asp.net mvc qr code

asp.net vb qr code

asp.net mvc qr code generator

asp.net vb qr code

asp.net ean 13, asp.net pdf 417, code 39 barcode generator asp.net, asp.net mvc qr code, asp.net ean 128, free barcode generator in asp.net c#, barcode 128 asp.net, asp.net upc-a, barcodelib.barcode.asp.net.dll download, barcode asp.net web control, barcode generator in asp.net code project, asp.net upc-a, code 128 barcode generator asp.net, asp.net pdf 417, asp.net code 39

asp.net mvc generate qr code,
asp.net mvc qr code,
asp.net create qr code,
asp.net vb qr code,
asp.net mvc qr code,
generate qr code asp.net mvc,
asp.net vb qr code,
asp.net qr code generator,
asp.net mvc generate qr code,
qr code generator in asp.net c#,
generate qr code asp.net mvc,
asp.net qr code generator,
asp.net vb qr code,
generate qr code asp.net mvc,
asp.net generate qr code,
asp.net create qr code,
asp.net mvc qr code generator,
asp.net mvc qr code,
asp.net vb qr code,
asp.net create qr code,
asp.net qr code generator open source,
asp.net generate qr code,
asp.net qr code,
generate qr code asp.net mvc,
asp.net create qr code,
generate qr code asp.net mvc,
asp.net qr code generator open source,
asp.net vb qr code,
qr code generator in asp.net c#,

Visual Field Defects The most familiar clinical abnormality resulting from a lesion of one occipital lobe, homonymous hemianopia, has already been discussed in Chap 13 Extensive destruction abolishes all vision in the corresponding half of each visual eld With a neoplastic lesion that eventually involves the entire striate region, the eld defect may extend from the periphery toward the center, and loss of color vision (hemiachromatopsia) often precedes loss of black and white Lesions that destroy only part of the striate cortex on one side yield characteristic eld defects that accurately indicate the loci of the lesions A lesion con ned to the pole of the occipital lobe results in a central hemianopic defect that splits the macula and leaves the peripheral elds intact This observation indicates that half of each macula is unilaterally represented and that the maculae may be involved (split) in hemianopia Bilateral lesions of the occipital poles, as in embolism of the posterior cerebral arteries, result in bilateral central hemianopias Unilateral quadrant defects and altitudinal eld defects due to striate lesions indicate that the cortex on one side, above or below the calcarine ssure, is damaged The cortex below the ssure is the terminus of bers from the lower half of the retina; the resulting eld defect is in the upper quadrant, and vice versa Most bilateral altitudinal defects are traceable to incomplete bilateral occipital lesions (cortex or terminal parts of geniculocalcarine pathways) Head and Holmes described several such cases due to gunshot wounds; embolic or thrombotic infarction is now the common cause As indicated in Chap 13, the homonymous hemianopia that results from ablation of one occipital lobe is not absolute In monkeys, visuospatial orientation and the capacity to reach for moving objects in the defective eld are preserved (Denny-Brown and Chambers) In humans also, ashing light and moving objects can sometimes be seen in the blind eld even without the patient s full awareness Weiskrantz and colleagues have referred to these preserved functions as blindisms or blindsight It is useful as a practical matter to note that the optokinetic responses are usually spared in hemianopic de cits of occipital origin, but our experience suggests that this is not always the case in occipital strokes, perhaps in part because of adjacent edema or hemorrhage caused by infarction Cortical Blindness With bilateral lesions of the occipital lobes (destruction of area 17 of both hemispheres), there is a loss of sight and a loss of re ex closure of the eyelids to a bright light or threat The degree of blindness may be equivalent to that which follows severing of the optic nerves The pupillary light re exes are preserved, since they depend upon visual bers that terminate in the midbrain, short of the geniculate bodies (see Fig 14-6) Usually no changes are detectable in the retinas, though van Buren has described slight optic atrophy in monkeys long after occipital ablations The eyes are still able to move through a full range, but.

.

optokinetic nystagmus cannot be elicited Visual imagination and visual imagery in dreams are preserved With rare exceptions, no cortical potentials can be evoked in the occipital lobes by light ashes or pattern changes (visual evoked response), and the alpha rhythm is lost in the electroencephalogram (EEG) (see Chap 2) Less complete bilateral lesions leave the patient with varying degrees of visual perception There may also be visual hallucinations of either elementary or complex types The mode of recovery from cortical blindness has been studied carefully by Gloning and colleagues, who describe a regular progression from cortical blindness through visual agnosia and partially impaired perceptual function to recovery Even with recovery, the patient may complain of visual fatigue (asthenopia) and dif culties in xation and fusion The usual cause of cortical blindness is occlusion of the posterior cerebral arteries (most often embolic) or the equivalent, occlusion of the distal basilar artery The infarct may also involve the mediotemporal regions or thalami, which share the posterior cerebral artery supply, with a resulting Korsakoff amnesic defect and a variety of other neurologic de cits referable to the high midbrain and diencephalon (drowsiness, akinetic mutism; see page 305) Hypertensive, eclamptic, and hypoxic-ischemic encephalopathy, Schilder s disease and other leukodystrophies, Creutzfeldt-Jakob disease, progressive multifocal leukoencephalopathy, cerebral infarctions following cardiac arrest, and in ltrating glioma are other causes of cortical blindness A transitory form of cortical blindness may occur with head injury, migraine, hypertensive encephalopathy, or the antiphospholipid antibody syndrome, as a consequence of intravascular dye injection and as a toxic effect of a number of drugs such as interferon-alpha or cyclosporine In the case of the latter drugs, imaging studies have disclosed a reversible posterior leukoencephalopathy, similar in appearance to what occurs in hypertensive encephalopathy Visual Anosognosia (Anton Syndrome) The main characteristic of this disorder is the denial of blindness by a patient who obviously cannot see The patient acts as though he could see, and in attempting to walk, collides with objects, even to the point of injury He may offer excuses for his dif culties: I lost my glasses, The light is dim, etc, or he may only evince indifference to his loss of sight The lesions in cases of negation of blindness extend beyond the striate cortex to involve the visual association areas Rarely, the opposite condition arises: a patient is able to see small objects but claims to be blind This individual walks about avoiding obstacles, picks up crumbs or pills from the table, and catches a small ball thrown from a distance Damasio suggests that this might be a type of visual disorientation but with suf cient residual visual information to guide the hand, and that the lesion will be in the visual association areas superior to the calcarine cortex Visual Illusions (Metamorphopsias) These may present as distortions of form, size, movement, or color In a group of 83 patients with visual perceptual abnormalities, Hecaen found that 71 fell under one of four headings: deformation of the image, change in size, illusion of movement, or a combination of all three Illusions of these types have been reported with lesions con ned to the occipital lobes but are more frequently due to shared occipitoparietal or occipitotemporal lesions; they are therefore also considered in earlier sections of this chapter as well as in Chaps 13 and 16 The right hemisphere appears to be involved more often than the left Illusions of movement occur more frequently with posterior tem-.

.

.