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hi all; in re several messages recently about 'glistening' phenomena in pd i dug up the following from our own pd list archives at: <http://james.parkinsons.org.uk/> ------------------------------------------------- Date:14/12/97 20:26 From: janet paterson Subject:BX: Algorithm 2/4 ADVANCING PARKINSON'S DISEASE... DYSAUTONOMIAS... THERMOREGULATION... The neurochemical and anatomic regulation of temperature is complex and poorly understood. Preoptic and hypothalamic areas appear to have thermoregulatory function. Noradrenergic, serotonergic, and cholinergic systems have an incompletely understood role in thermal homeostatais. Sweating is mediated by efferent sympathetic cholinergic fibers, which may be damaged in PD. Lewy bodies and cell loss in the hypothalamus have been implicated in PD-associated sweating abnormalities. Management. Abnormal sensations of heat or cold, impaired sweating responses, and hypothermia all can occur in the untreated patient. Excessive sweating of the head and neck in response to external heat has been associated with poor heat dissipation. Some of these phenomena disappear with levodopa treatment, which suggests a role for central dopaminergic systems in thermoregulation. Severe drenching sweats occur as an end-of-dose "off" phenomenon in patients with motor fluctuations, further supporting a role for dopamine systems in vasomotor tone and heat regulation. Dopamine agonist therapy may be of benefit to such patients. Although peak-dose chorea can cause sweating, it is rarely if ever as severe as that seen in the "off' state. For patients who experience it, however, a reduction in the dopaminergic medications may help but often at the price of more "off" time. These patients are more likely to respond to beta-adrenergic blockers than are patients with "off"-period sweating. Severe hyperpyrexia after levodopa withdrawal resembles the neureleptic malignant syndrome and needs to be treated promptly with reinstitution of dopaminergic agents. Other causes of excessive sweating must not be neglected simply because the patient has PD. Benign sweating can occur with either a visual, olfactory or gustatory stimulus. Ethanol and aspirin in high doses also can cause increased intermittent sweats. Therefore, taking a thorough history usually will clarify these situations. Thyrotoxicosis and postmenopausal states need to be considered and appropriate endocrine evaluation initiated. Finally, chronic infections such as tuberculosis must not be forgotten in the differential diagnosis. ------------------------------------------------- i have also found some relevant abstracts from pubmed at: <http://www.ncbi.nlm.nih.gov/PubMed/> ------------------------------------------------- Sweating dysfunction in Parkinson's disease. Sweating was measured with an evaporimeter in 5 different positions on both sides of the body in 23 patients with idiopathic Parkinson's disease and in 11 age-matched control subjects before and after a heating stimulus. Perspiration was increased significantly both before and after the heating provocation in the upper part of the body (the forehead, chest and forearm) of Parkinson patients in comparison with the control subjects (p less than 0.05). The increase of perspiration correlated significantly (p less than 0.05) with the severity of Parkinson's disease as estimated by the Webster scale. The results indicate wide and clear autonomic nervous system dysfunction in Parkinson's disease. PMID: 03816881 UI: 87133722 Eur Neurol 1987;26(1):1-7 Turkka JT, Myllyla VV ------------------------------------------------- Alterations of thermoregulation in Parkinson's disease. Sweating and superficial vasodilator responses were studied in 22 patients suffering from Parkinson's disease in order to evaluate the thermoregulatory function. Sweating was evaluated on different areas of the body with a colorimetric method (Minor's method). The superficial vasodilatation at the level of the face was assessed after oral intake of nitroglycerin by means of telethermography. Sweating and superficial vasodilatation were reduced in parkinsonian patients compared with control subjects. Asymmetries in sweating and superficial vasodilator responses were also observed between the left and right sides of the body in the patients. The decreased heat elimination was more apparent on the symptomatic side in patients with hemiparkinsonism. No relationship was found between the alterations of the thermoregulation and the other clinical features of Parkinson's disease. PMID: 01743543 UI: 92077466 Funct Neurol 1991 Jul-Sep;6(3):279-83 De Marinis M, Stocchi F, Testa SR, De Pandis F, Agnoli A La Sapienza University, Rome, Italy ------------------------------------------------- Sweat function in Parkinson's disease. Sweat function was studied in patients with Parkinson's disease and in normal adults by sympathetic skin response, the bromphenol blue printing method and the silicone mould method. In patients with Parkinson's disease, dysfunction of sweating was classified into two types: one type involved the postganglionic fibres and the other involved the preganglionic fibres or the central nervous system. The latter was observed in patients with milder disease and the former was observed in patients with severe disease. The progressive involvement of sweat function in Parkinson's disease may reflect spread from the central nervous system or preganglionic fibres to postganglionic fibres. In a few patients the results of sweat tests were normal. Ceruletide increased sweating in Parkinson's disease patients, and decreased the prolonged latency of the sympathetic skin response. It is hypothesized that ceruletide facilitates the preserved somatosympathetic reflex of sweating. PMID: 07836959, UI: 95138745 J Neurol 1994 Oct;241(10):573-6 Mano Y, Nakamuro T, Takayanagi T, Mayer RF Department of Neurology, Nara Medical University, Japan. ------------------------------------------------- janet paterson - 51 now /41 dx /37 onset - almonte/ontario/canada [log in to unmask]