A reader asks about/speculates that there "might be one form of “ADD” that is simply a phenotype of ADD but that is actually caused by narcolepsy and the patient's attempt to compensate for it. This might explain why modafinil has been occasionally known to improve ADD symptoms - the reasons to engage inthe ADD behavior are abolished by the absence of sleepiness."
The new edition of Principles and Practice of Pediatric Sleep Medicine has a good chapter on "Attention Deficit, Hyperactivity, and Sleep Disorders." Conditions such as obstructive sleep apnea that present with sleepiness in adults often present with inattention and hyperactivity in children. From Principles and Practice: "...increasing evidence suggests that a variety of childhood sleep disorders are associated with inattention, hyperactivity, and cognitive impairment that could have significantly adverse effects on such important outcomes as development and school performance."
Obstructive sleep apnea and restless legs syndrome are the 2 sleep disorders that have the most evidence linking them to ADHD symptoms.
As far as narcolepsy, Principles and Practice of Pediatric Sleep Medicine mentions that "Children with narcolepsy often have problems with inattention and hyperactivity that may improve upon treatment" and "Adults who have been diagnosed with narcolepsy frequently give a history of 'attention deficit disorder' in childhood."
I have never used Modafinil (Provigil) to treat ADHD, but a quick Medline search suggests that it is effective for ADHD symptoms.
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Inattention and hyperactivity can be symptoms of psychiatric disorders (including ADHD) and can be symptoms of sleep disorders. Multiple studies have linked inattention and hyperactivity to sleep disorders in children, but research is lacking in adults. However, I think it is quite possible for inattention to be a symptom of a sleep disorder in an adult.
Sunday, May 22, 2005
Monday, May 02, 2005
Grand Rounds 32
Grand Rounds 32, A Day in the Life of a Medical Student, is up at MudFud.
This carnival celebrates every aspect of medicine, from the student,to the surgeon and the patient on the table.
This carnival celebrates every aspect of medicine, from the student,to the surgeon and the patient on the table.
Sunday, May 01, 2005
Narcolepsy 3
Part 1, Part 2
This is 3rd in a series about narcolepsy.
In the last 5-6 years there has been a revolution in our understanding of narcolepsy. In 1999 hypocretin (orexin) was discovered. Most cases of human narcolepsy are due to a loss of hypocretin cells in the lateral hypothalamus, which results in very low levels of hypocretin in the cerebrospinal fluid. In contrast, narcolepsy in animal models (e.g. Doberman pinschers) is usually due to dysfunction of the hypocretin receptors.
Hypocretin neurons project to multiple areas in the brainstem and hypothalamus involved in the regulation of the alternation of sleep/wake and REM/non-REM cycles. There are 2 main theories about the function of hypocretin: 1) hypocretin promotes wakefulness and 2) hypocretin promotes stability of sleep/wake/REM/non-REM states. These 2 theories are not mutually exclusive.
Thus narcolepsy, a hypocretin deficient state, can be thought of as 1) a disorder of excessive daytime sleepiness in which a person has irresistable episodes of sleep and/or 2) a disorder of unstable sleep/wake/REM/non-REM states in which daytime wakefulness is interrupted by periods of sleep and nighttime sleep is frequently restless and fragmented (intrusion of wakefulness). Cataplexy can be explained in this model as a mixture of REM sleep and wakefulness- cataplexy is the intrusion of the muscle atonia (decreased/absent muscle tone) of REM sleep into wakefulness.
Hypocretin is also involved in appetite, feeding and metabolism. This is an area I know very little about, so I won't mention it further.
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That's it for now. I know I've been promising to talk more about Xyrem- I'll try to do this in part 4.
This is 3rd in a series about narcolepsy.
In the last 5-6 years there has been a revolution in our understanding of narcolepsy. In 1999 hypocretin (orexin) was discovered. Most cases of human narcolepsy are due to a loss of hypocretin cells in the lateral hypothalamus, which results in very low levels of hypocretin in the cerebrospinal fluid. In contrast, narcolepsy in animal models (e.g. Doberman pinschers) is usually due to dysfunction of the hypocretin receptors.
Hypocretin neurons project to multiple areas in the brainstem and hypothalamus involved in the regulation of the alternation of sleep/wake and REM/non-REM cycles. There are 2 main theories about the function of hypocretin: 1) hypocretin promotes wakefulness and 2) hypocretin promotes stability of sleep/wake/REM/non-REM states. These 2 theories are not mutually exclusive.
Thus narcolepsy, a hypocretin deficient state, can be thought of as 1) a disorder of excessive daytime sleepiness in which a person has irresistable episodes of sleep and/or 2) a disorder of unstable sleep/wake/REM/non-REM states in which daytime wakefulness is interrupted by periods of sleep and nighttime sleep is frequently restless and fragmented (intrusion of wakefulness). Cataplexy can be explained in this model as a mixture of REM sleep and wakefulness- cataplexy is the intrusion of the muscle atonia (decreased/absent muscle tone) of REM sleep into wakefulness.
Hypocretin is also involved in appetite, feeding and metabolism. This is an area I know very little about, so I won't mention it further.
-
That's it for now. I know I've been promising to talk more about Xyrem- I'll try to do this in part 4.
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