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PubMed2005

Narcolepsy in Singapore: is it an elusive disease?

INTRODUCTION: The aims of the study were to determine the demographic, clinical, and polysomnographic characteristics of narcolepsy, and to address the difficulties in diagnosing narcolepsy and cataplexy, which is a cardinal symptom. We also ventured to investigate the differences between narcolepsy with and without cataplexy. MATERIALS AND METHODS: Data were collected retrospectively from patients diagnosed with narcolepsy at the Sleep Disorder Unit of Singapore General Hospital over 5 years. Each patient had had a detailed clinical evaluation and overnight polysomnography (PSG) followed by a multiple sleep latency test (MSLT). RESULTS: A total of 28 cases were studied. Males made up 85.7% of the total and females, 14.3%. The mean age was 30.9 years. All had excessive daytime sleepiness. Other manifestations were cataplexy (48.1%), sleep paralysis (51.9%), hypnogogic hallucinations (84%), disturbed night sleep (29.2%), automatisms (17.4%) and catnaps (95.8%). The mean duration of symptoms was 7.24 years. In the MSLT, the mean values for mean sleep latency and number of sleep onset rapid eye movement (REM) periods (SOREMP) were 4.3 minutes and 2.7, respectively. Narcolepsy was associated with obstructive sleep apnoea and periodic limb movement disorder (35.7%). All the variables were compared between those who had narcolepsy with cataplexy and without cataplexy. The duration of presenting complaint, REM latency, respiratory disturbance index, number of SOREMPs and the presence of sleep paralysis were significantly different in the 2 groups. CONCLUSIONS: Narcolepsy predominantly affects young males. Concurrence of other sleep disorders is not uncommon. Some differences are evident between those who have narcolepsy with and without cataplexy.

Adolescent↗
PubMed1999

Narcolepsy.

Narcolepsy is a disabling, chronic sleep-wake disorder that typically starts in a patient's second or third decade of life. Its key features are hypersomnia and cataplexy. Sleep paralysis, hallucinations, and disrupted sleep are nonspecific symptoms and are not always present. Disability relates primarily to sleepiness- related cognitive impairment, accidents, and psychosocial problems. Treatment, which includes counseling, scheduled napping, and pharmacologic intervention, is effective for most patients. Hypersomnia is best treated with such indirect sympathomimetics as mazindol, pemoline, methylphenidate, and amphetamine. Modafinil may become the drug of choice because it has fewer side effects. Cataplexy, sleep paralysis, and hallucinations may be ameliorated by compounds, including clomipramine and imipramine, that suppress rapid eye movement (REM) sleep. Regular follow-up visits enable the clinician to recognize uncommon but serious side effects (tolerance, substance abuse, psychosis, and hypertension) and additional sleep disturbances (sleep apnea, periodic limb movements in sleep, REM sleep behavior disorder), which can be specifically treated.

Journal Article↗
PubMed1985

[Narcolepsy].

First described as a separate entity by Gelineau in 1880 and later considered as a symptom, narcolepsy has eventually been recognized as a disease on clinical and polygraphic grounds. Its prevalence stays between 0.04 and 0.06 percent. Age at onset varies from 5 to 50 with a peak in the second decade. Clinical symptoms include excessive daytime somnolence, overwhelming daytime sleep episodes, attacks of cataplexy, hypnagogic hallucinations, sleep paralysis and disturbed nocturnal sleep; sleep onset REM episodes are the main polygraphic feature. Natural history varies with the different symptoms. Excessive daytime somnolence never subsides completely. Cataplexy may disappear spontaneously. Hypnagogic hallucinations and sleep paralysis are not present in all patients and tend to be more transitory. A positive diagnosis of narcolepsy requires a minimum of one major symptom, daytime sleep episodes or cataplexy, together with documented sleep onset REM episodes. Prolonged polygraphic recordings or multiple sleep latency test are of special interest in difficult cases. Clinical variants can be grouped under three headings, incomplete, symptomatic and associated narcolepsies. The etiology of narcolepsy is not well understood. However the discovery of natural animal models of narcolepsy, mainly dogs, has prompted genetic, pharmacological and biochemical studies. The breeding of narcoleptic canine colonies has led to the evidence of a possible autosomal recessive model of inheritance in some species. Pharmacological and neurochemical analysis has shown an imbalance between monoaminergic and cholinergic mechanism. In man, extensive family studies suggest either a two-threshold multifactorial model of inheritance or a dominant mode of inheritance and immunologic studies have recently shown a strong association between HLA-DR2 and narcolepsy. Assays of CSF biogenic amines suggest a decreased bioavailability of dopamine to explain sleepiness and an imbalance between monoamines and acetylcholine to explain cataplexy. A disturbance of circadian rhythms has not been evidenced in narcoleptics. Treatment is still purely symptomatic. Amphetamines and tricyclic antidepressants have been extensively used. However they are not free of side-effects hence the need for alternative treatments.

Adolescent↗
PubMed1994

Laboratory-documented hallucination during sleep-onset REM period in a normal subject.

During an experiment on nocturnal sleep interruption, we observed a unique case of hallucination without sleep paralysis during the sleep-onset REM period in a normal individual. We documented the polysomnogram recorded during this hallucination. The polysomnogram showed a mixed pattern of Stages REM and W, with muscle-tone inhibition, rapid eye movements (REMs), slow eye movements (SEMs), and abundant alpha EEG trains. The blocking of alpha EEG trains by REMs appeared to reflect visual processing similar to that which occurs during waking. This hallucination was distinct from ordinary sleep-onset mentation in that it included strong emotional components and in that the subject simultaneously experienced both hallucinatory mentation and reality contact. This hallucination may resemble sleep paralysis with regard to its physiological and psychological background, and the discrimination of these two phenomena may depend on the subject's own awareness of muscle-tone inhibition.

Adult↗
PubMed1986

HLA-DR2 and Dw2 in narcolepsy and in other disorders of excessive somnolence without cataplexy.

Studies on HLA antigens were conducted in several patient populations with the following findings: (a) All 135 Japanese narcoleptic patients, eight of whom were considered to have "symptomatic" narcolepsy, were found to be HLA-DR2 and HLA-DQw1 positive. All 17 members of a subgroup of the original population were also found to be HLA-Dw2-positive. It was concluded that HLA-DR2 is a prerequisite for the development of narcolepsy and that the diagnosis of narcolepsy can be excluded if HLA-DR2 or HLA-Dw2 is negative. The distinction between idiopathic and symptomatic narcolepsy needs to be reconsidered. (b) Haplotype studies in three families with narcoleptic members enabled detection of children at high risk for narcolepsy. (c) Of the 54 patients with disorders of excessive daytime sleepiness other than narcolepsy, those with essential hypersomnia (EHS) had a higher frequency of HLA-DR2; the others had a lower frequency. The DR2-positive EHS group could include members with an incomplete form of narcolepsy; the DR2-negative EHS group had disorders essentially different from narcolepsy, although both positive and negative groups manifested hypnagogic hallucinations, sleep paralysis, and sleep onset REMs. Two further studies were conducted in subgroups of the original narcoleptic population studied. In a subgroup of 30 patients who underwent lymphocyte subset studies, no T-cell abnormalities were detected; it is unlikely that an autoimmune mechanism is involved in the development of narcolepsy. In a subgroup of 33 narcoleptic patients, Southern's blot analysis of DNA using a DQ beta probe revealed three specific restriction fragments. Further studies are necessary to locate the DNA locus that carries the susceptibility gene for narcolepsy.

Alleles↗
PubMed2003

Narcolepsy in the older adult: epidemiology, diagnosis and management.

Narcolepsy is a disorder of impaired expression of wakefulness and rapid-eye-movement (REM) sleep. This manifests as excessive daytime sleepiness and expression of individual physiological correlates of REM sleep that include cataplexy and sleep paralysis (REM sleep atonia intruding into wakefulness), impaired maintenance of REM sleep atonia (e.g. REM sleep behaviour disorder [RBD]), and dream imagery intruding into wakefulness (e.g. hypnagogic and hypnopompic hallucinations). Excessive sleepiness typically begins in the second or third decade followed by expression of auxiliary symptoms. Only cataplexy exhibits a high specificity for diagnosis of narcolepsy. While the natural history is poorly defined, narcolepsy appears to be lifelong but not progressive. Mild disease severity, misdiagnoses or long delays in cataplexy expression often cause long intervals between symptom onset, presentation and diagnosis. Only 15-30% of narcoleptic individuals are ever diagnosed or treated, and nearly half first present for diagnosis after the age of 40 years. Attention to periodic leg movements (PLM), sleep apnoea and RBD is particularly important in the management of the older narcoleptic patient, in whom these conditions are more likely to occur. Diagnosis requires nocturnal polysomnography (NPSG) followed by multiple sleep latency testing (MSLT). The NPSG of a narcoleptic patient may be totally normal, or demonstrate the patient has a short nocturnal REM sleep latency, exhibits unexplained arousals or PLM. The MSLT diagnostic criteria for narcolepsy include short sleep latencies (<8 minutes) and at least two naps with sleep-onset REM sleep. Treatment includes counselling as to the chronic nature of narcolepsy, the potential for developing further symptoms reflective of REM sleep dyscontrol, and the hazards associated with driving and operating machinery. Elderly narcoleptic patients, despite age-related decrements in sleep quality, are generally less sleepy and less likely to evidence REM sleep dyscontrol. Nonpharmacological management also includes maintenance of a strict wake-sleep schedule, good sleep hygiene, the benefits of afternoon naps and a programme of regular exercise. Thereafter, treatment is highly individualised, depending on the severity of daytime sleepiness, cataplexy and sleep disruption. Wake-promoting agents include the traditional psychostimulants. More recently, treatment with the 'activating' antidepressants and the novel wake-promoting agent modafinil has been advocated. Cataplexy is especially responsive to antidepressants which enhance synaptic levels of noradrenaline (norepinephrine) and/or serotonin. Obstructive sleep apnoea and PLMs are more common in narcolepsy and should be suspected when previously well controlled older narcolepsy patients exhibit a worsening of symptoms. The discovery that narcolepsy/cataplexy results from the absence of neuroexcitatory properties of the hypothalamic hypocretin-peptidergic system will significantly advance understanding and treatment of the symptom complex in the future.

Adult↗
PubMed1984

[Narcoleptic syndrome].

Only in the last century was the narcoleptic syndrome recognized as a distinct entity fundamentally different from epilepsy. It is characterized by increased daytime sleepiness, usually as short sleep attacks, and by cataplexy. The latter is reflected in attacks of fully or incompletely developed loss of muscle tone, and in distressing akinetic states (so-called sleep paralysis) which chiefly occur in transition states between wake and sleep. In about half the patients, excessive daytime sleepiness may manifest itself in twilight states of lowered vigilance with automatic behaviour and amnesia. Many narcoleptics suffer from hallucinations, which may occur as they are falling asleep, during sleep paralysis, cataplectic attacks, and daytime sleepiness. Knowledge of the pathogenesis of narcoleptic disturbances is still incomplete but has been essentially widened by the discovery of paradoxical sleep, because cataplexy, sleep paralysis and hypnagogic hallucinations may now be interpreted as dissociated paradoxical sleep phenomena. The treatment of narcolepsy comprises advice in appropriate daily regimen, nutrition and vocational orientation as well as medication by stimulating agents for hypersomnolence and by tricyclic drugs for cataplexy.

Arousal↗
PubMed1997

[Acoustic hallucinations as a symptom of a REM sleep-associated parasomnia].

This 52-year-old man suffered from auditory hallucinations that occurred during brief episodes of sleep paralysis at the end of REM sleep periods. During these episodes the patient experienced a dissociated state of consciousness with REM sleep intrusions into wakefulness. The occurrence of this mixed state, and of excessive sleep-onset REM periods during daytime polysomnography (MSLT = Multiple Sleep Latency Test), point to a disorder of REM sleep generation. The existence of narcolepsy could be ruled out. The observation of REM sleep-associated hallucinations has been reported earlier. In the presented polysomnographic sleep studies the existence of a REM sleep associated parasomnia characterised by hallucinations and sleep paralysis could be confirmed.

Acoustic Stimulation↗
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↗
PubMed2000

Is narcolepsy a REM sleep disorder? Analysis of sleep abnormalities in narcoleptic Dobermans.

Narcolepsy is a chronic sleep disorder marked by excessive daytime sleepiness, cataplexy, sleep paralysis, and hypnagogic hallucinations. Since the discovery of sleep onset REM periods (SOREMPs) in narcoleptic patients, narcolepsy has often been regarded as a disorder of REM sleep generation: REM sleep intrudes in active wake or at sleep onset, resulting in cataplexy, sleep paralysis, or hypnagogic hallucinations. However, this hypothesis has not been experimentally verified. In the current study, we characterized the sleep abnormalities of genetically narcoleptic-cataplectic Dobermans, a naturally occurring animal model of narcolepsy, in order to verify this concept. Multiple sleep latency tests during the daytime revealed that narcoleptic Dobermans exhibit a shorter sleep latency and a higher frequency of SOREMPs, compared to control Dobermans. The total amount of time spent in wake and sleep during the daytime is not altered in narcoleptic dogs, but their wake and sleep patterns are fragmented, and state transitions into and from wake and other sleep stages are altered. A clear 30 min REM sleep cyclicity exists in both narcoleptic and control dogs, suggesting that generation of the ultradian rhythm of REM sleep is not altered in narcoleptics. In contrast, cataplexy displays no cyclicity and can be elicited in narcoleptic animals anytime with emotional stimulation and displays no cyclicity. Stimulation of a cholinoceptive site in the basal forebrain induces a long-lasting attack of cataplexy in narcoleptic dogs; however, bursts of rapid eye movements during this state still occur with a 30 min cyclicity. Sites and mechanisms for triggering cataplexy may therefore be different from those for REM sleep. Cataplexy and a dysfunction in the maintenance of vigilance states, but not abnormal REM sleep generation, may therefore be central to narcolepsy.

Animals↗
PubMed1994

Characteristics of African-American and white patients with panic disorder and agoraphobia.

OBJECTIVE: The authors explored the clinical characteristics and treatment response of African-American and white patients with panic disorder and agoraphobia who presented for treatment at an anxiety disorders clinic. METHODS: One hundred white and 43 African-American patients were evaluated using a structured interview and completed a variety of standardized rating scales. In addition, data regarding clinical characteristics, psychiatric history, childhood history, life stressors, and treatment outcome were obtained by chart review. The incidence of isolated sleep paralysis was also assessed in a subsample of patients. RESULTS: The two groups had no significant differences in psychiatric symptoms. African-American patients were more likely to use a medical emergency room, to have had childhood separations, and to have had parents who abused substances. They also reported less separation anxiety, school phobia, and affective illness in family members. In addition, African Americans, both patients and nonclinical control subjects, were more likely to report that they experienced repetitive episodes of isolated sleep paralysis. Treatment outcome was moderately successful among both African-American patients and white patients. CONCLUSIONS: Although African-American and white patients show similar symptoms of panic disorder, African-American patients had more unnecessary psychiatric hospitalizations, a higher rate of medical emergency room visits, a higher incidence of isolated sleep paralysis, greater likelihood of childhood trauma, and a greater number of life stressors. Addressing these issues in treatment is critical in reducing the dropout rate and maintaining successful treatment.

Adult↗
PubMed2003

[Clinical and sleep EEG monitoring characteristics and long-term follow-up study on narcolepsy].

OBJECTIVE: Narcolepsy is a sleep disorder characterized by excessive daytime sleepiness, cataplexy, hypnagogic hallucination and sleep paralysis, with abnormal characteristics of shorter rapid eye movement (REM) sleep latency. The management of the patients is very important. The present study focused on the clinical characteristics, diagnostic methods and long-term prognosis of this particular syndrome. METHODS: The clinical data of 39 narcoleptic children were analyzed. Sleep EEG monitoring was performed in all patients. Among the 39 cases, 23 were followed up. RESULTS: All the patients manifested with excessive daytime sleepiness, with disrupted nocturnal sleep occurring in 35 cases. Cataplexy appeared in 36 cases, and sleep paralysis in 9, hypnagogic hallucination in 19, and automatic behavior in 6 cases, respectively. Sleep EEG monitoring demonstrated a short mean sleep latency (< 5 minutes) and two or more sleep onset REM periods (SOREMPs) in 38 cases. Twenty-three of the 39 cases were followed-up. Seventeen cases were followed-up for over one year. The longest follow-up duration was 14 years. Methylphenidate was administered in 10 cases. The excessive daytime sleepiness had been improved in 7 cases (70%). No obvious adverse effects were found. Psychosocial and academic problems appeared in most cases. CONCLUSION: Narcolepsy is a chronic neurological disorder. A definite diagnosis is established when the symptoms of cataplexy and excessive daytime sleepiness occur in association with the characteristic findings on sleep EEG monitoring. Appropriate drug therapy and psychosocial management are of help for such patients. Stimulant medication is an important component of the overall treatment program. A comprehensive approach is necessary to meet the needs of children with narcolepsy. Family education and emotional support are key elements in the management plan. The overall goal for managing childhood narcolepsy is to assist the child and family in achieving optimal quality of life.

Adolescent↗
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↗
PubMed2004

[Diagnosis of childhood narcolepsy and significance of HLA in its diagnosis].

OBJECTIVE: Narcolepsy is a lifelong sleep disorder characterized by excessive daytime sleepiness, and features of rapid eye movement (REM) sleep, such as cataplexy, sleep paralysis and hypnagogic hallucinations. The present study aimed to investigate the diagnostic basis of childhood narcolepsy and possible role of HLA Class II alleles in the onset of this disease. METHODS: The clinical data of 40 narcoleptic children were analyzed. All patients received Multiple Sleep Latency Test (MSLT) and they were analyzed in combination with clinical features. Polymerase chain reaction/sequence specific primers (PCR/SSP) methods were used to detect the HLA-DRB1 and DQB1 alleles. RESULTS: Narcolepsy was diagnosed in 40 children. The age range was 3 to 14 years (mean 8.5 +/- 2.5 years), 29 were male and 11 female. Their mean course of disease was 6.5 months, 14 patients (30%) were less than 3 months old, 21 patients (52%) were less than 6 months old. All the patients had excessive daytime sleepiness, cataplexy appeared in 37 cases, hypnagogic hallucination in 22 and sleep paralysis in 6. Mean sleep latency on MSLT was less than 5 min, the average number of sleep-onset rapid eye movement (SOREM) was 4.33 +/- 0.26 episodes (2-5 episodes), the latency of SOREM episodes were 4.0 +/- 1.8 min (0.25-4.9 min). Thirty-five patients were DRB1 1501 and DQB1 0602 positive (Pc < 0.01), 2 were DRB1 1502 and DQB1 0601 positive, while 3 were DRB1 15 and DQB1 6 negative. CONCLUSIONS: Some pediatric patients with narcolepsy were different from adult patients in that the pediatric cases had a sudden onset and shorter disease course. Diagnosis of this disease was based on the clinical manifestations, MSLT and absence of any medical or psychiatric disorder that could account for the symptoms. The authors demonstrated that DRB1 1501 and DQB1 0602 were susceptibility genes for narcolepsy and those who were DRB1 15 negative could not be excluded.

Adolescent↗
PubMed2005

Parkinsonism with excessive daytime sleepiness--a narcolepsy-like disorder?

BACKGROUND: Parkinsonian patients with excessive daytime sleepiness (EDS), hallucinations, REM sleep behavior disorder (RBD), short mean sleep latencies, and sleep-onset REM periods (SOREMP) on multiple sleep latency tests (MSLT) have been reported. In these patients a narcolepsy-like pathophysiology of sleep-wake disturbances has been suggested. PATIENTS AND METHODS: We studied 14 consecutive patients with Parkinsonism and EDS. Standard studies included assessment of duration and severity of Parkinsonism (Hoehn & Yahr score), Epworth sleepiness score (ESS), history of "REM-symptoms" (RBD/hallucinations/sleep paralysis/cataplexy-like episodes), polysomnography (PSG), MSLT, and measurement of cerebrospinal fluid (CSF) levels of hypocretin-1 (orexin A). RESULTS: There were 12 men and 2 women (mean age 69 years; range 54-82). The mean duration and the Hoehn&Yahr score were 6.3 years and 2.2, respectively. Diagnoses included idiopathic Parkinson's disease (IPD, n = 10), dementia with diffuse Lewy bodies (n = 3), and multisystem atrophy (n = 1). The ESS was > or = 10 in all patients (mean 12; range 10-18). "REM-symptoms" were reported by all but two patients (hallucinations: n = 9; RBD: n = 9). None of the patients reported cataplexy-like symptoms or sleep paralysis. On PSG sleep apnea (apnea hypopnea index > 10/h, n = 7), periodic limb movements during sleep (PLMS-index > 10/h, n = 6), and features of RBD (n = 5) were found. On MSLT mean sleep latency was < 5 minutes in 10 patients, and SOREMP were found in two patients. When compared with controls (n = 20, mean 497 pg/ml; range 350-603), CSF hypocretin-1 levels were normal in 8 patients and low in 2 patients (221 and 307 pg/ml, respectively). CONCLUSION: These findings do not support the hypothesis of a "final common pathway" in the pathophysiology of narcolepsy and Parkinsonism with EDS. Sleep apnea and PLMS may play a so-far underestimated role in the pathogenesis of EDS in Parkinsonian patients.

Aged↗
PubMed1994

Why is there an increased risk for sudden infant death in prone sleeping? Fear paralysis and atrial stretch reflexes implicated?

A number of recent reports have indicated a higher risk of sudden infant death syndrome (SIDS) in the prone sleeping position, compared with the supine position. However, the biological mechanisms for this increased risk have not been established. For this report, two biological explanations are proposed, each of which may be influenced by altered sleeping position in such a way that they may create conditions for increased triggering of SIDS.

Adrenergic Fibers↗
PubMed1995

Tranylcypromine in narcolepsy.

The narcolepsy syndrome consists of excessive daytime somnolence, cataplexy, hallucinations, and sleep paralysis. Data on the effects of tranylcypromine are scant. We report on a patient with severe narcolepsy in whom administration of tranylcypromine led to freedom from hallucinations, nightmares, sleep paralysis, and rapid eye movements (REM), with considerable amelioration of cataplexy and increased daytime alertness. Muscle atonia and low-voltage desynchronized cortical activity during REM sleep did not change. Tranylcypromine warrants further study in narcolepsy.

Adult↗