eMedicine Specialties > Physical Medicine and Rehabilitation > Movement Disorders
Parkinson Disease: Treatment & Medication
Updated: Mar 10, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Issues/Complications
Primary medical complications seen in patients with Parkinson's disease (PD) include autonomic dysfunction, cardiopulmonary impairment, dysphagia, and depression.
- Autonomic dysfunction is common in patients with PD.
- Orthostatic hypotension often becomes a concern during the later part of the disease process. Management techniques can include elevating the head of the bed, as well as having the patient arise slowly, use pressure garments, consume a high-salt diet, and use such medications as pseudoephedrine, mineralocorticoids, and midodrine.
- Impaired intestinal motility can lead to constipation, vomiting, and impaired absorption; treatment options include the employment of frequent, smaller meals; increased fiber; bulking agents; stool softeners; and suppositories.
- Urinary incontinence, retention, and bladder infection can occur. Treatment usually is based on the results of investigations, such as renal function studies, urinalysis, postvoid residuals, cystoscopy, and urodynamic studies.
- Erectile dysfunction is not uncommon. Treatment options include the use of sildenafil, prostaglandin injections, pumps, and prosthetic devices.
- Cardiopulmonary impairment
- The patient's flexed posture can lead to kyphosis, cause a reduction in pulmonary capacity, and produce a restrictive lung disease pattern.
- Breathing exercises, postural reeducation, and trunk exercises may be helpful.
- Institution of a general conditioning program can increase the patient's endurance.
- If pulmonary function progressively worsens, assisted coughing techniques, incentive spirometry, and respiratory therapy intervention may be required.
- Depression
- Depression can occur in approximately 50% of patients with PD and should not be overlooked, as its impact on disability can be significant.
- Depression may be related to a deficit in serotonergic neurotransmission or to decreased cortical levels of norepinephrine and dopamine.
- Serotonergic agents often are the first antidepressants of choice in PD. If this treatment regimen is ineffective, a tricyclic antidepressant with anticholinergic side effects (eg, desipramine, nortriptyline) may be recommended.
- Dysphagia
- If swallowing difficulties do not respond to conservative interventions by the speech therapist, more aggressive treatment may be required.
- Such aggressive management can include invasive procedures, such as nasogastric or gastrostomy feeding tube placement.
- Discussion should be initiated early on in the disease course to ascertain the patient's wishes about a feeding tube, in case dementia develops and the patient lacks the capacity for decision making when a feeding tube becomes medically indicated.
Surgical Intervention
Increased interest has been seen in the surgical management of Parkinson's disease (PD).11 Three main techniques currently in use are destructive therapy (lesioning), chronic deep brain stimulation, and transplantation.
- Destructive therapy
- Lesioning options include thalamotomy and pallidotomy.
- Ventral intermediate nucleus thalamotomy is quite effective at relieving tremor, but its effects on the other clinical manifestations of PD seem to be less significant and more variable. Thalamotomy usually is reserved for a relatively small percentage of patients with predominantly drug-resistant tremor.
- At present, pallidotomy is the surgical procedure most commonly used for advanced PD. The surgery employs lesioning to disrupt the abnormal activity in the globus pallidus; this disinhibits the motor thalamus and cortical motor areas,12 thereby improving motor functioning. Candidates for pallidotomy include patients who are disabled despite optimal medical management and who have responded to L-dopa therapy in the past but have developed complications from long-term L-dopa treatment. Rigidity, tremor, and bradykinesia all seem to respond to pallidotomy.
- Deep brain stimulation6
- Chronic deep brain stimulation seems to have emerged as an alternative to lesioning in patients with PD.
- Stimulation has the advantages of safety, reversibility, and adaptability (ie, stimulation parameters can be adjusted as the clinical features change over time).
- Stimulation sites include the ventral lateral thalamic nuclei (performed to decrease tremor, with a good response in 80-85% of patients), the globus pallidus (for bradykinesia, gait, speech, drug-induced dyskinesias), and the subthalamic nucleus13 (for bradykinesia, rigidity, tremor, gait/posture). A study of 6 male patients showed improved motor rating scores and reduced timing and spatial errors following deep brain stimulation of the internal globus pallidus.
- Earlier subthalamic nucleus stimulation (average of 7 years after diagnosis vs 14 years for control population) has been shown to improve results and patient quality of life.
- Subthalamic nucleus stimulation does not improve long-term mortality results.
- Bilateral subthalamic nucleus stimulation was linked in a case report with pathologic gambling.
- Transplantation
- Although stimulation and lesioning can improve symptoms, neither corrects the underlying pathology of the disease, which is a lack of dopamine from loss of substantia nigra neurons. Transplantation therapy offers the possibility of replacing these lost neurons.
- Clinical trials have examined the use of 3 types of transplants: autologous adrenal medulla transplants, fetal mesencephalon grafts, and xenografts.
- Adrenal medulla transplants are not in widespread use because of the high morbidity and mortality from adrenalectomy.
- Fetal mesencephalon grafts have shown promising early results. Trials continue, but ethical concerns, insufficient tissue, and procedural difficulties make it unlikely that the procedure will become commonplace.
- The most common xenograft used is the fetal pig mesencephalon. A trial currently is underway to determine the efficacy of this procedure.
- Human embryonic stem cell therapy and gene therapy
- Intrastriatal transplantation of human fetal mesencephalic tissue in PD patients has demonstrated clinical efficacy, but the limited availability of tissue precludes the systematic use of this procedure.
- Embryonic stem cells can differentiate into cells from the CNS. These cells could potentially provide a relatively unlimited source of cells for transplantation if protocols were developed to generate specific populations of neural cells.
- Ethical concerns also play a large role in this line of research.
- Initial results from the first human clinical trial of gene therapy for PD suggest the approach might significantly reduce symptoms of the disease and provide a 25% improvement in motor control.
Related eMedicine topic:
Surgical Treatment of Parkinson Disease
Surgical Treatment of Tremor
Consultations
Most commonly requested consultations for patients with Parkinson's disease are with neurologists, neurosurgeons, and psychiatrists.
- Consult with a neurologist for (1) initiation and management of medical therapy, (2) access to clinical medication trials if patient desires, and (3) management of side effects of L-dopa therapy.
- Consultation with a neurosurgeon may be indicated for a surgical opinion in patients who are resistant to standard medical therapy or who develop significant complications secondary to L-dopa therapy.
- Consult with a psychiatrist for management of depression in patients who do not respond to typical treatment options, such as the use of selective serotonin reuptake inhibitors (SSRIs), or who show evidence of contemplating suicide.
Rehabilitation Programs
Physical Therapy
Because Parkinson's disease (PD) is a progressive CNS disorder with progressive disability over time, the merits of therapy often are debated. Some studies have shown benefits in certain areas (eg, gait, independence in ADL, fine motor movements) in patients receiving therapy and medication versus those receiving only medication; however, the trials generally are quite small and improvements modest. Because the studies vary in the type of therapy and medications used, the reliability of combining the results of several trials is very small.
Physical therapy often is directed at the main causes of impairment and includes measures to decrease rigidity and increase range of motion (ROM), as well as to improve postural control, endurance, mobility, and gait. Treatment of bradykinesia and rigidity often includes daily stretching and ROM exercises, as well as task-specific activities. Gait and ambulation can be improved through a program of stretching and strengthening of the lower extremities that uses exaggerated steps and arm swings, marching steps (paced to the beat of a metronome), and mental rehearsal and imaging. The physical therapist should assess the need for ambulation aids (eg, walkers, canes) while completing gait training with the patient.
Exercises for the patient with PD should emphasize trunk extension, as well as lateral and rotational mobility, weight shifting, and balance training. Addressing how to fall safely and get up from the floor is important for patients with PD and their families. The physical therapist should instruct them in proper transfer techniques and try to improve their overall safety awareness during everyday activities. A general conditioning program also should be included in physical therapy to improve the patient's endurance. In addition, the physical therapist may instruct the patient and family members in a home exercise program.9,10
Occupational Therapy
Occupational therapy interventions for Parkinson's disease include providing exercises to improve upper extremity fine motor skills and dexterity, functional training in self-care and ADL, and appropriate aids and devices, such as dressing aids (eg, reachers, sock aid), railings, grab bars, and other environmental adaptations for the home. A home visit by the therapist may be helpful.
Speech Therapy
Speech therapy may be underemployed in patients with Parkinson's disease, given that speech and swallowing problems are common causes of disability in this population. Speech therapy seems to improve the quality of voice in patients with hypokinetic dysarthria. Therapy itself generally emphasizes better breath and rate control, as well as improved articulation and better volume. Beneficial effects of the therapy do not seem to persist after it has been discontinued.
Dysphagia tends to occur later in the disease process and can lead to drooling, aspiration, malnutrition, and inability to ingest medications. Speech therapy interventions can include positioning the neck in flexion, teaching a double swallow technique, using smaller amounts of food, or modifying the patient's diet and incorporating thickened liquids. A modified barium swallow analysis may be helpful in guiding the therapy plan and in monitoring the patient's progress.
Recreational Therapy
Because of the high level of impairment and disability seen in many patients with Parkinson's disease (PD), it is not surprising that avocational pursuits for these individuals often become more difficult. This change certainly can have a detrimental impact on a patient's overall quality of life. A recreational therapist may be helpful in identifying previous recreational interests and in helping the patient to pursue them once more, with or without assistance. If such pursuits are no longer possible, new interests can be identified and explored. The therapeutic value of social and recreational pursuits should not be underestimated in patients with PD, because many of these individuals can feel isolated and lonely because of the effects of the disease.
Medication
Medical management of Parkinson's disease (PD) can be quite complicated, as there are several classes of medications available, significant side effects to some of the medications, and no real consensus on which class of drug should be started at diagnosis. Different classes of medication often are combined to optimize symptom control. Medication management provides the most effective treatment of PD for the first 4-6 years. Thereafter, this disabling disease advances despite continuing medication management.
Currently, several trials are underway that are investigating potential medications for use in PD in the future.6 These are not yet approved for use in North America. They include symptomatic treatments targeting nondopaminergic areas,14 to avoid the motor complications seen with dopaminergic agents. Examples in this category include adenosine receptor antagonists and glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonists. Other agents have a neuroprotective or neurorestorative role.15,16 These include antioxidant coenzyme Q10; antiapoptotic agents, such as CEP-1347; and subthalamic glutamic acid decarboxylase, used in gene therapy.
In general, most clinicians start patients on selegiline (Eldepryl), a monoamine oxidase type B (MAO-B) inhibitor, at the time of diagnosis. This drug blocks one pathway in the breakdown of dopamine. When symptoms become more pronounced, therapy with L-dopa/carbidopa (Sinemet) or a dopamine receptor agonist (pergolide, bromocriptine) usually is instituted and is titrated as symptom control warrants, using the lowest dose required for adequate function.
Other options for medical management include anticholinergics (eg, benztropine [Cogentin]) and antivirals (eg, amantadine), which seem to have presynaptic and postsynaptic dopaminergic effects.
Some relatively new medications are available or are undergoing trials for treatment of PD. Two new dopamine agonists, ropinirole (Requip) and pramipexole (Mirapex), currently are available and may have fewer side effects than other dopamine agonists. They seem to be effective as monotherapy or in combination with other medications, such as L-dopa. A relatively new class of medications, catechol-O-methyltransferase (COMT) inhibitors, prevents peripheral degradation of L-dopa and allows a higher concentration to cross the blood-brain barrier. Medications in this class include tolcapone and entacapone. These medications are not widely available because of concern about elevated liver enzymes. Clinicians should see if they have been approved for use in the country where they practice.
Because of the often complicated drug regimens used by patients with PD, it is advisable to involve a neurologist with experience in management of this condition to assist with medication choice and side-effect management. Drug holidays have no basis and can be associated with significant morbidity due to a type of neuroleptic malignant syndrome.
Monoamine oxidase type B inhibitors
MAO-B inhibitors block one pathway in the breakdown of dopamine. This probably increases the amount of dopamine available in the brain and may prevent formation of hydrogen peroxide, offering a hypothetical neuroprotective benefit.
Selegiline (Eldepryl)
Used at time of diagnosis of PD before L-dopa therapy. May be useful as adjunct to L-dopa therapy.
Adult
10 mg/d divided PO bid (5 mg at breakfast; 5 mg at lunch) as monotherapy or in combination with L-dopa; not to exceed 10 mg/d
Pediatric
Not established
Can cause agitation and muscle rigidity and, rarely, death if taken in combination with meperidine; avoid concomitant administration of selegiline with SSRIs or TCAs; at least 5 wk should elapse between discontinuation of fluoxetine and initiation of MAOIs to prevent fatal interactions reported with MAO type A inhibitors; avoid administering MAOIs concomitantly with opioids; severe agitation, hallucinations, and death have occurred with concomitant administration of selegiline and meperidine
Documented hypersensitivity; extrapyramidal disorders, such as excessive tremor or tardive dyskinesia; severe psychosis; profound dementia
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
May experience exacerbation of L-dopa – associated side effects (may need to adjust L-dopa dose accordingly); adverse reactions associated with combination of selegiline and L-dopa include hallucinations (especially visual), nausea, abdominal pain, and confusion
Rasagiline (Azilect)
Irreversible MAO-B inhibitor that blocks dopamine degradation. Not metabolized to amphetamine derivatives. Main metabolite, aminoindan, has some activity and has been shown to improve motor and cognitive functions in experimental models. Indicated for Parkinson disease as initial monotherapy or as adjunctive therapy with levodopa.
Adult
Monotherapy: 1 mg PO qd
Adjunctive therapy with levodopa: 0.5 mg PO qd; may increase to 1 mg PO qd
Mild hepatic impairment or coadministration with CYP1A2 inhibitors: 0.5 mg PO qd
Pediatric
Not established
P450 CYP1A2 substrate; coadministration with drugs that inhibit CYP1A2 (eg, cimetidine, clarithromycin, erythromycin) may decrease elimination and increase toxicity; coadministration with TCAs, SSRIs, serotonin-norepinephrine reuptake inhibitors (SNRIs), nonselective MAOIs, or selective MAO-B inhibitors has caused severe CNS toxicity associated with hyperpyrexia and death; consuming tyramine-rich foods (eg, cheese, red wine, beer, sausage, avocado) may cause hypertensive crisis; also see Contraindications
Documented hypersensitivity; moderate-to-severe hepatic impairment (Child-Pugh score >6); concurrent use with meperidine, tramadol, methadone, propoxyphene; dextromethorphan, St. John's wort, mirtazapine, cyclobenzaprine, sympathomimetic amines (eg, pseudoephedrine, cocaine, ephedrine), other MAOIs, or local anesthetics containing epinephrine; pheochromocytoma
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
May cause dyskinesias, hallucinations, or hypotension; if emergent surgery is necessary, benzodiazepines, mivacurium, rapacuronium, fentanyl, morphine, or codeine may be used cautiously; melanoma may develop more frequently in those taking rasagiline than in matched controls
Dopaminergic agents
Because patients with Parkinson's disease (PD) suffer from a lack of dopamine, it follows that pharmacologic therapy is directed toward dopamine replacement. Dopamine does not cross the blood-brain barrier, but L-dopa, a precursor of dopamine, does.6 Increasing levels of striatal dopamine through the use of L-dopa is the mainstay of medical therapy in PD. L-dopa is combined with carbidopa, which is a decarboxylase inhibitor and helps to prevent breakdown of L-dopa, thus decreasing the need for large doses of L-dopa to achieve adequate brain dopamine levels.
Levodopa/carbidopa (Sinemet, Sinemet CR)
Given together with carbidopa (a decarboxylase inhibitor) to prevent breakdown of levodopa and increase bioavailability. Decreases the need for large doses of levodopa to achieve adequate brain dopamine levels. Medications often are used when symptom control is insufficient with selegiline alone. CR formulation can help prevent the on/off phenomenon in some patients. Sinemet tablets are available in a 4:1 ratio (Sinemet 100/25) and a 10:1 ratio (Sinemet 100/10 and 250/25) of levodopa to carbidopa. Sinemet CR tablets contain a 4:1 ratio of levodopa to carbidopa (100/25 or 200/50); daily dosage of Sinemet CR must be determined by careful titration.
Adult
Initial recommended dose is 1 tab of Sinemet CR 100/25 PO bid; in patients who require more levodopa, daily dose of 1-2 tab bid is generally well tolerated
Pediatric
Not established
Postural hypotension can occur when given with antihypertensive drugs; dose adjustment of antihypertensive drugs may be required; phenothiazines and butyrophenones may reduce therapeutic effects of levodopa; rare reports of adverse effects resulting from concomitant use of tricyclic antidepressants and Sinemet have been made; when general anesthesia required, Sinemet should be discontinued the night before
Documented hypersensitivity; do not administer MAOIs and Sinemet concomitantly; do not administer to patients with uncompensated cardiovascular, endocrine, hematologic, hepatic, pulmonary, or renal disease or to patients with narrow-angle glaucoma; because levodopa may activate malignant melanoma, do not administer to patients with suspicious or undiagnosed skin lesions or a history of melanoma
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
Periodic evaluations of hepatic, hematopoietic, cardiovascular, and renal function are recommended during extended therapy with Sinemet; absorption of Sinemet may be impaired in some patients on a high-protein diet
Dopamine receptor agonists
Dopamine agonists directly stimulate postsynaptic dopamine receptors, bypassing the need for conversion and storage as in L-dopa therapy. These medications usually are not as effective as L-dopa in controlling symptoms of Parkinson's disease and typically are considered third-line medications. The 2 most commonly used medications in this class are pergolide and bromocriptine.
Pergolide (Permax)
Believed to exert therapeutic effects by direct stimulation of postsynaptic dopamine receptors in the corpus striatum. Used as an adjunct with levodopa/carbidopa for management of PD. Not recommended for treatment of newly diagnosed patients or as sole medication in PD. Pergolide was withdrawn from the US market on March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. It is important not to abruptly stop pergolide. Health care professionals should assess patients' need for dopamine agonist therapy and consider alternative treatment. If continued treatment with a dopamine agonist is needed, another one should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.
Adult
0.05 mg single dose PO initially for first 2 d; gradually increase by 0.1-0.15 mg/d every third day for next 12 d; then increase dosage by 0.25 mg every third d until optimal dosage achieved; administer divided doses tid
Pediatric
Not established
Dopamine antagonists, such as the neuroleptics phenothiazines, butyrophenones, thioxanthenes, or metoclopramide, may diminish effectiveness of pergolide, a dopamine agonist; because pergolide mesylate is more than 90% bound to plasma proteins, exercise caution if pergolide is coadministered with other drugs known to affect protein binding
Documented hypersensitivity
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
Discontinue gradually, as abrupt discontinuation may cause hallucinations and confusion; dyskinesia may occur or worsen in patients receiving levodopa with pergolide; caution in cardiac dysrhythmias; may cause or exacerbate preexisting states of confusion and hallucinations or dyskinesia
Bromocriptine (Parlodel)
Used as adjunct therapy to levodopa in treatment of PD. Can facilitate use of lower doses of levodopa/carbidopa, thus decreasing risk of long-term complications, such as dyskinesias.
Adult
1.25 mg PO hs initially to establish tolerance; increase to 2.5 mg/d divided bid with meals; then increase dosage prn, adding an additional 2.5 mg/d, once q2-4wk taken in 2-3 divided doses with meals
Pediatric
Not established
Adverse effects may increase if coadministered with ergot alkaloids, erythromycin, or sympathomimetic agents; coadministration with dopamine antagonists (eg, metoclopramide), phenothiazines, butyrophenones (eg, haloperidol), pimozide, amitriptyline, imipramine, methyldopa, or reserpine may decrease efficacy
Documented hypersensitivity; coronary artery disease; severe cardiovascular disorders
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
May cause postural hypotension; periodic monitoring of blood pressure advisable; dizziness; caution patients about driving until response determined; few cases of GI bleeding and ulceration reported; discontinue medication if this occurs; safety not established in patients with severe hepatic or renal disease
Apomorphine (Apokyn)
Elicits dopamine agonist effect. Indicated to treat acute immobility episodes (hypomobility or "off-periods") in PD. These episodes consist of inability to rise from a chair, speak, or walk and may occur toward the end of the dose interval or may be spontaneous and unpredictable in onset. Approximately 10% of individuals with stage IV PD who do not respond to standard medications for acute immobility may respond to apomorphine.
Adult
Dosage is individualized
Test dose: 2 mg (0.2 mL) SC for 1 dose initially during hypomobility, if tolerated (ie, blood pressure remains stable), may use for subsequent hypomobility episodes
Establishing dose: If patient tolerates test dose and hypomobility responds, 2 mg is the dose to use for subsequent hypomobility episodes
If patient tolerates test dose but hypomobility does not respond to test dose, may increase dose by 1 mg (0.1 mL) q2-3 d until response is observed; not to exceed 6 mg (0.6 mL)/dose
Note: Administer only 1 dose per hypomobility episode, do not repeat dose; administer with antiemetic drug
Pediatric
Not established
Coadministration with 5HT3 antagonists used for emesis or irritable bowel syndrome (eg, ondansetron, dolasetron, granisetron, palonosetron, alosetron) may cause hypotension and loss of consciousness; coadministration with drugs that increase QTC interval (eg, thioridazine, quinidine, sotalol, erythromycin, dofetilide) may increase arrhythmia potential; metabolized by COMT, coadministration with COMT inhibitors (eg, entacapone, tolcapone) may decrease elimination
Documented hypersensitivity to apomorphine or metabisulfite
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
Causes severe nausea and vomiting and must be administered with an antiemetic drug (but not with antiemetic agents that are 5HT3 antagonists); may cause orthostatic hypotension, faintness, hallucinations, fluid retention, chest pain, increased sweating, flushing, pallor, dyskinesia, rhinorrhea, and extreme drowsiness (may fall asleep during waking hours without warning)
Rotigotine (Neupro)
April 2008: A recall was issued for Neupro patch in the United States because of crystal formation in the patch that resulted in decreased dopamine absorption transdermally. As of August 1, 2008, the patch was still unavailable, although the manufacturer is working to correct the defect and return the product to the market. For more information see Medscape News.
Dopamine agonist stimulating D3, D2, and D1 receptors. Improvement in Parkinson-related symptoms thought to be related to its ability to stimulate D2 receptors within the caudate putamen in the brain. Available as transdermal patch that provides continuous delivery for 24 h (2 mg/24 h [10 cm2], 4 mg/24 h [20 cm2], or 6 mg/24 h [30 cm2]). Indicated for symptoms of early Parkinson disease.
Adult
2 mg/24 h (10 cm2) transdermal qd initially; may increase qwk by 2 mg/24 h, not to exceed 6 mg/24 h
Remove previous day's patch before applying new patch; rotate application site each day between left and right sides of body and upper and lower parts of body
Pediatric
Indication not applicable to children
Dopamine antagonists (eg, antipsychotics, metoclopramide) may decrease effect
Documented hypersensitivity
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
Common adverse effects include dermal reactions at patch site, dizziness, nausea, vomiting, drowsiness, and insomnia; less common adverse effects that may be hazardous to patient include sudden sleep onset, hallucinations, and postural hypotension; weight gain secondary to fluid retention has been observed; rapid dose reduction or abrupt withdrawal may cause hyperpyrexia and confusion; apply to clean, dry, and intact skin on abdomen, thigh, hip, flank, shoulder, or upper arm
Anticholinergics
The most commonly used treatment for Parkinson's disease (PD) until the introduction of L-dopa; it probably works by blocking cholinergic receptors in the striatum and restoring the dopamine-acetylcholine balance; benztropine (Cogentin) is the most common anticholinergic agent in the treatment of PD.
Benztropine (Cogentin)
May be effective at any stage of disease process; helpful in patients resistant to other agents; reduces tremor and rigidity.
Adult
1-2 mg/d with range of 0.5-6 mg PO or parenterally; 0.5-1 mg hs; individualized treatment required; smaller doses likely in older or thinner patients
Pediatric
Not established
Decreases effects of levodopa; increases effects of narcotic analgesics, phenothiazines, quinidine, tricyclic antidepressants, and anticholinergics
Documented hypersensitivity; glaucoma
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
May cause weakness or inability to move particular muscle groups in larger doses; mental confusion and visual hallucinations may occur; tardive dyskinesia reported in long-term benztropine use; caution in hot weather because of anhidrosis; advise patient to report GI complaints, fever, or heat intolerance if concomitantly administered with phenothiazines, haloperidol, or other drugs with anticholinergic or antidopaminergic activity; paralytic ileus reported in patients taking benztropine in combination with phenothiazines and/or tricyclic antidepressants
Antivirals
Amantadine (Symmetrel) is the only antiviral used in the treatment of Parkinson's disease. The mechanism of action is unknown; it may trigger the release of brain dopamine from nerve endings.
Amantadine (Symmetrel)
Used alone and in combination with anticholinergic antiparkinsonian medications and with levodopa/carbidopa; maximal therapeutic benefit usually occurs within 1 wk, and initial benefits may decrease with continued dosing. May be useful as adjunct in patients who do not tolerate optimal doses of levodopa alone or in combined therapy with carbidopa. Amantadine may result in better control of PD in these patients and may decrease fluctuations in performance.
Adult
100 mg/d PO initially; after a few wk may be increased to 100 mg bid; increase to 300 mg/d divided dose may help some patients
Pediatric
Not established
Drugs with anticholinergic or CNS stimulant activity increase amantadine toxicity; the concurrent administration of hydrochlorothiazide plus triamterene with amantadine may increase plasma concentrations of amantadine
Documented hypersensitivity
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
Parkinsonian crisis may result from abrupt discontinuation; neuroleptic malignant syndrome associated with dose reduction or withdrawal of amantadine; reduce dose in patients with renal impairment and in patients aged 65 y or older; exercise care in patients with congestive heart failure, liver disease, orthostatic hypotension, or psychosis
More on Parkinson Disease |
| Overview: Parkinson Disease |
| Differential Diagnoses & Workup: Parkinson Disease |
 Treatment & Medication: Parkinson Disease |
| Follow-up: Parkinson Disease |
| Multimedia: Parkinson Disease |
| References |
| « Previous Page | Next Page » |
References
Lang AE, Lozano AM. Parkinson's disease. First of two parts. N Engl J Med. Oct 8 1998;339(15):1044-53. [Medline].
Stoessl AJ. Etiology of Parkinson's disease. Can J Neurol Sci. Aug 1999;26 Suppl 2:S5-12. [Medline].
Lang AE, Lozano AM. Parkinson's disease. Second of two parts. N Engl J Med. Oct 15 1998;339(16):1130-43. [Medline].
Driver JA, Logroscino G, Gaziano JM, et al. Incidence and remaining lifetime risk of Parkinson disease in advanced age. Neurology. Feb 3 2009;72(5):432-8. [Medline].
Grimes DA, Lang AE. Treatment of early Parkinson's disease. Can J Neurol Sci. Aug 1999;26 Suppl 2:S39-44. [Medline].
Thobois S, Delamarre-Damier F, Derkinderen P. Treatment of motor dysfunction in Parkinson's disease: an overview. Clin Neurol Neurosurg. Jun 2005;107(4):269-81. [Medline].
Stoessl AJ, Rivest J. Differential diagnosis of parkinsonism. Can J Neurol Sci. Aug 1999;26 Suppl 2:S1-4. [Medline].
Tolosa E, Gaig C, Santamaria J, et al. Diagnosis and the premotor phase of Parkinson disease. Neurology. Feb 17 2009;72(7 Suppl):S12-20. [Medline].
Sliwa JA. Neuromuscular rehabilitation and electrodiagnosis. 1. Central neurologic disorders. Arch Phys Med Rehabil. Mar 2000;81(3 Suppl 1):S3-12; quiz S36-44. [Medline].
Dombovy ML. Rehabilitation concerns in degenerative movement disorders of the central nervous system. In: Braddom RL, ed. Handbook of Physical Medicine and Rehabilitation. Philadelphia, Pa: WB Saunders; 1996:1088-99.
Honey C, Gross RE, Lozano AM. New developments in the surgery for Parkinson's disease. Can J Neurol Sci. Aug 1999;26 Suppl 2:S45-52. [Medline].
Chu J, Wagle-Shukla A, Gunraj C, et al. Impaired presynaptic inhibition in the motor cortex in Parkinson disease. Neurology. Mar 3 2009;72(9):842-9. [Medline].
Fogelson N, Kühn AA, Silberstein P, et al. Frequency dependent effects of subthalamic nucleus stimulation in Parkinson's disease. Neurosci Lett. Jul 1-8 2005;382(1-2):5-9. [Medline].
Poewe W. Treatments for Parkinson disease--past achievements and current clinical needs. Neurology. Feb 17 2009;72(7 Suppl):S65-73. [Medline].
Schapira AH. Molecular and clinical pathways to neuroprotection of dopaminergic drugs in Parkinson disease. Neurology. Feb 17 2009;72(7 Suppl):S44-50. [Medline].
Lim SY, Fox SH, Lang AE. Overview of the extranigral aspects of Parkinson disease. Arch Neurol. Feb 2009;66(2):167-72. [Medline].
Canadian Pharmacists Association. Compendium of Pharmaceuticals and Specialties. 25th ed. Toronto, Canada: Webcom Ltd; 2000.
Further Reading
Keywords
Parkinson's disease, Parkinson disease, Parkinson, tremors, tremor, dopamine, Parkinson's, deep brain stimulation, motor cortex, Parkinson's symptoms, dementia, L dopa, movement disorders, Parkinson's treatment, Parkinson's disease symptoms, parkinsonism, levodopa, bradykinesia, Parkinson's disease treatment, Parkinson disease symptoms, L-dopa, idiopathic Parkinson disease
