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In those with dopamine-responsive dystonia, symptoms typically dramatically improve with low-dose administration of levodopa, which is a biochemically significant metabolite of the amino acid phenylalanine, as well as a biological precursor of the catecholamine dopamine, a neurotransmitter. (Neurotransmitters are naturally produced molecules ...
Levodopa-induced dyskinesia has long been thought to arise through pathological alterations in pre-synaptic and post-synaptic signal transduction in the nigrostriatal pathway (dorsal striatum). [9] It is thought that the stage of illness, dosage of l-DOPA, frequency of l-DOPA treatment and the youth of the patient at the onset of symptoms ...
[170] [171] [note 1] Symptoms may become unresponsive to levodopa, with sudden changes between a state of mobility ("ON time") and immobility ("OFF time"). [173] Long-term levodopa use may also induce dyskinesia and motor fluctuations. Although this often causes levodopa use to be delayed to later stages, earlier administration leads to ...
Levodopa crosses the protective blood–brain barrier, whereas dopamine itself cannot. [3] [4] Thus, levodopa is used to increase dopamine concentrations in the treatment of Parkinson's disease, Parkinsonism, dopamine-responsive dystonia and Parkinson-plus syndrome. The therapeutic efficacy is different for different kinds of symptoms.
Levodopa (or L-DOPA) has been the most widely used treatment for over 30 years. [3] L-DOPA is transformed into dopamine in the dopaminergic neurons by dopa-decarboxylase. [3] Since motor symptoms are produced by a lack of dopamine in the substantia nigra, the administration of L-DOPA temporarily diminishes the motor symptoms. [3]
Motor symptoms in DLB appear to respond somewhat less to medications used to treat Parkinson's disease, like levodopa, and these medications can increase neuropsychiatric symptoms. [56] [65] Almost one out of every three individuals with DLB develops psychotic symptoms from levodopa. [56]
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