There are 12 paired cranial nerves, named and numbered according to the rostral-caudal order of attachment to the brain. They serve a variety of functions and predominantly provide the motor and sensory innervation to the head. The effects of a mononeuropathy depend on where in its pathway the nerve is affected and the etiology. The signs and symptoms of a cranial nerve mononeuropathy vary depending on which nerve is affected.
Summary
Olfactory (I)
Anatomy
- Olfaction begins with transduction of odorants from the air into the nasal mucosa. These odorants diffuse or are transported to bipolar receptor cells located in the olfactory neuroepithelium in the roof of the nasal chamber. Action potentials are induced in these cells, which synapse with olfactory bulb glomeruli.[1] The receptor cell axons project through the cribriform plate of the ethmoid bone and synapse within the glomerular layer of the olfactory bulb. The paired olfactory bulbs are located at the base of the frontal lobe overlying the cribriform plate.[2] The second-order neurons leave the olfactory bulb to synapse on the primary olfactory cortex. These areas encode characteristics of odor quality, identity, familiarity, and emotion.[3]
Function and disorders
- Changes in olfactory function frequently go unnoticed and often do not present to a clinician.[2] Patients may notice altered taste, rather than a loss of sense of smell.[4] Olfaction is critically important for safety, nutritional status, and quality of life. Disorders can manifest as a total loss of smell (anosmia), partial loss of smell (hyposmia), distortions (dysosmias), or spontaneous olfactory hallucinations (phantosmias).[2] Infrequently, olfactory dysfunction can be the presenting sign/symptom of neurodegenerative disorders (such as idiopathic Parkinson disease), or an intracranial mass lesion.
Nerve testing
- The diagnosis can usually be made clinically. Commercial odor identification tests are available, which require patients to identify several predefined smells.[5] These may be useful to confirm olfactory dysfunction. Psychophysical tests are useful to validate and classify olfactory dysfunction, but establishing the cause of olfactory loss relies heavily on the history. Olfactory evoked potentials are available in specialist centers.
Optic (II)
Anatomy
- Axons making up the optic nerve arise from retinal ganglion cells. These axons run toward the lamina cribrosa and merge in the optic papilla. At this point, they form the optic nerve. In the orbital apex, the nerve passes through the muscle origins and enters the optic canal. The nerve continues to course upward and inward until it meets with the contralateral nerve to form the optic chiasm superior to the sella and pituitary gland.[6] Action potentials are then carried to the lateral geniculate body. The intraorbital portion is surrounded by the subarachnoid space and dura that extends from the intracranial cavity. The central retinal artery and vein course through the middle of the nerve.
Function and disorders
- Humans have a highly developed visual system, which transmits information from the environment. The optic nerve carries millions of fibers from the retina into the central nervous system (CNS).[7] Vision is critical for human function and, as such, optic nerve pathology can severely affect quality of life.[6] Optic nerve lesions typically produce monocular visual loss, which can be sudden or gradual, and may or may not be associated with pain. The potential causes of optic neuropathy are diverse and include vascular, toxic, metabolic, traumatic, compressive, infectious, inflammatory, and idiopathic etiologies.
Nerve testing
- Symptoms of optic nerve damage can represent changes in visual acuity, contrast, brightness, or color.[6] A detailed description of visual dysfunction is essential and can narrow the differential. To define the degree of optic nerve dysfunction, the following tests are frequently performed.
- Visual acuity: this can be tested using a Snellen chart.[4] Optic nerve damage may result in central visual loss.
- Color vision: this can be assessed with a series of color plates. Patients with unilateral optic nerve impairment have great difficulty identifying colors between eyes (dyschromatopsia), and this is more affected than visual acuity.
- Pupillary testing: a relative afferent pupillary defect (RAPD) is the only objective test of optic nerve dysfunction.[6]
- Visual fields testing: a basic visual fields test can be performed at the bedside by comparing the patient's peripheral vision with the clinician's.[4] If a defect is identified, formal testing may be required, for example with Goldmann perimetry.
- Direct ophthalmoscopy: visualizing the optic nerve as it enters the back of the eye can reveal pallor (optic atrophy) or disk swelling (papillitis or papilledema).
Oculomotor (III), trochlear (IV), and abducens (VI)
Anatomy
- The third cranial nerve emerges from the midbrain nucleus that lies ventral to the sylvian aqueduct. One unpaired and 4 paired subnuclei can be distinguished. The most dorsal subnucleus contains the visceral Edinger-Westphal nucleus and the levator palpebrae nucleus. The Edinger-Westphal nucleus mediates pupillary constriction. Laterally the dorsal, intermediate, and ventral subnuclei provide innervation to the ipsilateral inferior rectus, inferior oblique, and medial rectus, respectively. The third nerve fascicles leave the nucleus and pass ventrally through the red nucleus before exiting just medial to the cerebral peduncles. In the subarachnoid space the third nerve passes between the superior cerebellar and posterior cerebral arteries. The nerve then enters the lateral wall of the cavernous sinus and divides into a superior and inferior branch as it enters the orbit through the superior orbital fissure.[8]
- The trochlear nucleus is located in the midbrain tegmentum at the level of the inferior colliculus. The nerve fascicles course posteroinferiorly to decussate at the anterior medullary velum before exiting from the dorsal aspect of the midbrain. The trochlear nerve is the only nerve to arise from the dorsal aspect of the brainstem. The fourth nerve traverses the brainstem cisterns close to the undersurface of the tentorial edge and pierces the dura to enter the lateral cavernous sinus. The trochlear nerve enters the orbit through the superior orbital fissure to innervate the superior oblique muscle.[8]
- The abducens nucleus contains motor neurons for the lateral rectus and interneurons traveling through the medial longitudinal fasciculus to the contralateral third nerve nucleus (to allow simultaneous movement of the contralateral medial rectus muscle). The nerve fascicles leave the nucleus and travel within the pontine tegmentum to leave the brainstem in the horizontal sulcus between the pons and medulla. The nerve enters the subarachnoid space and courses vertically along the clivus over the petrous apex of the temporal bone, where it is tethered in the Dorello canal. It then enters the cavernous sinus lateral to the internal carotid artery and finally enters the orbit through the superior orbital fissure.[8]
Function and disorders
- The third, fourth, and sixth cranial nerves are responsible for eye movements.
- The third cranial nerve controls most extraocular muscles, including the superior, inferior, and medial recti, and the inferior oblique muscles. In addition, it innervates the levator palpebrae superioris, which elevates the eyelid, and carries parasympathetic innervation to the pupil. Patients often present with paralysis of adduction, elevation, and depression, and when the pupil is involved a large unreactive pupil is noted. This presentation can suggest serious neurologic disorders, namely subarachnoid hemorrhage, cerebral aneurysms, uncal herniation, or meningitis, so prompt recognition and evaluation is needed.
- The fourth cranial nerve innervates the superior oblique muscle, which controls depression, intorsion, and adduction of the eye. It is the most common cause of vertical diplopia. The frequency of fourth nerve palsy is difficult to accurately report, but in one large series it was more common than both oculomotor and abducens palsies.[9] [10] The abducens nerve innervates the lateral rectus muscle and controls abduction. Patients typically present with horizontal double vision. It may be an isolated finding or part of a systemic disease.[8]
Nerve testing
- Simple bedside testing of eye movements can be performed to elicit a third, fourth, or sixth nerve palsy. The patient is asked to keep his or her head still and follow the examiner's index finger with the eyes. The examiner slowly moves his or her finger up and down and from side to side at eye level and observes eye movements.[4] The patient should report any diplopia. Diplopia is maximal in the direction of action of the paralyzed muscle. The outer image is the false image and disappears when the abnormal (paretic) eye is covered.[4]
Trigeminal (V)
Anatomy
- The trigeminal nerve has 3 main branches: ophthalmic (V1), maxillary (V2), and mandibular (V3).[11] V1 enters the cranial cavity through the superior orbital fissure, V2 through the foramen rotundum, and V3 through the foramen ovale. V1 and V2 traverse the cavernous sinus. The first-order cell bodies carrying modalities of pain, temperature, pressure, and light touch in all 3 branches are located in the trigeminal (gasserian) ganglion in the Meckel cave (near the petrous apex of the temporal bone). Proprioceptive fibers have their first-order cell bodies in the mesencephalic nucleus of the brainstem. From the trigeminal ganglion, the nerve fibers enter the pons and synapse in multiple trigeminal nuclei. From there, second-order neurons carry afferent information to the ventral posteromedial nucleus of the thalamus. Finally, third-order neurons relay to the primary sensory cortex. Efferent motor fibers originate in the motor nucleus of the trigeminal nerve in the midpons and travel with V3 through the foramen ovale to supply the muscles of mastication (masseter, temporalis, mylohyoid, medial and lateral pterygoid, and anterior belly of the digastric), as well as the tensor tympani and tensor veli palatini. The trigeminal nerve and its branches also mediate the afferent limbs of the corneal blink and lacrimal reflexes, and both afferent and efferent limbs of the jaw-jerk reflex.
Function and disorders
- The trigeminal nerve is the biggest cranial nerve.[4] It carries sensation from the face and mucosal surfaces, cornea, and supratentorial dura, as well as providing motor innervations to the muscles of mastication. The differential for a trigeminal neuropathy is very broad. Intra-axial pathology, particularly of the pons, can result in trigeminal dysfunction, but only rarely does this result in a mononeuropathy. Extra-axial lesions are more likely to affect the trigeminal nerve or its branches alone. Symptoms of trigeminal neuropathy depend on the location and etiology of the lesion and may include loss of sensation in the distribution of 1 or more trigeminal nerve branches, neuropathic pain, or weakness of the muscles of mastication.
Nerve testing
- Facial sensation can be tested by asking the patient to close his or her eyes and report where a stimulus is felt. Light touch with a cotton wool stick, pinprick with the end of a sterile needle, and warm and cold stimuli can be tested on each side of the face.[4] Contraction of the masseter and temporal muscles can be examined by visual inspection, and palpation of the masseter muscles can be examined when the patient is chewing.
- The jaw jerk can be tested as follows: with the patient's mouth slightly open, the mandible is tapped just below the lips in a downward direction. The masseter will move the mandible upward. Normally this reflex is weak, but it may be pronounced with upper motor neuron lesions.[4]
- The strength of the pterygoid muscles may be tested by asking the patient to open the jaw against resistance.[4]
- The corneal reflex can be tested with cotton wool (afferent-trigeminal, efferent-facial) and elicits an ipsilateral and contralateral blink response in normal individuals.[4]
Last updated
Citations
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