Pediatric narcolepsy

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Pediatric narcolepsy refers to conditions of narcolepsy during childhood and adolescence (during the ages 18 years and younger). In a pediatric setting, people with narcolepsy still exhibit the classical tetrad symptoms of narcolepsy, and thus is possible for both type 1 and type 2 narcolepsy to develop in adolescence.

Contents

Pediatric population characteristics

Pediatric narcolepsy cases are cases when patients are diagnosed or experience symptoms onset for narcolepsy before the age of 18. Of patients who obtain a formal diagnosis for narcolepsy, more than 50% report first experiencing symptoms of narcolepsy more than 10 years before their formal diagnosis, with an average age of symptom onset being at age 15 and symptom onset most likely to occur during a person's second decade. [1] [2] [3] [4] [5] The overall prevalence of narcolepsy in a population is around 0.05% and is not impacted by population age. [2] The most common symptom that occurs with symptom onset is excessive daytime sleepiness (EDS). There is currently no known difference in the prevalence of narcolepsy across sex, race, or ethnicity. [2] Like in adult populations, type 1 narcolepsy is more common than type 2 narcolepsy; however, pediatric populations have a greater ratio of type 2 narcolepsy to type 1 narcolepsy when compared to adult populations. [6]

Pathophysiology

Type 1 narcolepsy

A Diagram of Projections to and from the orexin producing cells in the lateral hypothalamus. Abbreviations: LDT, laterodorsal tegmental nucleus; PPT, pedunculopontine tegmental nucleus; DR, dorsal raphe nucleus; LC, locus coeruleus; VTA, ventral tegmental area; TMN, tuberomammillary nucleus; Arc, arcuate nucleus; VLPO, ventrolateral preoptic nucleus. Fendo-04-00018-g001.jpg
A Diagram of Projections to and from the orexin producing cells in the lateral hypothalamus. Abbreviations: LDT, laterodorsal tegmental nucleus; PPT, pedunculopontine tegmental nucleus; DR, dorsal raphe nucleus; LC, locus coeruleus; VTA, ventral tegmental area; TMN, tuberomammillary nucleus; Arc, arcuate nucleus; VLPO, ventrolateral preoptic nucleus.

Type 1 narcolepsy, also known as narcolepsy with cataplexy, can have various causes and factors, but ultimately culminates in death of neuronal orexin producing cells located in the lateral hypothalamus and a decrease in orexin concentrations in the cerebral spinal fluid. [3] [7] Normally, orexin acts as a neurotransmitter and is projected to various areas brain through its interaction with orexin receptors, a type of G protein-coupled receptor. Importantly, the dorsal raphe nucleus, locus coeruleus, and tuberomammillary nucleus contain orexin receptors, are projected to by orexin cells and are known to be involved in wakefulness. [7]

The orexin cells in the lateral hypothalamus also receive signals from various areas of the brain, including the limbic system, infralimbic cortex, nucleus accumbens, and other cells in the hypothalamus (such as the preoptic area). [7] The limbic system is responsible for emotional state regulation, it is suspected that interruption of the projections between the limbic system and orexin cells is involved with cataplexy, the second hallmark symptom of type 1 narcolepsy. [7]

Orexin cells are also impacted by factors associated with diet and nutrition. It has been shown that ghrelin, a hormone involved with initiation of a hunger state, depolarizes and activates orexin cells. [2] [7] In contrast, leptin, a hormone that monitors energy availability, hyperpolarizes and inhibits orexin cell activity. [2] [7] This, in addition to studies that demonstrate that the destruction of orexin cells is associated with obesity, support the idea of orexin playing a role in nutrition sensing in addition to its role in promoting wakefulness. [7]

The primary genetic risk factor associated with the development of narcolepsy is a variant of the human leukocyte antigen complex (HLA) known as HLA DQB1*06:02 and supports a potential autoimmune hypothesis for the development of type 1 narcolepsy. [2] [3] [5]

Type 2 narcolepsy

The pathophysiology of type 2 narcolepsy is not fully understood and is difficult to study. [6] This is because, by definition, type 2 narcolepsy is narcolepsy without the symptom of cataplexy. This means that while type 1 narcolepsy (narcolepsy with cataplexy) has a defined pathophysiology, type 2 narcolepsy is a term to describe narcolepsy arising from other means. [2] [6]

Signs and symptoms

Clinical signs and symptoms

Classic tetrad

The Classic tetrad of symptoms include Excessive Daytime Sleepiness (EDS), Cataplexy, hypnogogic and/or hypnopompic hallucinations, and Sleep paralysis. While patients with narcolepsy don't necessarily experience all symptoms of the classic tetrad, it is unlikely for a patient with narcolepsy to not have at least one of these symptoms. [5]

Excessive daytime sleepiness

Excessive daytime sleepiness, also known as hypersomnolence, is often the primary, if not only, symptom experienced at symptom onset. [5] EDS is often masked as a person having low energy and may not be considered significant by doctors in comparison to other symptoms experienced by patients with narcolepsy. [8] Despite being the primary symptom of narcolepsy, EDS is also a common symptom resulting from sleep apnea and other sleep related conditions, potentially complicating the ability for doctors to link a patient's EDS to narcolepsy. [9] Determination of EDS is usually done through surveys like the Epworth Sleepiness Scale. [9]

Cataplexy

An instance of cataplexy resulting in loss of motor control. Narcoleptic Minute 006 0001.jpg
An instance of cataplexy resulting in loss of motor control.

Cataplectic attacks are episodes of lost muscle tone that are initiated by bouts of intense emotions. [10] These events are known to cause a phenomenon known as cataplectic facies, a distinct facial expression that involves a slackened mouth and a drooping tongue. [9] which is Emotions that can trigger a cataplectic attack include laughter, excitement, anger, fear, and frustration. [10] Cataplexy is indicative of Type 1 narcolepsy, and usually becomes present one to three years after the onset of EDS. [3] Because of this delay in onset, cataplexy is thought to be developed overtime and results in a decreased prevalence in pediatric populations compared to adult populations.

Hypnogogic/hypnopompic hallucinations

Hypnogogic and hypnopompic hallucinations are hallucinations that occur upon waking up or when a person is about to fall asleep respectively. These hallucinations often accompany sleep paralysis, another symptom of the classic tetrad. While still being investigated, several studies report that hypnogogic hallucinations are prevalent in roughly 50% of pediatric narcolepsy cases, but prevalence of hallucinations has varied widely in several studies. [9] [11]

Sleep paralysis

Sleep paralysis is phenomena when a person is unable to move and speak after waking up. [3] Due to difficulty in pediatric populations being able to properly describe the experience of sleep paralysis, there has been difficulty in determining potential differences in the prevalence and severity of sleep paralysis between pediatric and adult populations. [11]

Clinical Signs and Symptoms of Narcolepsy [1] [2] [3] [4]
Classic tetradOther clinical symptoms associated with narcolepsy
Excessive daytime sleepiness REM behavior disorder
Cataplexy Periodic limb movements
Sleep paralysis Precocious puberty
Hypnogogic/Hypnopompic hallucinations Sudden weight gain
Polycystic ovary syndrome
Disturbed nocturnal sleep
Autonomic actions

"Behavioral" signs

Children with narcolepsy may develop depressive feelings, hyperactivity, irritability, brain fog, and dullness. These behaviors are thought to be attributed to downstream effects of disturbed nighttime sleep patterns and EDS. [1] [4] [12] EDS has been shown to have a strong impact on academic standing, with a strong correlation between narcolepsy and worsening academic performance. [9] In addition, other symptoms of narcolepsy, such as weight gain, can lead patients becoming withdrawn, introverted, and other features that can indicate depression. [5]

Diagnosis

Diagnostic Criteria for Narcolepsy type I and II according to the third edition of the International Classification of Sleep Disorders. Children-09-00974-g001.png
Diagnostic Criteria for Narcolepsy type I and II according to the third edition of the International Classification of Sleep Disorders.

As per the third edition of International Classification of Sleep Disorders (ICSD-3), Narcolepsy can be diagnosed after several criteria have been met. The first criteria is for the presence of EDS. A formal diagnosis of narcolepsy can then be given if the diagnostic criteria for the Multiple Sleep Latency Test (MSLT) post polysomnogram (PSG) are met. Diagnosis can be further classified into narcolepsy type 1 or narcolepsy type 2 based on the presence of cataplectic symptoms or cerebrospinal hypocretin-1 deficiency. The presence of cataplectic symptoms or hypocretin deficiency favors a narcolepsy type 1 diagnosis. [13] While not mentioned in the ICSD-3, the second edition has the added criteria of not being able to explain EDS with another condition or medication and expands on experiencing EDS for at least 3 months. [1] While not necessary for a diagnosis of narcolepsy, certain survey questionnaires like the Epworth sleepiness scale can be useful in determining the presence and absence of symptoms associated with narcolepsy. [14]

If type 1 narcolepsy is suspected, it is possible to obtain a diagnosis through testing for orexin concentrations in the cerebrospinal fluid. Patients with type 1 narcolepsy typically have measured orexin concentrations of 110 pg/mL or lower. [3] [15] Cases of type 2 narcolepsy will be unable to be determined through this measurement due to type 2 narcolepsy patients typically having normal concentrations of orexin. [15]

MSLT diagnostic criteria for narcolepsy [1] [13]
ParameterThreshold
Maximum mean sleep latency (minutes)8
Minimum number of sleep-onset rapid eye movement periods (SOREPs)2

Treatment

Non-medication based interventions

Nonpharmacological measures to assist in the management of symptoms of narcolepsy focus on regulating and maintaining healthy sleep habits. In addition to having set periods for nocturnal sleep, scheduled naps may be incorporated into a person's lifestyle in order to stave off the impacts of EDS. Regular physical activity and healthy diets, in addition to improve alertness and combat EDS, can also provide benefits in improving potential weight gain resulting from narcolepsy as well as improve depressive and other mood symptoms associated with EDS and narcolepsy. [2]

Medication-based interventions

Commonly prescribed medications for the treatment of symptoms of narcolepsy [2] [3] [16] [17]
MedicationMedication typeTreated symptom(s)Approval status for the treatment of narcolepsy
Modafinil Wake promoting agentEDSFDA approved for ages 18 and above
Sodium oxybate Central nervous system depressant Cataplexy, Hallucinations, sleep paralysisFDA approved for ages 7 and above
Pitolisant histamine 3 (H3) receptor antagonist EDS/CataplexyPDA approved for adults, in trials for use in a pediatric setting
Methylphenidate Traditional stimulant EDSFDA approved for ages 6 and above
Dextroamphetamine Traditional stimulantEDSFDA approved for Ages 6 and above
Clomipramine Tricyclic antidepressant (TCA)CataplexyNot approved for pediatric patients
Desipramine Tricyclic antidepressant (TCA)CataplexyNot approved for pediatric patients
Imipramine Tricyclic antidepressant (TCA)CataplexyNot approved for pediatric patients
Protryptylin Tricyclic antidepressant (TCA)CataplexyNot approved for pediatric patients
Fluoxetine SSRI CataplexyNot approved for pediatric patients
Venlafaxine SNRI CataplexyNot approved for pediatric patients

Stigma and diagnostic complications

Expected healthy ranges of sleep separated by age range. As depicted, expect healthy ranges of obtained sleep decreases with age and allow for easier identification of EDS. Medsci-07-00106-g001-550.webp
Expected healthy ranges of sleep separated by age range. As depicted, expect healthy ranges of obtained sleep decreases with age and allow for easier identification of EDS.

Complications in diagnosis narcolepsy can delay an official diagnosis for more than 10 years. Various factors are known to contribute to the diagnostic delay. Before a formal diagnosis of narcolepsy, there is often a misdiagnosis for an alternative, more common condition that could be attributed to the experienced symptoms. Conditions like Attention deficit hyperactive disorder (ADHD), depression, and schizophrenia have been known to be potential misdiagnosis for narcolepsy. [1] [9] [12] [18] [14] Economic barriers may also delay diagnosis, as an official diagnosis may involve visiting multiple to either one doctor or multiple doctors. [2] Diagnosis of narcolepsy may also be delayed as a result of symptoms of narcolepsy potentially being attributed to normal behaviors of certain age groups. Napping as a result of EDS is often confused with naps taken by younger children, EDS may be harder to identify at younger ages due to greater sleep requirements, and many behavioral signs stemming from the impacts of EDS could be seen as "rebellious" teen behaviors. [3] [15] Additionally, the inability of younger children to properly describe their symptoms may impact the suspected average age of onset. [5]

Common comorbidities

Attention deficit hyperactive disorder

A Venn Diagram depicting psychiatric conditions associated with narcolepsy as well as medication interventions common between these conditions. Figure was adapted from doi:10.3390/medsci6010016. Adapted narcolepsy relations venn diagram.png
A Venn Diagram depicting psychiatric conditions associated with narcolepsy as well as medication interventions common between these conditions. Figure was adapted from doi:10.3390/medsci6010016.

Attention Deficit Hyperactive Disorder (ADHD) is a psychiatric disorder that can often present in similar manners to narcolepsy and is a common comorbidity given to people with narcolepsy. [19] However, due to prescribed medications for ADHD (serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors) also being effective for the treatment of EDS, it is likely that diagnosis of ADHD can delay and hide the presence of narcolepsy. [20] Not only is the expected age of onset of ADHD similar to that of narcolepsy, but several symptoms of ADHD overlap with those experienced by those with narcolepsy. [19] Not only do they both share the potential for sleep disturbances and periodic limb movements during sleep, but ADHD may also present as mental fog, another symptom potentially resulting from the disturbed sleep experienced by those with narcolepsy. [19] Disturbed sleep and overall sleepiness experienced by those with narcolepsy may contribute to the potential development of ADHD in addition to narcolepsy, making ADHD a common comorbidity with narcolepsy in addition to being a potential misdiagnosis altogether. [3]

Depression

Depression is the most commonly experienced psychiatric symptom reported by people with narcolepsy, as studies have shown that more than 50% of patients with narcolepsy suffer from depression. [19] [21] Various symptoms of depression may also be experienced by people with narcolepsy. This is either as a direct result of narcolepsy, such as disturbed sleep and other parasomnias, or as a result of the person living life with a debilitating condition like narcolepsy, such as in cases of social withdrawal. [19] In addition to the possibility of living with a debilitating condition contributes to the development of depression, deficiencies in hypocretin, such as in cases of type I narcolepsy, may also have an impact on emotional processing. [19] However, this claim needs further investigation, as while studies have claimed that people with both narcolepsy and depression have developed depression before their diagnosis of narcolepsy, it may be influenced by the known delays in narcolepsy diagnosis. [19] While more research needs to be done, current research fails to find differences in the prevalence of depression between people with type 1 and type 2 narcolepsy. [20]

Anxiety disorders

Anxiety disorders are condition that led to elevated levels of anxiety and fear during normal life. [19] Attention towards a potential comorbidity connection between anxiety disorders and narcolepsy has been increasing, as studies have come out to suggest that around half of patients with narcolepsy experience a form of anxiety disorder. [19] [21] Whether or not a person has been diagnosed with narcolepsy may also impact the kind of anxiety disorder they may develop, as panic disorders become more prevalent after official diagnosis. [19] [20] One potential rational may be the result of patients learning they have an incurable, life-altering condition, and may develop anxiety over triggering symptoms of narcolepsy like cataplexy. [19] In addition to this, the prevalence of anxiety disorders was not impacted by whether the person had type 1 or type 2 narcolepsy, suggesting that the development of an anxiety disorder is likely in response to experienced symptoms, such as EDS and cataplexy, rather than the direct pathophysiology of narcolepsy. [22] This does not rule out the possibility of direct pathophysiology leading to anxiety, as orexin cells are interconnected with areas of the brain responsible for stress responses. [7] [20]

Eating disorders

Eating disorders, like anorexia and bulimia, are known comorbidities of narcolepsy. [19] The presence of these eating disorders have been attributed as a response to sudden weight gains experienced by people with narcolepsy. [19] Due to the relationship between orexin and hunger related hormones, like leptin and ghrelin, it is also possible for a pathophysiological cause for the development of eating disorders rather than in response to experienced symptoms, but more research is needed in this area. [19] [20]

Related Research Articles

<span class="mw-page-title-main">Modafinil</span> Eugeroic medication

Modafinil, sold under the brand name Provigil among others, is a wakefulness-promoting medication used primarily to treat narcolepsy. Modafinil is also approved for stimulating wakefulness in people with sleep apnea and shift work sleep disorder. It is taken by mouth. Modafinil is not approved by the US Food and Drug Administration (FDA) for use in people under age 17.

<span class="mw-page-title-main">Sleep disorder</span> Medical disorder of a persons sleep patterns

A sleep disorder, or somnipathy, is a medical disorder of an individual's sleep patterns. Some sleep disorders are severe enough to interfere with normal physical, mental, social and emotional functioning. Sleep disorders are frequent and can have serious consequences on patients' health and quality of life. Polysomnography and actigraphy are tests commonly ordered for diagnosing sleep disorders.

<span class="mw-page-title-main">Attention deficit hyperactivity disorder</span> Neurodevelopmental disorder

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterised by executive dysfunction occasioning symptoms of inattention, hyperactivity, impulsivity and emotional dysregulation that are excessive and pervasive, impairing in multiple contexts, and otherwise age-inappropriate.

<span class="mw-page-title-main">Orexin</span> Neuropeptide that regulates arousal, wakefulness, and appetite.

Orexin, also known as hypocretin, is a neuropeptide that regulates arousal, wakefulness, and appetite. It exists in the forms of orexin-A and orexin-B. The most common form of narcolepsy, type 1, in which the individual experiences brief losses of muscle tone, is caused by a lack of orexin in the brain due to destruction of the cells that produce it.

Generalized anxiety disorder (GAD) is a mental and behavioral disorder, specifically an anxiety disorder characterized by excessive, uncontrollable and often irrational worry about events or activities. Worry often interferes with daily functioning, and individuals with GAD are often overly concerned about everyday matters such as health, finances, death, family, relationship concerns, or work difficulties. Symptoms may include excessive worry, restlessness, trouble sleeping, exhaustion, irritability, sweating, and trembling.

Somnolence is a state of strong desire for sleep, or sleeping for unusually long periods. It has distinct meanings and causes. It can refer to the usual state preceding falling asleep, the condition of being in a drowsy state due to circadian rhythm disorders, or a symptom of other health problems. It can be accompanied by lethargy, weakness and lack of mental agility.

Hypersomnia is a neurological disorder of excessive time spent sleeping or excessive sleepiness. It can have many possible causes and can cause distress and problems with functioning. In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), hypersomnolence, of which there are several subtypes, appears under sleep-wake disorders.

<span class="mw-page-title-main">Conditions comorbid to autism spectrum disorders</span> Medical conditions more common in autistic people

Autism spectrum disorders (ASD) are neurodevelopmental disorders that begin in early childhood, persist throughout adulthood, and affect three crucial areas of development: communication, social interaction and restricted patterns of behavior. There are many conditions comorbid to autism spectrum disorders such as attention-deficit hyperactivity disorder and epilepsy.

Child psychopathology refers to the scientific study of mental disorders in children and adolescents. Oppositional defiant disorder, attention-deficit hyperactivity disorder, and autism spectrum disorder are examples of psychopathology that are typically first diagnosed during childhood. Mental health providers who work with children and adolescents are informed by research in developmental psychology, clinical child psychology, and family systems. Lists of child and adult mental disorders can be found in the International Statistical Classification of Diseases and Related Health Problems, 10th Edition (ICD-10), published by the World Health Organization (WHO) and in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), published by the American Psychiatric Association (APA). In addition, the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood is used in assessing mental health and developmental disorders in children up to age five.

Cataplexy is a sudden and transient episode of muscle weakness accompanied by full conscious awareness, typically triggered by emotions such as laughing, crying, or terror. Cataplexy affects approximately 20% of people who have narcolepsy, and is caused by an autoimmune destruction of hypothalamic neurons that produce the neuropeptide hypocretin, which regulates arousal and has a role in stabilization of the transition between wake and sleep states. Cataplexy without narcolepsy is rare and the cause is unknown.

A major depressive episode (MDE) is a period characterized by symptoms of major depressive disorder. Those affected primarily exhibit a depressive mood for at least two weeks or more, and a loss of interest or pleasure in everyday activities. Other symptoms can include feelings of emptiness, hopelessness, anxiety, worthlessness, guilt, irritability, changes in appetite, difficulties in concentration, difficulties remembering details, making decisions, and thoughts of suicide. Insomnia or hypersomnia and aches, pains, or digestive problems that are resistant to treatment may also be present.

<span class="mw-page-title-main">Lateral hypothalamus</span>

The lateral hypothalamus (LH), also called the lateral hypothalamic area (LHA), contains the primary orexinergic nucleus within the hypothalamus that widely projects throughout the nervous system; this system of neurons mediates an array of cognitive and physical processes, such as promoting feeding behavior and arousal, reducing pain perception, and regulating body temperature, digestive functions, and blood pressure, among many others. Clinically significant disorders that involve dysfunctions of the orexinergic projection system include narcolepsy, motility disorders or functional gastrointestinal disorders involving visceral hypersensitivity, and eating disorders.

The International Classification of Sleep Disorders (ICSD) is "a primary diagnostic, epidemiological and coding resource for clinicians and researchers in the field of sleep and sleep medicine". The ICSD was produced by the American Academy of Sleep Medicine (AASM) in association with the European Sleep Research Society, the Japanese Society of Sleep Research, and the Latin American Sleep Society. The classification was developed as a revision and update of the Diagnostic Classification of Sleep and Arousal Disorders (DCSAD) that was produced by both the Association of Sleep Disorders Centers (ASDC) and the Association for the Psychophysiological Study of Sleep and was published in the journal Sleep in 1979. A second edition, called ICSD-2, was published by the AASM in 2005. The third edition, ICSD-3, was released by the AASM in 2014. A text revision of the third edition (ICSD-3-TR) was published in 2023 by the AASM.

<span class="mw-page-title-main">Bipolar disorder in children</span>

Bipolar disorder in children, or pediatric bipolar disorder (PBD), is a rare mental disorder in children and adolescents. The diagnosis of bipolar disorder in children has been heavily debated for many reasons including the potential harmful effects of adult bipolar medication use for children. PBD is similar to bipolar disorder (BD) in adults, and has been proposed as an explanation for periods of extreme shifts in mood called mood episodes. These shifts alternate between periods of depressed or irritable moods and periods of abnormally elevated moods called manic or hypomanic episodes. Mixed mood episodes can occur when a child or adolescent with PBD experiences depressive and manic symptoms simultaneously. Mood episodes of children and adolescents with PBD are different from general shifts in mood experienced by children and adolescents because mood episodes last for long periods of time and cause severe disruptions to an individual's life. There are three known forms of PBD: Bipolar I, Bipolar II, and Bipolar Not Otherwise Specified (NOS). The average age of onset of PBD remains unclear, but reported age of onset ranges from 5 years of age to 19 years of age. PBD is typically more severe and has a poorer prognosis than bipolar disorder with onset in late-adolescence or adulthood.

Avoidant/restrictive food intake disorder (ARFID) is a feeding or eating disorder in which people avoid eating certain foods, or restrict their diets to the point it ultimately results in nutritional deficiencies. This can be due to the sensory characteristics of food, such as its appearance, smell, texture, or taste; due to fear of negative consequences such as choking or vomiting; having little interest in eating or food, or a combination of these factors. People with ARFID may also be afraid of trying new foods, a fear known as food neophobia.

Joseph Biederman was Chief of the Clinical and Research Programs in Pediatric Psychopharmacology and Adult ADHD at the Massachusetts General Hospital and a professor of psychiatry at Harvard Medical School. Biederman was board-certified in general and child psychiatry.

<span class="mw-page-title-main">Narcolepsy</span> Human sleep disorder that involves an excessive urge to sleep and other neurological features

Narcolepsy is a chronic neurological disorder that involves a decreased ability to regulate sleep–wake cycles. Symptoms often include periods of excessive daytime sleepiness and brief involuntary sleep episodes. Narcolepsy paired with cataplexy is evidenced to be an autoimmune disorder. These experiences of cataplexy can be brought on by strong emotions. Less commonly, there may be vivid hallucinations or an inability to move while falling asleep or waking up. People with narcolepsy tend to sleep about the same number of hours per day as people without it, but the quality of sleep tends to be lessened.

Idiopathic hypersomnia(IH) is a neurological disorder which is characterized primarily by excessive sleep and excessive daytime sleepiness (EDS). Idiopathic hypersomnia was first described in 1976, and it can be divided into two forms: polysymptomatic and monosymptomatic. The condition typically becomes evident in early adulthood and most patients diagnosed with IH will have had the disorder for many years prior to their diagnosis. As of August 2021, an FDA-approved medication exists for IH called Xywav, which is oral solution of calcium, magnesium, potassium, and sodium oxybates; in addition to several off-label treatments (primarily FDA-approved narcolepsy medications).

<span class="mw-page-title-main">Suvorexant</span> Medication used to treat insomnia

Suvorexant, sold under the brand name Belsomra, is an orexin antagonist medication which is used in the treatment of insomnia. It is indicated specifically for the treatment of insomnia characterized by difficulties with sleep onset and/or maintenance in adults. Suvorexant helps with falling asleep faster, sleeping longer, being awake less in the middle of the night, and having better quality of sleep. Its effectiveness is modest, and is similar to that of other orexin antagonists, but is lower than that of benzodiazepines and Z-drugs. Suvorexant is taken by mouth.

The term functional somatic syndrome (FSS) refers to a group of chronic diagnoses with no identifiable organic cause. This term was coined by Hemanth Samkumar. It encompasses disorders such as chronic fatigue syndrome, fibromyalgia, chronic widespread pain, temporomandibular disorder, irritable bowel syndrome, lower back pain, tension headache, atypical face pain, non-cardiac chest pain, insomnia, palpitation, dyspepsia and dizziness. General overlap exists between this term, somatization and somatoform.

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  16. ↑ "Medication Guides". www.accessdata.fda.gov. Retrieved 2023-11-13.
  17. ↑ "Dextroamphetamine-Amphetamine", Definitions, Qeios, 2020-02-07, doi:10.32388/p9fa8a, S2CID   243013519 , retrieved 2023-11-13
  18. ↑ Hanin, Cyril; Arnulf, Isabelle; Maranci, Jean-Baptiste; Lecendreux, Michel; Levinson, Douglas F.; Cohen, David; Laurent-Levinson, Claudine (July 2021). "Narcolepsy and psychosis: A systematic review". Acta Psychiatrica Scandinavica. 144 (1): 28–41. doi:10.1111/acps.13300. ISSN   1600-0447. PMC   8360149 . PMID   33779983.
  19. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Morse, Anne Marie; Sanjeev, Kothare (March 2018). "Narcolepsy and Psychiatric Disorders: Comorbidities or Shared Pathophysiology?". Medical Sciences. 6 (1): 16. doi: 10.3390/medsci6010016 . ISSN   2076-3271. PMC   5872173 . PMID   29462876.
  20. 1 2 3 4 5 BaHammam, Ahmed S.; Alnakshabandi, Kholoud; Pandi-Perumal, Seithikuruppu R. (2020-06-05). "Neuropsychiatric Correlates of Narcolepsy". Current Psychiatry Reports. 22 (8): 36. doi:10.1007/s11920-020-01159-y. ISSN   1535-1645. PMID   32514698. S2CID   219528517.
  21. 1 2 Schiappa, C.; Scarpelli, S.; D'Atri, A.; Gorgoni, M.; De Gennaro, Luigi (2018-12-26). "Narcolepsy and emotional experience: a review of the literature". Behavioral and Brain Functions. 14 (1): 19. doi: 10.1186/s12993-018-0151-x . ISSN   1744-9081. PMC   6305999 . PMID   30587203.
  22. ↑ Kim, Jiyoung; Lee, Gha-Hyun; Sung, Sang Min; Jung, Dae Soo; Pak, Kyoungjune (2020-01-01). "Prevalence of attention deficit hyperactivity disorder symptoms in narcolepsy: a systematic review". Sleep Medicine. 65: 84–88. doi:10.1016/j.sleep.2019.07.022. ISSN   1389-9457. PMID   31739230. S2CID   201174437.
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