From my experience of managing people with Parkinson’s disease (PD), although doctors tend to concentrate on the more visible motor symptoms, it’s often the non motor symptoms that have a more disruptive impact and are more troublesome for patients than the motor symptoms1. The non-specialist, whether in a Primary Care consulting room or indeed at the bedside in an acute trust is more likely to be requested to address the former. However, there is an incorrect assumption that restoration of dopamine levels will also address NMS. This article is meant to be a quick guide for generalists to help PD patients with some NMS issues across locales of care in a practical way.
It’s unsurprising that anxiety and depression symptoms are common in PD, particularly as dopamine is not the only neurotransmitter to be depleted in PD. Disruption of the serotonergic, cholingeric, and adrenergic pathways are implicit in the development of some of the non-motor complications such as anxiety, depression and cognitive decline and it’s important to be aware that these symptoms do not respond to doperminergic replacement therapy.
Confusingly however, some symptoms of depression and PD overlap. Experiencing anhedonia, defined as lowered ability to experience physical or social pleasure, is thought to be a useful discriminator, should you suspect the patient is experiencing depression as a result of their PD.(1,2). Anhedonia, is considered a good discriminating symptom to look for in this context to identify depression in PD.
For depression and anxiety in PD, Cognitive Behavioural Therapy is a valid approach but there maybe practicalities regarding access especially for patients with limited mobility. Pharmacological methods are also effective for PD associated affective disorders. Selective serotonin reuptake inhibitors (SSRI) are preferred given the adverse profile of drugs with cholinergic side effects such as Tricyclic Andidepressants (TCAs).
As ever benzodiazepines are best avoided as, in the longer term, they worsen the slurring of speech, drowsiness and gait disturbance.
Given the alterations that occur to the autonomic nervous system (ANS), which is responsible for regulating smooth muscle activity, it’s no surprise that PD can have a profound effect on the gut.
The motor effects of relative immobility, difficulty in chewing fibre, problems maintaining adequate fluids and trouble using abdominal musculature conspire to make about half of PD patients chronically constipated. Simple measures such as increasing fluids, changing food presentation to aid mastication and making fibre more palatable are useful initial steps. A review to eliminate anticholinergic drugs is also logical and useful. If epurients are indeed necessary, given the aspiration risk, avoid lactulose.
Disrupted sleep is a very common problem associated with Parkinson’s. Sleep symptoms, particularly parasomnias and REM Sleep Disorder, are often harbingers for the onset of PD and are worth inquiring about when the condition is suspected. Patients frequently lose their bed-partner to another room. Unfortunately, the sleep disorder symptoms can remain through the course of the illness. Paradoxically at least half of patients report that they have daytime sleepiness.
As ever, careful history taking is mandatory. Drugs such as Amantadine and Selegiline are stimulants and changing the dosing in relation to proposed sleep patterns is useful.
Practical issues such as a difficulty in turning over may make a patient in bed uncomfortable enough to stay awake. The use of “slippery” satin bed sheets can provide a useful solution. Or, if excessive sweating is a problem, then cotton sheets would be more appropriate. Occupational therapists can be invaluable in this kind of context.
This is a very tricky symptom to deal with. It exacerbates an already high risk of falls from motor symptoms. In addition, given the fact that orthostatic hypotension may predate motor symptoms, it can even be mistaken for cardiovascular disease.
Fludrocortisone remains the mainstay of pharmacological management but a review of existing medication is worthwhile. Reconsider drugs which may worsen matters such as TCAs. As ever non-pharmacological interventions such as balance classes or an Occupational Therapy led reappraisal of activities of daily living could be tried either alone or combined with drug treatment.
A review of all the facets of Pain in PD is an article, at least, in itself and only a few key points can be covered here. Up to half of PD patients have pain symptoms with a very wide spectrum of presentations. Careful history taking is important if only simply to avoid exacerbation of other PD symptoms through illjudged prescribing. PD medication can be sometimes culpable. For example, dopaminergic agonists such as Amantadine or Entacapone can cause headaches. Similarly, abrupt withdrawal of antiparkinsonian medication can cause pain alongside acute akinesia (or akinetic crisis). Be clear about the nature of the pain that is the problem.
Non-motor symptoms remain overlooked in PD but present sometimes a bigger impact to patients and their carers. Successful management involves careful history taking, reappraisal of medication, non-pharmacological methods and if necessary prescribing. It always fascinates me how sometimes the simplest measures can have the most profound effects. For example a couple of well placed handrails near a commode can sometimes do more good than a script of epurients for constipation. At the same time the same handrails can reduce falls in the bathroom during turning or transfers.
Parkinson’s UK has an excellent downloadable questionnaire (available on http://www.parkinsons.org.uk/content/non-motor -symptoms-questionnaire) to identify NMS. Listening, basic appraisal of medical knowledge and common sense will always be rewarded by the continuing gratitude of patients and their carers.
1. Truong, D, Bhidayasiri R Wolters E. Management of non-motor symptoms in advanced Parkinson’s disease. J Neurol Sci. 2008; 266, 216–228.
2. Rickards H. Depression in neurological disorders: Parkinson’s disease, multiple sclerosis, and stroke. J Neurol Neurosurg Psychiatr. 2005; 76:i48-i52