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Vestibular Sensory Organs Are Contained Within the Membranous Labyrinth
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The membranous labyrinth is filled with endolymph, an extracellular fluid resembling intracellular fluid in its ionic constituents: a high potassium concentration and a low sodium concentration (see Chapter 8). Vestibular receptor cells are hair cells, like auditory receptors, located in specialized regions of the semicircular canals (termed ampullae) (Figure 12–9, inset) and the saccule and utricle (termed maculae). The hair cells of the semicircular canals are covered by a gelatinous mass (termed the cupula) into which the stereocilia embed. Angular head movement induces the endolymph within the canals to flow, displacing the gelatinous mass, which in turn deflects the hair cell stereocilia. The utricle and saccule also have a gelatinous covering over hair cells in their maculae. Calcium carbonate crystals, embedded in the gelatin, rest on the stereocilia. Linear acceleration causes the crystals to deform the gelatinous mass, thereby deflecting the stereocilia. The saccule and utricle are sometimes called the otolith organs because otolith is the term for the calcium carbonate crystals. The semicircular canals, utricle, and saccule each have a different orientation with respect to the head, thereby conferring selective sensitivity to head movement in different directions. Benign positional vertigo is a condition in which calcium carbonate crystals move freely within the semicircular canals. Changing head position causes the crystals to stimulate the hair cells aberrantly, thereby causing vertigo.
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Vestibular hair cells are innervated by the peripheral processes of vestibular bipolar neurons, the cell bodies of which are located in the vestibular ganglion. The central processes of these bipolar neurons, which form the vestibular division of cranial nerve VIII, course along with the cochlear division and enter the brain stem at the lateral pontomedullary junction (see Figure AI–6). Some vestibular axons project directly to the cerebellum (see Chapter 13). In fact, the vestibular sensory neurons are the only primary sensory neurons that have this privileged access to the cerebellum because of the special role of the vestibular system in controlling eye, limb, and trunk movements.
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The Vestibular Nuclei Have Functionally Diverse Projections
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The vestibular nuclei (Figure 12–10) occupy the floor of the fourth ventricle in the dorsolateral medulla and pons (Figure 12–2). This region is termed the cerebellopontine angle. The posterior inferior cerebellar artery (PICA) supplies blood to the vestibular nuclei (see Chapter 4). Occlusion of this artery can produce vertigo, an illusion of movement—typically whirling—of the patient or his or her surroundings. The vestibular nuclei have extensive intrinsic interconnections with components of the nuclear complex on the same and opposite sides that are important in the basic processing of vestibular signals. The lateral vestibular nucleus (also termed Deiters' nucleus) gives rise to the lateral vestibulospinal tract, important in maintaining balance. The medial vestibular nucleus, with a lesser contribution from the superior and inferior vestibular nuclei, gives rise to the medial vestibulospinal tract, for head and neck control. The inferior, superior, and medial, but less so the lateral, vestibular nuclei also give rise to bilateral ascending projections to the thalamus. The vestibular nuclei also participate in the reflex stabilization of eye movements, the vestibuloocular reflex (Figure 12–6). Vestibular axons projecting to the extraocular motor nuclei travel in the MLF (Figures 12–10 and 12–11). Together with the cerebellum, the vestibular nuclei help to organize a blood pressor response to changes in gravity forces acting on the circulatory system.
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The Extraocular Motor Nuclei Are Located Adjacent to the MLF in the Pons and Midbrain
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The MLF is a myelinated pathway that runs close to the midline and beneath the fourth ventricle and cerebral aqueduct, throughout most of the brain stem. In the pons and medulla, it is closely associated with the extraocular motor nuclei: the abducens, trochlear, and oculomotor nuclei. The rostrocaudal course of the MLF can be seen on a parasagittal myelin-stained section close to the midline (Figure 12–11A2).
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Lesion of the oculomotor nucleus produces a down and out eye position
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The oculomotor nucleus (Figure 12–11B1) innervates the medial, inferior, and superior rectus muscles; the inferior oblique muscle; and the levator palpebrae superioris muscle, an eyelid elevator. The motor axons run in the oculomotor nerve, coursing through the red nucleus and basis pedunculi en route to exiting into the interpeduncular fossa (Figure 12–12B). Oculomotor nerve damage produces a "down and out" resting eye position ipsilaterally, resulting from the unopposed actions of the lateral rectus muscle (producing the outward position) and the superior oblique muscle (producing the downward position).
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There are three other important eye movement control centers in the midbrain. The first is the superior colliculus, essential for controlling saccadic eye movements (Figure 12–11B1). Receiving inputs directly from cortical eye movement control centers in the parietal and frontal lobes (Figure 12–7A), neurons in the deep layers of the superior colliculus project to the paramedian pontine reticular formation in the pons (for controlling horizontal saccades) and to the interstitial nucleus of the MLF (Figures 12–11B1 and 12–12A), the second midbrain control center. This nucleus organizes vertical eye movements through its connections with the oculomotor and trochlear nuclei. The third integrative center is the interstitial nucleus of Cajal (see Figure AII–15). This nucleus helps to coordinate eye and head movements, especially vertical and torsional movements. This nucleus contains neurons that project axons to the spinal cord (termed the interstitiospinal tract), for axial muscle control, and to the contralateral interstitial nucleus of Cajal (via the posterior commissure), for coordinating eye and axial muscle control bilaterally.
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Knowledge of regional midbrain anatomy is clinically important because damage of the ventral midbrain produces a complex set of neurological deficits that disrupt eye movement control, facial muscle function, and limb movements. Branches of the posterior cerebral artery supply the ventral midbrain, and when these branches become occluded, the oculomotor nucleus, the third nerve, and the basis pedunculi are affected. In addition to producing the "down and out" eye position because of third nerve involvement, this damage results in limb and lower facial muscle weakness on the contralateral side because of involvement of the corticospinal and corticobulbar tracts in the basis pedunculi. Limb tremor can also occur due to damage of the red nucleus (see Figure 10–11) and nearby axons that connect the red nucleus and the cerebellum.
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The trochlear nucleus is located in the caudal midbrain
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Trochlear motor neurons, found in the trochlear nucleus (Figure 12–11B2), innervate the superior oblique muscle contralateral to its origin. The nucleus is located in the caudal midbrain at the level of the inferior colliculus, nested within the MLF. Trochlear motor axons course caudally along the lateral margin of the cerebral aqueduct and fourth ventricle, in the periaqueductal gray matter. The axons decussate in the rostral pons (Figure 12–5A), dorsal to the cerebral aqueduct, and emerge from the dorsal brain stem surface (Figure 12–5B). Lesion of the trochlear nerve paralyzes the superior oblique muscle, resulting in slight outward rotation of the eye (or extortion) because of the unopposed action of the inferior oblique muscle. The eye elevates slightly because of the unopposed action of the superior rectus muscle. A patient with this lesion compensates by tilting his or her head away from the side of the paralyzed muscle.
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The abducens nucleus is located in the pons
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The abducens nucleus (Figure 12–11B4) contains the motor neurons that innervate the lateral rectus muscle. The nucleus is located just beneath the floor of the fourth ventricle and is partially encircled by facial motor axons on their way to the periphery (Figure 12–10A, inset). The abducens nerve fibers course toward the ventral brain stem surface and exit the pons at the pontomedullary junction, medial to the facial nerve. Lesion of the abducens nerve paralyzes the ipsilateral lateral rectus muscle and results in the inability to abduct that eye.
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Parasympathetic Neurons in the Midbrain Regulate Pupil Size
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The Edinger-Westphal nucleus mediates two reflexes: pupil constriction in response to light and pupil constriction together with lens accommodation in response to near focusing. The pupillary light reflex is the constriction of the pupil that occurs when light hits the retina. Visual input from the retina passes, via the brachium of superior colliculus, directly to the pretectal nuclei (Figure 12–12). The pretectal nuclei project bilaterally to the Edinger-Westphal nucleus, which contains parasympathetic preganglionic neurons; pretectal axons cross to the contralateral side in the posterior commissure. Axons from the Edinger-Westphal nucleus travel with the oculomotor fibers in their path to synapse in the ciliary ganglion in the periphery. From there, postganglionic neurons innervate the constrictor muscles of the iris. The bilateral projection of pretectal neurons to the parasympathetic preganglionic neurons in the Edinger-Westphal nucleus ensures that illumination of one eye causes constriction of the pupil on the ipsilateral side (direct response in the lighted eye) as well as on the contralateral side (consensual response). Pupillary reflexes are an important component of assessing brain stem function during clinical examination, including examination of the comatose patient.
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Pupillary dilation is mediated either by inhibition of the circuit for pupillary constriction or by the separate control of the iris by the sympathetic component of the autonomic nervous system (see Chapter 15). The pupillary dialator fibers join the third nerve close to the eye. As a consequence of this organization, damage to exiting fibers of the third nerve, such as by occlusion of a branch of the posterior cerebral artery, will spare the dilator fibers. Such a lesion produces pupillary dilation because of the unopposed action of the pupillary dilator fibers of the sympathetic nervous system, which are spared by the lesion.
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Parasympathetic preganglionic neurons in the Edinger-Westphal nucleus of the midbrain participate in a second visual reflex, the accommodation reflex, which is the increase in lens curvature that occurs during near vision. This reflex is usually part of the accommodation-convergence reaction, a complex response that prepares the eyes for near vision by increasing lens curvature, constricting the pupils, and coordinating convergence of the eyes. These responses involve the integrated actions of the visual areas of the occipital lobe, along with motor neurons in the oculomotor nucleus that innervate the extraocular muscles and parasympathetic preganglionic neurons. Central nervous system pathology can distinguish different components of the visual reflexes. For example, in neurosyphilis the accommodation reaction is preserved but the light reflex is impaired. Patients with this condition have a classic neurological sign, the Argyll Robertson pupils: Their pupils are small and unreactive to light but get smaller when the patients accommodate. Distinct portions of the midbrain are supplied by paramedian, short circumferential, and long circumferential branches of the posterior cerebral artery (see Figure 4–4B1).
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The action of levator palpebrae superioris muscle, an eyelid elevator, is assisted by the tarsal muscle, a smooth muscle under sympathetic nervous system control. Conditions that impair the functions of the sympathetic nervous system (see Chapter 15) can produce a mild drooping of the eyelid (pseudoptosis) resulting from weakness of the tarsal muscle. True ptosis is produced by weakness of the levator palpebrae muscle, the principal eyelid elevator. This effect can result from third nerve lesions or neuromuscular diseases, such as myasthenia gravis, an autoimmune disease that attacks the neuromuscular junction.
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Eye Movement Control Involves the Integrated Functions of Many Brain Stem Structures
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As discussed earlier, horizontal eye movements are controlled by signals from the frontal eye fields and superior colliculus to the paramedian pontine reticular formation that coordinate the actions of the lateral and medial rectus muscles. These circuits are well understood, so much so that lesions at different sites explain deficit horizontal eye movement control in humans (Figure 12–13). A lesion of the abducens nerve produces paralysis of the ipsilateral lateral rectus muscle, thereby preventing ocular abduction on the same side (Figure 12–13, lesion 1). The unopposed action of the medial rectus muscle can sometimes cause the affected eye to be adducted at rest (not shown in the figure).
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Deficits after an abducens nerve lesion differ from those after a lesion of the abducens nucleus (Figure 12–13, lesion 2). As with the nerve lesion, the ipsilateral eye cannot be abducted because of destruction of the lateral rectus motor neurons. Here, too, the resting position of the eye may be adducted because of the unopposed action of the medial rectus muscle. The nuclear lesion has a second effect: The patient cannot contract the contralateral medial rectus muscle on horizontal gaze in the same direction as the side of the lesion. Hence, the patient cannot gaze to the lesion side. This is called lateral gaze palsy, and it occurs because the lesion also destroys the internuclear neurons that coordinate the lateral and medial rectus muscles (Figure 12–7B).
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A more rostral lesion of the MLF, which spares the lateral rectus motor neurons but damages the axons of the internuclear neurons, produces internuclear ophthalmoplegia (Figure 12–13, lesion 3; at level of the pons in Figure 12–11B3). This lesion is characterized, on lateral gaze away from the side of the MLF lesion, by the lack of (or reduced) ability to contract the ipsilateral medial rectus muscle and thereby adduct that eye.
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For lesions at sites 2 and 3 (Figure 12–13), a clever way to verify that the affected medial rectus muscle is not paralyzed is to demonstrate that the patient can converge both eyes to view an object at close distance. This eye movement requires activation of both medial rectus muscles. The neural mechanisms that coordinate convergence involve the visual cortex and midbrain integrative centers, not the internuclear cells of the abducens nucleus.
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The Ventral Posterior Nucleus of the Thalamus Transmits Vestibular Information to the Parietal and Insular Cortical Areas
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The vestibular nuclei project bilaterally to the thalamus. This ascending projection originates primarily from the medial, inferior, and superior vestibular nuclei. Unlike the auditory and somatic sensory systems, there is no single tract through which the ascending vestibular projection travels. Some fibers travel in the MLF, some in the lateral lemniscus, and others scattered in the brain stem gray matter. The principal thalamic target of the ascending vestibular projection is the ventral posterior nucleus (Figures 12–2, 12–3B, and 12–14). Although this nucleus is familiar as a somatic sensory relay, it serves other functions. The rostral region of the nucleus, adjacent to the ventral lateral nucleus (for motor control; see Chapter 10), receives vestibular input and projects to area 3a of the somatic sensory cortex, to integrate proprioceptive vestibular information. More dorsal and posterior parts of the nucleus, and adjoining nuclei, also receive vestibular information but project to the posterior parietal lobe and the retroinsular cortex, a region near the posterior end of the lateral fissure (Figure 12–14). There does not seem to be a single "primary" vestibular cortex, like some of the other sensory modalities. Rather, the vestibular cortical areas are interconnected to form a network that integrates vestibular inputs with joint proprioceptive information such as posture, orientation, and perception (eg, acceleration, vertigo). Many of these areas have descending projections to the vestibular nuclei, which, in turn, project to the spinal cord for controlling axial and proximal muscles. The organization of this system—corticovestibulospinal—is similar to the indirect corticospinal pathways from the frontal motor areas (see Figure 10–2).
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Multiple Areas of the Cerebral Cortex Function in Eye Movement Control
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Eye movements are not controlled by the primary motor cortex but rather by multiple regions in the frontal and parietal lobes. The frontal eye fields, corresponding to a portion of area 8, are the principal frontal lobe regions engaged in circuits for both saccadic and smooth pursuit movements (Figures 12–7 and 12–8). Two other frontal lobe areas contain neurons important for saccadic eye movements, the supplementary eye fields and the dorsolateral prefrontal cortex (Figure 12–14B). The frontal lobe eye movement control centers work together with neurons in the caudate nucleus (Figure 12–14A), a component of the basal ganglia (see Chapter 14). The parietal lobe site important for saccadic eye movements is located in area 7. This region receives visual information from the "where" pathway (see Figures 7–15 and 7–16). Two nearby areas, the middle temporal and middle superior temporal, which are also part of the where pathway, transmit visual information for guiding pursuit movements.