Cranial nerves are usually an integral part of any neurological exami- nation; this is certainly the case in injuries and/or diseases that involve the head and neck. This chapter details their exit points (or, one could argue, the entrance points in the case of sensory nerves), their corre- sponding appearance in MRI, and examples of lesions causing deficits of eye movements in the horizontal plane and of brainstem lesions that include cranial nerve deficits.
This is, however, only part of a much larger picture that places cranial nerves in a functional context and views their connections in the periph- ery as well as within the central nervous system. Although these more comprehensive cranial nerve connections, and their corresponding func- tions, are illustrated in Chapter 8 in their appropriate systems context, they are briefly listed here to facilitate cross reference for those users wish- ing to consider cranial nerves in a more integrated format at this point.
The columns of cells within the spinal cord are rostrally con- tinuous with comparable cell columns in the brainstem that have similar functions. For example, general motor cell columns of the spinal cord are continuous with the groups of motor nuclei that inner- vate the tongue and the extraocular muscles; both cell columns inner- vate skeletal muscles. The same is the case for general sensation. Nuclei conveying special senses are found only in the brainstem and are associ- ated with only certain cranial nerves.
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Functional Components of Spinal and Cranial Nerves (see also Figures 6-1 and 6-2 on pp. 96–97)
The trigeminal nerve conveys sensory input from the face and oral cavity and provides motor innervation to the muscles of mastication. The spinal trigeminal tract and nucleus also receive general sensation via CNs VII, IX, and X. In this respect, the spinal trigeminal tract is the center for all general sensory sensations entering the brain- stem on all cranial nerves. In the same sense, the solitary tract and nucleus (Figure 8-9 on pp. 206–207) is the brainstem center for all vis- ceral sensation that enters the brainstem on CNs VII, IX, and X. Both of these cranial nerve brainstem nuclei convey information to the thala- mus and eventually to the cerebral cortex.
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Trigeminal Pathways and Deficits (see also Figures 8-7 and 8-8A, B on pp. 202–205)
The cerebral cortex influences cranial nerve nuclei via corti- conuclear fibers. In the neurological examination, this is most evident when testing motor functions of CNs VII, IX, X, XI, and XII. In many situations, the deficit is seen by the inability of the patient to per- form a movement “against resistance.” Comparing the deficit(s) of a lesion of these fibers to damage of cranial nerves within the brainstem, or the periphery, is essential to localizing the lesion within the central nervous system.
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Corticonuclear Pathways and Deficits (see also
Figures 8-13 and 8-14A, B on pp. 214–217)
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3: Cranial NervesCranial nerve nuclei are either motor to skeletal muscle or visceromotor to ganglia in the periphery. Lesions involving the nuclei, or roots, of motor nuclei result in paralysis of the muscles served, with the predictable deficits, such as weakness of the facial mus- cles or deviation of the tongue on protrusion. Lesions that damage the visceromotor fibers of a cranial nerve result in an expected visceromo- tor response, such as dilation of the pupil, or a decrease in secretory function or smooth muscle motility.
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Cranial Nerve Efferents (III–VII and IX–XII) and Deficits (see also Figures 8-19 to 8-22B on pp. 226–233)
Testing cranial nerve reflexes is a routine part of any com- plete neurological examination. This part of the neurological exam tests the integrity of the afferent and efferent limbs of the reflex.
Sometimes both of these are on the same cranial nerve; sometimes they are on different cranial nerves. In addition, deficits may be seen that reflect damage affecting cranial nerve function, but this damage is not in the afferent or efferent limbs of the reflex; this suggests a broader problem within the central nervous system.
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Cranial Nerve Reflex Pathways and Deficits (see also Figures 8-23 to 8-32 on pp. 234–240)
The pupillary reflex (commonly called the pupillary light reflex) has its afferent limb via the second cranial nerve and its efferent limb via the third cranial nerve. The reaction of the pupil when light is shined in one eye is a clear hint as to the location of the lesion. The optic nerve, chiasm, tract, and radiations and the visual cor- tex have a retinotopic representation throughout. Lesions of any of these structures result in visual deficits, such as a hemianopia or quad- rantanopia, that reflect the particular portion of the visual system that is damaged. Because visual pathways are widespread within the brain, lesions at various different locations may result in visual deficits.
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Pupillary and Visual Pathways and Deficits (see also Figures 8-44 to 8-47B on pp. 262–267)
The auditory portion of the eighth cranial nerve is concerned with the perception of sound. Damage to the cochlea itself, or the cochlear root, may profoundly alter one’s perception of sound or may result in deafness. The vestibular portion of the eighth cranial nerve functions in the arena of balance, equilibrium, and maintenance of posture. Damage to the semicircular canals, to the vestibular root, or to central structures that receive vestibular input, may result in vertigo, ataxia, difficulty walking or maintaining balance, and/or a variety of eye movement problems.
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Auditory and Vestibular Pathways and Deficits (see also Figures 8-49 to 8-50 on pp. 270–273)
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