Olfaction in dentistry.

Practitioners of oral medicine frequently encounter patients with complaints of taste disturbance. While some such complaints represent pathological processes specific to the gustatory system, per se, this is rarely the case. Unless taste-bud mediated qualities such as sweet, sour, bitter, salty, umami, chalky, or metallic are involved, 'taste' dysfunction inevitably reflects damage to the sense of smell. Such 'taste' sensations as chicken, chocolate, coffee, raspberry, steak sauce, pizza, and hamburger are dependent upon stimulation of the olfactory receptors via the nasopharynx during deglutition. In this paper, we briefly review the anatomy, physiology, and pathophysiology of the olfactory system, along with means for clinically assessing its function. The prevalence, etiology, and nature of olfactory disorders commonly encountered in the dental clinic are addressed, along with approaches to therapy and patient management.

Smell and taste disorders: a primary care approach.

Smell and taste disorders are common in the general population, with loss of smell occurring more frequently. Although these disorders can have a substantial impact on quality of life and may represent significant underlying disease, they are often overlooked by the medical community. Patients may have difficulty recognizing smell versus taste dysfunction and frequently confuse the concepts of "flavor" and "taste." While the most common causes of smell disturbance are nasal and sinus disease, upper respiratory infection and head trauma, frequent causes of taste disturbance include oral infections, oral appliances (e.g., dentures), dental procedures and Bell's palsy. Medications can interfere with smell and taste, and should be reviewed in all patients with reported dysfunction. In addition, advancing age has been associated with a natural impairment of smell and taste ability. A focused history and a physical examination of the nose and mouth are usually sufficient to screen for underlying pathology. Computed tomographic scanning or magnetic resonance imaging of affected areas, as well as commercially available standardized tests, may be useful in selected patients. The causes of olfactory dysfunction that are most amenable to treatment include obstructing polyps or other masses (treated by excision) and inflammation (treated with steroids). Enhancement of food flavor and appearance can improve quality of life in patients with irreversible dysfunction.

Chronic insomnia: a practical review.

Insomnia has numerous, often concurrent etiologies, including medical conditions, medications, psychiatric disorders and poor sleep hygiene. In the elderly, insomnia is complex and often difficult to relieve because the physiologic parameters of sleep normally change with age. In most cases, however, a practical management approach is to first consider depression, medications, or both, as potential causes. Sleep apnea also should be considered in the differential assessment. Regardless of the cause of insomnia, most patients benefit from behavioral approaches that focus on good sleep habits. Exposure to bright light at appropriate times can help realign the circadian rhythm in patients whose sleep-wake cycle has shifted to undesirable times. Periodic limb movements during sleep are very common in the elderly and may merit treatment if the movements cause frequent arousals from sleep. When medication is deemed necessary for relief of insomnia, a low-dose sedating antidepressant or a nonbenzodiazepine anxiolytic may offer advantages over traditional sedative-hypnotics. Longterm use of long-acting benzodiazepines should, in particular, be avoided. Melatonin may be helpful when insomnia is related to shift work and jet lag; however, its use remains controversial.

Olfactory testing as an aid in the diagnosis of Parkinson's disease: development of optimal discrimination criteria.

Since olfactory dysfunction is among the first signs of idiopathic Parkinson's disease (PD), olfactory testing may aid in the early of 'preclinical' diagnosis of this disorder. Indeed, the proportion of early-stage PD patients with olfactory dysfunction appears to be greater than the proportion of early-stage PD patients exhibiting some of the cardinal signs of PD. Because olfactory function varies in the general population and declines with age, empirically-based criteria are needed by the clinician to establish whether the degree of olfactory loss observed in a given patient is concordant with the presence of PD. In this study, we present cutoff criteria for the optimal assessment of olfactory dysfunction in the evaluation of PD. Specifically, we present scores for the University of Pennsylvania Smell Identification Test (UPSIT) that best discriminate between PD patients and age-matched controls. Receiver operating characteristic (ROC) curves, based upon sensitivity and specificity estimates, were computed for three age groups (< or = 60 yrs, 61-70 yrs, and > or = 71 yrs) and scores with highest sensitivity and specificity were determined. Sex- and age-related differences in the test scores were observed, with lower scores occurring for men and for the older patient groups.

Odor recognition memory is better under bilateral than unilateral test conditions.

Two odor memory tests were administered unilaterally (left and right) and bilaterally to the same set of 24 men and 24 women on two test occasions. These tests were (i) a "multiple-target" test (MTT) in which three target stimuli were selected, after 10-, 30-, and 60-sec retention intervals, from stimulus sets containing both target and distracter stimuli, and (ii) a 9-item "single-target" three-choice test (STT), in which single stimuli were selected from stimuli sets containing two distracters. Overall, odor memory scores were higher under bilateral than unilateral testing, and higher on the second than on the first test session. Unilateral testing resulted in a monotonic delay-related forgetting function. No differences were observed in the odor memory test scores of the left and right sides of the nose, and no significant correlations were present between these scores and scores on a battery non-olfactory memory tests. On the STT, the female, but not the male, subjects demonstrated better performance on the second, than on the first, test session. The results of this study imply that odor memory is facilitated centrally by bilateral activation, and that a memory system may exist for odors which is distinct from other memory systems.

Effect of carotid body denervation on arousal response to hypoxia in sleeping dogs.

We studied the arousal and ventilatory responses to hypoxia during sleep in three trained dogs, before and 1-4 wk after carotid body denervation (CBD). During the studies the dogs breathed through a cuffed endotracheal tube inserted via a chronic tracheostomy. Eucapnic progressive hypoxia was induced by a rebreathing technique, and arterial O2 saturation (Sao2) was measured with an ear oximeter. Sleep stage was determined by electroencephalographic and behavioral criteria. Following CBD, all dogs exhibited hypoventilation under resting conditions; hypoxic ventilatory responses during wakefulness, slow-wave sleep (SWS), and rapid-eye-movement (REM) sleep were less than 10% of control. Prior to CBD, hypoxic arousal occurred at Sao2 of 83.2 +/- 4.6% (mean +/- Se) during SWS and 70.6 +/-2.2% in REM sleep. Following CBD, arousal failed to occur during progressive desaturation to 60% in SWS and 50% in REM sleep, at which levels hypoxia was arbitrarily terminated. In a few studies following CBD where rebreathing was allowed to continue, the dogs occasionally failed to arouse at all and require active resuscitation. The results indicate a critical role for the carotid chemoreceptors in mediating the arousal response to hypoxia.

Role of the carotid body and of afferent vagal stimuli in the arousal response to airway occlusion in sleeping dogs.

We studied the independent effects of bilateral carotid body denervation and bilateral cold blockade of the vagus nerves on the arousal response to airway occlusion during sleep. Dogs breathed through a cuffed endotracheal tube inserted via a chronic tracheostomy, and airway occlusion was imposed at end-expiration and maintained until the moment of arousal. Arterial O2 saturation (SaO2) was measured with an ear oximeter, and sleep stage was determined by electroencephalographic and behavioral criteria. Mean +/- SE SaO2 values at arousal were 88.7 +/- 2.7% during slow-wave sleep, and 84.9 +/- 3.5% during rapid-eye-movement sleep (0.05 less than p less than 0.1). After carotid body denervation (2 dogs), arousal SaO2 values were less than 60% during slow-wave sleep and less than 50% during rapid-eye-movement sleep, at which time airway occlusion was arbitrarily terminated. In a few studies after denervation, when airway occlusion was maintained beyond these values, the dogs occasionally failed to arouse at all, and resuscitation was required. Bilateral cold blockade of the vagus nerves (2 dogs) resulted in no significant change in SaO2 at arousal. We concluded that the arousal response to airway occlusion is mediated primarily by the carotid bodies.