Postoperative parkinsonian tremor in a patient with a frontal meningioma.
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Female↗
Biomedical subjects
W Poewe
Publications and source records attributed to W Poewe.
Interference of rhythmic constraint on gait in healthy subjects and patients with early Parkinson's disease: evidence for impaired locomotor pattern generation in early Parkinson's disease.
Patients in the early stages of Parkinson's disease have been shown to walk slower with smaller steps, resembling the gait of normal elderly subjects, but specific disorders of dynamic equilibrium or rhythmic gait patterning have not yet been identified. In the present study, gait control in 22 healthy subjects and 22 patients with early Parkinson's disease was challenged by means of a paradigm requiring subjects to decrease their step rate (cadence) by 20% in response to a metronome signal (rhythmic constraint). Control subjects and patients were matched for age, sex, and body height. Eleven patients were receiving standard antiparkinsonian therapy and were assessed under their ongoing medication, whereas the remaining 11 patients had not yet been started on dopaminergic therapy ("de novo" Parkinson's disease). Gait parameters reflecting dynamic equilibrium (double-support time) and locomotor patterning (step length, stride duration) were recorded by means of a mechanical device (locometer). Sixteen patients and 16 control subjects were able to accomplish the task. Whereas regulation of step length became irregular during rhythmic constraint in both patients and control subjects, irregular timing of steps was only observed in patients suggesting disturbance of periodic locomotor activity generation.
Aged↗
Worsening of motor performance in patients with Parkinson's disease following transdermal nicotine administration.
Nicotine has been reported to have positive effects on motor performance in patients with Parkinson's disease. In this study, motor performance was evaluated in 16 patients with idiopathic Parkinson's disease during a practical off-period using the motor part of the Unified Parkinson's Disease Rating Scale after 12 hours' exposure to a transdermal patch containing 35 mg nicotine or placebo. The study was performed using a double-blind crossover design. In contrast to previous reports, nicotine exposure was followed by a worsening of symptoms compared with placebo. A negative response to subthreshold dopaminergic stimulation, resulting from an inhibitory effect of low striatal dopamine concentrations acting on a subset of dopamine receptors, might possibly account for this finding.
Administration, Cutaneous↗
Levodopa in the treatment of Parkinson's disease: a consensus meeting.
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Animals↗
Progression of falls in postmortem-confirmed parkinsonian disorders.
Although falls are known to occur in several parkinsonian disorders, such as Parkinson's disease (PD), multiple system atrophy (MSA), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP), differences in the evolution of this feature have not been studied systematically in pathologically confirmed cases. Seventy-seven cases with pathologically confirmed parkinsonian disorders (PD: n = 11, MSA: n = 15, DLB: n = 14, CBD: n = 13, PSP: n = 24), collected up to 1994, formed the basis for a multicenter clinicopathologic study organized by the National Institute of Neurological Disorders and Stroke to improve differential diagnosis of parkinsonian disorders. In the present study, we determined the time course, that is, the duration from first symptom to onset (latency) and duration from onset to death, of recurrent falls. Furthermore, we analyzed the diagnostic validity of a predefined latency to onset of recurrent falls within 1 year of symptom onset. Significant group differences for latency, but not duration, of recurrent falls were observed. Latencies to onset of falls were short in PSP patients, intermediate in MSA, DLB, and CBD, and long in PD. Recurrent falls occurring within the first year after disease onset predicted PSP in 68% of the patients. Our study demonstrates for the first time that latency to onset, but not duration, of recurrent falls differentiates PD from other parkinsonian disorders. Whereas early falls are important for the diagnosis of PSP, the addition of other features increases its diagnostic predictive value.
Accidental Falls↗
Trick maneuvers in cervical dystonia: investigation of movement- and touch-related changes in polymyographic activity.
Antagonistic gestures or trick maneuvers are well-known clinical features to reduce or abolish dystonic posturing in cervical dystonia (CD). The maneuvers typically consist of a finger touch to the facial skin but their physiology remains unknown. To determine the temporal profile of geste maneuver performance, 25 patients with idiopathic CD were studied by means of polymyography of six cervical muscles prior to any botulinum toxin treatment. Two piezoelectric elements fixed to a fingertip of the hand involved in the trick maneuver and to the facial target region, respectively, were used to relate the essential points of the trick maneuver time course (start of geste-arm movement, facial contact, end of contact, end of movement) to changes in polymyographic activity. Thirteen patients (52%) showed marked reductions of electromyographic (EMG) activity (> or =50% in at least one muscle) during arm movement, definitely prior to contact between fingers and facial target area; in the remaining 12 patients (48%), geste-related EMG effects were confined to facial-finger contact. These results might indicate different physiological mechanisms in clinically indistinguishable antagonistic gestures.
Adult↗
Neural transplantation in animal models of multiple system atrophy: a review.
Multiple system atrophy of the striatonigral degeneration (MSA-SND) type is increasingly recognized as major cause of neurodegenerative parkinsonism. Due to combined degeneration of substantia nigra pars compacta (SNC) and of striatum, antiparkinsonian therapy based on levodopa substitution eventually fails in more than 90% of patients. Animal models of MSA-SND are urgently required as test-bed for the evaluation of novel therapeutic interventions in this disorder such as neurotrophic factor delivery and neuronal transplantation. A number of well established rodent and primate models of Parkinson's (PD) and Huntington's (HD) disease replicate either nigral ("PD-like") or striatal ("HD-like") pathology and may therefore provide a useful baseline for the development of MSA-SND models. Previous attempts to mimick MSA-SND pathology in rodents have included sequential injections of 6-hydroxydopamine (6OHDA) and quinolinic acid (QA) into medial forebrain bundle and ipsilateral striatum, respectively ("double toxin-double lesion" approach). Preliminary evidence in rodents subjected to such lesions indicates that embryonic transplantation may partially reverse behavioural abnormalities. Intrastriatal injections of mitochondrial toxins such as 3-nitropropionic acid (3NP) and 1-methyl-4-phenylpyridinium (MPP+) in rodents result in (secondary) excitotoxic striatal lesions and subtotal neuronal degeneration of ipsilateral SNC, thus producing MSA-SND-like pathology by a simplified "single toxin-double lesion" approach. Comparative studies of human SND pathology and rodent striatonigral lesions are required in order to determine the rodent model(s) most closely mimicking the human disease process.
Animals↗
Validation of a mail questionnaire for parkinsonism in two languages (German and Italian).
As part of a larger epidemiological study [Neuro-Epidemiology Project South-Tyrol (NEPT)], we investigated the accuracy of a mail questionnaire for parkinsonism in two languages (German and Italian). We administered the instrument to 40 randomly selected subjects with parkinsonism (Italian-speaking, n = 20; German-speaking, n = 20), attending our Parkinson's disease clinic regularly. Each patient was matched by age, sex and language with a subject without parkinsonism residing in the same South-Tyrol Province in Northern Italy. Subjects free of parkinsonism were recruited randomly from two group practices collaborating in the NEPT study. A questionnaire containing nine symptom questions and two additional questions about the patient's diagnosis of parkinsonism and/or treatment was mailed to each subject's home. Forty subjects with parkinsonism and 36 without parkinsonism participated in the study. All nine symptom items showed significant differences between affected and unaffected individuals. A combination of any three questions yielded the best balance between sensitivity (95%) and specificity (89%). There were no differences between the German- and Italian-speaking groups. We demonstrated the usefulness of a simple questionnaire for validating the diagnosis of parkinsonism irrespective of the primary native language.
Adult↗
Reversible severe myopathy of respiratory muscles due to adult-onset type III glycogenosis.
Subacute severe myopathy of the respiratory muscles developed in a 47-year-old woman after a 3-week period of strict fasting. Histological and biochemical work-up of muscle biopsy specimens permitted the diagnosis of debrancher deficiency. The course of the disease was characterized by subacute respiratory failure and prolonged mechanical ventilation. After initiation of a high-protein diet the patient was successfully weaned from the respirator and recovered well. To our knowledge this is the first reported case of adult-onset debrancher deficiency myopathy presenting with subacute respiratory failure and responding to high-protein diet.
Age of Onset↗
Dopamine D4 receptor polymorphism and idiopathic Parkinson's disease.
Patients with idiopathic Parkinson's disease (IPD) are described as having markedly decreased novelty seeking characteristics. Since recent publications suggest an association between the dopamine D4 receptor polymorphism and novelty seeking, we investigated this polymorphism in a group of 122 patients with IPD and 127 healthy control subjects. We found similar allele and genotype frequencies in both groups and no association with the age of onset of symptoms. Therefore, the dopamine D4 receptor polymorphism does not confer genetic susceptibility to IPD and cannot explain the decreased novelty seeking in IPD patients.
Aged↗
Increased expression of apolipoprotein D following experimental traumatic brain injury.
Increasing evidence suggests that apolipoprotein D (apoD) could play a major role in mediating neuronal degeneration and regeneration in the CNS and the PNS. To investigate further the temporal pattern of apoD expression after experimental traumatic brain injury in the rat, male Sprague-Dawley rats were subjected to unilateral cortical impact injury. The animals were killed and examined for apoD mRNA and protein expression and for immunohistological analysis at intervals from 15 min to 14 days after injury. Increased apoD mRNA and protein levels were seen in the cortex and hippocampus ipsilateral to the injury site from 48 h to 14 days after the trauma. Immunohistological investigation demonstrated a differential pattern of apoD expression in the cortex and hippocampus, respectively: Increased apoD immunoreactivity in glial cells was detected from 2 to 3 days after the injury in cortex and hippocampus. In contrast, increased expression of apoD was seen in cortical and hippocampal neurons at later time points following impact injury. Concurrent histopathological examination using hematoxylin and eosin demonstrated dark, shrunken neurons in the cortex ipsilateral to the injury site. In contrast, no evidence of cell death was observed in the hippocampus ipsilateral to the injury site up to 14 days after the trauma. No evidence of increased apoD mRNA or protein expression or neuronal pathology by hematoxylin and eosin staining was detected in the contralateral cortex and hippocampus. Our results reveal induction of apoD expression in the cortex and hippocampus following traumatic brain injury in the rat. Our data also suggest that increased apoD expression may play an important role in cortical neuronal degeneration after brain injury in vivo. However, increased expression of apoD in the hippocampus may not necessarily be indicative of neuronal death.
Animals↗
Botulinum toxin A in the management of spastic gait disorders in children and young adults with cerebral palsy: a randomized, double-blind study of "high-dose" versus "low-dose" treatment.
The present study was performed to assess dose-response relationships of local botulinum toxin A (BtxA) treatment in children and teenagers with spastic gait due to cerebral palsy (CP) in a randomized, double-blind study employing a "high-dose" (200 units Botox per leg) and a "low-dose" (100 units Botox per leg) treatment arm in 33 patients with CP. Response parameters included changes in muscle tone assessed by the Ashworth scale at knee joint, range-of-motion (ROM) measurements at knee and ankle joint, objective analysis of longitudinal gait parameters as well as subjective assessments of improvement. Patients in the "high-dose" arm received 40-80 units Botox/muscle versus 20-40 units Botox/muscle in the "low-dose" group. Patients in both treatment arms showed significant improvement of Ashworth score (p<0.001) and ROM (p<0.01), while gait analysis revealed significant increase in gait velocity (p<0.01) and stride-length (p<0.001) over baseline. Subjects in the "high-dose" group showed significantly greater improvement on objective response measurements compared to "low-dose" patients. Also, children aged 7 years or less had greater functional benefit compared to the subgroup of patients older than 7 years. Incidence and severity of side-effects were similar in both treatment groups. The present study demonstrated dose-dependent functional improvement of dynamic deformities and spastic gait pattern in children and young adults with CP treated with local injections of botulinum toxin. A dose of 200 units Botox per leg distributed to 4 or 5 muscle bellies per leg is superior compared to 100 units Botox per leg without significantly affecting the risk of side-effects.
Adolescent↗
Antibodies against the myelin oligodendrocyte glycoprotein and the myelin basic protein in multiple sclerosis and other neurological diseases: a comparative study.
In experimental animal models of multiple sclerosis demyelinating antibody responses are directed against the myelin oligodendrocyte glycoprotein (MOG). We have investigated whether a similar antibody response is also present in multiple sclerosis patients. Using the recombinant human extracellular immunoglobulin domain of MOG (MOG-Ig) we have screened the sera and CSFs of 130 multiple sclerosis patients, 32 patients with other inflammatory neurological diseases (OIND), 30 patients with other non-inflammatory neurological diseases (ONND) and 10 patients with rheumatoid arthritis. We report that 38% of multiple sclerosis patients are seropositive for IgG antibodies to MOG-Ig compared with 28% seropositive for anti-myelin basic protein (MBP). In contrast, OIND are characterized by similar frequencies of serum IgG antibody responses to MOG-Ig (53%) and MBP (47%), whereas serum IgG responses to MOG-Ig are rare in ONND (3%) and rheumatoid arthritis (10%). Anti-MBP IgG antibodies, however, are a frequent finding in ONND (23%) and rheumatoid arthritis (60%). Our results provide clear evidence that anti-MOG-Ig antibodies are common in CNS inflammation. However, in OIND these antibody responses are transient, whereas they persist in multiple sclerosis. We demonstrate that the serum anti-MOG-Ig response is already established in early multiple sclerosis (multiple sclerosis-R0; 36%). In later multiple sclerosis stages frequencies and titres are comparable with early multiple sclerosis. In contrast, the frequency of anti-MBP antibodies is low in multiple sclerosis-R0 (12%) and increases during disease progression in relapsing-remitting (32%) and chronic progressive multiple sclerosis (40%), thus suggesting that anti-MBP responses accumulate over time. Finally we provide evidence for intrathecal synthesis of IgG antibodies to MOG-Ig in multiple sclerosis.
Adult↗
Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy.
Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.
Adult↗
Recent advances in the drug treatment of Parkinson's disease.
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Catechol O-Methyltransferase Inhibitors↗
Time course of symptomatic orthostatic hypotension and urinary incontinence in patients with postmortem confirmed parkinsonian syndromes: a clinicopathological study.
OBJECTIVE: Although both orthostatic hypotension and urinary incontinence have been reported in a number of parkinsonian syndromes, such as Parkinson's disease (PD), multiple system atrophy (MSA), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP), differences in the evolution of these features have not been studied systematically in pathologically confirmed cases. METHODS: 77 cases with pathologically confirmed parkinsonian syndromes (PD, n=11; MSA, n=15; DLB, n=14; CBD, n=13; PSP, n=24), collected up to 1994, formed the basis for a multicentre clinicopathological study organised by the NINDS to improve the differential diagnosis of parkinsonian disorders. The present study determined the time course-that is, latency to onset and duration from onset to death, of symptomatic orthostatic hypotension, and urinary incontinence in the NINDS series. Furthermore, the diagnostic validity of a predefined latency to onset within 1 year of disease onset of symptomatic orthostatic hypotension or urinary incontinence was analysed. RESULTS: Significant group differences for latency, but not duration, of symptomatic orthostatic hypotension and urinary incontinence were found. Latencies to onset of either feature were short in patients with MSA, intermediate in patients with DLB, CBD, and PSP, and long in those with PD. Symptomatic orthostatic hypotension occurring within the first year after disease onset predicted MSA in 75% of cases; early urinary incontinence was less predictive for MSA (56%). CONCLUSION: Latency to onset, but not duration, of symptomatic orthostatic hypotension or urinary incontinence differentiates PD from other parkinsonian syndromes, particularly MSA.
Age of Onset↗
Disturbances of dynamic balance in phasic cervical dystonia.
OBJECTIVE: To quantitatively assess control of balance under static and dynamic conditions in patients with tonic and phasic cervical dystonia. METHODS: Ten patients with purely tonic cervical dystonia with fixed postural deviation and 20 patients with cervical dystonia with phasic head movements were investigated at least 3 months after botulinum toxin injections. Seventeen age matched volunteers served as controls. Static posturography was performed on a force platform; dynamic equilibrium was studied on a stabilometer, which requires the subject to continuously adapt upright posture to an unstable tilting surface. Measurements of maximum amplitude and linear displacement of the pivot were taken with open and closed eyes. RESULTS: Sway path values in static posturography were not significantly different between patients with cervical dystonia and controls. On dynamic posturography, patients with phasic cervical dystonia showed significantly higher platform measures (maximum amplitude and linear displacement of the pivot) with eyes open and closed By contrast, none of the dynamic platform measures differed significantly between patients with tonic cervical dystonia and controls. CONCLUSIONS: Normal measures of dynamic equilibrium in tonic cervical dystonia argue against a primary abnormality of balance control in cervical dystonia. Impaired dynamic equilibrium in phasic cervical dystonia is likely to reflect a disruption of vestibular input due to repetitive, involuntary head oscillations.
Adult↗
Depression in Parkinson's disease: impediments to recognition and treatment options.
By some estimates, nearly half of patients with PD also suffer depression. Because features of PD frequently overlap with typical manifestations of major affective disorder (or mild dysthymia), both diagnosis and treatment of this comorbidity are challenging. Some of these interactive features include cognitive and speech deficits and impairments in emotional expression (e.g., PD-related facial masking) or processing. Parkinsonian depression probably is caused by an independent abnormality rather than as a maladaptive response to disease, in that the degree of depression is not correlated with PD severity. Prognostically, depressive features (e.g., introversion, inflexibility) may represent a subtle premorbid state heralding the onset of PD or an accelerated cognitive decline thereafter. Therapeutic mainstays for parkinsonian depression include psychosocial counseling at the time of PD diagnosis (and during advanced stages of PD) as well as appropriate medication regimens, the relative clinical efficacy of which remain a matter of ongoing clinical inquiry: levodopa, dopamine agonists, selegilene, tricyclic antidepressants, and selective serotonin reuptake inhibitors). This review formulates a rational treatment algorithm to assist in clinical management of parkinsonian depression, an enormously complex clinical entity.
Depressive Disorder↗