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Neuro-ophthalmology

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Abstract

This chapter considers disorders of vision, pupillary size, position and movement of the eyelids and globe, and lacrimation. The anatomical and physiological importance of these functions is presented alongside the principles and methods involved in their clinical assessment. This is followed by a discussion of the diseases and syndromes in which these manifestations occur.

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Figures

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19.1 Dorsal and sagittal views of the neuroanatomical pathway for conscious vision. The visual stimulus (here the left visual field is arrowed) is initiated in the retina of both eyes (1) and travels through the optic nerve (2) and optic chiasm (3) – where the majority of the fibres (65–75%) cross over – and continues along the optic tract (4). The stimulus is relayed from here to the lateral geniculate nucleus of the thalamus (5), then travels through the optic radiations (6), synapsing in the occipital cortex (7). A lesion in any part of this pathway can affect conscious vision. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.2 Dorsal and sagittal views of the neuroanatomical pathway for the menace response. The menacing stimulus is detected by the retina (1) and a resulting impulse travels through the optic nerve (2) and optic chiasm (3) to the contralateral optic tract. The stimulus is then relayed to the lateral geniculate nucleus of the thalamus (4), travels through the optic radiation and synapses in the occipital cortex (5). The signal then travels rostrally in association with interneurons and synapses in the motor cortex (6) and continues within projection fibres through the internal capsule, crus cerebri and longitudinal fibres of the pons and synapses in the pontine nucleus (7). The signal then proceeds within the transverse fibres of the pons, through the middle cerebellar peduncle and synapses in the cerebellar cortex (8). The signal then travels through the efferent cerebellar pathway and synapses on both facial nuclei (9). The signal is finally relayed through the left and right facial nerves (10; only one shown here), synapsing on the facial muscles (orbicularis oculi; 11) to cause muscular contraction and closure of the eyelids. A lesion in any part of the pathway can disrupt this response. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.3 Visual placing response in a cat. On approaching the surface of the table, the cat will reach out to support itself before the paw touches the table.
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19.4 Sagittal view of the neuroanatomical pathway for sympathetic innervation to the eye. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.5 Dorsal and sagittal views of the neuroanatomical pathway for the PLR. A bright light stimulus enters the retina and initiates an impulse (1) that travels through the optic nerve (2), optic chiasm (3) and optic tract (4). The stimulus is relayed to the pretectal nucleus within the rostral colliculus (6). The parasympathetic nucleus of the oculomotor nerve (7) is stimulated and the signal is transmitted through its parasympathetic branch (5), resulting in contraction of the iris sphincter muscle and constriction of the pupil. A lesion in any part of the pathway can disrupt the PLR. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.6 Dorsal and sagittal views of the proposed neuroanatomical pathway for the dazzle reflex. This reflex is similar to the PLR but differs in that the efferent pathway is mediated by the oculomotor nerve in the PLR pathway, whereas it is the facial nerve that carries the efferent information for the dazzle reflex. A very bright light stimulus enters the retina (1) and travels through the optic nerve (2), optic chiasm (3) and optic tract (4). The stimulus is relayed to the pretectal nucleus within the rostral colliculus (5). From here, the signal is transmitted to the ipsilateral facial nucleus in the brainstem (6). The facial nerve (7) then carries the efferent stimulus to the orbicularis oculi muscles of the eyelids, resulting in a reflex blink. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.7 Innervation of the extraocular muscles. Note that the retractor bulbi muscle is also innervated by the abducens nerve. (© Jacques Penderis and reproduced from the )
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19.8 The directions of pathological nystagmus. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.9 Peripheral visual pathway (outlined in red). This includes the retina, optic nerve, optic chiasm and the rostral portion of the optic tract. Lesions in the peripheral visual pathway generally affect the PLR. Central visual pathway (outlined in red). This includes the caudal portion of the optic tract, the lateral geniculate nucleus and the occipital cortex. Lesions in the central visual pathway typically spare the PLR. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.11 Approach to a case with unilateral blindness in the left eye, using the PLR and an ophthalmoscopic examination to determine lesion localization. The red shading depicts the possible locations of the lesion along the visual pathways. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.12 Approach to a case with sudden-onset bilateral blindness, using the PLR, an ophthalmic examination and, if indicated, electroretinography to determine lesion localization. The red shading represents possible locations of lesions along the visual pathways. Note that retinal disease may be primary or secondary to, for example, uveitis or glaucoma. ERG = electroretinogram; SARDS = sudden acquired retinal degeneration syndrome. (Redrawn after with permission from the publisher). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.15 Retinal detachment visible through the pupil on direct illumination in a dog. (Courtesy of D Gould)
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19.16 Fundus of a dog with optic neuritis. Note the poor optic nerve head demarcation associated with the peripapillary oedema, the pink discoloration of the optic nerve head caused by inflammation, and the change in direction of the superficial retinal blood vessels as they course over the elevated optic nerve head. (Courtesy of D Gould)
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19.17 Idiopathic left-sided Horner’s syndrome. Note the miosis, ptosis and protrusion of the third eyelid. (Courtesy of D Gould)
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19.18 A stepwise approach to localizing anisocoria based on the response of both pupils to light and darkness. Determining which pupil is abnormal can be achieved by checking the PLR and assessing whether the asymmetry in pupil size increases in bright light (suggesting parasympathetic dysfunction in the larger pupil) or in darkness (suggesting sympathetic dysfunction in the smaller pupil). Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.19 Evaluation of parasympathetic denervation using 0.1% pilocarpine. Rapid constriction of the pupil compared with the normal eye is observed with a postganglionic lesion due to denervation hypersensitivity. With a preganglionic lesion, constriction occurs more slowly, similar to the normal eye (20–30 minutes). A complete absence of pupillary response following administration of 0.1% pilocarpine to the affected eye probably suggests a non-neurological cause (e.g. iris atrophy)
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19.20 Evaluation of sympathetic denervation (Horner’s syndrome) using 1% phenylephrine. With a first order (upper motor neuron) or second order (preganglionic neuron) lesion, dilation occurs slowly or not at all. Rapid dilation of the pupil (within 20 minutes) is observed with a third order (postganglionic neuron) lesion due to denervation hypersensitivity. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.21 Lesion localization, differential diagnoses and diagnostic tests to perform in patients with anisocoria. CSF = cerebrospinal fluid; CT = computed tomography; MRI = magnetic resonance imaging; PLR = pupillary light reflex. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.22 Pupil size following head trauma can progress from normal and reactive to light (top), through miotic and pinpoint (middle) to dilated and unresponsive (bottom) as the pathology progresses. The onset of miosis is related to a brain injury that has caused damage to the sympathetic system responsible for pupil dilatation. As the injury progresses and causes transtentorial herniation, the oculomotor nucleus is affected and results in pupil dilatation. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
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19.23 MR images showing caudal transtentorial herniation (arrowed) in a dog with a brain tumour (arrowed). The miosis is progressing to mydriasis.
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19.25 Post-contrast transverse T1-weighted MR image of a meningioma (arrowed) within the left middle cranial fossa causing cavernous sinus syndrome (middle cranial fossa syndrome) in a dog.
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19.26 D-shaped pupil in a cat due to a lesion affecting the nasal ciliary nerve. (Courtesy of the Animal Health Trust)
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19.27 Dysautonomia in a dog with mydriasis in the left eye, bilateral mild third eyelid protrusion and xeromycteria (dry nose).
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19.28 Medial strabismus in the left eye of a dog with abducens nerve paralysis.
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19.30 Strabismus in a Shar Pei due to fibrosing extraocular muscle myositis. In this case, the condition was unilateral and led to severe esotropia and functional blindness in the right eye. (Courtesy of C Heinrich)
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19.31 Bilateral divergent strabismus in a kitten with congenital hydrocephalus. Affected kitten (left) with a normal littermate for comparison. Side view showing the domed appearance of the head due to the hydrocephalus. Bilateral exotropia is present. Note the bilateral scleral show. (Courtesy of P Oliveira)
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19.32 Transverse T2-weighted MR image of a retrobulbar mass (arrowed) within the left orbit causing lateral strabismus and exophthalmos in the left eye.
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19.33 Dorsal and transverse STIR MR images of a dog with masticatory muscle myositis. Note the areas of diffuse hyperintensity within the temporalis, masseter (arrowed) and pterygoid (arrowhead) muscles.
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19.34 Chronic masticatory muscle myositis.
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19.35 Unilateral right-sided masticatory muscle atrophy secondary to a trigeminal nerve sheath tumour.
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19.36 Post-contrast transverse T1-weighted MR image showing a trigeminal nerve sheath tumour (arrowed), which has caused atrophy of the temporalis (*) and masseter (arrowhead) muscles on the affected side.
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19.38 A dog with left-sided facial paralysis.
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19.39 Transverse T2 FLAIR MR image of left-sided otitis media (arrowed) causing facial nerve paralysis.
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19.40 Deviation of the nose to the left-hand side in a Springer Spaniel with chronic left-sided facial nerve paralysis. Chronicity results in muscle contracture and pulling of the nose to the affected side.
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19.41 Hemifacial spasm affecting the left side of the face in a dog with otitis media.
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19.42 Haw’s syndrome. (Courtesy of C Heinrich)

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