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The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment according to the progression of the degenerative process of the disease will diminishe aggravation. The following types of sleep-arousal disturbances have to be considered in PD patients: - Sleep Disturbances, Light Fragmented Sleep (LFS), Abnormal Motor Activity During Sleep (AMADS), REM Behavior Disorders (RBD), Sleep Related Breathing Disorders (SRBD), Sleep Related Hallucinations (SRH), Sleep Related Psychotic Behavior (SRPB). - Arousal Disturbances, Sleep Attacks (SA), Excessive Daytime Sleepiness (EDS), Each syndrome has to receive a score according to its severity. III. The specific therapy consists in: LFS: Benzodiazepines & Nondiazepines. AMADS: Clonazepam, Opioid, Apomorphine infusion; RBD: Clonazepam and dopaminergic agonists; SRBD: CPAP, UPPP, nasal interventions, losing weight; SRH: Clozapine, Risperidone; SRPD: Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual PD patient.

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A patient in stage 3-4 of the Unified Parkinson's Disease Rating Scale (UPDRS), or in stage 4-5 of Hoehn and Yahr staging scale, or a patient with 0-50% activities of daily living scale of Schwab and England is considered a Late Parkinson's Disease (LPD) patient. The prevalence of disturbed sleep in Parkinson's Disease (PD) was found to vary according to an objective rating, from 60 to 98%. The factors predicting the quality of life in PD patients are: depression, sleep disturbances and dependence. The present article proposes the insertion of the following items as a chapter in a revised UPDRS based on updated knowledge in sleep arousal disturbances in PD. V. SLEEP-AROUSAL DISTURBANCES: Sleep disturbances 43. Light fragment sleep (LFS) 44. Sleep-related breathing disorders (SRBD) 45. Restless legs-periodic leg movements during sleep (RLS-PLM) 46. REM behavioral disorders (RBD) 47. Sleep-related hallucinations (SRH) 48. Sleep-related psychotic behavior (SRPB) Arousal disturbances 49. Sleep attacks (SA) 50. Excessive daytime sleepiness (EDS). Approaching the treatment of disturbed sleep in LPD means postponement of the institutionalization of the LPD patient, allowing the spouse or the caregiver a quiet nights sleep. This approach consists of three steps, each one of major importance. (1) Correct diagnosis based on detailed anamnesis of the patient, of the spouse or of the caregiver; a one week recording on a symptom diary (log) by the patient or the caregiver; excluding co morbidities. Then choosing the most appropriate sleep test, if necessary: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), actigraphy or video-PSG. This first step allows the diagnosis of one of the above mentioned sleep-arousal disturbances. (2) The non-specific therapeutic approach consists of: (a) checking the sleep effect on motor performance: beneficial, worse or neutral. (b) Dopaminergic adjustment is necessary due to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals which alter the normal modulator mechanisms of motor centers in LPD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and non-REM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates LPD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. L-Dopa has also an arousal effect on Non-REM sleep, repeatedly awakening the patient and enhancing the fragmentation due to the involuntary movements. (c) Socio-physical assistance. (3) The specific therapy consists of: LFS-Sinemet CR, Tolcapone, Intranasal Desmopressin, Domperidon, Cisapride and neurosurgery; SRBD-CPAP, UPPP, nasal interventions, losing weight; RLS-PLM-Benzodiazepine (Clonazepam), Opioid, Apomorphine infusion; RBD-Clonazepam and dopaminergic agonists; SRH-Clozapine, Risperidone; SRPD-Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual LPD patient.

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Yawning is a complex event that depends largely on the autonomic nervous system. Microneurographic techniques were used to study the mechanism involved in yawning. A series of spontaneous yawns displayed by a healthy 39-year-old male offered us the opportunity to study the muscle sympathetic nerve activity (MSNA) during this phenomenon. It was found that 2 s of yawning inhibited the MSNA recorded at the right peroneal nerve in the lateral knee area, while 3 s of slow expiration succeeding a yawn provoked an MSNA discharge. Blood pressure decreased with each slow expiration by 5-6 mmHg, and increased again with the renewed MSNA discharge. We conclude that yawning is associated with a sympathetic suppression that favours a parasympathetic dominance, as indicated by the MSNA and the decrease in blood pressure. The slow expiration following a yawn is associated with a sympathetic activation marked by an MSNA discharge and an increase in blood pressure.

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During the 1991 Gulf War, we investigated the effect of missile attacks through two telephone surveys of a large sample of an urban population that evaluated self-reported sleep quality, stress, fear, depressed mood, fatigue and power of concentration. We surveyed 1,045 people during the Gulf War itself, and we interviewed them again (excluding the chronic insomniacs) 30 days after the war. During the war, 51% of the subjects claimed to be suffering from disturbed sleep. Whereas 13% of the survey population had been chronic insomniacs before the war, 38% developed insomnia during the war. The war provoked reported stress (67.5% of subjects), depressed mood (50.9%), difficulties in concentration (39.7%) and increased fatigue (25%). Four weeks after it ended, 19% of the previously normal subjects were still suffering from insomnia; 5% of the cases of insomnia were developed postbellum. Stress, depressed mood and impaired concentration were found to correlate significantly with subjectively evaluated insomnia. We concluded that modern missile warfare may induce long-lasting insomnia in one-third of the population under threat. A small percentage may develop insomnia postbellum. The risk of developing long-lasting insomnia is higher in those who reported experiencing prolonged stress and depressed moods.

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The present study was performed on 615 male subjects referred to the Sleep Medicine Center at Tel Hashomer, Israel, and polysomnographically recorded for a single night between January 1, 1990 and December 31, 1993. The study suggests the existence of a circannual rhythm of rapid eye movement (REM) sleep time with an acrophase during December-January and a nadir during July-September (single cosinor analysis: mesor = 49.7 +/- 0.9, amplitude = 5.9 +/- 1.2, p < 0.001). Both REM sleep time and REM sleep percentage were higher and REM sleep latency shorter during winter and spring than during summer and fall. No dependence of the seasonal REM sleep time rhythm upon age, apnea-hypopnea index or diagnosis type was detected. These data support, for a subtropical climate, results previously obtained in a temperate climate. It is possible that external temperature may be the principal factor influencing the phenomenon.

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Several paradigms of perceptual learning suggest that practice can trigger long-term, experience-dependent changes in the adult visual system of humans. As shown here, performance of a basic visual discrimination task improved after a normal night's sleep. Selective disruption of rapid eye movement (REM) sleep resulted in no performance gain during a comparable sleep interval, although non-REM slow-wave sleep disruption did not affect improvement. On the other hand, deprivation of REM sleep had no detrimental effects on the performance of a similar, but previously learned, task. These results indicate that a process of human memory consolidation, active during sleep, is strongly dependent on REM sleep.

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Two major sources of dissatisfaction with the quality of life among Parkinsonian patients are the "locomotor disability" and the "nature of their sleep". The main focus of research was directed towards the locomotor disability, but in the last two decades some progress has been made towards the understanding of sleep in PD patients. Sleep in Parkinson's disease is light and fragmented due to an increased skeletal muscle activity, disturbed breathing, impaired biological rhythm and REM-nonREM variations of the dopaminergic receptor sensitivity.

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Every new empiric observation made over two millenia fueled the dispute as to whether hiccup (Hc) is a digestive or a respiratory reflex. A review of the literature, focusing attention on the probable mechanism of Hc, shows Hc as a neurogenic dysfunction of the 'valve function' between the inspiratory complex and the glottis closure complex.

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Non-REM sleep transforms the waking alternating Parkinsonian tremor into subclinical repetitive muscle contractions whose amplitude and duration decrease as non-REM sleep progresses from stages I to IV. During REM sleep Parkinsonian tremor disappears while the isolated muscle events increase significantly.

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A wide range of elementary and complex motor activities are known to occur during sleep, but very little is known about the basic physiologic condition of the skeletal muscle during sleep. The present study provides evidence that a minute electric random activity constitutes the basic physiologic condition of the skeletal muscles during sleep. During the NonREM stages of each sleep cycle a regression of the continuous random minute activity occurs, followed by a sudden increase of the isolated motor unit action potentials during REM sleep. Particular structural features of the anterior tibial (AT) muscle make it the most active skeletal muscle during sleep. During wakefulness, at rest, the random muscle activity disappears.

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Four youngsters, between the ages of 13-27 years, presented dystonic foot. Two to three years following the appearance of the dystonic foot, cogwheel rigidity and tremor appeared on the dystonic foot side. Treatment with low doses of levodopa/carbidopa consistently reversed the symptoms. "On-off" phenomena appeared in the first years of treatment and persisted for the entire period of 5 to 15 years of illness. No parkinsonian signs were present when the dystonic foot appeared. Based on our observations and on a review of the literature, we conclude that responsiveness to low doses of L-dopa is the major marker of juvenile Parkinson's disease.

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Polysomnographic monitoring of a 16-year-old girl suffering from dopa-responsive dystonic parkinsonism showed a change in the distribution of muscle activity in thigh muscles during different stages of sleep. The hamstring muscles were hypertonic at sleep onset compared with the vastus lateralis of the quadriceps muscles. At the third sleep cycle of each of the 2 nights, the time at which sleep benefit becomes clinically evident, the hypertonia in the hamstring muscles was reversed and the vastus lateralis became more hypertonic. It is suggested that the muscle tonus inversion marks the moment at which the sleep process alleviates the dystonic parkinsonian state manifested at wakefulness as a circardian fluctuation. According to our data, the flexor-extensor tonus inversion during sleep was not yet described in the literature, and may be an associated feature of dopa-responsive dystonic parkinsonism.

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Despite the fact that yawning is a reality of everyday life, its study is not included in the curriculum of medical schools, and most medical textbooks barely mention its existence. Two factors may help to explain this puzzling situation: (a) yawning's borderline position between psychology and neurology, and (b) researchers' lack of understanding as to why people yawn. After review of the literature and personal observation, it is concluded that yawning is a complex arousal defense reflex located in the reticular brainstem with a peripheral and central arche, whose aim is to reverse brain hypoxia. Yawning occurs with loss of interest (boredom) and may or may not be associated with fatigue. By reversing drowsiness, yawning avoids a decreased concentration capacity resulting from borderline hypoxia. It is hoped that this article will stimulate further research on the phenomenon.

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