Sleep Disorders in Patients with Parkinson’s Disease

Sleep Disorders in Patients withParkinson’s DiseaseEpidemiology and Management

Jan P. Larsen and Elise TandbergDepartment of Neurology, Central Hospital of Rogaland, Stavanger, Norway

ContentsAbstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2671. Sleep and Sleep Disorders in Parkinson’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2682. Epidemiology and Management of Nocturnal Sleep Problems . . . . . . . . . . . . . . . . . . . . 269

2.1 Insomnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2692.1.1 Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2692.1.2 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269

2.2 Parasomnias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2712.2.1 Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2712.2.2 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272

3. Epidemiology and Management of Daytime Sleep Disorders . . . . . . . . . . . . . . . . . . . . . 2733.1 Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273

3.1.1 Excessive Daytime Sleepiness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2733.1.2 Sleep Attacks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273

3.2 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2744. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274

Abstract Patients with Parkinson’s disease can experience a number of sleep disorders,including insomnia, parasomnias and daytime somnolence [specifically, exces-sive daytime sleepiness (EDS) and sleep attacks].Insomnia is a frequent and important complaint of patients with the disease.

Both the pathology of Parkinson’s disease and dopaminergic drugs may contrib-ute to the much higher than expected frequency of sleep fragmentation and dis-rupted sleep among these patients. In addition, coexisting depression seems to bea major and frequent risk factor for insomnia in Parkinson’s disease.After recognising a sleep problem, the first step in management is to examine

and diagnose the type of insomnia and possible medical or psychological factorsthat may disturb nocturnal sleep. The next step is to give the patient appropriateadvice on sleep hygiene.Increasing the dosage of dopaminergic drug treatment will often increase sleep

disruption and should be avoided unless the patient’s sleep is primarily disturbedby the motor manifestations of parkinsonism during the night. Depression shouldbe looked for and if appropriate be treated in any patients with insomnia. If itbecomes necessary to treat the patient with an hypnosedative agent, it is importantto use a drug with a short half-life and that manifests as few adverse effects as

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possible the next morning. Up-to-date guidelines for the use of hypnosedativesshould be followed.Patients with Parkinson’s disease experience a wide range of parasomnias.

The majority of behaviours may be related to rapid eye movement (REM) sleepbehaviour disorder (RBD) or to a spectrum of symptoms ranging from vividdreaming to psychosis. RBD is effectively treated with clonazepam. In addition,the atypical antipsychotics have given physicians new and better treatment op-tions for psychotic symptoms in individuals with Parkinson’s disease.EDS is common in Parkinson’s disease, while sleep attacks seem to be rare

manifestations of the disease or its treatment. Significant EDS is found in 15%of patients with Parkinson’s disease compared with in 1% of healthy elderlypeople. Sleep attacks are observed in patients treated with all dopaminergic med-ications but have recently been brought to prominence because of their associa-tion with the newer dopamine agonists ropinirole and pramipexole. Patients withParkinson’s disease should be informed about the possibility of developing sleepproblems during the day when prescribed new drugs. Appropriate actions withregard to driving must be taken if significant and persistent daytime somnolenceor sleep attacks appear.

Parkinson’s disease is a common neurodegener-ative disorder, affecting more than 100 per 100 000of the population.[1,2] Patients with Parkinson’sdisease have a wide range of non-motor problemsthat accompany the motor manifestations of par-kinsonism. The nonmotor problems include, butare not limited to, cognitive impairment, auto-nomic dysfunction, psychiatric symptoms and sleepdisorders. These symptoms have received increas-ing interest and attention from physicians over re-cent years, and they may have a major influence onthe lives of patients and their caregivers. Studies ofhealth-related quality of life have shown that Par-kinson’s disease has a substantial impact on dis-tress in patients,[3] and that the variables that moststrongly predict increased disease-related distress aresymptoms of depression, impaired function and in-somnia.[4]Sleep disorders in Parkinson’s disease comprise

insomnia, daytime somnolence and parasomnias. Inthis article we provide a short overview of normalsleep and of the sleep disorders seen in individualswith Parkinson’s disease. We then discuss the epi-demiology and management of nocturnal sleepingproblems (insomnia and parasomnias) and the day-time sleep disorders [excessive daytime sleepiness

(EDS) and sleep attacks] in individuals with the dis-ease.

1. Sleep and Sleep Disorders inParkinson’s Disease

Sleep is a special activity of the brain, controlledby precise mechanisms that induce a specific sleeppattern, and that results in restoration of body andmind.[5] The normal sleep pattern consists of a suc-cession of identifiable states that by polysomno-graphy can be divided into 5 different stages. Sleepstages 1 to 4 include all stages of sleep from dozing(stage 1) to deep sleep (stages 3 and 4). These stagesare characterised by an increasing amount of slowEEG activity with low frequency (0.5 to 4 Hz) andhigh amplitude (delta activity). The fifth stage ofsleep is the rapid eye movement (REM) sleep.REM sleep is associated with the EEG pattern seenin stage 1 sleep. At the same time, rapid eye move-ments are observed along with arousal and fluctu-ations in the functions of the nervous, respiratory,cardiovascular, sexual and autonomic systems,while skeletal muscles are selectively inhibited. Incontrast, non-REM sleep (stages 1 to 4) consists ofa slowing down of all the previously mentionedfunctions.The sleep cycle is modulated by a number of

268 Larsen & Tandberg

© Adis International Limited. All rights reserved. CNS Drugs 2001; 15 (4)

neurochemical systems, each of which appears toinfluence a specific stage of sleep. Slow-wave sleepdepends, in part, on central serotonergic activityarising in cell bodies of the midline raphe nucleusof the pons.[6] REM sleep depends to some degreeon the integrity of the noradrenergic projectionsarising in the cell bodies of the locus ceruleus,[7]and the timing of the initial REM cycle is partiallydependent on cholinergic activity within the CNS.[8]In addition, evidence suggests that various pep-tidergic systems influence sleep behaviour.[9] Thecomplex interactions of these neurochemical sys-tems appear to be under the control of a circadian‘clock’ that synchronises the various systems invol-ved in the regulation of sleep.The neuropathology of Parkinson’s disease is

known to affect anatomical structures and centralneurotransmitters that are involved in the modula-tion of the physiological sleep cycle, including ab-normalities in the level of serotonin (5-hydroxy-tryptamine; 5-HT).[9] The treatment of Parkinson’sdisease also includes the use of agents that inducea number of alterations in central neurotransmittersystems and thus can cause sleep disturbances. Inaddition, there are both quantitative and qualitativechanges in sleep with increasing age.[10] It is there-fore expected that patients with Parkinson’s dis-ease, who in general are elderly, will have an in-creased risk for developing different types of sleepdisorders.

2. Epidemiology and Management ofNocturnal Sleep Problems

2.1 Insomnia

2.1.1 EpidemiologyNocturnal sleeping problems in Parkinson’s

disease are more widespread than would be ex-pected from the effect of ageing alone. A surveyby Nausieda et al.[11] in 1982 revealed prominentsleep complaints in 74 of 100 patients with Parkin-son’s disease. In 1988, Lees et al.[12] showed that215 of 220 individuals with Parkinson’s diseaseexperienced sleep disturbances. Insomnia is themost common symptom of sleep disturbance both

in the general population and among patients withParkinson’s disease.Insomnia can be separated into three different

symptom complexes that may coexist or may be pre-sent in isolation: sleep initiation insomnia, sleep frag-mentation, and early morning awakening. Sleep dis-orders in Parkinson’s disease have previously beenstudied in selected patient populations. These stud-ies have demonstrated that sleep fragmentation isthe most important problem for these patients.[11,12]This finding has been confirmed in a study of acommunity-based population of patients with Par-kinson’s disease from the county of Rogaland,Norway.[13] The study showed that 60% of this un-selected group of patients reported a nocturnalsleeping problem. This was significantly more fre-quent than among patients with diabetes mellitus(46%) and healthy controls (33%) with compara-ble age and gender distribution. About a quarter(27%) of the individuals with Parkinson’s diseaserated their overall night-time problem as moderateto severe. The most common sleep disorders repor-ted by the patients were frequent awakening (sleepfragmentation) and early awakening. Sleep frag-mentation was found in 38.9% of the patients ver-sus in 12% of healthy elderly controls. Problemswith sleep initiation or ability to fall asleep wereequally frequent among patients and controls. 40%of the patients with Parkinson’s disease were usingsleeping pills compared with 23% of the healthyelderly population.The correlations between the presence of noc-

turnal sleeping problems and a wide range of clin-ical and demographic patient characteristics in thisstudy population showed that the most importantrisk factor for developing insomnia in Parkinson’sdisease was co-existing symptoms of depression.[13]In addition, a longer duration of levodopa treat-ment showed significant correlation with noctur-nal sleep disorders.

2.1.2 ManagementInsomnia is common and distressing in patients

with Parkinson’s disease. It is therefore an impor-tant, but also difficult, task for the physician to

Sleep Disorders in Parkinson’s Disease 269


both recognise and develop management plans forinsomnia in these patients.

Diagnosis and RecognitionThe primary step in the management of insom-

nia in patients with Parkinson’s disease is to diag-nose or recognise the type of insomnia and possiblecauses of the problem. In addition to parkinsonismitself, several possible sleep-disturbing factors haveto be considered. Many of these may be treatable.Any physical illness that causes discomfort may

naturally disrupt sleep. Obvious examples are:• nocturnal dyspnoea• gastro-oesophageal reflux• constipation• nocturia caused by prostatism.Motor manifestations of parkinsonism such as

the inability to move in bed, ‘stiffness’, dystonicmovements and ‘cramps’ may also disturb normalsleep. These symptoms may be improved by in-creased dopaminergic treatment. An increase in thedopamimetic dosage may, however, disrupt the nor-mal sleep architecture, as discussed below.Symptoms of depression are frequent in individ-

uals with Parkinson’s disease,[14,15] and the presenceof depression is the strongest predictor of disturbedsleep.[13] It is therefore mandatory to evaluate de-pression in any patient with Parkinson’s disease whohas a nocturnal sleeping problem.Iatrogenic causes of insomnia include different

kinds of medication and consumption of alcoholand caffeine-containing drinks.

Sleep HygieneAfter identifying the nature of insomnia and as-

sessing any concurrent medical or psychologicalfactors that may contribute to the problem, the nextstep is counselling the patient in sleep hygienemeasures (see table I). For a review of these guide-lines, readers are referred to Zarcone.[16] Practisingsimple rules that promote better sleep habits is thecornerstone of the effective management of anysleep disorder. Sleep hygiene is, however, not alwaysenough to restore satisfactory nocturnal sleep, andpharmacological approaches may have to be con-sidered.

Dopaminergic MedicationsAdjustment of dopaminergic medication may

have a different impact on sleep in different patientsand situations; for example, levodopa has been re-ported to decrease, increase or even to have no ef-fect on REM sleep in Parkinson’s disease.[17]Dopaminergic drugs seem to influence sleep

through their effects on dopaminergic projectionsfrom the ventral tegmental area to the cerebral cor-tex. Stimulation of these neurons is associated witharousal,[18] and dopamine agonists produce arousaland suppress REM sleep.[19,20] High doses of apo-morphine reduce total sleep time and REM sleep,while low doses induce sleep.[21] In spite of this,treatment strategies with controlled-release formu-lations of levodopa and long-acting dopamine ag-onists are claimed to improve the overall nocturnalsleeping problems in patients with Parkinson’s dis-ease, if mobility is the issue.[22,23]van Hilten et al.[24] evaluated the controversial

effect of dopaminergic drugs on sleep in a recentstudy. They examined sleep disruption by contin-uous activity monitoring in 89 nondepressed pa-tients with Parkinson’s disease. They found that ahigher daily dose of levodopa was associated withhigher nocturnal activity levels, an increase in themovement time during the night, and a more dis-rupted sleep. The daily dose of levodopa or dopa-mine agonists, more than disease severity, was thestrongest predictor of sleep disturbance. Based ontheir findings, the authors postulated that dopamin-

Table I. Sleep hygiene measures

Regular sleep hours

Avoid excess time in bed

Have a regular get-up time, regardless of the quality of sleep

Avoid daytime naps

Use bed for sleep (and sexual activity) only

Regular pre-retirement routine

Schedule time to relax before bed (discuss relaxation techniques)

Take physical activity by day

Ensure sunlight exposure

Make the bedroom quiet, comfortable, correct temperature,adequately dark, and secure

Minimise stimulants, especially after 1700h

Avoid large evening meals



ergic drugs would cause sleep disruption in pa-tients with mild to moderate Parkinson’s disease.In more seriously affected patients, the beneficialeffect of dopaminergic drugs on disturbing noctur-nal motor manifestations of parkinsonism will out-weigh the adverse effects on sleep. More aggressivedopaminergic treatment of night-time problems inParkinson’s disease using long-acting dopamineagonists may therefore be indicated in a small andcarefully selected group of patients. However, inthe majority of patients this strategy will disruptand disturb the sleep even further.

AntidepressantsThe association between depression and fre-

quent and early awakening is well known. Treat-ment with antidepressant medication may be themost important drug strategy to overcome the in-somnia seen in individuals with Parkinson’s dis-ease. This is underlined by the high frequency (40to 50%) of symptoms of depression in Parkinson’sdisease[14,15] and their strong predictive value forinsomnia in these patients.The treatment of depression in patients with

Parkinson’s disease has been thoroughly discussedpreviously.[25] In ‘The Norwegian Recommenda-tions for Treatment of Parkinson’s Disease,’ wehave suggested the following strategy as the firstline of treatment for depression in those with Par-kinson’s disease: start with citalopram 20 mg/dayand increase the dosage to 30 mg/day if needed after2 weeks. If the treatment has not induced a satis-factory response after 1 month, we recommend thatcitalopram is combined with mianserin 10mg inthe evening and the dose may, if needed, be grad-ually increased to 30mg.This strategy is based on the need for a medica-

tion that is effective with as few adverse effects aspossible and that does not interact with widely usedantiparkinsonian drugs like selegiline (deprenyl).Citalopram has been used safely in combinationwith selegiline,[26] in contrast to other serotonin re-uptake inhibitors that have not been examined forinteractions with this antiparkinsonian agent.Mianserin has been shown to provide a substantialadditional antidepressant effect in patients with

Parkinson’s disease[27] and also to have a benefi-cial effect on insomnia by providing nocturnal se-dation when given in the evening. The sedative ef-fect of mianserin 10 to 30mg (and amitriptyline 10to 75mg) given in the evening can often be usefulin the treatment of insomnia.

HypnosedativesThe long term use of hypnosedatives in any pa-

tient population is not desirable. The major disad-vantage of these drugs in older people is that theycan impair daytime performance. Nonetheless, themajority of individuals with Parkinson’s diseasewhohave insomnia will at least at times require thesemedications. 40% of the patients in the community-based Parkinson’s disease population from Nor-way mentioned above[13] were using hypnotics orsedatives to improve their sleep.Physicians can optimise the use of hypnosed-

atives by applying the following guidelines: (i) usethe lowest effective dose; (ii) use intermittent (i.e.not every day) administration; (iii) prescribe med-ication for short term use only; (iv) discontinue themedication gradually; and (v) be alert for reboundinsomnia following discontinuation.[28]Several hypnotic and sedative drugs are avail-

able, and the preferred drug is based on the physi-cian’s personal experience and theoretical consid-erations, as there are no relevant drug trials that havecompared the usefulness of these drugs. The efficacyof benzodiazepines and newer compounds likezolpidem and zopiclone seems to be comparable.Zopiclonemay have advantages over the benzodia-zepines in terms of dependence and abuse potentialand effects on daytime performance, and is there-fore often the preferred drug. The standard initialdose in the elderly is 3.75mg, but a higher dose (5or 7.5mg) may be needed.

2.2 Parasomnias

2.2.1 EpidemiologyParasomnias include a variety of sleep-related be-

havioural phenomena. In patients with Parkinson’sdisease the major disorders are:• vivid dreams• altered dream content



• nightmares• night terrors with nocturnal vocalisations• REM sleep behaviour disorder (RBD)• nocturnal hallucinations• somnambulism.Accurate estimates of the frequencies of these

behaviours are not available, and the clinical diffe-rentiation of them is difficult. Some of these man-ifestations may also be different symptoms of thesame pathological processes.One distinct syndrome that has been clarified

and fully described during recent years is RBD.[29]Patients with this syndrome are executing exces-sive motor activity during dreaming and they havelost the normal and expected skeletal muscle atoniaof REM sleep. Among 93 consecutive patients withRBD from theMayo Sleep Disorder Center, 25 hadidiopathic Parkinson’s disease.[30] Multiple-sys-tem atrophy was diagnosed in 14 of the patients.Dementia with Lewy bodies is also associated

with RBD.[30] In these patients the syndrome wasnot associated with the use of drugs such as levo-dopa, and RBD developed before parkinsonism in52% of the patients with Parkinson’s disease. 32%of the patients had injured themselves and 64% hadassaulted their spouses during RBD.[30] These sit-uations are not uncommon among individuals withParkinson’s disease, but their frequency has not beenstudied.Vivid dreaming, nightmares and altered dream

content may represent the first steps in a progres-sive cascade of events leading to drug-induced hal-lucinations and psychosis in Parkinson’s disease.[31]This proposal is supported by longitudinal clinicalobservations in single patients and the high fre-quency of altered dreaming (60%) in patients withParkinson’s disease who experience hallucina-tions.[32] Sharf et al.[33] found that 30% of patientsreceiving long term levodopa therapy reported ‘newdream content’. van Hilten et al.[34] found that 24%of patients with Parkinson’s disease experienced‘altered dreams’. In the community-based Parkin-son’s disease population from Norway,[35] vividdreamswithout coexisting hallucinations were foundin 25.5% of the patients. In addition, 9.8% had hal-

lucinations with insight retained, and 6.0% had moresevere psychotic symptoms with hallucinations ordelusions.Both ‘benign’ and more severe hallucinations

are typically experienced in the late evening or dur-ing the night. These symptoms may profoundly dis-turb sleep for both the patient and caregiver, and arethe one single factor that most strongly predict nur-sing home placement for patients with Parkinson’sdisease.[36]

2.2.2 ManagementMany of the parasomnias experienced are only

mildly disturbing for the patient. It is, however, im-portant to also evaluate the distress and problems ex-perienced by the spouse when considering possibledrug therapies. On the other hand, the complaintshave to be balanced against adverse effects of newtherapies.

REM Sleep Behaviour DisorderThe syndrome of RBD may both be disturbing

to the spouse and be of danger to the patient. Sub-dural haematomas occurred in two of the 93 pa-tients with RBD described above in the Mayo Cen-ter population.[30] Other and more frequent injurieswere related to falling out of bed or bumping intofurniture or walls. For this syndrome, clonazepamhas been shown to be highly effective in nearly90% of patients.[37] Clonazepam may be started ata dose of 0.5mg in the evening and increased to 1.5or 2.0mg.

Vivid Dreams and HallucinationsVivid dreams and ‘benign’ hallucinations may

not be threatening and disturbing for the patient,and can be tolerated without pharmacological in-terventions. However, when needed, the first-linetreatment strategy for psychotic symptoms in pa-tients with Parkinson’s disease is to titrate the dop-aminergic therapy downward. However, this fre-quently leads to a worsening of parkinsonism.The novel atypical antipsychotics have pro-

vided a promising tool for treating psychotic symp-toms in Parkinson’s disease without worsening ofparkinsonism.[38] Clozapine has been available forseveral years, but may induce agranulocytosis in



about 1% of patients. This reaction is idiosyncraticand even low doses of clozapine can cause thisproblem. Weekly monitoring of the white cell countis necessary, and clozapine is therefore not used asthe treatment of first choice.Olanzapine and quetiapine are at present the

two preferred atypical antipsychotics for use in pa-tients with Parkinson’s disease who exhibit psy-chosis. Both are associatedwith a good response rate,but may also in some patients induce more severeparkinsonism. Initial low doses are mandatory, asthe risk for daytime sedation is high with thesedrugs in patients with Parkinson’s disease.[39] Newatypical antipsychotics will be available soon,making this a work in progress.

3. Epidemiology and Management ofDaytime Sleep Disorders

Sleep disorders during the day in patients with Par-kinson’s disease comprise excessive daytime sleep-iness (EDS) and sleep attacks.

3.1 Epidemiology

Sleep architecture and regulation change with in-creasing age. The need for a short nap during the dayis normal among older people. The daytime som-nolence observed in some patients with Parkinson’sdisease is, however, far more pronounced and in-capacitating.

3.1.1 Excessive Daytime SleepinessThere is no universally accepted definition of

the phenomenon of EDS. EDS represents a somno-lence that is related to pathology of general mech-anisms of the sleep-wake cycle, and the patient isoften asleep frequently and for hours during the day.There are few studies addressing EDS in indi-

viduals with Parkinson’s disease. Factor et al.[32]found that 49% of patients with Parkinson’s dis-ease experienced daytime sleepiness with napping,comparedwith 26% of controls. vanHilten et al.[34]found no significant difference between patientsand controls in terms of the incidence of EDS. In acommunity-based population of patients with Par-kinson’s disease, daytime somnolence was graded

as not present, mild somnolence and EDS.[40] Pa-tients with EDS fell asleep three or more times aday, or the total sleeping timewasmore than 2 hours.In this study, mild somnolence was found in about10% of both patients with Parkinson’s disease andcontrols. In contrast, EDS was found in 15.5% ofthe patients and in only 1% of healthy elderly con-trols. Compared with patients not reporting day-time somnolence, the patients with EDS had sig-nificantly higher staging of Parkinson’s disease,were more disabled, and showed a higher frequen-cy of cognitive decline and symptoms of depres-sion. They had also been using levodopa for alonger time and had significantly more hallucina-tions than patients without EDS.These clinical correlates suggested that patients

with Parkinson’s disease who have EDS havemorewidespread and severe brain disease, and that theirsleepiness is caused by the cerebral pathology ofParkinson’s disease. In contrast, the increased fre-quency of insomnia in Parkinson’s disease couldbe a natural explanation for the daytime somno-lence experienced by these patients. In the studyby Tandberg et al.,[40] the frequency of nocturnalinsomnia was, however, the same both among pa-tients with EDS and those without somnolence,therefore emphasising the importance of the pos-tulated role played by intrinsic neurobiologicalfactors. In addition, dopaminergic medications caninduce sedation and drowsiness in some patients[41]and increased alertness in others,[17] as discussed insection 3.1.2.

3.1.2 Sleep AttacksSleep attacks while driving were recently de-

scribed in 8 patients with Parkinson’s disease.[42,43]The episodes were said to be sudden and irrever-sible and were attributed to the new dopamine ag-onists pramipexole and ropinirole, because therewere no further episodes after the drugs were stop-ped. This description has led to a debate both onprescribing recommendations for these drugs andon the real nature of the described episodes.Olanow et al.[44] objected to the term ‘attack’,

and proposed that the patients fall asleep becausethey are continuously sleepy (i.e. they have EDS)



and are put in situations in which resistance to sleepis decreased.[44] Several detailed reports seem, how-ever, to support the notion that some of the reportedpatients fell suddenly and irresistibly asleep froma completely alert and awake mental state.[45,46]Sleep attacks seem thus to exist, but they have

been reported to occur with nearly all availabledopaminergic drugs.[42,45,47,48] The frequency ofthese true attacks, and not only napping in patientswith EDS, is not known. Most likely, true sleepattacks in idiopathic Parkinson’s disease are uncom-mon and many of the reports of such attacks havebeen in patients with atypical features of Parkin-son’s disease or with a diagnosis of multiple-sys-tem atrophy.

3.2 Management

EDS is common in individuals with Parkinson’sdisease, while sleep attacks are rare. There is noeffective medical therapy for either disorder. A re-duction in dosage of dopaminergic drugs may re-lieve somnolence in some patients and a changefrom dopamine agonists to levodopa (or vice versa)may for some patients be beneficial.The physician’s major task is to be aware of the

daytime sleep disorders that can occur in patientswith Parkinson’s disease and to diagnose them. Af-ter recognising these problems, management of thepatient depends on the severity of the somnolenceand the possible risks that the individual patientwith abnormal daytime sleep is exposed to in hisor her daily life.Car driving is an activity that necessitates spe-

cial concern. All individuals with Parkinson’s dis-ease who are prescribed dopaminergic medicationsmust be informed that daytime sleep episodes mayoccur, and they should also be advised about thedangers of driving while experiencing drowsiness,or if they have unexpected episodes of irresistiblesleepiness. If patients experience such episodesthey should refrain from driving and inform theirphysician. If satisfactory control of sedation is notobtained by dosage adjustments or a change inmedication, the patient should no longer be al-lowed to drive.

4. Conclusions

Insomnia has been shown to be more importantthan the severity of parkinsonism for reduced qual-ity of life in patients with Parkinson’s disease. In-somnia, parasomnias and daytime sleep disordersare all common in individuals with the disease. Theseproblems can be induced by the cerebral pathologyof the disease process itself and by antiparkinsoniandrugs.The management of sleep disorders in Parkin-

son’s disease is based on recognising and provid-ing a correct diagnosis of the causes and the kindof sleep disorder experienced by the individual pa-tient. The next step in management is counsellingthe patient and caregiver on sleep hygiene and pro-viding them with the relevant information on sleepproblems that can occur. Pharmacological therapiescan provide additional benefits in many patients.

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Correspondence and offprints: Prof. Jan P. Larsen, Depart-ment of Neurology, Central Hospital of Rogaland, PO Box8100, N-4068 Stavanger, Norway.



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Sleep Disorders in Patients with Parkinson’s Disease