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)

Vascular parkinsonism has not been well defined and the clinical correlation of vascular parkinsonism is still not clear. The aim of the study was to estimate prevalence of occurrence of vascular parkinsonism, analysis of risk factors leading to its development and to identify clinical features that suggest a vascular origin. 214 patients with Parkinson's disease were examined. Their ages ranged from 37 to 88 years (median 66.4 years). Evidence of vascular parkinsonism was assessed using a vascular rating scale previously described by Winikates and Jankovic. Statistical analysis was performed with Mann-Whitney U test, chi 2 Pearson test, chi 2 Yates test, Spearman rank correlation and Student's t test. Out of 214 patients 8 were proved to have developed Parkinson's disease due to vascular disease, what gave 3.74%. Out of risk factors for stroke 5 patients had hypertension, 3 had diabetes mellitus, 2 suffered from heart disease, 2 had infarctus myocardii, 1 had hyperlipidemia, 1 had atrial fibrillation. Additionally, those patients had neuroimaging (CT or MRI) evidence of vascular disease in one or more vascular territories. Patients with vascular parkinsonism were older, had shorter duration of disease, were more likely to present rigidity rather than tremor. Dementia and incontinence were more common in vascular group than in Parkinson's disease group. Patients with vascular parkinsonism were also significantly more likely to have corticospinal findings. Proving that Parkinson's disease had vascular etiology is extremely difficult. The test results are inconclusive.
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PMID:[Clinical correlation of vascular parkinsonism]. 1509 42

Lewy bodies (LB) are characteristic pathological findings for idiopathic Parkinson disease, and extracranial organs have also been known to exhibit these structures. Clinically, the possible involvement of LB in cardiac dysfunction has attracted attention based on the findings of studies using [123I] metaiodobenzyl guanidine (MIBG) scintigraphy. The purpose of the present study was to investigate the possible involvement of LB in heart disease. A total of 40 autopsy cases consisting of Lewy body disease and Parkinson syndrome were examined. The former were cases with intracranial LB regardless of clinical symptoms, and the latter were cases with parkinsonism but without intracranial LB. The presence of heart disease or an atrial arrhythmia and the results of an MIBG scintigraphy study were clinically examined. The sinoatrial node was examined microscopically and immunohistochemically. The results showed that heart disease and atrial arrhythmia complications were more frequent in cases with Lewy body disease than in cases with Parkinson syndrome and that LB were frequently found in extracranial organs, especially in the sinoatrial nodal ganglion, in cases with Lewy body disease. In the current report, we hypothesized that neuronal changes involving LB in the sinoatrial nodal ganglion may cause arrhythmia and ischemic heart disease as a result of vasoconstriction.
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PMID:Lewy bodies in the sinoatrial nodal ganglion: clinicopathological studies. 1536 36

Epidemiologic evidence has linked elevation of serum homocysteine to an increased risk of coronary artery disease, stroke, and dementia. An increase in homocysteine levels in Parkinson disease (PD) recently has been discovered. Although B vitamin status and genetic factors are important modifying influences determining the degree of this elevation, the main cause appears to be therapy with L-dopa. It has been suggested that breakdown of L-dopa by catechol-O-methyltransferase results in increased homocysteine formation. Therefore, there are reasons to suggest that management of PD may render patients at increased risk of stroke, heart disease, dementia, and even accelerated nigral degeneration. At present, no controlled prospective studies have evaluated this phenomenon, although they are ongoing.
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PMID:Homocysteine and levodopa: should Parkinson disease patients receive preventative therapy? 1536 41

Although chronic illness is likely to affect the well-being of patients' children, no assessment tools are currently available to measure this impact of parental illness. We therefore developed such an instrument based on interviews with children of patients with Parkinson's disease (PD). This questionnaire and other measures of psychological well-being were completed by 89 children, aged 12-48, years of patients with PD. Factor analysis revealed six domains with 38 questions. These six domains of the 'Parental Illness Impact Scale (Parkinson's disease)' or PIIS (PD) had satisfactory internal consistency and validity. Its six sub-scales correlated significantly and differentially with corresponding measures, including the Quality of Life in Epilepsy Inventory for Adolescents (QOLIE-AD-48; r = -0.2 to 0.85), the Beck Depression Inventory (r = -0.07 to -0.40) or Birleson Depression Self-Rating Scale (r = 0.04 to -0.62), and the Rosenberg Self-Esteem Scale (r = -0.01 to 0.33) as well as age (r = -0.37 to 0.28) and parent's disease duration (r = -0.31 to 0.34). The PIIS is the first instrument to assess the impact of parental illness on children. Its psychometric properties should be tested further in larger samples, including children of patients with other chronic disorders such as multiple sclerosis or chronic heart disease.
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PMID:Development of a measure of the impact of chronic parental illness on adolescent and adult children. The parental illness impact scale (Parkinson's disease). 1546 95

Elevated homocysteine is associated with increased risk of heart disease, stroke, and dementia. Therapy of Parkinson disease (PD) with levodopa elevates homocysteine. The authors conducted a 6-week, multicenter, randomized, double-blind, placebo-controlled trial to test whether folate 1 mg/vitamin B(12) 500 microg or entacapone reduced serum homocysteine in 35 levodopa-treated PD patients. Levodopa initiation caused a small elevation in homocysteine. Vitamin therapy, but not entacapone, resulted in a decrease in homocysteine compared to placebo.
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PMID:Vitamins and entacapone in levodopa-induced hyperhomocysteinemia: a randomized controlled study. 1745 98

Treatment of migraine presents special problems in the elderly. Co-morbid diseases may prohibit the use of some medications. Moreover, even when these contraindications do not exist, older patients are more likely than younger ones to develop adverse events. Managing older migraine patients, therefore, necessitates particular caution, including taking into account possible pharmacological interactions associated with the greater use of drugs for concomitant diseases in the elderly. Paracetamol (acetaminophen) is the safest drug for symptomatic treatment of migraine in the elderly. Use of selective serotonin 5-HT(1B/1D) receptor agonists ('triptans') is not recommended, even in the absence of cardiovascular or cerebrovascular risk, and NSAID use should be limited because of potential gastrointestinal adverse effects. Prophylactic treatments include antidepressants, beta-adrenoceptor antagonists, calcium channel antagonists and antiepileptics. Selection of a drug from one of these classes should be dictated by the patient's co-morbidities. Beta-adrenoceptor antagonists are appropriate in patients with hypertension but are contraindicated in those with chronic obstructive pulmonary disease, diabetes mellitus, heart failure and peripheral vascular disease. Use of antidepressants in low doses is, in general, well tolerated by elderly people and as effective, overall, as in young adults. This approach is preferred in patients with concomitant mood disorders. However, prostatism, glaucoma and heart disease make the use of tricyclic antidepressants more difficult. Fewer efficacy data in the elderly are available for selective serotonin reuptake inhibitors, which can be tried in particular cases because of their good tolerability profile. Calcium channel antagonists are contraindicated in patients with hypotension, heart failure, atrioventricular block, Parkinson's disease or depression (flunarizine), and in those taking beta-adrenoceptor antagonists and monoamine oxidase inhibitors (verapamil). Antiepileptic drug use should be limited to migraine with high frequency of attacks and refractoriness to other treatments. Promising additional strategies include ACE inhibitors and angiotensin II type 1 receptor antagonists because of their effectiveness and good tolerability in patients with migraine, particularly in those with hypertension. Because of its favourable compliance and safety profile, botulinum toxin type A can be considered an alternative treatment in elderly migraine patients who have not responded to other currently available migraine prophylactic agents. Pharmacological treatment of migraine poses special problems in regard to both symptomatic and prophylactic treatment. Contraindications to triptan use, adverse effects of NSAIDs, and unwanted reactions to some antiemetics reduce the list of drugs available for the treatment of migraine attacks in elderly patients. The choice of prophylactic treatment (beta-adrenoceptor antagonists, calcium channel antagonists, antiepileptics, and more recently, some antihypertensive drugs) is influenced by co-morbidities and should be directed at those drugs that are believed to have fewer adverse effects and a better safety profile. Unfortunately, for most of these drugs, efficacy studies are lacking in the elderly.
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PMID:Practical considerations for the treatment of elderly patients with migraine. 1687 31

It has been suggested that L-DOPA-induced hyperhomocysteinemia can increase the risk of stroke, heart disease, and dementia and is an additional pathogenetic factor involved in the progression of Parkinson's disease. In Chinese hamster ovary (CHO) cells stably cotransfected with adenosine A(2A) and dopamine D2 receptors, homocysteine selectively decreased the ability of D2 receptor stimulation to internalize adenosine A(2A)-dopamine D2 receptor complexes. Radioligand-binding experiments in the same cell line demonstrated that homocysteine acts as an allosteric D2 receptor antagonist, by selectively reducing the affinity of D2 receptors for agonists but not for antagonists. Mass spectrometric analysis showed that, by means of an arginine (Arg)-thiol electrostatic interaction, homocysteine forms noncovalent complexes with the two Arg-rich epitopes of the third intracellular loop of the D2 receptor, one of them involved in A(2A)-D2 receptor heteromerization. However, homocysteine was unable to prevent or disrupt A(2A)-D2 receptor heteromerization, as demonstrated with Fluorescence Resonance Energy Transfer (FRET) experiments in stably cotransfected HEK cells. The present results could have implications for Parkinson's disease.
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PMID:Allosteric modulation of dopamine D2 receptors by homocysteine. 1708 Oct 59

Embryonic stem cells (ESCs) offer a new and remarkable potential for treating and curing a wide range of genetic diseases such as diabetes and muscular dystrophy, degenerative diseases such as Parkinson's disease, renal disease and heart disease, and traumatic injury such as spinal cord injury. Therapeutic cloning, wherein patient-specific ESCs can be derived from pre-implantation stage embryos produced by somatic cell nuclear transfer, constitutes one approach of obtaining histocompatible cells for engraftment. Recent improvements in the production of cloned embryos in non-human primate models, combined with advances in the ability to establish human ESC lines and direct their differentiation along specific pathways support the notion that therapeutic cloning may soon be feasible. This review summarizes the status and current feasibility of the approach and the technical hurdles that must be addressed, and discusses the ethical issues that have arisen as a result.
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PMID:Therapeutic cloning: status and prospects. 1769 52

Restrictive valvular heart disease (VHD) has recently been reported in Parkinson's disease (PD) patients treated with ergot dopamine agonists. The aim of the present study was to detect valvular changes in our patients and to investigate their relationship to long-term use of pergolide. We examined 90 patients (mean age 60.8 +/- SD 9.5 years) with PD, average duration 10.0 +/- 5.1 years. Mean pergolide dose was 2.93 +/- 0.75 (range 0.75 to 5) mg per day. 36 subjects (mean age 55.0 +/- 12.8 years) served as controls. All subjects underwent transthoracic echo-Doppler examination. Valve morphology was rated as normal, fibrotic, restrictive, or degenerative. In addition, the mitral tenting area (TA) and tenting distance (TD) were assessed. In 40 out of 90 (45%) PD patients and in 13 out of 36 (36%) controls, mild mitral regurgitation was observed. In 1 PD patient, a moderate mitral regurgitation was recorded. However, no case of restrictive VHD was found. Neither the TA (1.44 +/- 0.24 cm(2) vs 1.33 +/- 0.44 cm(2)) nor the TD (0.73 +/- 0.10 cm vs. 0.72 +/- 0.30 cm) differed from controls. There were no correlations between the current or cumulative dose of pergolide and TA or TD. Discrete fibrotic changes on valves were found in 10 out of 90 (11%) patients. Degenerative changes of valves were found in 11 (12%) patients and in 7 (19 %) controls. Thus in contrast to earlier findings of restrictive VHD in up to one-third of PD patients on pergolide, we did not find any significant heart disease. We only observed mild to moderate mitral regurgitation and clinically insignificant valvular fibrosis. A possible reason for such a discrepancy is that the daily doses of pergolide in our patients were inferior to those reported previously. In conclusion, the prevalence of restrictive VHD has been lower than expected in our patients with PD, probably in relation to moderate daily doses of pergolide.
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PMID:Low incidence of restrictive valvulopathy in patients with Parkinson's disease on moderate dose of pergolide. 1875 89

Sporadic and chronic fatigue are common, but an underlying etiology is identified in only up to 10% of cases. Under-reporting makes fatigue's prevalence unknown. Some estimate up to 50% of elders suffer from mild fatigue. Causes vary, but prevailing theory links most fatigue as a secondary consequence to illness and medication. Fatigue is prominently linked to sleep disorders, depression, heart disease, Parkinson's disease, anemia, and cancer. Fatigue and its consequences should be assessed routinely. Empiric treatment is the norm, focusing on managing fatigue, and, when possible, selecting agents with fewer side effects. Exercise, diet, and promoting good sleep hygiene have beneficial effects in symptom management.
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PMID:Fatigue: implications for the elderly. 1771 1


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