Ординатура / Офтальмология / Английские материалы / Oxford American Handbook of Ophthalmology_Tsai, Denniston, Murray_2011

DIPLOPIA 657

Diplopia

Monocular

Abnormal refraction

•High ametropia, astigmatism, or edge effect from corrective lenses: usually correctable with appropriate refraction. Contact lenses may be more effective than glasses.

Abnormal cornea

•Opacity: associated with scarring (e.g., trauma, infection), edema (e.g., iIOP, decompensation), deposition (e.g., corneal dystrophies).

•Shape: peripheral thinning associated with ectasias (e.g., keratoconus), peripheral ulcerative keratitis, and other marginal disease.

Abnormal lens

•Opacity: cataract.

•Shape: lenticonus.

•Position: subluxation of lens (ectopia lentis) or implant (especially if complicated surgery).

Abnormal iris

•Defect: polycoria due to trauma (e.g., IOFB), peripheral iridotomy (laser or surgical), or disease (e.g., ICE syndrome).

Normal examination

•Not diplopia: “double vision” may be used by the patient to describe other visual anomalies (e.g., ghosting or blurring).

•Functional: this is a diagnosis of exclusion.

Binocular

Intermittent or variable

•Decompensating phoria: intermittent but usually predictable (e.g., when fatigued) with a constant pattern (e.g., only for distance, only horizontal); underlying phoria with variable to poor recovery.

•Myasthenia gravis: intermittent diplopia of variable orientation and severity that worsens with fatigue. It may be associated with ptosis progressive generalized muscular fatigue.

•Internuclear ophthalmoplegia: diplopia may only be noticed during saccades when the adducting eye is slower to refixate.

•Giant cell arteritis: intermittent diplopia may occur due to ischemia; may progress to become permanent.

Persistent

Neurogenic

In neurogenic lesions, the diplopia is worst when looking in the direction of the paretic muscle(s). Saccades are slowed in this direction; full sequelae will evolve with time. Forced duction test shows normal passive movements.

•Horizontal only: typically CN VI palsy lunderaction of LR lipsilateral reduced abduction ± convergent.

658CHAPTER 19 Aids to diagnosis

•Vertical/torsional only: typically, CN IV palsy with underaction of SO with ipsilateral hypertropia, extorsion, and reduced depression in adducted position.

•Mixed ± ptosis/pupillary abnormalities: typically, CN III palsy with underaction of any or all of LPS, SR, MR, IR, IO, and sphincter pupillae, resulting in anything from single-muscle involvement (rare) to complete ptosis obscuring a hypotropic divergent eye.

•Complex: unusual patterns may be due to brainstem lesions causing nuclear or supranuclear gaze palsies (often associated with other neurological signs), orbital pathology, or disorders of the neuromuscular junction (e.g., myasthenia gravis).

Mechanical

In mechanical lesions, the diplopia is worst when looking away from the restricted muscle(s); signs of restriction may include IOP increase, globe retraction, and pain when looking away from the restricted muscle(s). Ductions and versions are equally reduced but saccades are of normal speed. Sequelae are limited to underaction of contralateral synergist. Forced duction test shows restriction of passive movements.

•Congenital: these rarely give rise to diplopia unless progressive or decompensating.

•Acquired: associated with inflammation (e.g., thyroid eye disease, myositis, idiopathic orbital inflammatory disease), trauma (orbital wall/ floor fracture), or infiltration.

ANISOCORIA 659

Anisocoria

Anisocoria greatest in bright light

This implies that the larger pupil is the abnormal one.

Abnormal iris appearance (slit-lamp examination)

Vermiform movements

•Adie’s pupil: pupil is initially dilated, later abnormally constricted. Response to light is poor, response to near is initially poor, later tonic (exaggerated but slow), i.e., there is light-near dissociation. It will constrict with 0.1% pilocarpine because of denervation hypersensitivity.

Structural damage

•Iris trauma: dilated pupil (often irregular) due to a torn sphincter with associated anterior segment damage (e.g., transillumination defects).

•Iris inflammation: dilated pupil (often irregular) due to sectoral iris atrophy (typically with herpes group of viruses) or stuck down by posterior synechiae.

Normal iris appearance

Constricts to pilocarpine 1%

•Third nerve palsy: dilated pupil associated with other features of a CN III palsy (e.g., ptosis, oculomotor abnormality). It will constrict with 1% pilocarpine.

Does not constrict to pilocarpine 1%

•Pharmacological: dilated pupil resulting from anticholiergic mydriatics such as atropine (rather than adrenergics).

•Iris ischemia: dilated pupil occurring after angle-closure glaucoma or intraocular surgery (e.g., Urrets–Zavalia syndrome).

Anisocoria greatest in dim light

This implies that the smaller pupil is the abnormal one.

Abnormal iris appearance (slit-lamp examination)

Structural damage

•Iris inflammation: constricted pupil (may be irregular) stuck down by posterior synechiae.

Normal iris appearance

Dilates at normal speed in dim light

Both pupils dilate equally quickly when ambient light is dimmed.

•Physiological anisocoria: anisocoria is usually mild ( 1 mm) and only marginally worse in dim rather than bright light. Responses to light and near are normal. The degree of anisocoria varies from day to day and may reverse; pupil will dilate with 4% cocaine (cf. Horner’s syndrome).

Dilates in dim light but slowly (i.e., dilatation lag)

The smaller pupil is slower to dilate when ambient light is dimmed.

•Horner’s syndrome: constricted pupil, with mild ptosis. Iris hypochromia suggests congenital or very long-standing lesion; confirm with 4% cocaine test (a Horner’s pupil will not dilate).

NYSTAGMUS 661

Nystagmus

Early onset

Horizontal jerk

•Idiopathic congenital: very early onset (usually by 2 months of age); worsens with fixation; improves within null zone and on convergence; mild dVA.

•Manifest latent: fast phase toward fixing eye; worsens with occlusion of nonfixing eye, and with gaze toward fast phase; alternates if opposite eye takes up fixation; often associated with infantile esotropia.

Erratic

•Sensory deprivation: erratic waveform ± roving eye movements; moderate to severe dVA due to ocular or anterior visual pathway disease.

Late onset

Conjugate

Present in primary position

Sustained

•Peripheral vestibular: conjugate horizontal jerk nystagmus, improves with fixation and, with time, since injury; worsens with gaze toward fast phase (Alexander’s law) or change in head position.

•Cerebellar, central vestibular, or brainstem: conjugate jerk nystagmus that does not improve with fixation. It may be horizontal, vertical, or torsional:

•Horizontal type: e.g., lesions of the vestibular nuclei, the cerebellum, or their connections.

•Upbeat type: usually cerebellar or lower brainstem lesions (e.g., demyelination, infarction, tumor, encephalitis, Wernicke’s syndrome).

•Downbeat type: usually craniocervical junction lesions, (e.g., Arnold– Chiari malformation, spinocerebellar degenerations, infarction, tumor, demyelination).

Periodic

•Periodic alternating: conjugate horizontal jerk nystagmus with waxing– waning nystagmus; 90 sec in each direction with a 10 sec null period; usually associated with vestibulocerebellar lesions.

Present only in eccentric gaze

•Gaze evoked nystagmus (GEN): conjugate horizontal jerk nystagmus on eccentric gaze with fast phase toward direction of gaze.

•Asymmetric type: evoked nystagmus usually indicates failure of ipsilateral neural integrator or cerebellar dysfunction.

•Symmetric type: due to CNS depression (e.g., fatigue, alcohol, anticonvulsants, barbiturates) or structural pathology (e.g., brainstem, cerebellum).

OPHTHALMIC SIGNS: EXTERNAL 663

Ophthalmic signs: external

The patient

Consider the whole patient. Simple observation of the patient provides a vast amount of additional information and should be performed in all cases. Observe that the patient with juvenile cataracts and iIOP has severe facial eczema—he/she may not have thought to mention their topical corticosteroids when asked about their medication.

Note the rheumatoid hands of the patient in whom scleritis is suspected. Such information will also help with management (e.g., patient needs assistance with topical medication). Further hands-on systemic examination is directed according to clinical presentation.

Globe

Table 19.1 Ophthalmic signs—the globe

Sign Causes

Proptosis • Infection: orbital cellulitis

•Inflammation: thyroid eye disease, idiopathic orbital inflammatory disease, systemic vasculitis (e.g., Wegener’s granulomatosis)

•Tumors: capillary hemangioma, lymphangioma, optic nerve glioma, myeloid leukemia, histiocytosis, dermoid cyst

•Vascular anomalies: orbital varices, carotid–cavernous fistula

•Pseudoproptosis: ipsilateral large globe or lid retraction; contralateral enophthalmos or ptosis; facial asymmetry

Enophthalmos • Small globe: microphthalmos, nanophthalmos, phthisis bulbi, orbital implant

•Soft tissue atrophy: post-irradiation, scleroderma, cicatrizing tumors

•Bony defects: orbital fractures, congenital orbital wall defects

Lymph nodes

Table 19.2 Ophthalmic signs—lymph nodes

664 CHAPTER 19 Aids to diagnosis

Lids

Table 19.3 Ophthalmic signs—lids

Lid retraction • Congenital: Down syndrome, Duane syndrome

•Acquired: thyroid eye disease, uraemia, CN VII palsy, CN III misdirection, Marcus–Gunn

syndrome, Parinaud’s syndrome, hydrocephalus, sympathomimetics, cicatrization, lid surgery, large or proptotic globe

OPHTHALMIC SIGNS: ANTERIOR SEGMENT (1) 665

Ophthalmic signs: anterior segment (1)

Conjunctiva

Table 19.4 Ophthalmic signs—conjunctiva