© Geriatric Times. All rights reserved.
Parkinson's Disease and Pain
by Steven A. King, M.D., M.S.
| Geriatric Times |
 |
September/October 2000 |
|
Vol. I |
|
Issue 3 |
Any physician who treats geriatric patients is well acquainted with Parkinson's
disease (PD). Although PD can affect younger people, as demonstrated by the
recent publicity surrounding actor Michael J. Fox's struggle, PD still
primarily remains an illness of older age.
Many of the symptoms of PD-tremor, bradykinesia and akinesia, rigidity, and
stooped or flexed posture-are well-known and easily recognized by most
physicians. PD-associated pain, however, may affect 40% or more of PD patients
and often appears to go unrecognized (Chudler and Dong, 1995).
There are a number of reasons for this. Because patients are usually unaware
that pain is associated with PD, they may not report it to their physicians,
assuming it is related to another problem. Similarly, physicians often fail to
ask their patients with PD about pain.
The locations and types of PD pain add to confusion as to its etiology. The
most common pains associated with PD include muscle cramps or tightness in the
neck, back and legs; a dull pain in the head and neck; painful dystonias
especially in the feet; and neuropathic pain consisting of burning pain,
tingling or numbness (Chudler and Dong, 1995). Because these types of pain are
also associated with many other problems, patients with PD may undergo workups
before the PD is considered as the probable cause of the pain.
PD pain is often simply ascribed to abnormal movements. It appears, however,
that the pain is often more complicated and extends beyond being simply
secondary to them. For example, patients may develop pain before the onset of
these other symptoms. PD pain can be bilateral, or it can be unilateral, either
on the side where the motor symptoms are exhibited or the contralateral side
(Chudler and Dong, 1995). Furthermore, although PD pain often occurs in sites
that would be expected to be associated with abnormal or repetitive movements,
abdominal, oral and genital pain have also been reported (Chudler and Dong,
1995).
Another indication that PD pain may be associated with an underlying
neurochemical mechanism is that it occurs not only in cases of primary PD, but
also has been reported in neuroleptic-induced PD (Decina et al., 1992). Because
the drugs that cause this problem appear to exert their antipsychotic effects
by blocking dopamine receptors, it is possible that, at least to some degree,
PD pain may be related to reduced dopaminergic transmission (Chudler and Dong,
1995).
Other aspects of PD also suggest the role of a possible underlying
neurochemical mechanism in PD pain. Among these are what has been described as
the "on-off" mechanism (Quinn, 1998). One aspect of this process is that
patients being treated with levodopa may report a worsening of symptoms,
including pain, as the therapeutic level of the medication is reduced at the
end of the dosing period.
A potential neurochemical etiology of PD pain also is suggested by the
relationship between PD and depression. Depression is a common problem in both
chronic pain in general and in PD (Cummings, 1992; King, 1997). Although there
is limited literature examining the relationship between these three disorders,
Starkstein and colleagues (1991) reported that pain was more severe in PD
patients with major depression.
The key to evaluating and managing pain is to inquire about this problem in
all patients with PD. If the pain is believed to be associated with the PD, it
is important to insure that the PD itself is being adequately treated. If the
pain appears to be related to an "on-off" mechanism, a more frequent dosing
schedule or longer-acting medication, such as controlled-release
levodopa-carbidopa (Sinemet CR), may be efficacious (Quinn, 1998). This can
also potentially have a negative effect, however, because many of the
medications used to treat PD can themselves cause or exacerbate pain. For
example, levodopa can cause dystonias and hyperextension, each of which can
cause pain, and longer-acting medications can extend these symptoms over the
course of the day (Quinn, 1998).
Unfortunately, most of the literature on the management of PD pain consists
of case reports, making it difficult to compare therapeutic approaches. As with
other forms of chronic pain, opioids, non-steroidal anti-inflammatory drugs
(NSAIDs) and antidepressants are the first-line drugs for pain management
(Chudler and Dong, 1995). The decision as to which medications to use should be
based not only on what is most likely to be efficacious, but also what is least
likely to exacerbate other symptoms of PD.
For example, patients with PD may have reduced gastrointestinal motility due
to autonomic dysfunction (Jost, 1997). Opioids and certain antidepressants can
worsen this problem, and NSAIDs can increase the difficulties related to the
gastroesophageal reflux that may occur.
The anticholinergic effects of antidepressant medications may not only
exacerbate GI problems but also the cognitive impairment that can occur in PD
(Jost, 1997). Among the tricyclic antidepressants, which appear to be the most
analgesic, the best choice would be drugs such as desipramine (Norapramin) and
nortriptyline (Pamelor, Aventyl), which have the least anticholinergic
activity. Another antidepressant that appears to have an analgesic effect
without anticholinergic activity is venlafaxine (Effexor), and this should be
considered as an alternative if the tricyclics are contraindicated or are
poorly tolerated. The selective serotonin reuptake inhibitor antidepressants
appear to have less analgesic effect than the tricyclics, and it has been
reported that they may actually exacerbate the motor symptoms of PD (Caley,
1997).
Because selegiline (Selegeline), a commonly used PD medication, is a
monoamine oxidase inhibitor, if a tricyclic antidepressant is given as well,
hypertensive crisis can occur. The combination of SSRIs and selegiline can
result in serotonin syndrome, a potentially life-threatening problem. Its
symptoms include delirium, rigidity, hyperthermia, hypertension or hypotension,
and incoordination. Thus, it may be confused with the symptoms of PD itself.
Overall, it is safer to combine the tricyclics with selegiline than the SSRIs
(Ritter and Alexander, 1997).
When opioids are used, the least potent, such as codeine and oxycodone
(Roxicodone), should be tried first. Stronger opioids such as methadone
(Dolophine), however, may be required (Shang and King, 1991). Among the
non-medication therapies that may be employed are physical and occupational
therapy, transcutaneous electrical nerve stimulation, and acupuncture. All of
these can provide pain relief and improve functioning without exacerbating
other symptoms. Psychotherapy may also help patients to better cope with pain
and other PD-related problems.
At this time, there is little information on the analgesic effects of
surgical procedures for PD, such as pallidotomy and fetal tissue grafting.
Dr. King is professor of psychiatry and director of the division of pain
medicine at Temple University in Philadelphia.
References
Caley CF (1997), Extrapyramidal reactions and the selective
serotonin-reuptake inhibitors. Ann Pharmacother 31(12):1481-1489.
Chudler EH, Dong WK (1995), The role of the basal ganglia in nociception and
pain. Pain 60(1):3-38.
Cummings JL (1992), Depression and Parkinson's disease: a review. Am J
Psychiatry 149(4):443-454 [see comments].
Decina P, Mukherjee S, Caracci G, Harrison K (1992), Painful sensory
symptoms in neuroleptic-induced extrapyramidal syndromes. Am J Psychiatry
149(8):1075-1080.
Jost WH (1997), Gastrointestinal motility problems in patients with
Parkinson's disease. Effects of antiparkinsonian treatment and guidelines for
management. Drugs Aging 10(4):249-258.
King SA (1997), Depression and pain: assessment and therapeutic strategies.
Journal of Back and Musculoskeletal Rehabilitation 9:223-231.
Quinn NP (1998), Classification of fluctuations in patients with Parkinson's
disease. Neurology 51(suppl 2):S25-S29.
Ritter JL, Alexander B (1997), Retrospective study of
selegiline-antidepressant drug interactions and a review of the literature. Ann
Clin Psychiatry 9(1):7-13.
Shang AB, King SA (1991), Parkinson's disease, depression, and chronic pain.
Hosp Community Psychiatry 42(11):1162-1163.
Starkstein SE, Preziosi TJ, Robinson RG (1991), Sleep disorders, pain, and
depression in Parkinson's disease. Eur Neurol 31(6):352-355.