When given as adjuncts to levodopa, they may permit downward titration of the levodopa dosage. These drugs help decrease end-of-dose wearing off, “on-off” motor fluctuations (such as “freezing”), and dyskinesia.ĭopamine agonists also have neuroprotective effects. Dopamine agonistsĭopamine agonists stimulate dopamine receptors, allowing the brain to recognize it’s receiving dopamine. Stalevo combines L-dopa, carbidopa, and entacapone, a catechol-O-methyltransferase (COMT) inhibitor designed to inhibit end-of-dose “wearing off.” Unfortunately, clinical benefits of these drugs decline over time, necessitating additional doses, which in turn may cause dyskinesia. Levodopa is combined with carbidopa in various medications, including Sinemet, Sinemet CR, and Parcopa (orally disintegrating tablets). It takes effect within 15 to 30 minutes of administration. A peripheral decarboxylase inhibitor, carbidopa replaces the dopamine lost in PD. L-dopa is given in combination with carbidopa to minimize peripheral conversion, which allows more of the drug to reach the brain and thus prevent nausea. The immediate precursor of dopamine, L-dopa is converted to dopamine by decarboxylation both in the brain and peripheral tissues. Treatment focuses on symptom management, and levodopa (L-dopa) remains the gold standard. (See chart by clicking the PDF icon above.) Levodopa and carbidopa Also, many medications have adverse effects, and multiple drugs are needed to treat all aspects of the disease. But dopamine doesn’t cross the blood-brain barrier, so getting it to its intended target would require more than just dopamine administration. One might think that simply administering dopamine directly into the brain (if that were possible) would cure the disease. Treatment aims to slow disease progression and reduce disability while minimizing complications. Patients may exhibit compulsive behaviors, such as excessive gambling, hypersexuality, excessive eating and shopping, repetitive activities, and medication abuse. Psychological manifestations may include depression, dementia, memory loss, psychosis, fear, anxiety, and sleep difficulties. Some patients may complain of sensory symptoms, such as pain, itching, and numbness. PD also causes autonomic problems, such as genitourinary and GI dysfunction, thermoregulation problems, and orthostatic hypotension. Some patients have “freezing” episodes, which they describe as a feeling that their feet are stuck to the floor. Over time, they grow progressively worse and more debilitating, and may include cogwheel rigidity and postural instability leading to increased risk of falls. Signs and symptoms usually are asymmetric and commonly begin with a resting tremor. Some patients also have stooped posture, altered gait, dystonia, fatigue, muscle cramps, drooling, sexual dysfunction, masklike facial expression, dysphagia, and speech problems. AssessmentĬardinal features of PD are bradykinesia, resting tremor, and muscle rigidity. Another physiologic hallmark of PD is presence of Lewy bodies containing alpha-synuclein in this same brain region. As dopamine levels continue to fall, manifestations become more apparent and new signs and symptoms arise. Dopamine is integral to movement coordination once 70% of dopaminergic nerve cells are lost, PD signs and symptoms become evident. PD is characterized by loss of dopaminergic nerve cells in the substantia nigra of the basal ganglia in the brain’s lower region, on either side of the brainstem. Its cause isn’t known, although research now centers on genetic and environmental factors and brain trauma. Yet one in 20 patients is younger than 40 when diagnosed. Author Guidelines and Manuscript SubmissionĪmong the most common neurogenerative diseases, Parkinson’s disease (PD) most often affects people older than age 60.
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