Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By using diffusion-weighted imaging (DWI), we have recently shown abnormal diffusivity in the putamen of patients with the Parkinson variant of multiple system atrophy (MSA-P) which also correlated with disease severity, indicating the capability of putaminal diffusivity to serve as a marker for disease progression. We therefore performed a serial DWI study in 10 patients with MSA-P compared to 10 patients with Parkinson's disease (PD) to evaluate the dynamic evolution of diffusion properties in the basal ganglia including putamen, caudate nucleus and globus pallidum by means of the trace of the diffusion tensor (Trace(D)). For comparison, we have also analyzed the frequency and semiquantitative grading of MSA-P-related structural changes on conventional MRI including putaminal atrophy, lateral hyperintense margination of the putamen and putaminal signal hypointensity relative to the globus pallidum on T2 MR images. None of the Trace(D) values in the basal ganglia regions in the PD group changed significantly at follow-up compared to baseline. In MSA-P, a significant increase of the Trace(D) was found in the putamen, which correlated with motor progression as assessed by the Unified Parkinson's Disease Rating Scale (UPDRS). No significant change of any of the abnormal putaminal findings on routine MRI was obtained. We suggest that abnormal diffusivity in the putamen is sensitive to change over time in MSA-P and correlates with motor progression indicating that DWI may serve to monitor disease progression in MSA-P in an objective and quantitative manner.
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PMID:Progression of putaminal degeneration in multiple system atrophy: a serial diffusion MR study. 1644 75

Nicotinic acetylcholine receptors mediate the parasympathetic autonomic control of cardiac function. Aim of this study was the assessment of cardiac nicotinic acetylcholine receptor distribution with a novel (alpha4beta2) nicotinic acetylcholine receptor PET ligand (2-deoxy-2- [18F]fluoro-D-glucose-A85380) in humans. Five healthy volunteers without cardiac disease and six patients with either Parkinson's disease or multiple system atrophy without additional overt cardiac disease were evaluated with 2-deoxy-2-[18F]fluoro-D-glucose-A85380 PET-imaging to assess the cardiac parasympathetic innervation and the putative impact of both disorders. 2-deoxy-2- [18F]fluoro-D-glucose-A85380 whole body PET-scans were performed on a Siemens PET/CT biograph(TM) 75.4 min +/- 6.7 after i.v. injection of 371.2 +/- 58.1 MBq. Average count rate density of left ventricle ROI's and a standard ROI in the right lung were measured within three consecutive slices of 10.0 mm thickness. Heart-to-lung ratios were calculated in each volunteer and patient. Tracer uptake in the left ventricle could be measured in all of the five volunteers and the six patients. Heart-to-lung ratios in the volunteer group were not different from patients suffering from Parkinson's disease or MSA (3.2 +/- 0.5 vs 3.2 +/- 0.8 and 2.96+/-0.7, mean +/- SD), respectively. Human cardiac nicotinic acetylcholine receptors can be visualized and measured by 2-deoxy-2- [18F]fluoro-D-glucose-A85380 PET scans both in cardiac-healthy subjects and patients suffering from Parkinson's disease or multiple system atrophy. The heart- as well as the lung-tracer uptake was almost constant throughout all subjects leading to a good target-to-background ratio. These first results suggest no impact of either PD or MSA on cardiac nicotinic acetylcholine receptors.
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PMID:Feasibility of 2-deoxy-2-[18F]fluoro-D-glucose- A85380-PET for imaging of human cardiac nicotinic acetylcholine receptors in vivo. 1659 19

Clinical differentiation of parkinsonian syndromes such as the Parkinson variant of multiple system atrophy (MSA-P) and progressive supranuclear palsy (PSP) from Parkinson's disease is difficult in the early stage of the disease. In order to identify objective markers for differential diagnosis, we studied these three groups of patients with diffusion-weighted MRI (DWI). Sixteen MSA-P patients, 16 with PSP, 16 with Parkinson's disease and 15 healthy volunteers were studied. Regional apparent diffusion coefficients (rADC) were determined in different brain regions including basal ganglia, thalamus, white matter, pons and middle cerebellar peduncles (MCPs). rADC calculated in the MCP completely differentiated MSA-P patients (median: 0.93 x 10(-3) mm2/s) from PSP patients (median: 0.82 x 10(-3) mm2/s, P < 0.001), Parkinson's disease patients (median: 0.79 x 10(-3) mm2/s, P < 0.001) and healthy volunteers (median: 0.81 x 10(-3) mm2/s, P < 0.001). Other regions considered showed an overlapping among groups. DWI discriminates MSA-P from PSP and Parkinson's disease and healthy volunteers on the basis of MCP rADC values. These in vivo results confirm the pathological findings that the majority of MSA-P patients have moderate or severe degenerative changes not only in the nigrostriatal but also in the olivopontocerebellar systems. Our findings indicate that, in order to substantially contribute to the in vivo differential diagnosis of MSA-P, PSP and Parkinson's disease, rADC measurements should not be limited to the basal ganglia but should also include the MCP.
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PMID:Apparent diffusion coefficient measurements of the middle cerebellar peduncle differentiate the Parkinson variant of MSA from Parkinson's disease and progressive supranuclear palsy. 1681 75

We aimed to evaluate the potential of the cerebrospinal fluid (CSF) axonal damage biomarker NfH(SMI35) in the laboratory-supported differential diagnosis of parkinsonian syndromes. Patients with idiopathic Parkinson's disease (PD; n = 22), multiple-system atrophy (MSA; n = 21), progressive supranuclear palsy (PSP; n = 21), corticobasal degeneration (CBD; n = 6), and age-matched controls (n = 45) were included. CSF levels of NfH(SMI35) were measured using ELISA. Levels of CSF NfH(SMI35) were elevated in PSP compared to PD and controls (P < 0.05 each). They were also significantly higher in MSA than in PD and controls (P < 0.05 each). NfH(SMI35) differentiated PD from PSP with a sensitivity of 76.5% and a specificity of 94.4%. Axonal damage as measured by CSF NfH(SMI35) is most prominent in the more rapidly progressive syndromes PSP and MSA as compared to PD or CBD. CSF NfH(SMI35) may therefore be of some value for the laboratory-supported differential diagnosis of atypical parkinsonian syndromes.
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PMID:Neurofilament heavy-chain NfH(SMI35) in cerebrospinal fluid supports the differential diagnosis of Parkinsonian syndromes. 1701 9

Progressive supranuclear palsy (PSP) and the parkinsonian variant of multiple-system atrophy (MSA-P) may present with a similar phenotype. Magnetic resonance diffusion-weighted imaging (DWI) has been shown to be a sensitive discriminator of MSA-P from Parkinson's disease (PD). We studied 20 PSP, 11 MSA-P, 12 PD patients and 7 healthy controls in order to investigate whether regional apparent diffusion coefficients (rADCs) help distinguish PSP and MSA-P; whether rADCs are correlated with clinical disease severity scores; and the relationship between brainstem and cerebellar volumes and rADCs in PSP and MSA-P. The Unified Parkinson's Disease Rating Scale, Hoehn and Yahr score, Mini Mental State Examination, and frontal assessment battery were recorded in all patients. Regional ADCs were measured in the middle cerebellar peduncle (MCP), caudal and rostral pons, midbrain, decussating fibers of the superior cerebellar peduncle, thalamus, putamen, globus pallidus, caudate nucleus, corpus callosum, frontal and parietal white matter, as well as the centrum semiovale. In MSA-P, rADCs in the MCP and rostral pons were significantly greater than in PSP (P < 0.001 and 0.009) and PD (P < 0.001 and = 0.002). Stepwise logistic regression revealed that the MCP rADC distinguishes MSA-P from PSP with a sensitivity of 91% and a specificity of 84%. Increased brainstem rADCs were associated with motor deficit in MSA-P and PSP. Increased rADCs in the pons and MCP were associated with smaller pontine and cerebellar volumes in MSA-P. rADCs distinguish MSA-P from PSP. These have a clinical correlate and are associated with reduced brainstem and cerebellar volumes.
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PMID:Diffusion-weighted magnetic resonance imaging differentiates Parkinsonian variant of multiple-system atrophy from progressive supranuclear palsy. 1708 96

Camptocormia is defined as an abnormal, severe and involuntary forward flexion of the thoracolumbar spine, which becomes manifest during standing and walking and subsides in the recumbent position. It was originally described as a psychogenic disorder, particularly in soldiers involved in long-term trench service during World War 1. It is becoming increasingly recognized as a prominent and disabling phenomenon during the course of Parkinson's disease (PD). In our experience, there is no clear correlation between camptocormia and levodopa treatment. In a few patients, the abnormal posture improved and in others it was unaltered or even became worse following levodopa administration. In a minority of fluctuating patients, there was a temporary deterioration during the "off" periods, but in most, the severity of camptocormia was unchanged during the "on" and "off" phases. In some patients it is associated with back pains, whereas in others it is painless. It occurs in sporadic PD as well as in postencephalitic and parkin-gene mutation PD and in other parkinsonian syndromes such as MSA. The pathogenesis of this striking clinical sign is unknown. It is definitely not due to a primary vertebral disease causing kyphosis such as ankylosing spondylitis, as the bent spine disappears when the patient lies on his back. The muscles involved may be the abdominal, paravertebral or both. It may by due to a peculiar dystonia or to an extreme form of rigidity. Local myopathic changes were suggested as a possible cause, but these may rather be a secondary phenomenon. Treatment is currently unsatisfactory in most cases. Occasional patients may benefit from intramuscular botulinum toxin injections or from deep brain stimulation.
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PMID:Camptocormia in Parkinson's disease. 1713 Dec 21

We studied the response of the motor cortex to brief trains of suprathreshold repetitive transcranial magnetic stimulations (rTMS) in patients with the Parkinson-variant of multiple system atrophy (MSA-P) and compared it to patients with idiopathic Parkinson's disease (PD) and healthy controls. Eight subjects were studied in each group, and patients were matched for disease severity as assessed by Hoehn & Yahr stages. rTMS was delivered at rest and during low-level contractions in trains of 10 stimulations at 5 Hz, and stimulation intensity was set to result in an motor evoked potential (MEP) in the first dorsal interosseus muscle of 0.5 to 1.0 mV. In MSA-P, MEP amplitude at rest was already reduced after the second stimulus and remained so, while it did not change in PD and controls. During contraction, MEP size did not change during the train in any group. The silent period that followed the last stimulus was of similar duration as the first stimulus in MSA-P, but was increased in PD and controls. These findings indicate that abnormal inhibition occurs within the motor cortex in MSA-P, despite dopaminergic treatment and indicate differences in cortical dysfunction between MSA-P and PD. We suggest that these abnormalities reflect the motor cortex pathology found in MSA-P.
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PMID:Abnormal responses to repetitive transcranial magnetic stimulation in multiple system atrophy. 1713 17

The Parkinson variant of multiple system atrophy (MSA-P) is a distinct atypical parkinsonian disorder with a loss of dopaminergic neurons comparable to that found in Parkinson's disease (PD). The additional loss of striatopallidal projections is thought to account for levodopa unresponsiveness in MSA-P. Whereas histological features of MSA-P have been successfully reproduced in the double lesion rat model, loss of levodopa responsiveness has so far not been demonstrated. In the current study, 6-hydroxydopamine (6-OHDA) induced unilateral lesions of the substantia nigra produced a marked contralateral forelimb stepping deficit, which improved significantly after challenge with levodopa (P < 0.001). This response was abolished by the subsequent striatal quinolinic acid (QA) lesion. In the cylinder test, the marked asymmetry observed after 6-OHDA lesioning was reversed by levodopa to baseline levels. After QA, cylinder test performance under levodopa failed to reach baseline (P = 0.001) or 6-OHDA + levodopa (P = 0.002) levels. Nigral cell loss (90% +/- 5%) correlated with both stepping test (r = 0.608; P = 0.008) and cylinder test results (r = 0.656; P = 0.005). Lesion extent of the dorsal striatum correlated significantly with the loss of levodopa response (r = 0.593; P = 0.01) in the stepping test. These findings contribute further to the behavioral characterization of the double lesion rat model of MSA, improving its value in the evaluation of future neurorestorative strategies.
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PMID:Loss of dopaminergic responsiveness in a double lesion rat model of the Parkinson variant of multiple system atrophy. 1714 24

The objective was to develop a simple method for evaluating putaminal atrophy in patients with the Parkinson variant of multiple system atrophy (MSA-P). We used magnetic resonance imaging to study 9 patients with MSA-P, 24 patients with cerebellar variants of multiple system atrophy (MSA-C), 38 patients with Parkinson's disease (PD), and 27 healthy control subjects. Posterolateral linearization of the putaminal margin was semiquantitatively scored and the putaminal area per intracranial area was calculated as the adjusted putaminal area. There was a negative correlation between the linearization scores and adjusted putaminal areas (r = -0.43, P < 0.001), such that the mean adjusted putaminal area in the group without putaminal linearization (0.0148 +/- 0.0022) was greater than that of the group with linearization (0.0124 +/- 0.0029, P < 0.005). Moreover, the occurrence of putaminal linearization was significantly higher in MSA-P patients (88.8%) than in MSA-C (8.3%), PD (7.9%) and healthy subjects (7.4%; P < 0.005). Putaminal linearization was a highly sensitive (0.89) and specific (0.91) measure for differentiating MSA-P. Our results suggest that evaluating posterolateral putaminal linearization is useful for assessing putaminal atrophy and for differentiating MSA-P from MSA-C, PD, and healthy subjects.
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PMID:Evaluating posterolateral linearization of the putaminal margin with magnetic resonance imaging to diagnose the Parkinson variant of multiple system atrophy. 1726 Mar 43

In this study, we aimed to determine the progression of brain atrophy in the parkinson variant of multiple system atrophy (MSA-P). Voxel-based morphometry was applied to two consecutive high resolution MR images of 14 patients with probable MSA-P in comparison to 14 patients with Parkinson's disease (PD). The time interval between baseline and follow-up investigations (1.0 +/- 0.5 SD years in MSAP and 1.4 +/- 0.6 SD years in PD patients) was introduced as covariate in the statistical analysis. Additionally, correlation analyses were performed between the progression maps and clinical data. We observed marked progression of brain atrophy in the MSA-P cohort, the regions including striatum, mesencephalon, thalamus and cerebellum, but also cortical regions such as the primary sensorimotor cortex, supplementary motor area, lateral premotor cortex, medial frontal gyrus, middle frontal gyrus, orbito-frontal cortex,insula, posterior parietal cortex and hippocampus. Short disease duration was correlated with progression of atrophy in the striatum whereas longer disease duration was correlated with increasing atrophy in the cortical areas and cerebellar hemispheres. The UPDRS-III score was not significantly correlated with any brain region. Our data suggest that cortical atrophy is prominent in MSA-P and early degeneration of the basal ganglia drives late onset cortical atrophy.
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PMID:Progression of brain atrophy in multiple system atrophy. A longitudinal VBM study. 1733 61


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