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Entrapment Neuropathy of the Central Nervous System. Part II. Cranial

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Entrapment Neuropathy of the Central Nervous System. Part II. Cranial Entrapment neuropathy of the Cranial nerves central nervous system. Part II. Cranial nerves 1-IV, VI-VIII, XII HAROLD I. MAGOUN, D.O., F.A.A.O. Denver, Colorado This article, the second in a series, significance because of possible embarrassment considers specific examples of by adjacent structures in that area. The same entrapment neuropathy. It discusses entrapment can occur en route to their desti- nation. sources of malfunction of the olfactory nerves ranging from the The first cranial nerve relatively rare anosmia to the common The olfactory nerves (I) arise from the nasal chronic nasal drip. The frequency of mucosa and send about twenty central proces- ocular defects in the population today ses through the cribriform plate of the ethmoid bone to the inferior surface of the olfactory attests to the vulnerability of the optic bulb. They are concerned only with the sense nerves. Certain areas traversed by of smell. Many normal people have difficulty in each oculomotor nerve are pointed out identifying definite odors although they can as potential trouble spots. It is seen perceive them. This is not of real concern. The how the trochlear nerves are subject total loss of smell, or anosmia, is the significant to tension, pressure, or stress from abnormality. It may be due to a considerable variety of causes from arteriosclerosis to tu- trauma to various bony components morous growths but there is another cause of the skull. Finally, structural which is not usually considered. influences on the abducens, facial, The cribriform plate fits within the ethmoid acoustic, and hypoglossal nerves notch between the orbital plates of the frontal are explored. bone. Excessive medial compression, caused by trauma to the cranium, either unilaterally or bilaterally, can damp out the nerve function and lead to anosmia. In addition narrowing of the ethmoid notch crowds the ethmoidal and frontal sinuses, with the resulting congestion often causing chronic nasal drip (Fig. 1). The vulnerability of this area is revealed by As was shown in Part 1, entrapment neuro- the fact that, in embalming the dead, the pathy in the cranium can result from bony Egyptians used this avenue to remove the impingement, membranous tension, ligamen- brain without noticeably injuring the skull.2 tous pull, or the pressure of edema, venous The involvement may be with the frontal bone congestion, and so on. Lymphatic stasis im- alone or include others in the facial area such mediately outside of the skull at the foramina as the vomer, maxillae, or sphenoid. of exit should be included. Space-occupying Anosmia is relatively rare. However, such lesions have not been made a part of this thesis. a possible impingement may readily be dem- Specific examples of nerve involvement remain onstrated. With a finger inserted in the eth- to be considered. moid notch of even a dry, defatted laboratory The first four pairs of cranial nerves arise specimen, it is not difficult to compress the two from the cerebrum ; the last eight, from the orbital plates of the frontal bone sufficiently to hindbrain.1 Their point of emergence can be of feel the bind. Journal AOA/vol. 67, March 1968 779/101 Entrapment neuropathy fluid medium may make itself felt in the func- tion of the optic nerves. From the optic foramina to the cerebrum the nerve tracts are in contact with the sphenoid bone, a distance of about 18 mm., passing through between the roots of the lesser wings and then lying in grooves on the su- perior surface of that bone. Changes in the ETHMOID LATERAL ANGLE NOTCH position of the sphenoid, either of the pre- Fig. 1. The ethmoid notch may be slightly osseous elements before birth or the complete widened or narrowed (see arrows). If the latter, bone in later life, can lead to pathosis. In compression of the cribriform plate and thus the first cranial nerves can occur, as well as func- hyperopia both greater wings may have shifted tional disturbance in the ethmoidal and frontal forward, shortening the orbits and the eye- sinuses. balls, so that the focal point is behind the retina. In myopia the greater wings may be shifted backard, increasing the anteroposterior The second cranial nerve diameter, so that the focal point is in front of the retina. Should one greater wing move an- The optic nerves (II) are well protected in teriorly and the other posteriorly, one eyeball their short course to the brain. The first milli- will be prominent and the other recessive, meter of their length is intraocular and may be again disturbing optic nerve function (Fig. considered inviolable. The 30-mm. intraorbital 2). Diplopia may result from such traumatic portion is covered with a protective sheath malalignment. The child may use the domi- consisting of an extension of the cerebral nant eye exclusively with atrophy of the other meninges. It traverses the orbital fat and so is but this usually does not occur in adults. well cushioned. However, since there is a direct Astigmatism, a defective curvature of the perineural pathway for the cerebrospinal fluid refractive surface of the eye, can result from around the nerves, 1 at least as far as the sclera, the pressure or tension of structural alteration any chemical or trophic disturbance in that of the sphenoid or any of the other bones mak- ing up the orbit. Each orbit is a flexible, cone-shaped cavity with the optic foramen at the apex of the pyramid between the roots of the lesser wings of the sphenoid. The four walls are made up of seven bones for each orbit: the frontal, sphenoid, maxilla, zygoma, palatine, ethmoid, and lacrimal. Fixation of any of these con- stituents can be significant in eye malfunction because of the resulting venous stasis or dural Fig. 2. Prominent right eyeball and recessive left tension. Venous stasis can result from narrow- eyeball. Note also the difference in ear position. Both situations are due to structural trauma altering bone ing of the superior orbital fissure with the position and both may be pathogenic. greater wing crowded medially by the tern- 780/102 poral bone to approximate the lesser wing, or from narrowing of the inferior orbital fissure Crania l nerves with a change in the relationship between the greater wing and the maxilla. Occipitotemporal shifts can retard drainage through the jugular 111.•■• • foramina and so cause back-pressure in the 3/(1) orbits by way of the petrosal and cavernous • sinuses and the ophthalmic veins. This is a very common cause of pain behind the eyeballs. Aft(tglt Myopia may possibly be due to distortion of the occiput, as in the case of the Japanese who YE sleep on a wooden headrest and thus disturb the orbital centers in the occipital lobe near the 1pfernal Carotid calcarine fissure. ery In all races the great preponderance of ocu- Fig. 3. Cross section of the cavernous sinus showing lar defects requiring glasses attests to the vul- the relative position of the internal carotid artery and nerability of these nerves from many possible cranial nerves III, IV, V(1), and VI. causes. Careful evaluation of visual fields, acuity of vision, and the condition of the optic Within the orbit the third nerve is dis- fundi is the prerogative of the specialist but tributed to seven muscles. Parasympathetic faulty vision is one of the commonest afflic- fibers supply the sphincter of the iris and the tions among patients today. Therefore, along ciliary muscle, to regulate the size and shape with the other measures consideration of the of the pupil, its accommodation, and response structure by the general practitioner, as a cause to light. A branch goes to the levator muscle of the malfunction, is clearly indicated. of the upper eyelid, which arises from the Further eye problems may arise from faulty back of the orbit just above the optic foramen action of the orbital muscles due to entrap- and inserts into the tarsus of the upper lid. ment neuropathy of the third, fourth, and Thus the eye is opened by the third nerve but sixth cranial nerves. closed by the seventh. Twitching or ptosis of the lid indicates trouble in this part of the The third cranial nerve third nerve. A drooping eyelid may accompany Each oculomotor nerve (III) leaves the mesial Bells palsy, in which the seventh cranial nerve side of the cerebral peduncles and runs inferi- is at fault. orly, anteriorly, and laterally in the posterior More frequently involved in entrapment part of the cisterna basalis, and transverses neuropathy are the superior, medial, and in- three vulnerable areas en route : (1) as it ferior rectus muscles of the eyeball, as well as crosses the attached border of the tentorium the inferior oblique muscle. The rectus muscles cerebelli at the side of the dorsum sellae, (2) arise in the apex of the orbit from a dural as it passes forward in the outer wall of the sheath surrounding the optic foramen and cavernous sinus (Fig. 3), and (3) as it enters nerve. They insert anterior to the equator of the orbit through the superior orbital fissure. the eyeball. The inferior oblique muscle arises Anyone of these is a potential trouble spot. from the maxilla medially in the margin of Journal AOA/vol. 67, March 1968 781/103 Entrapment neuropathy the floor of the orbit and inserts posterior to the equator of the eyeball. Anterior clinoid process The action of these muscles supplied by the third cranial nerve may be outlined as follows : Petrosphenoid 8 ligament and Eye upward and inward—superior rectus posterior clinoid Eye medially—medial rectus Free border tentorium Eye downward and inward—inferior rectus Medulla Attached border Eye upward and outward—inferior oblique Eye directly upward—superior rectus and Tentorium inferior oblique Eye directly downward—inferior rectus and Fig.
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