bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spinal myoclonus induced by an intrathecal catheter
Authors: Ford Blair , Pullman Seth L. , Khandji Alexander , Goodman Robert 
Published: May 2005

AbstractWe report a case of spinal myoclonus induced by the tip of an intrathecal catheter in a 35‐year‐old patient with severe, adult‐onset, generalized dystonia of unknown cause, treated for 2 years using intrathecal baclofen. One month after a falling episode, the patient developed focal myoclonus of the right proximal leg whenever she stood up from a seated position. The electrophysiologic recordings were compatible with spinal segmental myoclonus, originating at a focus corresponding to the L2‐S2 segments. At this site, the tip of the intrathecal catheter was demonstrated by myelography to be in close proximity to the nerve roots and conus medullaris. The myoclonus resolved promptly once the catheter tip was withdrawn. We review the literature on spinal myoclonus and discuss the possible mechanisms of spinal myoclonus pertaining to the present case. This report represents an unusual complication of intrathecal catheter systems that, if recognized, can lead to prompt therapeutic intervention.
Cortical myoclonus in huntington's disease associated with an enlarged somatosensory evoked potential
Authors: Caviness John N , Kurth Mathias 
Published: May 2005

AbstractWe report the electrophysiologic findings of myoclonus in a patient with Huntington's disease (HD). This patient was studied postoperatively after a bilateral fetal cell transplant in his striatum. Incomplete transient improvement was seen in the myoclonus, followed by gradual deterioration. The myoclonus itself had a cortical correlate and was associated with an enlarged somatosensory evoked potential (SEP), consistent with the presence of cortical reflex myoclonus. An enlarged SEP has not been previously reported in myoclonus associated with HD. The postulated mechanisms for myoclonus, when it occurs in HD, have differed in the literature. The reason for the transient improvement of the myoclonus following transplantation is unclear, but this case raises the possibility that basal ganglia circuits may modulate cortical myoclonic activity.
Spinal rigidity following acute myelitis
Authors: Brown Peter , Quinn Niall P. , Barnes David , Wren Damien R. , Marsden C. David 
Published: May 2005

AbstractA patient with a 2½‐year history of painful spasms and rigidity of both lower limbs is described. Symptoms began after an episode of acute myelitis. The spasms—which were spontaneous and stimulus sensitive and occurred on voluntary action—involved the repetitive grouped discharge of motor units. Continuous motor unit activity was present at rest in the muscles of both legs, and cutaneomuscular reflexes were abnormal. This patient is similar to those recently reported as having stiffness and spasms of the legs due to a possible chronic spinal interneuronitis and provides further evidence that this kind of movement disorder may be caused by spinal cord pathology.
Botulinum toxin a improves muscle spasms and rigidity in stiff‐person syndrome
Authors: Liguori Rocco , Cordivari Carla , Lugaresi Elio , Montagna Pasquale 
Published: May 2005

AbstractWe studied the effect of botulinum toxin A (BTA) on painful muscular spasms and rigidity in two bedridden patients with clinical, electrophysiologic, and immunologic evidence of stiff‐person syndrome. We injected BTA of saline solution into several limb muscles with both the rater and patient blinded to the order of the injections. A physician, unaware of the treatment order, used an objective rating scale for rigidity and spasm frequency scale and independently assessed the treatment results. BTA administration significantly reduced rigidity and stopped the spasms in all limbs. Following BTA injection on one side, the spasm frequency decreased bilaterally possibly because of the spread of hematogenous toxin.
The shaking palsy, the first forty‐five years: A Journey through the british literature
Authors: Louis Elan D. 
Published: May 2005

AbstractThe authors examined the British medical literature published in the 45‐year‐period following Parkinson's treatise on the shaking palsy to determine the number and type of references to the shaking palsy or paralysis agitans during this particular period. Several sources suggest that Parkinson's 1817 treatise on the shaking palsy received little immediate attention in his native country, England, and that not until 1861, in France, did Charcot began to elucidate the clinical features of this entity, separating it from other Neurologic disorders (for example, multiple sclerosis), A review of the British medical literature from the 45‐year‐period 1817–1861 revealed a number of references to paralysis agitans, including those by Cooke (1820), Good (1824 and 1829), Elliotson (1827, 1829, 1830, 1831, and 1833), Gowry (1831), anonymous (1832), Todd (1833), Watson (1836), Gibson (1839), Hall (1838 and 1841), Thompson (1842), Graves (1843), Birkett (1853), Paget (1855), and Reynolds (1855). Many of these did not report new or personally observed cases, did not separate Parkinson's disease from other disease entities characterized by both “shaking” and “palsy” (for example, tonic‐clonic seizures), or misattributed motor signs to dysfunction of the pyramidal system rather than an extrapyramidal system (that is, attributing bradykinesia or rigidity to weakness). Although there were several references to “shaking palsy” in the early‐ to mid‐19th‐century British medical literature, there were few original case reports of Parkinson's disease. This may have contributed to the fact that during this period little was added to the original observations made by Parkinson in 1817. In particular, the separation of bradykinesia and weakness did not become apparent until later work by the French.
Depression in classic versus akinetic‐rigid Parkinson's disease
Authors: Starkstein Sergio E. , Petracca Gustavo , Chemerinski Erán , Tesón Alejandra , Sabe Liliana , Merello Marcelo , Leiguarda Ramón 
Published: May 2005

AbstractWe examined the prevalence of major depression and dysthymia in 78 patients with the classic variant of Parkinson's disease (PD) (that is, tremor plus rigidity and/or bradykinesia), and in 34 patients with the akinetic‐rigid variant. Although the prevalence of dysthymia was similar in both groups (classic PD, 31%; and akinetic‐rigid PD, 32%), patients with akinetic‐rigid PD had a significantly higher prevalence of major depression (38% versus 15%, respectively; p < 0.01). A stepwise regression analysis demonstrated that bradykinesia was the extrapyramidal sign with the highest correlation with Hamilton depression scale scores. Our findings demonstrate a significant association between major depression and the akinetic‐rigid type of PD.
Action tremor and weakness in Parkinson's disease: A study of the elbow extensors
Authors: Brown Peter , Corcos Daniel M. , Rothwell John C. 
Published: May 2005

AbstractWe have previously shown that action tremor persists during maximal wrist extension in patients with Parkinson's disease, and that this contributes to weakness at this joint by preventing the fully fused contraction of the forearm extensor muscles. Antiparkinsonian medication reduces the action tremor in torque and electromyographic (EMG) records, thereby improving strengh at the wrist. In the present experiments, peak torque and action tremor were recorded during maximal extension of the elbow in nine patients with Parkinson's disease while they were on and off antiparkinsonian medication, and in eight age‐ and sex‐matched healthy subjects. Peak torque and mean rectified EMG levels were reduced by 34% and 36%, respectively, during maximal elbow extension when patients off medication were compared to those in the treated state. Action tremor was visible in torque records and had a frequency of ∼ 10 Hz both in parkinsonian patients and in normal controls. Activity of a similar frequency was often detected in EMG records, especially in patients off therapy. The absolute amplitude of action tremor in torque (Atorque) and EMG (AEMG) records from the elbow was unaffected by therapy and was little different from that recorded in healthy controls. The relative action tremor in torque ([Atorque/peak torque] × 100) and EMG ([AEMG/mean rectified EMG] × 100) was reduced by treatment, but this was the result of the increase in peak torque and mean rectified EMG. Thus, in contrast to the results at the wrist, antiparkinsonian medication has little effect on the 10‐Hz action tremor at the elbow. Increased strength is produced by a different mechanism which allows recruitment of triceps motor units outside of this synchronizing influence.
Cerebral hypoperfusion and hypometabolism with altered striatal signal intensity in chorea‐acanthocytosis: A combined PET and MRI study
Authors: Tanaka Makoto , Hirai Shunsku , Kondo Susumu , Sun Xiayan , Nakagawa Toshiyuki , Tanaka Satoshi , Hayashi Kunihiko , Okamoto Koichi 
Published: May 2005

AbstractWe studied cerebral perfusion and oxygen metabolism in three patients with chorea‐acanthocytosis using positron‐emission tomography and oxygen‐15 labeled O2 and CO2. High‐field magnetic resonance imaging also was performed. Regional cerebral blood flow (rCBF) and oxygen metabolism (rCMRO2) were significantly reduced in the caudate and putamen when compared with seven control subjects. Mild but significant reductions of rCBF (lower than the normal control values ‐2 SD) were found in the bilateral frontal, left temporal and parietal, and bilateral thalamic areas; rCMRO2 was reduced in the bilateral frontal and left temporal areas. Magnetic resonance imaging showed increased signal intensity accompanied by scattered bright spots in the caudate head and putamen on T2‐weighted images; decreased signal intensity was shown at these sites on T1‐weighted images. These findings were not observed in 10 neurologically normal volunteers and are rare in the common hyperkinetic form of Huntington's disease. Reduced cerebral perfusion and oxygen metabolism seem to be related to the intellectual and personality changes that occur in chorea‐acanthocytosis. Combined positronemission tomography and magnetic resonance imaging studies may improve diagnostic accuracy in patients with choreaacanthocytosis and related disorders.
Changes in perfusion pattern using ECD‐SPECT indicate frontal lobe and cerebellar involvement in exercise‐induced paroxysmal dystonia
Authors: Kluge Andreas , Kettner Beatrice , Zschenderlein Rolf , Sandrock Dirk , Munz Dieter L. , Hesse Stefan , Meierkord Hartmut 
Published: May 2005

AbstractThe clinical features of exercise‐induced paroxysmal dystonia (EPD) are delineated in a pedigree including two affected members (both male) showing an autosomal‐dominant inheritance trait. Gait analysis using kinematic electromyography during the motor attacks revealed coactivation of antagonistic calf muscles characteristic of dystonia. In the interval, impaired muscular alternation was observed. To characterize further the pathophysiological basis of the condition, ictal and interictal cerebral perfusion SPECT studies using technetium 99m‐ethyl cysteinate dimer (ECD) were performed to establish whether cortical hyperactivity indicative of epilepsy is present during the motor attacks and to identify regional changes in the ictal perfusion pattern that could indicate an anatomic structure relevant to the disease. During the motor attacks, decreased ictal perfusion of the frontal cortex was found in both patients. In contrast, increased cerebellar perfusion was observed. The perfusion of the basal ganglia also decreased. No cortical hyperfusion indicative of an epileptic nature was seen. Cerebellar hyperactivity in connection with prominent frontal hypoactivity has also been described in both the idiopathic and the symptomatic forms of dystonia. Our findings therefore suggest that EPD represents a paroxysmal movment disorder rather than epilepsy. It is concluded that changes in frontal and in cerebellar function are relevant to the pathophysiology of EPD.
Asymmetric predominantly ipsilateral blepharospasm and contralateral parkinsonism in an elderly patient with a right mesencephalic cyst
Authors: Singer Carlos , Schatz Norman J. , Bowen Brian , Eidelberg David , Kazumata Ken , Sternau Linda , Shulman Lisa M. , Weiner William J. 
Published: May 2005

AbstractA 66‐year‐old woman presented with a 3‐year history of predominantly right‐sided blepharospasm and a 1‐year history of progressive predominantly left‐sided hemiparkinsonism manifested by a left upper extremity resting tremor and left‐sided bradykinesia. Magnetic resonance imaging of the brain revealed a large right mesencephalic cyst with mass effect. Positron emission tomography revealed bilateral striatal hypometabolism consistent with nigrostriatal dopaminergic dysfunction. The association of predominantly ipsilateral blepharospasm and predominantly contralateral hemiparkinsonism is very rare, and its association with a posterior fossa space‐occupying lesion has been reported only once. This is the second report of such an association and the first description of adult‐onset symptomatology.
Reversible chorea in primary antiphospholipid syndrome
Authors: Sundén‐Cullberg Jonas , Tedroff Joakim , Aquilonius Sten‐Magnus 
Published: May 2005

AbstractA 20‐year‐old woman with acute chorea induced by primary antiphospholipid syndrome was studied by using fluorodeoxyglucose and positron emission tomography (PET). PET sessions were conducted during an episode of severe chorea and after recovery. The symptoms predominantly affected the right side of her face and body, and PET demonstrated a corresponding increase in lentiform and caudate nucleus metabolism prevailing on the left side. After recovery, PET showed normal values in the regions previously studied. This study adds further evidence to support the theory that acute choreas are somehow the result of striatal hypermetabolism.
Pretreatment and posttreament positron emission tomographic scan imaging in a 20‐year‐old patient with Wilson's disease
Authors: Cordato Dennis J. , Fulham Michael J. , Yiannikas Con 
Published: May 2005

AbstractWilson's disease is an autosomal‐recessive inherited diorder that results in predominantly hepatic and neurologic manifestations. Neurologic abnormalities include tremor, ataxia, bradykinesia, rigidity, chorea, and dystonia. We report the clinical, radiologic, and serial FDG PET findings in a 20‐year‐old woman who presented with an asymmetric upper limb tremor caused by Wilson's disease. Reduced striatal and cerebral cortical glucose metabolism was demonstrated on a FDG PET study performed before the commencement of D‐penicillamine therapy. After 6 months of treatment, the patient had shown only minimal clinical improvement, despite an increase in striatal and cerebral cortical glucose metabolism on a repeat FDG PET study. After 14 months of treatment, however, a moderate clinical improvement was noted and there was further increase in glucose metabolism on FDG PET.
De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset
Authors: Pearce Ronald K. B. , Banerji Tara , Jenner Peter , David Marsden C. 
Published: May 2005

AbstractIn contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.
Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine
Authors: Gassen Michael , Gross Aviva , Youdim Moussa B. H. 
Published: May 2005

AbstractA significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D1/D2‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H2O2 (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H2O2 toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off L‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.
Asymmetry of basal ganglia glucose metabolism and dopa responsiveness in parkinsonism
Authors: Dethy Sophie , Van Blercom Nadège , Damhaut Philippe , Wikler David , Hildebrand Jerzy , Goldman Serge 
Published: May 2005

AbstractWe investigated, by positron emission tomography (PET) with [18F]fluoro‐2‐deoxy‐d‐glucose (FDG) (FDG‐PET), brain glucose metabolism in 19 patients with parkinsonian features. We compared local pattern of FDG uptake and asymmetry indexes in patients with therapeutic response to levodopa (L‐dopa) (group 1, presumed Parkinson's disease, n = 9) and patients without L‐dopa therapeutic response (group 2, presumed striatonigral degeneration, n = 10). Limb dystonia was present in 11% of patients in group 1 and in 40% of patients in group 2. Asymmetry in basal ganglia metabolism was distributed differently in the two groups (analysis of variance, p < 0.04). In superior and inferior putamen, superior and middle caudate, ventral striatum, and inferior thalamus, relative reduction in metabolism on the side contralateral to predominant parkinsonian signs was associated with L‐dopa unresponsiveness. On the contrary, in middle caudate, ventral striatum, and inferior thalamus, a relative increase in metabolism on the side contralateral to the predominant side, parkinsonian signs were found in L‐dopa‐responsive patients. Our FDG‐PET study using simple statistical procedures demonstrates inverse asymmetry of basal ganglia glucose metabolism in parkinsonian patients grouped on the sole basis of L‐dopa responsiveness.
Increasing striatal iron content associated with normal aging
Authors: Wayne Martin W. R. , Ye Frank Q. , Allen Peter S. 
Published: May 2005

AbstractFree‐radical‐mediated mechanisms may contribute to neuronal damage in Parkinson's disease (PD), other neurodegenerative conditions also associated with aging, and the aging process itself. Cytotoxic free radicals are generated in the brain by oxidation/reduction reactions that are catalyzed by transition metals such as iron. Any regional increase in brain iron concentration may increase the potential for local freeradical formation. The purpose of this study was to determine the relationship between age and basal ganglia iron content in 20 normal individuals ranging from 24 to 79 years of age. We used an in vivo magnetic resonance method to quantify the effects of paramagnetic centers sequestered inside cellular membranes, thereby enabling the determination of a quantitative index of local brain iron content. We observed a strong direct relationship between age and regional iron content in the putamen (r = 0.76, p < 0.0001) and caudate (r = 0.69, p < 0.001), but not in the globus pallidus (r = 0.32, p = 0.17) or thalamus (r = 0.13, p = 0.58). In conclusion, striatal iron content increases with advancing age. This increase may increase the probability of free‐radical formation in the striatum, therefore representing a risk factor for the development of neurodegenerative disorders such as PD in which nigrostriatal neurons may be affected by increased oxidant stress.
The offset cortical potential: An electrical correlate of movement inhibition in man
Authors: Rothwell John C. , Higuchi Kazuo , Obeso Jose A. 
Published: May 2005

AbstractNine normal subjects were asked to make either a brisk isometric pinch of a force transducer held between the forefinger and thumb, or to hold a pinch for approximately 15 s and then release the force suddenly without any overt antagonist contraction. EEG activity was averaged about the onset or offset of EMG activity, and movements were made in the subjects' own time. All subjects found the task simple. The EEG activity preceding offset of contraction (offset cortical potential) was significantly smaller in lateral leads than that seen before onset of contraction. Midline activation was similar in both tasks. We suggest that in the onset task, motor cortex activity related to the act to be performed contributes substantially to the EEG potentials in lateral leads. This activity is absent in the offset task which requires only withdrawal of tonic input to motor cortex. Midline activity, common to both onset and offset tasks, could reflect timing, attentional, or other processes. The results are discussed in relation to previous data from an isotonic relaxation task1.
Clozapine use in Parkinson's disease: A retrospective analysis of a large multicentered clinical experience
Authors: Trosch Richard M. , Friedman Joseph H. , Lannon Meg C. , Pahwa Rajesh , Smith D. , Seeberger Lauren C. , O'Brien Christopher F. , Lewitt Peter A. , Koller William C. 
Published: May 2005

AbstractWe conducted a multicentered, retrospective review of clozapine's (CZP) effects on a range of psychiatric, sleep, cognitive, motor, and sensory disorders in Parkinson's disease (PD). Therapeutic outcomes and adverse events were compared with varying prescribing practices at participating sites. The medical records of 172 consecutive PD patients treated with CZP at four movement disorder clinics were reviewed. Low‐dose CZP improved psychiatric symptoms of psychosis, anxiety, depression, hypersexuality, sleep disturbance, and akathisia. Tremor, torticollis, limb dystonia, and pain showed modest rates of improvement. Twenty‐three percent of patients withdrew as a result of adverse events or treatment failure. Inpatient CZP initiation did not improve therapeutic efficacy, or reduce adverse events or the withdrawal rate. Low‐dose CZP in the outpatient setting is generally an effective and well‐tolerated treatment for many of the psychiatric, sleep, motor, and sensory disturbances common to late‐stage PD.