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At least 127 records · Page 7Linked to original sources

PubMed1994

Fluoxetine suppresses human cataplexy: a pilot study.

We evaluated fluoxetine in six patients with poorly controlled cataplexy by beginning patients on a single 20 mg dose without any change in their current medications. Once benefit occurred, we discontinued or reduced other anticataplectic medication. Reduction in the number of cataplectic episodes per week after 20 weeks of treatment constituted the basis for efficacy determination. Patients experienced a mean reduction of 92% (a mean drop in frequency of 21.7 to 1.7 episodes per week). Although fluoxetine-induced headache occurred in one patient, the other five reported no side effects at the doses used. The results of this pilot study demonstrate that fluoxetine safely and effectively suppresses cataplexy and reduces the need for other, less desirable, anticataplectic agents.

Aged↗

PubMedDate not supplied

[Accidents prevalence in a group of patients with the narcolepsy- cataplexy syndrome].

INTRODUCTION: Recent studies have shown statistically that the proportion of accidents at work, at home and on the roads is greater in narcoleptic patients than in the general population. OBJECTIVE: The object of this study is to show the high prevalence of the risk of accidents in patients diagnosed as having the narcolepsy-cataplexy syndrome. PATIENTS AND METHODS: We studied a group of 35 patients of both sexes, diagnosed in the Sleep Pathology Unit of our hospital between 1994 and 1998 as having the narcolepsy-cataplexy syndrome. They filled out a questionnaire to find the prevalence of accidents. The data obtained regarding the type and number of accidents, their causes, gravity, legal and economic consequences were compared with those obtained in a group of 25 healthy subjects using the chi squared test. RESULTS: The results showed a higher risk of accidents in narcoleptic as compared with normal persons, with a statistically significant difference between the two groups. CONCLUSIONS: This study has shown the greater risk of accidents in these patients and the need for diagnosis as soon as possible so as to establish suitable treatment and thus improve their own personal safety and that of those around them.

Accidents, Traffic↗

PubMed2000

Systemic administration of hypocretin-1 reduces cataplexy and normalizes sleep and waking durations in narcoleptic dogs.

Recent work has implicated the hypocretin (orexin) system in the genesis of narcolepsy. In the current study we demonstrate that systemically administered hypocretin-1 (Hcrt-1) produces an increase in activity level, longer waking periods, a decrease in REM sleep without change in nonREM sleep, reduced sleep fragmentation and a dose dependent reduction in cataplexy in canine narcoleptics. Repeated administration of single daily doses of Hcrt-1 led to consolidation of waking and sleep periods and to a complete loss of cataplexy for periods of three or more days after treatment in animals that were never asymptomatic under control conditions. Systemic administration of Hcrt-1 may be an effective treatment for narcolepsy.

Animals↗

PubMed1979

Severe hypermotility during sleep in treatment of cataplexy with clomipramine.

A case of narcolepsy with marked cataplexy is described in detail. Clomipramine hydrochloride effectively controlled the cataplexy and partially alleviated the daytime sleep attacks. However, clomipramine treatment resulted in episodes of severe motor hyperactivity during sleep, which were most intense during rapid eye movement sleep.

Cataplexy↗

PubMed1998

[Hypersomnia. Narcolepsy-cataplexy (Gélineau syndrome)].

SIGNS AND SYMPTOMS: Narcolepsy is the most prevalent of the primary disorders of vigilance. It is relatively easy to identify in presence of clearcut cataplexy and other REM-sleep related symptoms, i.e. sleep paralysis and hypnagogic hallucinations. Otherwise, one must rely on demonstration of sleep onsets in REM during night and daytime polygraphy, and on the very strong association with the HLA gene DQB1*0602. TREATMENT: With the advent of modafinil, treatment of narcolepsy has been substantially modified. New strategies are an improvement over amphetamines both in terms of side effects and long-term outcome. Most cataplectic attacks can be controlled by tricyclics or other antidepressants. PATHOGENESIS: Major advances in pathophysiology and etiology have been obtained through an animal model of the disease, canine narcolepsy. Pharmacological studies point to the importance of alpha-1 adrenergic mechanisms in cataplexy, while dopaminergic systems seem more involved in generating sleepiness. As concerns genetics of this autosomal recessive disease, there is an equivalent of the human HLA association in the form of an immunoglobulin gene (mu-switch) linkage. Narcolepsy research is now looking for other genes, for which familial cases may give clues.

Animals↗

PubMed1982

Narcolepsy-cataplexy. I. Clinical and electrophysiologic characteristics.

The development, clinical course, and electrophysiologic characteristics of narcolepsy were evaluated in 50 adults who had a current complaint of sleep attacks and cataplexy. In most of the patients, the first symptoms, usually excessive daytime sleepiness and sleep attacks, developed during childhood or adolescence. The condition was invariably chronic. Patients frequently had family histories of some disorder of excessive daytime sleepiness. In nocturnal sleep or daytime nap recordings, all but three of the patients demonstrated a rapid-eye-movement (REM) period at sleep onset. Sleep apnea was found in only one patient. Our findings indicate that sleep laboratory recordings to detect a sleep-on-set REM period are of little diagnostic value when the narcoleptic patient has cataplexy. Furthermore, narcoleptic patients require sleep laboratory evaluation for sleep apnea only when the presence of apnea is suggested by the sleep history.

Adolescent↗

PubMed2005

Narcolepsy-cataplexy: how does recent understanding help in evaluation and treatment.

Narcolepsy is a substantially disabling disease with profound physical, mental, and social effects. The burden on patients is compounded by delayed and missed diagnoses and by the subsequent undertreatment of narcolepsy and associated symptoms such as cataplexy. The recent advances in the elucidation of the genetics of canine narcolepsy and the pathophysiologic role of hypocretin, in animals and humans, enhances current diagnostic capability and will provide better treatment modalities in the future. The varied symptoms of narcolepsy are challenging to manage and may require treatment with a combination of agents. The recent development of a markedly enhanced characterization of sodium oxybate in the treatment of the excessive daytime sleepiness, nocturnal sleep fragmentation, and cataplexy of narcolepsy offers the potential of treating multiple symptoms simultaneously and marks a dramatic advance in the treatment of narcolepsy.

Journal Article↗

PubMed2000

Presumed REM sleep behavior disorder arising from cataplexy and wakeful dreaming.

REM sleep behavior disorder (RBD) is an injurious parasomnia occasionally associated with narcolepsy. RBD usually occurs within REM sleep. We report a case of RBD in a narcoleptic patient arising from cataplexy and wakeful dreaming. The problem of state boundary control inherent in narcolepsy together with the pharmacological effects of tricyclic antidepressants used to treat cataplexy are usually the reason of RBD in narcoleptics. By similar mechanism our patient has presumed RBD out of REM intrusions into wakefulness.

Journal Article↗

PubMed1999

Clinico-polysomnographic diagnostics of narcolepsy-cataplexy.

INTRODUCTION: The introduction of polysomnography changed considerably our knowledge about narcolepsy. The aim of our study was to present the clinical picture and diagnostic criteria of narcolepsy based on our own research data. MATERIAL AND METHODS: The study comprises 22 consecutive patients with a mean age of 39.8 years, SD = 16.4, age range 7-78 years. The following methods were used: neurological, physical and mental status examination, specially designed questionnaires, nocturnal polysomnography, MSLT. RESULTS: The following clinical manifestations were observed: excessive daytime sleepiness (EDS) in 95.45% of the cases, cataplexy attacks (CA) in 77.27%, hypnagogic hallucinations (HH)--in 77.27%, sleep paralysis (SP)--in 54.54% and subjectively disturbed nocturnal sleep--in 72.72%. The mean ages of occurrence of the respective symptoms were as follows: EDS--32.14 +/- 10.15 years, CA--28.70 +/- 11.70 years, HH--36.70 +/- 8.82 years, SP--35.53 +/- 15.50 years and for the disease as a whole--39.82 +/- 15.50 years. At MSLT the mean sleep latency was 165.91 +/- 16.37 seconds and the mean REM latency--207.96 +/- 14.09 seconds. During the nighttime sleep the mean sleep latency was less than 5 minutes and the mean REM latency--less than 7 minutes. The sleep structure showed: NREM sleep, stage 1,2--66.30 +/- 4.1%, stage 3,4--5.52 +/- 4.1%, REM sleep--25.65 +/- 2.3%. The clinical picture presented 4 symptoms in 31.81%, 3 symptoms--in 50.00%, 2 symptoms--in 9.09% and 1 symptom in 9.09% of the cases. CONCLUSIONS: 1. The onset of narcolepsy is at about 30 years of age. 2. The clinical picture of narcolepsy is characterized by 2 major symptoms--excessive daytime sleepiness, attacks of cataplexy and 3 minor symptoms--sleep paralysis, hypnagogic hallucinations and disturbed nighttime sleep which may be found in various combinations. 3. Nocturnal polysomnography demonstrates characteristic changes in sleep structure. 4. MSLT ascertains shorter sleep latency and sleep onset rapid eye movements periods (SOREMs) of less than 5 minutes. 5. The presence of one of the major symptoms and SOREMs is sufficient for confirming the diagnosis of narcolepsy.

Adolescent↗

PubMed2006

Reduced hypothalamic gray matter in narcolepsy with cataplexy.

OBJECTIVES: Narcolepsy with cataplexy is associated with a loss of hypocretin. The question is, if there is an autoimmune or neurodegenerative process selectively killing the hypothalamic hypocretin-containing neurons or if these cells survive but fail to produce hypocretin. To support one of these hypothesis we aimed to detect structural changes in the hypothalamus of narcoletic patients. MATERIALS AND METHODS: Nineteen narcoleptic patients were compared to 16 healthy controls. We used voxel-based morphometry (VBM), an unbiased MRI morphometric method with a high sensitivity for subtle changes in gray and white matter volumes to investigate hypothalamic region in this condition. RESULTS: Classical MRI protocol revealed no structural abnormalities, but using VBM we found significant reduction in hypothalamic gray matter volumes between patients and controls. CONCLUSIONS: VBM showed hypothalamic gray matter loss in narcolepsy with cataplexy. This suggest that functional abnormalities of hypocretin neurons in narcolepsy are associated with structural changes of hypothalamus.

Adult↗

PubMed2004

Successful management of cataplexy with intravenous immunoglobulins at narcolepsy onset.

Hypocretin/orexin deficiency appears to be a consistent feature of narcolepsy with a putative autoimmune mechanism involved. We treated four hypocretin/orexin-deficient narcolepsy patients with intravenous immunoglobulins and assessed the efficacy by repeated polysomnographies and questionnaires. Three patients received the treatment within a few months after acute onset of narcolepsy. A clear improvement in the frequency and severity of cataplexy was obtained with a benefic effect up to 7 months without any anticataplectics drugs at follow-up. Our findings point to the importance of early diagnosis of narcolepsy, which once treated quickly may modify its long-term outlook.

Adult↗

PubMed1987

Differences between REM and NREM sleepiness measured by event-related potentials (P300, CNV), MSLT and subjective estimate in narcolepsy-cataplexy.

Differences between 'REM sleepiness' and 'NREM sleepiness' states in wakefulness studied respectively prior to REM-containing and NREM-only multiple sleep latency test (MSLT) naps were compared by complex evoked potentials (P300, CNV), subjective estimate (Stanford Sleepiness Scale, SSS) and MSLT measures in 12 untreated patients with narcolepsy-cataplexy. The EP paradigms lasted about 7 min each and were done during the 10 min immediately before MSLT naps at 10.00, 12.00, 14.00, 16.00 and 18.00 h. SSS forms were completed immediately before and after the EP studies and MSLT naps. Patients were studied on 2 days and performed either the P300 or CNV paradigm on each day. 'REM sleepiness' was found to be subjectively and objectively (shorter mean sleep latency on MSLT) greater. Although subjects were sleepier in REM sleepiness, the subsequent REM nap was relatively more refreshing and reduced SSS estimates to levels equivalent to those after NREM-only naps. EP measures also showed differences between the 2 sleepiness states. REM sleepiness was associated with a significantly larger P2 component (in both the P300 paradigm and the CNV paradigm), a strong but not significant trend towards reduced amplitude of the P3 component, and almost total suppression of the slow negative components of the CNV. REM sleepiness and NREM sleepiness therefore appear to be district and differentiable cerebral states.

Adult↗

PubMed1988

Ambulatory 24 hour sleep-wake monitoring in narcolepsy-cataplexy compared to matched controls.

Twenty-four hour ambulatory sleep-wake recordings were made in 10 untreated patients with narcolepsy-cataplexy and 10 matched controls. Nocturnal sleep of narcoleptics was similar to descriptions of laboratory based recordings and was characterized by frequent sleep onset REM periods, high variability of REM latency, increased amounts of wakefulness after sleep onset, and low sleep efficiencies. Daytime portions in narcoleptics showed greater drowsiness and sleep than in controls with significantly higher amounts of stages 1A, 1B, 3, 4 and REM, more sleep episodes longer than 1 and longer than 10 min in duration, and high intersubject variability. On average, only 1.2 daytime sleep episodes began with sleep onset REM periods. There was a strong tendency in both groups towards a long mid-afternoon sleep episode often containing slow wave sleep (SWS) and which was significantly longer in narcoleptics. The mean interval between the onset of nocturnal SWS and the main daytime SWS peak was 14.1 h for narcoleptics and 13.6 h for controls. Daytime waking portions in narcoleptics showed significantly less 'active wakefulness' than in controls. There was no correlation between MSLT measures of sleepiness and amount of daytime sleep in ambulant recordings.

Adult↗

PubMed1995

[Diagnosis of narcolepsy-cataplexy: importance of continuous recording in ambulatory EEG. Report of 20 cases].

Ambulatory EEG (A-EEG) allows longterm polygraphic recording over 24 hours or more and proves to be particularly useful in the diagnosis of narcolepsy-cataplexy (N/C). We performed A-EEG using the Medilog 9000-8 channel system over a total of 36 24-hour periods in 20 consecutive N/C patients and recorded an average of 3.5 daytime sleep episodes, of which 2.2 were with SOREMP, AND 21 evening SOREMP (58%). A MSLT was performed using A-EEG in 16 cases. Continuous A-EEG proved to be more informative than the MSLT, and may represent a valid alternative to the classic continuous polygraphic recordings performed in the sleep lab, that are more cumbersome and costly. Although a full-night polysomnographic recording is still necessary whenever other sleep disorders are suspected in association with N/C, A-EEG is a first-line, practical method for the confirmation of N/C, which remains a clinical diagnosis.

Adolescent↗

PubMed1981

Daytime performance deficits and physiological vigilance in untreated patients with narcolepsy-cataplexy compared to controls.

Ten patients, 7 female, 3 male, aged 17-65 years (mean 40) with narcolepsy-cataplexy were compared off treatment to matched controls on 4 performance tests. The tests were the 1 h Wilkinson auditory vigilance task, and 3 shorter tests including the 4-choice serial reaction time, the paced auditory serial addition task (PASAT) and digit span. Tests were counterbalanced and polygraphic recordings were done during all but the 4-choice serial RT. Subjective sleepiness was assessed by the 1-7 levels of the Stanford Sleepiness Scale and effort in the tests by a similar 1-7 scale. Practice sessions were held. Narcoleptics showed poorer performance on the more monotonous tests of auditory vigilance (fewer hits) and the 4-choice serial RT (longer reaction times, more 'gaps'). There were no significant differences between groups on the other performance tests. Narcoleptics were subjectively sleepier during all tests and over-all. But there was no good correlation between perceived degree of sleepiness and performance. They also expressed greater effort to perform the PASAT. The narcoleptics showed greater amounts of drowsiness and light sleep only during the 1 h vigilance test. For the detections of those signals (shorter times) occurring after 13 sec or more of polygraphic wakefulness, narcoleptics performed as well as controls.

Adolescent↗

PubMed2000

Narcolepsy -- cataplexy and psychoanalytic theory of sleep and dreams.

Narcolepsy had been documented some twenty years before the psychoanalytic movement, emphasizing the central role of sleep and dreams in the understanding of mental health, offered an entirely novel theory of its aetiology. And when the full range of the behavioral aspects of the condition were documented, it was obvious that intense psychoanalytic interest in it was inevitable. Unfortunately, even mainstream neurology, lacking any rival physiological explanation, for a time tended to entertain a definite role for such beliefs, at least in some cases. However, such a theory involving outre concepts of repressed, guilt-ridden sexual drives as an explanation of the behavioral aspects of narcolepsy-cataplexy, of necessity simply added to the burdens of the sufferer. For it became clear that the condition by itself produced enough psycho-social problems without further adding to them. This historical note details the persistence of this misconceived theory up to the later decades of this century, and the burden that it placed upon those who suffered from this condition.

Cataplexy↗

PubMed1985

Does memory impairment exist in narcolepsy-cataplexy?

Approximately one-half of patients with the narcolepsy-cataplexy syndrome suffer from subjective memory problems, mainly involving recent events. Ten untreated narcoleptic patients (7 male, 3 female, aged 28-65 years) with such problems and 10 matched controls were given a battery of tests to study the complaint. Tests included the digit span, Knox cube, recurring figures (verbal and nonverbal), visual reproduction, paired associates learning and logical memory test, plus naming and fluency tests to control for language capabilities. No significant intergroup differences were found. It is concluded that narcoleptics do not have a true organic memory deficit, but rather experience a subjective problem due to drowsiness which they are able to suppress during short testing sessions in a laboratory environment.

Adult↗

PubMed2004

Diagnostic ambiguities in a case of post-traumatic narcolepsy with cataplexy.

Narcolepsy arising from trauma can present particular problems of differential diagnosis. In this case study presentation the patient suffered a head trauma, without unconsciousness, and began to experience unusual episodic behaviours. Symptom presentation differed from the typical clinical manifestations of idiopathic narcolepsy leading to an 8-year search for a definitive diagnosis. Key relevant aspects that led to diagnostic ambiguities were the order of symptom development, negative for the antigen HLA DR2, significance of the Multiple Sleep Latency Test (MSLT) mean sleep latency versus number of sleep onset rapid eye movement periods, the somewhat atypical features of cataplexy, the coexistence of sleep apnoea, and the mildness of the original head injury. It is argued that cases of post-traumatic narcolepsy should be considered in the context of their clinical development over time and that practitioners should be aware that this form of narcolepsy can differ from the typical clinical history of idiopathic narcolepsy.

Adult↗