The cat is a successful predator with excellent special sense; the sense of smell is not as well-developed as that of dogs, but hearing is acute and tactile virbrissae allow the cat to manoeuvre with confidence under conditions of darkness. Cats are very hesitant in the dark if they lack tactile vibrissae and their presence helps to explain the uncanny abilities of cats to cope with severe disability and blindness.
The cat has an arrhythmic eye, which permits activity in a range of lighting conditions, but is particularly effective under conditions of low illumination because of a combination of optics, the presence of a tapetum cellulosum and a rod-dominated retina. Both a rod and cone electroretinogram can be demonstrated in the cat, green and blue absorbing photoreceptors are present and colour vision is somewhat rudimentary. The eyes are frontally placed and some 30% of retinal nerve fibres remain uncrossed - a prerequisite for binocular vision, stereopsis and conjugate eye movement.
The cat with ocular disease
A complete neurological examination is an essential, but challenging, part of the investigation of any cat with suspected neuro-ophthalmological disease. The aims of the neurological examination (the full neurological examination is detailed by Professor de Lahunta) are:
- Confirmation of neurological abnormalities: objective information is obtained to confirm or rule out the presence of neurological disease
- Localization of neurological disease: a single, focal site of disease within the central or peripheral nervous system should be sought that could account for the neurological abnormalities detected. If this is not possible, then a multifocal or diffuse disease may be present
- An assessment of the severity of the disease: based partly on historical features, and partly on the neurological examination. Because cats adapt well to gradual visual loss, the history may be crucial, particularly the owner's observations in relation to the cat in familiar and unfamiliar environments
- Differential diagnoses: the findings of the neurological examination, together with the ophthalmic examination, history and background details will allow appropriate differential diagnoses to be considered, and therefore facilitate a rational approach to the subsequent diagnostic investigations.
The value of repeat neurological examinations ( a few hours, or a day later) to demonstrate whether findings are genuine or artifactual should not be underestimated. This is particularly helpful when the initial findings suggest the presence of mild neurological deficits.
Observation of the cat (even if just for a few minutes) is important prior to commencement of the neurological examination to assess mental status, posture and gait. A full neurological examination incorporates careful assessment of cranial nerves, postural reactions, spinal reflexes and nociception. Aspects of the neurological examination relating specifically to ocular disease (cranial nerve examination and visual placing reactions) are outlined below, followed by some examples of neurological diseases with ocular manifestations.
Cranial nerve assessment
- Cranial nerve II (Optic)
- Cranial nerve III (Oculomotor)
- Cranial nerve IV (Trochlear) and VI (Abducens)
- Cranial nerve V (Trigeminal)
- Cranial nerve VII (Facial)
- Cranial nerve VIII (Vestibulocochlear)
Postural reactions include wheelbarrowing, the extensor postural thrust, hemi-standing and hemi-walking, hopping, proprioception and placing responses. The visual placing response is the only one of these that specifically includes an assessment of vision.
Light reflex pathway
Pupil size is controlled by the iris sphincter muscle (under cholinergic parsympathetic control) and the iris dilator muscle (under adrenergic sympathetic control, see below) and the balance between the two systems is in a constant state of flux. The light reflex, also known as the pupillary light response (PLR), originates in the retina following stimulation of receptors (probably the photoreceptors) by bright light and the afferent pathway begins in the ganglion cell layer. A proportion of the second-order neurones in the optic nerve carrying impulses derived from stimulation of receptor cells are pupillomotor fibres, which exit the optic tract to enter the midbrain where they synapse with third order neurones in the pretectal nucleus, which in turn synapse with the parasympathetic component of the oculomotor nucleus (known as the Edinger-Westphal nucleus in man). There is extensive crossover of both second-order neurones at the optic chiasm, and third-order neurones at the caudal commissure (between the pretectal and oculomotor nuclei) allowing a bilateral pupillary response to stimulation of light. Efferent parasympathetic fibres from the oculomotor nucleus are contained in the oculomotor nerve (CN III), they enter through the orbital fissure to synapse at the ciliary ganglion to the optic nerve, with post-ganglionic fibres passing in two short ciliary nerves (nasal or medial and malar or lateral) to innervate the iris musculature.
Sympathetic innervation to the iris originates in the hypothalamus. Upper motor neurones synapse with lower motor neurones at the T1-T3 level of the spinal cord, and their axons exit and travel in the thoracic and vago-sympathetic trunk to synapse in the cranial cervical ganglion close to the tympannic bulla. Postganglionic fibres pass through the middle ear and join the ophthalmic branch of the trigeminal nerve (CN V) ti innervate the iris dilator muscle and the smooth muscle of the periorbital muscles and eyelid.
Assessment of pupillary response
Pupillary assessment under a range of lighting conditions is a standard feature of neuro-ophthalmological examination. The shape, size and position of the pupils under normal conditions of illumination are examined first, then the examination is repeated with lights dimmed - a technique which helps in the differentiation of sympathetic and parasympathetic defects. In bright light, miosis caused by sympathetic dysfunction may be difficult to detect because of dominance of the parasympathetic system. In dim light, however, such a defect is obvious as the anisocoria becomes more marked, with the smaller pupil being on the affected side. Conversely, the mydriasis found in parasympathetic paralysis (e.g. traumatic damage to the ciliary ganglion), may be obvious in bright light, but difficult to detect in dim light.
The direct (ipsilateral) and consensual (indirect or contralateral) response to bright light is assessed next and this test is best performed in conditions of near darkness. Partial decussation of the optic nerve fibres at the optic chiasm and caudal commissures of the midbrain ensures that the normal pupil response to a bright light directed into one eye will be more intense miosis in the stimulated eye (dynamic contraction anisocoria), If the light is swung to stimulate the other eye then the pupil of this eye will, in turn, become more miotic and if the light is swung from one eye to the other, the miosis will alternate (alternating contraction anisocoria). This is the basis of the swinging flashlight test which can be used to detect the presence of a relative afferent pupillary defect (Marcus Gunn phenomenon). With a prechiasmal lesion, for example, when the light is swung to stimulate the other eye, the miotic pupil of this eye suddenly dilates while receiving direct illumination (a positive swinging flashlight test).
Pupil abnormalities with normal vision
- Pharmacological mydriasis and miosis
- Idiopathic anisocoria
- Unilateral miosis - Horner's syndrome
- Unilateral mydriasis
- Static anisocoria (Spastic pupil syndrome)
- Hemidilated pupil (partial internal ophthalmoplegia, 'D-shaped' pupil)
- Hepatic encephalopathy
- Feline spongiform encephalopathy (FSE)
- Thiamine deficiency
- Cavernous sinus syndrome
- Organophosphate poisoning
Pupil abnormalities with visual deficits
- Barnett, KC & Crispin, SM (2002) Feline ophthalmology: An atlas & text. WB Saunders, London