Disorders of pupil size and function

Pupil abnormalities, usually evident as alterations in pupil size, in the absence of visual loss may affect one or both pupils (Causes of alterations in pupil size and function that are not usually associated with loss of vision (with the exception of raised intracranial pressure)). Anisocoria results when only one pupil is affected. In this instance, evaluation of the PLRs is necessary in order to determine which pupil is abnormal. Before any neuro-ophthalmology assessment is performed it is essential first to ascertain whether the pupil abnormalities could be explained by non-neurological abnormalities of the iris (including iris atrophy, iris hypoplasia, uveitis and trauma) or globe (including lens luxation and glaucoma). Painful conditions of the cornea and conjunctiva may also cause miosis. Brief oscillations of pupillary size, referred to as hippus, may occur as a normal feature in response to light exposure. Very exaggerated hippus may be an indication of CNS disease, particularly if it occurs in conjunction with other neuro-ophthalmological abnormalities.

Causes of alterations in pupil size and function that are not usually associated with loss of vision (with the exception of raised intracranial pressure).

Condition Miosis or mydriasis Always bilateral?
Topical pharmacological agents Either No
Resting anisocoria Either No
Homer’s syndrome Miosis No
Static anisocoria (spastic pupil) Miosis No
Organophosphate toxicity Miosis Yes
Hemidilated pupil (D-shaped pupil) Mydriasis No
Cavernous sinus syndrome Usually mydriasis (or mid-range non-responsive) No
Pupillotonia Usually mydriasis No
Cerebellar disease Mydriasis No
Raised intracranial pressure progressing to herniation Initial miosis, later mydriasis (see Chapters 8 and 19) Initially may be unilateral, but usually bilateral
Dysautonomia Mydriasis Yes
Thiamine deficiency Mydriasis Yes

Pharmacological miosis and mydriasis

Pharmacological agents, accidentally or intentionally administered, may profoundly affect pupillary function. This includes pupillary dilation following administration of mydriatic (e.g. atropine) and cycloplegic (e.g. tropicamide) drugs and pupillary constriction following administration of miotic drugs (e.g. pilocarpine). Sys-temically administered anaesthetic agents may also have a profound effect on pupillary size, such as the miosis evident following systemic administration of some opioid agents in dogs ().

Resting anisocoria (idiopathic anisocoria)

Subtle resting anisocoria is a common observation, particularly in cats, and is of no clinical significance. The anisocoria is similar to physiological anisocoria seen in up to 20% of the human population () and is thought to be the consequence of an imbalance in basal sympathetic and parasympathetic tone between the two eyes.

Homer’s syndrome

Lesions affecting the sympathetic supply to the head will result in Homer’s syndrome () and loss of cutaneous vascular tone on the affected side with peripheral vasodilation. The loss of cutaneous vascular tone in dogs and cats is evident as increased cutaneous temperature (the pinna on the affected side being warmer than the unaffected side), hyperaemia and anhydrosis (decreased sweating on the affected side of the head). The effects of loss of cutaneous vascular tone on the eye include mild congestion of the scleral blood vessels and decrease in intraocular pressure. Horner’s syndrome describes the specific ophthalmic changes associated with loss of sympathetic innervation; these include:

  • Miosis (constriction of the affected pupil): avulsion of the brachial plexus nerve roots will usually cause only a partial Horner’s syndrome, often with miosis as the only feature. This is usually because only the T1 nerve root of the T1-T3 sympathetic outflow is affected by brachial plexus avulsions. Partial Horner’s syndrome (with miosis as the only feature) may also occur in dogs with acute and severe lateralized cervical spinal cord disease but the expectation would still be for the majority of cases to have a complete Horner’s syndrome ()
  • Enophthalmos: loss of sympathetic innervation leads to loss of orbital smooth muscle tone and sinking of the globe into the orbit
  • Protrusion of the third eyelid (nictitating membrane): while in the dog this occurs passively secondary to enophthalmos, in the cat the protrusion is due to a combination of enophthalmos and loss of third eyelid retraction • Ptosis (drooping) of the upper eyelid and decreased tone of the lower eyelid: this occurs as a result of loss of smooth muscle tone affecting the Muller’s muscle.

Horner’s syndrome is usually classified according to the level of the lesion along the sympathetic pathway () as first order, second order (pre-ganglionic) orthird order (post-ganglionic). Pharmacological testing or evidence of other neurological abnormalities can be used to localize the site of the lesion but the times to a response should only be treated as a guide to the site of the lesion and other neurological signs should be taken into consideration. In the majority of cases with apparent third order Horner’s syndrome (based on pharmacological testing) no underlying cause can be identified and these cases have historically been termed idiopathic Horner’s syndrome (). The prognosis depends to a large degree on the underlying neurological disease but is excellent in idiopathic Horner’s syndrome. The disorder in idiopathic Horner’s syndrome is largely cosmetic and in many cases may resolve spontaneously. Treatment is rarely required but in cases with bilateral Horner’s syndrome () and where vision is obscured by the third eyelid protrusion, topical 10% phenylephrine can be used to provide occasional, short-term alleviation of the symptoms. Maximal effect occurs for up to 2 hours and in some cases the effect may be maintained for up to 18 hours.

Pharmacological testing of Horner’s syndrome: In cases where Horner’s syndrome has been present for some time (usually at least 2 weeks), denervation hypersensitivity resulting from the sympathetic denervation allows prediction of the site of the lesion based on increased sensitivity to topical phenylephrine. The time to pupillary dilation, following administration of 1% phenylephrine topically in both eyes, is determined. Essentially, the shorter the time to pupillary dilation, the closer is the lesion to the iris.

  • • Less than 20 minutes suggests third order Homer’s syndrome.
  • • 20 to 45 minutes suggests second order Homer’s syndrome.
  • • 60 to 90 minutes suggests first order Homer’s syndrome or no sympathetic denervation of the eye.
  • • If 10% phenylephrine is used, mydriasis occurs in 5-8 minutes in post-ganglionic (third order neuron) lesions ().

Static anisocoria (spastic pupil syndrome)

Static anisocoria occurs in cats and is associated with FeLV infection, though it has been suggested to occur in association with other viruses, including FIV. However, few documented cases of static anisocoria or hemidilated pupils are recorded in the literature () and the majority of textbooks referring to the disorder provide largely anecdotal evidence. Cats with static anisocoria demonstrate moderate miosis (occasionally cats may demonstrate mydriasis) and anisocoria. The miosis typically only changes minimally, if at all, during dark adaptation. The clinical signs may be intermittent or change during the course of the disease and are thought to be the result of either viral infection or lymphosarcoma infiltration of the short ciliary nerves or ciliary ganglion. See also Hemidilated pupil (D-shaped pupil) below.

Hemidilated pupil (D-shaped pupil)

Hemidilated pupil is the consequence of vulnerability to paralysis of the ciliary nerves supplying the iris constrictor muscles in cats, in particular to FeLV-associated lymphosarcoma infiltration. Either of the two ciliary nerves, the lateral (malar) ciliary nerve or medial (nasal) short ciliary nerve, may be affected and, depending on which one is affected, this results in either a D-shaped or a reverse D-shaped pupil ().

Organophosphate and carbamate toxicity

Alterations in pupil size are a feature of a variety of toxins, with the most common being the marked miosis associated with organophosphate and carbamate toxicity. Both drugs inhibit cholinesterase and induce a variety of clinical signs, including salivation, gastrointestinal disturbances, muscle twitching, weakness and possibly seizures ().

Cavernous sinus syndrome

The paired cavernous sinuses are situated on the floor of the calvarium and adjacent to the pituitary gland. This area offers a convenient site for expansion of mass lesions (particularly tumours but also inflammatory lesions and vascular malformations) and, as it is the venous drainage from the frontal sinus and nose, there may be an increased likelihood of infectious and neoplastic diseases of these structures spreading to the cavernous sinus area. Neurological deficits develop when these lesions expand to incorporate the adjacent cranial nerves III, IV and VI (innervating the extraocular muscles, iris and ciliary muscle), the first two branches of the trigeminal nerve and the post-ganglionic (third order) sympathetic supply to the eye. It is reported that cavernous sinus syndrome affects the ophthalmic and maxillary branches of the trigeminal nerve () but in practice lesions may expand and involve the mandibular branch of the trigeminal nerve as well.

Mass lesions in this area may therefore result in paralysis of the extraocular muscles (external ophthalmoplegia), loss of iris and ciliary muscle function (mternal ophthalmoplegia), ipsilateral sensory deficits in the ophthalmic and maxillary branches of the trigeminal nerve and, with particularly large lesions, atrophy of the ipsilateral masticatory muscles (innervated by the mandibular branch of the trigeminal nerve) with associated sensory deficits. The potential for involvement of both the parasympathetic (CN III) and sympathetic innervation of the pupil can produce either a fixed mydriatic or a mid-range pupil. Paralysis of the extraocular muscles, the ciliary muscle and the parasympathetic and sympathetic supply to the iris is termed total ophthalmoplegia or panophthalmoplegia. Because the optic nerve is distant from the cavernous sinus, vision is not lost, but the loss of lens accommodation and eyeball movement would impair vision. Computed tomography (CT) or magnetic resonance imaging (MRI) of the brain should be performed in any animal with cavernous sinus syndrome, after retropulsion of the eyeball to ensure that the lesion is not retrobulbar.


Pupillotonia (defined as a pupil that is slow to react to light on both direct and consensual stimulation) has been reported in the dog due to a suspected immune-mediated cause (). This condition has not been reported since and may simply have represented a poor light source, fear or iris atrophy.

Cerebellar disease

Mydriasis of the contralateral pupil is an uncommon feature of the syndrome of clinical signs associated with asymmetrical cerebellar disease (). This may also serve to explain the intermittent mydriasis seen in cats with feline spongiform encephalopathy in addition to the diffuse cerebellar signs and altered behaviour.

Raised intracranial pressure

The oculomotor nerve, as it passes ventral to the brain and over the petroclinoid ligament, is vulnerable to compression as a result of dramatic increases in intracranial pressure (ICP) due to neoplastic, traumatic and inflammatory CNS lesions. Initial irritation of the oculomotor nerve as a result of raised intracranial pressure is evident as a miotic pupil, but this rapidly progresses to complete paralysis with a fixed dilated pupil with continuing elevation of intracranial pressure and herniation of the cortex under the tentorium. Such animals are usually comatose. Extensive lesions that affect the sympathetic innervation as well as the oculomotor nerve result in mid-position fixed pupils. See Chapters 8 and 19 for further information on the pathophysiology, assessment and treatment of raised ICP.


Bilateral pupillary dilation that is not responsive to light, protrusion of the third eyelids and decreased tear production, in the presence of normal vision, are features of canine and feline dysautonomia (also called Key-Gaskell syndrome in cats) (). The ocular changes are also associated with profound systemic signs of autonomic dysfunction (and, in particular, depression, anorexia, decreased saliva production, megaoesophagus, bradycardia and occasionally faecal and urinary incontinence). The canine and feline syndromes are both rare and occur sporadically. The treatment is purely supportive and the prognosis is guarded (). Pharmacological testing may be useful to confirm sympathetic and parasympathetic dysfunction.

Thiamine (vitamin B1) deficiency

Bilateral pupillary dilation with the occasional presence of non-specific fundus changes, including peripapillary oedema and papillary neovascularization, are evident in thiamine (vitamin B1) deficiency in cats. The ocular changes occur in conjunction with systemic changes of anorexia, ataxia and cervical ventroflexion. The prognosis is good with thiamine supplementation ().

Incoming search terms:

  • miosis dog neuro