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ease (ischemic optic neuropathy or occlusion of a branch of the retinal artery) are the usual ones. Orbital or retro-orbital tumors and infectious or granulomatous processes (e.g., sarcoid, retinal toxoplasmosis in AIDS) are other common causes. Certain toxic and malnutritional states are characterized by more or less symmetrical bilateral central scotomas (involving the xation point) or cecocentral ones (involving both the xation point and the blind spot). The cecocentral scotoma, which tends to have an arcuate border, represents a lesion that is predominantly in the distribution of the papillomacular bundle. However, the presence of this visual eld abnormality does not establish whether the primary defect is in the cells of the origin of the bundle, i.e., the retinal ganglion cells, or in their bers. Demyelinative disease is characterized by unilateral or asymmetrical bilateral scotomas. Vascular lesions that take the form of retinal hemorrhages or infarctions of the nerve- ber layer (cotton-wool patches) give rise to unilateral scotomas; occlusion of the central retinal artery or its branches causes infarction of the retina and, as a rule, a loss of central vision. As pointed out earlier, anterior ischemic optic neuropathy causes sudden monocular blindness or an altitudinal eld defect. Since the optic nerve also contains the afferent bers for the pupillary light re ex, extensive lesions of the nerve will cause a so-called afferent pupillary defect, which has been mentioned earlier and is considered further in Chap. 14. With most diseases of the optic nerve, as alluded to above, the optic disc will eventually become pale (atrophic). This usually requires 4 to 6 weeks to develop. If the optic nerve degenerates (e.g., in multiple sclerosis, Leber hereditary optic atrophy, traumatic transection, tumor of nerve, or syphilitic optic atrophy), the disc becomes chalk-white, with sharp, clean margins. If the atrophy is secondary to papillitis or papilledema, the disc margins are indistinct and irregular; the disc has a pallid, yellow-gray appearance, like candle tallow; the vessels are partially obscured; and the adjacent retina is altered because of the outfall of bers. As in the case of optic neuritis, visual evoked potentials from the stimulation of one eye may be slowed even if the optic disc appears normal and there is no perimetric abnormality.
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See the appendix for instructions on setting up and running these examples. These examples were all developed on Oracle BI Enterprise Edition 10.1.3.4. Oracle Virtual Directory (OVD) and Oracle Access Manager (OAM) were used as the Lightweight Directory Access Protocol (LDAP)and SSO systems, version 10.1.4. The Oracle Database-specific examples Virtual Private Database (VPD), DBMS_LDAP, and auditing were all tested on both Oracle 10g R2 and 11g R1.
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METHODS ITERATIVE
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Diplegia, 50, 505 cerebrocerebellar, 879 spastic, 876 Diplomyelia, 861 Diplopia, 230 233 monocular, 233 in multiple sclerosis, 779 Dipyridamole, for atheroembolic infarction and transient ischemic attacks, 697 Disabling positional vertigo, 261, 263 Disconjugate gaze, 222 Disconnection syndromes, 389 390, 391f, 409 410 Discriminative sensation, testing of, 137 Disjunctive gaze, 222 Disorganized schizophrenia, 1321 Disseminated intravascular coagulation (DIC), stroke complicating, 737 Disseminated myoclonus, 174 Dissociated nystagmus, 238 Disul ram (Antabuse), peripheral neuropathy due to, 1133 1134 Divergence eye movements, 222 Divergence paralysis, 233 Dix-Hallpike maneuver, 262f Dizziness. See also Vertigo with brain tumors, 553 de nition of, 256 psychiatric, 258 with stroke, 739 DJ-1, in Parkinson disease, 921 Docetaxel (Taxotere) intoxication, 1040, 1133 Doll s-head eye movements, 227 with brain herniation, 310 in comatose patient, 314 L-Dopa for Parkinson s disease, 921 922, 923 924 for progressive supranuclear palsy, 928 side effects of, 923 924 L-Dopa/carbidopa, for restless legs syndrome and periodic leg movements of sleep, 339 Dopamine, in basal ganglia, 59 60 Dopamine agonists, for Parkinson s disease, 922 Dopaminergic bers, 75 Dopa-responsive dystonia, 67 juvenile, 930 931 Dorsal horn, 113, 114f Dorsal midbrain syndrome, 227 Dorsal root ganglia, sensory syndromes involving, 139 140. See also Ganglionopathy; Neuronopathy
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Description AND returns true only if both of the operands are equal to true . If either of the operands is false, then the whole expression returns false. If either one of the operands is true, then the expression returns true. The expression will only return false if both of the operands are false. NOT simply returns the opposite of the evaluated expression. It reverses it so that the true becomes a false, or a false becomes a true.
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16 100 L2 25 64 L2 p 64 L 8 L The rectangle s length is 8 inches and its width is 8 3 6 inches. 4 5. The classroom s length is 14 feet more than its width, so L W 14. The diameter is 34 feet. The formula D2 L2 W 2 becomes 342 W 14 2 W 2 . 342 W 14 2 W 2 1156 W 14 W 14 W 2 1156 W 2 28W 196 W 2 1156 2W 2 28W 196 0 2W 2 28W 960 1 1 0 2W 2 28W 960 2 2 0 W 2 14W 480 0 W 16 W 30 W 16 0 W 16 W 30 0 (This does not lead to a solution.)
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590 Worked-Out Solutions to Exercises: s 1 to 9
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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