Recognition of Common Cranial Nerve Abnormalities in Dogs & Cats
ACVIM 2008
Jacques Penderis, BVSc, MVM, PhD, CVR, DECVN, MRCVS
Glasgow, UK, USA

Introduction

In contrast to the majority of neurological problems, the majority of the common cranial nerve disorders encountered in dogs and cats can readily be assessed and managed in the consulting room. Initial assessment of these conditions is both quick and simple, and in most cases does not require expensive or specialised equipment. Although not a cranial nerve as such, lesions affecting the eye's sympathetic supply (resulting in Horner's syndrome) are commonly encountered and will be discussed as part of the cranial nerves.

Figure 1.
Figure 1.

Schematic representation of the anatomical grouping and major functions of the cranial nerves.
 

I. Olfactory Nerve

This cranial nerve is difficult to evaluate and is only rarely evaluated in a clinical setting.

II. Optic Nerve

The optic nerve supplies:

 Vision: The optic nerve supplies sensory information for conscious perception of vision as well as for unconscious reflex pathways, including the papillary light reflex (PLR) and the dazzle reflex.

Clinical Signs

 Blindness and possible abnormalities of the pupillary light reflex.

Assessment

Vision should first be assessed in a 'hands-off' manner by observing the animal interacting with and negotiating a strange environment (usually the consulting room), navigate an obstacle course and by performing the tracking response (following moving, but silent, objects like a dropped piece of cotton wool.

The 'hands-on' assessment of vision includes the visual placing response, menace response, pupillary light reflex (PLR) and dazzle reflex.

Common Disorders

Based on the assessment of blindness by the menace response and the PLR, disorders of vision can be subdivided anatomically into:

 Decreased vision with PLR deficits (lesions of the: retina, optic disc, optic nerve, optic chiasm or optic tract), and

 Decreased vision with no PLR deficits (central visual pathway lesions: from the lateral geniculate nucleus to visual cortex).

III. Oculomotor Nerve, IV. Trochlear Nerve and VI. Abducent Nerve

These nerves supply:

 Motor: Extraocular muscles.

 Parasympathetic: Pupillary constrictor (oculomotor nerve).

Clinical Signs

 Dilated pupil.

 Abnormal eye position or paralysis of the extraocular muscles.

Assessment

 Pupillary light reflex.

 Evaluate for spontaneous nystagmus, strabismus, positional nystagmus and pupillary symmetry (also evaluates CN IV, VI and VIII).

 Assess normal vestibular eye movements (physiological nystagmus; also evaluates CN IV, VI and VIII).

IV. Trigeminal Nerve

The trigeminal nerve supplies:

 Sensory function to the face (via the ophthalmic, maxillary and mandibular branches).

 Motor function to the muscles of mastication.

Clinical Signs

Lesions may result in partial or complete sensory deficits, motor deficits or a combination of both ipsilateral to the lesion. When evaluating sensory lesions it may be difficult on first appearances to distinguish them from facial nerve lesions (CN VII)--where sensation is intact but due to motor paralysis the animal cannot respond appropriately (e.g., blink on stimulation of the medial canthus of the eye). However in facial nerve paralysis the animal should respond consciously to vigorous stimulation, e.g., by averting the head, demonstrating that sensory function (trigeminal nerve) is intact.

 Loss of facial and nasal sensation ipsilateral to the lesion.

 Ipsilateral neurogenic eye ulcers if the ophthalmic branch is damaged.

 Unilateral motor lesions: ipsilateral atrophy of the masticatory muscles.

 Bilateral motor lesions: dropped jaw (usually acute as a result of trauma or neuritis) followed by bilateral masticatory muscle atrophy a week later.

Assessment

 Assess jaw tone.

 Test skin sensation by tickling inside ear and nostril, pinch the lip fold and elicit a blink by tapping on the medial canthus or the cornea of the eye.

Common Causes

Trigeminal nerve lesions are less common than facial lesions but present with characteristic clinical signs and are therefore easy to identify. The two most common causes include:

 Mandibular paralysis (dropped jaw).

 Neoplastic and inflammatory lesions: usually causing unilateral and severe muscle atrophy (in this case particularly neoplasia affecting the peripheral portion) or sensory deficits.

V. Facial Nerve

The facial nerve supplies:

 Motor function to the muscles of facial expression.

 Parasympathetic function to the lachrymal gland and nasal secretory glands (less commonly affected).

 Some taste sensation and some sensation to the inner surface of the pinna.

Clinical Signs (In Partial Lesions, Only Some of the Clinical Signs May be Present)

 Ipsilateral facial paresis or paralysis.

 Decreased or loss of the blink on the affected side.

 Drooping of the lip on the affected side. This is often the feature that the owners notice due to the tendency for the dog to dribble saliva and drop food from the affected side, especially during the first days to weeks.

 Drooping of the ear on the affected side--more noticeable in dogs with erect ears.

 If parasympathetic function is affected a dry eye and dry nose (versus immune mediated keratoconjunctivitis sicca where only a dry eye is present) may be noticed on the affected side.

Assessment

 Look for drooping lip or ear with drooling saliva from affected side of mouth, inability to blink, deviation of the face to the unaffected side (in chronic stage this changes to the affected side) and/or dry eye and nose in combination.

Common Causes

The two most common causes of facial nerve paralysis in dogs and cats include idiopathic facial nerve paralysis and secondary to otitis media / interna. Other causes of facial nerve paralysis are less common and varied and facial nerve paralysis has been suggested as a component of hypothyroidism. Facial nerve paralysis may also occur secondary to trauma, especially iatrogenic following ear surgery. Brain stem lesions causing nerve paralysis are usually associated with central vestibular signs (see VIII--Vestibulocochlear Nerve) or other signs of brain stem disease. Furthermore the facial nerve may be affected by some polyneuropathies (including polyradiculoneuritis--where it is associated with profound generalised weakness--and an idiopathic cranial polyneuropathy complex) as well as disorders of the neuromuscular junction (including botulism and myasthenia gravis--where the blink reflex can be exhausted).

VI. Vestibulocochlear Nerve

The vestibulocochlear nerve supplies:

 Vestibular function.

 Hearing.

Clinical Signs of Vestibular Disease

Either only one or some of the clinical signs may be present, or in more severe or acute cases all the clinical signs may be present. Clinical signs evident with vestibular disease include: head tilt, nystagmus, strabismus, ataxia, circling or rolling, truncal deviation.

In cases with bilateral vestibular disease, instead of a head tilt, affected cases may demonstrate a side to side head sway, abnormal or absent vestibular eye movements may be evident and a ventrolateral strabismus may be present in both eyes (in contrast to just on the affected side in unilateral strabismus).

Differentiation of Central vs. Peripheral Vestibular Disease

Peripheral disease is by far the most common cause of vestibular dysfunction, and in the absence of any clinical signs to suggest the presence of central vestibular disease, the investigation should initially concentrate on causes of peripheral vestibular disease. The finding of postural deficits (in particular conscious proprioceptive deficits or hypermetria), vertical or positional nystagmus or other cranial nerve deficits (besides CN VII) is suggestive of central vestibular disease. Identifying ear disease and Horner's syndrome is suggestive of peripheral disease.

Table 1. Feature of vestibular disease that allow differentiation between central or peripheral disease include:

 

Peripheral

Central

Circling

No

Yes

Postural deficits (usually conscious
proprioceptive deficits or
hypermetria)

No

Yes

Trigeminal nerve lesions

No

Yes

Nystagmus
Vertical
Positional


No
No (except acute compensatory phase)


Yes
yes

Pain on opening the jaw or ear disease

Yes

No (except very extensive lesions)

Horner's Syndrome

Yes

No (except very extensive lesions)

Assessment

 Check vestibular eye movements (physiological nystagmus).

 Assess for signs of vestibular syndrome (loss of balance and head tilt).

Common Causes of Vestibular Disease

The most common cause of vestibular disease in both dogs and cats is idiopathic vestibular syndrome (in the dog also known as geriatric canine vestibular syndrome). Otitis media/interna is also an important cause, then followed by central vestibular disease (CNS neoplasia and inflammatory disease). Besides the above causes the potential for hypothyroidism, ototoxicity, metronidazole toxicity, thiamine deficiency and electrolyte disturbances as a cause of vestibular disease (among others) should be considered.

Assessment of Hearing

The clinical assessment of hearing is complicated by the difficulty of excluding conscious responses to auditory stimuli mediated through the opposite ear to the one being evaluated. Even in cases with bilateral deafness there may be a conscious response to visual cues or even vibrations making assessment difficult. The only objective way of assessing partial hearing loss and unilateral deafness is by electrodiagnostic means (the 'brainstem auditory evoked response' or BAER), but this requires specialised equipment.

Common Causes of Deafness

The three most common causes of deafness in dogs and cats include congenital sensorineural deafness in at risk breeds (in most cases seen in association with pigmentation genes for white coat breeds and particularly prevalent in white cats and the Dalmatian), acquired late-onset sensorineural deafness (usually manifested as age-related decline of hearing) and acquired late-onset conductive deafness (typically secondary to external and middle ear disease).

VII. Glossopharyngeal Nerve and X. Vagus

These nerves supplies (amongst others):

 Motor and sensory to the pharynx and larynx (the vagus also has important parasympathetic functions).

Clinical Signs

 Problems swallowing, aspiration pneumonia, coughing, change in bark.

Assessment

 Gag reflex.

VIII. Accessory Nerve

This cranial nerve is difficult to evaluate and is not routinely assessed in a clinical setting.

IX. Hypoglossal Nerve

The hypoglossal nerves supplies:

 Motor to the intrinsic and extrinsic tongue muscles.

Clinical Signs

 Bilateral lesion: tongue paralysis.

 Unilateral lesion: unilateral tongue atrophy and protrusion of tongue to affected side, although in some cases deviation towards the unaffected side.

Assessment

 Evaluating the licking response and the animal's ability to eat and drink.

 Manually retract the tongue and the dog should resist.

Sympathetic Lesions (Including Horner's Syndrome)

Although not a cranial nerve as such, lesions affecting the sympathetic pathway may result in ipsilateral Horner's syndrome, cutaneous vasodilation (evident as increased skin temperature and erythema) and decreased sweating (increased sweating in horses). Horner's syndrome comprises: miosis (pupillary constriction), enophthalmos (retraction of the globe), ptosis (narrowing of the palpebral fissure) and protrusion of the third eyelid. The most important diseases of the sympathetic and parasympathetic nervous system include Horner's syndrome (most commonly idiopathic, particularly in the Golden Retriever) and dysautonomia.

References

1.  Penderis J. In: Barnett et al. Canine ophthalmology, an atlas and text. 2002 pp 181-195;

2.  Penderis J. In Practice 2003 25:178-189;

3.  Penderis J. In Practice 2003 25:256-263;

4.  Penderis J. In Practice 2003 25:342-349;

5.  Penderis J. In: Platt and Olby (editors). BSAVA Manual of Canine and Feline Neurology, 3rd Edition. 2005 pp133-154;

6.  Penderis J. UK Vet 2005 10(1):89-96;

7.  Penderis J. UK Vet 2005 10(3):81-84.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Jacques Penderis, BVSc, MVM, PhD, CVR, DECVN, MRCVS
University of Glasgow
Glasgow, Scotland


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