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 activities of the aminotransferases, GOT and GPT, were determined in the serum and cerebrospinal fluid of patients with Parkinson's disease, Huntington's chorea, Wilson's disease, amyotrophic lateral sclerosis (ALS), Friedreich's ataxia, phenylketonuria, and head injuries. 1. In patients with Huntington's chorea the activity of SGOT was lower than in controls (P = 0.02); in Friedreich's ataxia LGPT activity was decreased (P less than 0.001); in patients suffering from ALS SGOT (P = 0.005), SGPT (P less than 0.001) and LGOT (P less than 0.001) activities were increased. 2. Long-term treatment of Parkinson's disease and Wilson's disease with L-dopa resulted in an increase in SGOT, LGOT, and SGPT activity over approximately 2 months, with subsequent normalization of these enzyme activities in spite of continued therapy. Guanidine treatment led to an increase in aminotransferase activities in patients with ALS. Penicillamine caused a decrease in SGOT and SGPT activities in Wilson's disease. These results illustrate the necessity of taking therapeutic measures into account in the interpretation of data on aminotransferase activities.
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PMID:[The activity of aminotransferases in serum and cerebrospinal fluid in neurological diseases (author's transl)]. 12 63

Rigidity in Parkinson patients can be easily quantitated by determining net work required to passively flex and extend the forearm through an arc of 100 degrees. Rigidity thus measured can be subdivided into two very distinct types, resting and activated. Resting rigidity, measured while the patient is relaxed, responds to all effective therapeutic agents and correlates closely to degree of clinical improvement. Activated rigidity, measured during voluntary activity, is not relieved by any presently available medical treatment. It remains unchanged at pre-therapy levels even in patients who may temporarily appear to have dramatic improvement in clinical symptomatology. Longitudinal measurements made in hundreds of parkinson patients over intervals ranging from 5 to 15 years show continuing high levels of activated rigidity through the entire period of study. In marked contrast to our wide experience with parkinson patients is a single, well documented case of Wilson's disease who appears to have recovered completely both by clinical examination and by all of our machine measurements. This patient had high levels of extrapyramidal deficit, repeatedly measured over a period of four months when penicillamine therapy was being investigated. He then suddenly reverted to normal and returned to full time employment. High values of resting rigidity activated rigidity, akinesia and resting tremor all reverted to normal and have remained normal for the past 6 years. The implication of this study is that L-dopa and related treatments only mask the symptomatology of Parkinson's disease and are not retarding the underlying pathological process. Penicillamine, on the other hand, probably does relieve the destructive process in Wilson's disease and may in early cases, permanently relieve the extrapyramidal dysfunction.
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PMID:Failure of L-dopa to relieve activated rigidity in Parkinson's disease. 93 Jul 49

123I-(S-)-2-hydroxy-3-iodo-6-methoxy-N[(1-ethyl-2-pyrrolidinyl) methyl]-benzamide (123I-IBZM) is a highly selective CNS D2 dopamine receptor ligand suitable for SPECT. This study reports on IBZM-SPECT findings in 60 patients including eight controls and 52 patients presenting with disorders of the dopaminergic system, including idiopathic Parkinson's syndrome (IPS) (n = 18), Parkinson's syndromes of other aetiology (PS) (n = 24) and Wilson's disease (n = 10). SPECT was performed 2 h p.i. of 185 MBq 123I-IBZM. For semiquantitative evaluation basal ganglia to frontal cortex ratios (BG/FC ratios) were calculated. In controls BG/FC ratios of 1.55 +/- 0.05 S.D. were observed. Findings in IPS patients (BG/FC ratio: 1.51 +/- 0.05) were not different from controls. In PS patients striatal IBZM binding (BG/FC ratio: 1.35 +/- 0.11) was significantly (P less than 0.001) lower compared to the control and IPS groups. Asymptomatic patients with Wilson's disease presented normal IBZM binding. In those with neurologic symptoms IBZM fixation was markedly reduced. IBZM-SPECT has shown to be a suitable means for in vivo imaging of striatal dopamine D2 receptors in controls and various disorders of the dopaminergic system. Our preliminary data suggest that IBZM-SPECT is potentially useful for discriminating between IPS and PS (sensitivity: 100%; specificity: 83%). In patients with Wilson's disease IBZM accumulation seems to correlate with the presence of neurologic symptoms.
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PMID:SPECT imaging of dopamine D2 receptors with 123I-IBZM: initial experience in controls and patients with Parkinson's syndrome and Wilson's disease. 183 42

Positron-emission tomography (PET), a noninvasive analytical method, made possible the detection of regional alterations in the central nervous system, thus demonstrating "in vivo" the presence of biochemical alterations and the organization of cerebral function in the pathological states. The study of glucose cerebral metabolism velocity, performed recently with the aid of PET, reveals that in the patients with thymic disorders the values recorded for the bipolar syndromes differ from those recorded the for unipolar ones. At the same time, the direct measurement of the activity of the neuroanatomic structures involved in schizophrenia and their response to neuroleptics was possible. This technique and the F-fluoro-desixiglucose method were also applied to the patients with Alzheimer's disease, multi-infarct dementia, Huntington's disease. Wilson's disease and Parkinson's disease. Suggestive alterations of glucose metabolism velocity were noticed and the neuroanatomic structures involved in the pathological manifestations could be specified.
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PMID:[The use of positron-emission tomography in psychiatry]. 198 25

We present a review on recent neuroimaging techniques, like x-ray computed tomography (XCT), magnetic resonance imaging (MRI), positron emission tomography (PET) and single photon emission tomography (SPECT) in dementia and related diseases. Significant new findings have been obtained using techniques reflecting proton density, regional brain perfusion and brain metabolism. In dementia of the Alzheimer type, for example, temporoparietal and sometimes also frontal reductions in cerebral blood flow and metabolism are characteristic. The infarctions found in multi-infarct dementia are especially well visualized on T2-weighted MRI images. Pick's disease is characterized by brain atrophy and decrease of radiotracer activity in the frontal lobes. In huntington's chorea the metabolic rate on PET scan in the area of the caudate nuclei may be reduced even before signs and symptoms become apparent. Furthermore, neuroimaging provides us with fairly typical finding in Creutzfeld-Jakob's disease, alcoholic dementia, Wilson's disease, hydrocephalus, Parkinson's disease, progressive supranuclear ophthalmoplegia, Fahr's disease, and the olivopontocerebellar ataxias. Neuroimaging techniques, however, have always to be interpreted in conjunction with clinical findings, thus disclosing their full range of information.
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PMID:[Diagnostic differentiation of dementia diseases by modern imaging procedures]. 227 95

Motor evoked potentials (MEPs) to transcranial stimulation (TCS) and somatosensory evoked potentials to median nerve stimulation (MN-SEPs) were examined in 74 patients affected by multiple sclerosis (MS = 49 cases), amyotrophic lateral sclerosis (ALS = 9 cases), cervical cord lesions (7 cases), Parkinson's disease (PD = 5 cases), Huntington's chorea (HC = 2 cases), Wilson's disease (WD = 1 case), subacute combined degeneration (SCD = 1 case). MN-SEPs were altered in 38% of arms in MS with a higher incidence in clinically affected than in clinically 'silent' arms (= 77.8% vs. 27.5%). MEP alterations were found in 54% of examined arms, mostly because of a prolongation of the motor CCT. This index was invariably altered in the affected arms, whilst it was involved in 40% of the 'silent' ones. Twelve out of 18 arms displayed abnormal MEPs in ALS. These were mainly due to an absent response, even if moderate motor CCT prolongation and 'giant' MEPs were also encountered. MN-SEPs were altered in 3/18 arms. By recording MEPs from proximal and distal upper limb muscles, cues on the level of abnormal propagation were obtained in patients suffering from 'focal' lesions of the spinal cord. Combining SEP records enhanced the diagnostic yield in this field. Both MEPs and SEPs were normal in patients with PD and HC, whilst abnormally prolonged CCTs were found in the case with WD. MEP and SEP recording revealed central propagation abnormalities coupled to a severe clinical picture of the peripheral nerve involvement (as in the case of SCD).
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PMID:Neurophysiological evaluation of the central nervous impulse propagation in patients with sensorimotor disturbances. 245 26

Technetium 99m hexamethylpropylene-amine oxime (HMPAO) is trapped by cerebral grey matter and the basal ganglia on its first pass through the brain. To assess its potential for studying patients with diseases of the basal ganglia, a study of 15 normal volunteers and 32 patients with known or suspected basal ganglia disease have been investigated. Sixteen patients with idiopathic Parkinson's disease showed no abnormality of the basal ganglia and varying degrees of cerebral underperfusion consistent with their intellectual status. Eight patients with Huntington's chorea showed a characteristic pattern of reduced or absent caudate nucleus uptake. Patients with diseases affecting the basal ganglia, such as Fahr's disease, Wilson's disease and hemibalismus had varying degrees of basal ganglia underperfusion as demonstrated by an HMPAO scan. We believe that this new radiopharmaceutical for the demonstration of cerebral blood flow shows significant potential for the diagnosis and management of patients with basal ganglia disease.
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PMID:Technetium-99m HMPAO imaging in patients with basal ganglia disease. 297 62

[3H]Spiperone binding to lymphocytes in Parkinson's disease (PD), Wilson's disease (WD), and age-matched control groups was studied. In the untreated PD group, [3H]spiperone binding was lower than in young controls, but did not differ from elderly healthy persons. After treatment with levodopa, the number of [3H]spiperone binding sites increased. In WD, lower binding of [3H]spiperone compared with age-matched controls was found. However, the magnitude of the differences in [3H]spiperone binding to lymphocytes in PD was too small to permit its use as a routine indicator of the disease state or the adequacy of pharmacological treatment in individual patients. [3H]Spiperone binding to lymphocytes decreases with age. Changes in [3H]spiperone binding to lymphocytes may be a general phenomenon for all states where dopamine is depleted, including normal aging. The nature of [3H]spiperone binding to lymphocytes remains unclear. The possible influence of dopamine on immune reactivity is discussed.
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PMID:[3H]spiperone binding to lymphocyte in extrapyramidal disease and in aging. 297 11

We describe a personal series of 60 cases of parkinsonism with onset under the age of 40 years. Known causes for early onset of secondary parkinsonism, such as Wilson's disease or encephalitis, were excluded in every case. Two groups were identified: those with onset after the age of 21 in whom no hereditary factors could be ascertained (56 cases), and those with onset before 21 years all of whom had familial parkinsonism. In neither group have we found any association with prematurely grey hair, hypertension, diabetes, pernicious anaemia, or thyroid disorder. Among their families, we have not found any association with diabetes, pernicious anaemia, or thyroid disorder. We propose that cases of apparent idiopathic Parkinson's disease beginning between age 21-40 years should be called "young onset Parkinson's disease." Twenty percent of such patients in our series had at least one first- or second-degree relative in the same or antecedent generations with parkinsonism, but only 1.5% of their relatives at risk had parkinsonism, which is similar to the prevalence in the general population. Ten percent of these patients had at least one relative with essential tremor, but only 1.6% of their relatives at risk had tremor, which again was similar to the prevalence in the population in general. These patients with young onset Parkinson's disease responded well to levodopa therapy. However, dyskinesias and response fluctuations occurred early and frequently. The prevalence of dyskinesias and response fluctuations was strongly correlated with the duration of levodopa treatment, but not with the duration (or probably the severity) of the disease before levodopa therapy was commenced. The involuntary movements often were severe and frequently were diphasic. Despite long disease duration, the incidence of dementia in young onset patients aged less than 65 years was negligible. We believe that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease. We have so far failed to identify any additional environmental factor which may have accelerated disease onset in these patients. In contrast, cases of parkinsonism beginning before age 21 years were invariably familial. We proposed that they should be called "juvenile parkinsonism." All affected relatives with parkinsonism also had young disease onset, and all but one were siblings. None of four such patients seen by us has demented, and computed tomography (CT) scan has been normal in all four. We believe that most such patients have some form of genetically determined secondary parkinsonism.
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PMID:Young onset Parkinson's disease. 350 66

Abnormal movements or postures often present a diagnostic and therapeutic challenge to the psychiatrist or neurologist. The authors review pertinent anatomy and physiology of disorders of the extrapyramidal system, suggest aspects of the clinical history and examination particularly important for diagnosis, and describe a range of abnormal movements. They review several syndromes in which abnormalities of behavior and movement may occur together, including Huntington's chorea, Wilson's disease, Parkinson's disease, and tardive dyskinesia.
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PMID:Movement disorders in the psychiatric patient. 623 96


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