Depression in Parkinson’s disease

Abstract

Depression is very common in Parkinson's disease (PD), but its severity and particular symptoms vary. It can often be difficult to diagnose because many of the symptoms typically associated with depression (eg, sleep difficulties, fatigue) can be seen in nondepressed patients with PD, and signs thought to represent depression (eg, lack of facial expression, slowness) can be produced by PD itself. Apathy, although a possible feature of depression, can exist apart from depression and is often associated with cognitive impairment. Therefore, when evaluating patients with PD for possible depression, one should concentrate on the psychological or ideational aspects of the illness. One must determine whether the patient feels sad or hopeless or has a marked inability to enjoy life. Once it has been determined that the patient has clinically significant depressive symptoms, it is important to let him or her know that depression is an aspect of PD requiring treatment, just like the motor manifestations of the disease. The idea of adding antidepressant medications and the possibility of psychotherapy should be introduced. A very reasonable first-choice antidepressant is either sertraline or paroxetine. Because of isolated case reports of worsening motor function associated with institution of a selective serotonin reuptake inhibitor (SSRI), one should keep track of when the medication was started so that the patient can be seen again within a month. It is important from a psychological perspective to have regular follow-up visits when treating depression. If the SSRIs are ineffective or not tolerated, nortriptyline is a good next choice. It has fewer anticholinergic effects and is less likely to cause or worsen orthostatic hypotension than other tricyclic antidepressants. Amitriptyline, although an old favorite of neurologists, is very sedating and has too much anticholinergic activity to be well tolerated in the higher doses needed to treat depression. If a patient could benefit from a dopamine agonist from a motor standpoint and his or her depressive symptoms are mild, consider using pramipexole, which may improve mood and motivation (although this has not yet been proven in a well-controlled trial). It is a good idea to keep patients on antidepressant therapy at least 6 months; many patients require long-term treatment. If a patient is severely depressed, he or she should be referred to a psychiatrist, who may consider admission to the hospital and possible electroconvulsive therapy.

Desipramine Protects Neuronal Cell Death and Induces Heme Oxygenase-1 Expression in Mes23.5 Dopaminergic Neurons

“…Furthermore, a number of PD patients who had subthalamic nucleus deep brain stimulation suffered from behavioral side effects including cognitive impairments and depression [51]–[53]. Treatment with TCAs is restricted by adverse effects, however, TCAs like desipramine are effective in treating depression in PD patients and may even reduce motor symptoms [54]. In this study, we used neurotoxins rotenone and 6-OHDA to induce dopaminergic neuron toxicity that mimics human neurodegenerative disease and neuropathological representative of PD.…”

Pramipexole and pergolide in the treatment of depression in Parkinson's disease: a national multicentre prospective randomized study

“…, 2000). Even though the incidence of depression shows no clear correlation with the severity of motor symptomatology (Richard, 2000), higher depression scores were shown to be associated with advancing disease severity, higher akinesia score and occurrence of falls (Schrag et al. , 2001).…”

“…It has already been shown in several studies that a substantial proportion of patients with PD has a less severe form of depression (Tandberg et al. , 1996; Leonard, 1999; Richard, 2000).…”

Apathy and cognitive performance in older adults with depression

“…The clinical profile of executive deficits, apathy and depression in older adults may indicate presence of brain lesions in frontal-subcortical regions from cerebrovascular disease, Alzheimer's disease, Parkinson's disease, head trauma and other frontal-subcortical neuro-degenerative diseases (Starkstein et al, 1993;Marin, 1996;Salloway et al, 1996;Alexopolous et al, 1997;Cummings and Benson, 1998;Levy et al, 1998;Gallarda, 1999;Richard, 2000;Andersson, 1999). Starkstein et al (1993) found that cerebrovascular lesions involving the posterior limb of the internal capsule were most often associated with major depression and apathy in patients with stroke and Marin et al (1994) found an association with left hemisphere stroke suggesting that there may be a vulnerable area of the brain for development of an apathy-depression syndrome.…”