Supplemental Reading

Barnard EA. The molecular biology of GABAA receptors and their structural determinants. In Biggio C, Sanna E, and Costa E (eds.). GABAa Receptors and Anxiety: From Neurobiology to Treatment. New York: Raven, 1992.

Costa E. From GABAA receptor diversity emerges a unified vision of GABAergic inhibition. Annu Rev Pharmacol Toxicol 1998;38:321-350.

Daval, J-L, Nehlig A, and Nicolas F. Physiological and pharmacological properties of adenosine: Therapeutic implications. Life Sci 1991;49:1435-1453.

Fredholm BB et al. International Union of

Pharmacology. XXV. Nomenclature and classification of adenosine receptors. Pharmacol Rev 2001;53:527-552.

Linden J. Structure and function of Aj adenosine receptors. FASEB J 1991;5:2668-2676.

Sieghart W. Structure and pharmacology of 7-aminobu-tyric acidA receptor subtypes. Pharmacol Rev 1995;47:181-234.

Smith GB and Olsen RW. Functional domains of GABAa receptors. Trends Pharmacol Sci 1995;16:162-168.

^ Case Study Daytime Sleepiness

W. M. is a 55-year-old highly successful businessman who often spends long hours at the office or in his automobile traveling to meet new clients and partners. Since his days in college, W. M. has had frequent episodes of daytime somnolence, which he attributed to overwork and fatigue. Over the past several years, the number of daytime episodes has begun to increase, and he recently began to lose mobility in his arms and legs during the periods of somnolence. He also barely avoided a significant automobile accident for which the local sheriff's deputy cited him for failure to maintain control of his vehicle. During questioning by the police, W. M. indicated that he had no memory of any of the events surrounding the incident; he tested negative for any intoxicating substances. As a result of this most recent episode, W. M. has come to you, his family physician, to determine the cause of the excessive daytime sleepiness (EDS) and to find a way to manage this condition. Your examination reveals an individual who is in otherwise excellent health and mentation with no apparent significant pathology. He indicates that he has several periods of EDS during the day and that the frequency of these events is beginning to increase. While he feels well rested upon waking, he is especially concerned about the recent loss of skeletal muscle function and fears that he may be developing some degenerative progressive disease that will leave him dis-

abled and unable to continue working. What types of pathological conditions can lead to excessive somnolence? What is the appropriate therapeutic management of these pathological conditions?

Answer: Three disorders are most often associated with EDS. Sleep apnea is characterized by pauses in respiration during sleep and usually excessive snoring. Patients with sleep apnea have EDS but often awake without feeling rested. Sleep apnea is managed by treating the nighttime episodes of apnea. Narcolepsy is characterized by episodic EDS. Patients with this pathology often exhibit periods of irresistible instantaneous REM sleep and may also progress to cataplexy, or sudden loss of tone in skeletal muscles (usually bilaterally). A final type of disorder that displays periods of EDS is idiopathic hypersomnia, in which patients usually have periods of EDS usually associated with non-REM sleep. W. M. most likely has narcolepsy, which could be more clearly defined by determining whether he has a specific human leukocyte antigen associated with the disorder (HLA-DR2). Management of narcolepsy is accomplished with psychomotor stimulants of the amphetamine type. Methylphenidate, modafinil, pemoline, and dextroamphetamine all are effective in managing the EDS periods, while imipramine and clomipramine can be used to manage any cataplexy.

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