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Clinical Pathways in Neuro-ophthalmology : An ... - E-Lib FK UWKS

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evaluation protocol, 183<br />

Vertical diplopia<br />

cranial nerve impairment, 237–238<br />

etiology, 234, 235–236<br />

exam<strong>in</strong>ation protocol, 232–234<br />

extraocular muscle disease, 238–240<br />

mechanical misalignment processes,<br />

240–245<br />

monocular elevator paresis, 234,<br />

236–237<br />

neuromuscular junction diseases, 238<br />

supranuclear processes, 234, 236–237<br />

Vertical gaze impairment<br />

anatomy, 321<br />

etiology, 322, 324–325<br />

evaluation protocols, 323, 325–326, 326<br />

lesion localization of palsies, 321–322,<br />

322–323<br />

Vertical jerk nystagmus, cl<strong>in</strong>ical features<br />

and etiology, 385–389<br />

Vertical ocular myoclonus, stuporous/<br />

comatose patients, 399<br />

Vertical pendular nystagmus, etiology,<br />

370<br />

Vertigo, b<strong>in</strong>ocular symmetric jerk<br />

nystagmus, 390–391<br />

Vistibular tone imbalance, nystagmus<br />

etiology, 367368 i368<br />

Visual acuity<br />

optical disc edema with macular star<br />

(ODEMA), 64<br />

pseudotumor cerebri syndrome, optic<br />

nerve sheath fenestration<br />

(ONSF) and, 150–155<br />

traumatic optic neuropathy (TON),<br />

121–122<br />

Visual field defects<br />

bilateral defects, cl<strong>in</strong>ical features, 192,<br />

193<br />

b<strong>in</strong>asal hemianospia, 196, 198<br />

bitemporal hemianopsia, 194, 195–196,<br />

196<br />

evaluation protocols, 190<br />

homonymous hemianopsia, 198<br />

lateral geniculate body lesion,<br />

199–200<br />

normal neuroimag<strong>in</strong>g, 205–207<br />

optic radiation, 201–202<br />

optic tract lesions, 198–199<br />

Index 485<br />

therapeutic management, 207<br />

junctional defects, 192–194<br />

monocular temporal cresent, 192<br />

occipital lesions, 202–205<br />

optic neuritis (ON), 35–36<br />

optic neuropathy, 191–192<br />

pseudotumor cerebri syndrome, 144<br />

ret<strong>in</strong>al lesions, 189, 191, 191<br />

topographical diagnosis, 189, 190<br />

unexpla<strong>in</strong>ed defects, 207–208<br />

unilateral defects, 189<br />

Visual loss<br />

giant cell arteritis (GCA), cl<strong>in</strong>ical<br />

diagnosis, 95–96, 96–98,<br />

98–99<br />

monocular nystagmus, 370<br />

transient visual loss (TVL)<br />

b<strong>in</strong>ocular TVL<br />

etiology, 179–183<br />

evaluation, 167, 169–170, 183<br />

etiology, 171–179, 177<br />

monocular TVL, duration of episodes,<br />

171–179<br />

monocular TVL, gaze positions, 168,<br />

168–169, 171<br />

patient history, 167<br />

prolonged read<strong>in</strong>g, 171<br />

Visually evoked potentials (VEPs), optic<br />

neuritis (ON), <strong>in</strong>dications for,<br />

47<br />

Visual prognosis<br />

nonarteritic anterior ischemic optic<br />

neuropathy (NA-AION), 79<br />

levodopa therapy, 82–83<br />

optic nerve sheath fenestration, 83,<br />

83–85<br />

optic disc edema with macular<br />

(ODEMS), 67, 69<br />

optic neuritis (ON), 49–50<br />

Visual recovery<br />

giant cell arteritis (GCA), therapeutic<br />

protocols, 106–108<br />

optic neuritis (ON), 49–50<br />

traumatic optic neuropathy (TON)<br />

corticosteroid therapy, 122–123<br />

natural history and progression,<br />

120–122<br />

Vitam<strong>in</strong> A, idiopathic pseudotumor<br />

cerebri etiology, 140–142, 141

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