Equine Cranial Nerves

The peripheral nervous system consists of the nerves that arise from the central nervous system. The cranial nerves are part of the peripheral nervous system.

Cranial nerves originate from the brain (in comparison to the spine, like the spinal nerves) inside the cranium. They leave the cranial cavity via various foramina.

There are 12 pairs of cranial nerves. They are short in structure and supply the structures of the head. However, this is on the exception of the vagus nerve (CN10) which is the longest nerve of the body.

It is important to remember that cranial nerves are P A I R S. Anatomical diagrams tend to show you one side of the skull for illustrative purposes. However, remember that the nerves are also present on the other side of the skull.

What type of nerve fibres do cranial nerves have?

Cranial nerves can have:

  • ONLY sensory fibres — these nerves will relay messages TO the brain.
  • ONLY motor fibres — these muscles will create and control muscle movement.
  • BOTH sensory and motor fibres — these are mixed fibres with mixed function.

How to the cranial neves leave the cranium?

All of the cranial nerves (apart from CNIV Trochlear) exit the brain from the ventral surface and then pass through small foramina (openings) in the skull. CNIV Trochlear exits the brain from the dorsal surface but immediately follows down to the bottom of the brain to unite with the other cranial nerves.

Cranial Nerves

CNI – Olfactory

CNII – Optic

CNIII – Oculomotor

CNIV – Trochlear

CNV – Trigeminal

CNVI – Abducens

CNVII – Facial

CNVIII – Vestibulocochlear

CNIX – Glossopharyngeal

CNX – Vagus

CNXI – Accessory

CNXII – Hypoglossal

Cranial nerves and their function

There is a mention of CN0 in some textbooks. This is in reference to the Nerves Terminalis (a nerve associated with smelling pheromones and triggering mating behaviour).

Cranial nerve anatomy


Monocular vision means that horses rely more heavily on chemical signals. This nerve is responsible for smell. Its receptors (located in the mucous membranes in the upper portion of the nasal cavity) are elongated nerve cells, specifically designed to analyse smells. These elongated nerve cells all join together to form the axon of CNI.

It runs from the nasal cavity through to the olfactory bulb (located in the forebrain). On its path, it passes through the cribiform plate and is surrounded by meningeal sheets. For this reason, CNI is a potential site of infection that can track towards the brain. Injury of CNI can result in anosmia (loss of smell), hyposmia (decreased sense of smell) and parosmia (perversion of sense of smell).

The function of CNI is to relay sensory data about smells that enter the nasal cavity to the brain.

Olfaction in canines is very well developed as they use it to orientate themselves.

By sniffing, a horse can intensify the currents of air in the nasal passages, providing more contact between the odour molecules and receptor cells and therefore more time for analysis.

Why do horses sniff more when they smell something?

CNI contains sensory nerve fibres that are formed into bundles known as olfactory filaments.

Locate underneath the nasal cavity is a secondary olfactory system known as the Jacobson’s organs. It is innervated by the vomeronasa 1 nerve. It has a tubular and cartilaginous structure lined with mucous membranes, and is about 12 cm long. It connects to the nasal passages via a nasopalatin duct. The Jacobson’s organs expand and contract like a pump when stimulated with strong odours (these odours are specific and strong enough to have their own pathway to the brain!). The purpose of this system is to work alongside the CNI and detect and analyse pheromones. The flehmen response helps to trap these pheromones scents for the Jacobson organs to closer analyse; the curling of the lip temporarily closes the nasal passages and holds the particles inside.

The flehmen response and its link to olfaction.

P A T H W A Y = nasal cavity –> cribriform plate (via various foramina) –> olfactory bulb (forebrain)

Process of Stimulation (action potential generation):

  1. Airborne chemicals and particles enter the nasal cavity and come into contact with the lipid and protein material of the mucous membrane.
  2. They interact with small hairs protruding from the receptor cells.
  3. Chemical substances are present and stimulate sensory neurones (these are the olfactory neurosensory cells that are found within the olfactory epithelium). This generates an action potential.
  4. The nerve impulse travels to the brain via sensory nerve fibres. This fibres represent CNI.

When chemical substances interact with our bodies, they stimulate sensory neurones that are specific to that chemical. If no specific sensory cell exists for that chemical substance, it will go undetected.

THE OLFACTORY BULB — this is a distinct area of the brain that is responsible for analysing scents. It is located at the front of the cerebrum (one on each lobe). The two olfactory bulbs are connected to the receptors in the nasal passage by CNI. The olfactory bulbs are also one of the few brain structures that do not cross over – the left nostril is paired with the left olfactory bulb.


The optic nerve connects the receptor cells of the retina to the diencephalon (a region of the forebrain). It contains sensory nerve fibres.

CNII works with CNIII to cause CNVII to respond to blinking. It singularly functions to carry information about sight from the eyes to the brain.

The optic nerve is susceptible to shearing injury after a head trauma leading to prechiasmal blindness.

P A T H W A Y = optic disc of retina (bipolar cells) –> retinal ganglion cells bundle together to form optic nerve –> enters skull via optic canal –> brain (diencephalon; occipital cortex).

Some (85-88%) of optic nerve fibres decussate (cross over) at the optic chiasm in the horse and ox. It is 75% in the dog.
The decussation of nerves at the optic chiasma ensures that both sides of the brain receives information from both eyes.

Optic nerve structure in canines versus equines

Indications of injury:

  • The pupils of the eye will point down and out during rest.
  • No response to bright light directed into the eye.
  • Paralysis of the oculomotor nerve results in a resting ventrolateral strabismus and an inability to rotate the eye upwards, downwards or inwards.

P A T H W A Y = synapse at ciliary ganglion of the eye –> orbital fissure –> pre-ganglionic nucleus in mesencephalon (ventral midbrain).


The trochlear nerve innervates the muscle of the head, especially the dorsal oblique muscle. It enables mastication by supplying nerve branches to the temporal and masseter muscles. It is comprised of motor nerves. It is the smallest of the cranial nerves, yet greatest in intracranial length. It is also the only cranial nerve that exits from the dorsal aspect of the brain stem

Indications of injury:

  • Dorso-lateral strabismus.
  • Loss of facial reflexes e.g. closure of the eyelid.
  • Headshaking (nerve can become damaged by a tumour or inflammation).

P A T H W A Y = orbit of the eye –> exits the orbit via superior orbital fissure –> along the lateral wall of the cavernous sinus –> orbital fissure dura matter –> subarachnoid space –> trochlear nucleus of the dorsal midbrain.


The trigeminal nerve is responsible for innervating structures that originate from the brachial arches. It has three branches: the opthalmic nerve, the maxillary nerve and the mandibular nerve. It originates from the pons and medulla oblongata of the brain (location of trigeminal nerve nuclei).

a. OPTHALMIC NERVE — a sensory nerve that supplies sensory fibres to the orbit of the eye. It travels from the orbit of the eye (where it further splits into other nerves), through the orbital fissure to the brain.

b. MAXILLARY NERVE — a sensory nerve. It travels from the brain through the round foramen and rostral alar canal, entering the infraorbital canal via the maxillary foramen. Whilst in the infraorbital canal, the maxillary nerve then branches off to innervate the teeth (sensory). When the maxillary nerve exits the infraorbital canal, it branches again into two nerves that supply the horn (zygomatic nerve) and the palate (pterygopalatine nerve).

c. MANDIBULAR NERVE — a nerve with mixed fibres; both sensory and motor. It travels from the brain and passes through the oval foramen, dividing into motor nerve branches (masticatory nerve, masseteric nerve and temporal nerve) to innervate the muscles of mastication, ventral throat and muscles of the palate.

This diagram explains how the nerve originates in the midbrain and medulla oblongata, and inserts into three sensory nuclei & one motor nuclei.

Indication of injury:

  • Reduced sensation in the sensory fibres results in loss of facial reflexes e.g. closure of the eyelid.
  • Headshaking – the nerve can be damaged by a tumor or inflammation.


The abducens nerve is a motor nerve that functions to control specific (lateral rectus & lateral portion of retractor bulbi) muscles of the eye. An indication that this nerve is damaged is that the affected eye is pulled medially.

P A T H W A Y = muscles of innervation –> orbital fissure –> medulla oblongata (brain)


The facial nerve is a mixed nerve. Motor nerve fibres innervate the ear canal, salivary glands (parasympathetic control), lacrimal glands, nasal cavity, muscles of facial expression and palate. Sensory nerve fibres innervate the rotary 2/3rds of the tongue.

Muscles of facial expression are superficial, flat and thin muscles that originate from bony landmarks of the skull and then radiate out around the skin.

Indications that this nerve is damaged include any facial paralysis, drooling or absence of blinding.

P A T H W A Y = variety of branches including palpebral nerve, internal auricular nerve, stylohyoid nerve… –> stylomastoid foramen (caudoventral aspect of skull) –> petrosal bone –> internal acoustic meatus, facial canal (here the nerve branches off), stylomastoid foramen–> medulla oblongata and second brachial arch.


The vestibulocochlear nerve is made of two components: the vestibular nerve and the cochlear nerve. It is a sensory nerve.

VESTIBULAR NERVE — this nerve is responsible for balance.

COCHLEAR NERVE — this nerve is responsible for hearing.

Indications that this nerve may be damaged include:

  • deafness
  • vomiting (canines, not equines)
  • vertigo
  • ipsilateral ventrolateral strabismus (the visual axes of the eyes are not parallel and the eyes appear to be looking in different directions)

P A T H W A Y = inner ear (vestibular apparatus and cochlear) –> internal acoustic meatus –> petrosal bone (like facial nerve) –> brain.


The glossopharyngeal nerve is part of the vagus group. It is a mixed nerve. It is responsible for swallowing and motor tongue movement and sensation.

P A T H W A Y = structures of the third brachial arch (carotid body, pharynx, stylopharyngess muscle, salivary glands, tongue…) –> a variety of nerve branches –> jugular foramen –> medulla oblongata.

Indication that this nerve may be damaged include:

  • Asymmetry
  • Drooling out of one side of the mouth
  • Difficulty drinking/eating
  • Partial paralysis of the tongue.

The vagus group encompasses the vagus, glossopharangel and accessory nerves as they pass through the jugular foramen.


The vagus nerve is part of the aforementioned vagus group. It has mixed fibres. Motor fibres innervate muscles of the larynx, pharynx, palate, oesophagus, abdominal and thoracic viscera. Sensory fibres innervate the base & root of the tongue, pharynx, larynx, epiglottis (taste), palate, external ear and dura matter. The vagus nerve has many functions; from the heart to the pharynx.

Indications that the nerve is damaged include:

  • Any changes related to gag reflxes, blood pressure/heart rate, voice or inspiratory dyspnoea.

To test for vagus nerve dysfunction:

  • observe and palpate swallowing
  • nasal tube for testing gag reflex
  • endoscopy

P A T H W A Y — structures of the fourth brachial arch –> jugular foramen –> brain.


Also known as the spinal accessory nerve, the accessory nerve is part of the aforementioned vagus group. The cranial root of CNXI contributes to the vagus nerve and striated muscles of the pharynx, larynx, palate and oesophagus. The spinal root CNXI also contributes to the cervical spinal cord via the foramen magnum to innervate the muscles of the neck. After emergence from the foramen magnum, CNXI branches into the dorsal branch (innervates the brachiocephalic, trapezius and omotransversarius) and ventral branch (sternocephalic). It is a motor nerve fundamental for thoracoscapular function and scapulohumeral rhythm.

Indications that the nerve is not functioning correctly are:

  • Weakness and atrophy of the trapezius muscle.
  • Reduced shoulder abduction
  • Drooped shoulder
  • Pain

CNXI is very vulnerable superficially and susceptible to injury (especially during surgery to the neck and lymph node biopsies).

P A T H W A Y — structures of the fourth brachial arch (this includes various structures of the neck from C5-C7) –> jugular foramen –> medulla oblongata

The accessory nerve starts off smaller and gets larger as more fibres are collected.


The hypoglossal nerve is responsible for movement of the muscles of the head. Due to its position (caudal location on the brain stem), it is partially considered as a cervical nerve. It is a motor nerve which controls the intrinsic and extrinsic muscles of the tongue. The muscular tone of the tongue is dependent on the function of CNXII.

Paralysis and atrophy of the tongue is indicative of malfunction of CNXII. This can be tested by grasping the tone and applying gentle traction. Inability to withdraw the tongue can suggest damage.

P A T H W A Y — muscles of the tongue –> hypoglossal canal –> medulla oblongata


Careful assessment of cranial nerve function is important since there are a number of diseases that may result in dysfunction of those nerves in addition to abnormalities found elsewhere. This can be found in particular with diseases such as polyneuritis equi and equine protozoal myeloencephalitis. Furthermore, if there are deficits noticed in multiple cranial nerves, there may be central disease for example in the area around the brainstem since that is where most cranial nerves originate. Deficits of the afferent pathways (sensory) would include reduced smell, taste, vision, hearing, or balance and specific proprioception. Deficits of the efferent pathways (motor) would include reduced ability to change pupil diameter, lesions of eyeball movement, reduced muscle of mastication mass, altered facial expression, reduced ear play, problems with swallowing, vocalization, and reduced tongue movement or tone. The most commonly seen deficits of cranial nerves in the horse include facial nerve paralysis, head tilt, laryngeal dysfunction, and dysphagia (Yvette and Not-Lomas).


Aspinal, M. and Cappello, M. (2015) Introduction to Veterinary Anatomy and Physiology Textbook.

Moretz, A. – Cranial Nerves of the Horse

WikiVet – Cranial Nerves

Proceedings of the 11th International Congress of the World Equine Veterinary Association (2009)

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