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Anti-Parkinson Drugs

Bradykinesia is slowness and poverty of movement. Anti-Parkinson Drugs... [Pg.283]

Dopaminergic System Anti-Parkinson Drugs a-Adrenergic System... [Pg.437]

Suggest a synthesis fpr the anti-Parkinson drug orphenadrine (23). [Pg.57]

More typical examples are the amino ethers (3) used as anti-histamine or anti-Parkinson drugs according to the substituents. These are obviously derived from the alcohols (4) which are made from an aryl Grignard reagent and a benzaldehyde. Either starting material may bear the substituent X the choice can be made according to availability and so that side reactions are avoided,... [Pg.94]

Toxicity is remarkably low for a compound of such activity. In mice, the LDso value is about three times that of chlorpromazine [166] while none of the effects of the latter drug on the myocardium, liver, skin or eye have appeared in the studies of oxypertine. It is, however, still too early to appraise its chronic toxicity in man. As indicated earlier, dangerous interactions are likely to follow concurrent use of a MAO inhibitor, though simultaneous use of anti-Parkinsonism drugs, for example, to control the relatively minor extra-pyramidal symptoms seems to present no unusual problems. Hypotension may occasionally occur with high doses. [Pg.25]

Youdim, M.B.H. (2006) The path from anti Parkinson drug selegiline and rasagiline to multifunctional neuroprotective anti... [Pg.294]

N. P. Quinn (1984). Anti-Parkinson drugs today. Drugs 28 236-262. [Pg.303]

Wesemann, W., Sturm, G., Funfgeld, E. W. Distribution of metabolism of the potential anti-Parkinson drug memantine in the human, J. Neural Transm. 1980, 16, Suppl., 143-148. [Pg.427]

The primary adverse effects associated with amantadine are orthostatic hypotension, CNS disturbance (e.g., depression, confusion, hallucinations), and patches of skin discoloration on the lower extremities (livedo reticularis). However, these side effects are relatively mild compared to those of other anti-Parkinson drugs and are usually reversed by altering the drug dosage. [Pg.128]

Controversy exists as to when specific anti-Parkinson drugs should be employed.1,16 Much of the debate focuses on when levodopa therapy should be initiated. Without question, levodopa is the most effective pharmacological treatment for reducing the motor symptoms of Parkinson disease. As mentioned previously, however, long-term use of levodopa poses several risks, and the effectiveness of this drug seems to diminish after several years of use. Consequently, some practitioners question whether levodopa therapy should be withheld until the parkinsonian symptoms become severe enough to truly impair motor function. In theory, this saves the levodopa for more advanced stages of this disease, when it would be needed the most.48... [Pg.129]

Anti-Parkinson Drugs, Dopamine Agonists (bromocriptine, pergolide, cabergoline)... [Pg.533]

The rationale for the need of recovery animals was frequently discussed. For drag substances which require chronic (live time) treatment (e.g. oral anti-diabetics, drags for treatment of hypertension, anti-Parkinson drugs, etc.) the question of recovery is less important than in the case of anti-infectives with, in most cases, short treatment periods where mild symptoms of intolerance, e.g. diarrhoea, are observed. However, inclusion of recovery animals is recommended in general because at the stage of development where first clinical studies are conducted, the whole set of indications is not finally known and line extensions can happen. One example is the use of quinolones and other anti-infectives for the treatment of cystic fibrosis. Another example is drugs used for chemotherapy of malignant diseases where recovery has to be studies anyway. [Pg.782]

Barnett A, Goldstein J (1975) Head-turning induced by electrical stimulation of the caudate nucleus and its antagonism by anti-parkinson drugs. J Pharmacol Exp Ther 194 296-302. [Pg.281]

Action on organs other than the target organ (e.g., peripheral tachycardic and hypertensive effects of dopamine after systemic application of the anti-Parkinson drug L-dopa, sedative side effects of lipophilic histamine Hj antagonists). [Pg.43]


See other pages where Anti-Parkinson Drugs is mentioned: [Pg.162]    [Pg.163]    [Pg.164]    [Pg.164]    [Pg.165]    [Pg.166]    [Pg.249]    [Pg.442]    [Pg.689]    [Pg.689]    [Pg.934]    [Pg.1070]    [Pg.1090]    [Pg.157]    [Pg.113]    [Pg.59]    [Pg.148]    [Pg.3]    [Pg.127]    [Pg.127]    [Pg.130]    [Pg.130]    [Pg.130]    [Pg.131]    [Pg.527]    [Pg.734]    [Pg.327]    [Pg.63]    [Pg.106]    [Pg.162]    [Pg.163]    [Pg.164]    [Pg.164]    [Pg.165]   
See also in sourсe #XX -- [ Pg.283 , Pg.285 , Pg.304 ]

See also in sourсe #XX -- [ Pg.283 , Pg.285 , Pg.304 ]




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