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Neuro-ophthalmic History



Introduction

Ophthalmology is a specialty in which diagnoses are most often made by using

visual clues. Ophthalmology residents are typically trained to concentrate on their

observational skills and to spend relatively less time obtaining the detailed

histories that are characteristic of other medical specialties.

In contrast, thorough history taking is the cornerstone of diagnosis in neuro-

ophthalmology. Without conversation with the patient, many details about the

patient's condition would be missed.

The neuro-ophthalmic history is not isolated from the rest of the patient's history

or physical examination. While conversing with the patient, note the following:

gait, visage, eyes, ocular adnexa, hands, clothing, and mannerisms.

Findings on physical examination often direct further questions. After one obtains

the patient's history and physical findings, the neuro-ophthalmic diagnosis is

usually apparent.



Identifying Data and Chief Complaint

Identifying data



Document the patient's age, sex, race, and occupation in the first sentence of the

chief complaint.

Chief complaint

When possible, document the chief complaint in the patient's own words. The

patient's conception of the problem may differ markedly from the referring

physician's diagnosis. Patients commonly are referred for a specific neuro-

ophthalmic problem, yet they may be unable to relate this to the physician.

Note the duration of the patient's symptoms and the lateralization or binocularity

of visual deficits.









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History of Present Illness

Document the onset, quality, severity, lateralization, temporal characteristics, and

associated features of the patient's visual symptoms. If the patient is unreliable,

family members, his or her medication list and past neuroimages, and results of

gestalt examination can guide the inquiry into the history of the present illness. In

patients who seem cognitively intact but do not or cannot provide details of their

visual problem, suspect functional visual loss. When questioned, patients with

functional visual loss often repeatedly state, "I don't know."

Unexplained visual loss is one of the most common reasons for neuro-

ophthalmic consultation.







Vital diagnostic elements.

Lateralization, location, duration, tempo, and presence or absence of pain

Determine if the patient's visual loss is monocular or bilateral by if they occlude 1

eye or the other. Patients frequently mistake homonymous visual loss as a deficit

confined to the eye that is ipsilateral to the field loss. Confirm that the patient

does not have a right homonymous hemianopsia.

If the visual loss is monocular, ascertain if horizontal respect to the visual loss is

present. If the visual loss is bilateral, exclude a homonymous or heteronymous

defect.

Document if the perceived vision loss is at distance fixation, near fixation, or

both. Patients often present to the neuro-ophthalmologist's office with complaints

of presbyopia.

Degree of recovery

The degree of recovery and the time until recovery after visual loss are other

important elements. Transient visual obscurations that last for seconds may be

due to increased intracranial pressure. Dry eyes can also cause transient visual

phenomena.

Painless unilateral visual loss that lasts several minutes may be embolic

(amaurosis fugax), especially if it respects the horizontal midline. Gaze-evoked

amaurosis may be due to a meningioma of the optic nerve sheath or another

tumor of the orbital apex.





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Transient visual loss with scintillations, , and movement that lasts 20-30 minutes

and then completely resolves suggests migraine. Migraine is a diagnosis of

exclusion, but it is the most common cause of transient visual loss in young

patients. Transient visual obscurations last only seconds. Amaurosis fugax

usually lasts seconds to minutes at the most.

Sudden-onset visual loss with little recovery suggests an ischemic event.

Subacute visual loss with almost complete recovery of vision after several weeks

or months is characteristic of optic neuritis. Slowly progressive visual loss may

be due to a compressive optic neuropathy. Painful visual loss may indicate optic

neuritis. Visual loss with headache in an elderly patient may be due to giant cell

arteritis.

.

Reading-related visual loss in older patients

When older patients complain of visual loss when reading, presbyopia is not

always the cause. Determine if the patient has difficulty seeing whole words,

finding the next line (possible left homonymous field loss), or reading the next

word (possible right homonymous field loss).

Diplopia

Diplopia is a common neuro-ophthalmic complaint. Document the following

features: monocular or binocular nature, , frequency of the diplopia, activities that

enhance the diplopia, and associated ptosis or known dysthyroidism.

Double vision that persists despite closing either eye but improves with pinhole

suggests the following: (1) monocular diplopia from uncorrected refractive error,

(2) optical aberrations of the ocular media, or (3) on occasion, retinal disorders

that distort the fovea.

Monocular diplopia that improves with blinking often is due to the irregular

astigmatism from dry eyes. Monocular diplopia that does not resolve despite

pinhole may be due to palinopsia (perseverance of visual images) from an

evolving cerebral lesion, often in the nondominant hemisphere.

Binocular diplopia with vertical or diagonal separation of objects, worse when the

patient is reading or climbing stairs and better with head tilt to 1 side, suggests

palsy of cranial nerve (CN) IV.

Binocular diplopia with horizontal separation that is worse in the distance

suggests CN VI palsy.



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Patients who develop complete CN III palsy may initially complain of diplopia.

They later indicate that the diplopia resolves, because ptosis occludes the visual

axis.

Variability or worsening of the diplopia as the day progresses with associated

ptosis suggests myasthenia gravis.







Periocular pain and headache

When patients present to the neuro-ophthalmologist, they frequently complain of

periocular pain or headache.

Always consider giant cell arteritis in older patients who present with headache,

scalp tenderness, or occipital tenderness.

Burning discomfort in a unilateral segment of the trigeminal nerve distribution

occasionally precedes the appearance of herpetic vesicles; at times, early

herpes zoster can be mistaken for temporal arteritis.

Migraine headaches, which often consist of several hours of throbbing

hemicranial and retro-orbital discomfort, are common. Migraine may be

accompanied by visual scintillations and fortification spectra, which resolve over

15-30 minutes. A family history of migraine is common, and trigger factors, such

as certain foods, may be noted.

Eye pain has several differential diagnoses. The number of patients with

keratitsicca who are referred for neuro-ophthalmic opinion is surprising. Dry eye

is the likely diagnosis in patients who complain of sandy eyes or sharp eye pain

that is worse in the evening than at other times.



Functional Inquiry

Headache may be associated with neuro-ophthalmic problems, such as

increased intracranial pressure, giant cell arteritis, migraine, and other neuro-

ophthalmic entities. Headaches associated with increased intracranial-pressure

are often associated with nausea and vomiting and usually worse in the morning,

in the supine position, or during a Valsalva maneuver than in other conditions.

Ophthalmologists must maintain a high index of suspicion for giant cell arteritis in

all elderly patients. In addition to headache, scalp tenderness, vision loss, or

diplopia, inquire about symptoms of polymyalgia rheumatica, jaw claudication

(pain with mastication that resolves with rest but returns after a period of

chewing), chills or fevers, weight loss, and malaise. Tongue claudication is a

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variant of jaw claudication. Erythrocyte sedimentation rate (ESR) results may be

normal in about 10% of patients..

Diabetes mellitus and hypertension are common diseases in patients with neuro-

ophthalmic problems. Be aware that many patients do not consider that they

have diabetes if their condition is controlled with diet or oral hypoglycemics.

Likewise, some patients with hypertension consider themselves cured, denying

that they have high blood pressure because they take antihypertensives.

Dysthyroidism is a common disorder that can cause neuro-ophthalmic problems,

such as proptosis, diplopia, or vision loss. Subtle cases of thyroid-related

ophthalmopathy and confirmatory symptoms of systemic dysthyroidism may be

overlooked unless patients are carefully examined for lid retraction.

A history of psychiatric problems ma yincrease the index of suspicion for

functional visual loss. However, the clinician must be wary to exclude an

accompanying component of organic disease in patients with such findings.







Medications and Allergies

Medications

Systemic or topical steroids may predispose patients to glaucomatous cupping of

the optic nerve.

Tetracycline, vitamin A, and other medications have been linked to pseudotumor

cerebri. The antituberculosis agents ethambutol, rifampin, and isoniazid can

cause a toxic optic neuropathy. Amiodarone-induced optic neuropathy has been

reported. Chronic hydroxychloroquine use may result in maculopathy. other

drugs have. Digoxin, even at therapeutic levels, may cause visual disturbances,

typically xanthopsia.

Allergies

Contrary Sulfonamide allergy may preclude the use of acetazolamide (Diamox)

in patients with pseudotumor cerebri.



Medical History

For patients who cannot remember their medical history, document the following

features: past surgery, hospital admissions, previous medications, reasons for

seeing a physician, results of past neuroimaging studies or blood tests, and



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trauma (eg, motor vehicle accidents). Whenever feasible, personally review the

patient's CT scans or MRIs.









Family History and Social History

Family history

The patients' family history helps delineate optic neuropathies.

A family history of glaucoma is helpful in patients with cupping of the optic nerve

that is not disproportionate to pallor. Likewise, a family history of multiple

sclerosis is a risk factor for optic neuritis.

Patients with dominant optic atrophy may have a supportive family history.

Blindness in a patient's brother or maternal uncles may indicate Leber hereditary

optic neuropathy





Social history

The social history is important, as it reveals the patient’s social situation, as well

as details of the disease.

. The patient's occupation may determine his or her work restrictions and ability

to continue work, as well as the need for vocational rehabilitation. Visual

dysfunction may have grave implications for patients who have jobs that involve

commercial driving, working at heights, or discharging firearms.

. A history of alcoholism raises the possibilities of nutritional amblyopia and

Wernicke alcoholic ophthalmoplegia.









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