Making a problem list, managing antiparkinsonian medications, and non-pharmacological approaches

Having negotiated a common framework and terminology for diagnosis and understanding, the next step is to produce a problem list, working systematically through the domains of motor, cognitive, neuropsychiatric, and autonomic functions, and sleep. Having established this list, the next step is to ask the patient and carer to identify the symptoms that they find most disabling or distressing and which carry the highest priority for treatment. There may be discrepant views about this which have to be resolved, for example a carer may complain that his/her sleep is being disrupted by the patient’s nocturnal restlessness, whereas the patient is more preoccupied with motor slowness through the day. Patients with a long-established history of PD will usually be familiar with the concept of trading benefits of treatment in one domain against potential adverse events in another, for example dyskinesias, worsening of nightmares, or emergence of hallucinations, as the cost of improved mobility with increased dopaminergic drug dose. What must also be stated is that some wearing off of dopaminergic drug responsiveness may occur as a consequence of disease progression at that same time as the emergence of side effects starts to become disproportionate to dose elevation. In other words chasing maintenance of motor function by continuing to increase antiparkinsonian drugs may not only become less effective than in the earlier stages of PD, but the risk of precipitating or exacerbating cognitive and psychiatric symptoms in particular is increased. The therapeutic ratio of these agents therefore begins to fall and the potential for unwanted symptoms to persist becomes greater, even after the medication which clearly precipitated their onset is withdrawn. This phenomenon of confusional states and visual hallucinations following closely on the heels of changes in antiparkinsonian treatments is generally interpreted as the symptoms having been ‘caused’ by medications. The reality is, however, that dementia and related symptoms in PD typically occur because of diffuse spread of the disease process, cortical involvement in particular producing a vulnerable cerebral substrate. Substances which affect neurotransmitter systems can under such circumstances ‘bring forward in time’ symptoms which were destined to emerge eventually, independent of such treatment. There is unlikely ever to be a randomized controlled trial of this proposition, but there is substantial corroborating clinical experience and circumstantial evidence.

In addition to providing adequate information to the patient and the family about the disease, non-pharmacological measures should be taken, including sufficient mental and physical activation and avoidance of aggravating factors such as undue sensory stimuli and inappropriate environmental factors. Other than these general measures cognitive-stimulation techniques can be employed in appropriate patients, although a systematic review of non-pharmacological and noninvasive therapies in PD revealed no studies in PD-D patients [9]. All together there were nine controlled trials, including six randomized controlled ones. Although five trials showed positive results, only one study of cognitive training achieved satisfactory grading for evidence of efficacy, demonstrating a significant benefit for cognitive training in the domains of attention, executive function, memory, and visuospatial function [10].

Before initiating a pharmacological treatment, other conditions which can trigger or aggravate mental dysfunction should be excluded. These include systemic abnormalities and diseases, depression, and adverse events of antiparkinsonian medication and treatment for concomitant diseases. Drugs which can aggravate mental dysfunction, such as anticholinergics, tricyclic antidepressants, and benzodiazepines, should be discontinued. Before reverting to medication the need for treatment, especially of behavioural symptoms, should be determined, based on the frequency, severity, and burden of symptoms. Whenever possible, one drug should be introduced at a time at a low dose and titrated up as needed. Non-specific treatment for behavioural symptoms should be tapered and discontinued once sufficient symptom control is attained.

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