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)

To determine whether MRI can reveal more vascular lesions in patients clinically suspected of having vascular parkinsonism, we compared 15 such patients with 15 patients who had idiopathic Parkinson's disease and 10 hypertensive controls. Patients with suspected vascular parkinsonism had significantly more subcortical lesions than those with Parkinson's disease or hypertension. The cutoff point that best distinguished patients with suspected vascular parkinsonism from patients with Parkinson's disease was a 0.6% level of lesioned brain tissue volume. There were two types of vascular parkinsonism: one had an acute onset and lesions located in the subcortical gray nuclei (striatum, globus pallidus, thalamus); the other had an insidious onset and lesions diffusely distributed in the watershed areas.
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PMID:MRI in patients with suspected vascular parkinsonism. 884 90

We report a 63-year-old woman who presented myotonia and parkinsonism. The patient was well until 15 years of the age when she noted that the ring finger of her left hand at times flexed when she did not intend to do so. She noted weakness in her left upper extremity at the age of 40, and difficulty in relaxing her hand grip at 45. She had an onset of tremor in her right foot at age 50, which was followed by difficulty in gait and hand writing. She was admitted to Juntendo University Urayasu Hospital when she was 63-year-old. Her mother, two sisters, and a son were affected with similar muscle weakness and myotonia. Although some of them developed stooped posture in the late stage of the disease, none of them had overt parkinsonism. General physical examination was unremarkable. Neurologic examination revealed an alert and oriented woman with some recent memory loss. She had bilateral ptosis, facial weakness, and a masked face. Myerson's sign was present. Her speech was small and monotonous. The sternocleidomastoid muscles were markedly atrophic and weak. The remaining of the cranial nerves were intact. She walked in small steps with freezing with support. She showed bradykinesia, retropulsion, and resting tremor in her right leg. Slight distal dominant weakness was noted in both upper and lower extremities more on the left. No cerebellar signs were noted. Muscle stretch reflexes were within normal limits in the upper extremities and diminished in the lower limbs. Sensation was intact. Routine laboratory findings were unremarkable. Cranial CT scan and MRI revealed slight cortical atrophy and leukoaraiosis. She responded to levodopa and she became able to walk by herself. She was transferred to another hospital one month after her admission. She had several bouts of airway obstruction with one episode of respiratory arrest. She expired six month after the transfer. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient suffered from myotonic dystrophy and Parkinson's disease which set in later years. Postmortem examination on the iliopsoas muscle revealed uneven muscle fiber diameters, central nuclei, and type 1 fiber predominance; the pathologic finding was consistent with myotonic dystrophy. The substantia nigra showed marked cell loss and Lewy bodies in the remaining neurons. The finding was consistent with Parkinson's disease. In myelin stain, diffuse myelin pallor was noted in the cerebral white matter which was the pathologic substrate of leukoaraiosis in this patient. Combination of these two disorders have never been reported in the literature to our knowledge. It appears to be that the coincidence is just a by-chance phenomenon, but it seems interesting to note that accelerated aging process appears to be present in both myotonic dystrophy and Parkinson's disease.
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PMID:[A 63-year-old woman with muscle weakness, myotonia, and parkinsonism]. 886 42

Three basic principles underlie the techniques of stereotactic cryosurgery for Parkinson's disease: (1) high-resolution MRI of the surgical target using thin sequential coronal, axial and sagittal views: (2) clinical-physiological verification of localization of the surgical target by reversible inhibition test, and (3) production of the cryosurgical freezing lesion in a conscious, cooperative patient. The cryosurgical lesion is created in the ventrolateral nucleus of the thalamus for control of tremor and rigidity, or in the posterior ventral area of the pallidum for control of rigidity and bradykinesia. An initially reversible inhibition is produced by cooling the probe tip to -10 degrees C. This cools the brain tissue within 3 mm of the probe to 2-15 degrees C. If parkinsonian symptoms are suppressed, the cryoprobe tip temperature is then lowered incrementally, resulting in a gradually enlarging lesion surrounded by a reversible buffer zone. The final temperature is that in which parkinsonian symptoms are abolished and/or side effects appear. After performing and evaluating over 1,000 cryothalamotomies and cryopallidotomies on patients for whom medical treatments had failed, the author concludes that cryosurgical techniques are safer and produce lesions that are better controlled for size and location than other techniques, resulting in lasting, successful therapeutic results.
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PMID:Role of cryosurgery and MRI for Parkinson's disease. 891 24

We report a 46-year-old man with right side dominant parkinsonism who died suddenly two years after the onset. The patient was well until the age of 42 years in January of 1993, when he noted an onset of difficulty in using his right hand and then the right leg. Soon after he noted nocturnal urinary incontinence. In January of 1994, a local doctor prescribed 200 mg of levodopa with benserazide and 5 mg of bromocriptine. The patient noted some improvement. Cystometry revealed 300 ml of residual urine. He visited our clinic on 24th of December, 1996. He was alert and oriented. BP was 106/60. He showed masked face and small voice. He walked in stopped posture dragging his feet; retropulsion was noted. He showed moderate bradykinesia and rigidity more on the right side. No resting tremor or cerebellar ataxia was noted. Ankle jerks were somewhat exaggerated but no Babinski sign was noted. He continued to show residual urine, but orthostatic hypotension was absent. Routine laboratory examination was unremarkable, however, his cranial MRI showed atrophy of the left putamen and a T2-linear high signal intensity lesion along the lateral border of the left putamen. On January 15, 1997, he ate certain amount of rice cake and drank alcohol. After coming back home and while changing his clothes, he suddenly complained of chest discomfort and lost consciousness. He was pronounced dead in the afternoon. The patient was discussed in a neurological CPC. Opinions were divided between Parkinson's disease and striatonigral degeneration. The chief discussed arrived at a conclusion that the patient had Parkinson's disease, because he responded to levodopa to some extent and except for nocturnal incontinence he did not have wide spread autonomic failure. Postmortem examination revealed marked loss of neurons and extensive gliosis in the left putamen. The right putamen did not show such changes. The substantia nigra showed gliosis in the lateral part on both side, however, neuronal loss was not apparent. The locus coeruleus was well retained. No Lewy bodies were found. The pontine nucleus and the cerebellum were intact. However, glial cytoplasmic inclusions were seen in oligodendrocytes of the cerebral white matter and the pontine base. The heart and lungs were intact and the cause of the sudden death could not be determined. The pathologic diagnosis is striatonigral degeneration. Such a marked asymmetry of the pathologic change is quite unusual. Probably, the death in the early stage of the disease is the reason for this asymmetry.
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PMID:[A 46-year-old man with right-side dominant parkinsonism, who suffered a sudden death]. 895

Patients with parkinsonism can be classified as clinical definite, probable, possible, or unlikely Parkinson's disease (PD). Possible PD includes patients with PD according to conventional diagnostic criteria and with at least a moderate response to dopamine agonists. However, these patients have clinical features that may reduce the probability for idiopathic PD. The objective of this study was to clinically characterize patients with possible disease in a prevalence study of PD and to indicate the frequency of idiopathic PD in this group of patients. The diagnostic re-evaluation was based on detailed MRI examinations and investigations of dopaminergic drug response after several years of treatment. In a community-based prevalence study in Norway, comprising 245 PD patients, we found 36 patients (15%) with clinical possible PD. The patients with possible disease had significant and clinically important differences in demographic and disease characteristics compared to patients with definite and probable PD. Possible PD patients were older at disease onset, more disabled, and had more neurobehavioral disorders. MRI examinations of 14 of the 36 patients with possible PD in the prevalence study revealed significant group effects compared to an age-matched control group, with reduced pars compacta width and increased cortical atrophy. In individual patients, signal attenuation consistent with vascular lesions of the basal ganglia contributed to diagnostic reclassification. Dopaminergic drug withdrawal revealed no response in 4 of 12 examined patients. Two of the remaining eight patients had a clear short-duration drug response. Six patients had only a varying degree of long-duration response. The re-evaluation of diagnosis indicates that probably less than half of the patients with clinical possible PD have idiopathic disease. Patients with atypical features and diagnosed as possible PD should thus be excluded from studies with a presumed high specificity for idiopathic PD.
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PMID:Patient characteristics, MRI examination, and dopaminergic drug response in clinical possible Parkinson's disease. 897 7

The brain glucose metabolism was studied by PET with 18F-FDG in 11 patients with multiple system atrophy (MSA) and 12 patients with idiopathic Parkinson's disease (PD). Seven of the 11 MSA patients were diagnosed as having olivopontocerebellar atrophy, two had striatonigral degeneration, while two demonstrated Shy-Drager syndrome. The glucose metabolic rates for each region in the PD patients showed no difference from the normal controls. The frontal, temporal and parietal cortical glucose metabolic rates and the caudate, the putaminal, the cerebellar and the brainstem glucose metabolic rates in the MSA patients decreased significantly from the controls. The atrophy of the cerebellum and the brainstem in the MSA patients were scored by MRI. The cerebellar and brainstem glucose metabolism in the MSA patients decreased as the atrophy score in such regions advanced in each group; however, some patients with no atrophy showed a decreased glucose metabolism. Although the cerebellar and the brainstem glucose metabolism decreased in all MSA patients, such a decrease was not observed in the SND patients. The decrease in the glucose metabolism for the non-cortical regions in the MSA patients seems to be due to a diffuse depletion of the neurons not restricted to the nigrostriatal neurons. Deafferentation to the cerebral cortices seems to result in a decreased cortical metabolism. The differences in the glucose metabolism between MSA and PD as assessed by PET may be caused by the pathophysiological differences between MSA and PD, and such differences therefore appear to be useful when making a differential diagnosis between MSA and PD. The relative sparing of the brainstem and cerebellar glucose metabolism is considered to be a feature of patients with SND.
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PMID:Glucose metabolism in the cortical and subcortical brain structures in multiple system atrophy and Parkinson's disease: a positron emission tomographic study. 899 7

We have investigated regional changes in dopamine metabolism within the basal ganglia with clinical progression of idiopathic Parkinson's disease, using coregistration of [18F]dopa-PET and MRI images and comparing six normal subjects with 15 Parkinson's disease patients in a cross-sectional study. We have demonstrated that [18F]dopa metabolism in the dorsal putamen is reduced to almost 50% of normal both caudally and rostrally early in the disease whilst the ventral putamen is not significantly affected. With progression of symptoms there is loss of dopa metabolism from the ventral putamen, the ventrocaudal putamen in advance of the ventrorostral putamen. Throughout the disease the ventrorostral putamen is relatively preserved; even in the most advanced group [18F]dopa uptake is reduced here by only 30%. We conclude that the progression of Parkinson's disease is associated with a focal process affecting only the dorsal putamen in its early (and preclinical) phase then affecting the ventral putamen with increasing disease severity.
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PMID:Regional changes in [18F]dopa metabolism in the striatum in Parkinson's disease. 901 13

Parkinson's disease (PD) is defined as a neurodegenerative disorder characterized pathologically by degeneration of substantia nigra and locus coeruleus with Lewy bodies in the remaining neurons and clinically by resting tremor, cogwheel rigidity, bradykinesia and loss of postural reflex. Parkinsonism may be defined as those who show at lest two of the major four features characterizing PD. We propose the following diagnostic criteria for PD, i.e., clinical criteria (resting tremor or at least two of the remaining cardinal features of PD), treatment criteria (good response to anti-parkinson drugs), image criteria (essentially normal cerebral MRI), and exclusion criteria (no history of encephalitis or exposure to parkinsonism-inducing substances or drugs). Patients must fulfil all four criteria for the diagnosis.
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PMID:[Concept and diagnostic criteria of Parkinson's disease and parkinsonism]. 901 17

In Parkinson's disease, both MRI and SPECT are usually normal. In striatonigral degeneration and olivo-ponto-cerebellar atrophy presenting as parkinsonism, MRI shows putaminal atrophy and SPECT shows hypoperfusion in the frontal lobe, basal ganglia and cerebellum. In progressive supranuclear palsy, MRI shows tegmental atrophy and SPECT shows hypoperfusion in the frontal lobe with intact cerebellar perfusion. In conclusion, MRI and SPECT seem to be useful for the differential diagnosis of Parkinson's disease and other neurodegenerative disorders presenting as parkinsonism.
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PMID:[The use of magnetic resonance imaging (MRI) and single photon emission computing tomography (SPECT) for the differential diagnosis of Parkinson's disease and other neurodegenerative disorders presenting as parkinsonism]. 901 21

Striatonigral degeneration (SND) is sporadic, middle-aged on set degenerative disease of the nervous system which etiology is unknown. SND is considered one of multiple system atrophy (MSA). Clinically parkinsonian symptom is dominant and then it is difficult to distinguish from idiopathic Parkinson's disease (PD). Pathologically neuron cell loss and gliosis are recognized principally striatum (mainly putamen) and substantia nigra. Putaminal hypointensity and slit-hyper intensity in the outer margin of putamen are often seen on T2-weighted 1.5 Tesla MRI. PET with [18 F] fluorodeoxyglucose indicates a considerably decreased glucose utilisation in the striatum of SND, whereas glucose utilisation are normal in PD. Striatal dopamine D1, D2 receptors are reduced. Response to Levodopa is poor or absent.
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PMID:[Striatonigral degeneration]. 901 34


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