Sleep-related Hallucinations Research Articles

Management of Excessive Daytime Sleepiness in Narcolepsy With Baclofen

BackgroundNarcolepsy is a disabling sleep-wake disorder characterized by the pentad symptoms of excessive daytime sleepiness, sleep paralysis, sleep fragmentation, sleep-related hallucinations, and cataplexy. There is no curative therapy for narcolepsy. Treatment is therefore symptom directed. Symptom management is generally directed at improving excessive daytime sleepiness, sleep fragmentation, and cataplexy. First-line treatment for excessive daytime sleepiness is typically daily use of wake-promoting agents, such as modafinil or armodafinil, or stimulant therapy, such as methylphenidate or amphetamines. Alternatively, sodium oxybate can be used nightly for improved cataplexy, sleep consolidation, and following day wakefulness. These therapies can be limited in some patients because of inadequate efficacy, poor tolerability, or side effects. MethodsWe describe five narcolepsy patients with severe excessive daytime sleepiness who had an inadequate response or experienced side effects with the initial therapies but had a positive response to treatment with baclofen. ResultsThese patients reported subjective improvement in sleep maintenance without fragmentation and daytime sleepiness. Average Epworth Sleepiness Scale assessment before treatment was 15.8 with post-treatment assessment being 10.4 (P < 0.05). ConclusionsBaclofen may be an effective treatment for excessive daytime sleepiness and sleep fragmentation in narcolepsy and warrants further study.

Therapeutic Symptomatic Strategies in the Parasomnias.

The purpose of this review was to discuss the currently available pharmacologic and non-pharmacologic treatment options for parasomnias. Recent pathophysiological findings about sleep structure in parasomnias helped understanding several drug mechanisms of action. Serotoninergic theory accounts for the effect of serotoninergic drugs. Study about spectral analysis of sleep showed the effect of clonazepam on spectral bands. Cannabinoids proved to be effective in some of parasomnias, as in many other neurological disorders. A series of therapeutic strategies were analyzed and compared. Benzodiazepines, antidepressant drugs, and L-5-hydroxytryptophan may be beneficial in DOA. SSRI and topiramate are effective in SRED. RBD responds to clonazepam, melatonin, and to a lesser extent to dopaminergic and anticholinergic agents. Prazosin and cannabinoids are effective in nightmare disorder. Sleep paralysis may respond to antidepressant agents. Tricyclic antidepressant may be effective in sleep-related hallucinations and exploding head syndrome. Sleep enuresis may be successfully treated with desmopressin, anticholinergic drugs, and imipramine.

On "Hearing" Voices and "Seeing" Things: Probing Hallucination Predisposition in a Portuguese Nonclinical Sample with the Launay-Slade Hallucination Scale-Revised.

The experience of hallucinations is a hallmark of psychotic disorders, but they are also present in other psychiatric and medical conditions, and may be reported in nonclinical individuals. Despite the increased number of studies probing the incidence of nonclinical hallucinations, the underlying phenomenological characteristics are still poorly understood. This study aimed to examine the psychometrics proprieties of the Portuguese adaptation of the 16-item Launay-Slade Hallucinations Scale (LSHS), the phenomenological characteristics of nonclinical hallucinatory experiences in a Portuguese sample, and the relationship between clinical symptoms and hallucination predisposition. Three-hundred-and-fifty-four European Portuguese college students completed the LSHS. Of those, 16 participants with high LSHS scores and 14 with low LSHS scores were further screened for clinical symptoms. A three-factor solution for the LSHS Portuguese version proved to be the most adequate. Intrusive or vivid thoughts and sleep-related hallucinations were the most common. Although, fundamentally perceived as positive experiences, all types of hallucinations were described as uncontrollable and dominating. However, the more pleasant they were perceived, the more controllable they were assessed. In addition, hallucination predisposition was associated with increased clinical symptoms. These results corroborate the lower severity of hallucinations in the general population compared to psychotic individuals. Further, they support an association between clinical symptoms and increased vulnerability to hallucinations. Specifically, increased schizotypal tendencies and negative mood (anxiety and depression) may be related to increased psychotic risk.

What Is the Link Between Hallucinations, Dreams, and Hypnagogic-Hypnopompic Experiences?

By definition, hallucinations occur only in the full waking state. Yet similarities to sleep-related experiences such as hypnagogic and hypnopompic hallucinations, dreams and parasomnias, have been noted since antiquity. These observations have prompted researchers to suggest a common aetiology for these phenomena based on the neurobiology of rapid eye movement (REM) sleep. With our recent understanding of hallucinations in different population groups and at the neurobiological, cognitive and interpersonal levels, it is now possible to draw comparisons between the 2 sets of experiences as never before. In the current article, we make detailed comparisons between sleep-related experiences and hallucinations in Parkinson's disease, schizophrenia and eye disease, at the levels of phenomenology (content, sensory modalities involved, perceptual attributes) and of brain function (brain activations, resting-state networks, neurotransmitter action). Findings show that sleep-related experiences share considerable overlap with hallucinations at the level of subjective descriptions and underlying brain mechanisms. Key differences remain however: (1) Sleep-related perceptions are immersive and largely cut off from reality, whereas hallucinations are discrete and overlaid on veridical perceptions; and (2) Sleep-related perceptions involve only a subset of neural networks implicated in hallucinations, reflecting perceptual signals processed in a functionally and cognitively closed-loop circuit. In summary, both phenomena are non-veridical perceptions that share some phenomenological and neural similarities, but insufficient evidence exists to fully support the notion that the majority of hallucinations depend on REM processes or REM intrusions into waking consciousness.

Isolated nocturnal auditory hallucinations: a case report

Sleep-related hallucinations (hypnagogic and hypnopompic) are transient and occur in normal individuals. Rarely, they are prominent and distressing and are associated with diverse conditions including narcolepsy. We report a case of prominent hypnopompic auditory hallucinations — which gradually became continuous and distressing with characteristics of schizophrenia-like hallucinations — that responded to a low dose of olanzapine.

Parasomnier

Parasomnias are undesirable experiences or motoric phenomena that occur in association with sleep. We have described characteristics of parasomnia subtypes. This review is based on the authors' research and clinical experience, and articles identified by non-systematic searches of Pubmed. Parasomnias are categorized into disorders of arousal (non-REM sleep parasomnias), e.g. sleepwalking, sleep terrors and confusional arousals, parasomnias associated with REM sleep, e.g. nightmare disorder, REM sleep behaviour disorder and recurrent isolated sleep paralysis, and other parasomnias, e.g. sleep-related groaning, exploding head syndrome, sleep-related hallucinations and sleep-related eating disorder. Prevalences for the subtypes vary. Most parasomnias are especially common in children. Drug treatment is seldom necessary, but may be indicated in severe cases.

Trying to understand sleep in Parkinson's disease patients*

The correct diagnosis of sleep disorders in Parkinson’s Disease (PD) patients consists in: detailed anamnesis of the patient and of the spouse or of the caregiver; 1 week recording on a symptom diary (log) by the patient or the caregiver; pointing out the co-morbidities and selection of the most appropriate sleep test such as: polysomnography, multiple sleep latency test, multiple wake latency test, Epworth Sleepiness Scale, actigraphy, or video-PSG. The sleep-arousal disturbances considered by the present article, in order to achieve a better quality of life for Parkinson’s disease patients are: light fragmented sleep; abnormal motor activity during sleep; REM behavior disorders; sleep related breathing disorders; sleep related hallucinations; sleep related psychotic behavior. The arousal disturbances to be described are: sleep attacks, and excessive daytime sleepiness.

Sleep disturbances in Parkinsonism.

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.

Approaching disturbed sleep in late Parkinson's Disease: first step toward a proposal for a revised UPDRS

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 fragmented sleep (LFS) 44. Sleep-related breathing disorders (SRBD) 45. Restless legs-periodic leg movements during sleep (RLS-PLM) 46. REM behavior 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.

The clinical spectrum of narcolepsy and idiopathic hypersomnia.

To better define the clinical spectra of narcolepsy and idiopathic hypersomnia, we retrospectively compared clinical and polygraphic findings and questionnaire results in groups of subjects with narcolepsy with or without cataplexy, idiopathic hypersomnia, insufficient sleep syndrome, mild sleep apnea, and excessive daytime sleepiness not otherwise specified. Sleep paralysis and sleep-related hallucinations were most frequent in narcolepsy-cataplexy, but their frequency did not differ between narcolepsy without cataplexy and idiopathic hypersomnia. Mean durations of nocturnal sleep, daytime naps, and morning grogginess were not increased in idiopathic hypersomnia compared with other groups. Among subjects without cataplexy, symptoms of sleep paralysis and sleep-related hallucinations were equally common in subjects with and without frequent sleep-onset REM periods. These findings suggest that the occurrence of these symptoms in subjects without classical narcolepsy-cataplexy is a function of factors other than a propensity for early onset of REM sleep and indicate a need to reevaluate diagnostic criteria for narcolepsy and idiopathic hypersomnia.