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A case of an adult female patient with jactatio capitis nocturnus evaluated in a sleep disorders center is reported. the unusual characteristics included symptoms initiating in early childhood and becoming more frequent with age, specifically observed during REM sleep. The occurrence in a 2-year-old son indicates the familial aspects of this syndrome.
The authors present a case of the Kleine-Levin syndrome, and review the literature to assess the various ways this illness can appear. Psychiatric manifestations not only obscure the diagnosis, but may lead to inappropriate treatment.
Six female rape victims with posttraumatic stress disorder (PTSD) were assessed for sleep disturbances. Five responded to cognitive-behavioral therapy (CBT) and one did not complete treatment. Sympatho-vagal balance was measured using heart rate variability (HRV) during rapid eye movement (REM) sleep. The treatment responders significantly decreased on HRV while the noncompleter increased. The responders also significantly decreased on sleep disturbances. The noncompleter remained unchanged. Thus a remission in PTSD symptoms following CBT accompanied a reduction in the HRV indicator of sympathetic predominance in REM sleep.
Shy-Drager syndrome (SDS) is associated with a myriad of autonomic and neurologic impairments, including sleep disturbances. A review of the literature reveals that there are no reports of SDS presenting with an abnormality of sleep. The following case report describes a patient who was diagnosed with SDS approximately one decade after initially presenting with a progressive, polysomnographically confirmed disturbance of sleep--specifically, an REM behavioral disorder (RBD).
Recent years have seen significant advances in sleep disorders medicine, including effective treatments for chronic psychophysiological insomnia and obstructive sleep apnea syndrome; greater understanding of biological rhythms and of the nature of sleep in depression, including seasonal affective disorder; and the discovery of REM behavior disorder. The author reviews selected developments in the sleep disorders field over the last three years. Developments are presented in the framework of the diagnostic classification of the American Sleep Disorders Association, with emphasis on areas relevant to the practice of psychiatry.
A 9-month-old, female Labrador retriever mix was presented for two types of seizure-like episodes, one of which occurred only during sleep. The two types of episodes were morphologically distinct. An electroencephalogram (EEG) demonstrated that the sleep-associated episodes occurred during rapid eye movement (REM) sleep, supporting a diagnosis of a REM behavior disorder. Based on their morphology and response to antiseizure medications, the waking episodes were diagnosed as seizures. The animal was also diagnosed with an obsessive-compulsive and generalized anxiety disorder. The REM behavior disorder and anxiety-related behaviors improved with tricyclic antidepressant therapy.
A subjective disturbance of sleep, including the occurrence of repetitive, stereotypical anxiety dreams, is characteristic of posttraumatic stress disorder (PTSD). The phenomenology of the PTSD anxiety dream has seemed most consistent with an underlying rapid eye movement (REM) sleep dysfunction. However, motor behavior reportedly can accompany PTSD dreams, and normal REM sleep typically involves a nearly total paralysis of the body musculature. As a means of understanding this discrepancy, anterior tibialis muscle activity during sleep was studied in a group of Vietnam combat veterans with current PTSD and in an age-matched normal control group. The PTSD subjects had a higher percentage of REM sleep epochs with at least one prolonged twitch burst; they also were more likely to have periodic limb movements in sleep, during nonrapid eye movement sleep. Both these forms of muscle activation also have been observed in REM behavior disorder (RBD), a parasomnia characterized by the actual enactment of dream sequences during REM sleep. The identification of RBD-like signs in PTSD adds to the evidence for a fundamental disturbance of REM sleep phasic mechanisms in PTSD.
BACKGROUND: Autosomal dominant spinocerebellar ataxia type 2 (SCA2) bears clinical and neuropathologic similarities to sporadic multisystem atrophy (MSA) or Parkinson disease, in which sleep pathology is well documented. However, those clinical entities have a marked variability of the reported sleep disturbances, and their etiology is heterogeneous. In contrast, the study of SCA2 provides an opportunity to examine a molecularly homogeneous patient group, in which disease stages can be defined not only based on disease duration and ataxia scores, but also with regard to modulatory effects of mutation size. OBJECTIVE: To examine the presence and progression of sleep pathology in SCA2. METHODS: We analyzed eight patients with disease durations of 3 to 31 years, all with medium size SCA2 expansions (CAG 38 to 49), using clinical scores, sleep interviews, and video-polysomnography (VPSG) recordings. RESULTS: Almost all patients reported good subjective sleep quality and negated incidents of REM behavior disorder (RBD). At early disease stages, however, REM without atonia in four patients' VPSG suggested subclinical RBD. This was accompanied by a consistent reduction of REM density. In three patients at later SCA2 stages, REM sleep was undetectable, whereas slow wave sleep (SWS) was markedly increased at the cost of light sleep. Periodic leg movements, apnea, or hypopnea were not prominent. CONCLUSIONS: Progressive loss of dream recall in spinocerebellar ataxia type 2 was found and correlated with stages of REM more than non-REM pathology in video-polysomnography. These stages correspond to the progressive atrophy from the pons, nigrostriatal projection, and locus ceruleus to the thalamus.
OBJECTIVE: Current guidelines for the treatment of children with obstructive sleep apnea (OSA) suggest that primary snoring (PS) in children is benign. However, PS has not been well evaluated, and it is unknown whether PS is associated with serious morbidity. This study investigated whether PS is associated with neurobehavioral deficits in children. METHODS: Parents of 5- to 7-year-old snoring children in public schools were surveyed about their child's sleeping habits. Children with a history of snoring and nonsnoring children were invited for overnight polysomnographic assessment and a battery of neurobehavioral tests. Only children who did not have a history of attention-deficit/hyperactivity disorder and were not considered hyperactive by parental report were tested. RESULTS: Children with a history of snoring, an obstructive apnea index of <1/hour of total sleep time (hrTST), an apnea/hypopnea index <5/hrTST, and no gas exchange abnormalities were classified as PS (n = 87). Control subjects were defined as children without a history of snoring, an obstructive apnea index <1/hrTST, an apnea/hypopnea index <5/hrTST, and no gas exchange abnormalities (n = 31). Although means for both groups were in the normal range, the PS children were found to perform worse on measures related to attention, social problems, and anxious/depressive symptoms. In addition, although within the normal range, both overall cognitive abilities and certain language and visuospatial functions were significantly lower for the PS group than for the control subjects. CONCLUSIONS: PS seems to be associated with significant neurobehavioral deficits in a subset of children, possibly related to increased susceptibility to sleep fragmentation. Larger studies are urgently required because current guidelines for treatment of snoring in children may require reevaluation.
The prevalence and role of sleep disorders in the sexual problems of diabetic patients remain unexplored. This study was conducted on 40 diabetic men carefully screened to exclude the confounding effects of other medical illnesses or drugs likely to impair sexual function and 40 age-matched healthy volunteers. They underwent an extensive psychosexual interview, medical and psychiatric evaluations, and three recorded nights in a sleep laboratory. Electroencephalogram, eye movements, muscle tone, and nocturnal penile tumescence were monitored continuously. Respiratory airflow and bilateral anterior tibialis recordings were obtained during the first sleep session. Diabetic men had significantly higher prevalences of respiratory and periodic leg movement disturbances during sleep. There was clinical, although not nocturnal penile tumescence, evidence suggesting that respiratory abnormalities during sleep are associated with erectile difficulties in diabetic men. Future studies should include blood oxygenation and respiratory effort measures to clarify the significance of sleep-related airflow disturbances in diabetic patients.
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Rapid eye movement (REM) sleep disturbance is associated with several psycho-behavioral disorders, hence, it is important to understand its neural mechanism of regulation. Although it was known that the noradrenergic (NA-ergic) neurons from locus coeruleus (LC) project to the pedunculopontine tegmentum (PPT), the role of noradrenaline (NA) alone and in association with GABA, an inhibitory neurotransmitter, in PPT for REM sleep regulation was not known and was investigated in this study in freely moving normally behaving rats. Rats were surgically prepared for electrophysiological sleep-wake recording and simultaneous bilateral microinjections into PPT. 200nl of prazosin (alpha1-antagonist) or clonidine (alpha2-agonist) or propranolol (beta-antagonist) or combination of picrotoxin (GABA-A antagonist) and clonidine or vehicle (control) was microinjected bilaterally into PPT using a remote-controlled pump and the effects on REM sleep compared. Prazosin, clonidine and propranolol increased the total time spent in REM sleep whereas co-injection of picrotoxin and clonidine did not affect REM sleep. The results suggest that NA in PPT tonically inhibits REM sleep, possibly by acting on the cholinergic REM-ON neurons, while GABA inhibits the release of NA for REM sleep regulation. A model of neural connections explaining such regulation has been presented.
The reexperiencing of a traumatic event in the form of repetitive dreams, memories, or flashbacks is one of the cardinal manifestations of posttraumatic stress disorder (PTSD). The dream disturbance associated with PTSD may be relatively specific for this disorder, and dysfunctional REM sleep mechanisms may be involved in the pathogenesis of the posttraumatic anxiety dream. Furthermore, the results of neurophysiological studies in animals suggest that CNS processes generating REM sleep may participate in the control of the classical startle response, which may be akin to the startle behavior commonly described in PTSD patients. Speculating that PTSD may be fundamentally a disorder of REM sleep mechanisms, the authors suggest several strategies for future research.
A 52 year-old male patient, had complaint of "restless sleep". His wife informed that for the past ten years the patient had presented intense and aggressive body movements, and sometimes, violent dreams. The patient also complained of excessive daytime sleepiness. His relevant previous medical history included a traumatic brain injury at the age of 28 which left him in coma for two months. A video-polysomnography showed periodic leg movements and, during REM sleep, aggressive and agitated behaviour. The multiple sleep latency test revealed extremely short latencies. Initially, he was treated with levodopa-benzerazide, 100/25 mg, 2 hours before bedtime. After 10 weeks his overnight behaviour pattern improved and leg movements diminished. This case supports the hypothesis of an association between cranial trauma and alterations in the dopaminergic pathways represented by periodic leg movements during sleep and a sleep behaviour disorder and proposes the possibility of hypothalamic hypocretin involvement in its pathophysiology.
BACKGROUND: Patients with PD can have disabling visual hallucinations associated with dopaminergic therapy. Sleep disorders, including vivid dreams and REM sleep with motor behaviors (RBD), are frequent in these patients. METHODS: The association of hallucinations and REM sleep both at night and during the day was examined in 10 consecutive nondemented patients with long-standing levodopa-responsive PD and hallucinations. Seven patients presented with paranoia and paranoid delusions. Overnight sleep recordings and standard multiple daytime sleep latency test were performed. The results were compared to those of 10 similar patients with PD not experiencing hallucinations. RESULTS: RBD was detected in all 10 patients with hallucinations and in six without. Although nighttime sleep conditions were similar in both groups, hallucinators tended to be sleepier during the day. Delusions following nighttime REM period and daytime REM onsets were observed in three and eight of the hallucinators, and zero and two of the others. Daytime hallucinations, coincident with REM sleep intrusions during periods of wakefulness, were reported only by hallucinators. Postmortem examination of the brain of one patient showed numerous Lewy bodies in neurons of the subcoeruleus nucleus, a region that is involved in REM sleep control. CONCLUSION: The visual hallucinations that coincide with daytime episodes of REM sleep in patients who also experience post-REM delusions at night may be dream imagery. Psychosis in patients with PD may therefore reflect a narcolepsy-like REM sleep disorder.
One theory about the pathogenesis of endogenous depression is that decreased serotonergic (5-HT) neurotransmission is involved in producing the disorder. A key component of brain 5-HT neurotransmission is the discharge rate of 5-HT neurons in the dorsal raphe nucleus (DRN), a major aggregation of 5-HT neurons. We tested the hypothesis that the discharge rate of 5-HT neurons in the DRN was decreased in a new animal (rat) model of human endogenous depression. In this model, rats are treated neonatally with the antidepressant chlorimipramine. When adult, these animals exhibit several behavioral, REM sleep, and treatment response features of the human disorder. We found in a single unit measurements in adult, pentobarbital-anesthetized rats that, compared with 'non-depressed' control rats, the 'depressed' rats had a lower discharge rate of 5-HT neurons in the DRN. This correlation is consistent with the theory that 5-HT neurotransmission is diminished in endogenous depression.
Headbanging is a rhythmic movement disorder (RMD) along with headrolling, bodyrocking and bodyrolling. The International Classification of Sleep Disorders defines RMD as a group of stereotyped, repetitive movements involving large muscles, usually of the head and neck, that typically occur immediately prior to sleep onset and are sustained into light sleep. The average onset is 9 months, and by 10 years of age the majority of subjects no longer complain of headbanging. If it continues, it is usually associated with mental retardation of autism. Headbanging is said to occur during presleep drowsiness or early non-rapid eye movement sleep. Often there is no need for treatment other than reassurance. Behavior modification has had little success. Benzodiazepines (such as oxazepam and diazepam) and tricyclic antidepressants have been used with variable success. We present two cases of headbanging with polysomnographic findings and treatment. The patients are two healthy adult males. They both experienced significant daytime somnolence and repeatedly wakened their partners. Only one of our patients had recorded head movements during his overnight sleep study. There was evidence of headbanging during stage 1 and stage 2 sleep but also during slow wave sleep. Headbanging was recorded during 14% of the epochs. Both patients responded to treatment with clonazepam (at a dose of 1.0 mg nightly) with decreased frequency and severity of headbanging. Although headbanging is most common in childhood, there may be significant number of cases that persist into adulthood. To our knowledge, this is the first report of the treatment of headbanging with clonazepam. Both patients benefited from this treatment.