Chapter 1
The Neuro-Ophthalmologic Case History: Elucidating the Symptoms
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Once again he would go over the points in the history, elucidating, elaborating. His own examination would follow—full, detailed, but without the tedious slowness of some other neurologists. A clinical point, or any unusual symptom or sign would attract his attention. He would perhaps send for a copy of his manual to verify an observation. Often he would produce his pocketbook and make some shorthand memorandum which at home would be simplified and indexed for later reference.

The basis of his assessment of the problem was hence solid and substantial. Aided by an adequate knowledge of neuropathology as it stood in his day, and by a thorough grounding in neuroanatomy, he interpreted his observations scientifically. Hence he did not have to rely on clinical memory, or clinical “instinct”—useful though they were to him. There was nothing flashy or meretricious therefore in his bedside technique.

Hence it was that his diagnostic accuracy proved uncanny.

M. Critchley: Sir William Gowers

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The case history remains one of the last strongholds of the clinician, besieged by dire predictions of its imminent replacement by continually refined neurologic imaging techniques. These computer-based procedures, and the thoroughness of the neuro-ophthalmologic examination, must raise doubts regarding the usefulness of the labor-intensive (supposedly anachronistic) elicitation of the detailed account of each patient's illness. Holmes,1 one of the great students of the eye and nervous system, succinctly rebutted similar doubts by affirming that “the final diagnosis is often as dependent on an accurate history as on a clinical examination.”

Holmes had a twofold approach to the medical history. First, he included a description of the illness in the patient's words, uninfluenced by the physician's leading questions. Second, the chronology or any ambiguous terminology was clarified by “a definite system of investigation… to determine: (a) the exact nature of each symptom; (b) its relations in space; (c) its relations in time; and (d) the factors which influence it.”1

Ideally, the history begins a process of diagnosis and directs the clinician to focus the examination on structures most likely to have caused particular neuro-ophthalmologic complaints. In addition to suggesting a tentative topographic localization, the patient's recollection of onset, progression, and recurrence of symptoms also may hint at etiology. Specific clinical paradigms (e.g., the sudden onset of visual loss stemming from optic nerve ischemia or inflammation, the fluctuating diplopia of myasthenia, or the indolent visual decline of tumoral compression of the anterior visual pathways) are invaluable leads to precise diagnosis. Circumstantial aspects of visual dysfunction, such as an inability to adapt visually in a darkened theater (pigmentary retinopathy), blurred vision during a hot bath (demyelinating optic neuropathy), or image degradation in bright light (posterior subcapsular cataracts), provide important etiologic clues.

The past medical background often sheds light on the acute complaint. In a patient with a prior history of diabetes or thyroid disease, the evaluation of acquired diplopia may be streamlined. Similarly, neuroradiologic studies are superfluous when slit-lamp detection of posterior subcapsular cataracts or ophthalmoscopic observation of pigmentary macular retinopathy confirms the cause of visual loss in the setting of chronic corticosteroid or thioridazine use, respectively. The details of personal and nutritional habits may prove critical: a puzzling progression of bilateral central visual loss is recognized as nutritional “amblyopia” with the revelation of excessive alcohol intake and an especially poor diet; an immunodeficient basis of cytomegalovirus retinopathy may be brought forward in the self-confessed intravenous drug abuser or homosexual.

The transition from appropriate inquiries to diagnostic precision is most readily conveyed by specific instances of history taking. In this chapter, the diagnostic choices prompted by frequently encountered historical paradigms and the symptom complexes of visual sensory or ocular motility disturbances, or of ocular/cephalic pain, are examined.

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As described by Traquair,2 the field of vision is “a portion of an immense hollow sphere upon the inner surface of which is spread a panoramic picture of external objects showing the central feature depicted with minute detail and vivid colouring, while objects at increasing distance from the centre are indicated with correspondingly diminished clearness and duller hues.” These external objects are not merely projected onto a static retina. James 3 likened peripheral areas to “sentinels, which when beams of light move over them, cry ‘Who goes there?’ and call the fovea to the spot.” The clinician must know that the dynamic process of normal vision is heir to transient and benign vagaries of function, such as fleeting constriction and dimming of the visual field periphery with relative retinal hypoperfusion induced by rapid postural changes. Some phenomena, such as suppression of vision 4 and visual masking during saccades, occur constantly and do not intrude on the observer's awareness. The extraretinal mechanism subserving saccadic suppression operates very early in the visual pathway, within the thalamus or possibly the primary visual cortex.5 Not only is vision suppressed during a saccade but many of the details of the view preceding the saccade are lost. This change-blindness also occurs with other brief visual disruptions, such as blinks, mud splashes on a windshield, or a camera cut in a film sequence.6 Other benign vision obscurations may be caused by the following:

  Tear film opacities
  Physiologic halos
  Vitreous floaters
  Retinal capillary circulation
  Orthostatic visual field constriction
  Phosphenes induced by the following:

  Mechanical pressure
  Saccadic eye movement
  Vitreous traction
  Cosmic particles

  Visual suppression during saccades
  Blank-out associated with Ganzfeld
  Monocular patching

Stimuli as diverse as a flashbulb ignition or a video display terminal can affect vision with afterimages of retinal7 or cerebral8 origin.

Intermittent darkening of the visual field (blank-out) can occur in patients undergoing bowl-type perimetry and is attributed to the effects of full-field illumination (Ganzfeld).9 Momentary loss of vision or “snowstorm” in the intact eye of patients wearing an eye patch may result from binocular rivalry suppression.10 Visual interference can occur as a result of images (entoptic phenomena) caused by the inherent structure of the eye. Bright lights may be encircled by entoptic halos that are produced by a normal lens and cornea but have a smaller diameter than the pathologic halo of glaucomatous corneal edema.11 When one observes a uniformly illuminated background, such as the sky, vitreous floaters consisting of a condensation of collagen fibrils are more readily perceived. The insidious or abrupt appearance of these muscae volitantes12 or the ringlike opacity of posterior vitreous peripapillary detachment usually is a benign concomitant of aging, although the sudden onset of many floaters and phosphenes may signify intravitreal hemorrhage or retinal detachment. Pinpoint luminosities, darting more rapidly than the gentle drift of vitreous floaters, probably represent cells moving within the retinal capillary circulation.

Phosphenes are luminous sensations that may be perceived spontaneously on eye closure, especially in children,13 or by astronauts exposed to high-energy, heavy cosmic particles.14 They also are caused by mechanical distortion of the retina induced by pressure on the globe, accommodation, rapid (saccadic) eye movement, or forward separation of the vitreous from the retinal surface. The latter phenomenon triggers the entoptic “lightning streaks” described by Moore,15 who emphasized their benign prognosis. These symptoms of posterior vitreous detachment16 alarm the patient and may prove difficult to distinguish from similar symptoms of less benign origin.

Pathologic disturbances of vision may be transient or permanent, simple or complex, and negative or positive. Patients detect a startling positive complex visual obscuration, such as a scintillating scotoma, more readily than a simple negative peripheral field defect. The ability to ignore small scotomata, or even more extensive visual depressions, is exemplified by the subjective imperception of the physiologic blind spot or of angioscotomata during monocular viewing conditions. Similarly, Helmholtz17 remarked on the deep inattention to visual defects occasionally encountered in “cases where one eye has gradually gone blind, and the patient lived for an indefinite time without knowing it, until through accidental closure of the healthy eye alone, the blindness of the other was brought to attention.” Nonawareness of homonymous hemianopsia may aid in cerebral localization, because such neglect may signify a large parietal lesion or lesions interrupting the associative pathways to the primary or secondary visual cortices. Partial or full awareness of hemianopia is more typical of purely occipital lesions.18 Alternatively, patients may attribute visual loss to one eye when in reality an ipsilateral hemianopia is present.

Transient pathologic visual loss can occur from events at any level of the afferent visual system, from the cornea to the occipital poles.19 The following lists give examples of these events.

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  Amaurosis fugax
  Retinal microembolization or hypoperfusion
  Retinal migraine
  Acute glaucoma (corneal edema)
  Reversible cataract (e.g., acute hyperglycemia)
  Aphakic dyschromatopsia
  Aphakic microhyphema (recurrent iris bleed)
  G force–induced “red out”
  Glycine urologic irrigating solution20 (retinal inhibition)
  Hemeralopia or “day blindness” (outer retinal dysfunction)
  Quinine, sildenafil, digitalis, clomiphene citrate21 (retinal toxicity)
  Primary marginal pigment epithelial iris cysts

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  Obscurations preceding ischemic optic neuropathy
  Photopsias with optic neuropathies
  Synesthesias (phosphenes induced by sound)
  Movement-induced phosphenes, with multiple sclerosis
  Uhthoff's phenomenon
  Optic disc swelling
  Retrobulbar tumors
  Intracranial hypotension22

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  Carotid or vertebrobasilar ischemia
  Contralateral diaschisis following occipital lobe cerebrovascular accident
  Classic migraine and variants
  Occipital lobe seizures23
  Occipital trauma
  Release and irritative hallucinations
  Osmotic disruption of occipital blood–brain barrier by angiographic contrast agents24

All too often, transient visual disturbances are attributed to extracranial carotid artery atheromatous disease, and further critical diagnostic analysis ceases when a normal study of the carotid bifurcation is obtained. The abrupt onset and transience (seconds to a few minutes) of a gray, monocular curtain or diaphragm-like constriction of the visual periphery, or positive visual phenomena in about one-third of patients,26 may herald embolism or momentarily decreased perfusion in the distribution of the internal carotid artery (see Chapter 5). These symptoms of amaurosis fugax (“fleeting blindness”) can be distinguished readily from the migraineurs' scintillating scotoma that expands into the visual periphery over a period of 15 to 25 minutes.27

Although light-induced periocular pain or photophobia is a nonspecific symptom of ocular or intracranial trigeminal irritation,28 other types of pain can reveal the origin of visual loss, as in angle-closure glaucoma that is characterized by attacks of nauseating ocular pain and vision obscured by halos around light sources, or reduced to mere perception of light.29 A several-day siege of central visual blurring and orbital ache aggravated by eye movement (possibly resulting from an inflamed dural sheath) is typical of demyelinating optic neuritis, and absence of pain is more typical of papillitis or ischemic optic neuropathy.30 Eye or supraorbital pain on the side contralateral to homonymous hemianopia may indicate ischemia of the occipital lobe and surrounding dural structures, which are innervated by the ophthalmic division of the trigeminal nerve.31 Temporal artery and scalp tenderness and jaw/lingual claudication point to giant-cell arteritis as the origin of permanent or (infrequently) transient monocular visual loss.

Other elucidating features of visual dysfunction include a worsening of central scotoma with exercise (Uhthoff's phenomenon) associated with demyelinating optic neuropathies. An enigmatic history of frequent, brief, painless visual obscuration with postural changes need not be investigated by angiography, but can be explained by ophthalmoscopic detection of swollen optic discs.32 These few examples should underscore the heterogeneity of “transient visual loss” and bolster the principle that meticulous history-taking may obviate the need for elaborate diagnostic devices or invasive neuroimaging procedures.

History-taking of complex visual disturbances may be hindered by a reluctance to disclose apparently bizarre symptoms or by a lack of insight (e.g., a patient who seeks a new refraction because he “can't read” but is found to be alexic). Other defective associative (suprastriate) visual processing includes visual agnosia, in which an object is clearly seen but cannot be recognized, and simultanagnosia, in which the details of a picture cannot be synthesized into an intelligible whole. The inability to recognize faces (prosopagnosia) and the inability to recognize colors, despite normal visual acuity and color matching, are further examples of selective “mind blindness” in which the clinical history merges into a battery of tests of higher cortical function. Visual perseveration in space and time may transform a moving light into a series of multiple discrete lights along its path (polyopia),33 or cause a visual afterimage to loom before the patient after gaze is directed elsewhere (palinopsia). It has been proposed that defects of object recognition34 such as visual agnosia, prosopagnosia, simultanagnosia, and cerebral achromatopsia result from an interruption of occipital–temporal projections, whereas disordered spatial location and motion perception (e.g., polyopia) are produced by an impairment of occipital–parietal pathways.

Hallucinations encompass a spectrum of false sensory impressions, ranging from unformed light to complex cinematic visions. The content of the latter may be sufficiently distressing that the patient may be coaxed to acknowledge “dreaming with the eyes open.” The clinical concept of equating calcarine cortex dysfunction with unformed positive visual phenomena, and more rostrally placed temporoparietal lesions with increasingly complex hallucinations, has been repeatedly criticized and supplanted by classifying hallucinations as irritative or release in origin. The former variety may allow tentative localization, but the latter can be formed or unformed in appearance regardless of the site of visual pathway lesions. Most non-psychiatric visual hallucinations are release hallucinations, and they are typically continuous and nonstereotypic. Cogan35 suggested that these originate when the “removal of normal visual impulses releases indigenous cerebral activity of the visual system.”

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Stability and fusion of binocular images are among the most demanding exercises of the central nervous system and are liable to disruption, as anyone who has experienced vertigo after sudden cessation of spinning, or diplopia after alcoholic intoxication,36 can attest. Momentary visual blurring or diplopia is a common complaint. Although causes such as decompensation of a preexistent phoria or physiologic diplopia37 often are invoked, other more precise explanations may not evolve. More persistent diplopia, or as the patient may call it, “seeing double,” is the most distressing and constant symptom of an ocular palsy. “It is due to failure of the images of the objects towards which the eyes are directed to fall on corresponding parts of the two retinae; the images are consequently projected separately into space, and the patient perceives them separately.”1

If the patient acknowledges that the diplopia disappears with closure of one eye, the origin of the symptom is a disturbance of motility. Double vision (subjectively perceived perhaps more accurately as “ghost images”) that persists despite closure of one eye is termed monocular diplopia and usually is caused by optical aberrations of the refractive media of the eyes, especially oil droplets in the tear film, excessive tearing, and corneal disease (e.g., keratoconus). Multirefractile cataracts are much more common causes of monocular diplopia than are retinal diseases, which physically distort or displace the fovea.38 Anomalous retinal correspondence is an uncommon sensory adaptation that occurs after strabismus surgery; it may be a rare cause of nonparetic diplopia.

The use of a pinhole should eliminate monocular diplopia (“ghost images”) caused by refractive errors of the ocular media. Persistence of monocular diplopia despite pinhole “refraction,” and without evidence of posterior visual pathway disease, is suggestive of a functional disorder. Similarly, binocular diplopia may have a functional origin, as in spasm of the near reflex,39 which can resemble bilateral abduction palsies but is accompanied by telltale accommodative miosis.

The process of identifying paretic extraocular muscles begins when the patient reports in which direction of gaze image separation is greatest or smallest; whether images are separated vertically, horizontally, or obliquely; and whether image separation is greater at near or far distances. For example, a report of image tilt or vertical diplopia that increases on down-gaze and is minimized by compensatory head tilt or tucking the chin down on the chest practically pinpoints a superior oblique palsy.

When an up-gaze attempt results in increasing vertical diplopia, then signs of lid retraction or proptosis should be sought. Restrictive myopathy of the inferior rectus resulting from Graves' ophthalmopathy is a likely cause of such spontaneously acquired vertical eye muscle imbalance. An acute onset of rather severe periorbital ache, horizontal diplopia with ptosis, dilated pupil, and exotropia may herald compression of the oculomotor nerve by distention or bleeding of a posterior communicating, internal carotid, or rostral basilar artery aneurysm.40 Pupil-sparing oculomotor palsy of benign vascular origin is much more common in the aging population. Other diagnostic maxims of diplopia include the diurnal fluctuations and ubiquitous ptosis of myasthenia, the confusion and ataxia accompanying Wernicke's alcoholic ophthalmoplegia, and the subjective bruit with chronic red eye of a carotid-cavernous or dural fistula.

Vertigo, oscillopsia (apparent shimmering movement of the environment), and visual tilt are symptoms of dynamic disturbances of ocular motility. Vertigo is the memorable illusory rotation of self or environment; the patient's recollection of the discomfort of vertigo, its induction by changes in head position, and its association with nausea or tinnitus can reliably localize disease of the semicircular canals or their central connections. Oscillopsia, the false perception of back-and-forth movement of the environment created by the repeated transit of images of stationary objects across the retina, can be caused by impairment of the vestibulo-ocular reflex, any acquired pathologic nystagmus, ocular fixation instability, superior oblique myokymia, or even “pseudonystagmus” induced by eyelid myokymia.41 The striking complaint of a 90-degree tilt, or complete inversion of the environment, is prompted by a distorted perception of gravity that arises from lateral medullary infarction damaging otolith connections.42

There may be inherent ambiguity in some patients' subjective descriptions of “blurry vision,” which can cover a multitude of conditions ranging from a central scotoma to subtle diplopia to impaired accommodation. Some patients complain more bitterly about narrowly separated double images, whereas paradoxically others can ignore the widely parted images produced by a large-angle heterotropia. Similarly, a patient who “can't see” may not be the victim of disease of the afferent visual system, but rather of the involuntary lid closure found in blepharospasm or of immobile globes found in chronic progressive external ophthalmoplegia.

Although most of these symptom complexes can be characterized easily by a few pertinent questions or even by “across-the-room” observations, a painstaking history may be required to assign relative values to multiple causes of visual disability and suggest avenues of therapy. A case in point is the complicated visual scenario of albinism: acuity is impaired by relative foveal hypoplasia, refractive error, photophobia, hemeralopia, and motor anomalies in the form of congenital pendular or jerk nystagmus and strabismus, probably related to misrouting of retinogeniculate projections.43

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Sherrington44 believed that pain was an integral component of nervous activity and proclaimed it to be “the physical adjunct of an imperative protective reflex.” Pain potentially serves as a guide to localization of disease and as an indicator of response to therapy. Pain is the overwhelming symptom in cluster headaches and in tic douloureux, where suffering appears disproportionately excessive from the minor degree of tissue injury. Conversely, a mildly painful compressive oculomotor palsy may lack the symptomatic “drama” appropriate to the life-threatening impending rupture of a posterior communicating artery aneurysm. In addition to the relatively well-known tic douloureux, there are infrequently encountered entities such as glossopharyngeal neuralgia in which burning throat pain may be triggered by swallowing. Pain in the distribution of the ear, palate, or occiput may arise from neuralgias of the geniculate ganglion, sphenopalatine ganglion, and greater occipital nerve, respectively.45 The somatic distribution and variations of neuralgias distinguish them from other sources of cephalic pain, such as temporomandibular joint syndrome, cranial arteritis, sinusitis, retrobulbar neuritis, and acute glaucoma.

A troublesome group of patients has facial pain lacking discernible origin, not conforming to any classic neuralgia or pain syndrome. Such atypical facial pain is characterized by the following:

  1. It is not limited to the somatic area supplied by a single cranial or cervical nerve.
  2. It is often bilateral.
  3. It is constant rather than occurring in paroxysmal attacks.
  4. External stimuli do not precipitate attacks.
  5. It is deep rather than superficial.
  6. The patient has a tendency for drug (or doctor) addiction.
  7. The patient suffers from depression or has a neurotic personality.46

Eye discomfort may be simply an indication of local ocular disease, running the gamut from the chronic irritation of relative tear deficiency or the acute foreign body sensation of corneal abrasion to the throbbing ache and photophobia of iritis or the nauseating agony of acute angle-closure glaucoma. Despite the common occurrence of these ocular disorders in the general population, other occult sources of “ocular pain” must be sought beyond the globe and adnexa.

Migraine may consist of several hours of throbbing hemicranial and retroorbital pain. This pain differs in degree from that of cluster headaches. The latter assail the patient with briefer but agonizing bouts of unilateral periocular pain accompanied by lacrimation and ipsilateral sympathetic paresis. Historical details such as a positive family history, “triggering” foodstuffs, a clocklike regularity of attacks, and visual scintillations lend credence to the diagnosis of vascular headache.

Physicians rarely encounter a disorder more distinctive than trigeminal neuralgia, with its lancinating pain affecting the mandibular, maxillary, or ophthalmic divisions (in decreasing order of frequency). During the crescendo agony, Wilson47 observed that the patient's face is “often screwed up, voluntarily or half-consciously, or becomes the seat of flickers or twitches (tic douloureux)…. As the paroxysm dies down it may leave behind it a nerve ‘on edge' which seems loath to cease its troubling.” Speaking, eating, or even the contact of a washcloth or breeze on the face may trigger a terrible spasm of facial pain. In addition to the demyelinative lesions or vascular compression that underlies some cases of tic douloureux, the trigeminal nerve is also prey to the neurotropism of herpes zoster. A complaint of steady, burning pain in a unilateral facial segment usually accompanies the appearance of herpetic vesicles emblazoning the cutaneous distribution of the affected trigeminal division. The further torturous course of postherpetic neuralgia, long after resolution of the cutaneous eruptions, is a common additional affliction.

Diplopia accompanied by pain should prompt a meticulous review of other symptoms, an assessment of nonocular cranial nerves, and a medical/surgical history. For example, the pain of self-limited ischemic oculomotor palsy can mimic an intracranial aneurysm, and diagnostic priorities may be assigned according to age-related general medical status (e.g., hypertension, diabetes), absence of meningismus, and typical pupillary findings.48 Other “painful ophthalmoplegias” may involve one of the ocular motor, trigeminal, or sympathetic nerves (or combinations of these nerves) and indicate a locus in the continuum of anterior orbit, posterior orbit (apex), superior orbital fissure, and cavernous sinus. However, the steady, boring eye pain associated with these lesions is insufficiently distinctive to accurately predict a neoplastic, aneurysmal, or inflammatory source.

Lastly, pain may herald a precise cause of visual loss, as is well known to the physician who confidently begins steroid therapy when confronted by an elderly individual with severe monocular visual loss, head and neck pain, and tenderness of the scalp and temporal arteries, and then commences the workup of giant-cell arteritis. The severe pain accompanying visual loss in angle-closure glaucoma and the eye movement that induces orbital ache of optic neuritis are specific admonitions against a nonsensical diagnosis of “painful amaurosis fugax” or the vagaries of “brain tumor.”

The linchpin of accurate diagnosis remains a detailed account of neuro-ophthalmologic disease as seen through the patient's eyes. Each individual's interpretation of visual experience is unique. As Carlyle49 observed, “To Newton and to Newton's dog Diamond, what a different pair of universes; while the painting on the optical retina of both was, most likely, the same!” The clinician in general and the neuro-ophthalmologist in particular must listen carefully to the patient's visual experiences so that they can proceed with effective diagnosis.

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1. Holmes G: Introduction to Clinical Neurology. Edinburgh: E&S Livingston, 1946

2. Traquair HM: An Introduction to Clinical Perimetry. London: Henry Kimpton, 1949

3. James W: The Principles of Psychlogy. Mineola, NY, Dover, 1950

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8. Rosner M, Belkin M: Video display units and visual function. Surv Ophthalmol 33:515, 1989

9. Fuhr PS, Hershner TA, Daum KM: Ganzfeld blankout occurs in bowl perimetry and is eliminated by translucent occlusion. Arch Ophthalmol 108:983, 1990

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11. Cavender JC: Entoptic imagery and afterimages. In Duane TD, Jaeger EA (eds): Biomedical Foundations of Ophthalmology, Vol 2, Chap 20, pp 1-22. Hagerstown, MD, Harper & Row,1982

12. Serpetopoulos C: Optical explanation of the gradual disappearance of flying dots in posterior vitreous detachment. Surv Ophthalmol 42:92, 1997

13. Oster G: Phosphenes. Sci Am 222:82, 1970

14. Fugii MD, Patten BM: Neurology of microgravity and space travel. Neurol Clin 10:999, 1992

15. Moore RF: Subjective “lightning streaks.”rdquo; Br J Ophthalmol 31:46, 1947

16. Meredith TA: Sensory experiences with posterior vitreous detachment. Am J Ophthalmol 121:687, 1996

17. Helmholtz H: Handbuch der Physiologischen Optik. Hamburg and Leipzig, Voss, 1910

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20. Barletta JP, Fanous MM, Hamed LM: Temporary blindness in TUR syndrome. J Clin Neurol Ophthalmol 14:6, 1994

21. Purvin VA: Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol 113:482, 1995

22. Horton JC, Fishman RA: Neurovisual findings in the syndrome of spontaneous intracranial hypotension from dural cerebrospinal fluid leak. Ophthalmology 101:244, 1994

23. Taylor I, Scheffer IE, Berkovic SF: Occipital epilepsies: Identification of specific and newly recognized syndromes. Brain 126:753, 2003

24. Lantos G: Cortical blindness due to osmotic disruption of the blood-brain barrier by angiographic contrast material: CT and MRI studies. Neurology 39:567, 1989

25. Horton JC, Trobe JD: Akinetopsia from nefazodone toxicity. Am J Ophthalmol 128:530, 1999

26. Goodwin JA, Gorelick P, Helgason C: Symptoms of amaurosis fugax in atherosclerotic carotid artery disease. Neurology 37:829, 1987

27. Hupp SL, Kline LB, Corbett JJ: Visual disturbances of migraine. Surv Ophthalmol 33:221, 1989

28. Trobe JD: Photophobia in anterior visual pathway disease. J Neuro-Ophthalmol 22:1, 2002

29. Ravits J, Seybold M: Transient monocular visual loss from narrow-angle glaucoma. Arch Neurol 41:991, 1984

30. Lepore FE: The origin of pain in optic neuritis. Determinants of pain in 101 eyes with optic neuritis. Arch Neurol 48:748, 1991

31. Knox DL, Cogan DG: Eye pain and homonymous hemianopsia. Am J Ophthalmol 54:1091, 1962

32. Sadun AA, Currie JN, Lessell S: Transient visual obscurations with elevated optic disks. Ann Neurol 16:489, 1984

33. Kampf D, Piper HF, Neundorfer B, et al: Palinopsia (visual perseveration) and cerebral polyopia: Clinical analysis and computed tomographic findings. Fortschr Neurol Psychiatr 51:270, 1983

34. Mishkin M, Ungerleider LG, Macko KA: Object vision and spatial vision: Two cortical pathways. Trends Neurosci 6:414, 1983

35. Cogan DG: Visual hallucinations as release phenomena. Graefes Arch Clin Exp Ophthalmol 188:139, 1973

36. Wilkinson IMS, Kime R: Alcohol and human eye movement. Trans Am Neurol Assoc 99:38, 1974

37. Trevor-Roper PD: The Eye and Its Disorders. Boston, Little, Brown, 1974

38. Lepore FE, Yarian DL: Monocular diplopia of retinal origin. J Clin Neuroophthalmol 6:181, 1986

39. Griffin JF, Wray SH, Anderson DP: Misdiagnosis of spasm of the near reflex. Neurology 26:1018, 1976

40. Bartleson JD, Trautman JC, Sundt TM: Minimal oculomotor nerve paresis secondary to unruptured intracranial aneurysm. Arch Neurol 43:1015, 1986

41. Krohel GB, Rosenberg PN: Oscillopsia associated with eyelid myokymia. Am J Ophthalmol 102:662, 1986

42. Wertenbaker C, Gutman I: Unusual visual symptoms. Surv Ophthalmol 29:297, 1985

43. Kinnear PE, Jay B, Witkow CJ: Albinism. Surv Ophthalmol 30:75, 1985

44. Sherrington C: The Integrative Action of the Nervous System. New Haven, CT, Yale University Press, 1947

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48. Jacobson DM: Pupil involvement in patients with diabetes-associated oculomotor nerve palsy. Arch Ophthalmol 116:723, 1998

49. Carlyle T: The French Revolution, New York, AL Burt, 19255

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