eMedicine Specialties > Psychiatry > Geriatric

Parkinson Disease Dementia: Treatment & Medication

Author: Margaret M Swanberg, DO, Assistant Professor of Neurology, Uniformed Services University; Chief of Neurobehavior Service, Walter Reed Army Medical Center; Assistant Chief, Department of Neurology, Walter Reed Army Medical Center
Coauthor(s): Raj K Kalapatapu, MD, Fellow in Geriatric Psychiatry, Mount Sinai School of Medicine
Contributor Information and Disclosures

Updated: Apr 15, 2009

Treatment

Medical Care

  • Although no specific therapy exists for dementia, the American Academy of Neurology recently evaluated the evidence regarding the use of cholinesterase inhibitors in Parkinson disease dementia (Parkinson's disease dementia, PDD). Based on their review, they suggested that rivastigmine (US Food and Drug Administration approved for Parkinson disease dementia) and donepezil are probably effective in treating the dementia. The risk of potentially exacerbating motor symptoms may limit their widespread use.
  • Focus treatment on managing the motor manifestations of Parkinson disease.
  • Anticholinergic drugs used for the treatment of motor manifestations of Parkinson disease may exacerbate memory impairment. When possible, avoid these medications.

Psychiatric care

  • Mood Disorders: For mood disorders, tricyclic agents, specifically the secondary amines (eg, nortriptyline, desipramine), heterocyclic agents, or serotonin reuptake inhibitors (SSRIs) are indicated.2,10,11 In severe refractory cases, electroconvulsive therapy may be effective.12 Psychotherapy can play an important role in the treatment of depression.5 Limited evidence shows any benefit with dopamine agonists13 and monoamine oxidase inhibitors14 . A randomized, controlled trial reported by Menza et al determined that depression in patients with Parkinson disease may be responsive to treatment with nortriptyline.15
  • Anxiety: SSRIs and venlafaxine can be beneficial. Buspirone is well tolerated, but has not been studied in this population. Benzodiazepines may help severe anxiety, but side effects such as cognitive impairment and balance problems may be concerning. Behavior modification techniques can play an important role in the treatment of anxiety.2,16
  • Psychosis: Any medications that might contribute to psychosis must be first eliminated.2 Medical conditions that may lead to psychosis must be treated.12 Atypical antipsychotics are preferred. Clozapine is the agent of choice, but its use may be limited because of adverse effects. Quetiapine has not been tried extensively. Olanzapine and risperidone worsen motor function.17 Dopamine agonists can lead to psychosis.10 Limited evidence shows any benefit with cholinesterase inhibitors.16,2
  • Sleep disturbances: Benzodiazepines can be helpful in the treatment of rapid eye movement sleep behavior disorder.18 Obstructive sleep apnea can be treated with positive airway pressure with either continuous pressure or bi-level pressure.18 Sleep hygiene techniques include avoiding stimulants/fluids near bedtime,  avoiding heavy late-night meals, and following a regular sleep schedule.16
  • Impulse control disorders: Because behaviors such as pathological gambling, hypersexuality, compulsive shopping, and binge eating may be related to the use of dopamine agonists, clinicians must closely monitor for such behaviors when using dopamine agonists. Doses may need to be decreased, or therapy may need to be completely discontinued.16,11,12,2

Surgical Care

Surgical treatment of Parkinson disease (eg, thalamotomy, pallidotomy, thalamic or subthalamic stimulation) improves some of the motor features of the disease but has no effect on cognitive deficits.

Consultations

The treatment of patients with Parkinson disease and dementia is best accomplished using a team approach.

  • Motor manifestations, especially those that develop late in the course of the disease, are best managed by neurologists or internists experienced in the treatment of patients with dementia disorders.
  • A psychiatrist who is familiar with the psychopharmacologic issues of Parkinson disease treatment should be part of the team, particularly when a mood disorder or psychosis complicates the course of illness.
  • Physical therapists should work with the patient to ensure optimal neuromuscular fitness.
  • A nutritionist can help ensure adequate energy intake, particularly when low-protein diets are needed to avoid adverse effects of levodopa.

Diet

Encourage patients to adopt a low-protein diet because such a diet may reduce fluctuations in dopamine levels.

Activity

Encourage patients to keep as active as possible. Recommend physical therapy to optimize motility.

Medication

Various medications are used to treat the movement disorders of Parkinson disease, but these agents do not usually help the psychiatric symptoms of the disorder. In fact, they may worsen cognitive and psychiatric symptoms. Patients with Parkinson disease dementia respond to cholinesterase inhibitors, but improvement observed in any dementing disorder, given the products available currently, is neither dramatic nor permanent.

Centrally acting acetylcholinesterase inhibitors

Used to palliate cholinergic deficiency.


Rivastigmine (Exelon)

Centrally acting inhibitor of AChE and BuChE.
US Food and Drug Administration approved for dementia of Parkinson's disease

Adult

1.5 mg PO bid for 1 mo, then 3 mg PO bid for 1 mo, then 4.5 mg PO for 1 mo, and 6 mg PO bid thereafter; medication must be given with largest meals

Pediatric

Not established

None reported; since drug metabolized by cholinesterases, no significant hepatic metabolism takes place

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Administer with large meals to minimize adverse effects; always titrate upward slowly


Donepezil (Aricept)

Centrally acting inhibitor of AchE but not of BuChE.

Adult

5 mg PO qd for 3-4 wk, followed by 10 mg PO qd

Pediatric

Not established

Increases effects of succinylcholine, cholinesterase inhibitors, or cholinergic agonists; may increase fluvoxamine levels

Documented hypersensitivity; sick sinus syndrome or other supraventricular cardiac conduction abnormalities; peptic ulcer disease; bladder outflow obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with seizures, asthma, sick sinus syndrome, or other supraventricular conduction abnormalities


Galantamine (Razadyne, Razadyne ER)

Enhances central cholinergic function; likely to inhibit AChE.

Adult

IR: 16-24 mg/d PO divided bid
ER: 16-24 mg PO qd

Pediatric

Not established

Can interfere with effect of anticholinergic medications; synergistic effect if given concurrently with other ChEIs, succinylcholine, other neuromuscular blocking agents

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Most frequent adverse events include nausea, vomiting, diarrhea, anorexia, and weight loss; dose titration needed in patients with hepatic and/or renal dysfunction; can cause bladder outflow obstruction; should be prescribed with care in patients with lung disease; could potentiate tendency toward seizures


Rivastigmine transdermal patch (Exelon patch)

Competitive and reversible acetylcholinesterase inhibitor. While mechanism of action unknown, may reversibly inhibit cholinesterase, which may, in turn, increase concentrations of acetylcholine available for synaptic transmission in CNS and thereby enhance cholinergic function. Effect may lessen as disease process advances and fewer cholinergic neurons remain functionally intact.
Available as 5-cm2 patch containing 9 mg (releases 4.6 mg/24 h) and 10-cm2 patch containing 18 mg (releases 9.5 mg/24 h). Indicated for dementia of Alzheimer disease and for dementia associated with Parkinson disease.

Adult

Apply patch to upper or lower back, upper arm, or chest
Initiating patch therapy (not switching from oral therapy): 4.6 mg/24 h patch (5 cm2) applied qd initially; if well tolerated and after minimum of 4 wk, increase to 9.5 mg/24 h patch (10 cm2) applied qd
Switching from oral administration to patch therapy:
Apply first patch on day following last oral dose
Total daily oral dose <6 mg/d: Switch to 4.6 mg/24 h patch
Total daily oral dose 6-12 mg/d: Switch to 9.5 mg/24 h patch

Pediatric

Not indicated

May reduce effects of anticholinergics; increases effects of cholinergic agonists and neuromuscular blockers; risk of bradycardia increases when administered concurrently with beta-blockers without ISA, the calcium channel blockers diltiazem or verapamil, and digoxin

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Apply patch to clean, dry, and hairless area of back, upper arm, or chest; area where patch is applied must be free of powder, oil, moisturizer, lotion, or other substances that would keep patch from adhering properly to skin; also, apply to areas free of cuts, rashes, or other irritation; may cause significant nausea, vomiting, anorexia, and weight loss if taken in doses higher than recommended; if significant adverse effects occur, patient should discontinue treatment for several doses, then restart at lowest dose; extrapyramidal symptoms may occur or be exacerbated (especially tremor); caution in history of peptic ulcer disease, sick sinus syndrome, urinary obstruction, pulmonary conditions (eg, COPD, asthma), and bradycardia or supraventricular conduction conditions

More on Parkinson Disease Dementia

Overview: Parkinson Disease Dementia
Differential Diagnoses & Workup: Parkinson Disease Dementia
Treatment & Medication: Parkinson Disease Dementia
Follow-up: Parkinson Disease Dementia
References
Further Reading

References

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  4. Goldmann Gross, R., Siderowf, A., & Hurtig, H. I. Cognitive impairment in Parkinson's disease and dementia with lewy bodies: a spectrum of disease. Neuro-Signals. 2008;16(1):24-34. [Medline].

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Keywords

Parkinson disease, PD, Parkinson's disease, parkinsonism, Alzheimer disease, AD, Alzheimer's disease, dementia, senility, palsy, cognitive deficits, cognitive impairment, cognitive dysfunction, neurodegenerative disorders

Contributor Information and Disclosures

Author

Margaret M Swanberg, DO, Assistant Professor of Neurology, Uniformed Services University; Chief of Neurobehavior Service, Walter Reed Army Medical Center; Assistant Chief, Department of Neurology, Walter Reed Army Medical Center
Margaret M Swanberg, DO is a member of the following medical societies: American Academy of Neurology and American Neuropsychiatric Association
Disclosure: Nothing to disclose.

Coauthor(s)

Raj K Kalapatapu, MD, Fellow in Geriatric Psychiatry, Mount Sinai School of Medicine
Raj K Kalapatapu, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

Medical Editor

Alan D Schmetzer, MD, Professor, Vice-Chair for Education, and Director of Residency Training in General and Addiction Psychiatry, Department of Psychiatry, Indiana University School of Medicine
Alan D Schmetzer, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Clinical Psychiatrists, American Academy of Psychiatry and the Law, American College of Physician Executives, American Medical Association, American Neuropsychiatric Association, American Psychiatric Association, and Association for Convulsive Therapy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

 
 
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