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)

The aim of this study was to analyze the recovery functions of median nerve somatosensory evoked potentials (SEPs) and to clarify changes in the somatosensory system of patients with Parkinson's disease (PD). The central and frontal SEPs and the nerve potential of the median nerve were examined. The latencies and amplitudes of SEPs produced by a single shock in patients with PD were normal. The recovery functions of central SEPs showed a low degree of suppression in patients with PD, although the recovery curve of the nerve potential in PD patients was almost normal. The change in recovery curves of SEPs in patients with sensory complaints were more noticeable than that in patients without sensory disturbance. A low degree of suppression of central SEPs might play a role in the sensory complaints of PD patients.
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PMID:Recovery functions of somatosensory evoked potentials in parkinsonian patients. 162 48

In order to assess quantitatively the state of the disease or the effect of drugs in parkinsonian patients, it would be helpful to have at our disposal mathematical models that reflect in their parameter values the deficiencies associated with the disease. This paper proposes a class of such models that are easily obtained in practice and lend themselves to useful interpretations. A pursuit manual tracking experiment is used to derive these models for patients with Parkinson's disease undergoing drug therapy and for normal controls. The input (one-dimensional visual target) and operator's output (manual tracking) are analyzed using a time series approach aiming at obtaining an auto-regressive moving-average (ARMA) model that minimizes the mean square error between the actual and model response. This mathematical model takes the form of a difference equation expressing, in discrete time, the present output value as a linear combination of past output values and past and present input values. Our experimental results indicate that a difference equation (ARMA model) involving the two previous output values and the present and past input values fits best both patient and control data. A comparison between the mean estimated model parameters for patients and controls shows a statistically significant difference in two of these parameters. The first parameter, which is significantly increased in patients, relates the current response of the patient to the immediately preceding response which represents an increased 'damping' of the motor dynamics, reflecting the muscular rigidity associated with the disease (motor disorder). The other parameter, which is significantly decreased in patients, represents the relative degree to which the current response of the patient is influenced by the target position information at the previous point in time which points to a deficiency in sensing/processing of this information (possible a sensory disorder). Our results also showed a marked reduction in the mean-square error of a second trial of the experiment in normal subjects but failed to do so for the patients, possibly indicating learning deficiencies associated with the disease.
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PMID:Quantifying deficiencies associated with Parkinson's disease by use of time-series analysis. 244 18

A case of familial juvenile parkinsonism with dementia, orthostatic hypotension, neurogenic bladder and constipation was reported. He had been in a good health until the age of 28 when a finger tremor occurred on effort to hold hands in a definite position, and disturbances in gait and speech were noted. These symptoms were relieved by levodopa treatment followed by dyskinesia and motor fluctuations. Three years later, he complained of faintness, constipation and urinary frequency. The neurological examination revealed mentally sound male with masked face, tremor and rigidity in his extremities, and short step gait with lateropulsion. Urodynamic study showed uninhibited bladder. In the following years, orthostatic hypotension, dysuria and urinary retention developed gradually. He became mentally loose and was unable to take medicines appropriately. When in the Nishiojiya Byoin National Sanatorium, he tried to snake out the hospital many times. His parents and a brother suffered from Parkinson's disease and juvenile parkinsonism, respectively, suggesting an autosomal dominant inheritance. On admission to our hospital, he was apathetic. He had masked face, bilateral postural tremor, frozen gait and dyskinesia in the right lower extremity. Little bradykinesia or rigidity was noted. His muscle tone and deep tendon reflexes were decreased but neither muscular wasting, weakness, ataxia nor sensory disturbance was observed. Laboratory data including ceruloplasmin, copper, dopamine-beta-hydroxylase and lysosomal enzyme activities were normal except for mild anemia. A cranial CT scan revealed mild cortical atrophy in the frontal and temporal lobes, but nerve conduction study and cortical evoked potentials showed no abnormality. While in the hospital, his mental functions deteriorated to the state of dementia and orthostatic hypotension became apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial juvenile parkinsonism with dementia and autonomic failure--a case report]. 833 79

Painful sensory complaints are known to occur in Parkinson's disease, but painful oral or genital syndromes have not been described. We report seven individuals with presumed idiopathic Parkinson's disease and one with atypical parkinsonism who experienced chronic severe oral or genital pains that appeared to be examples of a primary sensory disturbance related to the underlying parkinsonism. In each case, the pain syndrome overshadowed the other features of the parkinsonism. Five patients experienced oral pain and three patients, all women, had genital pain. No other definable organic cause was detected to explain the symptoms in any case. The genital pain tended to fluctuate in severity with the motor manifestations of the parkinsonism and could be abolished or reduced by levodopa. The recognition of painful oral or genital sensations in patients with parkinsonism should lead to further study regarding the prevalence, neurochemical basis, and treatment for these disabling symptoms.
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PMID:Oral and genital pain syndromes in Parkinson's disease. 881 22

Various sensory symptoms and disturbed sensory perception are often observed in patients with idiopathic Parkinson's disease (PD). The basis of sensory disturbance in PD is unknown but possibly reflects a role for the basal ganglia in sensory processing. To investigate the relationship between the sensory dysfunction and dopaminergic deficiency in PD, we measured spatial discrimination using the Grating Orientation Task in 21 drug-naive patients with PD, before and after long-term antiparkinson therapy, and 25 age-matched healthy controls. The grating orientation threshold was significantly higher in patients (3.03 +/- 0.84) than controls (2.03 +/- 0.79). After 3 to 10 months of antiparkinson therapy, the grating orientation threshold was significantly lowered (2.66 +/- 0.84), although it was still higher than that in controls. Improvement in the patients' sensory function was significantly correlated with motor improvement (r = 0.44). These results suggest that sensory dysfunction in Parkinson's disease is related at least in part to the dopaminergic deficit.
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PMID:Dopaminergic influence on disturbed spatial discrimination in Parkinson's disease. 1609 9

Nonmotor manifestations determine the life quality of patients with Parkinson's disease (PD). Identification of the nonmotor symptoms in PD as definite changes will represent a milestone in its diagnosis. Outcome measures that characterize nonmotor manifestations with specificity for dopaminergic deficiency are essential to that goal. Pain is a prevalent sensory disturbance in PD patients. The prevalence was reported to be up to 83%. Nociceptive stimuli under normal conditions elicit decreases in cerebral blood volume (CBV) in the striatum via dopaminergic neurotransmission. This nociception-induced CBV response is potentially to be defined as a characteristic of the pain symptom of PD. To validate this concept, steady-state CBV-weighted functional magnetic resonance imaging with iron oxide nanoparticles was employed to measure CBV changes in parkinsonian rats. Tyrosine hydroxylase immunohistology was used to identify the dopaminergic integrity to corroborate the imaging findings. Additional experiments that tested pain responses in parkinsonism were also carried out. The results revealed that the lesioned striatum exhibited a weakened CBV decrease in response to the nociceptive stimulus. This weakened CBV response occurred mainly in areas with dopaminergic denervation. A strong correspondence was observed between the distributions of the nociception-induced CBV responses and dopaminergic innervation. The persisting CBV signals in the striatum were abolished by the D2/D3 antagonist eticlopride. The findings of these behavioral, neuroimaging, immunohistological, and pharmacological experiments demonstrate that pain in a rat model of PD can be characterized by nociception induced striatal CBV signal changes with specificity for dopaminergic dysfunction.
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PMID:Dopaminergic imaging of nonmotor manifestations in a rat model of Parkinson's disease by fMRI. 2284 18

Parkinson's disease (PD) is one of common neurodegenerative diseases, which shows motor symptoms including tremor, bradykinesia, rigidity and postural instability. It also involves non-motor symptoms such as cognitive impairment, mental manifestation, autonomic disorder and sensory disturbance. Although treatments to improve the motor disability in PD are being assessed at present, the main challenge remains that is the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find approaches that can inhibit the progression of dopaminergic neurodegeneration. Astrocytes are known to play an important role in the maintenance of the neuronal environment and exert neuroprotective effects. Additionally, astrocyte dysfunction increases the susceptibility of neurons to cytotoxicity. We have demonstrated neuroprotective approaches in parkinsonian models in various studies targeting astrocytes. In this article, we summarize the neuroprotective function of astrocytes in the brain, involvement of astrocyte dysfunction in neurodegeneration, and experimental approaches to dopaminergic neuroprotection. We review findings reported in several papers including our own studies. We also address target molecules and pivotal pathways in astrocytes for dopaminergic neuroprotection. The review discusses new promising therapeutic strategies to prevent dopaminergic neurodegeneration in PD.
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PMID:Therapeutic Strategy of Targeting Astrocytes for Neuroprotection in Parkinson's Disease. 2869 20