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Show middle cranial fossa is probably congenital. The authors speculate that a prerequisite to the development of spontaneous CSF rhinorrhea from the middle cranial fossa is to have the bone in the base of these pits thinned and forming the roof of a laterally pneumatized sphenoid sinus. Thus, when studying patients with CSF rhinorrhea it is important to examine the full extent of the sphenoid sinuses, not just the anterior fossa. RO:'l'lldo D. Dia:, M. D. • • • I. Ref,'W/lt': Davis, P. C, Hoffman, J. C Jr., Tindall, G. T., and Braun, I. F.: Prolactin-secreting pituitary microadenomas: inaccuracy of high-resolution cr imaging. A./.N.R. 5: 721-726, 1984. Reprints: P. C Davis, M.D., Department of Radiology, Emory University School of Medicine and Emorv Clinic, 1365 Clifton Road, N.E., Atlanta, GA 3032i Fifty-one patients suspected of harboring a prolactin- secreting pituitary adenoma were studied with CT of the selJa and subsequently underwent transsphenoidal surgery. The surgical findings were retrospectively correlated with the CT findings. AlJ the patients had hyperprolactinemia (more than 25 nglml) with symptoms attributed to high prolactin levels such as amenorrhea, galactorrhea, infertility, and/or decreased libido. CT scans of the sella were performed in the coronal projection with continuous 1.5-mm sections immediately after a bolus of 100 ml of 60% intravenous contrast medium. After the bolus injection, a drip infusion of 30% intravenous contrast medium was kept open during the study. The bestknown indicators for diagnosing microadenomas by CT were evaluated. These were (1) a pituitary gland height greater than 8 mm, (2) a diffuse or focal, superiorly convexed diaphragma sellae, (3) a displaced infundibulum, (4) erosion of the sella floor, and (5) a focal lesion (either hyperdense or hypodense) within the enhancing pituitary gland. Of these, the only statistically Significant indicator for a microadenoma was a focal lesion. Nevertheless, six path<!llogically proven cases of microadenomas had normal CT scans, and a significant number of patients with surgically proven microadenomas had few of these findings. The authors conclude that these CT indicators are neither sensitive nor specific for microadenomas. Rosendo D. Diaz, M.D. • • • 8. Reference: Kapila, A., Steinbaum, S., and Chakeres, D. W.: Case report. Meckel's cave epidermoid with trigeminal neuralgia: cr findings. J. Comput. Assist. Tomogr. 8: 1172-1174, 1984. Reprints: A. Kapila, M.D., Department of Radiology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284. The authors describe a 42-year-old woman with throbbing right facial pain for 4 years. On physical examination she had two trigger points on the September 1985 Literature Abstracts right, one in the body of the mandible and the other in the nasolabial fold. She also had decreased pain sensation in the face and decreased corneal reflex, both on the right. CT showed a nonenhancing, lowattenuation ( - 66 HU) mass in the medial portion of the right middle cranial fossa extending into the posterior fossa over the right petrous apex. A CT metrizamide cisternogram accurately demonstrated the lesion within Meckel's cave. This mass was resected via a right subtemporal craniotomy, and the microscopic diagnosis was epidermoid with no dermal components. What is unique about this case is that, first, it is rare to find epidermoids with fat density. Actually, a negative CT attenuation is a feature used to differentiate dermoids and lipomas, typically having fat density, from epidermoids, which usually have a mixed CT attenuation. This is because of the relative concentration of high-denSity keratin and low-density cholesterol in epidermoids. Second, CT metrizamide cisternography showed the tumor to be within Meckel's cave, important preoperative information for the surgeon, since Meckel's cave is usually not in direct view. In this case, if significant tumor were left in Meckel's cave, the patient's trigeminal neuralgia could have persisted. Rosendo D. Diaz, M.D. • • • 9. Reference: Towle, V. L., Sutcliffe, E., and Sokol, S.: Diagnosing functional visual deficits with the P300 component of the visual evoked potential. Arch. Ophtha/mol. 103: 47-50, 1985. Reprints: V. L. Towle, M.D., Department of Neurology, Box 425, University of Chicago, 5841 Maryland Ave., Chicago, IL 60637. The authors attempt to show that a "cognitive component" of the visual evoked response called P300 (a positive deflection that occurs at about 300 ms) can be used to assess the validity of the patient's evoked response performance. The P300 wave is emitted when the brain is "identifying infrequently presented stimuli" and is not generated by visual cortex or degraded by poor fixation or blurred image. Horizontal and vertical stripes were used as stimuli, with the former presented 15% (i.e., infrequently) and the latter 85% of the time. Their traces first showed a normal subject's response when asked to either "attend" the horizontal stripes or simply to watch the TV. When attending, the P300 is readily evident. The same subject generated a P300 wave with a +11 diopter lens placed over the eye but not with a +45 diopter lens. Three patients with clinically diagnosed factitious visual loss were tested. Even when each claimed to be unable to see the horizontal stripes, a P300 wave was recorded, although the amplitude was less than in the normal subject and the timing and wave forms looked quite different on different tracings. The authors conclude that the presence of the P300 wave, when the patient denies being able to see the stimulus, bespeaks a functional visual loss, even though absence of the P300 wave does not confirm absence of vision. To the skeptic, this article offers a refinement in visual evoked response testing, 201 Literature Abstracts which seems only "possibly effective" in identifying malingering patients-and then only in the han?s of very good electrophysiologists. The actual tracmgs, however, are so variable that they may be unconvincing to the clinician. Lyn A. Sedwick, M.D. • • • 10. Referencl': Friedman, J. R., Kosmorsky, G. S., and Burde, R. M.: Stereoacuity in patients with optic nerve disease. Arch. Ophtha/mo/. 103: 37-38, 1985. Reprints: R. M. Burde, M.D., Department of Ophthalmology, Box 8096, 660 South Euclid Avenue, St. Louis, MO 63110. Thirteen patients with various optic nerve diseases and 11 patients with other ocular diseases were tested for near stereoacuity using the Titmus stereo acuity test. Visual acuity ranged from 20/20 in both eyes to asymmetry of 20/20 in one eye and 20/200 in the other. Stereoacuity scores were predicted based on visual acuity in each eye (the authors cite a previous study which set "normograms" for stereoacuity achieved by normal subjects with artificially degraded subnormal visual acuity, monocular and binocular). More than twice as many patients with optic nerve disease (76%) as other ocular diseases (27%) failed to achieve predicted stereoacuity scores. Data were not given regarding color vision, visual field, or details of motility examination, and quite variable optic nerve diseases were included. Most patients had good visual acuity. The authors concluded that good stereoacuity predicts good visual acuity, but that poor stereoacuity is not necessarily indicative of poor visual acuity (implicitly in patients with optic nerve disease); moreover, good stereoacuity with poor claimed visual acuity is probably indicative of malingering. Although these conclusions are probably valid, the patients tested seem too few with pathology too diverse to support them. Lyn A. Sedwick, M.D. • • • 11. Reference: Simonsz, D. M., Harting, F., de Waal, B. J., and Verbeeten, B. W. J. M.: Sideways displacement and curved path of recti eye muscles. Arch. Ophtha/mol. 103: 124-128, 1985. Reprints: D. M. Simonsz, Department of Ophthalmology, Academisch Ziekenhuis der Vrije Universiteit, De Boeleaan 1117, 1007 MB Amsterdam, Holland. The sideways displacement of the rectus eye muscles was examined by CT scanning of normal volunteers. The relaxed muscles assumed a curved path but straightened when contracted. The pictures of the scans themselves are very nice axial and coronal views of the orbits. One wonders why normal volunteers were subjected to radiation, as the prac- 202 tical application of this information is not readily apparent. Lyn A. Sedwick, M.D. • • • 12. Reference: rmes, R. K., Schatz, H., Hoyt, W..F., Monteiro, M. L. R., and Narahara, M.: Evolution of optociliary veins in optic nerve sheath meningioma. Arch. Ophtha/mo/. 103: 59-60, 1985. Reprints: W. F. Hoyt, M.D., Neuro-ophthalmology Unit, Room M-876, University of California Medical Center, San Francisco, CA 94143. A patient with a clinical course and CT s~an.consistent WIth optiC nerve sheath menmglOma was studied with serial fundus photographs over 8 years. These photographs docu,:,ent~d the onset of optociliary shunt vessels followmg dISC edema and the regression of these vessels with the development of optic atrophy. Very nice black and white disc photographs are included in the article. Lyn A. Sedwick, M.D. • • • 13. Reference: Zasorin, N. L., Yee, R. D., and Baloh, R. W.: Eye-movement abnormalities in ophthalmoplegia, ataxia, and areflexia (Fisher's syndrome). Arch. Ophtha/mol. 103: 55-58, 1985. Reprints: R. D. Yee, M.D., Jules Stein Eye Institute, 800 Westwood Plaza, Los Angeles, CA 90024. Three patients with the clinical diagnosis of Fisher's syndrome were studied, three by CT scan and two by eye movement recordings. The authors found that the ophthalmoplegia of these patients is consistent with a combination of supranuclear and peripheral cranial nerve palsies. Support for this view was provided by several pieces of evidence. The first was an abnormal computerized tomographic scan showing a right midbrain lucency in a patient with an up-gaze palsy, bilateral internuclear ophthalmoplegia, and bilateral ptosis. Eye movement recordings supplied information suggesting supranuclear and nuclearlinfranuclear patterns in the other two patients, which fit the clinical presentation. The authors reviewed 65 reported cases of Fisher's syndrome and 25 of brainstem encephalitis and found combinations of peripheral cranial neuropathy and supranuclear palsy in each group. Moreover, they postulated that the ataxia in Fisher's syndrome, as distinct from that of brainstem encephali'tis, is probably not due to long tract involvement but rather to cerebellar dysfunction, a conclusion that is suggested by eye movement abnormalities characteristic of lesions in the midline structures of the cerebellum, Le., impaired smooth pursuit, etc. This is an interesting article and a thoughtful addition to the literature about this unusual disorder. Lyn A. Sedwick, M.D. • • • Journal of Clinical Neuro-ophthalmology |
