Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 59-year-old man showed slowly progressive intentional tremor for 40 years prior to first visit to us in 1996. He was exposed to mercury vapor for about 3 years (1956-1959) and the diagnosis of chronic inorganic mercury poisoning was made. Hasegawa dementia scale-revised (HDS-R), mini-mental state (MMS) examination and P300 examination were performed. HDS-R and MMS were within normal range but the latency of P300 was remarkably prolonged. His tremor was considered to be due to chronic inorganic poisoning because there were no other causes and the frequency of his tremor was 3-4 Hz. which was lower than that in essential tremor. The prolonged P300 latency was also considered to be due to the same cause because there were no other causes and the head MRI were normal. Chronic inorganic mercury poisoning has been reported to produce organic changes in the brain and P300 is considered to be useful to detect these changes.
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PMID:[A case of chronic inorganic mercury poisoning with progressive intentional tremor and remarkably prolonged latency of P300]. 1034 50

We report a 73-year-old woman who had depression, dementia, and parkinsonism. She had postural tremor since her fortics. She was losing her weight since age 66 years. She noted difficulty in walk at age 72 (2001). She could not stand without assistance on July 2001, and she became hypobulic. On admission to our hospital on November 2001, she had dementia and revised Hasegawa dementia scale (HDS-R) was 8/30. She had mild limitation of the upward gaze, and rigidity in the neck, but not in the limbs. Postural tremor was seen. No muscle weakness was noted and tendon reflexes were normal. She was treated with levodopa/carvidopa, but she did not improve. She did not eat much. She was transferred to another hospital and she suddenly died on January 2002. The patient was discussed in a neurological CPC, and a chief discussant arrived at a conclusion that the patient had Parkinson disease with dementia. Some participants thought the diagnosis was progressive supranuclear palsy or diffuse Lewy body disease. The examination at autopsy revealed mild neuronal loss and Lewy bodies in the substantia nigra. Many Lewy bodies were observed in the cerebral cortex which corresponded to the neocortical type of DLB, and Lewy neurites were seen in the CA2 of the hippocampus by immunohistochemistry for alpha-synuclein. Spongy change was seen in the parahippocampus. Pathological diagnosis was diffuse Lewy body disease.
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PMID:[A 73-year-old woman with depression, dementia, and parkinsonism]. 1627 38

The cortical thickness has gained an extensive attention as a pathological alteration of sporadic Parkinson's disease (sPD), the alteration of pathological cortical thickness may distinctly contribute to the consistent clinical manifestations. Therefore, we investigated the cortical thickness correlates of clinical manifestations in the mid-stage sPD from the Han population of Chinese mainland (HPCM). A sample of 67 mid-stage sPD patients and 35 matched controls from HPCM were performed a corticometry of magnetic resonance imaging (MRI) and the assessment of clinical manifestations including the demographic and disease-related characteristics, and underwent the final analysis of the cortical thickness correlates with the clinical manifestations. In our result, we demonstrated that no significant differences in the demographic characteristics were found among the two groups. The tests of clinical disease-related characteristics demonstrated that the significant differences in the Hoehn and Yahr scale, the UPDRS Part I-IV, the symptom-dominant side (right/left/double), the tremor subscoree off (e), the tremor subscoref on (f), Webster, MMSE, HDS-R, DF, DB, SVFT, SDS, HAMD17, HAMD 24, CDT, CDR, LEDD and PDSI were observed between the mid-stage sPD patients and the controls. The analysis about the cortical thickness correlates with the clinical manifestations revealed that a significant correlation between UPDRS-I and Frontal-Sup-Orb-R and Rectus-R; DB and Frontal-Sup-Orb-R and Frontal-Inf-Orb-R; SDS and Frontal-Sup-Orb-R, Frontal-Mid-Orb-R, Rectus-R and Cingulum-Ant-R respectively in the mid-stage sPD patients from HPCM. Our data showed that the cortical thinning in the right frontal Orb, rectus and cingulum were the pathological base of some clinical manifestations including the cognitive impairment, hallucinations, psychosis, the depressed mood, the anxious mood, apathy, the sleep problems, the nighttime or/and daytime sleepiness, the short term memory stores and the central execution, as well as the sexual desire disorder in the mid-stage sPD patients, suggesting that the dysfunctions of brain regions of some cortical thinning are closely correlated with some clinical manifestations of the mid-stage sPD.
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PMID:The cortical thickness correlates of clinical manifestations in the mid-stage sporadic Parkinson's disease. 2772 Dec 6