Amantadine for parkinsonism

A Because CD is currently receiving amantadine for Parkinson s disease, he does not require additional prophylaxis with rimantadine because both medications are equally ef ive for the treatment and prophylaxis of influenza A. Zanamivir is unnecessary because he does not need additional prophylaxis for influenza B. In addition, zanamivir may cause bronchospasms in patients with asthma or chronic obstructive pulmonary disease. If CD requires zanamivir in the future, he should be instructed to use his beta-agonist inhaler prior to zanamivir. 

Note Fifty to 90% of patients receiving amantadine for Parkinsonism develop a more or less livedo reticularis ... 

Crosby NJ, Deane KH, Clarke CE. Amantadine for dyskinesia in Parkinson s disease. Cochrane Database SystRev. 2003 CD003467. 

Pad C, Thomas A, Onofrj M. Amantadine for dyskinesia in patients affected by severe Parkinson s disease. Neurol Sci. 2001 22 75-76. 

Amantadine a drug used for Parkinson s disease. It also has antiviral properties. 

CD is a 70-year-old man who resides in a nursing home. His PMH is significant for Parkinson s disease and COPD. His medications include carbidopa/levodopa, and amantadine, as well as ipratropium, albuterol, and triamcinolone inhalers. One of the residents is diagnosed with influenza A and all the residents now require prophylaxis for influenza A with rimantadine. Which of the following would be the most appropriate therapy for prevention of influenza A in CD ... 

Cardiovascular Does the patient have atrial fibrillation, a coronary artery disease history, or hyperlipidemia increasing stroke risk Could orthostatic hypotension be due to medications for Parkinson s disease treatment Is a medication such as amantadine causing peripheral edema ... 

Mrs Cooper is being treated with amantadine for her mild tremor and slowness of movement. While Mrs Cooper is managing quite well at home, her daughter is keen to know if there is anything she should be aware of regarding the treatment for Parkinson s disease. 

Bromocriptine is considered first line treatment for Parkinson s. It is effective in conjunction with a cholinergic-lowering drug (e.g., amantadine), and is also used as monotherapy in patients undergoing a drug holiday from therapy with L-dopa. It may also be used as a partial replacement for L-dopa, allowing the dose of L-dopa to be lowered. Bromocriptine is also used to ameliorate on-off phenomena. 

A 49-year-old woman was taking amantadine 200 mg daily, haloperidol 5 mg daily and flurazepam 30 mg at night was given phenelzine 15 mg twice daily for depression. Within 72 hours her blood pressure rose from 140/90 to 160/110 mmHg. The phenelzine was withdrawn, and 24 hours later, the amantadine and haloperidol were withdrawn. The blood pressure remained elevated for a further 72 hours. In contrast, a woman is reported to have been successfully and uneventfully treated with amantadine 200 mg daily for Parkinson s disease and phenelzine 45 mg daily for depression. ... 

Recent evidence points to a local release of catecholamines as the major mode of action of amantadine in parkinsonism. This is the most sensitive effect of amantadine reported to date and occurs at the lowest dose. Althou earlier clues pointed to this action, the results of Grelak et al. clarified this point. They reported that a small transient pressor effect of amantadine alone, intravenously in dogs, was markedly intensified by dopamine-priming. This suggested that amantadine released dopamine and/or other catecholamines from neuronal scores to cause Che peripheral pressor action. The effect was noted at very low amantadine doses. There was no evidence for block of dopamine uptake. Earlier Vernier reported that transient increases in myocardial contractile force occurred following moderate intravenous doses of amantadine. These also suggested local catecholamine release, since they were abolished by reserpinlzatlon and restored by norepinephrine infusion. 

Recently several laboratories have reported evidence for amantadine-induced release of radiolabelled catecholamine (mainly dopamine) from rat brain30,51)52. This seems to confirm In the central nervous system what was seen in the periphery. Although this may be the most likely major mode of action of amantadine in parkinsonism, the quantitative relations between this and ocher biochemical actions upon catecholamines remain to be worked out. 

A 52-year-old woman with Parkinson s disease who had taken amantadine for 6 years developed bilateral comeal edema for 2 months amantadine was withdrawn and the edema resolved amantadine was reintroduced and the corneal edema recurred amantadine was then permanently withdrawn and the comeal edema again resolved [277 ]. 

Observational studies In a retrospective observational study of 11 patients receiving amantadine for the treatment of Parkinson s Disease three patients reported side effects. Lower extremity oedema was reported in an 86-year-old man receiving amantadine (100 mg twice daily) after 5 months of treatment. This resolved when amantadine was discontinued. Hallucinations were reported in a 71-year-old man in the first 2 months of treatment with amantadine. A reduction in amantadine dosage from 100 mg twice daily to 100 mg once daily did not result in improvement and the drug was therefore discontinued, which resulted in resolution of symptoms. 

MaUcani R, Zadikoff C, Melen O, Videnovic A, Borushko E, Simuni T. Amantadine for freezing of gait in patients with Parkinson disease. 

Low affinity use-dependent NMDA recqrtor antagonists meet the criteria for safe administration into patients. Drugs like amantadine and memantine have modest effects on Parkinson s disease and are used as initial therapy or as adjunct to l-DOPA. Their adverse effects include dizziness, lethargy and sleep disturbance. 

AMANTADINE The nurse administers this drug for the prevention or treatment of respiratory tract illness caused by influenza A virus. Some patients are prescribed this drug to manage extrapyramidal effects caused by drugp used to treat Parkinsonism (See Chaps. 29 and 32). The nurse should protect the capsules from moisture to prevent deterioration. When the drug is administered for symptoms of influenza, it is important to start therapy within 24 to 48 hours after symptoms begin. 

Ms. Dennis, age 89 years, has Parkinson s disease and is taking amantadine daily. In discussing her care with the family, determine what information you would include in the teaching plan and what information would be most important for the family to understand. Explain your answer. 

Parkinson s disease 100 mg twice/day when used alone. Onset of action is usually within 48 h. Initial dose is 100 mg/day for patients with serious associated medical illnesses or those receiving high doses of other antiparkinson drugs. After one to several weeks at 100 mg once/day, increase to 100 mg twice/day, if necessary. Patients whose responses are not optimal at 200 mg/day may occasionally benefit from an increase up to 400 mg/day in divided doses supervise closely. Patients initially benefiting from amantadine often experience decreased efficacy after a few months. Benefit may be regained by increasing to 300 mg/day, or by temporary discontinuation for several weeks. Other antiparkinson drugs may be necessary. 

Amantadine has a long history in the symptomatic treatment of Parkinson s disease. Several recent double-blind, placebo-controlled studies have confirmed the impressive acute antidyskinetic effects of amantadine (Rajput et al. 1998 Verhagen Metman et al. 1998 Luginger et al. 2000 Del Dotto et al. 2001 Shoghi-Jadid et al. 2002). One study also indicates that amantadine s antidyskinetic benefit is maintained for at least 1 year (Metman et al. 1999). The related compound memantine was found, as in the MPTP monkey, to have no effect on dyskinesia in a double-blind study but it did improve parkinsonian symptoms (Merello et al. 1999). This indicates that the antidyskinetic effects of amantadine may be unrelated to NMDA receptor antagonism (Danysz et al. 1997). 

The Centers for Disease Control s (CDC) Immunization Practices Advisory Committee recommends annual vaccination as the method of choice in the prevention of influenza infection. However, when vaccination is contraindicated or early vaccination is not possible, amantadine and rimantadine are effective prophylactic agents that have been shown to protect approximately 70 to 90% of patients from influenza A infection. Since these drugs do not prevent the host immune response to influenza A, they may be used to prevent infection during the 2- to 4-week period required to develop immunity following vaccination. An additional use of amantadine, unrelated to its antiviral activity, is in the therapy of Parkinson s disease (see Chapter 31). 

Amantadine appears to work by blocking the N-methyl-D-aspartate (NMDA) receptor in the brain, thereby inhibiting the effects of excitatory amino acids such as glutamate.18,47 This suggests that excitatory neurotransmitters play a role in motor complications associated with advanced Parkinson disease.23,65 Future research may discover other ways of controlling these excitatory neurotransmitters, thus providing additional treatments for people with advanced Parkinson disease. 

Ketamine also shares a close chemical kinship to prescription drugs Tiletamine and Memantine. Tileta-mine is used in combination with zolazepam as a veterinary anesthetic under the brand names Zoletic and Tela-zol. Memantine is derived from the anti-influenza drug amantadine, and also works to block NDMA receptors. Memantine has been approved for use in Parkinson s disease and dementia in the elderly. It is also being used experimentally with AIDS patients for the treatment of HIV encephalopathy. 

In many viral infections the clinical symptoms appear late in the course of the disease at a time when most of the virus particles have replicated. [Note This contrasts with bacterial diseases in which the clinical symptoms are usually coincident with bacterial proliferation.] At this late, symptomatic stage of the viral infection, administration of drugs that block viral replication have limited effectiveness. However, some antiviral agents are useful as prophylactic agents. For example, amantadine [a MAN ta deen] and its congener, rimantadine [rih MAN ta deen] have been shown to be equally effective in preventing influenza A infections. [Note Amantadine is also effective in the treatment of some cases of Parkinson s disease (see p. 87).]... 

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