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Parkinson s disease levodopa

Ms. Whitman is taking two drugs for Parkinson s disease levodopa and carbidopa. Ms. Whitman questions you as to why she received two drugs while her friend with Parkinson s disease is taking only one drug. Discuss how you would explain this to Ms. Whitman. [Pg.272]

Levodopa is the amino precursor of dopamine. It is used to replenish depleted dopamine in Parkinson s disease. Levodopa may cause insomnia, reddish discoloration of urine and headache. [Pg.80]

All of the more recent compounds have been tested in randomized double-blind clinical trials using the Unified Parkinson s Disease Rating Scale (UPDRS). We do not however have studies comparing the different drugs nor different treatment durations. In addition, the length of these trials is totally different from that of the natural disease course (20 years). It is paradoxical that levodopa, developed in the sixties, remains today the mainstay treatment for Parkinson s disease (levodopa is always associated with a peripheral decarboxylase inhibitor, either car-bidopa or benzerazide). [Pg.691]

Therapeutic uses Levodopa in combination with carbidopa is a potent and efficacious drug regimen currently available to treat Parkinson s disease. In approximately two thirds of patients with Parkinson s disease, levodopa/carbidopa treatment substantially reduces the severity of the disease for the first few years of treatment. Patients then typically experience a decline in response during the third to fifth year of therapy. [Pg.97]

The harm may be life-destroying, as in the rare sudden death following an iajection of penicillin, rightly regarded as one of the safest of antibiotics, or the destruction of the quality of life that occasionally attends the use of drugs that are effective in rheumatoid arthritis (adrenocortical steroids, penicillamine), and Parkinson s disease (levodopa). [Pg.5]

Kondo T. Initial therapy for Parkinson s disease levodopa vs. dopamine receptor agonists. J Neurol 2002 249(Suppl 2) II25-9. [Pg.561]

Parkinson s disease Levodopa/carbidopa, dopamine agonists, amantadine, selegiline, COMT inhibitors, anticholinergics, surgery Dyskinesias, orthostatic hypotension, hallucinations, sedation, anticholineric effects, relief of symptoms... [Pg.588]

Phenol fragments are an integral part of drugs like analgetic, antipyretic (for example, acetaminophen, better known as paracetamol) and anti-inflammatory (Rowasa, Salsalate) agents, bronchodilators (Albuterol), semisynthetic antibiotics (Amoxyl) and for treatment of Parkinson s disease (levodopa, carbidopa) . ... [Pg.1349]

An 86-year-old man who developed Parkinson s disease dementia 8years after the diagnosis of Parkinson s disease. Levodopa had been started early after the diagnosis of Parkinson s disease, and after 6 years, he developed peak-dose choreic levodopa-induced dyskinesias and on-off phenomenon. He did not tolerate the use of rivastig-mine for Parkinson s disease dementia, and memantine was started, aimed at cognitive improvement. Memantine improved the motor fluctuation of this patient [74" ]. [Pg.198]

An example of a stereospecrfic process is the conversion of the drug levodopa to dopamine, a neuro transmitter in the brain. Levodopa (or L-dopa), the precursor of dopamine, is administered to treat Parkinson s disease. Levodopa has one chiral carbon atom. Therefore, it exists as either of two enantiomers. Only the enantiomer with the configuration shown below is transformed into dopamine. [Pg.245]

The main clinical use of COMT inhibitors is as adjunct (or additional adjunct) in the therapy of Parkinson s disease. The standard therapy of Parkinson s disease is oral L-dopa (as a drug levodopa) given with a dopa decarboxylase (DDC) inhibitor (e.g. carbidopa and benserazide), which does not reach the brain. When the peripheral DDC is inhibited, the concentration of 3-O-methyldopa (3-OMD), a product of COMT, in plasma is many times that of L-dopa. Since the half-life of 3-OMD is about 15 h, compared to about 1 h for L-dopa, the concentration of 3-OMD remains particularly high during chronic therapy, especially if new slow release L-dopa preparations are used. A triple therapy (L-dopa plus DDC inhibitor plus COMT-inhibitor) will... [Pg.336]

The immediate metabolic precursor to dopamine, l-DOPA (L-dihydroxphenylalanine) is converted to the active neurotransmitter dopamine by the action of the enzyme aromatic amine acid decarboxylase (AADC). l-DOPA (INN name Levodopa) is the main diug used to treat Parkinson s disease. [Pg.437]

Parkinson s disease (PD) 1. In a non-human primate model of PD endocannabinoid levels are elevated in the basal ganglia and may contribute to the generation of parkinsonian symptoms and/or to expression of levodopa-induced dyskinesia. The cerebrospinal fluid of untreated PD patients contains elevated levels of AEA 1. CB-) antagonists or biosynthesis inhibitors... [Pg.467]

Levodopa is a chemical formulation found in plants and animals that is converted into dopamine by nerve cells in the brain. Levodopa does cross die blood-brain barrier, and a small amount is dien converted to dopamine. This allows the drug to have a pharmacologic effect in patients witii Parkinson s disease (Pig. 29-1). Combining levodopa witii another drug (carbidopa) causes more levodopa to reach die brain. When more levodopa is available, the dosage of levodopa may be reduced. Carbidopa has no effect when given alone. Sinemet is a combination of carbidopa and levodopa and is available in several combinations (eg, Sinemet 10/100 has 10 mg of carbidopa and 100 mg of levodopa Sinemet CR is a time-released version of die combined drugs). [Pg.265]

Monoamine oxidase exists in two forms, MAOa and MAOb. The former is more active against NA and 5-HT than it is against DA, which is a substrate for both, even though, like S-phenylethylamine, it is more affected by MAOb. H seems likely that MAOb is the dominant enzyme in human brain and inhibitors of it, such as selegiline, have some value in the treatment of Parkinson s disease by prolonging the action of the remaining endogenous DA as well as that formed from administered levodopa. [Pg.142]

Figure 7.8 Dopamine and motor function. When nigrostriatal dopamine activity is normal so is motor function. Any reduction in this DA activity, as in Parkinson s disease, results in reduced motor activity, i.e. akinesia. By contrast, too much DA activity, as in Huntington s Chorea, produces abnormal motor function, i.e. dyskinesia. The latter may be controlled by neuroleptic drugs (DA antagonists) but they can swing the balance in DA activity sufficiently to produce akinesia (Parkinsonism). DA agonists (and levodopa) may overcome akinesia but can induce DA overactivity and dyskinesia (peak dose effect) (see Chapter 15)... Figure 7.8 Dopamine and motor function. When nigrostriatal dopamine activity is normal so is motor function. Any reduction in this DA activity, as in Parkinson s disease, results in reduced motor activity, i.e. akinesia. By contrast, too much DA activity, as in Huntington s Chorea, produces abnormal motor function, i.e. dyskinesia. The latter may be controlled by neuroleptic drugs (DA antagonists) but they can swing the balance in DA activity sufficiently to produce akinesia (Parkinsonism). DA agonists (and levodopa) may overcome akinesia but can induce DA overactivity and dyskinesia (peak dose effect) (see Chapter 15)...
Henry, B and Brotchie, JM (1996) Potential of opioid antagonists in the treatment of levodopa, induced dyskinesias in Parkinson s disease. Drugs and Ageing 9 149-158. [Pg.323]

A number of azetidine-based compounds have been disclosed in patent applications from Aventis Pharma for CBi-modulated treatment of diseases such as obesity, Parkinson s disease, schizophrenia, respiratory and neurological diseases [330-334]. Compound (556) was specifically claimed for use in two formulation patent applications [330, 331] for a stable semi-solid composition and oral emulsion composition, respectively. The optional coadministration of an agent that activates norepinephrinergic and se-rotoninergic neurotransmission (for example, sibutramine) or dopaminergic neurotransmission was also claimed for the treatment of obesity. The optional use of a dopamine agonist (for example, levodopa) was claimed... [Pg.301]

MH van Woert. Phenylalanine and tyrosine metabolism in Parkinson s disease treated with levodopa. Clin Pharmacol Ther 12 368-375, 1971. [Pg.72]

These symptoms are alleviated by administering levodopa (L-dopa), a precursor for dopamine. L-dopa is taken up by the axon terminals of dopaminergic neurons and used to form dopamine. Interestingly, in some patients, a side effect of dopamine replacement therapy is the development of symptoms characteristic of schizophrenia. (Recall that this mental disorder is caused by overactive dopaminergic neurons.) On the other hand, drugs used to treat schizophrenia — dopamine receptor antagonists — may elicit symptoms of Parkinson s disease. [Pg.43]

Dystonia due to identifiable structural or biochemical abnormalities ( secondary dystonia) often occurs weeks or months after strokes or other focal lesions, which commonly involve the basal ganglia, but may also involve the thalamus or cerebellum. Dystonia is also seen in children with cerebral palsy and in patients with abnormalities of dopaminergic transmission. For instance, dystonia may develop in the context of Parkinson s disease, either as an early parkinsonian sign, or in response to dopaminergic drugs. A particularly interesting inherited disease results in a combination of dystonia and parkinsonian features at a young age, which responds dramatically to treatment with low-dose levodopa ( dopamine-responsive dystonia ). [Pg.775]

Nonorganic and organometallic catalysts are also used to channel the reactions toward the chiral synthesis pathway. The drug called levodopa, (5)-3,4-dihydroxyalanine, is an effective drug against Parkinson s disease. It is stereoselectively manufactured using catalysts such as rhodium or ruthenium complexes. [Pg.338]

Dopamine-Boosting Medications. Levodopa/carbidopa (Sinemet), bromocriptine (Parlodel), pramipexole (Mirapex), and ropinirole (Requip) increase dopamine nenrotransmission in the brain by one or another mechanism. These medications do not reliably induce sleep, and in some patients are activating. They are certainly not true sedative-hypnotics. They are most often used by neurologists to treat Parkinson s disease. [Pg.272]

Bromocriptine is a dopamine agonist acting by direct stimulation of the dopamine receptors. In Parkinson s disease, it is reserved for use in patients who are intolerant to levodopa or in whom levodopa alone is not sufficient. Orphenadrine is an antimuscarinic indicated in Parkinson s disease. Antimuscarinics tend to be more effective than levodopa in targeting tremor rather than rigidity and bradykinesia. Moclobemide is an antidepressant referred to as a reversible monoamine oxidase inhibitor (RIAAA) type A. [Pg.253]

Co-careldopa is a combination of levodopa and the peripheral dopadecar-boxylase inhibitor. Co-careldopa is indicated in Parkinson s disease to improve bradykinesia and rigidity rather than tremor. Orphenadrine is an antimuscarinic agent indicated in patients with Parkinson s disease where tremor predominates. Trifluoperazine is a piperazine antipsychotic that should be used with caution in patients with Parkinson s disease as its use may exacerbate the condition. [Pg.300]

Recently we have been working on Parkinson s disease. This and other similar diseases are due to a depletion of dopamine in the corpus striatum. Direct addition of dopamine is not effective in the treatment presumably because it does not cross the blood-brain barrier. However, levodopa, the metabolic precursor of dopamine, does cross the blood brain barrier and is believed to then be converted to dopamine in the basal ganglia. [Pg.344]


See other pages where Parkinson s disease levodopa is mentioned: [Pg.78]    [Pg.126]    [Pg.78]    [Pg.126]    [Pg.166]    [Pg.1173]    [Pg.264]    [Pg.265]    [Pg.266]    [Pg.266]    [Pg.266]    [Pg.266]    [Pg.266]    [Pg.269]    [Pg.161]    [Pg.470]    [Pg.512]    [Pg.767]    [Pg.539]    [Pg.540]    [Pg.48]    [Pg.67]    [Pg.208]   
See also in sourсe #XX -- [ Pg.476 ]

See also in sourсe #XX -- [ Pg.93 ]

See also in sourсe #XX -- [ Pg.338 ]




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Levodopa/carbidopa in Parkinson’s disease

Parkinson’s disease

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