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Narcolepsy

Updated : August 22, 2023





Background

Narcolepsy is a sleep condition characterized by EDS (excessive daytime sleepiness), sleep fragmentation, and frequent uncontrolled sleep episodes, and it can be linked with hypnagogic hallucinations, cataplexy (muscle weakness), and sleep paralysis.

Narcolepsy is classified into type 1 (narcolepsy with cataplexy) and type 2 (narcolepsy without cataplexy). Nearly half of the individuals develop symptoms throughout their adolescence. The condition is exceptionally morbid, impairing intellectual and social function. Providentially, the condition responds to treatment.

 

 

 

Epidemiology

Narcolepsy type 1 has a 14 per 100,000 individuals, whereas narcolepsy type 2 has a prevalence of 65.4 per 100,000 persons.

According to data from 2008-2010, the incidence is significantly more significant in the late teens to early twenties, with a 50% larger female preponderance in the United States

 

 

 

Anatomy

Pathophysiology

Dopamine, histamine norepinephrine, and serotonin suppress REM (Rapid eye movement), but acetylcholine is elevated in REM and wakefulness. The RAS (Reticular activating system) also suppresses the sleep-promoting ventral lateral preoptic region, decreasing GABA, which promotes muscle tone and motor neuron activity.

Emotional intensity increases activity in the amygdala and, as a result, in orexin-containing neurons, which reduces REM. The wake and sleep-promoting mechanisms are often mutually inhibitory to enable complete transitions. Orexin levels drop during typical REM sleep, which reduces RAS activity and promotes atonia.

Without enough quantities of orexin, the mechanism that distinguishes waking from sleep becomes unstable in narcolepsy type 1. The RAS no longer constantly causes wake-promoting neurotransmitters to be released into the cortex and no longer consistently suppresses the VLPO. This causes fast transitions between sleep and alertness and permits REM-related events to enter consciousness.

 

 

 

Etiology

Narcolepsy type 1 is caused by the loss of nearly all neurons that carry orexin. HLA haplotype DQB1*0602 is found in 95% of narcolepsy type 1 patients; however, it is also found in roughly 20% of the general population. The exact etiology of narcolepsy type 2 is unknown.

Current possibilities include decreased orexin cell death, weaker orexin receptor signaling, and an unknown mechanism. Cataplexy is a symptom of clinical progression in people diagnosed initially with narcolepsy type 2. Trauma and tumors are less prevalent causes of narcolepsy.

Antibodies against streptococcal infections have also been linked to the emergence of type 1 narcolepsy. Although no autoantibody has been discovered that corresponds with the disease mechanism in narcolepsy, this suggests that maybe narcolepsy type 1 is an autoimmune condition.

 

 

 

Genetics

Prognostic Factors

Some individuals with narcolepsy type 2 will acquire cataplexy. Many people experience symptoms that intensify with time. Although symptoms are unlikely to resolve independently, they are often adequately controlled with a mix of behavioral therapies and medications.

There are also novel therapies being researched that may allow for immunomodulation or the delivery of orexin agonists tiny enough to traverse the blood-brain barrier. Children frequently struggle with poor academic achievement and social connections. Work impairment is widespread, and most patients are unable to work.

 

 

 

Clinical History

Clinical History:

The EDS (extreme daytime sleepiness), hypnagogic hallucinations, cataplexy, & sleep paralysis make up the typical tetrad of narcolepsy. All four symptoms are rarely seen in children. The main sign of narcolepsy, EDS, must be present for at least three months in order to support the diagnosis. It’s common to feel sleepy at times, and it always follows an extended period of awake.

Mild drowsiness is only noticeable in healthy people during monotonous, sedentary activities (e.g., watching television and falling asleep). Severe EDS in narcoleptics causes involuntary somnolence when performing tasks that call for focus, like eating, driving, or conversing. Narcolepsy sufferers may experience paroxysms during which they may suddenly fall asleep, resulting in acute and ongoing sleepiness (i.e., sleep attacks).

Narcoleptic patients frequently take short, revitalizing naps (REM-style naps) throughout the day. Dreams could accompany their midday naps. Many people with narcolepsy have problems falling asleep at night. Patients may also engage in nocturnal compulsive activities, such as nocturnal smoking & eating disorders related to sleep. Another typical aspect of narcolepsy is obesity. Obstructive sleep apnea may be made worse by the presence of narcolepsy and obesity.

Cataplexy

Cataplexy, which is a momentary decrease of muscular tone, is an example of REM sleep interruption when awake. It could result in a fall if it is serious and widespread. Less obvious kinds may simply result in a substantial loss of tone (e.g., knee buckling & head nod). Movements of the lungs and eyes are retained. The most distinguishing trait of cataplexy is that it frequently results from emotional triggers (especially anger & laughter). About 70% of narcolepsy sufferers experience cataplexy. Its presence along with EDS substantially supports the narcolepsy diagnosis.

Sleep Disturbances

Narcoleptic patients may develop sleep paralysis, which is the unable to move after awakening and, less frequently, after dozing off while still conscious. It frequently comes with hallucinations. Muscles in the eyes and the lungs are unaffected. When people are uncomfortable while they sleep, sleep paralysis is less common. Sensory inputs like chatting to them or touching them can help to relieve it.

Hallucinations associated with sleep may be hypnagogic (occurring at the beginning of sleep) or hypnopompic (i.e., at the time of awakening). These hallucinations are typically of the vivid (dreamlike) kind and sensory in character. Narcolepsy frequently includes disturbed night-time sleep as one of its symptoms. As a result of daytime naps, narcoleptic individuals’ overall amount of sleep in a 24-hour period remains basically unaltered.

Young children

In young children, the typical narcolepsy image could look a little different. EDS may be denied by kids out of embarrassment. In certain cases, agitation and excessive motor activity are dominant. There is a high prevalence of academic decline, inattentiveness, & emotional lability. Children with cataplexy & narcolepsy may have a variety of motor abnormalities in the beginning of the condition that may not fit the traditional criteria of cataplexy.

Later in the course of the condition, these motor disturbances—which may be negative (hypotonia) and active (e.g., perioral motions, dyskinetic-dystonic movements, and stereotypic movements)—might go away. 51 prepubertal narcolepsy patients were studied, and both the first complaints and the typical misdiagnoses differed with age. Children under the age of five frequently experienced sudden object drops, “drop attacks,” aggressive conduct, & sudden irritability. In this age group, atonic seizures were the most often misdiagnosed condition.

The most frequent initial complaint in kids between the ages of 5 and 10 was inattentiveness, which was then followed by chronic tiredness and then difficulties waking up in the morning that was linked to aggressive behavior and sudden drops in academic performance. These kids were frequently given incorrect diagnoses of depression, ADHD, learning disabilities, or other neurological conditions. Poor academic achievement was a typical complaint among kids aged 10 to 12. Additional symptoms that were evident were an inappropriately low level of alertness, sleeping throughout class, and difficulty waking up in the morning.

Questionnaires

There are various surveys that can be used to gauge sleepiness. The 8-question Epworth Sleepiness Scale is the most often employed of these. The lowest possible total score is 0, and the highest possible score is 24. Patients react to each question with a numerical score ranging from 0 (not at all likely to fall asleep) to 3 (extremely likely to fall asleep). Although there is some debate regarding the exact threshold for atypical drowsiness, it is generally agreed that total scores greater than 10 call for further study.

 

 

Physical Examination

Physical examination

Patients with narcolepsy exhibit normal physical examination results. To rule out other potential explanations of the patient’s condition, such as an underlying structural anomaly, a thorough neurologic examination should be conducted.

Although there are no distinct physical signs that point to narcolepsy, the illness may be linked to obesity. Patients often exhibit atonia of the neck and limb muscles as well as lack of deep tendon reflexes during an episode of cataplexy.

 

 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Differential diagnosis:

Cataplexy

Seizures (particularly atonic seizures)

Syncope

  • Neurogenic
  • Orthostatic
  • Cardiogenic

Periodic paralysis

Psychogenic

Excessive sleepiness during the day

  • Poor sleeping hygiene and the reduced sleep syndrome
  • Idiopathic hypersomnia
  • Symptoms of sleep apnea
  • Syndrome of protracted weariness
  • Disordered movement during sleep (restless leg syndrome, periodic limb movement disorder, etc.)
  • Long-sleeping individuals (Normal variation in which the patient needs more sleep than usual to feel rested while undergoing otherwise normal tests)
  • Psychiatric (factitious disorder, depression, conversion disorder, malingering, etc.)
  • Addiction-related sleep problem (antihistamines, narcotics, antihistamines, benzodiazepines, beta-blockers, anticonvulsants, antipsychotics, etc.)
  • Hypersomnia accompanied by menstruation.
  • A medical ailment (Parkinson’s, multiple sclerosis, etc.) that causes hypersomnia.
  • Kleine-Levin syndrome

 

 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

With between 15- and 20-minute naps strategically timed during the day and upholding a sufficient nocturnal sleep schedule, behavioral therapy can be successful. For excessive morning sleepiness, modafinil (twice daily dose) and armodafinil are the first-line pharmaceutical treatments (once-daily dosing). Amphetamines would be the second method of treatment. Gamma-hydroxybutyrate, or GHB, in the form of sodium oxybate, is the first-line medication for cataplexy.

Due to the short duration of sleepiness—generally 5 to 15 minutes—the medicine is taken while lying in bed. After 2.5 to 4 hours, a second dose is administered. A central pharmacy distributes the restricted drug Xyrem. Although there are worries regarding sodium oxybate abuse, dependence, & illicit usage, post-market studies has not shown that these worries are warranted. Protriptyline, clomipramine, and SNRI/SSRIs (fluoxetine, venlafaxine) have also been used to treat cataplexy with modest success.

Alternative medicine therapies

In addition to promoting excellent sleep hygiene, the following actions are crucial:

  • Inform them on the dangers of drinking and using illicit drugs.
  • Help acquiring drugs & completing disability documents.
  • Counsel on mental health is provided.
  • Provide emotional assistance.

Drug therapy:

Although there are a number of CNS inhibitors used to treatment narcolepsy, none are completely successful in all patients. The sleep-improving advantages of methylphenidate are mixed with undesirable side effects such headaches, anxiety, & irritability. Although modafinil does cause drowsiness, its safety in young children has not yet been determined.

Armodafinil has similar side effects to methylphenidate and is also effective for treating narcolepsy. The sole FDA-approved medication for cataplexy is sodium oxybate, which shouldn’t be taken with some other CNS depressants and alcohol. Pitolisant, a histamine H3 blockers, was just recently licenced by the FDA for the treatment of narcolepsy. Early research suggests that it can enhance sleep. At this time, the FDA has not approved any medications for use in children.

 

 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Medication

 

amphetamine

Immediate release::

5 - 60

mg

once a day

in divided doses



dextroamphetamine

Extended release::

Initial dose: 10 mg oral capsule once or twice a day
Increase 10 mg at weekly intervals until the required response is achieved (preferred to be given in intervals of 4 to 6 hours at the early morning)
5 to 60 mg/day in divided doses
Immediate release:
Initial dose: 10 mg oral tablet/solution once or twice a day
Increase 10 mg at weekly intervals until the required response is achieved (preferred to be given in intervals of 4 to 6 hours in the early morning)
5 to 60 mg/day in divided doses



armodafinil

150 - 250

mg

Tablet

Oral

once a day

in the morning



modafinil

200

mg

single daily dose in the morning
Increase to 400 mg if well tolerated



pitolisant

8.9

mg

Orally 

once a day for 1 week and increase to 17.8 mg/day for another week (Maximum dose: 35.6 mg/day)



ephedrine

25 mg-50 mg IM or subcutaneously or 5 mg-25 mg IV administered slowly repeat the dose in 5-10 minutes as needed



sodium oxybate 

4.5

g

Solution

Orally 

dose divided every 4 hours

2.25g half strength and 2.25g taken 2.5-4 hours later
increase up to 1.5g/night at weekly intervals
Do not exceed 9g/night



amphetamine/dextroamphetamine 

(immediate-release) initial oral dose is 10 mg per day, which is usually divided into multiple doses throughout the day
dose may be raised by 10 mg per week



solriamfetol 

Upon awakening take 75mg orally everyday
The dose can be doubled at least every three days.
Maximum dose-150mg orally everyday



 

amphetamine

Immediate release::

For 6 to 11 years: 5 mg/day initially in divided doses, increase 5 mg/day weekly until required response achieved
For >12 years: 10 mg/day initially in divided doses, increase 10 mg/day weekly until required response achieved
Maintain dose between 5 to 60 mg/day once a first response is achieved (max. 60 mg/day)



dextroamphetamine

Immediate release::

For 6 to 11 years: 5 mg/day initially in divided doses, increase 5 mg/day weekly until required response achieved (NMT 60 mg/day)
For >12 years: 10 mg/day initially in divided doses, increase 10 mg/day weekly until required response achieved (NMT 60 mg/day)



ephedrine

Body surface area (BSA): 0.5 mg/kg or 16.7 mg/m2 IM or SC every 4-6 hours



sodium oxybate 

<7 years: Safety and efficacy not established
≥7 years
<20 kgs: Start with a lower dose
20 to <30kgs:
Initial dose- ≤1g orally/day
Maintenance dose- increase by 0.5g/dose
Maximum dose-3g/day
30 to <45kgs:
Initial dose-≤1.5g orally/day
Maximum dose- 3.75g/day
≥45 kgs:
Initial dose- ≤2.25g orally/day, divided into two doses
Maximum dose- 4.5g/day



amphetamine/dextroamphetamine 

(immediate-release) Age: 6-11 Years: Starting dose is 5 mg per day, taken orally and divided into multiple doses throughout the day
dose may be increased by 5 mg every week until the desired therapeutic response is achieved
Age: >12 Years: initial oral dose of this medication is 10 mg per day, divided into several doses throughout the day
dose may be gradually increased by 10 mg per week until the desired therapeutic effect is attained



 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK459236/

https://emedicine.medscape.com/article/1188433-clinical#b3

 

 

ADVERTISEMENT 

Narcolepsy

Updated : August 22, 2023




Narcolepsy is a sleep condition characterized by EDS (excessive daytime sleepiness), sleep fragmentation, and frequent uncontrolled sleep episodes, and it can be linked with hypnagogic hallucinations, cataplexy (muscle weakness), and sleep paralysis.

Narcolepsy is classified into type 1 (narcolepsy with cataplexy) and type 2 (narcolepsy without cataplexy). Nearly half of the individuals develop symptoms throughout their adolescence. The condition is exceptionally morbid, impairing intellectual and social function. Providentially, the condition responds to treatment.

 

 

 

Narcolepsy type 1 has a 14 per 100,000 individuals, whereas narcolepsy type 2 has a prevalence of 65.4 per 100,000 persons.

According to data from 2008-2010, the incidence is significantly more significant in the late teens to early twenties, with a 50% larger female preponderance in the United States

 

 

 

Dopamine, histamine norepinephrine, and serotonin suppress REM (Rapid eye movement), but acetylcholine is elevated in REM and wakefulness. The RAS (Reticular activating system) also suppresses the sleep-promoting ventral lateral preoptic region, decreasing GABA, which promotes muscle tone and motor neuron activity.

Emotional intensity increases activity in the amygdala and, as a result, in orexin-containing neurons, which reduces REM. The wake and sleep-promoting mechanisms are often mutually inhibitory to enable complete transitions. Orexin levels drop during typical REM sleep, which reduces RAS activity and promotes atonia.

Without enough quantities of orexin, the mechanism that distinguishes waking from sleep becomes unstable in narcolepsy type 1. The RAS no longer constantly causes wake-promoting neurotransmitters to be released into the cortex and no longer consistently suppresses the VLPO. This causes fast transitions between sleep and alertness and permits REM-related events to enter consciousness.

 

 

 

Narcolepsy type 1 is caused by the loss of nearly all neurons that carry orexin. HLA haplotype DQB1*0602 is found in 95% of narcolepsy type 1 patients; however, it is also found in roughly 20% of the general population. The exact etiology of narcolepsy type 2 is unknown.

Current possibilities include decreased orexin cell death, weaker orexin receptor signaling, and an unknown mechanism. Cataplexy is a symptom of clinical progression in people diagnosed initially with narcolepsy type 2. Trauma and tumors are less prevalent causes of narcolepsy.

Antibodies against streptococcal infections have also been linked to the emergence of type 1 narcolepsy. Although no autoantibody has been discovered that corresponds with the disease mechanism in narcolepsy, this suggests that maybe narcolepsy type 1 is an autoimmune condition.

 

 

 

Some individuals with narcolepsy type 2 will acquire cataplexy. Many people experience symptoms that intensify with time. Although symptoms are unlikely to resolve independently, they are often adequately controlled with a mix of behavioral therapies and medications.

There are also novel therapies being researched that may allow for immunomodulation or the delivery of orexin agonists tiny enough to traverse the blood-brain barrier. Children frequently struggle with poor academic achievement and social connections. Work impairment is widespread, and most patients are unable to work.

 

 

 

Clinical History:

The EDS (extreme daytime sleepiness), hypnagogic hallucinations, cataplexy, & sleep paralysis make up the typical tetrad of narcolepsy. All four symptoms are rarely seen in children. The main sign of narcolepsy, EDS, must be present for at least three months in order to support the diagnosis. It’s common to feel sleepy at times, and it always follows an extended period of awake.

Mild drowsiness is only noticeable in healthy people during monotonous, sedentary activities (e.g., watching television and falling asleep). Severe EDS in narcoleptics causes involuntary somnolence when performing tasks that call for focus, like eating, driving, or conversing. Narcolepsy sufferers may experience paroxysms during which they may suddenly fall asleep, resulting in acute and ongoing sleepiness (i.e., sleep attacks).

Narcoleptic patients frequently take short, revitalizing naps (REM-style naps) throughout the day. Dreams could accompany their midday naps. Many people with narcolepsy have problems falling asleep at night. Patients may also engage in nocturnal compulsive activities, such as nocturnal smoking & eating disorders related to sleep. Another typical aspect of narcolepsy is obesity. Obstructive sleep apnea may be made worse by the presence of narcolepsy and obesity.

Cataplexy

Cataplexy, which is a momentary decrease of muscular tone, is an example of REM sleep interruption when awake. It could result in a fall if it is serious and widespread. Less obvious kinds may simply result in a substantial loss of tone (e.g., knee buckling & head nod). Movements of the lungs and eyes are retained. The most distinguishing trait of cataplexy is that it frequently results from emotional triggers (especially anger & laughter). About 70% of narcolepsy sufferers experience cataplexy. Its presence along with EDS substantially supports the narcolepsy diagnosis.

Sleep Disturbances

Narcoleptic patients may develop sleep paralysis, which is the unable to move after awakening and, less frequently, after dozing off while still conscious. It frequently comes with hallucinations. Muscles in the eyes and the lungs are unaffected. When people are uncomfortable while they sleep, sleep paralysis is less common. Sensory inputs like chatting to them or touching them can help to relieve it.

Hallucinations associated with sleep may be hypnagogic (occurring at the beginning of sleep) or hypnopompic (i.e., at the time of awakening). These hallucinations are typically of the vivid (dreamlike) kind and sensory in character. Narcolepsy frequently includes disturbed night-time sleep as one of its symptoms. As a result of daytime naps, narcoleptic individuals’ overall amount of sleep in a 24-hour period remains basically unaltered.

Young children

In young children, the typical narcolepsy image could look a little different. EDS may be denied by kids out of embarrassment. In certain cases, agitation and excessive motor activity are dominant. There is a high prevalence of academic decline, inattentiveness, & emotional lability. Children with cataplexy & narcolepsy may have a variety of motor abnormalities in the beginning of the condition that may not fit the traditional criteria of cataplexy.

Later in the course of the condition, these motor disturbances—which may be negative (hypotonia) and active (e.g., perioral motions, dyskinetic-dystonic movements, and stereotypic movements)—might go away. 51 prepubertal narcolepsy patients were studied, and both the first complaints and the typical misdiagnoses differed with age. Children under the age of five frequently experienced sudden object drops, “drop attacks,” aggressive conduct, & sudden irritability. In this age group, atonic seizures were the most often misdiagnosed condition.

The most frequent initial complaint in kids between the ages of 5 and 10 was inattentiveness, which was then followed by chronic tiredness and then difficulties waking up in the morning that was linked to aggressive behavior and sudden drops in academic performance. These kids were frequently given incorrect diagnoses of depression, ADHD, learning disabilities, or other neurological conditions. Poor academic achievement was a typical complaint among kids aged 10 to 12. Additional symptoms that were evident were an inappropriately low level of alertness, sleeping throughout class, and difficulty waking up in the morning.

Questionnaires

There are various surveys that can be used to gauge sleepiness. The 8-question Epworth Sleepiness Scale is the most often employed of these. The lowest possible total score is 0, and the highest possible score is 24. Patients react to each question with a numerical score ranging from 0 (not at all likely to fall asleep) to 3 (extremely likely to fall asleep). Although there is some debate regarding the exact threshold for atypical drowsiness, it is generally agreed that total scores greater than 10 call for further study.

 

 

Physical examination

Patients with narcolepsy exhibit normal physical examination results. To rule out other potential explanations of the patient’s condition, such as an underlying structural anomaly, a thorough neurologic examination should be conducted.

Although there are no distinct physical signs that point to narcolepsy, the illness may be linked to obesity. Patients often exhibit atonia of the neck and limb muscles as well as lack of deep tendon reflexes during an episode of cataplexy.

 

 

Differential diagnosis:

Cataplexy

Seizures (particularly atonic seizures)

Syncope

  • Neurogenic
  • Orthostatic
  • Cardiogenic

Periodic paralysis

Psychogenic

Excessive sleepiness during the day

  • Poor sleeping hygiene and the reduced sleep syndrome
  • Idiopathic hypersomnia
  • Symptoms of sleep apnea
  • Syndrome of protracted weariness
  • Disordered movement during sleep (restless leg syndrome, periodic limb movement disorder, etc.)
  • Long-sleeping individuals (Normal variation in which the patient needs more sleep than usual to feel rested while undergoing otherwise normal tests)
  • Psychiatric (factitious disorder, depression, conversion disorder, malingering, etc.)
  • Addiction-related sleep problem (antihistamines, narcotics, antihistamines, benzodiazepines, beta-blockers, anticonvulsants, antipsychotics, etc.)
  • Hypersomnia accompanied by menstruation.
  • A medical ailment (Parkinson’s, multiple sclerosis, etc.) that causes hypersomnia.
  • Kleine-Levin syndrome

 

 

With between 15- and 20-minute naps strategically timed during the day and upholding a sufficient nocturnal sleep schedule, behavioral therapy can be successful. For excessive morning sleepiness, modafinil (twice daily dose) and armodafinil are the first-line pharmaceutical treatments (once-daily dosing). Amphetamines would be the second method of treatment. Gamma-hydroxybutyrate, or GHB, in the form of sodium oxybate, is the first-line medication for cataplexy.

Due to the short duration of sleepiness—generally 5 to 15 minutes—the medicine is taken while lying in bed. After 2.5 to 4 hours, a second dose is administered. A central pharmacy distributes the restricted drug Xyrem. Although there are worries regarding sodium oxybate abuse, dependence, & illicit usage, post-market studies has not shown that these worries are warranted. Protriptyline, clomipramine, and SNRI/SSRIs (fluoxetine, venlafaxine) have also been used to treat cataplexy with modest success.

Alternative medicine therapies

In addition to promoting excellent sleep hygiene, the following actions are crucial:

  • Inform them on the dangers of drinking and using illicit drugs.
  • Help acquiring drugs & completing disability documents.
  • Counsel on mental health is provided.
  • Provide emotional assistance.

Drug therapy:

Although there are a number of CNS inhibitors used to treatment narcolepsy, none are completely successful in all patients. The sleep-improving advantages of methylphenidate are mixed with undesirable side effects such headaches, anxiety, & irritability. Although modafinil does cause drowsiness, its safety in young children has not yet been determined.

Armodafinil has similar side effects to methylphenidate and is also effective for treating narcolepsy. The sole FDA-approved medication for cataplexy is sodium oxybate, which shouldn’t be taken with some other CNS depressants and alcohol. Pitolisant, a histamine H3 blockers, was just recently licenced by the FDA for the treatment of narcolepsy. Early research suggests that it can enhance sleep. At this time, the FDA has not approved any medications for use in children.

 

 

amphetamine

Immediate release::

5 - 60

mg

once a day

in divided doses



dextroamphetamine

Extended release::

Initial dose: 10 mg oral capsule once or twice a day
Increase 10 mg at weekly intervals until the required response is achieved (preferred to be given in intervals of 4 to 6 hours at the early morning)
5 to 60 mg/day in divided doses
Immediate release:
Initial dose: 10 mg oral tablet/solution once or twice a day
Increase 10 mg at weekly intervals until the required response is achieved (preferred to be given in intervals of 4 to 6 hours in the early morning)
5 to 60 mg/day in divided doses



armodafinil

150 - 250

mg

Tablet

Oral

once a day

in the morning



modafinil

200

mg

single daily dose in the morning
Increase to 400 mg if well tolerated



pitolisant

8.9

mg

Orally 

once a day for 1 week and increase to 17.8 mg/day for another week (Maximum dose: 35.6 mg/day)



ephedrine

25 mg-50 mg IM or subcutaneously or 5 mg-25 mg IV administered slowly repeat the dose in 5-10 minutes as needed



sodium oxybate 

4.5

g

Solution

Orally 

dose divided every 4 hours

2.25g half strength and 2.25g taken 2.5-4 hours later
increase up to 1.5g/night at weekly intervals
Do not exceed 9g/night



amphetamine/dextroamphetamine 

(immediate-release) initial oral dose is 10 mg per day, which is usually divided into multiple doses throughout the day
dose may be raised by 10 mg per week



solriamfetol 

Upon awakening take 75mg orally everyday
The dose can be doubled at least every three days.
Maximum dose-150mg orally everyday



amphetamine

Immediate release::

For 6 to 11 years: 5 mg/day initially in divided doses, increase 5 mg/day weekly until required response achieved
For >12 years: 10 mg/day initially in divided doses, increase 10 mg/day weekly until required response achieved
Maintain dose between 5 to 60 mg/day once a first response is achieved (max. 60 mg/day)



dextroamphetamine

Immediate release::

For 6 to 11 years: 5 mg/day initially in divided doses, increase 5 mg/day weekly until required response achieved (NMT 60 mg/day)
For >12 years: 10 mg/day initially in divided doses, increase 10 mg/day weekly until required response achieved (NMT 60 mg/day)



ephedrine

Body surface area (BSA): 0.5 mg/kg or 16.7 mg/m2 IM or SC every 4-6 hours



sodium oxybate 

<7 years: Safety and efficacy not established
≥7 years
<20 kgs: Start with a lower dose
20 to <30kgs:
Initial dose- ≤1g orally/day
Maintenance dose- increase by 0.5g/dose
Maximum dose-3g/day
30 to <45kgs:
Initial dose-≤1.5g orally/day
Maximum dose- 3.75g/day
≥45 kgs:
Initial dose- ≤2.25g orally/day, divided into two doses
Maximum dose- 4.5g/day



amphetamine/dextroamphetamine 

(immediate-release) Age: 6-11 Years: Starting dose is 5 mg per day, taken orally and divided into multiple doses throughout the day
dose may be increased by 5 mg every week until the desired therapeutic response is achieved
Age: >12 Years: initial oral dose of this medication is 10 mg per day, divided into several doses throughout the day
dose may be gradually increased by 10 mg per week until the desired therapeutic effect is attained



https://www.ncbi.nlm.nih.gov/books/NBK459236/

https://emedicine.medscape.com/article/1188433-clinical#b3

 

 

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