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Levodopa can be combined with other therapies, such as serotonergic drugs, which improve depressive symptoms but which are ineffective in the treatment of cognitive and other symptoms.
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People often mistake this movement as a symptom of the disease itself, but it's actually a side effect of levodopa that can be as disabling as the PD itself.
These symptoms result primarily from the loss of dopaminergic neurons in the substantia nigra and can be reduced by levodopa, which replenishes dopamine, and dopamine agonists.
The genotypes with very low TH activity are at the edge of the DA cliff and, interestingly, these genotypes sometimes show a dystonia [ 38], involuntary muscle contractions that affect posture, brought about by low levels of extracellular DA that can be alleviated by levodopa.
It is a frequent cause of falls and can be only partially relieved by levodopa therapy.
Dopamine agonists can be used as an alternative initial levodopa therapy, to delay the onset of motor complications, but at the expense of more dopaminergic adverse effects; poorer control of motor symptoms; and increased cost.
3 However, the long-term use of levodopa is limited by treatment-emergent motor fluctuations and dyskinesias that can be both challenging to manage and a significant source of disability for patients.
The lack of significant differences can be explained by the great differences observed in the pharmacokinetic behaviour of levodopa in each patient.
Patients can be switched directly from CL with or without entacapone without having to decrease the levodopa dose.
Additionally, longer-acting sustained-release carbidopa/levodopa regimens can be used during sleeping hours if awakenings are accompanied by immobility [ 22].
Motor fluctuations can be improved by the addition of drugs such as entacapone or monoamine oxidase inhibitors, which extend the half-life of levodopa or dopamine, respectively.
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CEO of Professional Science Editing for Scientists @ prosciediting.com