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)

Retroperitoneal fibrosis is a rare complication of pergolide therapy. This complication can be easily missed, so it is essential to have a high index of suspicion. We describe a case of well controlled Parkinson's disease who presented with shortness of breath and oedema.
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PMID:Pergolide-induced retroperitoneal fibrosis. 1109 16

We experienced 2 patients of valvular heart disease in Parkinson's patients taking cabergoline. Patient 1 was a 79-year-old woman who began taking 4 mg cabergoline daily after being diagnosed with Parkinson's disease (PD) in June 2003. She presented with dyspnea in November 2005. The patient had cardiomegaly, pulmonary congestion, and pleural effusion, and an echocardiogram showed valvular heart disease in the form of aortic regurgitation (AR) (grade I), tricuspid regurgitation (TR) (grade I), and mitral regurgitation (MR) (grade III). Cabergoline was thought to have caused these phenomena, so it was replaced with pramipexole, and after administration of diuretics and angiotensin-converting enzyme inhibitors (ACEIs) the patient's symptoms gradually disappeared. MR, AR and TR also disappeared 3 months later. Patient 2 was a 74-year-old woman who presented with sluggish movement in April 2001 and subsequently developed Parkinson's. While being administered 700 mg levodopa (Menesit) and 4 mg cabergoline, the patient presented with shortness of breath in April 2005. An echocardiogram showed valvular heart disease in the form of MR (grade I) and TR (grade I). Heart function improved with the administration of diuretics. However, heart function again worsened in November 2005, and the patient presented with edema of the lungs and lower limbs. An echocardiogram in January 2006 showed worsening MR (grade III) and TR (grade II), and the patient also had pulmonary hypertension. ACEIs were administered along with diuretics and cabergoline was replaced with pramipexole, but the patient also developed malignant syndrome and disseminated intravascular coagulation (DIC) and later died. Patient 2 is the first case in Japan of death due to heart failure caused by the side effects of cabergoline. Caution is usually needed when treating a Parkinson's patient for valvular heart disease due to a dopamine agonist, and periodic checks for heart murmurs and echocardiography are crucial. When signs of heart failure develop during treatment with an ergot preparation of dopamine agonist, it is essential to immediately either stop the administration of the ergot preparation or change to a non-ergot preparation of dopamine agonist.
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PMID:[Two cases of patients with Parkinson's disease developing valvular heart disease while taking cabergoline]. 1871 82

Although levodopa is considered the gold standard for Parkinson's disease therapy, prolonged use of this drug can result in motor complications such as a 'wearing-off' phenomenon. This outcome is seen in a significant number of patients with Parkinson's disease taking levodopa and, in some cases, is observed only a few hours after intake of the last dose of levodopa. Patients experiencing the wearing-off period may present with sensory, autonomic, psychiatric and motor fluctuations. Although infrequent, shortness of breath is an important non-motor wearing-off symptom experienced by patients with Parkinson's disease. In addition to being a symptom induced by wearing off, other causes of shortness of breath include pulmonary diseases, coronary artery disease and anxiety. Thus, it is important to identify the cause of shortness of breath to ensure that the appropriate treatment is initiated. We report here on a patient with Parkinson's disease who was taking levodopa and developed both shortness of breath and hyperventilation during wearing-off periods. He underwent extensive pulmonary and cardiac investigations that were unremarkable. His shortness of breath was determined to be a wearing-off phenomenon and his condition improved with the addition of a catechol-O-methyltransferase inhibitor (entacapone).
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PMID:Shortness of breath, a 'wearing-off' symptom in Parkinson's disease. 1971 85

Bilateral vocal cord paralysis leading to stridor is a known but rare complication of Parkinson's disease (PD) and a recognised complication of multiple system atrophy (MSA). Tracheostomy is a commonly offered treatment, leading to substantial adaptations and lifestyle changes for the patient. Patients can struggle to manage a tracheostomy due to the tremor and bradykinesia associated with their parkinsonism. We report a case of bilateral vocal cord paralysis leading to significant stridor in a patient with atypical parkinsonism (probable MSA). To avoid tracheostomy, our patient underwent successful right-sided laser arytenoidectomy and posterior cordotomy as a day-case procedure. At follow-up, he had a weaker voice but complete recovery from the shortness of breath and stridor. He was very satisfied with the outcome. We conclude that, despite resulting in a weaker voice, this procedure offers an option to the patient that improves quality of life.
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PMID:Laser arytenoidectomy and posterior cordotomy in a patient with bilateral vocal cord paralysis due to multiple system atrophy. 2593 70

Nutritional protein may decrease levodopa absorption and has resulted in withdrawal and neuroleptic malignant-like syndromes in critically ill patients. A 72-year-old male was admitted with shortness of breath. His medical history included Parkinson's disease for over 30 years for which he took carbidopa/levodopa 5 times daily. The patient's home medications were continued. On day 2, he was intubated and transferred to the intensive care unit (ICU). He was extubated the next day and reintubated on day 4. Enteral nutrition was initiated at 85 mL/h overnight. The patient's carbidopa/levodopa was administered to limit coadministration with nutrition. Throughout his ICU stay, the patient did not demonstrate changes in mental status. Despite resolution of his pneumonia, he developed fever after administration of one dose overlapping with nutrition, with defervescence throughout the rest of the day. On hospital day 10, that dose was empirically increased. After this dosing change, the patient failed to develop fever during the rest of his hospital stay. On day 16, the patient was discharged to a long-term care facility without any other complications. Our case highlights the interaction between levodopa and enteral nutrition and the potential of fever as the sole sign of withdrawal.
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PMID:Levodopa Withdrawal Presenting as Fever in a Critically Ill Patient Receiving Concomitant Enteral Nutrition. 2680 58

Respiratory dysfunction has been associated with Parkinson's disease since it was first described in 1817. The respiratory symptoms observed in Parkinson's disease patients vary greatly. Most patients remain asymptomatic, whereas others present with acute shortness of breath and even stridor. In August 2016, an electronic literature search was conducted using PubMed and Google Scholar. Results were screened and studies reporting on respiratory dysfunction associated with Parkinson's disease were included. Respiratory dysfunction is due to a combination of factors including restrictive changes, upper airway obstruction, abnormal ventilatory drive and response to medications. Much debate surrounds the mechanism underlying respiratory dysfunction in Parkinson's disease, its prevalence and the effect of levodopa on respiration. It is clear from this review that larger studies, comparing patients of similar disease duration and severity using the same pulmonary function parameters, are required to provide a better understanding of the pathophysiology underlying respiratory dysfunction in Parkinson's disease.
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PMID:Respiratory dysfunction in Parkinson's disease. 2856 80

Anosmia, stroke, paralysis, cranial nerve deficits, encephalopathy, delirium, meningitis, and seizures are some of the neurological complications in patients with coronavirus disease-19 (COVID-19) which is caused by acute respiratory syndrome coronavirus 2 (SARS-Cov2). There remains a challenge to determine the extent to which neurological abnormalities in COVID-19 are caused by SARS-Cov2 itself, the exaggerated cytokine response it triggers, and/or the resulting hypercoagulapathy and formation of blood clots in blood vessels throughout the body and the brain. In this article, we review the reports that address neurological manifestations in patients with COVID-19 who may present with acute neurological symptoms (e.g., stroke), even without typical respiratory symptoms such as fever, cough, or shortness of breath. Next, we discuss the different neurobiological processes and mechanisms that may underlie the link between SARS-Cov2 and COVID-19 in the brain, cranial nerves, peripheral nerves, and muscles. Finally, we propose a basic "NeuroCovid" classification scheme that integrates these concepts and highlights some of the short-term challenges for the practice of neurology today and the long-term sequalae of COVID-19 such as depression, OCD, insomnia, cognitive decline, accelerated aging, Parkinson's disease, or Alzheimer's disease in the future. In doing so, we intend to provide a basis from which to build on future hypotheses and investigations regarding SARS-Cov2 and the nervous system.
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PMID:Neurobiology of COVID-19. 3253 57