The vestibulocochlear nerve or cranial nerve eight (CN VIII) consists of two nerves originating from distinct nuclei in the brain: vestibular and the cochlear nerve. The vestibular nerve is responsible for maintaining body balance and eye movements, while the cochlear nerve conveys neural impulses related to hearing.
Vestibulocochlear nerve injuries are the result of pathological processes or injuries involving the pontocerebellar angle, the internal acoustic meatus, or the inner ear. In such cases, symptoms such as vertigo and nystagmus may occur due to the involvement of the vestibular part, and tinnitus and hypacusis occur due to the involvement of the cochlear component of CN VIII.
The peripheral sensory origin of the cochlear nerve is from the spiral organ of Corti, also known as the cochlear ganglion. The spiral or cochlear ganglion is located at the spiral canal of the modiolus. Nerve fibers originate from the spiral ganglion and travel to the edge of the osseous spiral lamina. Few nerve fibers reach the outer hair cells, while the majority travel to the basal and middle coils. The spiral ganglion gives rise to two types of cell types: type 1 and type 2 cells. Type 1 cells (large bipolar cells that are myelinated with axons in cranial and caudal directions) account for the majority of cochlear nerve cells (90%) and are afferent for the inner hair cells. Type 2 cells are smaller, nonmyelinated cells, and are afferent for the outer hair cells.
Neuronal projections from the cochlear ganglion form the cochlear nerve as they pass through the internal acoustic meatus. The central projections enter the brainstem laterally at the pontomedullary junction, where they synapse on ventral and dorsal cochlear nuclei.
Cochlear nuclei are organized tonotopically, located at the dorso-lateral side of the brainstem. The cochlear afferents that carry impulses from the base of the cochlea send high-frequency signals toward the dorsomedial nuclei. The afferents coming from the apex of the cochlea send signals transmitting low-frequency tones toward the ventrolateral cochlear nuclei. From the nuclei mentioned above, transverse fibers are born: dorsal acoustic striae, intermediate acoustic striae, and ventral acoustic striae.
The ventral cochlear nucleus plays a fundamental role in humans in the auditory pathways and from which the ventral striae are derived; these give rise to the trapezoid body once crossed the bridge in the ventral portion of the tegmen. The trapezoid body (in which we find the nucleus of the trapezoid body and the upper olivary complex) continues with an ascending path through the lateral lemniscus.
The vestibular nerve has complex functions. Its ganglion in the internal acoustic meatus, called the vestibular ganglia of Scarpa, is the formation of the upper and lower vestibular nerve. These ramifications derive from the sensory cells of the labyrinth, in the ampullary crest of the semicircular canals, and in the sensory macula of the utricle and the saccule. These cells, called ciliated cells, are stimulated by the inertial fluids of the endolymph during rotational head movements (ampullar crest) and linear movements (the utricle for vertical movements and the saccule for the horizontal ones).
The post-ganglionic extension forms the vestibular nerve that enters the brainstem, reaching the vestibular nuclear complex. This complex occupies an area located under the floor of the fourth ventricle, in a lateral position and between the bulb and the bridge. A small axonal contingent heads towards the cerebellum, forming the vestibulocerebellar pathway. The vestibular complex comprises four nuclei: the upper or Bechterew nucleus; the medial nucleus; the lateral nucleus or Deiters; and the lower nucleus.
The afferents deriving from the ampullary crest affect all four nuclei; from the saccule, they will arrive at the inferior nucleus; from the utricle, they will direct information to the lower and medial nucleus. This complex at the rostral level is mainly concerned with the movements of the head and eyes while the caudal area is more involved in the posture and tone of the muscles. In addition to the labyrinthine area of the ear, the vestibular system receives information from the cerebellum and has a direct connection to the medial longitudinal fasciculus by which relationships are created with the thalamus and cortex, making a part of the conscientious vestibular information.
Through the medial longitudinal fasciculus, the vestibular system creates an upward preferential relationship with the nerves connected to the eye and the retina (II, III, IV, and VI) or vestibulo-oculomotor reflex. The fibers that instead go caudally through the longitudinal fasciculus will go to pass information of the cervical muscles within the vestibulo-nuchal reflex.
Continuing in the descent, the vestibular fibers will be put in contact with lumbar spinal and dorsal neurons, facilitating the extension movement, through the vestibulospinal beam. We could hypothesize that a previous dysfunction of the vestibule, due for example to a whiplash, could influence the vertebral muscular attitude, altering the muscular behavior from a morphological and phenotypic point of view.
Not only is the vestibular system essential for posture and standing but also for the auditory system as it has been shown that the same sound affects the postural control. The vestibular system interacts for the control of blood pressure, using sympathetic communication and the baroreceptors of the carotid and the aortic arch.
The embryological reference sheet is the ectoderm, the outer layer of the embryo. Cranial nerve motor neurons originate from the neural plaque, while sensory neurons arise from the neural crest, such as nerve VIII. The cranial nerves derived from the ectoderm appear from the fourth week of gestation.
At the closure of the neural tube and by induction of this, appear on the coating ectoderm, in well-localized areas, pairs of thickening called placodes (olfactory, crystalline, otic, and epibranchial placodes) linked to the formation of sense organs.
The placodes evolve into dimples, and therefore, vesicles that deepen, become independent of the epiblast and connect to the nervous system.
The olfactory placodes are made up of sensory cells from which the olfactory nerve axons that connect with the telencephalon originate.
The crystalline placodes do not form neurons but the lens or crystalline of the eye.
The otic placodes form the sensory epithelium of the inner ear and the neurons of the vestibulocochlear ganglion.
The epibranchial placodes differ in three other small placodes (geniculate, petrous, nodose) that give rise, respectively, to sensory neurons of the facial nerves, glossopharyngeal and vague.
The vestibular and vestibulocochlear artery (branches of the internal auditory artery), and the superolateral cerebellar vein or Dandy vein are closely related to nerve VIII.
Bilateral direct ascending projections (through the medial longitudinal fasciculus) lead to the oculomotor, trochlear and abducent nerve nuclei that innervate the extrinsic musculature of the eyes, generating the vestibulo-oculomotor reflex.
Projections descending from the medial vestibular nucleus give rise to the medial vestibulospinal fascicles, which descend bilaterally giving rise to the alpha and gamma motoneurons of the cervical region to create the vestibular-nuchal reflex responsible for the stability of the head during movements.
From the lateral vestibular nucleus the lateral vestibulospinal fasciculus arises, with a somatotopic organization (the fibers that arise cranially are directed to more rostrally arranged muscles and so on), dedicated to the vestibulospinal reflex that allows correction of the posture in response to vestibular stimuli.
Nerve VIII conditions the motoneurons of the muscles of the skull and the muscular districts of the body.
There does not appear to be any physiological variation of nerve VIII, but rather, a variety of genetic malformations leading to pathology.
Acoustic neuroma is a benign tumor. Treatment modalities include microsurgical removal or radiotherapy. In some special cases, a waiting policy may be advisable. In its growth, the tumor can reach large dimensions and affect the nearby cranial nerves or the brain stem. Acoustic neuroma originates from the lining sheaths of the eighth cranial nerve. The causes that determine the growth of a neurinoma are not currently known. Only in cases of type II neurofibromatosis can a genetic cause be attributed.
The main and most important possible risks of nerve VIII surgery are from tumors (meningiomas, lipomas, acoustic neurinoma or schwannomas). Symptoms may include:
The most effective instrumental examination in making an immediate diagnosis is magnetic resonance imaging.
The pathologies that can affect the cranial nerve VIII are multiple, from direct trauma to the nerve to problems associated with vascular compression and congenital malformations. Dysfunction of the cochlear nerve can occur anywhere in its path, central and peripheral, and be associated with a decrease in hearing, partial, total mono lateral or bilaterally. One can go from frank deafness to auditory hallucinations, from paracusia (the sound is felt for a few seconds even after its termination) to autophony (exaggerated resonance of one's voice).
Another classic symptom is tinnitus, that is the perception of sounds in the absence of acoustic stimuli. The clinical evaluation of hearing is the responsibility of the otolaryngologist, but some clinical evaluations are simple to perform. One can check for bone and air conduction in the office using the tuning fork with relative ease.
The problems and pathologies affecting the vestibular nerve are highlighted with disturbances of balance, postural tonic deviations, vertigo, and nystagmus. Some tests can be performed to understand if the nerve is compromised. The patient is made to walk with his/her eyes closed; if a change of direction occurs (or a positive Romberg test) it may be indicative of a unilateral vestibular lesion.
Another test that can be performed is to observe the nystagmus according to how it behaves; this may be done by varying the position of the head and keeping it steady for 30 seconds (first sitting, then lying on the side, and keeping the head out of the bed slightly extended). If the nystagmus is persistent and changes direction with changes in the position of the head, it could mean an injury to the brainstem or posterior cranial fossa. If instead, the nystagmus disappears quickly and does not repeat itself in the other directions of the head, it should result in evidence of benign postural vertigo.
Also, the involvement of the facial nerve due to its proximity should not be excluded during the exam.
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