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At least 685 records · Page 38Linked to original sources
PubMed1990

Disorder of excessive daytime somnolence: a case series of 1,000 patients.

Symptoms of excessive daytime somnolence range from mild to severe. In mild cases, there may be minimal interference with normal daytime function. The hypersomnia can be disabling. When severe the patient finds it difficult to remain awake at times when physically inactive. Excessive daytime somnolence is the chief complaint of the majority of our adult patients. In this paper, we present the findings for 1,000 consecutive patients (755 males and 245 females) who were seen at the Humana Hospital Audubon Sleep Disorders Center. Patients ranged in age from 15 to 83. All patients had a sleep history, medical history and physical, psychological evaluation, polysomnographic evaluation, and other laboratory tests as indicated. Obstructive sleep apnea syndrome was the most prevalent diagnosis for males (84.2%) and females (59.6%). It accounted for over three-fourths of all diagnoses. Hypersomnia secondary to a psychiatric disorder was the next most frequent diagnosis overall (6.1%). A psychiatric disorder was second for females and third for males. Narcolepsy was diagnosed for 5.8% of all patients. This was the second most prevalent diagnosis for males and third for females. Eighteen males (47.4% of all males with a diagnosis of narcolepsy) and 9 females (45.0%) had cataplexy. Nocturnal myoclonus was the primary diagnosis in 2.5% of all patients with excessive daytime somnolence. An additional 49 patients with sleep apnea syndrome and 18 patients with narcolepsy also had periodic leg movements during sleep. A diagnosis of obstructive sleep apnea and narcolepsy was made for 1.3% of patients. The narcolepsy component of this diagnosis was typically made only after the obstructive sleep apnea had been resolved (eg, nasal CPAP, tracheostomy).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

[Naltrexone in narcolepsy. Initial experience].

The administration of 550 mg naltrexon in the course of 13 days did not four patients with narcolepsy-cataplexy to improvement of symptoms of the disease and did not improve their appetite or increase their body weight. No side-effects of naltrexon were observed.

Adult↗
PubMed1989

Current concepts in narcolepsy.

Narcolepsy, a disabling disorder, has been underdiagnosed. The classic tetrad of symptoms includes sudden sleep attacks, cataplexy, sleep paralysis, and hypnogogic hallucinations. Diagnosis and treatment will restore a normal quality of life.

Amphetamines↗
PubMed1987

Narcolepsy. Diagnosis, treatment, and management.

Narcolepsy is a syndrome of unknown origin characterized by the irresistible urge to sleep. Other important features are disturbed nocturnal sleep and abnormal manifestations of REM sleep such as cataplexy, sleep paralysis, and abnormal sleep-onset REM periods. Narcolepsy is not a rare condition. With a prevalence between 2 and 10 per 10,000 individuals, it is about as common as multiple sclerosis. Like multiple sclerosis, narcolepsy can be disabling and have profound consequences for job capability, public safety, sense of self-worth, and social image.

Animals↗
PubMed1988

Medullary regions mediating atonia.

Electrical stimulation studies have implicated the medial medulla in the inhibition of muscle tone. In the present report we present evidence for suppression of muscle tone by chemical activation of the medial medulla. We find 2 distinct zones within the classically defined medial medullary inhibitory area. A rostral region corresponding to the nucleus magnocellularis (NMC) is sensitive to glutamate. Atonia produced by activation of this region is mediated by non-NMDA receptors. A caudal region, corresponding to the nucleus paramedianus (NPM) is sensitive to ACh. Atonia produced by activation of this region is mediated by muscarinic receptors. Activation of these regions both in acute decerebrate and intact cats suppresses muscle tone. We find that the cholinoceptive dorsolateral pontine region, previously implicated in atonia control, can be activated by glutamate-sensitive non-NMDA receptors. Microinjection of atropine into the NPM or of glutamylglycine into the NMC blocks atonia elicited by pontine carbachol injection. The medullary regions identified here are hypothesized to mediate the suppression of muscle tone that occurs in rapid eye movement sleep and in cataplexy and may have a role in postural control in waking.

Acetylcholine↗
PubMed1988

Sleep paralysis: a study in family practice.

Over a period of two years, five patients with sleep paralysis referred themselves to four family practices in Israel serving a population of 6800. None of the patients suffered from daytime sleep attacks or cataplexy and all were from the oriental (sephardi) community. The two who were tissue typed had HLA haplotypes different from those which are exclusively associated with narcolepsy and one of them who also underwent polysomnography had a normal tracing. There was considerable delay in consulting a physician despite the physical and mental anguish caused by the disorder and some improvement was noted once the diagnosis was explained. The serious nature of the components of the differential diagnosis - myocardial infarction, seizure disorder, cardiac arrest, anaesthetic accident - makes it important that sleep paralysis be more widely recognized.

Adult↗
PubMed1985

[Advances in the psychopharmacological management of the narcoleptic patient].

Sleep attacks, cataplexy, sleep paralysis and hypnagogic hallucinations are the cardinal signs of narcolepsy. However most patients present only with sleep attacks at disease onset. Animal and human studies on the psychopharmacology and neurochemistry of narcolepsy, suggest abnormalities on rapid eye movement (REM) sleep. Thus, most drugs used on its treatment, such as tricyclic antidepressants and psychostimulant agents, are aimed to reduce REM sleep. However, there is growing evidence that some drugs that can alleviate fragmentation of sleep rather than suppress REM sleep can also be clinically effective for this condition. The authors review the subject and comment on their experience with clonidine, an imidazoline derivative marketed as an antihypertensive agent, and suggest that REM suppression is not always necessary for narcoleptics to improve.

Animals↗
PubMed1984

Narcolepsy in a Brahman bull.

Behavioral, electrophysiologic, and pharmacologic tests were performed on a 2 1/2-year-old Brahman bull suspected of having narcolepsy. Placement on a tilt table or electroejaculation induced apparent sleep and cataplexy. Electrophysiologic recordings during the episodes revealed the low-voltage, high-frequency electroencephalogram, reduced electromyogram amplitude, and rapid eye movements in the electrooculogram associated with rapid eye movements sleep. Physostigmine salicylate appeared to elicit and potentiate the episodes, whereas atropine sulfate and imipramine reduced or blocked them. The combined results of the tests supported the diagnosis of narcolepsy.

Animals↗
PubMed1984

A quantitative polygraphic study of daytime somnolence and sleep in patients with excessive diurnal sleepiness.

The authors propose a method of quantitative evaluation of excessive diurnal sleepiness intensity. They perform in each patient a 45-minute polygraphic examination to evaluate the occurrence of manifestations of wakefulness as well as all forms and stages of sleep, together with their latencies and total durations. In this way it is possible to describe the patients' sleepiness both quantitatively and qualitatively. The above test was used in the study of 8 healthy controls, 8 patients with narcolepsy-cataplexy, 8 patients with idiopathic hypersomnia and 8 patients suffering from the syndrome of hypersomnia with sleep apnea. All three groups of patients differed significantly from the control group showing deeper sleep stages of shorter latency and longer total duration. The three groups of patients differed also in some aspects from each other.

Circadian Rhythm↗
PubMed1982

Narcolepsy with concomitant features of obstructive sleep apnea.

A 17-year-old man presented with daytime sleepiness, episodic attacks of sleep and probable cataplexy. His EEG showed rapid eye movements and central sawtooth waves at sleep onset, and supported the clinical impression of narcolepsy. He improved with methylphenidate but died suddenly, and had cardiomegaly, right ventricular enlargement, and pulmonary hypertension at autopsy. These findings suggested concomitant features of sleep apnea which were not evident by history or examination.Central apneas have been frequently described in the sleep of narcoleptic patients. Few patients have had indications of obstructive or mixed apneas. This patient's course suggests that ventilation during sleep should be included in the polygraphic assessment of patients with suspected narcolepsy, as the agents used for treatment of narcolepsy may aggravate the cardiac complications of sleep apnea.

Adolescent↗
PubMed1981

[The place of Gelineau's syndrome (narcolepsy) among diurnal attacks of sleep and somnolence (author's transl)].

A clinical and electroencephalographic study was conducted in 41 patients (25 men and 16 women) complaining of diurnal attacks of sleep, and the results were compared with those obtained in 15 control subjects (7 men and 8 women) of the same age. EEG tracings were recorded during 33 hours in each subject. The total duration of the various phases of nocturnal sleep and the mean duration of each phase were the same in both groups. The incidence of EEG peculiarities, such as short delay in the onset of sleep and in the first stage of desynchronized sleep, and prolonged nocturnal periods of vigilance, was assessed in both groups, but no correlation was found between clinical and electrical data. The three criteria of Gelineau's syndrome (irresistible sleepiness, cataplexy and onset of sleep in desynchronized phase) were present in 35% of the patients.

Adult↗
PubMed1980

The use of clomipramine as an REM sleep suppressant in narcolepsy.

Clomipramine is known to suppress REM sleep, and this property may be of value in treating certain features of narcolepsy. In a case reported here, clomipramine produced relief of cataplexy, sleep paralysis and hallucinations with considerable subjective improvement. Although the sleep attacks were little changed, the time spent asleep increased, leaving clearer intervals of wakefulness.

Clomipramine↗
PubMed1980

Timing of REM and stages 3 + 4 sleep during temporal isolation in man.

During nonentrained sleep--wake conditions in man, healthy adult subjects spontaneously develop "long" biological days (greater than 35 hr) in addition to the normal, approximately 25 hr day. The ratio of sleep to total time remains constant (approximately 0.30), with long sleep episodes occurring approximately 180 degrees out of phase with the short sleep episodes. The timing and amount of REM sleep advance to an earlier time within the sleep episode during free-running, whereas stage 3 + 4 sleep is related to the initiation and course of the sleep process itself. The REM--NREM cycle length does not change, comparing entrained and nonentrained conditions. The study of the chronophysiology of humans under nonentrained conditions may serve as a model of the chronopathology of sleep--wake changes which occur in sleep disorders associated with depression, narcolepsy--cataplexy, sleep--wake dyssomnias, delayed sleep phase insomnia, and aging.

Adult↗
PubMed1995

[Narcolepsy disclosing neurosarcoidosis].

A 37-year-old man developed excessive daytime sleepiness, sleep attacks and cataplexy revealing an hypothalamic tumour. Multiple Sleep Latency Tests (MSLT) were characteristics of narcolepsy. Tissue typing was positive for HLA DR2 and DQ1. Most cases of narcolepsy are idiopathic without any evidence of brain pathology. Although symptomatic narcolepsy may occur occasionally with diencephalic lesions. The relationship between narcolepsy with diencephalic lesions is unsettled and will be discussed.

Adult↗
PubMed1994

Neurochemical studies of human narcolepsy: alpha-adrenergic receptor autoradiography of human narcoleptic brain and brainstem.

Studies of human and canine narcolepsy-cataplexy syndrome suggest that noradrenergic function may be abnormal. We used quantitative autoradiography to assess noradrenergic alpha-1 and alpha-2 receptors in several regions of seven human narcoleptic and 18 control brains using [3H]prazosin to evaluate alpha-1 receptors, and [3H]UK14304 and [3H]rauwolscine to evaluate alpha-2 receptors. Specific blocking agents were used in combination with the tritiated ligands to assess alpha-1 and alpha-2 receptor subtypes. Although we found few statistically significant differences between narcoleptic and control brains, there were a number of trends. [3H]Prazosin binding to sites in the amygdala, globus pallidus and putamen was reduced by 22-68%, whereas binding was increased by 40% to the inferior olive and by 84% to portions of the dorsal pons. Binding was similar to control values in other regions. In all seven brainstem regions that were evaluated, the ratio of alpha-1b receptor binding to alpha-1a receptor binding was increased. Binding of [3H]UK14304 was increased by 35-74% in the caudate nucleus, putamen and portions of the amygdala and pons. [3H]rauwolscine binding data suggested that increase of alpha-2 receptor binding in the dorsal pons were not due to effects at the imidazole receptor. findings suggest that noradrenergic function may be altered in specific regions of the brain and brainstem in human narcolepsy, although the absence of statistical significance indicates that these trends should be considered preliminary. The trend toward a relative increase of alpha-1b receptor binding in narcoleptic brainstem is consistent with data from studies of canine narcolepsy and suggests that altered activity at this receptor may contribute to the pathogenesis of human narcolepsy. Studies of additional brains will be required to confirm these findings.

Adult↗
PubMed1994

Practice parameters for the use of stimulants in the treatment of narcolepsy. Standards of Practice Committee of the American Sleep Disorders Association.

Narcolepsy is a disorder of the central nervous system characterized by excessive sleepiness, cataplexy, and other rapid-eye-movement (REM)-sleep phenomena such as sleep paralysis and hypnagogic hallucinations. Although stimulants are the only effective treatment for the sleepiness of narcolepsy, no clinical guidelines on the use of stimulants in the treatment of narcolepsy have been published that address the following factors: appropriate doses; development of tolerance; potential for side effects, adverse reactions and abuse; and use in children and pregnant or breast-feeding women. These practice parameters from the American Sleep Disorders Association provide the first clinical guidelines on the appropriate use of stimulants in the treatment of narcolepsy.

Adolescent↗
PubMedDate not supplied

Effective treatment of narcolepsy with codeine in a patient receiving hemodialysis.

A 64-year-old man with narcolepsy could not take stimulant drugs due to coronary heart disease. In the past he noted improvement in alertness when taking codeine for pain, but this was eventually discontinued. After he developed end-stage renal disease, and because the use of stimulants in this setting may be difficult, treatment with codeine was again initiated. This resulted in dramatic improvement in alertness and substantial reduction of cataplexy. Because it is simple to use and familiar to most physicians, codeine may be the drug of choice for narcoleptic patients who are undergoing hemodialysis.

Codeine↗
PubMed1995

[A case of HLA-DR2, DQw1 negative post-traumatic narcolepsy].

We reported a case of a 24-year-old man who had frequent sleep attacks beginning 4 years after a head trauma. He showed frequent episodes of excessive daytime sleepiness and cataplexy which were triggered by emotional excitement. He also complained of sleep paralysis and hypnagogic hallucination. An overnight polysomnography revealed the sleep onset REM stage as typically observed in narcoleptic patients. The HLA typing was negative for DR2 and DQw1. He was diagnosed as having HLA-DR2 and DQw1 negative-post-traumatic narcolepsy. Peroral pemoline suppressed excessive daytime sleepiness, sleep paralysis and hypnagogic hallucination with dramatic relief of cataplectic attacks by the addition of imipramine. It has been reported that more than 90% of narcoleptic patients are HLA-DR2 and-DQw1 positive. About 10% of the narcolepsy patients were regarded as symptomatic due to brain tumors, cerebrovascular disorders, head trauma, multiple sclerosis, encephalitis and so on, which mainly affect the brainstem or diencephalon. Thus far, narcolepsy is considered to develop depending on both the genetic background including HLA types, and exogenous factors. According to reported cases with narcolepsy, sporadic cases were HLA-DR2 positive even more frequently than familial cases. To date, however, there have been only three previous reports of a symptomatic narcolepsy patient without association of HLA-DR2 and DQw1. In conclusion, the present report suggests that typical symptomatic narcolepsy could be HLA-DR2 or DQw1 negative.

Adult↗