Dementia in Parkinson's Disease.
One of the more recently recognized problems in treatment of patients with Parkinson's disease (PD) is development of cognitive dysfunction and, in many cases, frank dementia. As patients with PD live longer, because of improved care and treatment of motor symptoms, dementia in PD is becoming a major contributor to morbidity in the illness. Prevalence studies suggest that up to 30% of patients with PD develop dementia. Dementia in PD patients is often a multifactorial condition. Neuropathologic changes caused by PD itself may cause memory loss. However, some patients with PD and memory decline also have pathologic changes that are more consistent with Alzheimer's disease. Many PD patients have a mix of the two types of pathology. Other factors, such as underlying illnesses, medication side effects, and interaction of therapeutic agents, may contribute to cognitive changes in PD patients. Predictors of development of dementia in PD include advancing age and severity of neurologic symptoms, which may interact with one another to produce this effect. Recent work suggests that tobacco use also may increase risk of PD dementia, despite its possible protective effect against development of PD itself. Presence of psychiatric illness, especially depression, may interfere with cognition and exacerbate memory loss. Reduction in the dose of dopaminergic agents and of other medications may be helpful in partially improving cognitive function in some cases. The balance between improvement of motor function and preservation of cognitive abilities must be weighed, and it is important for clinicians to discuss this trade-off with patients and their families. At this time, there is no US Food and Drug Administration-approved pharmacologic treatment for dementia in PD. However, medication used to treat Alzheimer's disease, such as acetylcholinesterase inhibitors, may slow progression of memory loss in some PD patients. Based on work from small double-blind studies, open-label trials, and case reports, cholinesterase inhibitors may be tried for treatment of dementia in PD, as long as the patient and caregivers understand that these agents are being used on an off-label basis. Surgical intervention, such as deep brain stimulation of the subthalamic nucleus or globus pallidus internus, although useful for treatment of motor symptoms in some PD patients, does not improve cognitive function in most cases and may actually worsen cognition in patients with pre-existing dementia. There is no specific exercise regimen or dietary guidelines for patients with PD who develop dementia. However, patients should be encouraged to lead a healthy lifestyle; this may improve overall well-being, which could impact positively on cognition function. Similarly, although assistive devices have not been developed for people with PD who have memory loss, any aid that increases mobility will probably improve mental and physical function. Clinicians should be mindful of the increased caregiver burden posed by PD patients who also have dementia. They should intervene appropriately to prevent caregiver distress and "burn out." Herbal and nutritional supplements have not been shown in clinical trials to be beneficial for treatment of any type of dementia, and thus are not recommended for PD patients with cognitive decline.
Anderson
Karen E.
KE
Department of Neurology, Movement Disorders Division, University of Maryland School of Medicine, 22 South Greene Street, Baltimore, MD 21201, USA. kanderson@psych.umaryland.edu