Acta neurologica Scandinavica. Supplementum最新文献

{"title":"Current strategies in the drug treatment of advanced Parkinson's disease--new modes of dopamine substitution.","authors":"L Schelosky,&nbsp;W Poewe","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Oral levodopa treatment remains the most efficacious treatment of Parkinson's disease, but the majority of patients treated with a levodopa monotherapy for more than 5 years will develop fluctuations and/or dyskinesias. Important pathophysiological mechanisms are peripheral factors resulting in fluctuating levodopa blood concentrations and central pharmacodynamic changes, possibly due to chronic pulsatile stimulation of dopamine receptors. Continuous dopaminergic stimulation is able to smooth out a fluctuating response to oral levodopa and reduce 'off period' dystonia and the intensity of 'peak dose' dyskinesias. New drug delivery techniques include 'slow release' levodopa preparations and subcutaneous infusions of apomorphine. Future methods of transcutaneous or intramuscular application of dopamine agonists are under development. These methods may help to improve the results of long-term levodopa treatment of parkinsonian patients.</p>","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"146 ","pages":"46-9"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19094794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strategies in the treatment of early Parkinson's disease.","authors":"U K Rinne","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Over recent years I have been studying whether dopamine agonist treatment alone, or in early combination with levodopa, might institute a better long-term treatment in Parkinson's disease than levodopa alone. Indeed, early combination of levodopa with bromocriptine, pergolide or lisuride has indicated that this kind of treatment results in better management of Parkinson's disease with fewer fluctuations in disability, especially end-of-dose disturbances and dyskinesias, than treatment with levodopa alone. Furthermore, similar results were obtained by using lisuride in combination with selegiline and levodopa. Thus, it appears advisable to initiate the dopaminergic treatment in early Parkinson's disease by using a combination of selegiline, levodopa and a dopamine agonist. There are many ways of building up this kind of treatment. Instead of levodopa, it is possible to use initially a dopamine agonist and to add selegiline and levodopa when the therapeutic response becomes insufficient. Another alternative would be to start with selegiline alone, then to add a dopamine agonist and, finally, levodopa when clinically indicated.</p>","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"146 ","pages":"50-3"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19093896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computer-aided decision-making for epilepsy and sleep diagnostics.","authors":"L Korpinen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The main objective of the study was first to develop two prototypes of decision support systems for epilepsy and sleep disorder diagnostics. The second goal was to examine medical decision-making with the help of these program examples and further to assess what requirements should be set to decision support systems for them to find their place in clinical work. Requirements were first defined for the systems to be developed. The requirements were, for the most part, successfully taken into consideration during the development process. Epilepsy Expert, a decision support system based on the International Classification of Epilepsies and Epileptic Syndromes (51) was then developed. An epilepsy expert was in a central role in the development work due to the nature of the classification. For sleep disorders Sleep Expert, a decision support system, was developed based on the International Classification of Sleep Disorders (52). In the developing of the system the role of experts in sleep disorders was minor as the international classification provided a good foundation for program knowledge. The knowledge of the programs was validated as follows. First, three experts were requested to provide 10 case descriptions, and then they made diagnoses of their colleagues' patients. On the basis of these diagnoses a majority agreement, 'the right diagnosis', was reached. From the same epilepsy cases the author made diagnoses with the aid of the decision tree of Epilepsy Expert. Two other physicians, who were not experts in sleep disorders, made diagnoses for sleep disorders using Sleep Expert. In the validation Epilepsy Expert proved partly incomplete, which was due in part to the weakness of the international classification. However, the section of the program whose diagnostics was based on clinical findings only was as good as the experts. In the validation of Sleep Expert the physicians who used the program did not achieve as good results as the experts. The functionality of the programs was evaluated with questionnaires. According to this limited inquiry Sleep Expert could be used in clinical work, whereas Epilepsy Expert was regarded as being weaker. As a whole Sleep Expert was better than Epilepsy Expert. The conclusions to be drawn from the study are: In the development phase factors related to users, knowledge, problem definition and the environmental adaptation of the system need to be taken into account. If international classifications are to be used as a basis for the systems' knowledge, classification should be sufficiently clear and precise in respect of individual diagnoses.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"144 ","pages":"1-101"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19308613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered mitochondrial function, iron metabolism and glutathione levels in Parkinson's disease.","authors":"P Jenner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The mechanisms underlying dopamine cell death in substantia nigra in Parkinson's disease remain unknown. Current concepts of this process suggest the involvement of free radical species and oxidative stress. Indeed, in postmortem tissues from patients dying with Parkinson's disease there is evidence for inhibition of complex I of the mitochondrial respiratory chain, altered iron metabolism and decreased levels of reduced glutathione. However, alterations in iron levels in substantia nigra are not specific to Parkinson's disease but also occur in other basal ganglia degenerative diseases. So, alterations in iron may be a response to, rather than a cause of nigral cell death. This is further suggested by a failure to find any alterations in iron metabolism in cases of incidental Lewy body disease (presymptomatic Parkinson's disease). Similarly, in these tissues no significant alteration in complex I activity is apparent. However, there is a reduction in the levels of reduced glutathione in substantia nigra in incidental Lewy body disease of the same magnitude as occurs in advanced Parkinson's disease. This would suggest that alterations in glutathione function are an early marker of pathology in Parkinson's disease and may be a clue to the primary cause of nigral cell death.</p>","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"146 ","pages":"6-13"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19320144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New approaches to the pathophysiology and treatment of Parkinson's disease. Proceedings of a symposium at the 2nd Congress of the Paneuropean Society of Neurology. Vienna, December 1991.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"146 ","pages":"5-53"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19094795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotinamide adenine dinucleotide (NADH)--a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application.","authors":"J G Birkmayer,&nbsp;C Vrecko,&nbsp;D Volc,&nbsp;W Birkmayer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The reduced coenzyme nicotinamide adenine dinucleotide (NADH) has been used as medication in 885 parkinsonian patients in an open label trial. About half of the patients received NADH by intravenous infusion, the other part orally by capsules. In about 80% of the patients a beneficial clinical effect was observed: 19.3% of the patients showed a very good (30-50%) improvement of disability, 58.8% a moderate (10-30%) improvement. 21.8% did not respond to NADH. Statistical analysis of the improvement in correlation with the disability prior to treatment, the duration of the disease and the age of the patients revealed the following results: All these 3 parameters have a significant although weak influence on the improvement. The disability before the treatment has a positive regression coefficient (t value < 0.01). The duration of the disease has a negative regression coefficient (< 0.01) and so has the age a negative regression coefficient (t value < 0.05). In other words younger patients and patients with a shorter duration of disease have a better chance to gain a marked improvement than older patients and patients with longer duration of the disease. The orally applied form of NADH yielded an overall improvement in the disability which was comparable to that of the parenterally applied form.</p>","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"146 ","pages":"32-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19094793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracranial blood flow, pain and tenderness in migraine. Clinical and experimental studies.","authors":"K Jensen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Migraine pain has traditionally been ascribed to dilatation of primarily extracranial arteries. Such dilatation has, however, not been demonstrated so far. Studies of microcirculation reveal no major hyperperfusion or ischemia in the temporal muscle or the subcutaneous tissue in the temporal region during attacks of migraine. However, a reduction in the orthostatic reactivity of the subcutaneous arterioles was observed on the side of the headache. Increased tenderness of the pericranial myofascial tissues is observed during migraine attacks, particularly on the side of the headache. Increased tension of pericranial muscles on the other hand is not a constant finding and migraine attacks are not induced by experimentally increased tension of the temporal and masseter muscles. Extracranial pain and tenderness may, however, be induced experimentally by intramuscular injections of hypertonic saline and potassium chloride as well as of endogenous substances like bradykinin with 5-hydroxytryptamine and bradykinin with substance P. The extracranial arteries and myofascial structures are both supplied by unmyelinated trigeminal sensory nerve fibers containing a variety of neuropeptides which are released during migraine attacks. Axonal reflexes between extracranial arteries and neighbouring myofascial tissues as well as referred pain mechanisms may account for the observed tenderness during migraine attacks.</p>","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"147 ","pages":"1-27"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18696198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoreactive T and B cells in nervous system diseases.","authors":"J B Sun","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>Abnormal autoimmunity could play a role in the pathogenesis of multiple sclerosis (MS), in analogy with its model experimental allergic encephalomyelitis (EAE) which can be transferred by T cell lines directed to myelin basic protein (MBP) and myelin proteolipid protein (PLP), and worsened with antibody to myelin oligodendrocyte glycoprotein (MOG). Whether T and B cell reactivities to these autoantigens, and to myelin-associated glycoprotein (MAG) which is another possible target for autoimmune attack, occur in MS and then especially in the cerebrospinal fluid (CSF) with its close relation to the nervous tissue, is not clear. Myasthenia gravis, a prototype for autoimmune disease in humans, is characterized by IgG antibodies to acetylcholine receptor (AChR) in serum, but it is not known whether an augmented T cell response to AChR occurs in this disease. Nerve trauma has been speculated upon to be associated with exacerbations of MS; if nerve trauma recruits augmented autoimmune T and B cell responses is not known. High numbers of anti-myelin protein and anti-AChR antibody secreting cells have been described in cord blood, but whether corresponding T cell reactivities occur remains to be settled.</p><p><strong>Methods: </strong>Antigen specific T cell responses in blood and CSF are studied regarding specificity, quantity and functional differentiation by counting numbers of cells which, upon antigen stimulation, respond by secretion of interferon-gamma (IFN-gamma). Similarly, the B cell responses to autoantigens are evaluated by counting cells which, in presence of antigen, secrete specific antibodies of IgG, IgA and IgM isotypes.</p><p><strong>Results: </strong>MS is characterized by elevated numbers of T cells recognizing MBP, PLP, MAG and MOG as well as the synthetic MBP amino acid sequences 1-20, 63-88, 89-101, 96-118, 110-128 and 148-165, without immunodominance for any of these components. PLP, MOG and MAG reactive T cells are strongly enriched in the patients' CSF, as previously also shown for MBP reactive T cells. Similarly, elevated numbers of B cells with these specificities and enriched in CSF were found in MS. No preferential autoimmune T cell response was apparent after subdivision of the MS patients according to their HLA-DR genotype. A majority of patients with myasthenia gravis had AChR and alpha-subunit reactive T cells in peripheral blood, and also anti-AChR antibody secreting cells of the IgG, less frequently IgA and IgM isotypes. Peripheral nerve trauma in form of diagnostic sural nerve biopsy is accompanied by transient elevation in blood of T cells recognizing MBP and MAG which are common to the central and peripheral nervous system, and to the peripheral nerve myelin proteins P0 and P2. Myelin protein and AChR reactive T and B cells occur also in patients with other neurological diseases and tension headache, and in healthy subjects, but less frequently and at lower numbers than in MS and myas","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"142 ","pages":"1-56"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19368723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epileptic equivalents in psychiatry: some 19th century views.","authors":"B Schmitz,&nbsp;M Trimble","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"140 ","pages":"122-6"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12612412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of initial brain ischemia in subarachnoid hemorrhage following aneurysm rupture. A pathophysiological survey.","authors":"M Jakobsen","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75395,"journal":{"name":"Acta neurologica Scandinavica. Supplementum","volume":"141 ","pages":"1-33"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12646235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}