The Hands-On Evaluation - Cranial Nerves

Testing of the cranial nerves should be done in conjunction with the assessment of mentation, gait, postural reaction, and segmental spinal reflexes to determine whether there is brainstem disease versus peripheral nerve disease.  For a more detailed and animated overview of the functional anatomy responsible for the cranial nerve examination, please head over to our clinical neuroanatomy page.

The menace response

How to perform – the menace response is elicited by making a threatening gesture at the eye tested.  The expected response is a closure of the eyelid.  The contralateral eye must be blindfolded with the other hand to assess each eye separately.  Care must be taken not to touch the eyelashes or to create air currents that might stimulate the face (CN V, trigeminal nerve) and elicit a palpebral or corneal reflex (see below).  

How to interpret - This reaction is a learned response that may not be developed until 10 to 12 weeks in puppies and kittens.  The afferent arc of this response involves the following neurons:  the first neuron in this arc is the bipolar cell of the retina.  This receives impulses from the neuroepithelial cells of the retina (rods and cones).  The second afferent neuron is the ganglion cells of the retina.  Its axons lie in the optic nerve and continue through the optic chiasm and proximal part of the optic tract of the opposite side of the eye being menaced.  This second neuron synapses with neuron three in the lateral geniculate nucleus.  The axons then project to the visual cortex (mostly occipital cortex) in a band of fibers called the optic radiation.  The efferent arc of this response is not well understood.  The information generated in the optic cortex (contralateral to the eye stimulated) is forwarded to the motor cortex via association fibers.  The cortico-bulbar pathways to the facial nerve nucleus (CN VII) then transmit the motor information.  This response requires an intact facial nerve function.  This function should be separately evaluated using the palpebral reflex (see below).  There is some experimental and clinical evidence for cerebellar involvement in the menace response efferent pathways: unilateral cerebellar lesions can lead to an ipsilateral menace response loss with retention of normal vision.  The neuronal pathways through the cerebellum are however not precisely known.  

The menace response is shown below in this normal dog

Evaluation of pupil size

Immediately after the menace response testing, the pupil size and response to light and darkness should be evaluated.  Pupillary abnormalities are frequent following intracranial trauma or vascular compromise.  The size of the pupils represents a balance of the parasympathetic system which is responsive to the amount of light entering the eye and the sympathetic system which is responsive to the emotional state of the animal.  Through the parasympathetic nerve pathways that innervate the iris, the pupil regulates the amount of light that reaches the retina.  The parasympathetic component of the oculomotor nerve (CN III) is involved in the control of pupillary constriction while the somatic efferent component of the oculomotor nerve is responsible for the motor innervation of the levator palpebrae superioris (elevation of the upper eyelid) ipsilateral dorsal, ventral and medial recti extraocular muscles as well as the ventral oblique muscle (movement of the eyeball).  The tone of the iris dilator muscle is maintained by the sympathetic system which keeps the pupil partially dilated under normal conditions and dilates it during periods of stress, fear, and painful stimuli.  The ocular sympathetic nervous system also innervates and provides tone to the smooth muscle of the periorbita and eyelids.  This tone keeps the eyeball protruded, the palpebral fissure widened and the third eyelid retracted.  

How to perform - Assessment of pupillary size and equality should be determined in ambient light as well as in darkness.  

Using a light source in a darkened room can help provide enough ambient light to see the pupils without stimulating their constriction and can then be used to directly stimulate each pupil for the pupillary light reflex (see below).

How to interpret - Normally, the pupil of each eye should be symmetrically shaped and equal to each other in size.  Animals with pupils of unequal size (anisocoria) or shape (dyscoria) must be found free of primary or secondary anatomic or mechanical abnormalities (iris atrophy, uveitis, or glaucoma) before consideration is given to neurologic dysfunction.  Determining which pupil is abnormal is achieved by checking the pupillary light reflex and determining if the asymmetry in pupil size increases in bright light or in complete darkness (dark adaptation test).

Note the asymmetrical dilation of this dog's right eye when both are evaluated in ambient light.

Pupillary light reflex (PLR)

How to perform – The PLR is tested by shining a bright light into the pupil and assessing for pupillary constriction (direct reflex).  The opposite pupil should constrict at the same time (consensual or indirect reflex).  A slight dilation usually follows the initial pupillary constriction (pupillary escape) as a consequence of light adaptation of photoreceptors.

How to interpret - The pupillary light reflex (PLR) involves an afferent arm and an efferent arm.  The afferent arm of this reflex shares some common pathways (ipsilateral retina, optic nerve, optic chiasm and contralateral optic tract) with part of the afferent arm of the menace response and visual placing. These tests use different integration centers within the brain and different efferent pathways.  The PLR does not test the animal’s vision and the cerebrum is not involved in the PLR pathway. The efferent arm of the PLR reflex is mediated by the parasympathetic portion of CN III.  While axons involved in vision reach the conscious level after synapse with the lateral geniculate nucleus, the axons involved in the PLR synapse with a third neuron in the pretectal nucleus.  Most of the axons arising from this nucleus decussate again and synapse in the parasympathetic component of the oculomotor nucleus (ipsilateral to the stimulated eye) in the mesencephalon.  Some neurons do not decussate and which project to the oculomotor nucleus on the contralateral side of the stimulated eye.  The proportion of axons that decussate is higher than the ones that do not decussate, explaining why the direct response (constriction in the eye receiving the light stimulus) is greater than the consensual response (constriction in the eye not receiving the light stimulus).  Combining the results of the menace response, visual placing, and PLR testing helps to localize the lesion as being within these common pathways or not.

The dark adaptation test consists of allowing the eyes to dark-adapt in complete darkness for a couple of minutes to allow complete relaxation of the pupillary sphincter muscle. 

Each eye is tested individually and then at the same time in this dog below.

Evaluation of eye position and movement

How to perform – Observe the animal’s head in a normal position for a deviation of one or both globes in the orbit(s).

How to interpret – Cranial nerves III, IV, and VI aid vision by maintaining the globe in a central position. Deviation of the globe from its central axis indicates dysfunction in one or more of these nerves: ventrolateral – CN III, dorsolateral – CN IV, and medial – CN VI.

The palpebral reflex

How to perform – Touch the medial canthus of the normal eyelid and watch the response.

How to interpret – The normal eyelid should close. Cranial nerve V (trigeminal nerve) is responsible for facial sensation, whereas the motor response to facial sensory stimulation is generally provided by the facial nerve (CN VII). Facial paresis presents as a drooping of the facial muscles, most notably the lips and the eyelids. It may also be detected as a reduction or absence in the blink response.

A normal palpebral reflex is shown below.

Evaluation of jaw tone

How to perform – Observe the patient for a dropped lower jaw and/or an inability to eat. Assess the strength of the jaw safely by manually opening the mouth and evaluating the resistance to opening.

How to interpret – The mandibular branch of CN V provides motor function to the jaw. A dropped lower jaw or the inability to chew can indicate damage to CN V.

A normal jaw can be assessed as seen below. Ideally, gloves should be worn and caution should be taken not to get bitten, especially in regions where rabies is a possibility.

The oculocephalic reflex / physiological nystagmus

How to perform – Move the head from side to side in a horizontal plane and observe the resulting movement of the eyes.

How to interpret – In normal animals, a physiological nystagmus will be induced, with the fast phase in the direction of head movement. This reflex tests the integrity of CN VIII (vestibulocochlear nerve), which is the sensory arm of this reflex, and CNs III, IV, and VI, which are responsible for the motor movement of the eyes. Clinical signs of peripheral vestibular disease are manifest after damage to the inner ear or vestibular branch of CN VIII, which effectively gives unbalanced input to the intact central vestibular system. In the absence of head motion, spontaneous horizontal nystagmus is consistent with CN VIII damage, with the fast component away from the side of the lesion. Unilateral peripheral disease may cause a head tilt and circling to the side of the lesion.

Laryngeal, pharyngeal and tongue function

Because of their proximity in the brainstem, the glossopharyngeal (CN IX) and vagus (CN X) nerves share sensory (nucleus solitarius) and motor nuclei (nucleus ambiguus).  CN IX innervates the musculature of the pharynx and palatine structures.  It provides sensory innervation to the caudal third of the tongue and pharyngeal mucosa (taste).  Its parasympathetic component innervates the parotid and zygomatic salivary glands.  CN X controls the motor function of the larynx (recurrent laryngeal branch), pharynx, and esophagus (cervical esophagus innervated by the pharyngeal and recurrent laryngeal branches while the thoracic esophagus is innervated by the vagal branches).  It provides sensory function to the larynx, pharynx, and thoracic and abdominal viscera.  Its parasympathetic component provides innervations to all thoracic and abdominal viscera, except those of the pelvic region.

The pharyngeal reflex can assess CN IX and X function.  This reflex is also known as the swallowing or gag reflex. 

How to perform - It is evaluated by applying external pressure to the hyoid bones to stimulate swallowing or by stimulating the pharynx with a finger to elicit a gag reflex.  It can also be evaluated by watching the animal eat and/or drink and by opening the mouth wide: the animal will usually close its mouth, swallow and lick its nose, allowing simultaneous evaluation of the tongue. The parasympathetic innervation of CN X can be evaluated by testing the oculocardiac reflex.  This is achieved by applying digital pressure to both eyeballs and observing simultaneously a reflex bradycardia (mediated as well by CN V).  

CN IX dysfunction results in dysphagia, an absent gag reflex, and reduced pharyngeal tone.  Animals frequently cough after drinking and swallow repeatedly because of an accumulation of saliva in their pharynx. CN X abnormality includes dysphagia, inspiratory dyspnea (due to laryngeal paralysis), voice changes, and regurgitation (due to megaoesophagus in case of bilateral vagal disorder).  The pharyngeal and oculocardiac reflexes are absent.

CN XII provides motor innervation to the muscles of the tongue.  The nucleus is in the caudal medulla and can therefore be affected by high cervical lesions.  This cranial nerve exits by the hypoglossal foramen.  CN XII function can be evaluated by inspecting the tongue for atrophy, asymmetry or deviation to one side.  Manually stretching the tongue and observing a voluntary retraction can assess the tongue’s tone.  Applying food paste to the nose and observing the animal licking can assess its movement.  Lesions affecting CN XII can result in problems with prehension, mastication, and deglutition.  With unilateral and recent lesions, the tongue tends to deviate toward the contralateral side.  With unilateral and chronic lesions, the tongue protrudes toward the side of the lesion, and atrophy is observed ipsilaterally. Muscle fasciculations may be obvious on the affected side in the denervated tongue.

In the dog below, the dog's left side of the tongue is atrophied and there is deviation toward this side.