Evidence-Based Reviews

Psychiatric symptoms in Parkinson’s disease: A team approach to successful management

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How can you make sound treatment decisions when almost no evidence exists on the use of psychotropics in patients with Parkinson’s disease? A psychiatrist and a neurologist argue that collaboration is key to treating PD patients’ psychiatric symptoms.



Depression, anxiety, and psychosis are common complications of Parkinson’s disease (PD) and of the medications used in antiparkinsonian treatment. These psychiatric problems impair patients’ functioning throughout the course of the chronic degenerative disease.

Because medication side effects often call for adjustments and trade-offs in PD treatment, a team effort by the psychiatrist, neurologist, patient, and caregiver is the most effective approach to decision-making. From our experience in such collaborations, here’s what you need to know about PD to be a most-valuable player on that treatment team.

Presentation of PD

The classic triad of PD features consists of a pill-rolling tremor, rigidity, and bradykinesia or slowness of movement. Other common features include postural instability, flexed posture, and other motor-freezing phenomena.

Freezing phenomena occur in the later stages of PD, as the response to dopaminergic therapy becomes erratic and unpredictable. Freezing can range from hesitation—such as when the patient tries to turn or is in a doorway—to transient episodes of total inability to move. These episodes are extremely distressing for both patients and caregivers.

Patients rarely present with the full complement of symptoms, but the presence of tremor at rest and/or bradykinesia is essential for the diagnosis. While motor signs dominate the presentation, cognitive symptoms such as shortened attention span, visuospatial impairment, personality changes, and dementia are also frequently present.

Average age of diagnosis is 60, and more men are affected than women (male-to-female ratio is 3:2). Many causative factors—including genetics and environmental toxins—have been implicated, but the disorder’s etiology remains unknown.

Drug treatment side effects

PD results from the loss of neurons in the substantia nigra that produce the neurotransmitter dopamine. Pharmacologic treatment emphasizes dopamine replacement, dopamine receptor stimulation, or prevention of enzymatic breakdown of dopamine in the synaptic cleft. As treatment of PD is symptomatic and not curative, medications are instituted only when the disease begins to cause functional impairment.

Treatment begins with dopamine agonists (Table). As dopamine agonist monotherapy becomes less effective, levodopa therapy is initiated. Blocking the enzymatic breakdown of dopamine with catechol-O-methyltransferase inhibitors is the next therapeutic strategy.

Within 5 years of starting levodopa therapy 75% of patients experience unsatisfactory motor response, from unpredictable fluctuations to wearing-off phenomena (in which a dose of levodopa does not last as long as it once did). Treatment of advanced PD is complicated by the emergence of psychiatric symptoms, such as hallucinations and psychosis, as dopamine levels are increased in an attempt to smooth the motor response.

The significantly distressing level of disability associated with the prominent side effects of pharmacologic treatment has led to interest in surgical interventions. These range from pallidotomy to implantation of basal ganglia stimulators to transplantation of fetal striatal neurons. The possibility of neuroprotection has also been extensively investigated, with mixed results.

Psychiatric complications of PD

Depression. Clearly, the stress of anticipating and coping with a relentless degenerative disease helps to trigger depression and anxiety in patients with PD. Depression is the most common psychiatric syndrome, with prevalence in PD as high as 42%.1 Patients with a history of depression are at particular risk.2 Those with recent deterioration or advancing severity of PD, akinesia, history of falls, or cognitive impairment are also at increased risk for depression.



Medication classExampleIndication for use
MAO-B inhibitorSelegiline? Neuroprotection
Anticholinergic agentsTrihexyphenidyl, benztropine, biperiden, hyoscyamine, diphenhydramineTremor
Dopamine agonistPramipexole, pergolide, ropinirole? Neuroprotection Treatment of movement disorder
Dopamine replacementCarbidopa-levodopaTreatment of movement disorder
Catechol-O-methyltransferase inhibitorEntacapone, tolcaponeSmooth motor fluctuations

Depression correlates well with the patient’s perception of his or her degree of PD-related disability. Depression symptoms seem to peak early in the illness following diagnosis and in advanced disease.3

Patients may present with symptoms meeting diagnostic criteria ranging from dysthymic disorder to minor depression to major depressive disorder.1,4 Although they will frequently endorse suicidal ideation, patients with PD have a low rate of suicide. Diagnosing depression, however, may be difficult because its symptoms overlap with those of the underlying neurologic disease:

  • Diminished affect and psychomotor slowing may be secondary to the motor features of parkinsonism.
  • Diminished concentration may be secondary to cognitive decline rather than depression.

Patients also frequently have a chief complaint of diminished energy or fatigue that should trigger further investigation into other depressive symptoms.4,5

In addition to the obvious additional suffering it causes, depression in PD predicts impaired social, physical, and role functioning.6 Depression in the PD patient also results in higher distress for caregivers.7 In one study, depression was identified as a risk factor for development of psychosis in PD patients.8

Anxiety is a frequent problem for PD patients, with a prevalence of 33 to 40%.9,10 Anxiety in PD typically presents with symptoms of panic disorder, generalized anxiety disorder, or social phobia.11 It is comorbid with depression in up to 92% of cases and—like depression—frequently predates the onset of motor symptoms.12


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