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Idiopathic Parkinson's Disease (idiopathic + parkinson's_disease)

Distribution by Scientific Domains

Medical Sciences	94%
2 Other Domains	6%

Selected Abstracts

Differences in age at onset and familial aggregation between clinical types of idiopathic Parkinson's disease

MOVEMENT DISORDERS, Issue 9 2004
Alexei Korchounov MD
Abstract Idiopathic Parkinson's disease (PD) can be subdivided by its patterns of motor symptoms into tremor-dominant (TDT), akinetic-rigid (ART), and mixed type (MT). Our objective was to determine whether age at onset and family history are different in these three types. In total, 366 patients with PD were assigned in a standardized approach to one of the three subtypes. Age at onset and family history were obtained in all patients and all presumably affected family members were examined. Mean ages at disease onset were similar in all three groups, but distribution of age at onset was markedly different: monophasic in TDT with a peak around 60 years, biphasic in ART with two peaks, one in the middle of the sixth decade (earlier onset, ART-EO), another during the first half of the seventh decade (later onset, ART-LO), and increasing with age only in MT patients A positive family history was significantly associated only with TDT (odds ratio = 5.7) and ART-EO (odds ratio = 7.8), but not with MT or ART-LO patients. Segregation analysis suggested an autosomal recessive mode of transmission in ART-EO and an autosomal dominant mode of transmission in TDT. © 2004 Movement Disorder Society [source]

Major and minor depression in Parkinson's disease: a neuropsychological investigation

EUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2006
A. Costa
Previous studies have failed to distinguish the differential contribution of major and minor depression to cognitive impairment in patients with idiopathic Parkinson's disease (PD). This study was aimed at investigating the relationships among major depression (MD), minor depression (MiD) and neuropsychological deficits in PD. Eighty-three patients suffering from PD participated in the study. MD and MiD were diagnosed by means of a structured interview (SCID-I) based on the DSM-IV criteria, and severity of depression was evaluated by the Beck Depression Inventory. For the neuropsychological assessment, we used standardized scales that measure verbal and visual episodic memory, working memory, executive functions, abstract reasoning and visual-spatial and language abilities. MD patients performed worse than PD patients without depression on two long-term verbal episodic memory tasks, on an abstract reasoning task and on three measures of executive functioning. The MiD patients' performances on the same tests fell between those of the other two groups of PD patients but did not show significant differences. Our results indicate that MD in PD is associated with a qualitatively specific neuropsychological profile that may be related to an alteration of prefrontal and limbic cortical areas. Moreover, the same data suggest that in these patients MiD and MD may represent a gradual continuum associated with increasing cognitive deficits. [source]

The importance of educational and psychological factors in Parkinson's disease quality of life

EUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2002
E. Cubo
Objective: ,To define the factors correlated with quality of life (QoL) in patients with idiopathic Parkinson's disease (PD). Background: PD has a substantial impact on QoL. Although several clinical factors have been associated with QoL in PD, the influence of patient's education still remains controversial. Methodology: ,A consecutive series of patients with PD were examined using the unified Parkinson's Disease Rating Scale (UPDRS part I, II, III), Schwab and England (SE), and Hoehn and Yahr stage (H&Y). QoL was rated with the PDQ-39, cognition with the Mini-Mental State examination (MMSE), and the presence of depressive symptoms with the geriatric depression scale (GDS). Patient's characteristics, estimated cumulative levodopa dose (CLD), UPDRS, H&Y, MMSE and GDS were correlated with the PDQ-39 using univariate and multiple regression analysis. Results: ,A total of one hundred 58 patients (68 men, 90 women) with a mean age of 65.6 ± 9.3 years, PD duration of 8.1 ± 10.6 years, and education of 6.6 ± 3.9 years were included. The mean PDQ-39 was 48.8 ± 27.8, mean MMSE was 25.7 ± 4, and mean GDS was 11.7 ± 6.8. Using stepwise multiple regression analysis, the most important predictive factors were depression, UPDRS part I, UPDRS part II, and educational background, which accounted for a 61% of the variability of the PDQ-39 scores. Conclusions: ,In our PD sample, educational, behavioural, and psychological factors influenced life satisfaction more than physical ones. [source]

A two-fold difference in the age-adjusted prevalences of Parkinson's disease between the island of Als and the Faroe Islands

EUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2000
L. Wermuth
With the aim of comparing the previously found high prevalence of idiopathic Parkinson's disease (PD) in the Faroe Islands with the prevalence of PD in an area of Denmark, we used the same case-finding methods for case ascertainment and the same strict criteria to diagnose PD on the island of Als. During the last year before the prevalence date (1 January 1998), we found in various registries from pharmacies, hospital, private neurologist and general practioners 121 patients with suspected Parkinsonism out of 56 839 inhabitants on the island of Als. After exclusion of those who had other diseases, a total of 79 patients were left for further examinations. Among these we found 58 with PD. The overall prevalence of PD was estimated to be 102.0 and the age-adjusted prevalence to be 98.3 per 100 000 persons compared with 187.6 and 209.0 in the Faroe Islands. Compared with the previous results from the Faroe Islands (prevalence date 1 July 1995) we found an even lower mean age at onset of PD symptoms and at onset of treatment, a lower proportion of definite PD and a lower average dose of levodopa. We therefore conclude that the two-fold higher prevalence in the Faroe Islands than on the island of Als was not due to an early diagnosis and a higher ascertainment of cases with mild PD, which was suggested as being one possible explanation for our previous finding of a high prevalence of PD in the Faroe Islands. [source]

PGE2 receptor EP1 renders dopaminergic neurons selectively vulnerable to low-level oxidative stress and direct PGE2 neurotoxicity

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 14 2007
Emilce Carrasco
Abstract Oxidative stress and increased cyclooxygenase-2 (COX-2) activity are both implicated in the loss of dopaminergic neurons from the substantia nigra (SN) in idiopathic Parkinson's disease (PD). Prostaglandin E2 (PGE2) is one of the key products of COX-2 activity and PGE2 production is increased in PD. However, little is known about its role in the selective death of dopaminergic neurons. Previously, we showed that oxidative stress evoked by low concentrations of 6-hydroxydopamine (6-OHDA) was selective for dopaminergic neurons in culture and fully dependent on COX-2 activity. We postulated that this loss was mediated by PGE2 acting through its receptors, EP1, EP2, EP3, and EP4. Using double-label immunohistochemistry for specific EP receptors and tyrosine hydroxylase (TH), we identified EP1 and EP2 receptors on dopaminergic neurons in rat SN. EP2 receptors were also found in non-dopaminergic neurons of this nucleus, as were EP3 receptors, whereas the EP4 receptor was absent. PGE2, 16-phenyl tetranor PGE2 (a stable synthetic analogue), and 17-phenyl trinor PGE2 (an EP1 receptor,selective agonist) were significantly toxic to dopaminergic cells at nanomolar concentrations; EP2- and EP3-selective agonists were not. We challenged dopaminergic neurons in embryonic rat mesencephalic primary neuronal cultures and tested whether these receptors mediate selective 6-OHDA toxicity. The nonselective EP1,3 receptor antagonist AH-6809 and two selective EP1 antagonists, SC-19220 and SC-51089, completely prevented the 40%,50% loss of dopaminergic neurons caused by exposure to 5 ,M 6-OHDA. Together, these results strongly implicate PGE2 activation of EP1 receptors as a mediator of selective toxicity in this model of dopaminergic cell loss. © 2007 Wiley-Liss, Inc. [source]

Differentiating vascular parkinsonism from idiopathic Parkinson's disease: A systematic review,,

MOVEMENT DISORDERS, Issue 2 2010
Seema Kalra MRCP
Abstract Vascular parkinsonism (VP) remains a loose constellation of various clinical features. We systematically reviewed studies comparing clinical, neuroimaging and other investigations that might distinguish VP from idiopathic Parkinson's disease (PD). Medline, Embase, Cinahl (R), and PsycINFO were searched by querying appropriate key words. Reports were included if the study population contained comparative findings between patients with VP and PD. Twenty-five articles fulfilled the selection criteria. Patients with VP were older, with a shorter duration of illness, presented with symmetrical gait difficulties, were less responsive to levodopa, and were more prone to postural instability, falls, and dementia. Pyramidal signs, pseudobulbar palsy, and incontinence were more common in VP. Tremor was not a main feature of VP. Structural neuroimaging was more likely to be abnormal in VP (90,100% of cases) than in PD (12,43% of cases), but there was no specific abnormal structural imaging pattern for VP. Two studies of presynaptic striatal dopamine transporters (using single photon emission computed tomography) showed a significant reduction in striatal uptake ratios in PD but not in VP, whereas another study found that only the mean asymmetry index was significantly lower in VP. Various other investigations, including alternative imaging techniques, electrophysiological, and neuropsychological studies, are reported, but the diverse diagnostic criteria used makes it difficult to reach any firm conclusions. The development of accepted international diagnostic criteria for VP is urgently needed to facilitate further studies. © 2010 Movement Disorder Society [source]

Hereditary parkinsonism: Parkinson disease look-alikes,An algorithm for clinicians to "PARK" genes and beyond,,

MOVEMENT DISORDERS, Issue 14 2009
Christine Klein MD
Abstract In the past decade, a number of genetic causes of parkinsonism have been identified. As a consequence, clinicians have to consider an increasing range of differential diagnoses when confronted with a patient with parkinsonism with a positive family history. While well-established monogenic forms with PARK acronyms have been reviewed extensively, less emphasis has been placed on other inherited conditions that may also present with signs of parkinsonism or even mimic idiopathic Parkinson's disease clinically. In this review, we focus on three different scenarios in patients with an overall early age of onset of parkinsonism: (i) atypical features in patients with mutations in one of the "PARK" genes; (ii) classical parkinsonism due to mutations in "other than-PARK" genes or yet other genes where parkinsonism may be a well-recognized, concomitant, or even an isolated feature; (iii) atypical parkinsonism in other genetic disorders which are, however, typically characterized by features other than parkinsonism. Atypical features in patients from Group I include, for example, a slower disease course (PARK2, PARK6, PARK7) or dementia (PARK1/4, PARK14). Conditions in Group II have been designated by a DYT or SCA acronym (for example, DYT5 or SCA3) and also include patients with heterozygous GBA mutations, mitochondrial gene mutations. Group III comprises mutations in the FMR1, MAPT, GRN, ATP7B, PANK2, FBXO7, CHAC, FTL1, Huntingtin, JPH3 genes, and a number of even rarer, miscellaneous conditions. © 2009 Movement Disorder Society [source]

Restless legs syndrome, rapid eye movement sleep behavior disorder, and hypersomnia in patients with two parkin mutations,

MOVEMENT DISORDERS, Issue 13 2009
Nadège Limousin MD
Abstract Parkin gene mutations cause a juvenile parkinsonism. Patients with these mutations may commonly exhibit REM sleep behaviour disorders, but other sleep problems (insomnia, sleepiness, restless legs syndrome) have not been studied. The aim of this study was to evaluate the sleep-wake phenotype in patients with two parkin mutations, compared with patients with idiopathic Parkinson's disease (iPD). Sleep interview and overnight video-polysomnography, followed by multiple sleep latency tests, were assessed in 11 consecutive patients with two parkin mutations (aged 35,60 years, from seven families) and 11 sex-matched patients with iPD (aged 51,65 years). Sleep complaints in the parkin group included insomnia (73% patients versus 45% in the iPD group), restless legs syndrome (45%, versus none in the iPD group, P = 0.04), and daytime sleepiness (45%, versus 54% in the iPD group). Of the parkin patients, 45% had REM sleep without atonia, but only 9% had a definite REM sleep behavior disorder. All sleep measures were similar in the parkin and iPD groups. Two parkin siblings had a central hypersomnia, characterized by mean daytime sleep latencies of 3 min, no sleep onset REM periods, and normal nighttime sleep. Although the patients with two parkin mutations were young, their sleep phenotype paralleled the clinical and polygraphic sleep recording abnormalities reported in iPD, except that restless legs syndrome was more prevalent and secondary narcolepsy was absent. © 2007 Movement Disorder Society [source]

Levodopa affects functional brain networks in parkinsonian resting tremor,

MOVEMENT DISORDERS, Issue 1 2009
Bettina Pollok PhD
Abstract Resting tremor in idiopathic Parkinson's disease (PD) is associated with an oscillatory network comprising cortical as well as subcortical brain areas. To shed light on the effect of levodopa on these network interactions, we investigated 10 patients with tremor-dominant PD and reanalyzed data in 11 healthy volunteers mimicking PD resting tremor. To this end, we recorded surface electromyograms of forearm muscles and neuromagnetic activity using a 122-channel whole-head magnetometer (MEG). Measurements were performed after overnight withdrawal of levodopa (OFF) and 30 min after oral application of fast-acting levodopa (ON). During OFF, patients showed the typical antagonistic resting tremor. Using the analysis tool Dynamic Imaging of Coherent Sources, we identified the oscillatory network associated with tremor comprising contralateral primary sensorimotor cortex (S1/M1), supplementary motor area (SMA), contralateral premotor cortex (PMC), thalamus, secondary somatosensory cortex (S2), posterior parietal cortex (PPC), and ipsilateral cerebellum oscillating at 8 to 10 Hz. After intake of levodopa, we found a significant decrease of cerebro-cerebral coupling between thalamus and motor cortical areas. Similarly, in healthy controls mimicking resting tremor, we found a significant decrease of functional interaction within a thalamus,premotor,motor network during rest. However, in patients with PD, decrease of functional interaction between thalamus and PMC was significantly stronger when compared with healthy controls. These data support the hypothesis that (1) in patients with PD the basal ganglia and motor cortical structures become more closely entrained and (2) levodopa is associated with normalization of the functional interaction between thalamus and motor cortical areas. © 2008 Movement Disorder Society [source]

Participation of the subthalamic nucleus in executive functions: An intracerebral recording study

MOVEMENT DISORDERS, Issue 4 2008
Marek Balá
Abstract The objective of our work was to find whether the subthalamic nucleus (STN) is directly involved in cognitive activities, specifically in executive functions. Ten patients with idiopathic Parkinson's disease had P3 potentials recorded by externalized deep brain electrodes that were implanted in the STN or in its immediate vicinity. Two contacts of each electrode were positioned inside the STN according to clinical effect, perioperative microrecording, and stimulation. The P3 waves were recorded following the auditory stimulus in a standard oddball paradigm. They were compared with the P3 waves elicited from a protocol modified by a dual task with an increased demand on executive functions. The P3 potentials with a steep amplitude gradient evoked by the modified protocol were detected by the contacts in 8 of the 14 available electrodes, located either inside the STN or in its immediate vicinity. The modified protocol led to an increased latency of the P3 potential in 8 of 14 electrodes. No local field potentials of the standard P3 potentials were recorded. The P3 potentials related to the increased demand on executive functions were detected by the STN contacts known to have the best effect on Parkinsonian motor signs. This could suggest that the STN takes part in the executive function processing. © 2007 Movement Disorder Society [source]

Olfactory loss may be a first sign of idiopathic Parkinson's disease

MOVEMENT DISORDERS, Issue 6 2007
Antje Haehner MD
Abstract Recent studies support the idea of olfactory dysfunction as a very early sign of idiopathic Parkinson's disease (IPD). Aim of the present study was to clinically follow-up patients with idiopathic hyposmia to find out the percentage of patients developing IPD after 4 years time. At baseline, olfactory tests had been combined with transcranial sonography of the substantia nigra and 123I-FP-CIT SPECT imaging. At the present neurological examination, 7% of the individuals with idiopathic hyposmia had developed clinical IPD. Altogether, 13% presented with abnormalities of the motor system. Our data suggest that a combination of olfactory testing and other tests may constitute a screening tool for the risk to develop IPD. © 2007 Movement Disorder Society [source]

Parkinson's disease due to the R1441G mutation in Dardarin: A founder effect in the basques

MOVEMENT DISORDERS, Issue 11 2006
Javier Simón-Sánchez BSc
Abstract The recent discovery of mutations in Dardarin (LRRK2) have been related to the appearance of Parkinson's disease in several families. Notably, one single mutation in this gene (R1441G) not only appeared in familial, but also in apparently sporadic Parkinson disease (PD) patients of Basque descent. A clinical population was ascertained, and subjects were classified into Basque and non-Basque descent according to their known ancestry. The R1441G mutation was assayed using an allele-specific polymerase chain reaction, and several single nucleotide polymorphisms surrounding this mutation were analyzed by direct sequencing. In addition to 22 members of the original Basque families where R1441G was identified, we observed 17 carriers of the mutation who were apparently related through a common ancestor. From a clinical perspective, the disease observed in mutation carriers is indistinguishable from that in noncarriers. The R1441G mutation causes a form of Parkinson's disease that is equivalent to that observed in idiopathic Parkinson's disease. This mutation appears in 16.4% and 4.0% of familial and sporadic PD in this Basque population, respectively. © 2006 Movement Disorder Society [source]

Pyramidal tract imaging in multiple-system atrophy

MOVEMENT DISORDERS, Issue 11 2005
Nicole Limberg MBBS
Abstract A new radiological finding of T2 FLAIR hyperintensities in the pyramidal tracts is described in a patient clinically thought to have idiopathic Parkinson's disease but histologically proven to have multiple-system atrophy. © 2005 Movement Disorder Society [source]

Emergency hospital admissions in idiopathic Parkinson's disease

MOVEMENT DISORDERS, Issue 9 2005
Henry Woodford BSc
Abstract Little is known about the hospital inpatient care of patients with idiopathic Parkinson's disease (PD). Here, we describe the features of the emergency hospital admissions of a geographically defined population of PD patients over a 4-year period. Patients with PD were identified from a database for a Parkinson's disease service in a district general hospital with a drainage population of approximately 180,000. All admissions of this patient subgroup to local hospitals were found from the computer administration system. Two clinicians experienced in both general medicine and PD then reviewed the notes to identify reasons for admission. Admission sources and discharge destinations were recorded. Data regarding non-PD patients was compared to PD patients on the same elderly care ward over the same time period. The total number of patients exposed to analysis was 367. There was a total exposure of 775.8 years and a mean duration of 2.11 years per patient. There were 246 emergency admissions to the hospital with a total duration of stay of 4,257 days (mean, 17.3 days). These days were accounted for by 129 patients (mean age, 78 years; 48% male). PD was first diagnosed during 12 (4.9%) of the admissions. The most common reasons for admission were as follows: falls (n = 44, 14%), pneumonia (n = 37, 11%), urinary tract infection (n = 28, 9%), reduced mobility (n = 27, 8%), psychiatric (n = 26, 8%), angina (n = 21, 6%), heart failure (n = 20, 6%), fracture (n = 14, 4%), orthostatic hypotension (n = 13, 4%), surgical (n = 13, 4%), upper gastrointestinal bleed (n = 10, 3%), stroke/transient ischemic attack (n = 8, 2%), and myocardial infarction (n = 7, 2%). The mean length of stay for the PD patients on the care of elderly ward specializing in PD care was 21.3 days compared to 17.8 days for non-PD patients. After hospital admission, there was a reduction in those who returned to their own home from 179 to 163 and there was an increase in those requiring nursing home care from 37 to 52. Infections, cardiovascular diseases, falls, reduced mobility, and psychiatric complications accounted for the majority of admissions. By better understanding the way people with PD use hospital services, we may improve quality of care and perhaps prevent some inpatient stays and care-home placements. © 2005 Movement Disorder Society [source]

Chronic bilateral subthalamic deep brain stimulation in a patient with homozygous deletion in the Parkin gene

MOVEMENT DISORDERS, Issue 12 2004
Marianna Capecci MD
Abstract Chronic subthalamic nucleus deep brain stimulation (STN-DBS) is an efficacious treatment for idiopathic Parkinson's disease (PD) that cannot be further improved by medical therapy. We present a case of an individual with juvenile parkinsonism caused by homozygous deletion of exon 3 in the parkin gene with disabling long-term side-effects from levodopa who underwent bilateral STN neuromodulation. Parkin-linked parkinsonism may show clinical features different from sporadic PD, yet it shares levodopa responsiveness. Because levodopa responsiveness is a predictor of STN-DBS efficacy, we argued that this kind of surgical approach might be efficacious in hereditary parkin-linked juvenile parkinsonism. We evaluated clinical and functional assessment before and 12 months after surgery. The results showed that the Unified Parkinson Disease Rating Scales Motor score improved by 84% in our patient, the levodopa equivalent daily dose medication (LEDD) was reduced by 66%, and, finally, disabling and severe dyskinesias disappeared. © 2004 Movement Disorder Society [source]

Differences in age at onset and familial aggregation between clinical types of idiopathic Parkinson's disease

Diagnostic considerations in juvenile parkinsonism

MOVEMENT DISORDERS, Issue 2 2004
Dominic C. Paviour MRCP
Abstract Juvenile parkinsonism (JP) describes patients in whom the clinical features of parkinsonism manifest before 21 years of age. Many reported cases that had a good response to levodopa have proved to have autosomal recessive juvenile parkinsonism (AR-JP) due to mutations in the parkin gene. With the exception of parkin mutations and dopa-responsive dystonia, most causes are associated with the presence of additional neurological signs, resulting from additional lesions outside of the basal ganglia. Lewy body pathology has only been reported in one case, suggesting that a juvenile form of idiopathic Parkinson's disease may be extremely rare. © 2003 Movement Disorder Society [source]

Role of dopamine transporter imaging in routine clinical practice

MOVEMENT DISORDERS, Issue 12 2003
Vicky Marshall MRCP
Abstract Functional imaging of the dopamine transporter (DAT) defines integrity of the dopaminergic system and has its main clinical application in patients with mild, incomplete, or uncertain parkinsonism. Imaging with specific single positron emission computerised tomography ligands for DAT (FP-CIT, ,-CIT, IPT, TRODAT) provides a marker for presynaptic neuronal degeneration. Striatal uptake correlates with disease severity, in particular bradykinesia and rigidity, and monitoring of progression assists in clinical trials of potential neuroprotective drugs. DAT imaging is abnormal in idiopathic Parkinson's disease, multiple system atrophy and progressive supranuclear palsy and does not distinguish between these disorders. Dopamine loss is seen even in the earliest clinical presentations of true parkinsonism; a normal scan suggests an alternative diagnosis such as essential tremor, vascular parkinsonism (unless there is focal basal ganglia infarction), drug-induced parkinsonism, or psychogenic parkinsonism. Congruence between working clinical diagnosis and DAT imaging increases over time in favour of baseline DAT imaging results. Additional applications are characterising dementia with parkinsonian features (abnormal results in dementia with Lewy bodies, normal in Alzheimer's disease); and differentiating juvenile-onset Parkinson's disease (abnormal DAT) from dopa-responsive dystonia (normal DAT). © 2003 Movement Disorder Society [source]

Paroxysmal exercise-induced dystonia as a presenting feature of young-onset Parkinson's disease

MOVEMENT DISORDERS, Issue 12 2003
Maria Bozi MD
Abstract Paroxysmal exercise-induced dystonia (PED) is a rare, typically idiopathic familial condition, although sporadic and secondary cases have been reported. We present 2 cases where PED was the presenting feature of young-onset idiopathic Parkinson's disease (PD), preceding the onset of parkinsonian symptoms by 1.5 and 5 years, respectively. Initially, the dystonic symptoms occurred after prolonged exercise and were unilateral, affecting the foot in both patients. Over time, symptoms occurred with minimal exercise. We conclude that PED can rarely be the first and only feature of PD. © 2003 Movement Disorder Society [source]

Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease

MOVEMENT DISORDERS, Issue 9 2003
Paul S. Fitzmaurice PhD
Abstract The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [,30%], PSP [,21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [,20%]). GSH levels were normal in all examined normal and degenerating extra-nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (,19 to ,30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD. © 2003 Movement Disorder Society [source]

Olfaction in neurodegenerative disorder

MOVEMENT DISORDERS, Issue 4 2003
Christopher Hawkes MD
Abstract There has been an increase of interest in olfactory dysfunction since it was realised that anosmia was a common feature of idiopathic Parkinson's disease (PD) and Alzheimer-type dementia (AD). It is an intriguing possibility that the first sign of a disorder hitherto regarded as one of movement or cognition may be that of disturbed smell sense. In this review of PD, parkinsonian syndromes, essential tremor, AD, motor neurone disease (MND) and Huntington's chorea (HC) the following observations are made: 1) olfactory dysfunction is frequent and often severe in PD and AD; 2) normal smell identification in PD is rare and should prompt review of diagnosis unless the patient is female with tremor-dominant disease; 3) anosmia in suspected progressive supranuclear palsy and corticobasal degeneration is atypical and should likewise provoke diagnostic review; 4) hyposmia is an early feature of PD and AD and may precede motor and cognitive signs respectively; 5) subjects with anosmia and one ApoE-4 allele have an approximate 5-fold increased risk of later AD; 6) impaired smell sense is seen in some patients at 50% risk of parkinsonism; 7) smell testing in HC and MND where abnormality may be found, is not likely to be of clinical value; and 8) biopsy of olfactory nasal neurons shows non-specific changes in PD and AD and at present will ot aid diagnosis. © 2003 Movement Disorder Society [source]

Memory and executive function impairment predict dementia in Parkinson's disease

MOVEMENT DISORDERS, Issue 6 2002
Gilberto Levy MD
Abstract We analyzed the association of neuropsychological test impairment at baseline with the development of dementia in idiopathic Parkinson's disease (PD) patients. A cohort of nondemented PD patients from northern Manhattan, NY was followed annually with neurological and neuropsychological evaluations. The neuropsychological battery included tests of verbal and nonverbal memory, orientation, visuospatial ability, language, and abstract reasoning. The association of baseline neuropsychological tests scores with incident dementia was analyzed using Cox proportional hazards models. The analysis controlled for age, gender, education, duration of PD, and the total Unified Parkinson's Disease Rating Scale motor score at baseline. Forty-five out of 164 patients (27%) became demented during a mean follow-up of 3.7 ± 2.3 years. Four neuropsychological test scores were significantly associated with incident dementia in the Cox model: total immediate recall (RR: 0.92, 95% CI: 0.87,0.97, P = 0.001) and delayed recall (RR: 0.73, 95% CI: 0.59,0.91, P = 0.005) of the Selective Reminding Test (SRT), letter fluency (RR: 0.87, 95% CI: 0.77,0.99, P = 0.03), and Identities and Oddities of the Mattis Dementia Rating Scale (RR: 0.85, 95% CI: 0.73,0.98, P = 0.03). When the analysis was performed excluding patients with a clinical dementia rating of 0.5 (questionable dementia) at baseline evaluation, total immediate recall and delayed recall were still predictive of dementia in PD. Our results indicate that impairment in verbal memory and executive function are associated with the development of dementia in patients with PD. © 2002 Movement Disorder Society [source]

Effect of medication on EMG patterns in individuals with Parkinson's disease

MOVEMENT DISORDERS, Issue 5 2002
Julie A. Robichaud PT
Abstract Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation. © 2002 Movement Disorder Society [source]

Levodopa-induced dyskinesia in an autopsy-proven case of progressive supranuclear palsy,

MOVEMENT DISORDERS, Issue 5 2002
Jong-Min Kim MD
It is common for patients with idiopathic Parkinson's disease to develop levodopa-induced dyskinesia. This report provides what we believe is the first videotape presentation of levodopa-induced dyskinesia in a patient with progressive supranuclear palsy. To our knowledge, there is only one previous report of an autopsy-proven case of this kind. © 2002 Movement Disorder Society [source]

Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study

MOVEMENT DISORDERS, Issue 4 2002
José Berciano PhD
Abstract We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation. © 2002 Movement Disorder Society [source]

Bimanual coordination in Parkinson's disease: Deficits in movement frequency, amplitude, and pattern switching

MOVEMENT DISORDERS, Issue 1 2002
Winston D. Byblow BHK
Abstract Six patients with idiopathic Parkinson's disease (PD) and six age-matched controls participated in a variety of rhythmic bimanual coordination tasks. The main goal of the task was to perform inphase or antiphase patterns of pronation and supination of the forearms at a specified tempo, and to switch from one pattern to the other upon presentation of a visual cue. The availability of advance information was varied to examine whether deficits would emerge under choice versus pre-cue constraints. In pre-cue conditions, the subjects knew in advance which hand would be cued to initiate pattern change. In choice conditions, the cued hand was not known until the imperative stimulus was presented. Overall, the PD patients made movements with significantly lower frequencies and smaller amplitudes relative to controls. Patients exhibited spontaneous pattern switching from antiphase to inphase at significantly lower movement frequencies than controls. During intentional switching trials, the control group was significantly faster at initiating pattern change. PD and control groups differed in the time to initiate pattern switching to a greater extent under choice conditions, suggesting that patients used advance information to increase the speed of their response. The control group exhibited a preference for spontaneous switching and intentional switching through the subdominant hand. Patients exhibited a switching preference using the impaired limb (whether or not it was subdominant). The control group made more correct responses when the subdominant side was either pre-cued or presented in choice conditions. The patients maintained the subdominant/impaired side advantage under pre-cue conditions but not choice. In the maintenance of rhythmic movement, individuals with PD were able to use advance information in terms of both speed and accuracy. © 2001 Movement Disorder Society. [source]

Insights into yeast adaptive response to the agricultural fungicide mancozeb: A toxicoproteomics approach

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 3 2009
Pedro M. Santos
Abstract Toxicogenomics has the potential to elucidate gene,environment interactions to identify genes that are affected by a particular chemical at the early stages of the toxicological response and to establish parallelisms between different organisms. The fungicide mancozeb, widely used in agriculture, is an ethylene-bis-dithiocarbamate complex with manganese and zinc. Exposure to this pesticide has been linked to the development of idiopathic Parkinson's disease and cancer. Given that many signalling pathways and their molecular components are substantially conserved among eukaryotic organisms, we used Saccharomyces cerevisiae to get insights into the molecular mechanisms of mancozeb toxicity and adaptation based on expression proteomics. The early global response to mancozeb was analysed by quantitative proteomics using 2-DE. The target genes (e.g. TSA1, TSA2, SOD1, SOD2, AHP1, GRE2, GRX1, CYS3, PRE3, PRE6, PRE8, PRE9, EFT1, RPS5, TIF11, HSP31, HSP26, HSP104, HSP60, HSP70 -family) and the putative main transcription activators (e.g. Yap1, Msn2/Msn4, Met4, Hsf1, Aft1, Pdr1, Skn7, Rpn4p, Gcn4) of the complex mancozeb-induced expression changes are related with yeast response to stress, in particular to oxidative stress, protein translation initiation and protein folding, disassembling of protein aggregates and degradation of damaged proteins. Our results also suggest that this study provided powerful indications that may be useful to expand the knowledge obtained in yeast not only to the global response to mancozeb toxicity in phytopathogenic fungi but also to humans. [source]

Effectiveness of aripiprazole in a patient with presumed idiopathic Parkinson's disease and chronic paranoid schizophrenia

PSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 1 2010
Junya Fujino md
No abstract is available for this article. [source]

Paranoid schizophrenia and idiopathic Parkinson's disease do coexist: A challenge for clinicians

PSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 5 2006
CHRISTINE WINTER md
No abstract is available for this article. [source]

Orthostatic heart rate variability analysis in idiopathic Parkinson's disease

ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2006
E. Mihci
Objectives ,, We evaluated time and spectral analyses of 24-h heart rate variability (HRV) and the heart rate responses to passive tilt in patients with idiopathic Parkinson's disease (IPD) in order to investigate cardiovascular autonomic functions. Material and methods ,, Twenty-three subjects with IPD without autonomic symptoms and 15 age-matched healthy controls were enrolled. Frequency- and time-domain HRV parameters were studied during resting and passive head-up tilt (HUT) test. Results ,, All time-domain parameters were found to be low in patients with IPD. In patients with IPD, both low frequency (LF) and high frequency (HF) decreased during HUT period and no significant change in LF to HF ratio was noted. Both time- and frequency-domain HRV indices showed no correlation with age, disease severity and duration, and with l -dopa medication. Conclusion ,, The results indicate that impairment of autonomic nervous system function in IPD without autonomic symptoms is frequent, and does not show clear association with clinical stage and the age of the patients. [source]