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79 Cards in this Set
- Front
- Back
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projects to the most posterior portion of the visual cortex
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he central region of the visual field (macula)
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projects to the most posterior portion of the visual cortex
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he central region of the visual field (macula)
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Because the central retinal artery subsequently divides into superior and inferior retinal branches, vascular disease of the retina tends to produce
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altitudinal (i.e., superior or inferior) visual field deficits.
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Because the central retinal artery subsequently divides into superior and inferior retinal branches, vascular disease of the retina tends to produce
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altitudinal (i.e., superior or inferior) visual field deficits.
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Because the central retinal artery subsequently divides into superior and inferior retinal branches, vascular disease of the retina tends to produce
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altitudinal (i.e., superior or inferior) visual field deficits.
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With a complete nerve III lesion, the eye is
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partially abducted and there is an inability to adduct, elevate, and depress the eye; the eyelid droops (ptosis), and the pupil is nonreactive.
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With a complete nerve III lesion, the eye is
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partially abducted and there is an inability to adduct, elevate, and depress the eye; the eyelid droops (ptosis), and the pupil is nonreactive.
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With a complete nerve III lesion, the eye is
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partially abducted and there is an inability to adduct, elevate, and depress the eye; the eyelid droops (ptosis), and the pupil is nonreactive.
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The nuclei of the oculomotor and trochlear nerves are located in the
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dorsal midbrain, ventral to the cerebral aqueduct (of Sylvius), while the abducens nerve nucleus occupies a similarly dorsal and periventricular position in the pons.
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The nuclei of the oculomotor and trochlear nerves are located in the
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dorsal midbrain, ventral to the cerebral aqueduct (of Sylvius), while the abducens nerve nucleus occupies a similarly dorsal and periventricular position in the pons.
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The nuclei of the oculomotor and trochlear nerves are located in the
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dorsal midbrain, ventral to the cerebral aqueduct (of Sylvius), while the abducens nerve nucleus occupies a similarly dorsal and periventricular position in the pons.
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The nuclei of the oculomotor and trochlear nerves are located in the
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dorsal midbrain, ventral to the cerebral aqueduct (of Sylvius), while the abducens nerve nucleus occupies a similarly dorsal and periventricular position in the pons.
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The nuclei of the oculomotor and trochlear nerves are located in the
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dorsal midbrain, ventral to the cerebral aqueduct (of Sylvius), while the abducens nerve nucleus occupies a similarly dorsal and periventricular position in the pons.
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In disorders affecting the abducens nerve nucleus rather than the nerve itself, lateral rectus paresis is often associated with
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facial weakness, paresis of ipsilateral conjugate
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In disorders affecting the abducens nerve nucleus rather than the nerve itself, lateral rectus paresis is often associated with
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facial weakness, paresis of ipsilateral conjugate
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In disorders affecting the abducens nerve nucleus rather than the nerve itself, lateral rectus paresis is often associated with
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facial weakness, paresis of ipsilateral conjugate
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In disorders affecting the abducens nerve nucleus rather than the nerve itself, lateral rectus paresis is often associated with
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facial weakness, paresis of ipsilateral conjugate
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In disorders affecting the abducens nerve nucleus rather than the nerve itself, lateral rectus paresis is often associated with
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facial weakness, paresis of ipsilateral conjugate
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enters that control horizontal and vertical gaze are located
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in the pons and in the pretectal region of the midbrain, respectively, and receive descending inputs from the cerebral cortex that allow voluntary control of gaze
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enters that control horizontal and vertical gaze are located
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in the pons and in the pretectal region of the midbrain, respectively, and receive descending inputs from the cerebral cortex that allow voluntary control of gaze
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enters that control horizontal and vertical gaze are located
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in the pons and in the pretectal region of the midbrain, respectively, and receive descending inputs from the cerebral cortex that allow voluntary control of gaze
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enters that control horizontal and vertical gaze are located
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in the pons and in the pretectal region of the midbrain, respectively, and receive descending inputs from the cerebral cortex that allow voluntary control of gaze
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Each lateral gaze center, located in the
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Located in the paramedian pontine reticular formation (PPRF) adjacent to the abducens nerve nucleus, mediates ipsilateral, conjugate,
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Each lateral gaze center, located in the
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Located in the paramedian pontine reticular formation (PPRF) adjacent to the abducens nerve nucleus, mediates ipsilateral, conjugate,
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Each lateral gaze center, located in the
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Located in the paramedian pontine reticular formation (PPRF) adjacent to the abducens nerve nucleus, mediates ipsilateral, conjugate,
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Each lateral gaze center, located in the
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Located in the paramedian pontine reticular formation (PPRF) adjacent to the abducens nerve nucleus, mediates ipsilateral, conjugate,
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Each lateral gaze center, located in the
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Located in the paramedian pontine reticular formation (PPRF) adjacent to the abducens nerve nucleus, mediates ipsilateral, conjugate,
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Right homonymous inferior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left parietal lobe.
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Right homonymous inferior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left parietal lobe.
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Right homonymous inferior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left parietal lobe.
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Right homonymous inferior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left parietal lobe.
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Right homonymous inferior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left parietal lobe.
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Right homonymous superior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left temporal lobe (Meyer loop).
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Right homonymous superior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left temporal lobe (Meyer loop).
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Right homonymous superior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left temporal lobe (Meyer loop).
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Right homonymous superior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left temporal lobe (Meyer loop).
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Right homonymous superior quadrantanopia caused by partial involvement of the optic radiation by a lesion in the
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left temporal lobe (Meyer loop).
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Right homonymous hemianopia (with macular sparing) resulting from
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posterior cerebral artery occlusion.]
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Right homonymous hemianopia (with macular sparing) resulting from
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posterior cerebral artery occlusion.]
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Right homonymous hemianopia (with macular sparing) resulting from
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posterior cerebral artery occlusion.]
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Right homonymous hemianopia (with macular sparing) resulting from
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posterior cerebral artery occlusion.]
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Right homonymous hemianopia (with macular sparing) resulting from
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posterior cerebral artery occlusion.]
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n early papilledema (Figure 4-11), the retinal veins appear engorged and spontaneous venous pulsations are
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absent
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n early papilledema (Figure 4-11), the retinal veins appear engorged and spontaneous venous pulsations are
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absent
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n early papilledema (Figure 4-11), the retinal veins appear engorged and spontaneous venous pulsations are
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absent
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The macula, a somewhat paler area than the rest of the retina, is located about
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two disk diameters temporal to the temporal margin of the optic disk. It can be visualized quickly by having the patient look at the light from the ophthalmoscope. Ophthalmoscopic examination of the macula can reveal abnormalities related to visual loss from age-related macular degeneration, from macular holes, or from hereditary cerebromacular degenerations.
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The macula, a somewhat paler area than the rest of the retina, is located about
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two disk diameters temporal to the temporal margin of the optic disk. It can be visualized quickly by having the patient look at the light from the ophthalmoscope. Ophthalmoscopic examination of the macula can reveal abnormalities related to visual loss from age-related macular degeneration, from macular holes, or from hereditary cerebromacular degenerations.
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The macula, a somewhat paler area than the rest of the retina, is located about
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two disk diameters temporal to the temporal margin of the optic disk. It can be visualized quickly by having the patient look at the light from the ophthalmoscope. Ophthalmoscopic examination of the macula can reveal abnormalities related to visual loss from age-related macular degeneration, from macular holes, or from hereditary cerebromacular degenerations.
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The macula, a somewhat paler area than the rest of the retina, is located about
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two disk diameters temporal to the temporal margin of the optic disk. It can be visualized quickly by having the patient look at the light from the ophthalmoscope. Ophthalmoscopic examination of the macula can reveal abnormalities related to visual loss from age-related macular degeneration, from macular holes, or from hereditary cerebromacular degenerations.
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The macula, a somewhat paler area than the rest of the retina, is located about
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two disk diameters temporal to the temporal margin of the optic disk. It can be visualized quickly by having the patient look at the light from the ophthalmoscope. Ophthalmoscopic examination of the macula can reveal abnormalities related to visual loss from age-related macular degeneration, from macular holes, or from hereditary cerebromacular degenerations.
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Tonic pupil— The tonic (Adie) pupil (see Table 4-1) is
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larger than the contralateral unaffected pupil and reacts sluggishly to changes in illumination or accommodation. Because the tonic pupil does eventually react, anisocoria becomes less marked during the time of the examination. This abnormality is most commonly a manifestation of a benign, often familial disorder that frequently affects young women (Holmes-Adie syndrome) and may be associated with depressed deep tendon reflexes (especially in the legs), segmental anhidrosis (localized lack of sweating), orthostatic hypotension, or cardiovascular autonomic instability. The condition may be bilateral. The pupillary abnormality may be caused by degeneration of the ciliary ganglion, followed by aberrant reinnervation of the pupilloconstrictor muscles.
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Tonic pupil— The tonic (Adie) pupil (see Table 4-1) is
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larger than the contralateral unaffected pupil and reacts sluggishly to changes in illumination or accommodation. Because the tonic pupil does eventually react, anisocoria becomes less marked during the time of the examination. This abnormality is most commonly a manifestation of a benign, often familial disorder that frequently affects young women (Holmes-Adie syndrome) and may be associated with depressed deep tendon reflexes (especially in the legs), segmental anhidrosis (localized lack of sweating), orthostatic hypotension, or cardiovascular autonomic instability. The condition may be bilateral. The pupillary abnormality may be caused by degeneration of the ciliary ganglion, followed by aberrant reinnervation of the pupilloconstrictor muscles.
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Tonic pupil— The tonic (Adie) pupil (see Table 4-1) is
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larger than the contralateral unaffected pupil and reacts sluggishly to changes in illumination or accommodation. Because the tonic pupil does eventually react, anisocoria becomes less marked during the time of the examination. This abnormality is most commonly a manifestation of a benign, often familial disorder that frequently affects young women (Holmes-Adie syndrome) and may be associated with depressed deep tendon reflexes (especially in the legs), segmental anhidrosis (localized lack of sweating), orthostatic hypotension, or cardiovascular autonomic instability. The condition may be bilateral. The pupillary abnormality may be caused by degeneration of the ciliary ganglion, followed by aberrant reinnervation of the pupilloconstrictor muscles.
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Tonic pupil— The tonic (Adie) pupil (see Table 4-1) is
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larger than the contralateral unaffected pupil and reacts sluggishly to changes in illumination or accommodation. Because the tonic pupil does eventually react, anisocoria becomes less marked during the time of the examination. This abnormality is most commonly a manifestation of a benign, often familial disorder that frequently affects young women (Holmes-Adie syndrome) and may be associated with depressed deep tendon reflexes (especially in the legs), segmental anhidrosis (localized lack of sweating), orthostatic hypotension, or cardiovascular autonomic instability. The condition may be bilateral. The pupillary abnormality may be caused by degeneration of the ciliary ganglion, followed by aberrant reinnervation of the pupilloconstrictor muscles.
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Tonic pupil— The tonic (Adie) pupil (see Table 4-1) is
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larger than the contralateral unaffected pupil and reacts sluggishly to changes in illumination or accommodation. Because the tonic pupil does eventually react, anisocoria becomes less marked during the time of the examination. This abnormality is most commonly a manifestation of a benign, often familial disorder that frequently affects young women (Holmes-Adie syndrome) and may be associated with depressed deep tendon reflexes (especially in the legs), segmental anhidrosis (localized lack of sweating), orthostatic hypotension, or cardiovascular autonomic instability. The condition may be bilateral. The pupillary abnormality may be caused by degeneration of the ciliary ganglion, followed by aberrant reinnervation of the pupilloconstrictor muscles.
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Horner syndrome (Tables 4-1 and 4-2) results from a lesion of the central or peripheral sympathetic nervous system and consists of a small (miotic) pupil associated with mild ptosis (Figure 4-13 A) and sometimes
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loss of sweating (anhidrosis).
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Horner syndrome (Tables 4-1 and 4-2) results from a lesion of the central or peripheral sympathetic nervous system and consists of a small (miotic) pupil associated with mild ptosis (Figure 4-13 A) and sometimes
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loss of sweating (anhidrosis).
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Horner syndrome (Tables 4-1 and 4-2) results from a lesion of the central or peripheral sympathetic nervous system and consists of a small (miotic) pupil associated with mild ptosis (Figure 4-13 A) and sometimes
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loss of sweating (anhidrosis).
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Horner syndrome (Tables 4-1 and 4-2) results from a lesion of the central or peripheral sympathetic nervous system and consists of a small (miotic) pupil associated with mild ptosis (Figure 4-13 A) and sometimes
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loss of sweating (anhidrosis).
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Horner syndrome (Tables 4-1 and 4-2) results from a lesion of the central or peripheral sympathetic nervous system and consists of a small (miotic) pupil associated with mild ptosis (Figure 4-13 A) and sometimes
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loss of sweating (anhidrosis).
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Oculosympathetic pathways— The sympathetic pathway controlling pupillary dilation (Figure 4-13 B) consists of an uncrossed three-neuron arc:?
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hypothalamic neurons, the axons of which descend through the brainstem to the intermediolateral column of the spinal cord at the T1 level; preganglionic sympathetic neurons projecting from the spinal cord to the superior cervical ganglion; and postganglionic sympathetic neurons that originate in the superior cervical ganglion, ascend in the neck along the internal carotid artery, and enter the orbit with the first (ophthalmic) division of the trigeminal (V) nerve. Horner syndrome is caused by interruption of these pathways at any site.
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Oculosympathetic pathways— The sympathetic pathway controlling pupillary dilation (Figure 4-13 B) consists of an uncrossed three-neuron arc:?
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hypothalamic neurons, the axons of which descend through the brainstem to the intermediolateral column of the spinal cord at the T1 level; preganglionic sympathetic neurons projecting from the spinal cord to the superior cervical ganglion; and postganglionic sympathetic neurons that originate in the superior cervical ganglion, ascend in the neck along the internal carotid artery, and enter the orbit with the first (ophthalmic) division of the trigeminal (V) nerve. Horner syndrome is caused by interruption of these pathways at any site.
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Oculosympathetic pathways— The sympathetic pathway controlling pupillary dilation (Figure 4-13 B) consists of an uncrossed three-neuron arc:?
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hypothalamic neurons, the axons of which descend through the brainstem to the intermediolateral column of the spinal cord at the T1 level; preganglionic sympathetic neurons projecting from the spinal cord to the superior cervical ganglion; and postganglionic sympathetic neurons that originate in the superior cervical ganglion, ascend in the neck along the internal carotid artery, and enter the orbit with the first (ophthalmic) division of the trigeminal (V) nerve. Horner syndrome is caused by interruption of these pathways at any site.
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Oculosympathetic pathways— The sympathetic pathway controlling pupillary dilation (Figure 4-13 B) consists of an uncrossed three-neuron arc:?
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hypothalamic neurons, the axons of which descend through the brainstem to the intermediolateral column of the spinal cord at the T1 level; preganglionic sympathetic neurons projecting from the spinal cord to the superior cervical ganglion; and postganglionic sympathetic neurons that originate in the superior cervical ganglion, ascend in the neck along the internal carotid artery, and enter the orbit with the first (ophthalmic) division of the trigeminal (V) nerve. Horner syndrome is caused by interruption of these pathways at any site.
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Oculosympathetic pathways— The sympathetic pathway controlling pupillary dilation (Figure 4-13 B) consists of an uncrossed three-neuron arc:?
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hypothalamic neurons, the axons of which descend through the brainstem to the intermediolateral column of the spinal cord at the T1 level; preganglionic sympathetic neurons projecting from the spinal cord to the superior cervical ganglion; and postganglionic sympathetic neurons that originate in the superior cervical ganglion, ascend in the neck along the internal carotid artery, and enter the orbit with the first (ophthalmic) division of the trigeminal (V) nerve. Horner syndrome is caused by interruption of these pathways at any site.
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When Horner syndrome has been present since infancy, the ipsilateral iris is
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lighter and blue (heterochromia iridis).
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When Horner syndrome has been present since infancy, the ipsilateral iris is
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lighter and blue (heterochromia iridis).
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When Horner syndrome has been present since infancy, the ipsilateral iris is
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lighter and blue (heterochromia iridis).
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When Horner syndrome has been present since infancy, the ipsilateral iris is
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lighter and blue (heterochromia iridis).
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When Horner syndrome has been present since infancy, the ipsilateral iris is
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lighter and blue (heterochromia iridis).
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Relative afferent pupillary defect (Marcus Gunn pupil)— In this condition...
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one pupil constricts less markedly in response to direct illumination than to illumination of the contralateral pupil, whereas normally the direct response is greater than the consensual response. The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil (Gunn pupillary test). Relative afferent pupillary defect is commonly associated with disorders of the ipsilateral optic nerve, which interrupt the afferent limb and affect the pupillary light reflex (Figure 4-12). Such disorders also commonly impair vision (especially color vision) in the involved eye.
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Relative afferent pupillary defect (Marcus Gunn pupil)— In this condition...
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one pupil constricts less markedly in response to direct illumination than to illumination of the contralateral pupil, whereas normally the direct response is greater than the consensual response. The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil (Gunn pupillary test). Relative afferent pupillary defect is commonly associated with disorders of the ipsilateral optic nerve, which interrupt the afferent limb and affect the pupillary light reflex (Figure 4-12). Such disorders also commonly impair vision (especially color vision) in the involved eye.
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Relative afferent pupillary defect (Marcus Gunn pupil)— In this condition...
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one pupil constricts less markedly in response to direct illumination than to illumination of the contralateral pupil, whereas normally the direct response is greater than the consensual response. The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil (Gunn pupillary test). Relative afferent pupillary defect is commonly associated with disorders of the ipsilateral optic nerve, which interrupt the afferent limb and affect the pupillary light reflex (Figure 4-12). Such disorders also commonly impair vision (especially color vision) in the involved eye.
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Relative afferent pupillary defect (Marcus Gunn pupil)— In this condition...
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one pupil constricts less markedly in response to direct illumination than to illumination of the contralateral pupil, whereas normally the direct response is greater than the consensual response. The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil (Gunn pupillary test). Relative afferent pupillary defect is commonly associated with disorders of the ipsilateral optic nerve, which interrupt the afferent limb and affect the pupillary light reflex (Figure 4-12). Such disorders also commonly impair vision (especially color vision) in the involved eye.
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Relative afferent pupillary defect (Marcus Gunn pupil)— In this condition...
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one pupil constricts less markedly in response to direct illumination than to illumination of the contralateral pupil, whereas normally the direct response is greater than the consensual response. The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil (Gunn pupillary test). Relative afferent pupillary defect is commonly associated with disorders of the ipsilateral optic nerve, which interrupt the afferent limb and affect the pupillary light reflex (Figure 4-12). Such disorders also commonly impair vision (especially color vision) in the involved eye.
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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The abnormality is detected by rapidly moving a bright flashlight back and forth between the eyes while continuously observing the suspect pupil
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