Excessive daytime sleepiness (EDS) is characterised as involuntary drowsiness or an inability to stay awake throughout the day, affecting one's capacity to operate. The prevalence of EDS in the general population is difficult to assess because to the subjectivity involved with self-reported EDS.
According to a recent population-based research, 33% of participants self-reported EDS at baseline, and 28% of those who did not have EDS at baseline acquired EDS throughout the 5-year study period.
The degree of EDS changed with time, and younger age and depression were independent predictors of incident EDS. EDS and hypersomnolence are often used interchangeably, despite the fact that EDS is a symptom and hypersomnolence is a disease process.
EDS has a negative influence on quality of life and adds to dangerous work and home situations, as well as putting public safety on the road in jeopardy. Insufficient sleep condition is the most prevalent cause of EDS. EDS, on the other hand, is a frequent symptom of medical conditions and a side effect of a variety of prescription and over-the-counter drugs.
Obstructive sleep apnea (OSA), alveolar hypoventilation, restless leg syndrome, periodic limb movement disorder, circadian rhythm disorder, narcolepsy, idiopathic hypersomnia, and Kleine-Levin syndrome are all examples of sleep disorders that may show as EDS.
Hypothyroidism, renal/hepatic failure, neurodegenerative disorders such as Parkinsonism, stroke, myotonic dystrophy, multiple sclerosis, structural brain lesions, traumatic brain injury, and psychiatric disorders such as depression, anxiety, and substance abuse are all medical conditions in which EDS is a clinical symptom. Sedative-hypnotics, beta blockers, antihistamines, anticonvulsants, antidepressants, and opiates are among the medications linked to EDS.
Multiple risk factors overlapping in a single patient might create a diagnostic conundrum. If the patient does not react to the first treatment, further diagnosis for EDS should be sought. Residual drowsiness in OSA patients who have been properly treated might be complex, necessitating additional evaluation and care.
In 1998, two groups of researchers discovered the same gene in animal models, which led to a breakthrough in the aetiology of narcolepsy. This novel gene was given the names hypocretin by Lecea et al. and orexin by Sakurai et al. The neuropeptide hypocretin/orexin is generated in the lateral posterior hypothalamus.
It's important for controlling the sleep/wake cycle, as well as neurocognitive and metabolic activities. Type 1 narcolepsy (NT1) is defined by the loss of hypocretin/orexin-producing neurons and low levels of hypocretin/orexin in the cerebrospinal fluid (CSF).
Though no direct proof has been uncovered, the loss of these particular neurons is assumed to be linked to an autoimmune process. The evidence for this notion is based on a significant relationship between NT1 and the HLA-DQB1*0602 allele and polymorphisms.
Seasonal fluctuation in the prevalence of NT1 supports infectious etiologies, with an increased incidence of NT1 in Scandinavia after the introduction of the Pandemrix influenza vaccine for the H1N1 virus. There's additional evidence that NT1 is linked to Streptococcus infections, with greater antibody titers to Streptococcus pyogenes seen in comparison to controls.
The aetiology of type 2 narcolepsy (NT2), in contrast to NT1, is unclear, while it is considered to be caused by less significant hypocretin/orexin impairment. The majority of NT2 individuals have normal hypocretin levels; nonetheless, NT2 seems to be a heterogeneous illness with subgroups.
To further explain the genetic tendency to narcolepsy, 86–98% of NT1 patients had the HLA-DQB1*0602 allele, albeit this is not enough to cause the condition. In the general population, this allele is found in 5–38 percent of people. Some studies have shown that this allele is more common in NT2 than in the general population, however the evidence is limited.
Increased BMI in individuals with narcolepsy/cataplexy was not linked with CSF hypocretin levels in a short study of 26 participants. Other metabolic pathways might explain the link between fat and narcolepsy, according to this report. A greater BMI was linked to a later diagnosis in another research.
Animal studies suggest that weight gain is caused by the loss of hypocretin neurons rather than the loss of hypocretin itself. According to certain research, the dietary choices of NT1 patients compared to controls may also contribute to weight gain. Binge eating, nocturnal eating, and carbohydrate desire have all been described in NT1 individuals, therefore this might reflect impaired reward motivation and processing.
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According to a recent population-based research, 33% of participants self-reported EDS at baseline, and 28% of those who did not have EDS at baseline acquired EDS throughout the 5-year study period.
The degree of EDS changed with time, and younger age and depression were independent predictors of incident EDS. EDS and hypersomnolence are often used interchangeably, despite the fact that EDS is a symptom and hypersomnolence is a disease process.
EDS has a negative influence on quality of life and adds to dangerous work and home situations, as well as putting public safety on the road in jeopardy. Insufficient sleep condition is the most prevalent cause of EDS. EDS, on the other hand, is a frequent symptom of medical conditions and a side effect of a variety of prescription and over-the-counter drugs.
Obstructive sleep apnea (OSA), alveolar hypoventilation, restless leg syndrome, periodic limb movement disorder, circadian rhythm disorder, narcolepsy, idiopathic hypersomnia, and Kleine-Levin syndrome are all examples of sleep disorders that may show as EDS.
Hypothyroidism, renal/hepatic failure, neurodegenerative disorders such as Parkinsonism, stroke, myotonic dystrophy, multiple sclerosis, structural brain lesions, traumatic brain injury, and psychiatric disorders such as depression, anxiety, and substance abuse are all medical conditions in which EDS is a clinical symptom. Sedative-hypnotics, beta blockers, antihistamines, anticonvulsants, antidepressants, and opiates are among the medications linked to EDS.
Multiple risk factors overlapping in a single patient might create a diagnostic conundrum. If the patient does not react to the first treatment, further diagnosis for EDS should be sought. Residual drowsiness in OSA patients who have been properly treated might be complex, necessitating additional evaluation and care.
In 1998, two groups of researchers discovered the same gene in animal models, which led to a breakthrough in the aetiology of narcolepsy. This novel gene was given the names hypocretin by Lecea et al. and orexin by Sakurai et al. The neuropeptide hypocretin/orexin is generated in the lateral posterior hypothalamus.
It's important for controlling the sleep/wake cycle, as well as neurocognitive and metabolic activities. Type 1 narcolepsy (NT1) is defined by the loss of hypocretin/orexin-producing neurons and low levels of hypocretin/orexin in the cerebrospinal fluid (CSF).
Though no direct proof has been uncovered, the loss of these particular neurons is assumed to be linked to an autoimmune process. The evidence for this notion is based on a significant relationship between NT1 and the HLA-DQB1*0602 allele and polymorphisms.
Seasonal fluctuation in the prevalence of NT1 supports infectious etiologies, with an increased incidence of NT1 in Scandinavia after the introduction of the Pandemrix influenza vaccine for the H1N1 virus. There's additional evidence that NT1 is linked to Streptococcus infections, with greater antibody titers to Streptococcus pyogenes seen in comparison to controls.
The aetiology of type 2 narcolepsy (NT2), in contrast to NT1, is unclear, while it is considered to be caused by less significant hypocretin/orexin impairment. The majority of NT2 individuals have normal hypocretin levels; nonetheless, NT2 seems to be a heterogeneous illness with subgroups.
To further explain the genetic tendency to narcolepsy, 86–98% of NT1 patients had the HLA-DQB1*0602 allele, albeit this is not enough to cause the condition. In the general population, this allele is found in 5–38 percent of people. Some studies have shown that this allele is more common in NT2 than in the general population, however the evidence is limited.
Increased BMI in individuals with narcolepsy/cataplexy was not linked with CSF hypocretin levels in a short study of 26 participants. Other metabolic pathways might explain the link between fat and narcolepsy, according to this report. A greater BMI was linked to a later diagnosis in another research.
Animal studies suggest that weight gain is caused by the loss of hypocretin neurons rather than the loss of hypocretin itself. According to certain research, the dietary choices of NT1 patients compared to controls may also contribute to weight gain. Binge eating, nocturnal eating, and carbohydrate desire have all been described in NT1 individuals, therefore this might reflect impaired reward motivation and processing.
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