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PubMed1975

Altered states of consciousness in disorders of daytime sleepiness.

Patients with daytime sleepiness present altered states of consciousness. The occurrence of these states impairs their professional, social and familial activities and may threaten life itself. The automatic behavior syndrome is characterized by continuation of mechanical activity and complete amnesia. Episodes lasting from a few seconds to several hours are correlated with repetitive micro-sleep periods. During cataplectic attacks, patients may have a meshing of reality with hallucinatory dream contents. Sleep-induced apnea may lead to abnormal movement and abnormal ambulation during sleep as well as hallucinations in the early morning. These altered states of consciousness must be considered as diagnostic indexes in differentiating epileptic syndromes from syndromes of daytime sleepiness.

Adult↗
PubMed1992

HLA-DR2 negative narcolepsy in Australian Caucasians: clinical features, serology and sequence specific oligonucleotide typing.

An almost invariable association with HLA-DR2 and DQw1 has previously been reported in Japanese and caucasian narcoleptics. We performed HLA typing in 18 Australian narcoleptics using serological techniques and sequence specific oligonucleotide probes. HLA-DQw1 was present in 15 patients and DR2 in 12; 3 patients with cataplectic narcolepsy were DR2-negative. The serological haplotype most strongly associated with narcolepsy was DRw15 (a subtype of DR2), DQw1. DRw15-positive patients were positive for the alleles DRB1*1501 and DQB1*0602 defined with oligonucleotide probes. We conclude that the association of narcolepsy with DR2 and DQw1 is not as strong as previously reported and the absence of DR2 or DQw1 does not preclude the diagnosis of classical narcolepsy, at least in caucasians. Secondly, DR2-positive narcoleptics possess characteristic serological subtypes and alleles defined with oligonucleotide probes that are also found in normals. Thirdly, the occurrence of DR2-negative cataplectic narcoleptics points to the existence of more than one narcolepsy susceptibility gene.

Adult↗
PubMed1991

Radioligand binding to adenosine receptors and adenosine uptake sites in different brain regions of normal and narcoleptic dogs.

The present study compares the characteristics of radioligand binding to adenosine receptors and adenosine uptake sites in 100- and 50-day-old normal and narcoleptic dogs. Binding to A1 receptors was quantified using a selective A1 agonist ([3H]N6-[(R)-1-methyl-2-phenylethyl] adenosine, [3H]R-PIA) and an antagonist ([3H]dipropyl-8-cyclopentyl-xanthine, [3H]CPX). Differences in the binding of [3H]R-PIA and that of [3H]5'-ethylcarboxamide adenosine ([3H]NECA), which binds to both A1 and A2 receptors with similar affinities, were used to quantify A2 receptors. Nucleoside transport sites were labeled with [3H]nitrobenzylthioinosine ([3H]NBTI), a potent inhibitor of nucleoside transport systems. The present study offered no evidence that either adenosine A1 receptors and adenosine uptake sites in the frontal cortex or adenosine A2 receptors in the putamen were altered in narcoleptic dogs. However, we found that adenosine A1 receptors in the dog exist in different affinity states and that the affinity state in which the receptor is found depends on the brain region examined. A characterization of these low- and high-affinity sites was performed and results indicated that these sites cannot be explained by a single interaction of the A1 receptor with a single G-protein population.

Adenosine↗
PubMed2005

Lack of cataleptogenic potentiation with non-imidazole H3 receptor antagonists reveals potential drug-drug interactions between imidazole-based H3 receptor antagonists and antipsychotic drugs.

Since H3 receptor (H3R) antagonists/inverse agonists can improve cognitive function in animal models, they may have the potential to be used as add-on therapy in the treatment of schizophrenia, a disease with significant cognitive deficits. However, a recent study showed potentiation of haloperidol-induced catalepsy by ciproxifan, an imidazole-containing H3R antagonist/inverse agonist, suggesting there is a potential risk of exacerbating extrapyramidal symptoms (EPS) if H3R antagonists were used as adjunctive treatment [Pillot, C., Ortiz, J., Heron, A., Ridray, S., Schwartz, J.C. and Arrang, J.M., Ciproxifan, a histamine H3-receptor antagonist/inverse agonist, potentiates neurochemical and behavioral effects of haloperidol in the rat, J Neurosci, 22 (2002) 7272-80]. In order to clarify the basis of this finding, we replicated this result and extended the work with another imidazole and two non-imidazole H3R antagonists. The results indicate that ciproxifan significantly augmented the effects of haloperidol and risperidone on catalepsy. Another imidazole H3R antagonist, thioperamide, also potentiated the effect of risperidone on catalepsy. In contrast, no catalepsy-enhancing effects were observed when selective non-imidazole H3R antagonists, ABT-239 and A-431404, were coadministered with haloperidol and/or risperidone. As ciproxifan and thioperamide are inhibitors of cytochrome P450 enzymes, responsible for metabolizing risperidone and haloperidol, the possibility that the augmentation of antipsychotics by imidazoles resulted from drug-drug interactions was tested. A drug metabolism study revealed that an imidazole, but not a non-imidazole, potently inhibited the metabolism of haloperidol and risperidone. Furthermore, ketoconazole, an imidazole-based CYP 3A4 inhibitor, significantly augmented risperidone-induced catalepsy. Together, these data suggest the potentiation of antipsychotic-induced catalepsy may result from pharmacokinetic drug-drug interactions and support the potential utility of non-imidazole H3R antagonists in treatment of cognitive impairment in schizophrenia without increased risk of increased EPS in patients.

Animals↗
PubMed2006

Possible confusion between primary hypersomnia and adult attention-deficit/hyperactivity disorder.

We explored the possibility of diagnostic confusion between hypersomnias of central origin (narcolepsy and idiopathic hypersomnia, IH) and the adult form of attention-deficit/hyperactivity disorder (ADHD). We included 67 patients with narcolepsy, 7 with IH and 61 with ADHD. All patients completed the Epworth Sleepiness Scale and the ADHD Rating Scale. We found that 18.9% of the hypersomnia patients fulfilled the self-reported criteria for ADHD in adulthood, compared with 77% of the ADHD patients. A score > or =12 on the Epworth Sleepiness Scale (usually regarded to indicate excessive daytime sleepiness) was found in 37.7% of the ADHD patients compared 95.9% of the hypersomnia patients. In ADHD patients, inattention scores correlated with the excessive daytime sleepiness score. We conclude that one should be aware of possible diagnostic confusion between narcolepsy or IH and adult ADHD when using self-report questionnaires. The high percentage of symptom overlap found in our study raises questions about possible misdiagnosing of both conditions, comorbidity with sleep problems in adult ADHD, and the validation of the used scales. It remains unclear whether our findings indicate pathophysiological overlap.

Adult↗
PubMed2004

Concomitant use of modafinil and tranylcypromine in a patient with narcolepsy: a case report.

This is a case report of a patient with narcolepsy treated simultaneously with modafinil and tranylcypromine. The concurrent use of these two medications is normally contraindicated based on theoretical concerns. To our knowledge this is the first report of the combined use of these two medications in a patient for any reason. This combination of medications was particularly effective in the treatment of the patient's narcoleptic symptoms and was well tolerated, with no evidence of the potential cardiovascular side effects. Due to modafinil's lack of sympathomimetic activity and unique pharmacological profile, it may be well tolerated with monoamine oxidase inhibitor's (MAOI's) in humans with respect to hemodynamic parameters and concerns of hypertensive crisis. Further investigation would help clarify cardiovascular safety issues in using this combined therapy. We believe that with proper informed consent from the patient and careful monitoring, a combination of an MAOI and modafinil may be a viable treatment alternative in refractory cases of narcolepsy.

Benzhydryl Compounds↗
PubMed2004

Functional status in patients with narcolepsy.

OBJECTIVE: To describe health and functional status in treated narcolepsy patients and to compare it with normative data and with patients with another cause of sleepiness, the obstructive sleep apnea/hypopnea syndrome (OSAHS) patients. METHODS: A functional status survey in narcolepsy patients and in symptomatic untreated and CPAP treated OSAHS patients with an apnea-hypopnea index (AHI) >5 was assessed using the UK Short Form 36 (SF-36) questionnaire, the Functional Outcomes of Sleep Questionnaire (FOSQ) and the Epworth Sleepiness Scale (ESS). SF-36 scores in narcoleptics were compared to age and sex matched controls. Narcolepsy patients also replied to a psychosocial aspects questionnaire. Health history and demographic data were obtained via a review of medical records and postal survey. RESULTS: Forty-nine treated narcolepsy patients, 56 untreated OSAHS and 48 CPAP treated OSAHS patients attending the sleep disorders clinic were recruited for this study. Narcoleptics presented significantly lower scores in all SF-36 domains compared to normative data. No difference in SF-36 scores was found between narcoleptics and untreated OSAHS patients but narcoleptics were sleepier and had lower FOSQ scores. These treated narcolepsy patients had lower scores in two dimensions of the SF-36 and in all FOSQ domains compared to CPAP-treated OSAHS patients. CONCLUSIONS: Functional status in treated narcoleptics is poor.

Activities of Daily Living↗
PubMed2004

Pharmacotherapy for excessive daytime sleepiness.

Excessive daytime sleepiness (EDS) has recognized detrimental consequences such as road traffic accidents, impaired psychological functioning and reduced work performance. EDS can result from multiple causes such as sleep deprivation, sleep fragmentation, neurological, psychiatric and circadian rhythm disorders. Treating the underlying cause of EDS remains the mainstay of therapy but in those who continue to be excessively sleepy, further treatment may be warranted. Traditionally, the amphetamine derivatives, methylphenidate and pemoline (collectively sympathomimetic) psychostimulants were the commonest form of therapy for EDS, particularly in conditions such as narcolepsy. More recently, the advent of modafinil has broadened the range of therapeutic options. Modafinil has a safer side-effect profile and as a result, interest in this drug for the management of EDS in other disorders, as well as narcolepsy, has increased considerably. There is a growing school of thought that modafinil may have a role to play in other indications such as obstructive sleep apnea/hypopnea syndrome already treated by nasal continuous positive airway pressure but persisting EDS, shift work sleep disorders, neurological causes of sleepiness, and healthy adults performing sustained operations, particularly those in the military. However, until adequately powered randomised-controlled trials confirm long-term efficacy and safety, the recommendation of wakefulness promoters in healthy adults cannot be justified.

Amphetamines↗
PubMed1997

REM sleep disinhibition at sleep onset: a comparison between narcolepsy and depression.

Shortened REM latency and increased REM density are frequently observed in both narcolepsy and depression, suggesting a common mechanism of REM sleep disinhibition in these disorders. We compared night sleep recordings of 24 depressive and 24 narcoleptic patients. The amount of REM sleep and REM density did not differ between the patient groups; however, REM latency distributions differed significantly. Whereas in narcoleptic patients REM episodes started either immediately at sleep onset or following at least 60 min of non-REM sleep, in depressives two thirds of REM latencies were in the range from 1 to 60 min. In narcoleptic patients, short as compared to long REM latencies were associated with longer total sleep time, greater sleep efficiency, reduced amounts of wakefulness, and increased amounts of slow-wave sleep. In depressive subjects the reverse pattern was seen. We conclude that a common mechanism of REM sleep disinhibition in narcolepsy and depression is very unlikely.

Adult↗
PubMed1986

The management of drop attacks.

From the preceding it is evident that drop attacks can result from a myriad of causes. As in all situations, the patient's history and the clinical picture are the most important factors in arriving at the appropriate diagnosis. However, understanding the neurophysiologic basis of posture should prove significantly helpful in this endeavor.

Aged↗
PubMed1997

Comparison of the results of the Epworth Sleepiness Scale and the Multiple Sleep Latency Test.

The Epworth Sleepiness Scale (ESS), which asks patients to estimate the likelihood that they would doze off or fall asleep in sedentary situations, has been proposed to be a quick, inexpensive way to assess sleepiness. We analyzed relations among ESS scores, mean sleep latencies on the Multiple Sleep Latency Test (MSLT), and subjective assessments of severity of sleepiness in 60 patients (34 women) with suspected excessive daytime sleepiness. Mean scores were 14.2 +/- 5.9 on the ESS and 8.3 +/- 5.2 minutes on the MSLT. ESS scores correlated negatively, but not strongly, with MSLT scores (rho = -0.37, p = 0.0042) and ESS scores of 14 and above predicted a low mean sleep latency on the MSLT. The ESS score correlated with the degree to which patients complained of sleepiness and may be useful as an otherwise elusive link between patients' complaints and their objective findings on MSLT.

Adolescent↗