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Trigeminal receptor cells are also stimulated by odorant molecules, but at a higher threshold than the olfactory receptor cells. The perceived intensity of a persistent odor decreases or disappears with time (olfactory adaptation). External factors such as an arid environment, cold, or cigarette smoke impair the ability to smell; diseases affecting the nasopharyngeal cavity impair both smell and taste. The perception of smell may be qualitatively changed (parosmia) because of autonomic (hunger, stress) and hormonal changes (pregnancy) or disturbances such as ozena, depression, traumatic lesions, or nasopharyngeal empyema. Olfactory hallucinations can be caused by mediobasal and temporal tumors (focal epilepsy), drug or alcohol withdrawal, and psychiatric illnesses such as schizophrenia or depression. One nostril is held closed, and a bottle containing a test substance is held in front of the other. In this subjective test, odor perception per se is more important than odor recognition. Odor perception indicates that the peripheral part of the olfactory tract is intact; odor recognition indicates that the cortical portion of the olfactory pathway is also intact. Because there is bilateral innervation, unilateral lesions proximal to the anterior commissure and cortical lesions may not cause anosmia. Viral infections (influenza), heavy smoking, and toxic substances can damage the olfactory epithelium; trauma (disruption of olfactory nerves, frontal hemorrhage), tumors, meningitis, or radiotherapy may damage the olfactory pathway. Parkinson disease, multiple sclerosis, Kallmann syndrome (congenital anosmia with hypogonadism), meningoencephalocele, albinism, hepatic cirrhosis, and renal failure can also cause olfactory disturbances. Cranial Nerves 76 Olfactory Disturbances (Dysosmia) Olfactory disturbances can be classified as either quantitative (anosmia, hyposmia, hyperosmia) or qualitative (parosmia, cacosmia). Taste buds are found on the margins and furrows of the different types of gustatory papillae (fungiform, foliate, and vallate) and are specific for one of the four primary tastes, sweet, sour, salty, and bitter. Stimulation of the gustatory cell at its receptors by the specific taste initiates a molecular transduction process, resulting in depolarization of the cell. Each taste bud responds to multiple qualities of taste, but at different sensitivity thresholds, resulting in a characteristic taste profile. Complex tastes are encoded in the different patterns of receptor stimulation that they evoke. Sensory impulses from the tongue are conveyed to the brain by three pathways: from the anterior two-thirds of the tongue via the lingual nerve (V/3) to the chorda tympani, which arises from the facial nerve (nervus intermedius); from the posterior third of the tongue via the glossopharyngeal nerve; and from the epiglottis via the vagus nerve (fibers arising from the inferior ganglion). Sensory impulses from the soft palate travel via the palatinate nerves to the pterygopalatine ganglion and onward through the greater petrosal nerve and nervus intermedius. All gustatory information arrives at the nucleus of the solitary tract, which projects, through a thalamic relay, to the postcentral gyrus. The gustatory pathway is interconnected with the olfactory pathway through the hypothalamus and amygdala. It has important interactions with the autonomic nervous system (facial sweating and flushing; salivation) and with affective centers (accounting for like and dislike of particular tastes). For example, chocolate pudding can be identified as "sweet" but not as "chocolate. Taste thresholds on each side of the tongue are tested with the tongue outstretched. The patient is then asked to point to the corresponding region of a map divided into "sweet", "sour", "salty" and "bitter" zones. The test solutions contain glucose (sweet), sodium chloride (salty), citric acid (sour), or quinine (bitter). Electrogustometry can be used for precise determination of the taste thresholds but it is time-consuming and requires a high level of concentration on the part of the patient. Lesions of the chorda tympani producing unilateral gustatory disturbances are seen in patients with peripheral facial palsy, chronic otitis media, and cholesteatoma.

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Hypoxanthine and xanthine are both purine bases, and the monophosphates are nucleotides. Because allopurinol inhibits xanthine oxidase, the 6-mercaptopurine will not be deactivated as rapidly. The 2 chromosomes in each diploid pair are said to be homologs, or homologous chromosomes. They contain the same genes, but because one is of paternal origin and one is of maternal origin, they may have different alleles at some loci. The regions that are homologous are sometimes referred to as pseudoautosomal regions. During meiosis-1 of male spermatogenesis, the X and Y chromosomes pair in the pseudoautosomal regions, allowing the chromosomes to segregate into different cells. When a specific site on a chromosome has multiple alleles in the population, it is said to be polymorphic (many forms). Throughout human history there have been many mutations in the -globin gene, and each mutation has created a new allele in the population. Some alleles cause no clinical disease, but others, like the sickle cell allele, are associated with significant disease. Included among the disease-causing alleles are those associated with sickle cell anemia and several associated with -thalassemia. When mutations occur in cells giving rise to gametes, the mutations can be transmitted to future generations. Missense mutations result in the substitution of a single amino acid in the polypeptide chain. Nonsense mutations produce a stop codon, resulting in premature termination of translation and a truncated protein. When the number of inserted or deleted bases is a multiple of 3, the mutation is said to be in-frame. If not a multiple of 3, the mutation is a frameshift, which alters all codons downstream of the mutation, typically producing a truncated or severely altered protein product. Mutations can occur in promoter and other regulatory regions or in genes for transcription factors that bind to these regions. Mutations that cause a missing protein product or cause decreased activity of the protein are termed loss-of-function. Those that produce a protein product with a new function or increased activity are termed gain-of-function. Recurrence risk the recurrence risk is the probability that the offspring of a couple will express a genetic disease. For example, in the mating of a normal homozygote with a heterozygote who has a dominant disease-causing allele, the recurrence risk for each offspring is 1/2, or 50%. It is important to remember that each reproductive event is statistically independent of all previous events. Therefore, the recurrence risk remains the same regardless of the number of previously affected or unaffected offspring. Determining the mode of inheritance of a disease 304 Chapter 1 Single-Gene Disorders. The first affected individual to be identified in the family is termed the proband. Note that, by convention, the dominant allele is shown in uppercase (A) and the recessive allele is shown in lowercase (a).

Further, reliance on human scorers using visual pattern recognition requires intensive and ongoing training to achieve high reliability (Whitney et al. Visual scoring also may not maximally utilize the spectral components of the electrophysiological data, which may provide useful information on sleep architecture. Currently there are only 2,198 certified technicians to monitor and score sleep tests, far below the need (Association of Polysomnographic Technologists, 1999). Summary of Formal Evaluation Reviews Three recent in-depth reviews have been performed to examine the effectiveness of portable monitoring devices (Ross et al. As described above, these reports were largely aimed at evaluating the literature regarding the accuracy of clinical diagnosis relative to reference in lab polysomnography, with some attempt at also evaluating the literature relative to cost-effectiveness and clinical prediction. The review concluded that at the time there was insufficient evidence to make firm recommendations for use of portable monitoring for the diagnosis of sleep apnea (Ross et al. The review committee also recognized the need for further development of portable devices and suggested several goals for future research. The evidence review committee recommended that future studies should include more diverse populations, other than patients with sleep apnea, that are not subject to selection bias. Additional recommendations were that future studies should address clinical predictive algorithms in combination with portable monitoring in the diagnosis of sleep apnea, and study design should assess the cost-effectiveness and outcomes associated with different diagnostic and management strategies. They determined that only the first two criteria had been met, but the last three were not. Evaluating Daytime Sleepiness There is also a need to improve diagnostic procedures aiming at the quantification of excessive daytime sleepiness and the diagnosis of narcolepsy and hypersomnia. It is also unknown whether these tests may not be more valid after a night at home and verification of sleep with actigraphy or other procedures, a modification that would reduce cost in some cases. Finally, performance tests such as the psychomotor vigilance task, used commonly to evaluate performance after sleep deprivation, may have applications in this area (Dauvilliers and Buguet, 2005), especially if those tests can be adjusted to be used in ambulatory situations. Biochemical and imaging research aiming at discovering biomarkers of sleep debt and sleepiness is also needed. Other Diagnostic Technologies In addition to the development of ambulatory strategies, efforts are also currently under way to utilize other techniques to diagnose individuals who suffer chronic sleep loss or sleep disorders. Tests such as the standardized immobilization test or biochemical/imaging measures of brain iron metabolism are being developed to assist in the diagnosis and quantification of severity in restless leg syndrome (Allen and Earley, 2001; Garcia-Borreguero et al. Actigraphy and other methods are also used to estimate leg movement frequency in outpatients (Kazenwadel et al. Video technologies may also be of value, especially in the diagnosis of individuals with night terrors. Finally, there is a need to establish novel procedures to objectively identify abnormalities in insomnia beyond the changes generally observed using sleep questionnaires, logs, and polysomnography (Roth and Drake, 2004). Improvement in portable monitoring techniques will likely enhance access to sleep diagnostic services. With the inadequate availability of sleep centers and sleep technicians, not only in the United States but more so worldwide, access to portable diagnostic screening procedures and streamlining initiation of treatment would clearly be advantageous. Research in the design and evaluation of existing and novel diagnostic technologies is also needed in the area of insomnia, hypersomnia, and restless legs syndrome and periodic limb movements. This should include consideration of the extent to which data from new technologies complement those from other techniques. Use of wrist activity for monitoring sleep/wake in demented nursing-home patients. Upper airway size analysis by magnetic resonance imaging of children with obstructive sleep apnea syndrome. Executive summary on the systematic review and practice parameters for portable monitoring in the investigation of suspected sleep apnea in adults. Effects of problem-based scheduling on patient waiting and staff utilization of time in a pediatric clinic. Functional imaging of the sleeping brain: Review of findings and implications for the study of insomnia.

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Adverse effects on family cohesiveness, in turn, can lead to severe family turmoil and divorce. Similarly, sleep disruption of family caregivers has broader societal effects by contributing to hospitalization or nursing home placement of ill family members for whom they provide care. Further, in a large population-based sample of older individuals, bed partners report poor health, depressed mood, poor mental health, and marital unhappiness (Strawbridge et al. At least four studies have addressed this question, with three showing improvement. Two of the studies that demonstrated a benefit were nonrandomized and used a before versus after study design. The improvement in sleep efficiency (percentage of time asleep while in bed) translated to an extra hour of sleep per night. These effects were independent of the effects of obesity and other health factors. In a separate study, 60 percent of bed partners reported that they slept apart versus 20 percent of controls. A common complaint of parents is being awakened by a young child with a sleep problem. Sleep loss is indeed reported more frequently by parents after the birth of a child than during pregnancy (Gay et al. Previously, controlled clinical trials had shown that parent training and extinction are effective for treating young children (Mindell, 1999; Ramchandani et al. Sleep disturbances in chronic illness, whether in the affected individual or in the caregiver, affect decisions about hospital or nursing home placement. One area of future study is whether treating sleep problems (in either the patient or the caregiver) can delay institutionalization. Counseling of caregivers-although not explicitly targeted to their sleep disturbance or that of the patient-has been shown, in a separate randomized trial, to delay nursing home placement (Mittelman et al. Within nursing homes, behavioral and pharmacological therapies are effective at improving sleep problems (Alessi et al. There are limited data on the economic impact of insomnia, sleepdisordered breathing, and narcolepsy; the economic impact of other sleep disorders has not been analyzed. As will be discussed in further detail in Chapters 5 and 8, the lack of sufficient data result from inadequate reporting and surveillance mechanisms. Increased Health Care Utilization Daytime sleepiness, inadequate sleep time, insomnia, and other sleep disorders place a significant burden on the health care system through increased utilization of the health care system (see below). Patients in the highest quartile of the Epworth Sleepiness Scale are associated with an 11 percent increase in health care utilization, and individuals with sleepdisordered breathing or sleepiness and fatigue are associated with a 10 to 20 percent increase in utilization (Kapur et al. Their activity is more limited (Simon and VonKorff, 1997), and they are significantly more likely to access medical and psychiatric care than are individuals that do not have a sleep or psychiatric disorder (Weissman et al. Individuals with insomnia who also have an associated psychiatric disorder are more likely to seek treatment for emotional problems (14. The burden insomnia place on the health care system is long-term-the majority of individuals with either mild (59 percent) or severe (83 percent) insomnia continue to suffer symptoms of insomnia 2 years after initial diagnosis (Katz and McHorney, 1998). Consequently, individuals suffering from insomnia place a significant economic burden on society resulting in increased health care costs (see below). This was associated with an increase in cost of services-$49,000 to $99,000 (Kryger et al. The realized savings would likely be much larger in the United States due to higher associated health care costs. Direct Costs of Sleep Loss and Sleep Disorders Billions of dollars are spent each year in the United States on the direct costs of sleep loss and sleep disorders. These medical costs include expenses associated with doctor visits, hospital services, prescriptions and over-thecounter medications. Further, based on the costs associated with a laboratory-based polysomnogram, it would cost over $17. Although it is predicted that the advent of more effective portable monitoring devices (Chapter 6) will decrease the costs associated with testing and diagnosis of sleep disorders, the total direct costs will still remain high and be a burden. As is the case with direct costs, for each of these categories further analysis is required to determine the complete indirect costs of sleep loss and sleep disorders.