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Objective To describe the unique case of a middle-aged woman with severe insomnia recurring with a regular infradian period without any other significant clinical condition. To infer the existence of a circadian dysfunction modeled according to the physical phenomenon of the “beats.” Patient/Methods A two-year prospective observation by means of a sleep log was performed during the patient’s normal life. She underwent one month of motor activity recording and also polysomnography, circadian rhythm of body core temperature and psychiatric evaluation during periods with and without insomnia. Results Visual inspection of the 293-day plot of the sleep log disclosed a regular 42-day rhythm of insomnia recurrence confirmed by a Discrete Fourier Transform. During the periods of insomnia, lasting 5–7 days, only moderate mood symptoms (depressive overlapping hypomaniac symptoms) were present. Treatment with sodium valproate was effective in curtailing insomnia. Conclusion The wax and wane infradian modulation of the sleep length suggested the presence of a basic mechanism similar to the physical phenomenon of the “beats,” i.e., a long period modulation of the amplitude of an oscillating system due to the interference of two uncoupled oscillators with a slightly different oscillation frequency. Hypothesizing a dysfunction of the circadian component of sleep, namely two uncoupled circadian cycles, a simple mathematical model estimated the difference of their periods of oscillation |34 ± 2 min| and reproduced the sleep-log data of the drug-free period of observation.

We investigated the prevalence of nocturnal eating (sleep-related eating disorder-SRED or night-eating syndrome-NES) in patients with restless legs syndrome (RLS). One hundred RLS patients living in Emilia-Romagna (Northern Italy) and 100 matched controls randomly selected from the general population received two telephone interviews, and were investigated for socio-demographic characteristics, general health status, and presence of nocturnal eating. Additionally, subjects underwent interviews for psychopathological traits [by means of the Eating Disorder Inventory-2 (EDI-2), the Maudsley Obsessive-Compulsive Inventory (MOCI), the Beck Depression Inventory (BDI)], excessive daytime sleepiness (EDS), and subjective sleep quality. Compared with controls, RLS patients had more frequently pathological MOCI scores (24% versus 10%, P = 0.03), used significantly more drugs for concomitant diseases and had more nocturnal sleep impairment and EDS. SRED was more prevalent in RLS patients than controls (SRED: 33% versus 1%, P < 0.001). Medication use and pathological MOCI scores were more prevalent in RLS patients with SRED than among RLS patients without SRED. Use of dopaminergic or hypnotic drugs for RLS was not correlated with the presence of SRED. We demonstrate an association between RLS and SRED. Prospective studies are needed to establish the mechanisms underlying such association and whether it is causal.

Peduncular hallucinosis (PH) consists of formed and coloured visual images, which the patient knows are unreal; it is often associated with lesions of the pons, midbrain and diencephalon. A 72-year-old man had noted the sudden onset of visual hallucinations one year before, specifying the time and body position in a 4-week, 24-h diary. Thereafter, he underwent video-polysomnography (VPSG), brain magnetic resonance imaging (MRI), angiography (MRA), proton spectroscopy ((1)H MRS), and single photon emission tomography (SPECT). Patient's diaries and VPSG showed a strong clustering of hallucinatory experiences during the evening/night time while lying in supine position, similar to hypnagogic hallucination and sleep paralysis in supine position. Repeated episodes of REM sleep behaviour disorder (RBD) occurred during the night. MRI and MRA showed an elongated and dilated left internal carotid artery displacing the left subthalamus upwards, and (1)H MRS relatively decreased N-acetyl-aspartate in the left subthalamus. Brain SPECT during PH revealed hypoperfusion in the right temporal region and hyperperfusion in the left occipital and right opercular regions (the latter possibly related to the patient's awareness of unreality). PH resolved with serotonergic (citalopram) therapy.

Autonomic nervous system activity changes have been described during cataplexy as playing a role in triggering it. To confirm these previous findings, we investigated the time course of sympathetic and cardiovascular activities during cataplexy. We made for the first time microneurographic recordings of 10 cataplectic episodes in three patients with hypocretin-deficient narcolepsy. During microneurography, muscle sympathetic nerve activity (MSNA) was recorded simultaneously with heart rate (HR), respiratory movements, arterial finger blood pressure (BP), electroencephalography, electro-oculogram and superficial electromyogram. Results showed no significant autonomic changes before the onset of the cataplectic episodes. Cataplexy was associated with a significant increase in MSNA and BP compared with baseline, whereas HR was markedly decreased. An irregular breathing pattern mainly characterized by apnea typically occurred during the attacks. In conclusion, our findings did not show significant changes in autonomic activity prior to cataplexy onset, ruling out a triggering role of the autonomic system. However, cataplexy was associated with co-activation of sympathetic and parasympathetic autonomic systems, a pattern reminiscent of that reported during the vigilance reaction in animals.

We report the case of a 47-year-old man with idiopathic central sleep apnoeas recurring during wake-sleep transitions at night or at diurnal naps. Symptoms associated with central apnoeas were sudden awakening with shortness of breath, sleep fragmentation and daytime tiredness. Following the failure of CPAP and BiPAP, we treated the patient with zolpidem which reduced central apnoea events, improved sleep and eliminated the patient's nocturnal disturbing symptoms. Beneficial effects were still present after two years of treatment. Our case demonstrates that zolpidem may be beneficial in the long term treatment of idiopathic central sleep apnoea syndrome.

We describe a patient with a paraproteinemic anti-myelin-associated glycoprotein (anti-MAG) antibody polyneuropathy and concomitant axial myoclonic jerks. Neurophysiological investigation revealed that axial jerks were asymmetrical and exaggerated by lying in bed. They disappeared during mental arousal and sleep. Analysis of axial myoclonus showed that the first activated muscle was the left rectus abdominis with subsequent rostral and caudal propagation of a propriospinal type. Plasmapheresis substantially reduced the frequency and intensity of axial myoclonic jerks. In our patient, propriospinal myoclonus was associated with anti-MAG polyneuropathy, but the causal relationship remains unclear.

Objective We present two patients, a 52-year-old man and a 56-year-old woman, with rapid eye movement sleep behaviour disorder (RBD) since the age of 50. Method In both the patients RBD was videopolysomnographically documented. Results Both patients developed, with time, autonomic and motor symptoms consistent with the diagnosis of multiple system atrophy. During the course of the disease RBD episodes diminished in frequency but the patients’ sleep became even more abnormal, with nearly continuous motor and verbal abnormal behaviours and ambiguous and rapid oscillations of state-determining polysomnographic variables, now consistent with status dissociatus (SD). Conclusion If SD represents the evolution and most extreme form of RBD it should be investigated longitudinally in neurodegenerative diseases.

Electrophysiological investigations of restless legs syndrome (RLS) have found spinal circuits impinging on motoneurones. We evaluated the H reflex threshold, latency, the Hmax/Mmax ratio, and the short latency autogenic inhibition in 7 patients with RLS and 10 age-matched controls by testing the excitability changes in soleus H reflex Ib interneuron function. A significant reduction in Ib inhibition at 4 (P 0.043), 5 (P 0.007), and 6 ms (P 0.001) of H reflex conditioning interstimulus interval was found in RLS patients. Data support the hypothesis that altered group I nonreciprocal inhibition is implicated in enhancing the spinal circuitry excitability of RLS, and are consistent with the view of an abnormal supraspinal drive to spinal interneurons in RLS. © 2007 Movement Disorder Society

SUMMARY The aim of this study was to investigate the relationships among sympathetichyperactivity, excessive daytime sleepiness (EDS) and hypertension in obstructive sleepapnoea syndrome (OSAS). Ten newly diagnosed OSAS patients with untreated EDSand daytime hypertension underwent polysomnography (PSG) and daytime measure-ments of plasma noradrenaline (NA), ambulatory blood pressure (BP), musclesympathetic nerve activity (MSNA) by microneurography and objective assessmentof EDS before and during 6 months of compliance-monitored continuous positiveairway pressure (CPAP) treatment. One month after the start of CPAP, BP, MSNAand NA were significantly lowered, remaining lower than baseline also after 3 and6 months of treatment. CPAP use caused a significant improvement of sleep structures,and reduced EDS. A statistical correlation analysis demonstrated that EDS was notcorrelated with sleep measures obtained from baseline PSG (% sleep stages, apnoea andarousal index, mean oxygen saturation value), whereas daytime sleepiness wassignificantly correlated with MSNA. Furthermore, MSNA and BP showed nocorrelation. Our data obtained from selected patients suggest that the mechanismsinducing EDS in OSAS are related to the degree of daytime sympathetic hyperactivity.Additionally, resting MSNA was unrelated to BP suggesting that factors other thanadrenergic neural tone make a major contribution to OSAS-related hypertension. Theresults obtained in this pilot study need, however, to be confirmed in a larger studyinvolving more patients.keywords continuous positive airway pressure, hypertension, muscle sympatheticnerve activity, obstructive sleep apnoea syndrome, sleepiness

Objective We describe six patients affected by frequent episodes from sleep associated with compulsive smoking and/or eating. Patients woke up with a desire to smoke and/or eat because of an “inner” drive. Method Video-polysomnography (VPSG) was performed in three patients. Results VPSG documented a normal sleep structure with an increased arousal index. Conclusion Compulsive eating during sleep has been classified as sleep-related eating syndrome or Nocturnal eating syndrome, but its association with compulsive smoking has not been previously reported.

Summary: Purpose: Nocturnal frontal lobe epilepsy (NFLE) may be associated with sleep fragmentation and reduced sleep efficiency. Daytime sleepiness and disturbed sleep quality have been reported in some patients. We investigated the occurrence of daytime sleepiness-related symptoms and subjective sleep quality in patients with NFLE in comparison with matched controls. Methods: Patients with NFLE at a single epilepsy center and matched controls randomly selected from the general population self-administered questionnaires on daytime sleepiness-related symptoms and subjective sleep quality [Epworth sleepiness scale (ESS), Bologna questionnaire on sleepiness-related symptoms (BQS), Berlin questionnaire]. Results: Thirty-three patients with NFLE and 27 controls were enrolled. “Tiredness after awakening” and “spontaneous mid-sleep awakenings” were more frequent in NFLE patients than in controls (36.4% versus 11.1%, p = 0.04, and 50.0% versus 22.2%, p = 0.03). The frequency of excessive daytime sleepiness (EDS) did not differ between groups. Posthoc analysis showed that patients with a complaint of “midsleep awakenings” had higher ESS and BQS scores than those without (7.3 versus 4.3, p = 0.004, and 5.0 versus 2.2, p = 0.001, respectively) and more frequent “tiredness after awakening” (56.3% versus 18.8%, p = 0.03). Conclusions: Patients with NFLE have no pathological level of EDS with respect to controls. However, daytime sleepiness-related symptoms could be more frequent in a subgroup of patients with subjective disturbed sleep quality, irrespective of the perceived frequency of seizures.

Restless legs syndrome (RLS) augmentation, defined as a kind of suppression of the circadian rhythm of the disease in which sensory and motor symptoms appear earlier during the day (and over previously unaffected body parts), with a progressive phase advance until, backwards, the symptoms may cover the entire day, has been described only after treatment with dopaminergic drugs. We report clinical and polysomnographic accounts of a patient developing RLS augmentation after long-term treatment with tramadol, an opioid agonist with selectivity for mu-receptor and added norepinephrine and serotonin reuptake inhibition properties. Polysomnographic measures showed an improvement of RLS and a disappearance of diurnal sensory and motor RLS symptoms after tramadol was stopped. Our case confirms a recent retrospective report of augmentation of RLS after treatment with tramadol, and begs the question whether augmentation is truly restricted to dopaminergic drugs.

Seizures, namely in certain epileptic conditions, may be precipitated by sleep. Nocturnal frontal lobe epilepsy seizures, characterized by bizarre motor behaviour and autonomic activation, appear almost exclusively during sleep. The differential diagnosis between this condition and sleep-related non-epileptic paroxysmal motor phenomena, in particular the parasomnias, is arduous. Moreover, accepted criteria for the diagnosis of nocturnal frontal lobe seizures are lacking and even ictal scalp EEG recording could fail to disclose paroxysmal abnormalities. The clinical and polygraphic features of the different types of seizures in nocturnal frontal lobe epilepsy and of the more common non-epileptic paroxysmal events during sleep are described. The main differentiating features characterizing nocturnal frontal seizures are: onset at any age, several attacks per night at any time during the night, brief duration (s) with stereotyped motor pattern. As video-polysomnographic recordings of the attack, the gold-standard for diagnosis, are expensive and not readily available everywhere, home-made video recordings may be helpful. Further investigations on pathophysiology, genetics and epidemiology are needed to clarify the relationship between epileptic and non-epileptic sleep related paroxysmal phenomena.

Objective To evaluate the structure and quality of sleep and the circadian rhythm of body core temperature (BcT degrees ) in patients with drug-resistant chronic cluster headache (CH) before and during deep brain stimulation (DBS) of the posterior hypothalamus. Background Chronic CH is a severe primary headache and frequently associated with disturbances in sleep. Posterior hypothalamus DBS is performed as an effective treatment of drug-resistant chronic CH. The effects of posterior hypothalamus DBS on sleep and the circadian rhythm of BcT degrees are unknown. Methods Three male patients with chronic drug-resistant CH underwent 48-hour consecutive polysomnography (PSG) by means of the VITAPORT system with determination of BcT degrees by means of a rectal probe. Recordings were done before electrode implantation in the posterior hypothalamus and after optimized DBS of posterior hypothalamus. Results Before electrode implantation PSG showed nocturnal CH attacks, reduced sleep efficiency, fragmented sleep and increased periodic limb movements in sleep (PLMS). During DBS nocturnal CH attacks were abolished and sleep efficiency and PLMS improved. BcT degrees circadian rhythm was normal both before and during DBS. Conclusions Our data show that DBS of posterior hypothalamus in drug-resistant chronic CH is effective in curtailing nocturnal CH attacks, and is associated with improved sleep structure and quality. Chronic CH displays a normal circadian rhythm of BcT degrees, unchanged during hypothalamic DBS.

Previously referred to as “nocturnal myoclonus”, periodic limb movements in sleep (PLMS) is regarded as a distinct nosologic entity, although it overlaps a great deal with restless legs syndrome and other sleep disorders. While there is a lack of complete consensus on this matter, PLMS are regarded as pathological if more than five events occur per hour of sleep, and as a disorder (PLMD) if there is comorbid insomnia or daytime sleepiness in the absence of other symptoms. PLMS are common in healthy elderly individuals and have been reported to increase with age. The pathogenesis of PLMS is not clear. Lesion, imaging and laboratory studies indicate neuronal hyperexcitability with involvement of brain stem and spinal cord structures, in particular the central pattern generator for gait, and decreased dopaminergic transmission. Dopaminergic drugs, dopamine agonists, opiates, benzodiazepines and anticonvulsants are all used, with dopaminergic drugs or dopamine agonist regarded as first-line treatment.

Sleep-disordered breathing and sleep-related motor phenomena are part of the clinical spectrum of multiple system atrophy (MSA). Stridor has been attributed to denervation of laryngeal muscles or instead to dystonic vocal cord motion. We studied 3 patients with nocturnal stridor in the setting of MSA. All patients underwent nocturnal videopolysomnography (VPSG) with breathing and heart rate, O(2) saturation and intra-esophageal pressure recordings, and simultaneous EMG recordings of the posterior cricoarytenoid, cricothyroid, and thyroarytenoid muscles and continuous vocal cord motion evaluation by means of fiberoptic laryngoscopy. VPSG/EMG and fiberoptic laryngoscopy documented normal vocal cord motion without denervation during wake and stridor only during sleep when hyperactivation of vocal cords adductors appeared in the absence of significant O(2) desaturation. All patients had tachycardia and tachypnea and paradoxical breathing during sleep, erratic intercostalis and diaphragmatic EMG activity and Rem sleep behavior disorder. One of the patients had restless legs syndrome with periodic limb movement during sleep and excessive fragmentary hypnic myoclonus. In conclusion, our patients with MSA had nocturnal stridor due to sleep-related laryngeal dystonia. Stridor was associated with other abnormal sleep-related respiratory and motor disorders, suggesting an impairment of homeostatic brainstem integration in MSA.

Objective Periodic limb movements during sleep (PLMS) in Restless Legs Syndrome (RLS) are associated with arousals and stereotyped EEG and heart rate (HR) changes. We investigated PLMS-related EEG and HR variations in multiple system atrophy (MSA) in order to detect possible abnormalities in cortical and autonomic arousal responses. Methods Ten patients with MSA were contrasted against ten patients with primary RLS. Cortical (EEG) and autonomic (HR) variations associated with PLMS during NREM sleep were analysed by means of Fast Fourier Transform and HR analysis. In addition, we analysed the cyclic alternating pattern (CAP) during sleep, CAP representing a measure of the spontaneous arousal oscillations during NREM sleep. Results PLMS in RLS were associated with tachycardia and spectral EEG variations, beginning about 2 s before the onset of PLMS, and peaking 1–4 s after. The HR and spectral EEG variations were strikingly reduced or absent in MSA. MSA patients also had significantly lower CAP rate compared to RLS patients. Conclusions Blunted HR and EEG spectral changes adjacent to PLMS indicated impaired cortical and autonomic arousal responses during sleep in MSA patients. Significance PLMS, when present, may represent a useful means to study the arousal responses during sleep.

Study objectives To describe the clinical and videopolysomnographic characteristics of nocturnal eating episodes in sleep-related eating disorder. Design Descriptive study of outpatients prospectively enrolled in 2 sleep centers. Setting Videopolysomnographic recordings done in the sleep laboratory. Patients Thirty-five consecutive drug-free patients with nocturnal eating. Interventions N/A. Measurements and results Clinical interviews disclosed abnormal compulsory nocturnal eating episodes in all patients associated with a clinical report of sleepwalking (in 1), somniloquy (in 5), restless legs syndrome (in 8), and periodic limb movements during sleep (in 4). Videopolysomnography documented 45 episodes of nocturnal eating in 26 patients. Eating always occurred after complete awakenings from non-rapid eye movement sleep and only in 1 patient from REM sleep and was characterized by electroencephalographic alpha activity with no dissociated features of state-dependent sleep variables. Patients interviewed during the eating episodes were fully conscious and remembered the events the next day. Pathological periodic limb movements during sleep index was recorded in 22 and restless legs syndrome dyskinesias in 5 patients. Recurring chewing and swallowing movements during sleep were a feature in 29 patients, associated in about half of the events with electroencephalographic arousals. Conclusions In our patients, eating episodes occurred with normal consciousness and recall. Chewing or swallowing movements during sleep occurred frequently, resembling rhythmic masticatory-muscle activity in bruxism patients. The presence of periodic limb movements during sleep and chewing activity, the reported efficacy of dopaminergic medications, and the compulsory food-seeking behavior all argue for a dopaminergic dysfunction underlying the pathogenesis of sleep-related eating disorder.

Obtructive sleep apnoea syndrome (OSAS) is a common disorder in the general population with an estimated prevalence in an adult population of 2% in women and 4% in men. Although several studies have suggested that headaches, particularly morning headaches, are more common in patients with OSAS than in normal subjects, others have yielded contradictory findings. When the sleep-related breathing disorder was treated with success, the headache generally disappeared, supporting a causal role of the sleep disorder for headache. Several hypotheses have been proposed to explain the relationship between OSAS and the occurrence of headache, particularly on awakening. Night-time fluctuations of oxygen saturation during the night with hypercapnia, vasodilatation, increased intracranial pressure and impaired sleep quality are all considered contributing factors. However the exact mechanisms of headache pathogenesis and the relationship between OSAS, headache and morning headaches in particular remain controversial.

Augmentation, defined as a loss of circadian recurrence with progressively earlier daily onset and increase in the duration, intensity, and anatomy of symptoms, not compatible with the half-life of the drug, is associated with dopaminergic treatment in restless legs syndrome (RLS) patients. The pathogenesis of augmentation is unclear. We describe a patient with idiopathic RLS who developed augmentation after 8 months of levodopa treatment. Videopolysomnographic and pharmacokinetic studies with monitoring of plasma levodopa levels demonstrated marked motor hyperactivity during augmentation, with anarchic discharges of motor unit potentials, tonic grouped discharges and flexor spasms, associated with painful dysesthesia. Symptoms and signs of augmentation were related to low plasma levodopa levels, abating 75 minutes after oral levodopa administration and reappearing after 3 hours, closely mirroring the rapid rise and fall of plasma levodopa concentration. This case is the first report in which RLS augmentation is shown to be characterized by motor hyperkinesias paralleling levodopa plasma pharmacokinetic profile.

Studies comparing the efficacy of continuous positive airway pressure (CPAP) versus surgery in correcting cardiovascular abnormalities in OSAS are lacking. We describe an OSAS patient with hypertension who responded favorably to CPAP treatment, whereas subsequent uvulopalatopharyngoplasty (UPPP) was less successful. While CPAP markedly lowered daytime muscle sympathetic nerve activity (MSNA) and blood pressure (BP), findings after UPPP were comparable to pre-treatment baseline. Thus, parallel changes in MSNA and BP demonstrated treatment efficacy.

Different pathological conditions may lead to somnambulic automatisms arising from nocturnal sleep. Video polysomnography represents the diagnostic tool but, due to the difficulty of capturing complex episodes in the sleep laboratory, audio-video recordings at home of the episodes may help in the differential diagnosis also. Sleepwalking is a disorder of arousal in which the subject arises from deep sleep, even displaying long complex behaviour, including leaving the bed and walking, with memory impairment of the event. Disordered arousal mechanisms with an inability of the brain to fully awaken from slow-wave sleep are thought to lead to these motor automatisms. REM sleep behaviour disorders begin during REM sleep and are accompanied by features of REM sleep. The motor behaviour may be violent and injurious to the patient and/or bed partner. In some patients, however, the behaviour may be similar to that observed in sleepwalking and some patients have an overlap syndrome. In nocturnal frontal lobe epilepsy in particular, and in complex partial seizures in general, stereotypic and repetitive motor attacks may recur, at any time, on the same night and on different nights, with a continuum between minimal or minor attacks and major or prolonged episodes up to agitated epileptic nocturnal wanderings.

Three patients presented with a 25-, 15-, and 5-year history of restless legs syndrome (RLS) and periodic limb movements during sleep (PLMS). For 1, 4, and 5 years, they reported additional involuntary trunk and limbs jerks preceding falling asleep and occasionally during intrasleep wakefulness. Videopolysomnography revealed jerks during relaxed wakefulness arising in axial muscles with a caudal and rostral propagation at a slow conduction velocity, characteristic of propriospinal myoclonus (PSM). Jerk-related EEG-EMG back-averaging did not disclose any preceding cortical potential. During relaxed wakefulness preceding falling asleep and during intrasleep wakefulness, PSM coexisted with motor restlessness and sensory discomfort in the limbs. PSM disappeared when spindles and K-complexes appeared on the EEG. At this time, typical PLMS appeared every 20 to 40 seconds, especially during light sleep stages. PLMS EMG activity was limited to leg, especially tibialis anterior muscles, and did not show propriospinal propagation. In one patient, alternating leg muscle activation was also present. Jerks with a PSM pattern represent another motor phenomenon associated with RLS and different from the more usual PLMS.

Objective To ascertain the presence of abnormalities of sleep in patients with continuous motor unit activity with and without symptoms of central nervous system involvement. Methods Five patients with isolated neuromyotonia (Isaacs' syndrome) and 1 patient with Morvan syndrome underwent 24-h videopolysomnographic recording to investigate sleep structure, motor activities and autonomic variables during sleep. Results Macro- and microstructural organization of sleep and of the attending autonomic variables were substantially normal in patients with Isaacs' syndrome. On the contrary, sleep structure was severely disrupted with subcontinuous dream enactment and hallucinations in the patient with Morvan syndrome. The pattern of the neuromyotonic discharges, however, was not different between the patients with Isaacs' syndrome compared to Morvan syndrome, the EMG discharges persisting throughout the 24 h of recording and affecting wakefulness and sleep equally. Conclusions Neuromyotonia is compatible with normal organization of sleep. The severe sleep abnormalities observed in Morvan syndrome cannot be simply attributed to the effects of neuromyotonia of peripheral origin. Significance Even though neuromyotonia is common to both Isaacs' and Morvan syndromes, the two conditions differ significantly in regard to CNS involvement with sleep abnormalities and lumping the two conditions together is not justified on clinical and neurophysiological grounds.

Sleep-related eating disorder (SRED) is characterized by recurrent arousals from sleep associated with compulsive ingestion of food. No controlled therapeutic trials are available for SRED. We assessed the safety, tolerability and efficacy of pramipexole, a dopamine D3-receptor agonist, in the treatment of SRED. Eleven consecutive patients with SRED in the absence of concurrent daytime eating disorders underwent actigraphic recording and subjective sleep diary evaluation for a week before and every week for 2 weeks of treatment with pramipexole 0.18-0.36 mg or placebo, administered in a double-blind crossover randomized sequence. The primary outcomes of the trial were actigraphic measures of night sleep parameters (sleep efficiency, motor activity mean and median, number and duration of wake episodes), secondary outcomes were the number of good sleep nights/weekly, number and duration of nocturnal awakenings/night, and visual analogue preference score. Pramipexole was well tolerated without any patient withdrawing from the study. Pramipexole reduced night-time activity median (P = 0.02) and increased the number of nights of good sleep/week (P = 0.02). All other measurements remained unaffected. Pramipexole at low doses was well tolerated, improving some measures of sleep quality and reducing median night activity in SRED. Further studies with higher dosages and for longer time-periods are warranted.

We describe the clinical, neurophysiological and polysomnographic characteristics of some involuntary motor nocturnal events occurring during sleep or at the transition from wakefulness to sleep.

A patient with nocturnal frontal lobe epilepsy characterized by paroxysmal motor attacks during sleep had brief paroxysmal arousals (PAs), complex episodes of nocturnal paroxysmal dystonia, and epileptic nocturnal wandering since childhood. Ictal SPECT during an episode of PA demonstrated increased blood flow in the right anterior cingulate gyrus and cerebellar cortex with hypoperfusion in the right temporal and frontal associative cortices.

After surgery for a tegmental ponto-mesencephalic cavernoma, a patient developed sleep-related excessive fragmentary myoclonus, diffuse myoclonic jerks, simple quasipurposeful movements of the limbs, and rapid eye movement (REM) sleep behaviour disorder as motor features of status dissociatus, a condition in which elements of one state of being (wake, NREM and REM sleep) pathologically intrude into another.