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Levo-dopa

Mecfianism of Action Levodopa is converted to dopamine in the basal ganglia thus increasing dopamine concentration in brain and inhibiting hyperactive cholinergic activity. Carbidopa prevents peripheral breakdown of levodopa, allowing more levo-dopa to be available for transport into the brain. Therapeutic Effect Reduces tremor and other symptoms of Parkinson s disease. [Pg.193]

Because bupropion is metabolized in the liver, medications that alter hepatic enzyme metabolism, such as carbamazepine or cimetidine, may effect blood concentrations. Bupropion should not be administered in combination with the MAOIs because of risk of hypertensive crisis. Levo-dopa use in conjunction with bupropion has been associated with confusion, hallucinations, and dyskinesia. Although generally well tolerated, there are case reports documenting that the... [Pg.302]

Tolcapone [TOLE ka pone] is a nitrocatechol derivative that represents a new class of anti-Parkinson s drugs. It selectively and reversibly inhibits both peripheral and central catechol-O-methyl-transferase (COMT) (Figure 8.11). Normally, the methylation of levo-dopa by COMT to 3-O-methyldopa is a minor pathway for levodopa metabolism. However, when peripheral dopamine decarboxylase activity is inhibited by carbidopa, a significant concentration of 3-O-methyldopa is formed that competes with levodopa for active transport into the CNS. Inhibition of COMT by tolcapone leads to decreased plasma concentrations of 3-O-methyldopa, increased central uptake of levodopa, and greater concentrations of brain dopamine. Tolcapone has been demonstrated to reduce the frequency of the on-off phenomenon. [Pg.455]

L-Dopa. Dopamine itself cannot penetrate the blood-brain barrier however, its natural precursor, L-dihydroxyphenylalanine (levo-dopa), is effective in replenishing striatal dopamine levels, because it is transported across the blood-brain barrier via an amino acid carrier and is subsequently decarboxy-lated by dopa decarboxylase, present in striatal tissue. Decarboxylation also takes place in peripheral organs where dopamine is not needed and is likely to cause undesirable effects (vomiting hypotension p.116). Extracerebral production of dopamine can be prevented by inhibitors of dopa decarboxylase (carbidopa, benserazide) that do not penetrate the blood-brain barrier, leaving intracerebral decarboxylation unaffected. [Pg.188]

An 81-year-old woman took sertraline 100 mg/day for depression and 6 months later presented with tremor and difficulty in moving her right arm and leg (3). A diagnosis of right hemiparkinsonism was made and the sertraline was withdrawn. Her extrapyramidal symptoms resolved within 3 months, but 14 months later she developed parkinsonism and was treated with levo-dopa and carbidopa. [Pg.72]

Three Japanese women aged 78-87 years who had taken amantadine 100-200 mg/day for 1 month to 5 years, in two cases together with co-careldopa, developed multifocal myoclonus and two were confused (13). Amantadine concentrations were high in the two patients in whom they were measured, at over 3000 ng/ml a concentration over 1000 ng/ml is regarded as toxic. Amantadine was withdrawn and the myoclonus disappeared within 1-2 weeks and did not recur. Cortical myoclonus has also been described with levo-dopa and bromocriptine, but the mechanism is not known. [Pg.106]

A less radical and much less expensive approach to the management of motor fluctuations has been described in 14 patients with advanced Parkinson s disease and levo-dopa-induced motor disorders (69). Amantadine (mean dose 350 mg/day) reduced the severity and duration of dyskinesias by 33-75%, depending on the parameter measured. The rationale was that amantadine blocked iV-methyl-D-aspartate receptors. [Pg.2045]

Lisi P. Pemfigo eritemosa indotto dall associazione levo-dopa-carbidopa. Ann Ital Dermatol Clin Sper 1983 37. [Pg.2047]

Clarke CE, Speller JM, Clarke JA. Pramipexole for levo-dopa-induced comphcatiorrs in Parkitrson s disease. Cochrane. Database Syst Rev 2000 (3) CD002261. http // www.cochrane.org/cochrane/revabstr/ab002261.htm. [Pg.2908]

Antithyroid medications methimazole, methylthiouracil Antihypertensives beta blockers, captopril, enalapril Levo-dopa... [Pg.2368]

ACE inhibitors captopril, enalapril Carbamazepine Chemotherapeutic agents Cigarette smoking Diuretics Levo-dopa Phenylbutazone Metallic taste Allopurinol Ciguatoxin... [Pg.2368]

Parkinson s disease is caused by the oxidative stress-induced loss of dopaminergic neurons and can be effectively treated with levo-dopa in combination with dopa decarboxylase inhibitors such as carbidopa or catechoi-0-methyltransferase inhibitors such as tolca-pone. Levodopa is well known to increase the life spans of patients with Parkinson s disease. It may do this by enhancing brain dopamine levels and inhibiting tyrosine hydroxylase, which produces oxygen radicals. Several dopamine receptor agonists are available for use in Parkinson s disease and are extensively used in patients suffering from the adverse effects of levodopa. Anticholinergics such as trihexyphenidyl are also used in Parkinson s disease. [Pg.674]

Nearly 40 years after its introduction, levo-dopa or L-dopa (1 Fig. 12.4) remains an effective pharmacotherapy in PD (8,11,13,80,81). [Pg.721]

Many of the side effects (e.g. granulocytopenia) encountered with racemic DOPA were not seen with levo-DOPA and therefore can be attributed to the (+)-enantiomer. For this reason the racemate is no longer given. Post-anesthesia reactions to the anesthetic and analgesic agent ketamine are overwhelmingly associated with the R(-) antipode. ... [Pg.543]

A retrospective study of patients with Parkinson s disease taking selegiline 5 to 10 mg daily (and other antiparkinsonian drugs such as levo-dopa/carbidopa, bromocriptine, amantadine, pergolide, and... [Pg.691]

A retrospective study of patients with Parkinson s disease taking selegiline 5 to to mg daily (and other anti-parkinson drugs such as levo-dopa/carbidopa, bromocriptine, amantadine, pergolide, and antimuscarinics) noted that the addition of trazodone 25 to 150 mg daily caused no adverse effects and the patients appeared to obtain overall benefit, including some improvement in parkinsonian symptoms. ... [Pg.691]

Wanamaker WM, Wanamaker SJ, Celesia GG (1976) Thrombocytopenia associated with long term levo-dopa therapy. JAMA 235 2217 Ward AM, Udnoon S, Watkins J (1976) Immunological mechanisms in the pathogenesis of vinyl chloride disease. Br Med J 1 936... [Pg.132]

It is Interesting to note that several authors have shown that levo-dopa may release amines in the brain, specifically serotonin, which may imply that it shaires a somewhat similar action with amantadine ... [Pg.47]

Bonnici A, Ruiner CE, St-Laurent L, Hornstein D. An interaction between levo-dopa and enteral nutrition resulting in neuroleptic malignant-like syndrome and prolonged ICU stay. Ann Pharmacother 2010 44(9) 1504-7. [Pg.540]

Selegiline [(/ )(-)-W,a-dimethyl-W-(2-propynyl)benzeneethanamine, Elde-pryl. Deprenyl, 1] is a phenethylamine derivative which is pharmacologically active in the levo form. It is indicated as adjuvant treatment with levo-dopa in Parkinson s disease, and is supplied as a 5 mg tablet of selegiline hydrochloride. It belongs to the class of type B inhibitors of monoamine oxidase (MAOI-B). At high doses (>40 mg/day in man), selegiline loses its MAOI-B specificity and also inhibits MAO-A. [Pg.39]


See other pages where Levo-dopa is mentioned: [Pg.19]    [Pg.587]    [Pg.2201]    [Pg.2780]    [Pg.245]    [Pg.247]    [Pg.330]    [Pg.347]    [Pg.125]    [Pg.677]    [Pg.453]    [Pg.454]    [Pg.125]    [Pg.537]    [Pg.1352]    [Pg.152]    [Pg.508]    [Pg.509]    [Pg.21]    [Pg.488]    [Pg.489]   


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