Cranial Nerves and Nuclei I

The reticular formation | Main Anatomy Index | Cranial nerves and nuclei II

Click here for the gross anatomy of the cranial nerves (First Year Medicine ANAT1006).

• Although the tracts and nuclei of the cranial nerves are intricate, they can be systematised in terms of their function components contained within each nerve.
• Spinal nerves contain both motor and sensory components.
• Some of each kind may be related to visceral or somatic structures.

• A given nerve fibre can thus be put into the following categories:

• Afferent
1. General Somatic Afferent (GSA)
• These fibres are related to the receptors for pain, temperature, and mechanical stimuli in somatic structures such as skin, muscle and joints.
2. Special Somatic Afferent (SSA)
• These fibres are related to the special senses of sight, hearing and equilibrium.

• Efferent
1. General Somatic Efferent (GSE)
• These fibres innervate skeletal muscle (i.e., they are the axons of the alpha and gamma motor neurons).

• Afferent
1. General Visceral Afferent (GVA)
• These fibres are related to the receptors of the visceral structures such as the walls of the digestive tract.
2. Special Visceral Afferent (SVA)
• These fibres are related to the special senses of smell and taste.

• Efferent
1. General Visceral Efferent (GVE)
• These are fibres that are the preganglionic autonomic fibres.
2. Special Visceral Efferent (SVE)
• These fibres innervate certain striated muscles with a special embryological origin.
• They are referred to as the branchiomeric muscles.
• Structures that develop into gill arches in fish develop instead into various structures near or in the head and neck (muscles of the face, larynx and pharynx).
• Although these muscles are identical to normal striated muscle, neurons for branchiomeric muscles have a distinctive location in the brainstem.

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• The locations of the cell bodies where cranial nerve afferents terminate or cranial nerve efferents originate, can be predicted to some extent from the embryology of the brainstem.
• The walls of the neural tube spread apart

• in the medulla and pons and form the floor of the 4th ventricle.

• The sulcus limitans runs longitudinally along the floor of the adult ventricle.
• It still separates the sensory alar plate derivatives (now lateral) and the motor basal plate derivatives (now medial).
• The cell concerned with visceral function tend to be located nearer the sulcus limitans.

• Ideally, the cell columns of the special components of the cranial nerves would be located adjacent to those for the corresponding general components.
• The actual arrangement is not so simple, however, because:

1. The cell columns are not continuous with those of the spinal cord.
• They are interrupted and form a series of nuclei.
• All components may not be present in one transverse plane.
2. In a few instances, portions of the cell columns migrate away from their expected locations.
• For example, most SVE neurons are located in the ventrolateral part of the tegmentum rather than on the floor of the ventricle, adjacent to the other efferent neurons.

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• No cranial nerve contains all seven functional components.
• There are 3 types of cranial nerves:

1. Those that contain GSE fibres and little or nothing else (e.g., CN III, IV, VI and XII) and are referred to as somatic efferent nerves;
2. Those that contain special sensory fibres (SSA or SVA) and nothing else (e.g., CN I, II and VIII);
3. And the remaining nerves that are more complex, contain several components including the innervation of the branchial arch musculature (e.g., CN V, VII, IX, X and XI). These nerves are called branchiomeric nerves.

Table is from Nolte, The Human Brain 3rd Ed. p. 180 Table 6

• Cranial nerves I and II are not attached to the brainstem, but are directly related to the forebrain.

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• This includes the oculomotor (CN III), trochlea (CN IV), abducens (CN VI) and hypoglossal (CN XII) nerves.
• These nerves are the simplest of the cranial nerves as each contains only one functional component (GSE fibres).
• The exception is for CN III, which has a small but important complement of GVE fibres.

• The nuclei of origin of all these nerves are located adjacent to the midline near the aqueduct or the floor of the 4th ventricle.

• This supplies the levator palpebrae superioris and all the internal and external muscles of the ipsilateral eye.
• The exception are the lateral rectus, the superior oblique and dilator pupillae.

• The fibres originate from the wedge-shaped oculomotor nucleus.
• This is located at the ventral edge of the periaqueductal grey in the rostral midbrain.
• They then proceed ventrally and arch through the midbrain tegmentum in several bundles.
• These join the nerve as they emerge into the interpeduncular fossa.

• This consists of a series of longitudinal cell columns or subnuclei.
• The column supplying:

1. The levator palpebrae superioris is located in the midline and innervates this muscle on both sides;
2. The superior rectus projects to the contralateral eye;
3. The medial rectus, inferior rectus, and inferior oblique all project to the ipsilateral eye;

• This column includes preganglionic parasympathetic neurons (GVE).
• It straddles the midline and projects to the ipsilateral ciliary ganglion.
• The ciliary ganglion then innervates the sphincter pupillae and the ciliary muscle.

• Although the oculomotor nerve has a partly-crossed, uncrossed nature, this is of limited clinical significance.
• This is as the two nuclei are so close together, that a central lesion in this vicinity is likely to damage both nuclei.

• However, once a given oculomotor nerve leaves the brainstem, it supplies only ipsilateral muscles.
• Thus, a lesion to the nerve affects only one eye.

• Therefore, unilateral nuclear damage is extremely rare (paralysis of superior rectus on one side and of the other extraocular muscles on the other).

• Damage to the oculomotor nerve cause:

1. Lateral strabismus, as medial rectus is paralysed and the lateral rectus is unopposed;
2. Diplopia, double-vision as one of the eye deviates from the midline;
3. Inability to move the eye medially or vertically;
4. Ptosis as the ipsilateral levator palpebrae superioris is paralysed;
5. Mydriasis (dilated pupil of affected side) and unresponsiveness to light as the sphincter pupillae is non-functional and the dilator pupillae is unopposed;
6. Inability for the affected eye to focus on near objects as the ciliary muscles have also been paralysed.

• Along the course of the oculomotor nerve from the brainstem to the orbit, the GVE fibres of the Edinger-Westphal nucleus travel in a superficial location.
• They are especially susceptible to external pressures.
• Thus a dilated pupil and unresponsiveness to light may be the first clinically detectable sign of something pressing on the third nerve.

• Note: on Third Nerve Damage vs. Horner's Syndrome.

• Third Nerve Damage: ptosis and same side larger pupil.
• Horner's Syndrome: ptosis and same side smaller pupil.

• Also, with third nerve damage, ptosis is more pronounced, and is usually accompanied with defective eye movements and lateral strabismus.

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• This supplies the superior oblique muscle.
• Its cell bodies are located in the contralateral trochlear nucleus.

• This is a small nucleus located at the level of the inferior colliculus.
• Here, it indents the medial longitudinal fasciculus (MLF).
• Fibres leaving the nucleus turn caudally in the periaqueductal grey.
• They then arch dorsally to decussate and leave the brainstem at the pons-midbrain junction.

• The trochlear nerve is unique in that:

1. It is the only cranial nerve attached to the dorsal aspect of the brainstem;
2. It is the only one to originate completely from the contralateral nucleus.

• Damage to the trochlear nerve result in much less drastic and noticeable deficits than damage to the oculomotor or abducens nerves.

• The superior oblique muscle helps to move the eye downward and laterally.
• Attempted movements in these directions (e.g., reading or walking down stairs) may cause diplopia.

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• This supplies the lateral rectus muscle.
• The fibres originate from the ipsilateral abducens nuclei.
• This is located in the caudal pons, beneath the floor of the 4th ventricle.

• Medial to the nucleus is two bundles of fibres.
• The more medial of the two is the MLF.
• Between the MLF and the abducens nuclei are the motor fibres of the facial nerve.

• The facial fibres project dorsomedially and wrap around the abducens nucleus.
• They then turn back ventrally to exit from the brainstem.
• Here, the fibres are known as the internal genu of the facial nerve.

• The abducens nuclei along with the internal genu are responsible for the facial colliculus in the floor of the 4th ventricle.

• This causes medial strabismus (the affected eye deviates medially by the unopposed action of the medial rectus muscle).
• The individual may be able to move the affected eye to the midline, but no further, by relaxing the medial rectus muscle.

• This has the same deficit as damage to the sixth nerve with a significant addition.
• Not only is it impossible to move the ipsilateral eye laterally, but now also the contralateral medially.
• This is called lateral gaze paralysis.

• This is as internuclear neurons are also affected.
• These neurons normally project to the MLF to the motor neurons controlling the contralateral medial rectus muscle.
• This is so that we normally have co-ordinated lateral gaze (i.e., if we want to look left, our left eye turns laterally and simultaneously, our right eye turns medially).

• This condition is known as internuclear ophthalmoplegia (INO).

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• This nerve supplies the muscles of the tongue.
• The fibres originate in the ipsilateral hypoglossal nucleus.

• This extends from the caudal medulla to the rostral part of the rostral medulla.
• This nucleus is situated in the midline just beneath the floor of the 4th ventricle.
• Here it forms the hypoglossal trigone, a triangular elevation.

• Hypoglossal axons proceed ventrally and emerge as a series of rootlets in the groove between the pyramid and the olive.

• This will cause weakness of one side of the tongue.
• As this is a lower motor neuron lesion, that side of the tongue will also atrophies.

• This weakness is easily demonstrated by the patient protruding his or her tongue.
• The tongue is deviated to the side of the lesion.

• Bilateral hypoglossal lesions may cause difficulties in both speaking and eating.

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