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Parkinson's disease — medical education and psychosocial aspects
pATiENl EdUCATjoN
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ELSEVIER
Patient Education and Counseling 26 (1995) 71-79
Parkinson’s disease - medical education and psychosocial aspects Wolfgang H. Oertel*“, Heiner Ellgringb “Department
of Neurology,
Klinikum Grosshadern Ludwig-Maximilians-University, bDepartment of Psychology, University of Wuerzburg,
Marchioninistrasse 15, D-81377 Wuecburg, Germanq
Munich,
German?
Abstract This article describesthe attempt to develop educationalmaterial for patients suffering from Parkinson’sdisease (PD) and for their partners. The material relatesto the neuropathology of PD. The extent of the degenerationof dopaminergicneuronsin the substantianigra, presentat the outbreak of the disease,is illustrated to the patient. The substantianigra is explainedasa TV-broadcastingsystem,the nerve fibers to the so-calledstriatum ascablesand the striatum itself is explainedasa TV-set with 2 channels(calleddopamineD l-receptor and dopamineD 2-receptor). The action of anti-Parkinsonianagentsis exemplifiedwith the substanceL-DOPA, a precursor of the transmitter dopamine.The patient and his partner are introduced to the time-courseof the L-DOPA concentrationin blood after oral intake of the substance(the pharmacokineticsof L-DOPA). The pharmacokineticscan explain the clinical improvementand the long-term effectsof L-DOPA therapy. The secondpart reports on psychosocialproblemsthat Parkinsonianpatients and their spousesencounter and how psychologicalinterventions may help to solve someof thesepsychosocialproblems. Parkinson’s disease;Education; Neuropathology; Pharmacologicaltreatment; L-DOPA; Psychosocial problems;Partners; Patients Keywords:
1. Introduction 1.1. Medical background Parkinson’s disease (PD) is associated with a degeneration of dopaminergic neurons in the substantia nigra located in the midbrain. These do-
*Correspondingauthor, Phone:004989 70953678; Fax: 0049 89 70953677.
paminergic neurons project with their nerve fibers to the striatum, a subnucleus of the so-called basal ganglia. The basal ganglia are responsible for performing automatized programmed movements (for other functions, see [2]). The loss of dopaminergic nigral neurons leads to a reduction of the neurotransmitter dopamine in the striatum. Biochemically, PD therefore can - slightly simplified - be defined as a dopamine deficiency syndrome in the striatum. A second neuropatho-
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/ Paiient
logical feature for Parkinson’s disease is the presence of so-called Lewy-bodies in the substantia nigra (eosinophilic intracytoplasmic inclusion bodies) [3]. The cardinal clinical features of Parkinson’s disease are akinesia (reduction up to lack of movement), rigidity (increased muscular tone this feature leads to a stooped posture with flexed arms and lack of swing of the arms at walking; when a joint is passively extended, the so called cog-wheel sign is experienced by the investigator), and rest tremor. Rest tremor is enhanced by any stressful situation, whether it be negative or positive [l]. One aspect of akinesia is lack of facial expression and of spontaneous movements when talking (body language). Thus, the patient has a reduced capability for non-verbal communication. In addition, he suffers from speech disturbances due to uncoordinated movement of laryngeal, pharyngeal and respiratory muscles. Thus, on one hand the patient loses non-verbal communication (a typical feature of human beings), and on the other hand, he shows impairment of verbal communication. The clinical symptoms impair interpersonal communication. As facial expression is lacking, people think that Parkinsonian patients are stupid, demented, bored, boring, not interested or even drunk. The patient is fully aware of this attitude. He also is aware that this attitude is shared by most of his neighbours, friends, relatives, and even in part by the partner. Stress in any form will enhance symptoms of Parkinson’s disease, in particular rest tremor. This sign stigmatizes the Parkinsonian patient even further. In addition, Parkinsonian patients have a lack of drive and quite a high percentage suffers from depression (may it be reactive, a part of the disease or both). Thus, all these symptoms stigmatize the Parkinson patient. The partner is also stigmatized, because he is identified in public to live together with a patient suffering from a visible neurological disorder (for a list of frequent psychosocial problems, see Table 2).
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2. The medical education of Parkinson and their partners
patients
The following material is presently in use at the out-patient clinic for movement disorders at the Department of Neurology, Klinikum Grosshadern, (Ludwig-Maximilians-University, Munich, Germany). It is based on numerous attempts to explain the medical basis of PD and the different aspects of pharmacological therapy to Pdrkinsonian patients and their spouses. The preliminary character of the material is to be stressed. If a Parkinsonian patient consults a physician for the first time, he either has no idea what he suffers from or he has been pointed to the potential diagnosis of PD by relatives, friends or the media. In general, the Parkinsonian patient or the partner will ask ‘what is the matter with me ?‘. Following a standardized and detailed clinical neurological investigation, a neurologist is able to give the diagnosis ‘Parkinson syndrome’ with a high degree of certainty. Parkinson syndrome means, that a patient exhibits all the features, characteristic for PD, but the clinician is not certain whether the pathology, typical for PD, is present in the brain of the patient. According to a (retrospective) clinical pathological correlation, only about 70-80% of patients diagnosed during their life time to suffer from Parkinson’s disease, showed at post-mortem the neuropathological features of PD [3]. A further cardinal feature of PD is the prompt and marked response of the clinical symptoms to the administration of LDOPA, the precursor of dopamine. Provided that the patient expresses only the cardinal features akinesia, rigidity and/or rest tremor (at least 2 out of 3) and no further clinical neurological signs (according to the UK brain bank criteria) [3], the physician can tell the patient that he suffers from PD with a chance of about 80-85%. 2.1. Lesson No. 1: What is Parkinson’s disease The patient now will ask ‘What is PD ?’ At this point, the Parkinson patient and his partner have to learn 4 words: 1, substantia nigra; 2, striatum; 3, dopamine; 4, L-DOPA. He is then presented with a scheme (see Fig. la), illustrating the substantia nigra, the striatum, and the nigro-striatal
W.H.
Oertel,
H. Ellgring
1 Patient
Educ Counsel
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,-y---F-.-,
a
b
Fig. 1. The nigrostriatal system can be compared with a TV-broadcasting system. (la) Scheme of the substantia nigra (SN), the nigrostriatal nerve fibers (NSF) and the striatum (ST). The substantia nigra can be compared with a TV-broadcasting station, which broadcasts via a cable system (nigrostriatal nerve fibers-NSF) 2 programs called dopamine-1 (0) and dopamine-2 (0). These 2 programs are received by the striatum (ST), which is compared to a TV-set. This TV-set has 2 channels (dopamine-1 and dopamine-2), which can recognize the appropriate dopamine-1 or dopamine-2 program. (lb) Parkinson’s disease is a progressive, bilateral, generally asymmetric disease associated with a loss of dopaminergic nerve cells in the substantia nigra. The neurons in SN degenerate and therefore the nerve fibers to the striatum slowly disappear. ‘The quality and amplitude of the broadcasting of the programs dopamine-1 and dopamine-2 are severely impaired’.
pathway. The substantia nigra is introduced as a powerful TV-broadcasting system of the brain, which provides power to move properly. This TV-station broadcasts via a cable system to the striatum. The striatum is introduced as the TV-set (receiver or receptor). The TV-station (substantia nigra) can send 2 programmes, called dopamine 1 and dopamine 2. When broadcasting, the cables release the transmitter ‘dopamine’, the substance which carries information from the cable to the TV-set. The TV-set can receive both programmes via a specific receptor or ‘channel’. Dopamine interacts now with the receptor (channel) dopamine 1 and the receptor (channel) dopamine 2. Simultaneous activation of the 2 channels leads to
perfect movement. To illustrate the extent of the damage to the substantia nigra neurons, the patient is presented with Fig. lb. It illustrates a marked asymmetric degeneration of the connection (cable system) from the substantia nigra nerve cell bodies to the striatum, as is already present at the outbreak of the symptoms in brain of Parkinson’s disease patients. To stress the extent of the lesion already present at the manifestation of PD, a second example is introduced. The substantia nigra is compared with a car fitted with an g-cylinder engine. At the outbreak of PD, about 5 cylinders of the engine have been damaged or destroyed. As no g-cylinder engine is able to provide smooth driving, when only 3 cylinders
14
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Time
Blood concentration of L-Dopa . . . . . Early stage of Parkinson’s Disease (2a) - -. Intermediate stage of Parkinson’s Disease (2 b) - - - - Advanced stage of Parkinson’s Disease (2~) Fig. 2. Pharmacokinetics of L-DOPA in the early, intermediate and advanced stage in Parkinson’s disease. A single oral dose of L-DOPA will lead to a rise and fall of the L-DOPA serum concentration, with a half-life of approximately l-2 h. (2a) Early stage of PD; the brain can store L-DOPA for many hours and converts it to dopamine. The mobility of the patient is improved for more than 4 h, despite the fact that at this time L-DOPA is hardly present in the blood any more. (2b) Intermediate stage of PD; the storage capacity of the brain for L-DOPA becomes lessened. The mobility of the patient is only improved for 3-4 h, but still longer than L-DOPA is present in blood. 2c. Advanced stage of PD-the brain has virtually lost its storage capacity for L-DOPA. The increase and fall in L-DOPA concentrations in blood is reflected by the disappearance (‘on’) and reappearance (‘off) of the symptoms of PD. The phase of good mobility lasts as long as L-DOPA is present in blood.
are left, the patient realizes the extent of the lesion at the very early phase of PD. This example also allows to advise patient and partner ‘not to fight’ against PD, but rather to accept the disease, as non-acceptance of the disease will put extra pressure on the remaining substantia nigra neurons (remaining ‘cylinders’). In addition, the remaining dopaminergic neurons help in the therapy of Parkinson’s disease, as they can store the presently most effective anti-Parkinsonian agent, L-DOPA. The more nigro-striatal fibers are left, the longer the action of L-DOPA per dose will be (Fig. 2).
At this time the patient is asked: Do you have any questions? By experience, the patient asks at least the following questions: Will I die of Parkinson’s disease? Is Parkinson’s disease hereditary? Can you help me? The answers to the first 2 questions are ‘no’(although linkage analyses in patients with PD suggest the possibility, that a small hereditary component may play a role in the aetiology of PD) [4]. The answer to the third question is ‘yes’. Before the patient is offered the perspective of a long-term effective pharmacological therapy, he is given a sequence of bad and good news (Table 1). The bad news is given first, according to the principle described by Dunn et
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Table I Bad news and good news on Parkinson’s disease Bad news
Good news
It is a progressive disorder I do not know where it comes from I cannot cure it
I know what you suffer from I know what is missing I know how to treat it, although side-effects of therapy may occur I will help you to cope with side-effects, if necessary Research will improve PD therapy in the near future
1 cannot stop it I cannot even slow it down
al. [5]. The patient is then introduced to the 5 groups of substances, presently available in the pharmacy for the therapy of Parkinson’s disease. These groups subsume amantadine-derivatives, anticholinergics, dopamine agonists, L-DOPA, and monoaminoxidase-B (MAO-B) inhibitors
Fl.
In the last part of lesson 1, the physician explains the action and effect of the most effective anti-Parkinsonian agent, L-DOPA. L-DOPA is the precursor for dopamine, i.e. as ‘grapes are used for the production of wine’, so is L-DOPA converted in the brain to dopamine. Dopamine will then act on the 2 receptors (‘channels’ dopamine 1 and dopamine 2) located in the striatum. LDOPA has the best ratio of beneficial effects to adverse effects of all known anti-Parkinsonian agents. Modern nuclear medical techniques, such as iodobenzamide-single-photon-emission computed tomography (IBZM-SPECT) can help to improve confidence in the promised effective therapy of the disabling symptoms. IBZM-SPECT allows to demonstrate in vivo to each patient whether he has a normal number and distribution of the channel type 2 (dopamine-D2-receptor) in the striatum. This method predicts to more than SW, that the patient will respond to L-DOPA, provided the IBZM-SPECT-binding is normal [7]. The patient is then offered a short course of L-DOPA treatment. He and/or the spouse are asked either to come or to call back and to report on the effect of the offered therapy.
2.2. Lesson 2: How to understand L-DOPA therapy?
In lesson 2, the patient learns the advantages and some disadvantages of L-DOPA therapy. LDOPA will improve symptoms of Parkinson’s disease, especially in the early phase. Its effect will in principle last and will ameliorate the cardinal motor symptoms for 7-10 years. This means that the patient will be in a similar state of disability under L-DOPA therapy in 7- 10 years, he presents at the first time of manifestation of PD in the untreated stage. In the next step, the patient and the spouse learn the principles of the pharmacokinetics of L-DOPA. L-DOPA, when orally administered, passes through the oesophagus and the stomach to the duodenum. After a latency of 30-40 min, mainly due to the passage of L-DOPA through the stomach, L-DOPA is absorbed through the mucosa of the duodenum into the blood. From here, L-DOPA is transported to the blood vessels of the brain. L-DOPA is then actively transported from the blood to the brain via an uptake mechanism. At this moment the patient learns the following sentence: ‘The striatum is a sink with one water-tap and 2 outlets.’ The meaning of this sentence is illustrated by Fig. 3. According to the comparison ‘the striatum is a sink’, L-DOPA is brought into the brain via opening the water-tap (oral intake of L-DOPA). L-DOPA is now converted to dopamine. It remains in the brain until it has disappeared via breakdown of dopamine by the 2 enzymes monoaminoxidase-B catechol-O-methyl-transferase (MAO-B) and (COMT). These 2 degrading pathways (MAO-B and COMT) are illustrated as outlets in Fig. 3.
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As already indicated in Fig. 2, in the early stage of PD L-DOPA can be stored in the brain over several hours. This stored L-DOPA is continuously converted to dopamine. As long as dopamine is produced in the striatum, the patient is nearly normally mobile. This phenomenon is observed despite the fact that L-DOPA in blood is only present for 2-3 h (Fig. 2a). When the disease progresses to an intermediate stage, the timecourse of the presence of L-DOPA in blood will remain the same. However, the storage capacity
L-DOPA
. .
. .
..
Dopamlne
l-1,’
M/Q-B
Inhibition
COMT Inhibition
/ ! / , i ‘\ 0
/
..I~...:~..
.,-x-,-x-
Fig. 3. ‘The striatum is a sink with one water-tap and 2 outlets’. The dopamine deficit in the striatum of PD patients is substituted by intake of L-DOPA (‘L-DOPA comes into the striatum through the water-tap’). L-DOPA is converted to dopamine. Dopamine is destroyed by 2 proteins, the enzyme monoaminooxidase-B (MAO-B) and the enzyme Catechol-O-MethylTransferase (COMT). Blocking one outlet, for example MAOB with a MAO-B-inhibitor (. .), leads to a small increase of the dopamine concentration in the striatum. Blocking the other outlet by inhibitors of (COMT-inhibitor - note that COHTinhibitors are clinically not available in 1994) will lead to a marked increase of dopamine in the striatum (- - - -).
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for L-DOPA in brain becomes reduced and conversion of L-DOPA to dopamine in brain lasts shorter than that of the early phase (3-4 h) (Fig. 2b). In the advanced stage, storage of L-DOPA in brain is not possible any more and the timecourse of improvement of motor symptoms nearly reflects the time-course of L-DOPA in blood. Thus, in the early phase of PD, intake of LDOPA (100 mg) 3 times per day leads to a continuous disappearance of motor symptoms (‘on’). In the intermediate phase, the patient notices a short lasting appearance of motor symptoms (‘off) just before the intake of the next dose. Uninformed Parkinson patients blame in fact the next L-DOPA dose to be responsible for the appearance of the ‘off-phase. The educated Parkinson patient realizes, however, that he has reached the intermediate phase of the disease and that storage of L-DOPA in brain becomes shorter. In fact, numerous educated Parkinson patients or their partners suggest at this stage to reduce the time between each L-DOPA dose in order to again achieve a continuous response to the drug. In the advanced stage, the patient will experience the so-called response ‘fluctuation’, i.e. an ‘off-phase before the first L-DOPA dose and an ‘on’-phase after each L-DOPA intake lasting for 1.5-2 h, followed by an interdose ‘off-phase. This clinically experienced and theoretically explainable phenomenon can now be used to introduce to the patient combination therapy with either a blocker of MAO-B (see Fig. 3; outlet on the left side) or with a dopamine agonist. The additional administration of an MAO-B-inhibitor together with L-DOPA will close one outlet of the sink, thereby inducing an increased level of dopamine in brain. Subsequently, the patient will experience a prolongation of ‘on’-phase and a reduction in the duration and severity of the ‘off -phase. Dopamine-agonists are substances which act like dopamine on the dopamine 1- and/or dopamine 2-receptor without the need for conversion to the active compound. Dopamine agonists are explained as immediately active substances to the patient. In the model of the substantia nigra as a TV-broadcasting station and the striatum as a TV-set with 2 channels, the dopamine agonist
W.H.
Oertrl,
H. Ellgring
/ Putient
represents a programme broadcasted not via cable as in Fig. 1, but via satellite. So the dopamine agonist will directly act by itself either on channel 1 (dopamine l-receptor-agonist) or on channel 2 (dopamine 2-receptor-agonist). If a dopamine agonist with a long half-life (defined as the time in which the blood concentration of the dopamine agonist drops by 50% of the initially present concentration) is administered in an effective dosage without causing too many side-effects, the patient may experience a markedly reduced ‘offphase in respect to duration and severity and an increase in the time spent in the ‘on’ phase. 2.3. Creuting hope developments
future
thrrctpeuticul
At this stage of the disease and experience with therapy patients have either become members of the Parkinson’s Disease Society or have tried to inform themselves about the possibilities of the presently available treatment for Parkinson’s disease. They have seen other patients in various stages of the disorder including those with marked side-effects associated with long-term L-DOPA therapy. In addition to the already mentioned response fluctuations, these neuropsychiatric sideeffects include phases of abnormal hyperactivity during ‘on’-time, so called dyskinesias and dopaminometica induced psychosis. Numerous patients and their partners also know the limited effectiveness of Parkinson therapy in the late stage of the disease. It is therefore of importance to provide information on new developments in drug therapy. One of the present clinically-tested substances can be explained by the scheme in Fig. 3. In this scheme, the sink (striatum) has 2 outlets, One of the 2 is governed by the enzyme COMT. It is possible to block this major degrading pathway for L-DOPA in brain (Fig. 3). The so-called COMT-inhibitors lead to a marked increase of the dopamine concentration in brain. This biochemical fact is reflected in the clinical observations obtained in so far short-term clinical testing of COMT-inhibitors: Parkinsonian patients, who previously showed marked response fluctuations under L-DOPA therapy alone, expressed a nearly continuous ‘on’-time under combination therapy with L-DOPA and a COMT-inhibitor ([8]; Eich-
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horn and Oertel, unpublished observation). Based on this example and other unmentioned developments in basic and clinical neuroscience, it is justified to offer patient and spouse a positive perspective on the future therapy of PD.
3. Psychosocial aspects of Parkinson’s psychological intervention
disease -
Medical therapy without doubt improves the motor symptoms and, in part, the mood of Parkinsonian patients. Nevertheless, numerous patients still feel to be stigmatized by the fact that they suffer from PD, despite regained mobility under effective treatment. We have therefore postulated, that psychosocial problems impair the quality of life of Parkinsonian patients and their partners. These psychosocial problems are considered to be secondary to the primary organic neurological symptoms. In 1989, a group of neurologists and psychologists at the Department of Neurology, Klinikum Grosshadern, LudwigMaximilians-University, Munich and the MaxPlanck-Institute of Psychiatry, Munich, started a project on psychosocial problems of Parkinsonian patients and their partners. In collaboration with a specialised clinic (Paracelsus-Elena-Klinik, Kassel) for Parkinsonian patients and the German Parkinson’s Disease Society (lay organisation) we sent out an extensive questionaire on psychosocial problems to 325 patients in various cities of the German Federal Republic and asked the patient and the spouse to separately fill out one questionaire each. The results of this questionaire-based survey are summarized in Table 2. To solve these reported psychosocial problems, different types of psychological interventions were developed and offered to Parkinsonian patients and their spouses. These psychological interventions include individual counseling, short time counseling, group counseling and counseling of partners. Group counseling consisted of different and various psychotherapeutical techniques including situational analysis, cognitive restructuring, prac- ticing social skills, role playing, stress inoculation, relaxation techniques, and practicing these techniques outside the group. Table 3 ad-
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/ Patient
Table 2 Common psychosocial problems, expressed by Parkinsonian patients” Patients experiencing stress (‘%I)
Type of stress
Lack
of’ eficiency
Slowness Reduced motivation and drive Anxiety
and
psychological
96 90
distress
Anxiety about helplessness 93 Increase of symptoms under minimal stress 90 Psychological
stress
from
bodily
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Therefore, counseling of partners is as important as advice to the patient, This counseling should address the anxiety of partners related to the progression of the disease and to the anxiety related to partner’s own health. It should indicate how this partner could support the patient to keep the still available, although limited self-independence. Most important the partner has to (re-) learn to lead an independent life (‘keep time for yourself). The effect of counseling partners of Parkinsonian patients is presently assessed.
syn~ptorns
Reduced manual skills Reduced gestures and body language Social
Educ
97 86
4. Conclusion
interacfion
Inability to cope with many people Insecurity in social interactions Partnership lfbr 241
and fivnil~ patients with
84 83
partnrrs)
Fewer activities Anxiety about stress for partner
83 70
“Adapted from Ellgring et al. [9].
dresses some practical problems trained during patients seminars. A re-evaluation of patients who had participated in these seminars, revealed that 44% were still able to use the learned techniques of cognitive restructuring and relaxation techniques for longer than 3 months in public. Another 20% still used one of the mentioned 2 methods. Long-term effects of such seminars, however, remain to be demonstrated [9]. A largely neglected aspect of Parkinson’s disease is the psychosocial situation of the partner. The partner is stigmatized as a person, who lives together with a person suffering from a chronic disabling neurological disorder. Partners face multiple problems related to day-to-day aspects of life such as financial problems, career planning, change of life situation and loss of hobbies and activities. Caring for a Parkinsonian patient means psychological and physical problems in addition to her or his own problems. The responsibility for the partner’s life can be overwhelming. Feelings of guilt, insufficiency, anger and aggression occur and have been observed to a remarkable degree in seminars offered to partners of PD patients.
This article describes how the same group of medical care providers tries to explain patients the medical background of PD in simple terms and on the other hand to work on psychosocial problems of Parkinsonian patients and their partners. After establishing the extent and variation in psychosocial problems of Parkinsonian patients, one can now design psychological interventional strategies to train patients in techniques which may help the patient to solve these psychosocial problems. The same strategy can be used in the psychological support of partners of Parkinsonian patients. The presented educational material on medical aspects of PD has to be considered as preliminary. It is necessary to perform controlled studies in order to find out whether the sequence of the presentation of information makes a difference to the well-being of the Parkinsonian patient and his partner. It may be useful to analyse whether such an educational programme will improve compliance or even may influence the outcome of the disease. It remains to be studied whether educational programmes related to medical aspects and whether participation in psychological interventional strategies also influence the health status of the partner. A further study should investigate the effect of such a programme on health costs. Research on a number of the above-mentioned questions has been performed in the area of diabetes mellitus. It is hoped, that neurologists, psychiatrists, psychologists, and other professionals engaged in the provision of health care to Parkinsonian patients and their partners may benefit
W.H. Oertel, H. Ellgring 1 Patient Educ Counsel 26 (1995) 71- 79
79
Table 3 Practical problems trained during seminars” Main focus
Public situation
Private situation
Cognition and emotions
Anxiety about being perceived negatively by others Eating in a restaurant
Anxiety about being helpless, depressive tendencies Less contact with friends because invitations are refused
Behaviour <‘Adapted from Ellgring et al. [9]
from the available experience in the chronic endocrinological/metabolic disease. References [I] Selby G. Clinical features. In: Stern GM ed. Parkinson’s Disease. London: Chapman and Hall Medical, 1990; 333-388. [2] Alexander GE, Crutcher MD. Functional architecture of basal ganglia circuits: Neural substrates of parallel processing. Trends Neurosci 1990; 13: 266-271. [3] Hughes AJ, Daniel SE, Kilford L. Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinice-pathological study of I00 cases. J Neurol Neurosurg Psychiatr 1992; 55: 181-184. [4] Smith CA, Cough AC, Leigh PN, Summers BA, Harding AE, Maranganore DM, Sturman SC. Schapira AH, Williams AC, Spurr NK. Debrisoquine hydroxylase gene polymorphism and susceptibility to Parkinson’s disease. Lancet 1992; 339: 1375-1377. [5] Dunn S, Taylor J, Fowler P, Steinbeck K, Kearns M, Yue
D. The elfects of complications information on anxiety and perceived vulnerability and severity: a randomized trial of information sequence. Melbourne: Proc. Annual Scientific Meeting, Australian Diabetes Society and Australian Diabetes Educators Association, (abstract), 1989. (61 Oertal WH, Quinn NP. Parkinsonism. In: Brandt Th, Caplan L, Dichgans J, Diener C eds. Neurological Disorders: Course and Treatment. Academic Press. [7] Schwdrz J, Tatsch K, Arnold G, Gasser T, Trenkwalder C, Kirsch CM, Oertel WH. “‘I-IodobenzamideSPECT predicts dopaminergic responsiveness in patients with ‘de novo’ Parkinsonism. Neurology 1992; 42: 556561. [8] Roberts JW, Cora-Locatelli G, Bravi D, Amantea MA. Mouradian MM, Chase TN. Catechol-O-methyltransferase inhibitor tolcapone prolongs levodopa/carbidopa action in Parkinsonian patients. Neurology 1993; 44: 2685-2688. [9] Ellgring H, Seiler S, Perleth B, Frings W, Gasser T, Oertel WH. Psychosocial aspects of Parkinson’s disease. Neurology 1993: 43 (Suppl. 6): S4l-S44.
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ELSEVIER
Patient Education and Counseling 26 (1995) 71-79
Parkinson’s disease - medical education and psychosocial aspects Wolfgang H. Oertel*“, Heiner Ellgringb “Department
of Neurology,
Klinikum Grosshadern Ludwig-Maximilians-University, bDepartment of Psychology, University of Wuerzburg,
Marchioninistrasse 15, D-81377 Wuecburg, Germanq
Munich,
German?
Abstract This article describesthe attempt to develop educationalmaterial for patients suffering from Parkinson’sdisease (PD) and for their partners. The material relatesto the neuropathology of PD. The extent of the degenerationof dopaminergicneuronsin the substantianigra, presentat the outbreak of the disease,is illustrated to the patient. The substantianigra is explainedasa TV-broadcastingsystem,the nerve fibers to the so-calledstriatum ascablesand the striatum itself is explainedasa TV-set with 2 channels(calleddopamineD l-receptor and dopamineD 2-receptor). The action of anti-Parkinsonianagentsis exemplifiedwith the substanceL-DOPA, a precursor of the transmitter dopamine.The patient and his partner are introduced to the time-courseof the L-DOPA concentrationin blood after oral intake of the substance(the pharmacokineticsof L-DOPA). The pharmacokineticscan explain the clinical improvementand the long-term effectsof L-DOPA therapy. The secondpart reports on psychosocialproblemsthat Parkinsonianpatients and their spousesencounter and how psychologicalinterventions may help to solve someof thesepsychosocialproblems. Parkinson’s disease;Education; Neuropathology; Pharmacologicaltreatment; L-DOPA; Psychosocial problems;Partners; Patients Keywords:
1. Introduction 1.1. Medical background Parkinson’s disease (PD) is associated with a degeneration of dopaminergic neurons in the substantia nigra located in the midbrain. These do-
*Correspondingauthor, Phone:004989 70953678; Fax: 0049 89 70953677.
paminergic neurons project with their nerve fibers to the striatum, a subnucleus of the so-called basal ganglia. The basal ganglia are responsible for performing automatized programmed movements (for other functions, see [2]). The loss of dopaminergic nigral neurons leads to a reduction of the neurotransmitter dopamine in the striatum. Biochemically, PD therefore can - slightly simplified - be defined as a dopamine deficiency syndrome in the striatum. A second neuropatho-
0738-3991/95/$09.50 0 1995ElsevierScienceIrelandLtd. All rightsreserved SSDI
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W.H.
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H. E&ring
/ Paiient
logical feature for Parkinson’s disease is the presence of so-called Lewy-bodies in the substantia nigra (eosinophilic intracytoplasmic inclusion bodies) [3]. The cardinal clinical features of Parkinson’s disease are akinesia (reduction up to lack of movement), rigidity (increased muscular tone this feature leads to a stooped posture with flexed arms and lack of swing of the arms at walking; when a joint is passively extended, the so called cog-wheel sign is experienced by the investigator), and rest tremor. Rest tremor is enhanced by any stressful situation, whether it be negative or positive [l]. One aspect of akinesia is lack of facial expression and of spontaneous movements when talking (body language). Thus, the patient has a reduced capability for non-verbal communication. In addition, he suffers from speech disturbances due to uncoordinated movement of laryngeal, pharyngeal and respiratory muscles. Thus, on one hand the patient loses non-verbal communication (a typical feature of human beings), and on the other hand, he shows impairment of verbal communication. The clinical symptoms impair interpersonal communication. As facial expression is lacking, people think that Parkinsonian patients are stupid, demented, bored, boring, not interested or even drunk. The patient is fully aware of this attitude. He also is aware that this attitude is shared by most of his neighbours, friends, relatives, and even in part by the partner. Stress in any form will enhance symptoms of Parkinson’s disease, in particular rest tremor. This sign stigmatizes the Parkinsonian patient even further. In addition, Parkinsonian patients have a lack of drive and quite a high percentage suffers from depression (may it be reactive, a part of the disease or both). Thus, all these symptoms stigmatize the Parkinson patient. The partner is also stigmatized, because he is identified in public to live together with a patient suffering from a visible neurological disorder (for a list of frequent psychosocial problems, see Table 2).
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2. The medical education of Parkinson and their partners
patients
The following material is presently in use at the out-patient clinic for movement disorders at the Department of Neurology, Klinikum Grosshadern, (Ludwig-Maximilians-University, Munich, Germany). It is based on numerous attempts to explain the medical basis of PD and the different aspects of pharmacological therapy to Pdrkinsonian patients and their spouses. The preliminary character of the material is to be stressed. If a Parkinsonian patient consults a physician for the first time, he either has no idea what he suffers from or he has been pointed to the potential diagnosis of PD by relatives, friends or the media. In general, the Parkinsonian patient or the partner will ask ‘what is the matter with me ?‘. Following a standardized and detailed clinical neurological investigation, a neurologist is able to give the diagnosis ‘Parkinson syndrome’ with a high degree of certainty. Parkinson syndrome means, that a patient exhibits all the features, characteristic for PD, but the clinician is not certain whether the pathology, typical for PD, is present in the brain of the patient. According to a (retrospective) clinical pathological correlation, only about 70-80% of patients diagnosed during their life time to suffer from Parkinson’s disease, showed at post-mortem the neuropathological features of PD [3]. A further cardinal feature of PD is the prompt and marked response of the clinical symptoms to the administration of LDOPA, the precursor of dopamine. Provided that the patient expresses only the cardinal features akinesia, rigidity and/or rest tremor (at least 2 out of 3) and no further clinical neurological signs (according to the UK brain bank criteria) [3], the physician can tell the patient that he suffers from PD with a chance of about 80-85%. 2.1. Lesson No. 1: What is Parkinson’s disease The patient now will ask ‘What is PD ?’ At this point, the Parkinson patient and his partner have to learn 4 words: 1, substantia nigra; 2, striatum; 3, dopamine; 4, L-DOPA. He is then presented with a scheme (see Fig. la), illustrating the substantia nigra, the striatum, and the nigro-striatal
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,-y---F-.-,
a
b
Fig. 1. The nigrostriatal system can be compared with a TV-broadcasting system. (la) Scheme of the substantia nigra (SN), the nigrostriatal nerve fibers (NSF) and the striatum (ST). The substantia nigra can be compared with a TV-broadcasting station, which broadcasts via a cable system (nigrostriatal nerve fibers-NSF) 2 programs called dopamine-1 (0) and dopamine-2 (0). These 2 programs are received by the striatum (ST), which is compared to a TV-set. This TV-set has 2 channels (dopamine-1 and dopamine-2), which can recognize the appropriate dopamine-1 or dopamine-2 program. (lb) Parkinson’s disease is a progressive, bilateral, generally asymmetric disease associated with a loss of dopaminergic nerve cells in the substantia nigra. The neurons in SN degenerate and therefore the nerve fibers to the striatum slowly disappear. ‘The quality and amplitude of the broadcasting of the programs dopamine-1 and dopamine-2 are severely impaired’.
pathway. The substantia nigra is introduced as a powerful TV-broadcasting system of the brain, which provides power to move properly. This TV-station broadcasts via a cable system to the striatum. The striatum is introduced as the TV-set (receiver or receptor). The TV-station (substantia nigra) can send 2 programmes, called dopamine 1 and dopamine 2. When broadcasting, the cables release the transmitter ‘dopamine’, the substance which carries information from the cable to the TV-set. The TV-set can receive both programmes via a specific receptor or ‘channel’. Dopamine interacts now with the receptor (channel) dopamine 1 and the receptor (channel) dopamine 2. Simultaneous activation of the 2 channels leads to
perfect movement. To illustrate the extent of the damage to the substantia nigra neurons, the patient is presented with Fig. lb. It illustrates a marked asymmetric degeneration of the connection (cable system) from the substantia nigra nerve cell bodies to the striatum, as is already present at the outbreak of the symptoms in brain of Parkinson’s disease patients. To stress the extent of the lesion already present at the manifestation of PD, a second example is introduced. The substantia nigra is compared with a car fitted with an g-cylinder engine. At the outbreak of PD, about 5 cylinders of the engine have been damaged or destroyed. As no g-cylinder engine is able to provide smooth driving, when only 3 cylinders
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Time
Blood concentration of L-Dopa . . . . . Early stage of Parkinson’s Disease (2a) - -. Intermediate stage of Parkinson’s Disease (2 b) - - - - Advanced stage of Parkinson’s Disease (2~) Fig. 2. Pharmacokinetics of L-DOPA in the early, intermediate and advanced stage in Parkinson’s disease. A single oral dose of L-DOPA will lead to a rise and fall of the L-DOPA serum concentration, with a half-life of approximately l-2 h. (2a) Early stage of PD; the brain can store L-DOPA for many hours and converts it to dopamine. The mobility of the patient is improved for more than 4 h, despite the fact that at this time L-DOPA is hardly present in the blood any more. (2b) Intermediate stage of PD; the storage capacity of the brain for L-DOPA becomes lessened. The mobility of the patient is only improved for 3-4 h, but still longer than L-DOPA is present in blood. 2c. Advanced stage of PD-the brain has virtually lost its storage capacity for L-DOPA. The increase and fall in L-DOPA concentrations in blood is reflected by the disappearance (‘on’) and reappearance (‘off) of the symptoms of PD. The phase of good mobility lasts as long as L-DOPA is present in blood.
are left, the patient realizes the extent of the lesion at the very early phase of PD. This example also allows to advise patient and partner ‘not to fight’ against PD, but rather to accept the disease, as non-acceptance of the disease will put extra pressure on the remaining substantia nigra neurons (remaining ‘cylinders’). In addition, the remaining dopaminergic neurons help in the therapy of Parkinson’s disease, as they can store the presently most effective anti-Parkinsonian agent, L-DOPA. The more nigro-striatal fibers are left, the longer the action of L-DOPA per dose will be (Fig. 2).
At this time the patient is asked: Do you have any questions? By experience, the patient asks at least the following questions: Will I die of Parkinson’s disease? Is Parkinson’s disease hereditary? Can you help me? The answers to the first 2 questions are ‘no’(although linkage analyses in patients with PD suggest the possibility, that a small hereditary component may play a role in the aetiology of PD) [4]. The answer to the third question is ‘yes’. Before the patient is offered the perspective of a long-term effective pharmacological therapy, he is given a sequence of bad and good news (Table 1). The bad news is given first, according to the principle described by Dunn et
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Table I Bad news and good news on Parkinson’s disease Bad news
Good news
It is a progressive disorder I do not know where it comes from I cannot cure it
I know what you suffer from I know what is missing I know how to treat it, although side-effects of therapy may occur I will help you to cope with side-effects, if necessary Research will improve PD therapy in the near future
1 cannot stop it I cannot even slow it down
al. [5]. The patient is then introduced to the 5 groups of substances, presently available in the pharmacy for the therapy of Parkinson’s disease. These groups subsume amantadine-derivatives, anticholinergics, dopamine agonists, L-DOPA, and monoaminoxidase-B (MAO-B) inhibitors
Fl.
In the last part of lesson 1, the physician explains the action and effect of the most effective anti-Parkinsonian agent, L-DOPA. L-DOPA is the precursor for dopamine, i.e. as ‘grapes are used for the production of wine’, so is L-DOPA converted in the brain to dopamine. Dopamine will then act on the 2 receptors (‘channels’ dopamine 1 and dopamine 2) located in the striatum. LDOPA has the best ratio of beneficial effects to adverse effects of all known anti-Parkinsonian agents. Modern nuclear medical techniques, such as iodobenzamide-single-photon-emission computed tomography (IBZM-SPECT) can help to improve confidence in the promised effective therapy of the disabling symptoms. IBZM-SPECT allows to demonstrate in vivo to each patient whether he has a normal number and distribution of the channel type 2 (dopamine-D2-receptor) in the striatum. This method predicts to more than SW, that the patient will respond to L-DOPA, provided the IBZM-SPECT-binding is normal [7]. The patient is then offered a short course of L-DOPA treatment. He and/or the spouse are asked either to come or to call back and to report on the effect of the offered therapy.
2.2. Lesson 2: How to understand L-DOPA therapy?
In lesson 2, the patient learns the advantages and some disadvantages of L-DOPA therapy. LDOPA will improve symptoms of Parkinson’s disease, especially in the early phase. Its effect will in principle last and will ameliorate the cardinal motor symptoms for 7-10 years. This means that the patient will be in a similar state of disability under L-DOPA therapy in 7- 10 years, he presents at the first time of manifestation of PD in the untreated stage. In the next step, the patient and the spouse learn the principles of the pharmacokinetics of L-DOPA. L-DOPA, when orally administered, passes through the oesophagus and the stomach to the duodenum. After a latency of 30-40 min, mainly due to the passage of L-DOPA through the stomach, L-DOPA is absorbed through the mucosa of the duodenum into the blood. From here, L-DOPA is transported to the blood vessels of the brain. L-DOPA is then actively transported from the blood to the brain via an uptake mechanism. At this moment the patient learns the following sentence: ‘The striatum is a sink with one water-tap and 2 outlets.’ The meaning of this sentence is illustrated by Fig. 3. According to the comparison ‘the striatum is a sink’, L-DOPA is brought into the brain via opening the water-tap (oral intake of L-DOPA). L-DOPA is now converted to dopamine. It remains in the brain until it has disappeared via breakdown of dopamine by the 2 enzymes monoaminoxidase-B catechol-O-methyl-transferase (MAO-B) and (COMT). These 2 degrading pathways (MAO-B and COMT) are illustrated as outlets in Fig. 3.
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As already indicated in Fig. 2, in the early stage of PD L-DOPA can be stored in the brain over several hours. This stored L-DOPA is continuously converted to dopamine. As long as dopamine is produced in the striatum, the patient is nearly normally mobile. This phenomenon is observed despite the fact that L-DOPA in blood is only present for 2-3 h (Fig. 2a). When the disease progresses to an intermediate stage, the timecourse of the presence of L-DOPA in blood will remain the same. However, the storage capacity
L-DOPA
. .
. .
..
Dopamlne
l-1,’
M/Q-B
Inhibition
COMT Inhibition
/ ! / , i ‘\ 0
/
..I~...:~..
.,-x-,-x-
Fig. 3. ‘The striatum is a sink with one water-tap and 2 outlets’. The dopamine deficit in the striatum of PD patients is substituted by intake of L-DOPA (‘L-DOPA comes into the striatum through the water-tap’). L-DOPA is converted to dopamine. Dopamine is destroyed by 2 proteins, the enzyme monoaminooxidase-B (MAO-B) and the enzyme Catechol-O-MethylTransferase (COMT). Blocking one outlet, for example MAOB with a MAO-B-inhibitor (. .), leads to a small increase of the dopamine concentration in the striatum. Blocking the other outlet by inhibitors of (COMT-inhibitor - note that COHTinhibitors are clinically not available in 1994) will lead to a marked increase of dopamine in the striatum (- - - -).
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for L-DOPA in brain becomes reduced and conversion of L-DOPA to dopamine in brain lasts shorter than that of the early phase (3-4 h) (Fig. 2b). In the advanced stage, storage of L-DOPA in brain is not possible any more and the timecourse of improvement of motor symptoms nearly reflects the time-course of L-DOPA in blood. Thus, in the early phase of PD, intake of LDOPA (100 mg) 3 times per day leads to a continuous disappearance of motor symptoms (‘on’). In the intermediate phase, the patient notices a short lasting appearance of motor symptoms (‘off) just before the intake of the next dose. Uninformed Parkinson patients blame in fact the next L-DOPA dose to be responsible for the appearance of the ‘off-phase. The educated Parkinson patient realizes, however, that he has reached the intermediate phase of the disease and that storage of L-DOPA in brain becomes shorter. In fact, numerous educated Parkinson patients or their partners suggest at this stage to reduce the time between each L-DOPA dose in order to again achieve a continuous response to the drug. In the advanced stage, the patient will experience the so-called response ‘fluctuation’, i.e. an ‘off-phase before the first L-DOPA dose and an ‘on’-phase after each L-DOPA intake lasting for 1.5-2 h, followed by an interdose ‘off-phase. This clinically experienced and theoretically explainable phenomenon can now be used to introduce to the patient combination therapy with either a blocker of MAO-B (see Fig. 3; outlet on the left side) or with a dopamine agonist. The additional administration of an MAO-B-inhibitor together with L-DOPA will close one outlet of the sink, thereby inducing an increased level of dopamine in brain. Subsequently, the patient will experience a prolongation of ‘on’-phase and a reduction in the duration and severity of the ‘off -phase. Dopamine-agonists are substances which act like dopamine on the dopamine 1- and/or dopamine 2-receptor without the need for conversion to the active compound. Dopamine agonists are explained as immediately active substances to the patient. In the model of the substantia nigra as a TV-broadcasting station and the striatum as a TV-set with 2 channels, the dopamine agonist
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represents a programme broadcasted not via cable as in Fig. 1, but via satellite. So the dopamine agonist will directly act by itself either on channel 1 (dopamine l-receptor-agonist) or on channel 2 (dopamine 2-receptor-agonist). If a dopamine agonist with a long half-life (defined as the time in which the blood concentration of the dopamine agonist drops by 50% of the initially present concentration) is administered in an effective dosage without causing too many side-effects, the patient may experience a markedly reduced ‘offphase in respect to duration and severity and an increase in the time spent in the ‘on’ phase. 2.3. Creuting hope developments
future
thrrctpeuticul
At this stage of the disease and experience with therapy patients have either become members of the Parkinson’s Disease Society or have tried to inform themselves about the possibilities of the presently available treatment for Parkinson’s disease. They have seen other patients in various stages of the disorder including those with marked side-effects associated with long-term L-DOPA therapy. In addition to the already mentioned response fluctuations, these neuropsychiatric sideeffects include phases of abnormal hyperactivity during ‘on’-time, so called dyskinesias and dopaminometica induced psychosis. Numerous patients and their partners also know the limited effectiveness of Parkinson therapy in the late stage of the disease. It is therefore of importance to provide information on new developments in drug therapy. One of the present clinically-tested substances can be explained by the scheme in Fig. 3. In this scheme, the sink (striatum) has 2 outlets, One of the 2 is governed by the enzyme COMT. It is possible to block this major degrading pathway for L-DOPA in brain (Fig. 3). The so-called COMT-inhibitors lead to a marked increase of the dopamine concentration in brain. This biochemical fact is reflected in the clinical observations obtained in so far short-term clinical testing of COMT-inhibitors: Parkinsonian patients, who previously showed marked response fluctuations under L-DOPA therapy alone, expressed a nearly continuous ‘on’-time under combination therapy with L-DOPA and a COMT-inhibitor ([8]; Eich-
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horn and Oertel, unpublished observation). Based on this example and other unmentioned developments in basic and clinical neuroscience, it is justified to offer patient and spouse a positive perspective on the future therapy of PD.
3. Psychosocial aspects of Parkinson’s psychological intervention
disease -
Medical therapy without doubt improves the motor symptoms and, in part, the mood of Parkinsonian patients. Nevertheless, numerous patients still feel to be stigmatized by the fact that they suffer from PD, despite regained mobility under effective treatment. We have therefore postulated, that psychosocial problems impair the quality of life of Parkinsonian patients and their partners. These psychosocial problems are considered to be secondary to the primary organic neurological symptoms. In 1989, a group of neurologists and psychologists at the Department of Neurology, Klinikum Grosshadern, LudwigMaximilians-University, Munich and the MaxPlanck-Institute of Psychiatry, Munich, started a project on psychosocial problems of Parkinsonian patients and their partners. In collaboration with a specialised clinic (Paracelsus-Elena-Klinik, Kassel) for Parkinsonian patients and the German Parkinson’s Disease Society (lay organisation) we sent out an extensive questionaire on psychosocial problems to 325 patients in various cities of the German Federal Republic and asked the patient and the spouse to separately fill out one questionaire each. The results of this questionaire-based survey are summarized in Table 2. To solve these reported psychosocial problems, different types of psychological interventions were developed and offered to Parkinsonian patients and their spouses. These psychological interventions include individual counseling, short time counseling, group counseling and counseling of partners. Group counseling consisted of different and various psychotherapeutical techniques including situational analysis, cognitive restructuring, prac- ticing social skills, role playing, stress inoculation, relaxation techniques, and practicing these techniques outside the group. Table 3 ad-
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Table 2 Common psychosocial problems, expressed by Parkinsonian patients” Patients experiencing stress (‘%I)
Type of stress
Lack
of’ eficiency
Slowness Reduced motivation and drive Anxiety
and
psychological
96 90
distress
Anxiety about helplessness 93 Increase of symptoms under minimal stress 90 Psychological
stress
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Therefore, counseling of partners is as important as advice to the patient, This counseling should address the anxiety of partners related to the progression of the disease and to the anxiety related to partner’s own health. It should indicate how this partner could support the patient to keep the still available, although limited self-independence. Most important the partner has to (re-) learn to lead an independent life (‘keep time for yourself). The effect of counseling partners of Parkinsonian patients is presently assessed.
syn~ptorns
Reduced manual skills Reduced gestures and body language Social
Educ
97 86
4. Conclusion
interacfion
Inability to cope with many people Insecurity in social interactions Partnership lfbr 241
and fivnil~ patients with
84 83
partnrrs)
Fewer activities Anxiety about stress for partner
83 70
“Adapted from Ellgring et al. [9].
dresses some practical problems trained during patients seminars. A re-evaluation of patients who had participated in these seminars, revealed that 44% were still able to use the learned techniques of cognitive restructuring and relaxation techniques for longer than 3 months in public. Another 20% still used one of the mentioned 2 methods. Long-term effects of such seminars, however, remain to be demonstrated [9]. A largely neglected aspect of Parkinson’s disease is the psychosocial situation of the partner. The partner is stigmatized as a person, who lives together with a person suffering from a chronic disabling neurological disorder. Partners face multiple problems related to day-to-day aspects of life such as financial problems, career planning, change of life situation and loss of hobbies and activities. Caring for a Parkinsonian patient means psychological and physical problems in addition to her or his own problems. The responsibility for the partner’s life can be overwhelming. Feelings of guilt, insufficiency, anger and aggression occur and have been observed to a remarkable degree in seminars offered to partners of PD patients.
This article describes how the same group of medical care providers tries to explain patients the medical background of PD in simple terms and on the other hand to work on psychosocial problems of Parkinsonian patients and their partners. After establishing the extent and variation in psychosocial problems of Parkinsonian patients, one can now design psychological interventional strategies to train patients in techniques which may help the patient to solve these psychosocial problems. The same strategy can be used in the psychological support of partners of Parkinsonian patients. The presented educational material on medical aspects of PD has to be considered as preliminary. It is necessary to perform controlled studies in order to find out whether the sequence of the presentation of information makes a difference to the well-being of the Parkinsonian patient and his partner. It may be useful to analyse whether such an educational programme will improve compliance or even may influence the outcome of the disease. It remains to be studied whether educational programmes related to medical aspects and whether participation in psychological interventional strategies also influence the health status of the partner. A further study should investigate the effect of such a programme on health costs. Research on a number of the above-mentioned questions has been performed in the area of diabetes mellitus. It is hoped, that neurologists, psychiatrists, psychologists, and other professionals engaged in the provision of health care to Parkinsonian patients and their partners may benefit
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Table 3 Practical problems trained during seminars” Main focus
Public situation
Private situation
Cognition and emotions
Anxiety about being perceived negatively by others Eating in a restaurant
Anxiety about being helpless, depressive tendencies Less contact with friends because invitations are refused
Behaviour <‘Adapted from Ellgring et al. [9]
from the available experience in the chronic endocrinological/metabolic disease. References [I] Selby G. Clinical features. In: Stern GM ed. Parkinson’s Disease. London: Chapman and Hall Medical, 1990; 333-388. [2] Alexander GE, Crutcher MD. Functional architecture of basal ganglia circuits: Neural substrates of parallel processing. Trends Neurosci 1990; 13: 266-271. [3] Hughes AJ, Daniel SE, Kilford L. Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinice-pathological study of I00 cases. J Neurol Neurosurg Psychiatr 1992; 55: 181-184. [4] Smith CA, Cough AC, Leigh PN, Summers BA, Harding AE, Maranganore DM, Sturman SC. Schapira AH, Williams AC, Spurr NK. Debrisoquine hydroxylase gene polymorphism and susceptibility to Parkinson’s disease. Lancet 1992; 339: 1375-1377. [5] Dunn S, Taylor J, Fowler P, Steinbeck K, Kearns M, Yue
D. The elfects of complications information on anxiety and perceived vulnerability and severity: a randomized trial of information sequence. Melbourne: Proc. Annual Scientific Meeting, Australian Diabetes Society and Australian Diabetes Educators Association, (abstract), 1989. (61 Oertal WH, Quinn NP. Parkinsonism. In: Brandt Th, Caplan L, Dichgans J, Diener C eds. Neurological Disorders: Course and Treatment. Academic Press. [7] Schwdrz J, Tatsch K, Arnold G, Gasser T, Trenkwalder C, Kirsch CM, Oertel WH. “‘I-IodobenzamideSPECT predicts dopaminergic responsiveness in patients with ‘de novo’ Parkinsonism. Neurology 1992; 42: 556561. [8] Roberts JW, Cora-Locatelli G, Bravi D, Amantea MA. Mouradian MM, Chase TN. Catechol-O-methyltransferase inhibitor tolcapone prolongs levodopa/carbidopa action in Parkinsonian patients. Neurology 1993; 44: 2685-2688. [9] Ellgring H, Seiler S, Perleth B, Frings W, Gasser T, Oertel WH. Psychosocial aspects of Parkinson’s disease. Neurology 1993: 43 (Suppl. 6): S4l-S44.