NEUROLOGIC CAUSES OF REDUCED VISION in Microsoft Office

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NEUROLOGIC CAUSES OF REDUCED VISION
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Certain anatomic and physiologic facts are requisite for an interpretation of the neurologic lesions that affect vision Visual stimuli entering the eye traverse the inner layers of the retina to reach its outer (posterior) layer, which contains two classes of photoreceptor cells the ask-shaped cones and the slender rods The photoreceptors rest on a single layer of pigmented epithelial cells, which form the outermost surface of the retina The rods and cones and pigmentary epithelium receive their blood supply from the capillaries of the choroid and, to a smaller extent, from the retinal arterioles The rod cells contain rhodopsin, a conjugated protein in which the chromophore group is a carotenoid akin to vitamin A The rods function in the perception of visual stimuli in subdued light (twilight or scotopic vision), and the cones are responsible for color discrimination and the perception of stimuli in bright light (photopic vision) Most of the cones are concentrated in the macular region, particularly in its central part, the fovea, and are responsible for the highest level of visual acuity Specialized pigments in the rods and cones absorb light energy and transform it into electrical signals, which are transmitted to the bipolar cells of the retina and then, in turn, to the super cially (anteriorly) placed neurons, or ganglion cells (Fig 13-1) There are no ganglion cells in the fovea The axons of the retinal ganglion cells, as they stream across the inner surface of the retina, pursue an arcuate course Being unmyelinated, they are not visible, although uorescein retinography shows a trace of their outlines; an experienced examiner, using a bright light and deep green lter, can visualize them through direct ophthalmoscopy The axons of ganglion cells are collected in the optic discs and then pass uninterruptedly through the optic nerves, optic chiasm, and optic tracts to synapse in the lateral geniculate nuclei, the superior colliculi, and the midbrain pretectum (Figs 13-1 and 13-2) The bers derived from macular
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CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE
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eye that is due to the optic nerve lesion, as shown in Fig 13-2B The optic chiasm lies just above the pituiInternal limiting tary body and also forms part of the Anterior membrane anterior wall of the third ventricle; Nerve fiber layer hence the crossing bers may be compressed from below by a pituiGanglion cell tary tumor, a meningioma of the tublayer erculum sellae, or an aneurysm and from above by a dilated third ventriInner plexiform cle or craniopharyngioma The relayer sulting eld defect is bitemporal (Fig 13-2C); if one optic nerve is Amacrine cell also implicated, there will be a loss M ller cell of full- eld vision in that eye Optic Bipolar cells Inner nuclear tract lesions, in comparison with chiHorizontal cell layer asmatic and nerve lesions, are relatively rare Surprisingly, in albinism, Outer plexiform there is an abnormality of chiasmatic layer decussation, in which a majority of the bers, including many that would Outer nuclear not normally cross to the other side, layer decussate How this relates to the albinic defect in the pigment epitheExternal limiting lium is not known membrane About 80 percent of the the bers of the optic tract terminate in the Layer of rods lateral geniculate body and synapse and cones with the six laminae of its neurons Three of these laminae (1, 4, 6), Pigmented layer which constitute the large dorsal nucleus, receive crossed (nasal) bers Posterior Figure 13-1 Diagram of the cellular elements of the retina Light entering the eye anteriorly passes through from the contralateral eye, and three the full thickness of the retina to reach the rods and cones ( rst system of retinal neurons) Impulses arising (2, 3, 5) receive uncrossed (temporal) in these cells are transmitted by the bipolar cells (second system of retinal neurons) to the ganglion cell layer bers from the ipsilateral eye The The third system of visual neurons consists of the ganglion cells and their axons, which run uninterruptedly geniculate cells project to the visual through the optic nerve, chiasm, and optic tracts, synapsing with cells in the lateral geniculate body (Courtesy (striate) cortex of the occipital lobe, of Dr E M Chester) also called area 17 or V1 (Fig 13-4) Other optic tract bers terminate in the pretectum and innervate both Edinger-Westphal nuclei, which subserve pupillary constriction cells form a discrete bundle that rst occupies the temporal side of and accommodation (see Fig 14-7) A small group of bers terthe disc and optic nerve and then assumes a more central position minate in the suprachiasmatic nuclei in animals and presumably within the nerve (papillomacular bundle) These bers are of also in humans These anatomic details explain several useful clinsmaller caliber than the peripheral optic nerve bers It is important ical signs If there is a lesion in one optic nerve, a light stimulus to keep in mind that the retinal ganglion cells and their axonic to the affected eye will have no effect on the pupil of either eye, extensions are, properly speaking, an exteriorized part of the brain although the ipsilateral pupil will still constrict consensually, ie, and that their pathologic reactions are the same as in other parts of in response to a light stimulus from the normal eye This is termed the CNS an afferent pupillary defect The vascular supply of the lateral geIn the optic chiasm, the bers derived from the nasal half of niculate body is from both the posterior and anterior choroidal and each retina decussate and continue in the optic tract with uncrossed thalamogeniculate arteries; it is therefore rarely infarcted temporal bers of the other eye (Figs 13-2 and 13-3) Thus, interIn their course through the temporal lobes, the bers from the ruption of the left optic tract causes a right hemianopic defect in lower and upper quadrants of each retina diverge The lower ones each eye, ie, a homonymous (left nasal and right temporal) eld arch around the anterior pole of the temporal horn of the lateral defect (Fig 13-2D) In partial tract lesions, the visual defects in the ventricle before turning posteriorly; the upper ones follow a more two eyes are not exactly congruent, since the tract bers are not direct path through the white matter of the uppermost part of the evenly admixed A variable bundle of bers from the inferior nasal temporal lobe (Fig 13-2) and possibly of the adjacent parietal lobe part of the optic nerve turns anteriorly into the opposite optic nerve Both groups of bers merge posteriorly at the internal sagittal straas it crosses in the chiasm (Wilbrand s knee) Lesions at this junctum For these reasons, incomplete lesions of the geniculocalcarine tional point of the optic nerve and the chiasm, generally compathways cause visual eld defects that are partial and often not pressive in nature, may therefore cause a contralateral quadrantic fully congruent (Fig 13-2E and F) defect in addition to the expected central scotoma in the ipsilateral
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