generate barcode in c# asp.net DISORDERS OF SMELL AND TASTE in Microsoft Office

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DISORDERS OF SMELL AND TASTE
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The wide diversity of these transmembrane proteins permits subtle differentiation of thousands of different odorant molecules, as outlined by Young and Trask This speci city for molecules is encoded neuroanatomically Different odorant molecules activate speci c olfactory receptors Each olfactory neuron expresses only one allele of one receptor gene Moreover, each olfactory glomerulus receives inputs from neurons expressing only one type of odorant receptor In this way, each of the glomeruli is attuned to a distinct type of odorant stimulus Presumably, this encoding is preserved in the olfactory cortex Something is to be learned from olfaction in lower vertebrates, which have a second, physically distinct olfactory system (the vomeronasal olfactory system or organ of Jacobson), in which the repertoire of olfactory receptors is much more limited than in their main olfactory system This functionally and anatomically distinct olfactory tissue is attuned to, among other odorants, pheromones and thereby importantly in uence menstrual, reproductive, ingestive, and defensive behavior (see review of Wysocki and Meredith) The vomeronasal receptors employ different signaling mechanisms than other olfactory receptors and project to the hypothalamus and amygdala via a distinct accessory olfactory bulb
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Table 12-1 Main causes of anosmia Nasal Smoking Chronic rhinitis (allergic, atrophic, cocaine, infectious herpes, in uenza) Overuse of nasal vasoconstrictors Olfactory epithelium Head injury with tearing of olfactory laments Cranial surgery Subarachnoid hemorrhage, meningitis Toxic (organic solvents, certain antibiotics-aminoglycosides, tetracyclines, corticosteroids, methotrexate, opiates, L-dopa) Metabolic (thiamine de ciency, adrenal and thyroid de ciency, cirrhosis, renal failure, menses) Wegener ganulomatosis Compressive and in ltrative lesions (craniopharyngioma, meningioma, aneurysm, meningoencephalocele) Central Degenerative diseases (Parkinson, Alzheimer, Huntington) Temporal lobe epilepsy Malingering and hysteria
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Clinical Manifestations of Olfactory Lesions
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Disturbances of olfaction may be subdivided into four groups, as follows: 1 Quantitative abnormalities: loss or reduction of the sense of smell (anosmia, hyposmia) or, rarely, increased olfactory acuity (hyperosmia) Qualitative abnormalities: distortions or illusions of smell (dysosmia or parosmia) Olfactory hallucinations and delusions caused by temporal lobe disorders or psychiatric disease Higher-order loss of olfactory discrimination (olfactory agnosia)
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Anosmia or Loss of the Sense of Smell (Table 12-1) This is the most frequent clinical abnormality, and, if unilateral, will not be recognized by the patient Unilateral anosmia can sometimes be demonstrated in the hysterical patient on the side of anesthesia, blindness, or deafness Bilateral anosmia, on the other hand, is a not uncommon complaint, and the patient is usually convinced that the sense of taste has been lost as well (ageusia) This calls attention to the fact that taste depends largely on the volatile particles in foods and beverages, which reach the olfactory receptors through the nasopharynx, and that the perception of avor is a combination of smell, taste, and tactile sensation This can be proved by demonstrating that such patients are able to distinguish the elementary taste sensations on the tongue (sweet, sour, bitter, and salty) The olfactory defect can be veri ed readily enough by presenting a series of nonirritating olfactory stimuli (vanilla, peanut butter, coffee, tobacco, etc), rst in one nostril, then in the other, and asking the patient to sniff and identify them If the odors can be detected and described, even if they cannot be named, it may be assumed that the olfactory nerves are relatively intact (humans can distinguish many more odors than they can identify by name) If they cannot be detected, there is an olfactory defect Ammonia and similar pungent substances are unsuitable stimuli because they do not
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test the sense of smell but have a primary irritating effect on the mucosal free nerve endings of the trigeminal nerves A more elaborate scratch-and-sniff test has been developed and standardized by Doty and colleagues (University of Pennsylvania Smell Identi cation Test) In this test the patient attempts to identify 40 microencapsulated odorants and his or her olfactory performance is compared with that of age- and sex-matched normal individuals Unique features of this test are a means for detecting malingering and amenability to self-administration Air-dilution olfactory detection is a more re ned way of determining thresholds of sensation and of demonstrating normal olfactory perception in the absence of odor identi cation The use of olfactory evoked potentials is being investigated in some electrophysiology laboratories, but their reliability is uncertain These re ned techniques are essentially research tools and are not used in neurologic practice The loss of smell usually falls into one of three categories: nasal (in which odorants do not reach the olfactory receptors), olfactory neuroepithelial (due to destruction of receptors or their axon laments), and central (olfactory pathway lesions) In an analysis of 4000 cases of anosmia from specialized clinics, Hendriks found that three categories of pathology viral infection of the upper respiratory tracts (the largest group), nasal or paranasal sinus disease, and head injury accounted for most of the cases Regarding the nasal diseases responsible for bilateral hyposmia or anosmia, the most frequent are those in which hypertrophy and hyperemia of the nasal mucosa prevent olfactory stimuli from reaching the receptor cells Heavy smoking is probably the most frequent cause of hyposmia in clinical practice Chronic atrophic rhinitis; sinusitis of allergic, vasomotor, or infective types; nasal polyposis; and overuse of topical vasocontrictors are other common causes Biopsies of the olfactory mucosa in cases of allergic rhinitis have shown that the sensory epithelial cells are still present, but their cilia are deformed and shortened and are buried under other mucosal cells In uenza, herpes simplex, and hepatitis virus infections may be followed by hyposmia or anosmia due to destruction of receptor cells; if the basal cells are also destroyed, this may be
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