Basic Design, Development: the rhombomeres
cranial nerve nuclei, ascending and descending nerve tracts, reticular formation
Cranial Nerve Nuclei:
motor: somatic efferents (dorsomedial), special visceral efferent (branchiomotor), general visceral efferent;
sensory: general somatic afferents, general visceral afferent, special visceral afferents, special somatic afferents
Singly monosynaptic reflex: myotatic reflex of the masicatory muscles
Nuclei Associated with the Cerebellum:
nuclei pontis, inferior olive, lateral reticular nucleus
1) median/paramedian group extends through the entire length of the brainstem: the raphe nuclei
2) medial gigantocellular nuclei extends through the pontomedullary tegmentum, lateral to the raphe nuclei, upward: n. reticularis tegmenti pontis oralis and caudalis, n. cuneiformis, n. locus coeruleus, dorsal and deep tegmental nuclei, midbrain periaqueductal gray (PAG)
3) lateral nuclei extend from the medullocervical region into the midbrain, just lateral to the magnocellular group: The midbrain also contain the interpeduncular nucleus. Other nuclei : lateral and medial parabrachial nuclei, nucleus tegmentalis pedunculopontinus
4) specialized regions of the RF: periaqueductal gray; serotoninergic (B1-B6); noradrenergic (A1-A7); dopaminergic (A8-A9); adrenergic (C1-C3) cholinergic (Ch5-6) groups; parabrachial nuclei; autonomic regulatory centers
††††††††††† Recent studies have conclusively shown that the† precursur cells in the brainstem are arranged in an axially repeated set of similar modules (rhombomeres). The rhombomeres, a series of eight subdivisions that partition the hindbrain neuroepithelium, are true metameric units that play a crucial role in patterning this region, thus that specialization of cell type and pattern can be generated as local variations on the repetetive theme. Namely, several investigators noticed that combination of certain genes are expressed in banded patterns in the developing chick NS, especially in the hindbrain. These genes were called hoemotic genes because they were able to convert segments one one sort to those of another. The homebox, is a 180-base-pair DNA sequence that is common to the homeotic genes in the fruit fly. The homebox encodes of 60 amino acids, called the homeodomain, that forms the part of proteins that binds to specific segments of DNA. These specific binding mechanisms regulate where and when genes are "turned on" in the developing embryo. A gene which is turned on in a particular part of the body is said to be expressed there. Consistent with their serving a similar function in vertebrates, the homologs of these genes, the Hox family of homebox genes, retain a clustered chromosomal organization in which the relative position of a gene in the cluster reflects its boundary of expression along the A/P axis (principle of colinearity). These genes were all products of gene duplications at different times in the evolutionary past and were derived ultimately from a primordial gene in the common ancestor.
††††††††††† The overlapping distribution of Hox gene transcripts in the hindbrain region suggests that their proteins may act in a combinatorial manner to set the positional value of individual rhombomeres and thereby control their identity and phenotypic specializations. Loss of function mutations of rostrally expressed Hox genes in mice may result in malformations that are consistent with transformation of regional identity. In the Hoxb-1 knockout mouse, for example, r4 (where the gene is normally expressed at high level) loses its r4 specific characters and takes on those of r2, r6 and other rhombomeres where the gene is not normally expressed.
††††††††††† The expression of the homeobox genes in the hindbrain is controlled by the concentration of a chemical signal, retinoic acid (RA). Retinoic acid is the biologically active from of vitamin A.† RA exerts its effect on development by controlling target gene transcription via multiple types of RA receptors, members of the nuclear receptor superfamily. RA-bound receptors are transcription factors that binds as homo or heterodimers to RA response elements in the promoters of target genes. The most anteriorly expressed homebox gene in the hindbrain is the most sensitive to RA, and the sensitivity decreases in a stepwise fashion toward the spinal cord. Thus, the genes are turned on from anterior to posterior in a stepwise fashion as the concentration of RA is increased. The experimental application of RA in the developing embryo has the effect of advancing the expression of particular homebox genes and transforming anterior rhombomeres into the pattern normally found more posteriorly. RA has a similar role in the developing eye as well as in the limbs. Becuase RA is a morphogen the ingestion of excessive amounts of vitamin A by pregnant woman can alter the development of the fetus and produce severe birth defects. Hensen's node and the isthmus region is a rich source of retinoids, and node-derived RA may act as a morphogen conferring positional information on cells at different A/P positions by differently regulating Hox expression.
Neural crest, branchial arches, Pax genes
††††††††††††††† The spinal nerves that form a ladder-like array on either side of the spinal cord are an obvious manifestation of segmentation. But here, in contrast to the intrinsic patterning mechanism that operates in the hindbrain, the segmentation process is under the direct control of the paraxial mesoderm. The segmental pattern of dorsal root ganglia and ventral root nerves is imposed by a serially reitarated asymmetry in the sclorotomal component of the somites. Despite extensive searches, no segmental patterns of neuronal differeniation or clear evidence of cell lineage restriction along the A/P axis of the spinal cord has been found in higher vertebrates.
††††††††††† The cranial mesoderm of the avian embryo is not organized into segmental blocks; yet there is obvious segmentation of the cranial sensory ganglia. In the head ectodermal placods contribute neurons to sensory ganglia, whereas the neural crest contribute both neurons, glia, the parasympathetic ganglai and the bulk of skeletal connective tissue; it also has an important role in patterning mesoderm-derived muscle cells.
††††††††††† The Hox genes, expressed in the premigratory neural crest populations in their parent rhombomeres, may also confer identity on neural crest cells, which would then migrate from the neural tube in an orderly and predictable way, carrying preassigned positional information into the apropriate arch. The combinatorial expression of Hox genes, a Hox code, could control the morphogenetic program for patterning the branchial arches. Consitent with this idea, rhombencephalic crest cells emigrate from discrete segmental levels of the avian hindbrain; the crest cells from r1 and r2 migrate into the first (mandibular) arch, from r4 into the second (hyoid) arch, and from r6 and r7 into the third arch, whereas the premigratory crest is massively depleted in the intervening rhombomeres, r3 and r5, by apoptosis.
††††††††††† †Pax genes encode positional value on the D/V axis in much the same way as Hox genes on the A/P axis, but here the positional signal that could direct Pax gene expression is unknown.
In the pons and medulla, approximately the medial two-thirds of the RF consists of many large cells, in part so called giant cells. The lateral one-third contains almost exclusively small cells. Tract-tracing methods have shown that the medial parts send out many long ascending and descending fibers, whereas the lateral small-celled part receives most of the afferents coming to the RF.
††††††††††† Studies with the Golgi method give evidence of how complexly the RF is organized. The long ascending and descending efferent fibers give off numerous collaterals on their way through the brainstem. The collaterals run primarily in the transverse plane. Most dendrites of reticular cells have the same preferential orientation, so that the RF may be described as consisting of numerous transversely oriented disks. In fact, it was the Golgi studies of the Scheibels (1958) in which the fundamental (stacked-discs) principle of the entire neuraxis was recognized.
††††††††††† Efferents. The RF sends fibers to four main regions: thalamus, spinal cord, brainstem nuclei and the cerebellum. The descending reticular fibers end primarily on interneurons, which in turn can influence motorneurons. This is both crossed and uncrossed system and via the connection of the tectum the tecto-reticular-spinal pathway is of particular importance for postural mechanisms, for the orientation of the head and body toward external stimuli and for voluntary movements of proximal body parts.
††††††††††† The ascending fibers from the RF end in the intralaminar thalamic nuclei.† Some fibers also end in the hypothalamus. The ascending reticular connections are of particular importance for the general level of activity of the cerebral cortex.
††††††††††† Afferents. Spinoreticular fibers. They ascend in the ventral part of the lateral funciculus together with the spinothalamic tract, but diverge in the lower medulla.† Among other destinations, the fibers and in the parts of the RF giving off long ascending axons to the thalamus. This provides a spinoreticulothalamic pathway that is anatomically and functionally different from major sensory pathways. Some of the spinoreticular fibers end in areas where neurons send axons back to the spinal cord, thus establishing feedback loops between RF and the spinal cord.
††††††††††† Corticoreticular fibers arise mainly in the cortical areas that give origin to teh pyramidal tract. They end mainly in the region of the RF sending axons to the spinal cord. Therefore, a cortico-reticulo-spinal pathway exist. It is known to be of importance for the control of voluntary and autonomic movements.
††††††††††† Fibers from the superior colliculus makes it possible for integrated somatosensory and visual information to influence the RF.
††††††††††† In addition to spinal neurons that send their axons only to the RF, many secondary sensory neurons send colaterals to the RF.
††††††††††† Fibers from the hypothalamus ending in parts of the RF serve to coordinate the activity of different peripheral parts of the autonomic NS. Fibers from the basal ganglia (substantia nigra) send fibers tio the mesencephalic locomotor region. Limbic structures, notably the amygdala, also send fibers to the RF. Such connections probaly mediate emotional effects on autonomic and somatomotor functions. Fibers from the PAG is related to defensive reactions. Finally, the RF receive fibers from the cerebellum, via which the cerebellum influences the alpha and gamma neurons.
1)somatomotor control: postural reflexes, muscle tone (reticulospinal, corulospinal tracts) voluntary and reflex eye movements, including vestibulo-ocular refelex arc, orienting movements of the head and body in response to vestibular and optic stimuli. Premotor networks.†
2)somatosensory control: sensory gating mechanism (e.g. pain)
3)viscero-motor control: reflexes of the gastrointestinal, respiratory and urogenital tracts (upper gastroint. and resp. reflexes: cougphing, sneezing, swallowing, vomiting, hiccuping, chewing, sucking, swallowing, salivation)
4)homeostatic functions: cardiovascular, electrolytic balance
5)breathing (volational, emotional and homeostatic [O2/CO2)components])
7)organized behavior functions: various columns in PAG organizing defensive, reproductive (lordosis) behaviors,
Action on skeletal muscles. Early experiments led to the identoification of two regions within th eRF than influence the tone of the skel;etal muscles. Stimualtion of a region in the medulla† that sends particularly strong connections to the spinal cord could inhibit stretch reflexes. Thi sregion was called the inhibitory region. A region with opposite effects, the facilitatory region, wa sfound rostral to the inhibitory one. It extends rostrally into the mesencephalon and is located somewhat more laterally than the inhibitory region. The action is exeretd both via the alpha and gamma motorneurons. Since the cerebral cortex, the cerebellum, the basal ganglia send fibers to the RF, it is not unexpected that muscle tone can be influenced from these parts as well. It should be recalled, however, that other than the RF have direct access to the motorneurons, notably the vestibular nuclei with their strong facilitatoryt effects on muscle tone.
††††††††††††††† In addition to the rather diffuse effects on miuscle tone, present studies emphasizes the role of RF in control of more specific motor tasks (rhytmic locomotor movements, premotor networks)†††††††
Respiration. The early invetigations with stimulation of the RF indicated that inspiratory movements are evoked from a region that coincides roughly with inhibitory region. Expiratory movements were produced by stimulation within the facilitatory region in the medulla. Later studies with microelectrodes have shown, however, that neurons with respiratory movement related activity are found in several regions of the RF, and not only in the medulla. Furthermore, a clear-cut separation of an inspiratory and an expiratory region appears not to be tenable. The current view is that respiration is controlled by a network formed by several cell groups in the RF of the ventrolateral medulla. The neurons of the network change their activity in relation to specific phases of the breathing rhythm. This network has properties in common with other rhythm generators, for example those producing locomotor movements.
Longitudinal Organization of Cranial Nerve Nuclei
††††††††††† The specific sensory and motor (also vegetative) nuclei of the cranial nerves are subdivided into separate entities in the brainstem, but the continuity of sensory and motor columns can still be recognized and traced upward until the mesencephalon.
††††††††††† A fundamental change of the design occured with the appearance in the lower brainstem of larger nuclear masses connecting the longitudinal arrangement of the neuraxis with higher centers, notably the cerebellum and the tectum, which have developed, even in very early stages of vertebrate phylogeny, for auxilliary (althogh very highly specialized) and essential functions. The two main nuclear formations for conenctions with these higher centers are the inferior olive and the nuclei of the pons.
††††††††††† According to the traditional view, two main groups of somatomotor nuclei can be separated, both arranged more or less in a column of individual nuclei that are interrupted in stringlike fashion. The so called dorsomedial column consists in the caudocranial direction of the hypoglossus, the abducens, the trochlear, and the oculomotor nuclei. The position of the nuclei and the courses of the axons remain fairly stable in the phylogeny of the vertebrates. The ventrolateral column is built of the branchial motor nuclei, in caudocranial direction of the accessorius, vagus, glossopharyngeus, facial and trigeminal nucleus.† The position of thes nuclei, the shape and dendritic arborization pattern of their motorneurons, and the initial courses of their axons, are subject to major changes during the phylogenesis from amphibia to the mammalians.
Sensory Components of the Cranial Nerves
V. Trigeminal. General somatic afferent component:
††††††††††† From the face and scalp as far as the top of the head, conjunctiva, bulb of the eye, mucous membranes of paranasal sinuses, and nasal and oral cavities including tongue and teeth, part of the external aspect of the tympanic membrane.
††††††††††† The trigeminal sensory fibres enter into nucleus of the spinal tract of the trigeminal nerve and the pontine trigeminal nucleus. The former nucleus is thought to be concerned primarily with the perception of pain, temperature and some tactile information. The main tactile nucleus is the pontine trigeminal nucleus†
††††††††††† Axons of secondary neurons project to a variety of targets in the brain. Principal targets are the reticular formation, and the sensory cortex via the crossed ventral trigeminothalamic tract. A small ipsilateral projection reaches the ipsilateral thalamus. Tertiary neurons in the thalamus project through the internal capsule to the lower third of the postcentral gyrus of the ipsilateral cerebral cortex.
VII. Facial. Special sensory afferents from the anterior two third of the tongue and the hard and soft palates carry taste afferents. Peripheral processes of these cells for taste run with the lingual nerve and then separate from it to join the chorda tympani. The cell bodies of the special sensory neurons for taste are located in the geniculate ganglion. From the ganglion fibres enter the brainstem to terminate in the rostral part of the nucleus tractus solitarius. Ascending sensory fibers from this nucleus project bilaterally via the central tegmental tract to reach the ipsilateral and contralateral ventral posterior nuclei of the thalamic. Axons of thalamic† (tertiary) neurons then project through the posterior limb of the internal capsule to cortical area of taste (insular cortex)
IX. Glossopharyngeus. General Somatic afferent (pain, temperature, touch, pressure). Provides general sensation from the posterior one-third of the tongue, upper pharynx. Cell bodies: superior and inferior glossopharyngeal ganglia. The central processes for pain descend in the spinal trigeminal tract to end on the caudal part of this nucleus. From here axons of secondary neurons end in the contralateral VP of the thalamus.
Special sensory for taste from the posterior third of the tongue. Cell bodies: inferior glossopharyngeal ganglion. Central processes of these neurons enter the medulla to terminate in the rostral part of the solitary nucleus.
X. Vagus. Visceral afferents from the larynx, trachea, base of the tongue, aryepiglottic folds, travels in the internal laryngeal nerve. Below the vocal folds, visceral sensation (esophagus, lungs, chemoreceptors [blood oxygen tension] in the aortic bodies adjacent to the arch) is carried in the recurrent laryngeal nerves. Cell bodies: inferior vagal ganglion. Axons enter the caudal nucleus tractus solitarius.
General somatic afferents from larynx, pharynx, external surface of the tympanic membrane. Cell bodies: both superior and inferior vagal ganglion. These fibers end in the descending spinal trigeminal nucleus.
In summary, the general somatosensory fibers from these territories terminate in the spinal trigeminal nucleus, while the viscerosensory and special sensory (taste) and the aortiic chemoreceptors (blood O2 tension) send their terminals to the nucleus tr, solitarius (NTS).
Stabilizing the retina with regard to the outside world and aligning the retina with moving or stationary targets is a critical challenge to effective vision. Effective retinal stabilization is achieved by gaze stabilization and gaze shifting. The former is found in all animals with visual systems, but the latter is found only in primates with foveal specialization.
Gaze Stabilization Mechanisms
Gaze stabilization mechanisms fall into two subclasses: the vestibulo-ocular and the optokinetic systems.† The vestibulo-ocular (VOR) system relies on the semicircular canals to determine the precise rate at which the head is rotated in any direction. The optokinetic system relies on information from the photoreceptors themselves to compute the speed and direction at which the visual world is shifting across the retina. The vestibulo-ocular system is most efficient at higher speed of rotation, where the vestibular apparatus most accurately measures head velocity. In contrast, the optokinetic system operates most efficiently at low speed of rotation, where the photoreceptors accurately determine the speed and direction of image motion. Both systems compensate by activating the extraocular muscles. The result is that the line of sight remains constant with respect to the environment, despite movement of the head.
The extremely precise cooperation among the individual ocular muscles that moves the eye in various diirection requires a close interrelationship among all nuclei of the nerves† in charge of the ocular movements. Such intimate connections are provided by the medial longitudinal fascicle, which runs bilaterally paralell to the midline from the tegmentum of the midbrain down to the cervical cord. It interconnects the nuclei of the motor nerves of the eye muscles. It also receives impulses from the cervical cord (anterior and posterior neck muscles), from the vestibular nuclei, and the reticular formation controlling pontine and midbrain gaze centers, the cerebral cortex and the basal ganglia. The eyes can be moved both voluntarily and by reflex. They can, however, move only jointly (conjugately). In whatever direction the eyes move, all eye muscles participate, in part by increasing muscular tension (agonists), in part by relaxation (anatagonists).
The vestibulo-ocular reflex. The VOR is the neuronal system by which rotations of the head are detected by the semicircular canals of the vestibular organs, and the eyes are counterrotated in their sockets an equal amount in the opposite direction to stabilize the line of vision. This reflex is in constant use. Whenever you walk, for example, the VOR is engaged, compensating for the small visually disruptive movement of the head that are produced during locomotion.
††††††††††† To compensate for head rotation, the VOR rotates the eyes. If the head continues to rotate, of course, the eyes cannot continue to counter rotate without being pointed backward in the orbit. To overcome this limitation, the eye is often reset to a central position in the orbit during a vestibular eye movement. After this resetting is complete, the compensatory counter rotation resumes. The compensatory movements and the† quick resetting mechanism constitute the two phases of the† VOR. This characteristic pattern of alternating quick and slow phases during sustained rotation is called nystagmus. A leftward nystagmus is one in which the quick phase shift gaze to the left. Note that only the slow phase compensates for head rotation; the quick phase simply returns the eye to the center of the orbit.
The optokinetic system. Like the VOR, the optokinetic system activates the oculomotor musculature to stabilize gaze during rotation of the head. Unlike, the VOR, however, the optokinetic system uses visual information, extracting from the global pattern of visual stimulation a measure of how fast and in what direction the visual world is moving across the retina. This movement is called the retinal slip. Like the VOR, the optokinetic system produces nystagmus: a slow phase, during which the eyes compensate for movement of the visual world, is followed by a quick phase that moves the eyes back from the limits of their orbital rotation to a more central position. Pretectal neurons encode the velocity and direction of retinal slip. They project directly to the vestibular nuclei via the pontine and medullary relays. In fact, many vestibular neurons can be activated by both vestibular and visual stimuli, suggesting that the two types of stimuli access a common circuitry for eye velocity control. This common motor circuitry may also integrate the optokinetic velocity signals to calculate the static force necessary to hold the eye at its new position.
Gaze-shifting mechanisms can be divided into the main groups: saccadic systems, which rapidly shifts gaze from one point to another and the smooth pursuit system, which allows the fovea to track a moving target as it slides across a stationary background. The saccadic and smooth pursuit system together are often referred to as versional systems.
Saccadic movements. Saccades are conjugated movements that change the optical axis of the eye (line of gaze) from one point of fixation to another with maximal speed. Saccades can be voluntary, as when we look at a stationary landscape and fix the gaze at one point of a moment, and then move on to another point of fixation. Saccades can also be reflex, as with vestibular or optokinetic nystagmus. When awake, we perfrom saccades all the time, often several per second. The saccadic system uses visual, somatosensory, and auditory information to compute the eye rotation necessary to align the line of gaze with a visual target. The system controlling† the saccades are composed of the neurons of the pontine gaze center in the paramedian reticular formation (burst and omnipause neurons), neurons in the nucleus prepositus hypoglossus, and neurons of the superior colliculus and the frontal eye field. Higher level saccadic system include also the parietal cortex, the basal ganglia and the cerebellum. Saccadic eye movements become inaccurate and uncoordinated following damage to the cerebellum; they overshoot or undershoot the target, and multiple saccades are necessary to fixate a novel† target. In Parkinsonís disease, the increase of activity of nigral reticular neurons lead to decrease of activity of collicular burst neurons which cause paucity of eye movements and increase in their latency.
Smooth pursuit movements.. If attention is paid to a visual object, its images are fused in both eyes in the area of greatest acuity. Regardless in which direction the object moves, its image is always kept in both foveas by finely tuned sequences of movements. As the images leave the foveas, messages are sent by the retinas via the visual pathways to the calcarine cortices and from here via the occipitotectal fibers to the nuclei of the ocular motor nerves. The result is that the images are brought back into the foveas by the optokinetic process. In this process the eyes perform a jerking movements. Such nystagmus occurs when one is looking out of a moving train or experimentally, when one focuses on a slowly turning cylinder displaying alternating black and white stripes. The jerks of the eyes occur in a direction opposite to the movement of the gaze. The circuitry of the Spm is less well understood. It is suggested that the nucleus prepositus hypoglossi, the cerebellum, the dorsolateral pontine nucleus, the vestibular nuclei are involved. Signals that indicate target motion appears to be provided to the pursuit system by the cortical motion system, which is composed in part of areas MT and MST . These areas compute the direction and speed of moving stimuli throughout the visual field and pass this information to the dorsolateral pontine nucleus directly and via the posterior parietal cortex and the frontal eye fields.
Vergence movements change the visual axes of the eyes in relation to each other when the point of fixation moves away or toward the eyes. This is necessary to keep the image on corresponding points of the retina. Vergence movements are a prerequisite for fusion of the two images and for stereoscopic vision.† Convergence of the optic axes, which takes place when an object is approaching the eyes, depends primarily on the activity of the medial rectus muscles. Convergence movements are accompanied† by acomodation and pupillary constriction.
Fixation reflex. Holding the image of the object in the retinal area of most acute vision is called the fixation reflex. Any object entering the field of vision attracts attention, and vison is involuntarily directed to it. As the object moves, the eye follows involuntarily in an attempt to keep the image of the object continuously in the area of most acutre vision, the fovea of both maculae. If we voluntarily focus on an object of interest, the eye is automatically kept on it, even if we as well as the object of interest moving. Thus, all voluntary eye movements are appended by involuntary reflex movements.
††††††††††††††† The afferent portion of this reflex runs from the retina over the visual pathway to the visual cortex (area 17). from here the impulses are transmitted to areas 18 and 19. The efferent fibers probably originate in these areas and temporarily join the optic radiation on their course to the contralateral mesencephalic and pontine centers of oculomotion. From here they join the corresponding nuclei of the oculomotor nerves. The rest of the fibers make a detour over Brodmann area 8.
††††††††††††††† Special portion of the reticular formation contained in the anterior portion of the midbrain and pons regulate individual direction of vision. The prestitial nucleus in the posterior wall of the third ventricle regulates upward movements; the nucleus of the posterior commissure, dawnward movements; and the interstitial nuclei of Cajal and Darkschewitsch, rotatory eye movements. The pontine centers are involved in conjugate lateral eye movements. ††††††††††††††
Voluntary eye movements are triggered in the frontal eye field of Br area 8, located in front of the precentral gyrus. A conjugate† movement of the eyes toward the opposite side is the most frequent response to stimulation of this teriotory. The movement of the eyes is sometimes accompanied by a movement of the head toward the opposite side. Unilateral destruction of area 8 creates a predominance of the contralateral area, producing a conjugate movement toward the side of the lesion (the patient looks towards the paralysing focus). This deviation abates with time. The situation is reversed with pontine lesions, because the corticopontine pathway† is crossed. A pontine paralysis of gaze is seldom followed by full recovery. The fibers from the area 8 accompany the corticonuclear tract on its way to the internal capsule and cerebral peduncle. They do not terminate directly in the nuclei of the cranial nerves, however. It appears that their impulses arrive at the nuclei via intercalated neurons in the RF and via the mlf.
††††††††††††††† All voluntary movements of the eyes are under the influence of reflex arcs. Some of these afferent arcs belong to the optical and others to the acoustic, vestibular and proprioceptive reflex arcs (originating in the neck muscles and transmitted via the spinotectal tract and the mlf).
††††††††††††††† After unilateral destruction of the frontal eye field, the eyes for a time cannot be turned voluntarily to the opposite side, but such movement is still possible by reflex action. The patient is able to pusue with his eye an object that moves slowly through his field of vision even if he/she is not able to follow its direction voluntarily.
††††††††††††††† In contrast, if the occipital fields are destroyed, the reflex movements of the eyes are abolished. The patient can move his eyes voluntarily in every direction, but he cannot pursue an object. It immediately escapes from the area of highest acuity and must be searched for again by voluntary eye movements.
Convergence, Accomodation, Constriction of† Pupils
Convergence: Both medial rectus muscles become innervated simulatenously, so that the axes of both eyes are directed toward the object. This process places the images of the object precisely on corresponding portions of the retinas, that is on the areas of gretast acuity.
Accomodation. Because of the contraction of the ciliary muscle, the lens relaxes and becomes more rounded. By this mechanism the retinal image of an approaching object is continuously kept in focus. Looking into the distnce relaxes the ciliary muscle, and this produces a flattening of the lens.
Constriction of the pupils. Narrowing of the pupil permits the retinal image of the object to remain sharpley outlined, just as a narrowing of the paerture in a photographic camera increases the sharpness of the object image.
††††††††††††††† All three reactions can be triggered by voluntary fixation on a nearby object. They also take place by reflex if a distant object suddenly approaches. The afferent impulses travel from the retina to the calcarine cortex. From here the efferent impulses proceed over the area pretectalis. Impulses from these nuclear complexes go to the neurons innervating both medial rectus muscles (convergence), the Edinger-Westphal nuclei and from here via the ciliary ganglion to the ciliary muscles (accomodation) and the sphincter pupillae (narrowing of the puplis).
Pupillary Light Reflex
When light falls on the retina, the diameter of the pupil changes. This pupillary light reflex has the same effect as an automatic adjustment of the diaphragm of a photographic camera: it protects the retina and its photoreceptors against exposure to an overdose of light and sharpens the image of a visual object projected on the retina. The reflex arc does not involve cortex. Therefore, the pupillary reactions do not enter the level of consciousness.
††††††††††† The afferent fibers of the reflex arc accompany the optic nerve and tract and leave the tract near the LGB as its medial bundle, which proceed toward the superior colliculi and terminate in the pretectal area. Intercalated neurons connect with the EW nuclei of both sides, causing the light reflex consensual; that is light falling into one eye causes narrowing of the pupil also in the contralateral, unilluminated eye.
††††††††††† The efferent motor fibers originate in the EW nuclei accompany the oculomotor nerve into the orbit. Here the parasympathetic preganglionic fibers become independent and enter the ciliary ganglion, where the impulses are transmitted to short postganglionic fibers. The fibers enter the eye and innervate the sphincter muscle of the pupil.
††††††††††† The sphincter muscle is paralyzed if the ipsilateral oculomotor nerve, preganglionic fibers, or ciliary ganglion is damaged.† As a result, the light reflex is extinguished, and the pupil is dilated because it is now solely under the influence of the sympathetic innervation.† Interruption of the afferent fibers along the course of the optic nerve abolishes the light reflex in both the ipsilateral and the contralateral eye, because the consensual reaction is interrupted. If in such a case the contralateral eye is exposed to light, however, the light reflex functions bilaterally.
††††††††††† The width of the pupil is not controlled only by light reflex; extraocular stimuli may have an influence. Severe pain, partiularly pain involving the musculature in the neck, and strong emotional recations may produce a widening of the pupils. It has been assumed that this kind of mydriasis result from a predominance of sympathetic impulses that cause contraction of the dilator muscle of the pupil.
Sympathetic Innervation of the Eye
The area of the sympathetic nuclei (ciliospinal center), is located in the lateral horn of the spinal gray matter of C8-T2. From here preganglionic fibers ascend to the superior cervical ganglion, from which postganglionic fibers emerge. The postganglionic fibers adjoin the internal carotid artery and accompany it up to the level of the orbit. Here, the fibers proceed to the dilator muscle of the pupil. The ciliospinal center may receive indirect light related information via the the retinohypothalamic system and the further descending fibers from the hypothalamus.
††††††††††††††† An interruption of impulses in the ciliospinal center or its efferents produces Horner's syndrome. The sympathetic nerve iinervates the smooth fibers of pupillary dilator, the superior and inferior tarsal and the orbital muscles, and in addition, the sweat glands and the blood vessels of the corresponding half of the face. The symptoms are as follows: 1)narrowing of the palpebral fissure; 2) miosis; 3)enophtalmus and 4)anhydrosis
Protective Blink Reflex
An object suddenly appearing in front of the eyes causes an immediate reflex closure of the lids, or blink reflex. The afferent impulses of the reflex extend from the retina directly to the tectum of the midbrain and proceed from there via the tectonuclear tract to the nuclei of the facial nerves that innervate the orbicularis oculi muscles.
††††††††††† The motor nucleus of the facial nerve is located in the ventrolateral portion of the lower pontine tegmentum near the medulla oblongata. While still in the tegmentum of the pons, the axons of the neurons first proceed toward the floor of the fourth ventricle near the midline, then loop around the abducense nerves (inner knee) and proceed toward the pontocerebellar angles, where they emerge at the pontomedullary junction just in front of the cranial nerve VIII. Within the facial canal the nerve continue up to the level of the geniculate ganglion.† Here the facial canal makes a sharp turn in caudal direction. Because the facial nerve follows the canal, it also makes such a turn, which is called the outer or external knee. At the end of the canal the facial nerve leaves the cranium through the foramen stylomastoideum. From this point the motor fibers spread over the face. The muscles innervated by the VII serve facial expression and are derivatives of the second branchial arch.
††††††††††† The motor nucleus of the facial nerve is part of several reflex arcs. Some related to optical impulses (Corneal, blink reflex). Acoustic impulses reach the nucleus via the dorsal nucleus of the trapezoid body. Depending on the intensity of the noise, this reflex arc produces either relaxation or tension of the stapedius muscle (in the middle ear).
††††††††††† The supranuclear innervation of the forehead musculature is located in both hemispheres, whereas the remaining facial musculature is innervated only from the contralateral precentral gyrus. Consequently, a unilateral interruption of the corticonuclear tract by a lesion, such as an infarct, leaves the innervation of the frontal muscles intact (central paralysis). If however, a lesion involves the nucleus or the peripheral nerve, the entire ispilateral facial nucleus is paralyzed (peripheral paralysis).
††††††††††† The facial nuclei also receive impulses from the thalamus and basal ganglia.† If these or other parts of the extrapyramidal system are diseased, there may be a decrease in or absence of facial expression (hypomimia) as in Parkinson's disease or a hyperkinetic reaction causing a mimetic facial spasm.
††††††††††† The nuclei of the hypoglossal nerves are located in the lower medulla oblongata on either side of the midline and next to the floor of the fourth ventricle, where they produce the hypoglossal trigobne. Developmentally, the neurons are identical to the motorneurons of the spinal anterior horns. The hypoglossal axons proceeds ventrally toward the anterior lateral sulcus between the pyramid and the inferior olive. The nerves leave the cranium through its own canal, the canalis hypoglossi, above the lateral margin of the foramen magnum. Deep within the neck it passes in between the internal jugular vein and the internal carotid artery and is accompanied by fibers of the three upper cervical segments (ansa hypoglossi). These fibers do not unite with the hypoglossal nerve, rather, they soon separate and innervate the muscles of the hyoid bone.
††††††††††† The hypoglossal nerve innervates the muscles of the tongue. Voluntary innervation travels via the corticonuclear tract, which coming from the precentral cortex, accompanies the corticospinal tract on its way through the internal capsule.
††††††††††† The hypoglossus nucleus receives impulse from the conralateral corticonuclear tract. In addition, afferent fibers from the RF, the tectum, from the solitary tract and trigeminal nuclei, subserving swallowing, chewing, sucking and licking.
††††††††††† A unilateral supranuclear interruption of innervation has no major consequences, because the nuclei also receive some ipsilateral impulses, although the extended tongue usually deviates slightly to the paretic side. The two geniglossus muscle move the tongue forward. If one of them weak, the stronger, healthy muscle pushes the tongue to the paretic side. In the presence of hemiplegia there is some initial dysarthria, but no disorder of swallowing (dysphagia). If the supranuclear paralysis is bilateral, tehre is severe impairment of speaking and swallowing (pseudobulbar palsy).† Causes of supranuclear plasy are, among others, hematoma, infarct, tumor. Peripheral hypoglossus lesion is caused by basal fracture of the skull, aneurysm, tumor, and diverse toxic substances (alcohol, etc).
Progressive bulbar paralysis. This syndrome develops in the course of amyotrophic lateral sclerosis and syringobulbia, which is often a rostral extension of cervical syryngomyelia. The underlying pathologic change consists of a degenerative loss of motor nuclei of several cranial nerves, mainly IX-XII. A disorder o speach (dysarthria) is usually the first sign. Soon swallowing becomes impaired (ambiguus nucleus), the tongue develops atrophy with fasciculation, and sign such as nystagmus, ptosis and facial paresis follows.
Pseudobulbar paralysis. This syndrome stems from bilateral interruption of the corticonuclear tracts, most often cuased by cerebral arteriosclerosis. The results is bilateral spastic paresis of the motor cranial nerevs IX-XII. Dominat signs are dysarthria and dysphagia. There is a tendency to forced laughter and crying.
Alternating lesions. The term alternating refers to the fact that the signs of interruption of long tracts alternate with (i.e. are on the opposite side of) the cranial nerve signs. Interruption of a cranial nerve in the brainstem causes ipsilateral LMN paralysis. Interruption of the pyramidal tract, which will decussate, or of a long sensory tract, which has decussated, causes contralateral signs.
Weber syndrome (peduncle of the midbrain): akinesia (substantia nigra, parkinsonism); contralateral spasic hemiplegia (pyramidal tract), contarlateral facial and hypoglossal paralysis (corticonuclear fibers); contralateral ataxia (corticopontine fibers to the cerebellum); ipsilateral oculomotor paralysis with wide fixed pupils.
Dejerine syndrome (medial medullary syndrome): nystagmus (med. long. fascicle); contralateral decrease of touch, vibration and position sensation (medial lemniscus); ipsilateral paralysis of hypoglossal nerve with atrophy (hypoglossal nucleus); contralateral hemiparesi with positive Babinski reflex (pyramidal tract).
Wallenberg (dorsolateral medulla syndrome): nystagmus and ipsilateral inclination to fall (inferior vestibular nucleu); tachycardia and dyspnea (dorsal m. n. X);† ataxia (inferior cerebellar peduncle, ventral spinocerebellar tract); dysphagia, dysarthria (ambiggus nucleus: ipsilateral paralysis of the palata, larynx and pharynx); ipsilateral thermanesthesia of face, loss of corneal reflex (n.sp. n. V.); contralateral hypesthesia for pain and temperature for trunk and extermities (spinothalamic tract); Horner syndrome (central sympathetic pathway: ptosis, myosis, anhydrosis; vasodilatation in face).