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Algorithm For The Management Of Parkinson's Disease 8 |
Exacerbated by anxiety. Regardless of the type or pattern. choreodystonic dyskinesias can be unmasked or worsened by anxiety-provoking situations. If this is a frequent problem for the patient, intervention directed at neuropsychiatric issues may be appropriate.
Dystonic movements. Dystonia in the absence of chorea is common in PD and can be caused by the disease process, per se, rather than a medication effect. Dystonia is commonly related to drug action, however. Prototypic is the isolated dystonic deviation of the toes or cramping of the legs that occasionally occurs in undertreated patients. Often, this will occur with other signs of undertreated parkinsonism. In this case, the usual strategies for improving PD motor control are appropriate. In certain patients, painful dystonia of the lower extremities is particularly a problem upon awakening in the morning (early morning foot dystonia), before the initial morning dose of carbidopa-levodopa can take effect. One option is to administer a dose of CR carbidopa-levodopa at bedtime. The effects may not be sufficiently long-lasting to carry the patient to the following morning, however. Administration of a dose of carbidopa-levodopa in the early morning, before the patient is scheduled to rise from bed, can be effective but requires the patient to set an alarm to awaken. The addition of bromocriptine or pergolide, with their longer-lasting effects, also may prove beneficial, particularly if one of the doses is administered at bedtime. Some patients experience painful or uncomfortable dystonia at the end of their levodopa response cycle. Several options are available, as described in the section "Optimal peak response but "wearing off." This is also one circumstance, apart from tremor, in which an anticholinergic drug may be helpful. Lithium may be helpful for painful "off"-period dystonia and can be tried when all other methods have failed. Botulinum toxin injection can be used to treat sustained focal dystonias of the foot. In some patients dystonia may be secondary to their medications. If it is present at the time of peak levodopa effect, a reduction in the individual doses of carbidopa-levodopa should result in resolution. If it occurs during the "off" period as a "wearing-off" phenomenon, strategies can be employed to increase "on" time (see the section "Optimal response but wearing off").
NEUROPSYCHIATRIC PROBLEMS
The neuropsychiatric manifestations of PD and of the medications used to treat it can be ever more disabling than the motoric dysfunction seen in this illness. In approaching the management of this group of symptoms, it is important to keep in mind that some of them, such as hallucinations, usually are induced by medication, while others, such as depression and "off"-period anxiety, typically are not directly related to drugs. Still a third group of neuropsychiatric symptoms, most notably memory loss, confusion, and agitation occur independent of medication in some patients but can be caused or exacerbated by antiparkinsonian agents in others. Thus, in devising a rational approach to the treatment of these behavioral syndromes, a critical decision must be made as to whether to add psychoactive medications, reduce the dosage of antiparkinsonian agents, or do both.
COGNITIVE IMPAIRMENT. The incidence of dementia in patients with PD has been variously estimated, but most studies place it in the range of 15 to 20%[125,126] in a typical clinic population. Its prevalence increases with disease duration and with advancing age and contributes to mortality. In one recent study,[125] dementia developed in 65% of patients with PD by the time they reached 85 years of age. Memory loss is one of the most noticeable manifestations of dementia in patients with PD.[127] Some patients also manifest the phenomenon of bradyphrenia a slowing of cognitive processes that is out of proportion to their general level of cognitive function.[128] Not only does primary dementia appear in patients with PO but these individuals especially those over age 65, may also suffer from other dementing illnesses, such as Alzheimer's disease or multi-infarct dementia. Unlike drug-induced cognitive symptoms, those caused by PD itself are not amenable to therapy (breakout 19). However, parkinsonian patients with dementia are especially prone to experience further memory loss or confusion when treated with antiparkinsonian drugs. As I will discuss, reduction or cessation of these drugs is a valid therapeutic option in this circumstance. Drug-induced cognitive impairment can take the form of impaired memory or confusion. Memory deficit as a manifestation of antiparkinsonian drugs is almost always caused by agents having anticholinergic properties--most notably drugs such as trihexyphenidyl or benztropine, but also agents such as amantadine and the tricyclic antidepressants. This effect appears to be especially prominent in the elderly, which suggests that the primary antiparkinsonian anticholinergic drugs should be avoided in this group and that even these agents with milder anticholinergic effects should he used with great caution. The management of medication-induced memory deficit consists of reducing or elimination the offending medication. In patients who take more than one class of anticholinergic preparation, the agent with the most potent anticholinergic properties-the anticholinergic antiparkinsonian agents-should be eliminated or reduced first, followed by the tricyclic antidepressants and finally amantadine. A tricyclic antidepressant such as amitriptyline occasionally can be replaced with one with less anticholinergic potency, such as nortriptyline, but just as often, total discontinuance of drugs with any anticholinergic effect, however mild, is required. Confusion can be induced by anticholinergic medications and by those which are dopaminergic, as well. Thus, selegiline, the dopamine agonists (bromocriptine and pergolide), and carbidopa-levodopa must be considered as potential causes of this symptom. When confusion develops in a patient taking several of these preparations, a decision must be made as to which should be discontinued or reduced first. A reasonable guideline is to discontinue first the agent that has the greatest potential for causing confusion but has a relatively smaller impact on the motoric symptoms of PD. In this approach, the anticholinergic preparations should he the first to be discontinued, followed by selegiline, tricyclic antidepressants, amantadine, and then the dopamine agonists. If confusion persists despite discontinuance of these preparations, or if the patient has not been receiving any of them, the carbidopa-levodopa dosage must then be reduced.
In most patients with moderate to advanced PD, total discontinuance of carbidopa-levodopa is not feasible because of the reemergence of severely disabling motoric symptoms. Instead, a gradual downward titration of dosage is recommended, aiming at an amount low enough to relieve confusion but high enough to provide some benefit for motor skills and ambulation. Unfortunately, in some patients confusion is a direct consequence of the disease process and no medication adjustment is adequate to reduce these symptoms.
PSYCHOSIS. Psychosis in PD can take many forms[129] and is almost always drug-induced. Two of the most common psychotic manifestations are vivid dreams and hallucinations (breakout 20). The management of the former is handled in the "Sleep disorders" algorithm. The latter is covered under a separate heading in the "Neuropsychiatric problems" algorithm.
BEHAVIORAL IMPAIRMENT. Behavioral impairment in PD can take the form of agitation, depression, anxiety, and panic attacks (breakout 21). Agitation. Agitation can occur spontaneously in PD or result from virtually any of the antiparkinsonian medications.
* Primary. The treatment of agitation, when it occurs without relation to antiparkinsonian medication, involves the administration of anxiolytic agents. The benzodiazepines, especially alprazolam, are particularly useful. Diazepam and lorazepam can he used for this purpose, as well. Buspirone, a 5-HTia serotonin agonist, is also an effective anxiolytic, but because of its dopamine-blocking potential it probably should not be the first agent used in a patient with PD.
* Medication induced. When it appears that agitation is an adverse effect of medication, adjunctive antiparkinsonian agents should be discontinued in order of their potential to have caused this syndrome. Selegiline, especially in a patient already receiving levodopa, should be discontinued first, followed by amantadine, dopamine agonists, and anticholinergic agents. It is worth noting because of their profound effect on cognitive processes, are the first to be discontinued when memory loss is the target symptom but are among the last to be discontinued when agitation is the problem. If none of these preparations is in use, or if all have been discontinued without improvement in agitation, then carbidopa-levodopa must be carefully titrated downward, in hope of improving agitation without allowing the reemergence of serious motor disability.; In addition to these measures, a careful review should be made of other non-PD medications that may have the potential to produce or enhance agitation. Certain patients who are receiving inadequate dosages of dopaminergic medications or who are experiencing "wearing off" of the levodopa effect become very anxious and might appear agitated. This must be distinguished from primary agitation.
Depression. Depression is extremely common in PD. In a recent study the incidence of depression in PD was found to be 47%.[130] The diagnosis of an affective disorder in PD can be difficult, however, because many of the clinical manifestations of depression--such as slowness, poor concentration, sleep disturbance, and loss of energy--can be signs of PD itself. Starkstein et al.[131] confirmed that motor retardation, loss of energy, and early morning awakening were no more common in nondepressed than depressed patients with PD. On the other hand, depressive symptoms--such as worrying, brooding, loss of interest, suicidal tendencies, social withdrawal, loss of libido, and initial or middle insomnia--among others, were more common in depressed than nondepressed patients.
