OCR Text |
Show Journal of Neuro- Ophthalmology 20( 1): 63- 65, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Letters to the Editor • f To the Editor: Balcer and Galetta ( 1) included our article on anterior visual pathway meningiomas ( 2) in their article on the pregeniculate afferent visual system. I would like to correct their article in that the Mayo Clinic where the study took place is in Rochester, Minnesota, not Rochester, New York. The reason the title of our article specifies Mayo Clinic Rochester is to distinguish it from our affiliates, Mayo Clinic Scottsdale ( Arizona) and Mayo Clinic Jacksonville ( Florida), which are part of the Mayo Foundation. Jacqueline A. Leavitt, MD Rochester, Minnesota REFERENCES 1. Balcer LJ, Galetta SL. Neuro- ophthalmology of the pregeniculate afferent visual system: part II: June to December 1998. J Neuro- Ophthalmol 1999; 19: 207- 16. 2. Stafford SL, Perry A, Leavitt JA, et al. Anterior visual pathway meningiomas primarily resected between 1978 and 1988: the Mayo Clinic Rochester experience. J Neuro- Ophthalmol 1998; 18: 206- 10. Publisher's Reply To the Editor: The error reported by Dr. Leavitt that appeared in the article by Drs. Balcer and Galetta was entirely our own and occurred after the authors' careful page proof review. The publisher apologizes to Drs. Leavitt, Balcer, and Galetta for any inconvenience this error has caused. To the Editor: In an interesting and challenging article by Safran and Landis ( 1), " From cortical plasticity to unawareness of visual field defect," the authors reiterate the findings of Gilbert et al. and Murakami et al. ( references 1 and 20), which indicated that while binocular cortical plasticity and remapping were evident a few months after bilateral homologous retinal lesioning, monocular retinal lesion-ing did not produce neuronal reorganization. The article also implies that structural changes in the primary visual cortex, which result from sensory alteration, are probably comparable in adults and children. While I agree with the notion of cortical remapping and filling- in phenomena in adults, I found the topic of the article confusing because the term " cortical plasticity" does not appear to be concerned with visual field defects as described by the authors. Furthermore, " cortical plasticity" is markedly different between children and adults and perhaps requires different terminology. Cortical plasticity in children is characterized by the following findings, which have no analogs in adults: 1. Alteration of sensory input in children usually results in amblyopia, changes in binocularity, and inability to develop fusion and stereopsis, probably by anomalous wiring of the eye's connections at the visual cortex during the critical period ( 2); 2. It has been suggested that cortical plasticity, and therefore the critical period, is dependent on visual input. Thus, total- dark rearing represents complete visual deprivation and prolongs susceptibility to monocular deprivation beyond its normal limit. No such changes can be demonstrated in adults; 3. Alteration in sensory input in children may lead to competitive suppression and profound deficits in developmental anatomy, psychology, behavior, and neurochemistry ( 3); 4. The sensory deficit in infants who mainly possess brainstem predominance ( depth indifferent - r depth insensitive = pyknostereopsis) are different from adults who exhibit cortical predominance. Therefore, infants with crude spatial resolution often exhibit exo-tropic/ esotonic conflict until the delicate balance of precise bifixation leads to fine stereoacuity and maturity; 5. Bilateral suturing of the infant eyelids lead to disintegration of the cortical receptive fields; 6. The loss of ocular dominance and orientation columns are very clear in children with amblyopia ( 2), and absent in adults; 7. There are many other changes and deficits of the visual function in children as a result of alteration of sensory inputs, such as high spatial frequency, grating acuity, contrast sensitivity, visual evoked response, receptive field changes, vernier acuity, and binocular summation( 4). Summation of binocular light pupillary reaction also is reduced in people with amblyopia, which is probably the result of efferent reduction from the cortex to the pretectal regions. Critical period varies for different visual tasks; for example, the critical period begins and ends earlier for magnocellular than parvocellular functions ( 5). These cortical deficits, if treated early, are reversible in children. On the contrary, if these deficits are left alone, they will cause irreversible changes, such as amblyopia, latent fixation nystagmus, dissociated vertical deviation, face turn, abduction deficit, and, usually, esotropia. None of these conditions are observed in adults. These abnormalities are extremely different from Troxler phenomenon, angioscotoma, or abnormal glaucomatous scotomata, as mentioned by the au- 63 64 LETTERS TO THE EDITOR thors. Additionally, stereomotion scotomata is a binocular phenomenon that might occur in many individuals who have normal visual fields in each eye( 6). I would be interested in the authors' comments on this type of scotomata. Moreover, we may be overlooking an important aspect of the visual system, which can be called " subconscious vision or visceral vision." In this respect, I have presented for the first time " nonseeing photoreceptors," and I have enumerated its potential trophic, hormono-humoral, and metabolic effects on the visual system( 7). It is likely that such a system will constitute a critical aspect of cortical growth and development, particularly in children and possibly in adults. This aspect of vision is also important for cycles of rest and activity, sleep and waking, deep body temperature, sexual behavior, and many other visceral and hypothalamic activities that may affect visual functions. In view of the above information, an explanation from the authors would be greatly appreciated. AH A. Kashani, MD Beverly Hills, California REFERENCES 1. Safran AB, Landis T. From cortical plasticity to unawareness of visual field defect. J Neuroophthalmol 1999; 19: 84- 8. 2. Hubel DH, Wiesel TN, LeVay S. Plasticity of ocular dominance columns in monkey striate cortex. Philos Trans R Soc Lond B Biol Sci 1977; 278: 377^ i09. 3. Rose SPR. Early visual experience, learning and neurochemical plasticity in the rat and the chick. Philos Trans R Soc Lond B Biol Sci 1997; 278: 307- 18. 4. Legge GE. Binocular contrast summation 1: detection and discrimination. Vision Res 1984; 24: 373- 83. 5. Tychsen L. Motion sensitivity and the origins of infantile strabismus. In: Simons K, ed. Infant vision: basic and clinical research. New York: Oxford University Press, 1993: 364- 90. 6. Regan D, Erkelens CJ, Collewijin H. Visual field defects for ver-gence eye movements and for stereomotion perception. Invest Ophthalmol Vis Sci 1986; 27: 806- 19. 7. Kashani AA. The triplex hypothesis of vision. Ann Ophthalmol 1993; 25: 125- 32. Authors' Reply To the Editor: We read with interest the letter from Dr. Kashani concerning our paper " From cortical plasticity to unawareness of visual field defects" ( 1). Dr. Kashani has addressed a variety of issues. In reply, we wish to focus on the main point stressed in his letter- namely, whether reorganization occurring in the adult cortex should be referred to as cortical plasticity. The concept of cortical plasticity was originally applied to cortical changes occurring during so- called " critical periods" of postnatal maturation of the visual system, as exemplified in the 1977 paper by Hubel et al. ( 2), quoted in Dr. Kashani's letter. Over the past few years, however, our understanding of plasticity in the visual system has changed dramatically. In particular, it has been established that neuronal receptive fields in the adult cortex can reorganize, following either activation or an alteration in the pattern of activation, leading to changes in cortical topography. The last 2 decades of research have shown that, in contrast to previous widely held views, cortical maps are not static in adults, but show plastic changes ' in response to both visual stimuli and experience throughout life. Within certain limits, the cortex allocates areas in a use-dependent manner. The terms " cortical plasticity" and " synaptic plasticity" have been widely used when referring to these processes ( for recent reviews, see references [ 3] and [ 4]). Indeed, both during development and in adult life, structural synaptic and dendritic plasticity are implicated in a variety of physiologically and behaviorally induced changes in neural organization ( 4). Therefore, different types of learning are associated with synaptic addition and/ or loss. Moreover, in adults, the concept of cortical plasticity has been applied to pathologic conditions involving a variety of sensory modalities. This is clearly seen following limb amputation, in which massive shifts of cortical representation zones correlate with perceptual changes. Clinical observations of visual distortion of spatial perception in adults suffering from recently acquired visual field defects reflect the visual counterparts of such phenomena ( 5). Network reorganization has been found to be extensive, inaccurate, and fluctuating, rather than hardwired. As a result, modifications in the ability to induce subsequent synaptic plasticity, such as long- term potentiation or depression, have given rise to the newly defined concept of " plasticity of plasticity" ( 6). As stated by Turrigiano ( 7), the nervous system is subject to opposing requirements: the need for change and adaptation, and the need for stability. Indeed, given the variety of forms of activity- dependent mechanisms promoting changes, neuronal networks need to maintain some degree of constancy in their fundamental characteristics. Recent research has shown homeostatic mechanisms that promote stability in neural activity, resulting in the emerging concept of " homeostatic plasticity" in neuronal networks ( 7). As recently emphasized by Blight ( 8), some functions of the adult nervous system remain plastic throughout life, whereas others seem to be fixed from childhood. We are, in fact, recognized as individuals partly because of the constancy of our behavior. We certainly agree, however, with Dr. Kashani's statement that cortical plasticity occurring in childhood, during so- called " critical periods," differs in many respects from adaptation processes occurring later in life. It is true that we need to distinguish between these various forms of adaptation. Nevertheless, different processes, whether physiologic or pathologic in nature, are presently referred to under the general term of " cortical plasticity." Avinoam B. Safran, MD Theodor Landis, MD Geneva, Switzerland J Neuro- Ophthalmol, Vol. 20, No. I, 2000 LETTERS TO THE EDITOR 65 REFERENCES 1. Safran AB, Landis T. From cortical plasticity to unawareness of visual field defect. J Neuroophthalmol 1999; 19: 84- 8. 2. Hubel DH, Wiesel TN, LeVay S. Plasticity of ocular dominance columns in monkey striate cortex. Philos Trans R Soc London Ser B Biol Sci 1977; 278: 377. 3. Buonomano DV, Merzenich MM. Cortical plasticity: from synapses to maps. Anna Rev Neurosci 1998; 21: 149- 86. 4. Klintsova AY, Greenough WT. Synaptic plasticity in cortical systems. Curr Opin Neurobiol 1999; 9: 203- 8. 5. Safran AB, Achard O, Duret F, Landis T. The thin man phenomenon: a manifestation of cortical plasticity following homonymous paracentral scotomas. Br J Ophthalmol 1999; 83: 137^ 2. 6. Knecht S, Henningsen H, Hohling C, et al. Plasticity of plasticity? Changes in the pattern of perceptual correlates of reorganization after amputation: part 4. Brain 1998; 121: 717- 24. 7. Turrigiano GG. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same. Trends Neurosci 1999; 22: 221- 7. 8. Blight AR. Containing plasticity: neurite inhibitory factors of myelin. Nat Neurosci 1998; 1: 87- 8. To the Editor: To the Editor: Dr. Miller is right. An eye with an adrenergic mydriasis when stimulated in the dark will receive a large retinal dose of light because the pupil is initially wide open. Retinal illumination, and therefore the ensuing pupillary response, will depend on the amount of light that gets into the eye during the first few milliseconds of the stimulus, and it doesn't matter how the pupil got to be that size. However, during the alternating light test, most adrenergically dilated pupils will have constricted a fair amount because of the light stimulus in the other eye; thus, the actual amount of anisocoria during the test will indeed be expected to be less in a patient with a purely adrenergic anisocoria and also in other patients whose anisocoria diminishes in light ( e. g., patients with Horner syndrome or simple anisocoria). We left these three groups out of our study because it was already evident that small anisocorias did not induce much relative afferent pupillary defect ( RAPD), and because we were trying to simplify an already complex question. It should be emphasized that the anisocoria- induced RAPD is on the borderline of clinical significance. It is, of course, in the eye with the smaller pupil, and in general it seems to be on the order of a decibel ( 0.1 log unit) of RAPD for each millimeter of anisocoria. This kind of afferent pupillary defect only reaches the level of clinical significance when there are special circumstances: 1. When the anisocoria is very large ( over 2 mm in diameter). The work of Kawasaki et al. ( 1,2) has shown that the RAPD is " a moving target" that cannot be measured precisely, even with an expensive instrument, unless many repetitions are averaged, and that the closest that a clinician can expect to get with a single measurement is ± 0.2 log units; 2. When the smaller pupil is very small ( less than 3 mm in diameter). We suspect that this is because the percentage difference in pupillary area between the two eyes is amplified when one pupil is small, and this amplifies the difference in retinal illumination during the alternating light test; 3. When the eyes are dark adapted. Steady room light or daylight tends to gradually bleach the exposed retina behind the larger pupil more than the retina behind the smaller pupil, and this asymmetric light adaptation tends to even out the anisocoria- induced RAPD during the alternating light test. Note that in the first experiment which was performed in darkness ( Fig. 1), the RAPD grew with unilateral mydriasis to well over 1.2 log units, because in between the light stimuli, the eyes returned to darkness, and there was no chance for a state of light adaptation to accumulate. For example, a patient is struck in the right eye with a golf ball, an ambulance is called, both eyes are patched, and you see the patient in your examining chair 40 minutes later. You remove the patches and see that the right eye has an apparent traumatic iridoplegia, with the right pupil at 8 mm and the left pupil at 4 mm. One of your concerns is whether damage has been done to the right retina, so you promptly look for an afferent pupillary defect. If, by watching the pupil that moves, you see no pupillary input asymmetry at this moment when both retinas are equally dark-adapted and a lot more light is getting into the injured eye, then the anisocoria ( which is creating an RAPD in the eye with the smaller pupil) may be masking an afferent pupillary defect in the injured right eye. Byron L. Lam, MD, and H. Stanley Thompson, MD REFERENCES 1. Kawasaki A, Moore P, Kardon RH. Variability of the relative afferent pupillary defect. Am J Ophthalmol 1995; 120: 622- 33. 2. Kawasaki A, Moore P, Kardon RH. Long- term fluctuation of relative afferent pupillary defect in subjects with normal visual function. Am J Ophthalmol 1996; 122: 875- 82. I read with interest the article by Lam and Thompson ( An anisocoria produces a small relative afferent pupillary defect in the eye with the smaller pupil. J Neuroophthalmol 1999; 19: 153- 9) in which they elegantly showed that an anisocoria produces a small relative afferent pupillary defect ( RAPD) in the eye with the smaller pupil. The subjects studied by Lam and Thompson, both normal individuals and patients with a preexisting RAPD, all had anisocoria induced by a combination of a parasympatholytic agent and a sympathomimetic agent. I would assume that aniscoria induced by a sympathomimetic agent alone, like physiologic ( simple, central) anisocoria, would not be associated with an RAPD, because the parasympathetic system would not be affected, and the pupil should still constrict sufficient to light, as to eliminate or at least substantially reduce any asymmetry of light intensity reaching the retinas of the two eyes. I would like to know if the authors tested any subjects with physiologic anisocoria or if they tested any of their normal subjects with only a sympathomimetic agent? Neil R. Miller, MD Baltimore, Maryland Authors' Reply J Neuro- Ophthalmol. Vol. 20, No. I, 2000 |