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)

Ten free monoamines and their metabolites in plasma and cerebrospinal fluid (CSF) were simultaneous measured in 6 levodopa-untreated (LU), 18 levodopa-treated (LT) and 37 levodopa-withdrawn (LW) Chinese patients with Parkinson's disease (PD) and 26 controls. We found that the levels of these substances in LW patients were not significantly different from those in LU patients. In LU- and LW-PD patients, CSF epinephrine (EPI) was higher (P < 0.05) than that of the controls. 3-methoxy-DOPA (3-OMDOPA) might not inhibit the accumulation of 3,4-dihydroxyphenylalanine (DOPA) and dopamine metabolites in CSF. Levodopa treatment might change the dopaminergic and serotoninergic neuronal systems, but not the noradrenergic or adrenergic neuronal systems, in CNS of PD patients. Benserazide (a peripheral decarboxylase inhibitor) in Madopar might decrease the levels of serotonin (5-HT) and norepinephrine (NE), but not those of DOPA and homovanillic acid (HVA), in plasma. HVA, NE and EPI in plasma were not good indices for those in CSF. Otherwise, our results were consistent with some other studies by showing a significantly lower level (P < 0.01) of HVA in CSF of LU- and LW-PD patients than that of the controls, while no difference for NE, 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxyindole acetic acid (5-HIAA) or 3-OMDOPA was noted. The severity of clinical disability was related to the deficiency of CSF HVA and DOPAC in LU- and LW-PD patients; however, there was no relationship between clinical symptoms of tremor, rigidity-bradykinesia, autonomic dysfunction, dementia, depression or levodopa-induced dyskinesia and CSF monoamines or their metabolites.
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PMID:Monoamines and their metabolites in plasma and lumbar cerebrospinal fluid of Chinese patients with Parkinson's disease. 833 58

We report a 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty in eye-lid opening, and marked pseudo-bulbar palsy. He felt difficulty of it, hand movement at 59 years old. When he was 60 years old, monotonous speech and slowness of movement appeared. He visited a neurologist who noted vertical gaze palsy, neck rigidity, and bradykinesia. He was diagnosed as progressive supranuclear palsy (PSP) and given 300 mg L-Dopa/Benserazide by the neurologist. This medication improved his rigidity and bradykinesia. At 62 years of the age, his eye-lids closed involuntary and it was difficult to open. In addition, he began to complain of wearing-off, autonomic symptoms, and dysphagia. Anti-parkinsonian drugs were increased, but his bradykinesia progressed. At 64 years of the age, he was admitted to the Neurology Service of Juntendo Hospital. On admission, he was alert and not demented. No aphasia, apraxia, or agnosia was noted. In the cranial nerves, upward and downward gaze were markedly restricted. His face was hypomimic and seborrhoic. It was difficult to swallow liquid or solid for him. No weakness was noted, but he walked in small steps with freezing and falling tendency to backward. Rigidity was noted on his extremities and stronger on his left side than right. Tremor was absent. Bradykinesia of his body and extremities was marked. No cerebellar ataxia was noted. Deep tendon reflexes were within normal range. Planter response was flexor bilaterally. Myerson's sign was noted. Sensory and autonomic function were normal. He was treated with L-Dopa, Pergolide, and Bromocriptine. However, these medications improved his bradykinesia and gait disturbance only slightly, dysphagia became progressively worse. He developed aspiration pneumonia when he was 65 years old and admitted to Juntendo Hospital. A large amount of sputum was aspirated from his trachea. Two days after from admission, he was found dead on his bed. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had progressive supranuclear palsy (PSP). Other differential diagnoses included Parkinson's disease, pallido-nigroluysian atrophy (PNLA), multiple system atrophy (MSA), and corticobasal degeneration(CBD). Many participants considered that PSP or PNLA was most likely. Post-mortem exmination revealed marked nigral neuronal loss and gliosis. The globus pallidus and the luysian body changed mildly. However, the frontal cortex was relatively spared, there were many ballooned neurons in the cortical layer. Other parts were spared. With sliver (Bodian and Gallyas-Braak) and anti-phsphorylated tau stain, abundant astrocytic plaques, neurofibrillary tangles, and argyrophilic threads on the frontal cortex, striatum, and substantia nigra were seen. There was no tufted astrocyte which was hallmark of diagnosis of PSP. In addition, several Lewy bodies were seen in the brainstem. Because astrocyte plaque was considered specific for pathology of CBD, the pathologist revealed that the pathological diagnosis of this patient was CBD. Nevertheless, discussion was focused on the relatively mild degeneration of the frontal cortex for CBD.
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PMID:[A 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty of eye-lid opening, and marked pseudo-bulbar palsy]. 1578 4

We report a 67-year-old man with rt. hand resting tremor and rigidity after lt. putaminal hemorrhage. He had hypertension and alcoholic liver cirrhosis as past history. When he was 62 years old, he realized rt. hemiplegia suddenly and admitted in Juntendo Urayasu hospital. Brain CT showed intracranial hemorrhage in lt. putamen. He was treated with neurosurgery operation for rejecting hemorrhage. Mild rt. hemiparesis remained but he could live independently. He was medicated sulpiride for depression after cerebrovascular accident. On 63 years old, resting tremor and rigidity appeared on his rt. hand. His doctor stopped sulpiride and treated with L-Dopa/Benserazide and trihexiphenidyl. His parkinsonism was stable with this treatment for four years. His doctor considered that he was Parkinson's disease or drug-induced parkinsonism. On 67 years old, he became akinetic-mutism state suddenly and admitted in the hospital. His consciousness turned alert soon and discharged after two weeks. This episode was considered as epilepsy. After one week from discharge, he was found cardio-pulmonary arrest and confirmed dead in the hospital. Post-mortem examination revealed necrosis in the posterior-lateral part of lt. putamen due to hemorrhage. However, there was no degenerative change of the striatum or the substantia nigra and no Lewy bodies in his brain. Other pathological changes were also not found. His parkinsonism might be caused putaminal pathology due to hemorrhage.
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PMID:[A 67-year-old man with rt. hand resting tremor and rigidity after lt. putaminal hemorrhage]. 1591 60