M. , Stahl S. , Jenner P. , Marsden C. D. 
Published: January 2005

AbstractAdministration of MPTP (1–4 mg/kg ip daily for 5–7 days) to common marmosets induced persistent parkinsonian motor deficts. The subcutaneous adminstration of (+)‐PHNO [(+)‐4‐propyl‐9‐hydroxynaphtoxazine; 1–4 μ/kg] caused a dose‐dependent reversal of the akinesia and incoordination of movement. Similarly, oral administration of (+)‐PHNO (5–20 μ/kg) caused an equivalent reversal of the motor abnormalities. No dyskinetic phenomena were induced by (+)‐PHNO on oral or subcutaneous administration. Oral or subcutaneous administration of (+)‐PHNO to normal control marmosets also increased the usual repetoire of motor behaviour, but this was not as marked as in MPTP‐treated animals. (+)‐PHNO is a potent dopamine agonist drug of potential use in the treatment of Parkinson's disease.
Antiparkinsonian activity of single oral dose of PHNO
Authors: Grandas F. , Quinn N. , Critchley P. , Rohan A. , Marsden C. D. , Stahl S. M. 
Published: January 2005

AbstractPHNO, a new D‐2 agonist, was investigated in five patients with Parkinson's disease. In an acute, open, oral, dose‐ranging study comparing benefit from single doses, 4 mg of PHNO was found to be equivalent to one tablet of Sinemet 25/250 mg. Adverse reactions were those anticipated for a dopaminomimetic agent. Because of its novel structure and apparent transcutaneous penetration, further studies on PHNO are desirable.
Neuroleptic malignant‐like syndrome induced by metoclopramide
Authors: Samie M. Reza 
Published: January 2005

AbstractA prompt recognition of neuroleptic malignant‐like syndrome is essential because of its high morbidity and mortality. A similar condition is described associated with metoclopramide, an agent with dopamine receptorblocking properties. An increased index of suspicion for early diagnosis of this condition and adjustment of metoclopramide dosing in patients with renal failure are emphasized.
Blepharospasm accompanying hypoxic encephalopathy
Authors: Palakurthy Prasad R. , Iyer Vasudeva 
Published: January 2005

AbstractSevere bilateral blepharospasm with left hemiplegia occurred in a 50‐year‐old woman, who developed cardiac arrest following ventricular aneurysmectomy. The blepharospasm was present constantly, even during sleep, and increased during attempts at voluntary eye opening. CT scan revealed multiple hypodense areas involving basal ganglia bilaterally and the right perisylvian area. The blepharospasm improved gradually over a 6‐month period, although the left hemiplegia remained unchanged.
PHNO, a novel dopamine agonist, in animal models of parkinsonism
Authors: Koller William , Herbster Gregory , Gordon John 
Published: January 2005

AbstractPHNO, a naphthoxazine compound, was investigated in animal models of central dopaminergic activity. The drug in doses of 5–300μg/kg when administered subcutaneously, or transdermally, induced stereotypic behavior in rats which was blocked by haloperidol but not by reserpine pretreatment. In rats with unilateral 6‐hydroxydopamine lesions of the substania nigra PHNO induced dose‐dependent contralateral turnings. The drug caused emesis in dogs and hypothermia in mice. PHNO bound to D‐2 dopamine receptors in the rat striatum. Chronic injection with PHNO did not induce behavioral super‐sensitivity of increase dopamine receptor density. These data indicate that PHNO is a direct acting dopamine agonist that is highly potent. PHNO differs from other dopaminergic drugs and may be useful in the treatment of Parkinson's disease.
A double‐blind evaluation of ciladopa in Parkinson's disease
Authors: Weiner William J. , Factor Stewart A. , Sanchez‐Ramos Juan , Berger Joseph 
Published: January 2005

AbstractWe evaluated 32 patients with Parkinson's disease in a double‐blind, parallel group, placebo‐controlled study with ciladopa (a troponylpiperazine derivative). The dosages administered were 5 mg b.i.d. and 15 mg b.i.d. Significant improvement was found in the gait scores and in the total disability scores in the high dose group (p<0.05). In addition, there was a trend toward improvement, though not significant, in the bradykinesia and rigidity scores in the high dose group and in the disability scores in the low dose group. Four patients in the low dose group and five patients in the high dose group decreased their Sinemet doses while no patients increased their Sinemet dose. There were no adverse effects observed in this study. These findings suggest that ciladopa may be an efficacious agent in Parkinson's disease. The low incidence of adverse effects with this agent suggests that higher doses may be utilized and may prove to be more effective.
Levodopa‐induced regional cerebral blood flow changes in normal volunteers and patients with Parkinson's disease
Authors: Montastruc J. L. , Celsis P. , Agniel A. , Demonet J. F. , Doyon B. , Puel M. , Marc‐Vergnes J. P. , Rascol A. 
Published: January 2005

AbstractSingle photon emission computed tomography was used to measure regional cerebral blood flow in six normal subjects and 12 patients with Parkinson's disease, before and after acute oral administration of levodopa. The drug induced a significant increase in cerebral blood flow both in controls and patients. Before levodopa, there was no significant difference between the groups, either in flow values or in their pattern. The clinical effects of levodopa were not related to the hemodynamic changes. The results suggest that measuring the flow response to levodopa is not appropriate to demonstrate variations in central dopaminergic receptor sensitivity in man.
The effect of intracerebroventricular infusion of (+)‐4‐propyl‐9‐hydroxynapthoxacine (PHNO) through a totally implanted drug delivery system in rats with dopamine deficiency
Authors: de Yebenes Justo G. , Fahn Stanley , Jackson‐Lewis Vernice , Mena Maria Angeles 
Published: January 2005

AbstractRats with experimentally induced DA deficiency were trated with intracerebroventricular administration of (+)‐4‐propyl‐9‐hydroxynaphthoxacine (PHNO) through a totally implanted chronic delivery system which delivered PHNO, 0.9μg/h, continuously for up to 2 weeks. Rats with 6‐OH‐DA induced unilateral nigrostriatal lesion showed, after PHNO infusion, a potent and persistent contralateral turning behavior (8–11 turns/min) which was not present in vehicle‐infused animals. The intensity of spontaneous and apomorphine‐induced rotation did not decrease after 2 weeks of continuous infusion, suggesting that tolerance to PHNO or to other dopamine agonists did not develop. The magnitude of the spontaneous turning behavior in PHNO‐infused animals correlated well with the baseline response to apomorphine (r = 0.505, p < 0.025). Rats implanted with pumps delivering PHNO or vehicle were treated with reserpine, 0.5 mg/kg/day for 14 days. Vehicle‐infused, reserpinized animals had a severe akinesia and weight loss during the experimental period (motor activity, measured in counts per minute was reduced to 5–10% of baseline levels, and body weight to 50% of baseline levels). PHNO‐infusion partially restored activity to 60% of baseline counts and reduced the severity of weight loss. PHNO effects were observed for as long as the infusion was maintained. No side effects were observed. Intracerebroventricular infusion of PHNO may be an alternative experimental approach to untreatable motor fluctutations in Parkinson's disease.
Torticollis following radiation therapy
Authors: Landan Ivan , Cullis Paul A. 
Published: January 2005

AbstractA patient with adenocarcinoma in the apical portion of the lung producing a Pancoast's syndrome developed torticollis a few months after receiving a course of radiation therapy (5,040 rad) to his upper chest and neck. We describe this case, in which local radiation fibrosis of the neck muscles and perhaps segmental demyelination of the 11th cranial nerve resulted in peripheral nervous system lesion causing torticollis.
The effect of carbidopa on plasma and muscle levels of L‐dopa, dopamine, and their metabolites following L‐dopa administration to rats
Authors: Rose S. , Jenner P. , Marsden C. D. 
Published: January 2005

AbstractAdministration of L‐dopa (L, 4‐dihydroxyphenylalanine) (200mg/kg p.o.) to rats produced elevated plasma and muscle concentrations of both L‐dopa and 3‐O‐methyldopa (3‐OMD). This effect was potentiated by simultaneous administration of carbidopa (25 mg/kg p.o.) both L‐dopa and 3‐OMD accumulated in muscle after administration of L‐dopa with or without carbidopa. Elevated dopamine levels were detected in both muscle and plasma after treatment with L‐dopa alone. Concurrent administration of carbidopa only diminished dopamine levels in plasma, and the duration of raised dopamine levels in muscle was increased. Carbidopa administration had no effect on the elevated plasma concentrations of 3,4‐dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) caused by L‐dopa administration. In muscle, carbidopa treatment tended to prolong the duration of raised metabolite levels. Muscle appears to accumulate L‐dopa at a site where decarboxylation is not totally prevented by concurrent carbidopa administration, and where dopamine is not degraded as actively as in other tissues. The muscle sink for L‐dopa may influence the plasma profile of the amino acid, which has implications for the therapeutic response to L‐dopa in Parkinson's disease.
Chorea and dystonia: A remote effect of carcinoma
Authors: Albin Roger L. , Bromberg Mark B. , Penney John B. , Knapp Robert 
Published: January 2005

AbstractA 45‐year‐old women with an acquired multifocal neurologic syndrome, including chorea, dystonia, cerebellar dysfunction, multiple cranial neuropathies, and pure sensory neuropathy, was found at autopsy to have oat cell carcinoma. Neuropathologic examination revealed serveral features typically associated with remote effects of malignancy on the nervous system. We believe that this is the first described case of chorea as a remote effect of malignancy.
Decrease of serotonin‐S2 receptors in temporal cortex of patients with Parkinson's disease and progressive supranuclear palsy
Authors: Maloteaux J. M. , Laterre E. C. , Laduron P. M. , Javoy‐Agid F. , Agid Y. 
Published: January 2005

AbstractThe number of serotonin‐S2 receptors was decreased in the temporal cortex of patients with Parkinson's disease and progressive supranuclear palsy (PSP). There was no significant modification of these receptors in the frontal cortex or in the hippocampus and putamne in both diseases. The decrease in mumber of receptors in PSP was unexpected, because the cerebral cortex is thought to be spared in this disease. There was no correlation between the decrease in number of serotonin‐S2 receptors and the degree of dementia in Parkinson's disease, suggesting that these receptors are not directly involved in the deterioration of cognitive functions.
Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington's chorea
Authors: Agostino R. , Berardelli A. , Cruccu G. , Pauletti G. , Stocchi F. , Manfredi M. 
Published: January 2005

AbstractBlink and corneal reflexes were studied in 11 patients with Huntington's chorea and the results compared with the severity of the disease. The latency of the R2 component of the blink reflex was delayed and the duration of R2 and of the corneal reflex (CR) prolonged. A greater habituation of the R2 component was found in the patients with involuntary movements in the face, and in some patients a long‐lasting depression of R2 was present. A correlation was found between: (a) severity of involuntary face movements and R2 and CR latency and (b) severity of involuntary movements in the neck and latency of R2.
Comparison between L‐Dopa and lisuride intravenous infusions: A clinical study
Authors: Ruggieri Stefano , Stocchi Fabrizio , Carta Angelico , Bravi Daniele , Bragoni Maura , Giorgi Luigi , Agnoli Alessandro 
Published: January 2005

AbstractL‐Dopa is still the most effective drug for the treatment of Parkinson's Disease, but after 5 years or more of therapy fluctuations in motor performance and abnormal involuntary movements commonly appear. Continuous intravenous infusions of L‐Dopa abolish or strikingly reduce such fluctuations. Unfortunately, this is not suitable for daily treatment because of the low solubility of L‐Dopa. Lisuride is a potent dopamine agonist and is very soluble in water. In this study the clinical effects of L‐Dopa and lisuride continuous intravenous infusions were compared in a group of 20 fluctuating parkinsonian patients L‐Dopa controlled fluctuations in almost all the subjects, whereas only seven patients were continuously mobile while taking lisuride. Another seven patients showed a fluctuating response and the remaining six did not satisfactorily respond to lisuride. Dyskinesias were present in all patients during “on” phases, with both levodopa and lisuride treatment.
Dopamine and memory function in Parkinson's disease
Authors: Mohr Erich , Fabbrini Giovanni , Williams Jill , Schlegel Jerry , Cox Christiane , Fedio Paul , Chase Thomas N. 
Published: January 2005

AbstractResponse fluctuations in motor function, complicating long‐term dopaminomimetic therapy of Parkinson's disease, may extend to the cognitive realm. To evaluate the effect of levodopa treatment both on attention as well as acquisition and retrieval of memory tasks, parkinsonian patients were examined neuropsychologically both while medicated with levodopa/carbidopa (“on”) and when the medication's antiparkinsonian effect had worn off (“off”). Significant cognitive differences emerged only on the delayed recall of complex verbal materials, where patients when “on” performed better compared with their “off” state. Comparison of change scores across states (administration or withholding of levodopa/carbidopa between acquisition and retrieval, “off” to “on” to “off”), revealed no substantial differences as a function of dopaminomimetic therapy. These results support the view that slight changes in cognition are associated with dopaminomimetic therapy of Parkinson's disease, but that these changes may be task‐specific.
Volitional control of involuntary movements
Authors: Koller William C. , Biary Nabil M. 
Published: January 2005

AbstractVoluntary suppressibility of abnormal movements is helpful in the classification of movement disorders because this ability appears to be a common component of tics. However, there has been no systematic study of voluntary suppressibility in other movement disorders. We have therefore assessed 146 patients with tremors and dyskinetic disorders as to their ability to suppress movements by mental concentration. Patients were videotaped while trying to stop their movements, and the length of time they could suppress their abnormal movements was recorded. One hundred percent (10 of 10) of patients with tics could suppress movements for an average of 2.5 min. Two percent (1 of 50) of essential tremor patients could suppress the tremor, and the tremor of 24% (12 of 50) was made worse by mental concentration. Eighty percent (4 of 5) of neuroleptic‐induced tremor could be improved mentally. Seventy percent (35 of 50) of patients with parkinsonian tremor could voluntarily diminish their tremor for an average of 48 s. Fifty percent (8 of 16) of chorea (tardive dyskinesia, Huntington's disease, postencephalitic) was reduced. Dystonia was suppressible in 20% (3 of 15). It is concluded that movement disorders besides tics can be voluntarily suppressed and that suppressibility should not be used to classify movement disorders. Tics, however, are easier to suppress and can be suppressed for a longer time.
CQP 201‐403 in Parkinson's disease: An open‐label pilot study
Authors: Pfeiffer Ronald F. , Herrera Leonel H. , Glaeske Carolyn S. , Hofman Ruth E. 
Published: January 2005

AbstractThe dopamine agonist, CQP 201–403, was administered to 10 patients in an open label fashion with rapid dosage escalation during hospitalization. Assessed over an average of 20 days, significant improvement occurred in bradykinesia, rigidity, and postural instability. Tremor did not occur in sufficient frequency in this group of patients to be accurately assessed. The most serious adverse effect encountered was prolonged confusion with psychosis. This study suggests that CQP 201‐403 may be of value in the treatment of Parkinson's disease.
Induction of chorea and dystonia in parkinsonian primates
Authors: Boyce S. , Clarke C. E. , Luquin R. , Peggs D. , Robertson R. G. , Mitchell I. J. , Sambrook M. A. , Crossman A. R. 
Published: January 2005

AbstractAdministration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine in primates induced a parkinsonian syndrome that could be reversed by levodopa treatment. Animals quickly developed an apparent restlessness (“akathisia”) of the lower limbs after as little as five doses. After 4–10 weeks of regular levodopa therapy, animals developed “peak dose” choreiform movements in the lower limbs that spread, with time, to involve the upper limbs and orofacial musculature. With further treatment (5–21 months), animals developed “peak dose” dystonia that variably involved the limbs and orofacial musculature. These conditions represent novel models of levodopa‐induced chorea and dystonia in humans. They depend on the same underlying neuropathology and treatment regimen as their human counterparts. It is to be anticipated that these models of dyskinesia will be useful in determining the mechanisms underlying chorea and dystonia in humans and are ideally suited for experimental evaluation of new treatment strategies.
Neural mechanisms of dystonia: Evidence from a 2‐deoxyglucose uptake study in a primate model of dopamine agonist‐induced dystonia
Authors: Mitchell I. J. , Luquin R. , Boyce S. , Clarke C. E. , Robertson R. G. , Sambrook M. A. , Crossman A. R. 
Published: January 2005

AbstractThe neural mechanisms that mediate dystonia were investigated in a novel experimental primate model of dopamine agonist‐induced dystonia. This condition was produced by long‐term (15 months) dopamine agonist therapy of a macaque monkey that had been rendered hemiparkinsonian by unilateral infusion of 1–methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine into the right common carotid artery. The 2–deoxyglucose (2–DG) metabolic mapping technique was applied to the animal during the expression of active unilateral dystonia, and regional brain uptake of 2–DG was assessed autoradiographically. The results demonstrate that dystonia is associated with marked increases in 2–DG uptake in the constituent nuclei of the basal ganglia (caudate nucleus, putamen, medial and lateral segments of the globus pallidus) and in the subthalamic nucleus, but decreased uptake in the structures that receive output of the basal ganglia (ventral anterior/ventral lateral thalamic complex and lateral habenula). Based on these findings it is suggested that dystonia is characterized by increased activity in the putaminopallidal and pallidosubthalamic pathways, and decreased activity in the subthalamopallidal and pallidothalamic pathways.
Cortical mechanisms mediating asterixis
Authors: Artieda J. , Muruzabal J. , Larumbe R. , de Casasola C. García , Obeso José A. 
Published: January 2005

AbstractWe describe a patient with chronic renal failure who suffered multifocal action‐induced jerks. Electromyography (EMG) recorded the typical silence of asterixis. Back‐averaging the EEG activity preceding the EMG silent periods in the forearm showed a biphasic wave antedating the asterixis by 23 ms. Somatosensory evoked potentials (SEPs) after median nerve stimulation were pathologically enlarged on both hemispheres. Brain‐mapping of the biphasic wave preceding asterixis and the giant SEPs indicated a common origin in the sensorimotor cortex. This observation provides further documentation of a cortical origin for some types of asterixis in humans.
Choreoathetosis in acquired immune deficiency syndrome patients with cerebral toxoplasmosis
Authors: Maggi P. , de Mari M. , De Blasi R. , Arminise S. , Romanelli C. , Andreula C. , Zimatore G. , Angarano G. 
Published: January 2005

AbstractThe aim of our study was to evaluate both the incidence and the pathologic and clinical features of extrapyramidal disorders in a population of acquired immune deficiency syndrome (AIDS) patients with cerebral toxoplasmosis. Of 240 AIDS patients evaluated in the 1985–1994 period, 50 of them were diagnosed to have cerebral toxoplasmosis on the basis of the following criteria: occurrence of specific antibodies, computed tomography and/or magnetic resonance imaging (MRI), and regression of the symptoms after specific therapy. Three of 50 (6%) had hemichoreoathetosis. In the first case, the disorder began as a dyskinesia of the left hand that subsequently spread to the whole ipsilateral arm and assumed the features of choretic athetotic movements. The other two cases were characterized by left hemisomatic distal choreic movements. Therapy with pyrimethamine and sulfadiazine led to a complete recovery of the extrapyramidal signs in two cases and to improvement in the third. According to our observations, the onset of these movement disorders could not be related to the dimension of the lesion or to the edema, but to a specific localization in subthalamic nucleus, in subthalamic/pallidal, and pallidal/thalamic pathways. MRI seems the elective tool to perform a more accurate study of the anatomic areas involved in this pathway and to verify their integrity. Cerebral toxoplasmosis in AIDS can be considered as a new etiopathogenic cause of choreoathetosis.
Adult‐onset acid maltase deficiency: A postmortem study
Authors: Dimauro Salvatore , Stern Lawrence Z. , Mehler Mark , Nagle Raymond B. , Payne Claire 
Published: January 2005

AbstractIn a postmortem study of a patient with adult‐onset acid maltase deficiency (AMD), morphological abnormalities were confined to skeletal muscle and consisted of a vacuolar myopathy. Acid maltase activity, however, was approximately 6% of normal in muscle, liver, and brain, and 3% of normal in heart. Kinetic characteristics, and inhibition by antibodies and Zn++, showed that the residual activity was “authentic” acid maltase. Neutral maltase activity was normal in muscle and liver, but decreased in brain (55% of normal) and heart (19% of normal). Although the relative decrease of acid maltase was similar in different tissues, absolute residual activity was lowest in skeletal muscle: this may explain the selective involvement of this tissue in late‐onset AMD.