Complications
Develop as a result of advanced disease and the inability of the dopaminergic cells in the substantia nigra to buffer exogenous levodopa. The excess dopamine results in excessive movements. Management involves lowering dopaminergic medication dosages and/or lengthening dosing intervals. If this results in decreased efficacy, amantadine can be used in lieu of reducing dopaminergic medications. Disabling refractory dyskinesias can be treated with deep brain stimulation to the subthalamic nucleus or globus pallidus interna.
Advancing disease and inability to buffer exogenous dopamine explains this complication. Institution of a catechol-O-methyltransferase (COMT) inhibitor as an adjunct to carbidopa/levodopa is the first-line treatment. Long-acting carbidopa/levodopa can be effective in extending response time. Unexpected wearing off can be treated with injectable apomorphine. Deep brain stimulation to the subthalamic nucleus or globus pallidus interna is an effective treatment.
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Constipation is a common pre-motor symptom of PD that many patients have well before they are diagnosed.[71] Prevalence tends to increase with disease progression, and PD medication may make it worse. Recognizing and treating constipation is important to prevent complications (e.g., intestinal occlusion) and to ensure an optimal response to levodopa.[207]
Bladder symptoms (e.g., nocturia, urgency, daytime frequency, urinary incontinence) are common in patients with PD, with reported prevalence between 38% and 71%.[208] These symptoms have a major negative impact on quality of life of patients and are not levodopa-responsive. Medications with antimuscarinic effects can be used to treat lower urinary tract symptoms, but the possible anticholinergic side effects of these medications should be carefully monitored. Other commonly prescribed medications to treat lower urinary tract symptoms include oxybutynin, trospium, tolterodine, mirabegron, and darifenacin.[209] Solifenacin may be effective for treating urinary symptoms, but more evidence is needed.[124][210]
Orthostatic hypotension (defined as a drop in systolic blood pressure of >20 mm Hg and of diastolic blood pressure of 10 mmHg within 3 minutes of standing) is a common nonmotor symptom of PD that may precede the appearance of motor symptoms. Nonpharmacologic (medication review, lifestyle changes) and pharmacologic (mineralocorticoid, short-acting pressor agent, droxidopa) treatment options are available.[211][212][213]
Sleep disorders are common in patients with PD, and may include impaired sleep initiation, fragmented sleep, and daytime fatigue. Nonpharmacologic treatment options include cognitive behavioral therapy, exercise, and bright light therapy.[214] Modafinil and sodium oxybate are recommended for the treatment of hypersomnia secondary to PD in adults.[215] Possible pharmacologic treatments for insomnia include rotigotine, eszopiclone, and melatonin, although evidence is limited.[124]
Maintaining a safe sleeping environment is important to prevent injury in patients with secondary rapid eye movement sleep behavior disorder; pharmacologic treatment may be considered.[216] See Parasomnias in adults.
Dysphagia is a common complication of PD, with a reported prevalence of between 11% and 87%. Treatments for PD should be optimized to minimize impact on swallowing function. Conventional swallowing therapy is recommended. Botulinum toxin injection may be considered for treating upper esophageal sphincter impairment.[103]
Clozapine has been shown to be effective for treating psychosis in PD patients, but risk of agranulocytosis and need for frequent WBC monitoring can limit its use.[124][197][199] Quetiapine may improve symptoms, although evidence is lacking.[124][200] Pimavanserin, a selective serotonin 5-HT2A inverse agonist, has been shown to be efficacious over the short term (6 weeks) for treating psychosis in patients with PD.[124] One meta-analysis showed a low impact on motor function for clozapine and little impact for pimavanserin.[201][202][203]
Depression has been reported to affect up to 25% to 35% of patients with PD.[124][125] Referral to a psychiatrist may be required. There is evidence for effectiveness of cognitive behavioral therapy for treating depression in patients with PD.[127][128] Selective serotonin reuptake inhibitors (SSRIs) are often used to manage depression in patients with PD; the dopamine agonist pramipexole may also be effective.[124] Although there is evidence of efficacy for tricyclic antidepressants, adverse effects limit use.[197]
Screening tools are being developed to assist in identifying impulse control disorder. Reported risk factors include younger age, male sex, smoking, longer PD duration, dopamine agonist use, and higher doses of levodopa.[204] If present, dopamine agonist should be reduced or discontinued. Appropriate psychological and social support should be provided.[205][206]
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