Journal of Neuro-Ophthalmology, September 1991, Volume 11, Issue 3

Insight into the recent European literature. A review of studies concerning the visual pathways.

loumal or Clinical Nt" uro-" l'hfllf1l"',,!<' gy 11( 3): 190-- 197. 1991 Insight into the Recent European Literature A Review of Studies Concerning the Visual Pathways Avinoarn B, Safran, M. D. © \ 99\ Raven Press, Ltd., New York This review refers to articles published in 1990. For obvious practical reasons, only some of these studies are reviewed here. Should the tenn " papillomacular bundle" be abandoned? In a systematic and critical way, Plant and Perry ( 1) attempted to demonstrate that using the term papillomacular bundle is inappropriate, for both anatomical and physiological reasons. To account for the vulnerability of the central retinal projec­tion in certain disease processes, it has commonly been held that papillomacular bundle is distin­guished by a number of anatomical features, in­cluding rectilinear projection of the foveal fibers, small diameter of axon fibers or specific cell types, fiber or ganglion cell density, specific glial content of fiber bundles, regional variations in the vascu­lature of the inner retinal layers, distribution of precapillaries, and unique location of fibers within the optic nerve. Plant and Perry stated that all these are oversimplifications, based on autopsy findings in abnormal subjects generally suffering from toxic amblyopia, and not on normal anatomy. They suggested that the term papillomacular bun­dle be abandoned. Astigmatism and optic nerve hypoplasia A higher prevalence of astigmatism was found in patients with optic nerve hypoplasia than in From the Neuro- ophthalmology Unit, Department of Oph­thalmology, Geneva University Hospital, Geneva, Switzerland. Address correspondence and reprint requests to Dr. Avi­noam B. Safran at Neuro- ophthalmology Unit, Geneva Univer­ · _, t\' Ho'p, tal. 1211 Geneva 4. Switzerland. 190 controls. This conclusion was reached by Zeki ( 2), who performed retinoscopy in 31 patients with iso­lated optic nerve hypoplasia or septo- optic hy­poplasia. Two patients showed segmental optic nerve hypoplasia. Results were compared with those of 20 controls ( p < 0.001). Mean astigmatism in patients with hypoplasia was 1.52 diopters. The axis was oblique in 37% of the eyes with both hy­poplasia and astigmatism. A trend toward myopia was observed in affected patients, mean total spherical power being 30% lower than in the nor­mal subjects. Occurrence of tilt in the optic nerve head is not mentioned. The association of astigma­tism with optic nerve hypoplasia highlights the im­portance of carefully identifying and correcting er­rors of refraction in these patients in order to re­duce the risk of their developing refractive amblyopia. The article is followed by a review pa­per by the same author ( 3), an optic nerve hy­poplasia. Morning glory syndrome is definitely not a coloboma of the optic nerve It has been postulated that morning glory syn­drome is a mesodermal congenital lesion and does not result from a neuroectodermal closure defect. This suggestion is supported by a new histopath­ological report by Manschot ( 4). He gives a de­scription of the inner wall of the staphyloma as being lined by a single uninterrupted layer of nor­mal retinal pigment epithelium and provides fur­ther evidence that the dysplasia does not result from a neuroectodermal closure defect. The globe described in this study was made available for his­tological examination because computerized to­mography ( CT) revealed a retrobulbar cyst con­nected with the sclera. Because the cyst was sus- RECENT EUROPEAN LITERATURE 191 pected of being a retinoblastoma, enucleation was eventually performed. Natural history of delayed visual maturation Using acuity cards, a quantified evaluation of the natural history of delayed visual maturation was performed by Tresidder et al. ( 5) in 26 consec­utive cases. Ages at which visual improvement commenced were as follows: in patients with de­layed visual maturation as the major abnormality ( group 1), 7- 24 weeks; in patients with obvious neurodevelopmental abnormalities ( group 2), 22­78 weeks; in patients showing nystagmus and oc­ular problems ( group 3), 13- 28 weeks. All the pa­tients of group 3 developed a horizontal nystag­mus of the " congenital" type, within a week or so of the onset of visual improvement. In group 1, patients attained normal acuities between 12 and 47 weeks; no infant of group 2 reached normal acuity; in group 3, infants attained acuities at the lower end of the normal range between 20 and 40 weeks. The massive visual deficit initially found with delayed visual maturation is attributed to a defect in the extrageniculate visual system. It is considered that both the relatively narrow age range over which the visual function commences and the onset of nystagmus ( in infants of group 3) might indicate the emergence of the geniculostri­ate function. Considering the contradictions in previous observations of pupillary responses to light stimulation in the early stages of the condi­tion, it is worth mentioning that all infants in this study showed normal pupillary responses. Retinal dystrophy and cerebellar atrophy A family with autosomal dominant cone dystro­phy and cerebellar atrophy is described over five generations by Neetens et al. ( 6). Visual deteriora­tion usually starts in childhood and precedes cer­ebellar ataxia by many years. Ophthalmologic changes include bull's- eye macula and progressive alteration of both cones and rods over the entire retina. As a rule, the neurological picture is char­acterized by gait and truncal ataxia, discrete kinetic ataxia, and eventually pyramidal signs. Later, ves­tibular areflexia occurs, as well as dysarthria and dysphagia, the latter sometimes resulting in fatal bronchopneumonia. Data from angiographic, functional, and histopathological evaluation of the eye are provided, as well as neuropathological findings. Modifications are suggested in the Har­ding classification of autosomal dominant cerebel­lar atrophies. Visual recovery and mutation of mitochondrial DNA in Leber's optic neuropathy In patients with Leber's optic neuropathy, mu­tation of mitochondrial DNA at base pair 11778 appears to be associated with poorer visual recov­ery. Holt et al. ( 7) analyzed mitochondrial DNA in eight families with Leber's optic atrophy and found mutation in four of them. In contrast with affected males presenting with the mutation, four of five affected males without the mutation recov­ered useful vision during a follow- up period of 4 years or more. Analyzing mitochondrial DNA might help in detecting the small number of af­fected patients who have a better chance of recov­ering vision. It was also demonstrated that all but one subject with the mutation had a variable mix­ture of mutant and normal mitochondrial DNA in peripheral blood. The relative proportions might be correlated with the risk of developing or trans­mitting the disease. Increased intraocular pressure in anterior ischemic optic neuropathy . .. In some patients, anterior ischemic optic neu­ropathy might be related to raised intraocular pres­sure. The statement is from Katz et al. ( 8), who prospectively evaluated the changes in intraocular pressure throughout the day in 16 patients pre­senting with nonarteritic anterior ischemic optic neuropathy and compared the results with those obtained from 15 normal controls. The mean peak intraocular pressure was 19.9 mmHg in affected patients, as compared with 17.6 mmHg in the con­trols ( p = 0.034). Seven of the 16 patients showed values exceeding 21 mmHg during the study pe­riod. ... and survival prognosis of affected patients There is increasing evidence that nonarteritic an­terior ischemic optic neuropathy is associated with an increase in mortality. This is supported by the results of a study by Sawle et al. ( 9), who obtained information about 63 affected patients over an av­erage period of 5.3 years. A significant increase in mortality rate was found in comparison with the general population for both cardiac and cerebro­vascular diseases ( p < 0.002). Nineteen patients ( 27%) died during the follow- up period ( expected deaths 8.44), 9 from myocardial infarction ( 2.67 ex­pected) and 4 from cerebrovascular conditions ( 0.93 expected). JClin Neuro- ophlhalmol. Vol. 11. No. 3. 1991 192 A. B. SAFRAN The sequence of events in lesion of multiple sclerosis: An MRl study Discrepancies between magnetic resonance Im­aging ( MRl) and clinical findings in multiple scle­rosis ( MS) were studied by Kermode et al. ( 10). In a number of patients, Gd- DTPA enhancement was found to occur either before other evidence of white matter involvement or before the develop­ment of clinical signs. Detection of breakdown of the blood- brain barrier with normal surrounding tissue suggests that inflammation is a primary event in the development of acute lesions in MS and not a secondary phenomenon. Conversely, the presence of important clinical deficit with min­imal MRl changes was also observed. This was at­tributed to lesions either bevond the resolution of the present imager or resulting from wallerian de­generation ( in the chronic progressive cases). In MS presenting as progressive spastic paraplegia, it is thought that many of the lesions inducing dis­abilitv are located in the spinal cord, where imag­ing i~ less satisfactory than in the brain. Ability to read television subtitles in multiple sclerosis It was stated in a study by Stenager and Jensen ( 11) that, in patients with MS, inability to read tele­vision subtitles might be a simple indicator of de­laved visual evoked potential ( VEP) latency. This in" cludes a number of patients with 20/ 20 visual acuity. These conclusions resulted from a study invoiving 25 randomly selected MS patients. Oc­casionally, patients were found reluctant to admit their inability to read television subtitles for fear of appearing stupid. Degree of visual loss in multiple sclerosis The importance of clinical classification as a pre­dictor of visual dysfunction in MS patients was emphasized by Honan et al. ( 12), who studied vi­sual function in 58 affected patients. In contrast to clinical disease duration, which was a poor predic­tor of visual dysfunction, comparison of clinical classification categories revealed significantly fewer visual abnormalities in the suspected MS category ( 31 ( lc) than in the early probable and clin­ically definite categories ( 75-- 100CJc). Contrast sensitivity versus VEP Contrast sensitivity emerged as the most useful (", q for detecting visual disorders, when compared to the YEP and partial Farnsworth- Munsell 100 Hue tests in MS. This conclusion was reached by Ashworth et al. ( 13), in a study involving 126 af­fected patients. Contrast sensitivity was abnormal in 92.2( lc of eyes, YEP was delayed in 35%, and color vision was found altered in less than a third. Loss of temporal sensitivity following optic neuritis, in relation to eccentricity Variations in the pattern of temporal modulation sensitivity in eves recovering from optic neuritis were fou~ d to be related to the eccentricity of the tested locations. In 12 affected patients, Edgar et al. ( 14) demonstrated that, in comparison with normal controls, there was a loss of sensitivity at all temporal frequencies at 0 and 2.5 degrees ec­centricity, especially in medium- to- lower temporal frequen~ ies, whereas at 5 degrees losses were lim­ited medium frequencies. In contrast, at 10 degrees eccentricitv no significant loss was found. These findings ~ ere attributed to a greater effect of de­myelination on small diameter fibers. It is sug­g~ sted that affected patients may also show losses of spatial contrast sensitivity, which diminishes with eccentricity. Monocular paracentral scotoma in occipital lobe infarction Nijssen et al. ( 15) reported a 38- year- old patient with right occipital lobe infarction and a small paracentral visual field defect only in the left eye. Repeated perimetric evaluation failed to reveal any paracentral scotoma in the right eye. Although a definitive explanation of the " extreme incongru­encv" of this retrochiasmatic " homonymous" def~ ct is still lacking, the authors suggest several possible mechanisms: ( a) an anatomical variation of the fiber crossing at the optic chiasma; ( b) in­volvement in the occipital lobe of fibers carrying input only from the left retina, based on the Hubel and Wiesel observation that visual responses from the left and right eye are separated until layer IVc of the visual cortex; and ( c) the existence of mech­anisms compensating only for visual defects lo­cated in the right half- field. Use of CT in children with cortical visual impainnent The importance of CT in the diagnosis of cortical visual impairment was assessed by Flodmark et aI. ( 16) in 95 affected children, in what might be the largest study on the subject. The commonest eti- RECENT EUROPEAN LITERATURE 193 ology was sustained perinatal asphyxia. Following such an event, the premature brain develops an hypoxic- ischemic injury located in the periventric­ular white matter, whereas in children born at term the susceptible watershed areas are found in the cortex. Unless secondary hemorrhage had oc­curred, periventricular leucomalacia was difficult to diagnose in the neonatal period, using either CT or sonography. Most patients born at term had various degrees of multicystic encephalomalacia. The visual pathway and the cortex appeared to become more resistant with increasing age. Chil­dren with hydrocephalus developed cortical visual impairment following shunt failure. It was found that occipital infarcts involving the visual cortex occurred in all children presenting with cortical vi­sual impairment and a history of shunt failure. Computed tomography demonstration of bilateral occipital infarcts supports the etiology of transten­torial herniation. A number of patients with dam­age that was apparently restricted to one hemi­sphere were initially blind. They eventually recov­ered, but they were left with a dense, unilateral, homonymous hemianopia and visual- motor per­ceptual difficulties. With normal or mildly abnor­mal CT, affected children often recovered visual acuity, especially after a hypoxic- ischemic insult in full- term neonates or children. The visual progno­sis is usually poor when little or no sight is found for more than 12 months after the CNS insult. The amount of residual vision could not be predicted from the imaging alone. Detection of isolated occipital lobe lesions in early childhood using VEP Subtle visual field defects resulting from occipi­tal lobe lesions cannot easily be recognized in pre­verbal children. Lambert et al. ( 17) reported two cases in which recording YEP from a horizontal array of occipital electrodes helped in detecting discrete lesions in the occipital lobes. Lightgazing in visually impaired children as an indicator of lesions in the posterior visual pathways Almost 60% of children with cortical visual im­pairment stare into light as a form of compulsive behavior. This unexpectedly high prevalence of blind mannerism was found by Jan et al. ( 18) in a study involving 153 affected children. In contrast, the same authors found a 1.8% prevalence of light­gazers in another series of children with ocular dis­orders. Lightgazing was occasionally used by par-ents to calm affected children, who would report­edly " stare into a flashlight until the battery ran out." Lightgazers preferred " concentrated" light ( i. e., lamps or fluorescent lights) to diffuse light. A number of these children flicked their fingers in front of their eyes against a light source. All light­gazers suffered from bilateral disturbances of the visual cortex and/ or posterior visual pathways. This behavior did not, however, appear to be re­lated to the etiology of the disorder. Lightgazing was more frequent in children with congenital rather than with acquired disorders. With recovery from visual impairment, lightgazing tended to re­gress. Whereas in some patients it completely re­solved, it was nevertheless observed in others whose visual acuity was nearly normal. While the eye- pressing phenomenon seems to be a rather specific sign of severe, bilateral visual defects re­sulting from ocular disorders, lightgazing strongly suggests bilateral retrogeniculate involvement of visual pathways. Head shaking Jan et al. ( 19) studied a series of 260 children with visual impairment and 13 children with nystagmus considered to be motor in nature. They observed head shaking in 18 children. Thirteen of these ( 72%) suffered from disorders involving the retina. Head shaking was never found in totally blind children. Distance visual acuity ranged from 20/ 50 to finger counting. Unexpectedly, 8 children showing head shaking had problems with spatial and/ or sequential interpretation; these difficulties are unusual in neurologically normal visually im­paired children. Head shaking occurs upon in­tense visual fixation, and it can be turned on and off at will. Neurological examination did not show evidence that head shaking was a tremor or a neu­rological extension of the nystagmus. Although eye movement could not be recorded, it was felt that the clinical findings supported the hypothesis that head shaking improves foveation time. Differ­ential diagnosis from spasmus nutans is discussed. Visual input and visual attention in normal and neurologically impaired children Over the first few months of life, there appears to be an increase in ability to shift visual attention to events occurring in the peripheral field. This results either from an improvement in sensory dis­crimination, the postnatal emergence of cortical mechanisms controlling visual attention, or both. Hood and Atkinson ( 20) first examined fixation JClin Neuro- ophthalmol, Vol. 11, No. 3, 1991 194 A. B. SAFRAN shifts to visual targets in 1- and 3- month- old nor­mal subjects and correlated results of behavioral tests with visual evoked responses to peripheral events. It was found that younger infants demon­strated poorer shift of attention when a central fix­ating target remained visible during the presenta­tion of a peripheral target. In addition, younger infants, unlike most 3- month- olds, do not produce a significant VEP with peripheral stimuli. How­ever, the fact that 1- month- olds can refixate the same single target in the periphery suggests a dis­sociation in the mechanism controlling VEP output and orienting at this age. In a group of 16 children suffering from various eNS disorders, subjects were found capable of visual tracking, with an in­tact peripheral sensory input as indicated by VEP recordings, but they were unable to reliably shift attention to the peripheral targets. Visual neglect: location . .. It is admitted that behavioral manifestations of neglect are usually located mainly in the space con­tralateral to hemisphere lesions, most often in the left hemispace. There is also clinical evidence that bilateral damage to parietal lobes can lead to alti­tudinal neglect ( 21). More recently, Shelton et al. ( 22) observed that in man, attention is spatially directed in three orthogonal axes: horizontal, ver­tical, and radial. In normal subjects, attention ap­pears to be unequally distributed in each of these axes. Neglect can occur in either the horizontal, vertical, or radial axes. ... and physiological basis To explain the unilateral spatial neglect found in patients with right brain damage, Heilman et al. ( 23) assumed that attentional neurons of the right parietal cortex have bilateral receptive fields, whereas the homologous cells of the left parietal cortex have only contralateral receptive fields. This hypothesis remains controversial. Kashiwagi et al. ( 24) reported a clinical observa­tion which may support this hypothesis. They re­ported on a right- handed patient with a callosal lesion due to cerebral infarction, demonstrating left hemispatial neglect in right- hand performance such as line bisection, and in verbal performance such as reading aloud a multiple digit number, but with little or no neglect in tasks performed with the left hand. In contrast, results from the study by Gainotti et aL ( 25) apparently did not corroborate the hypoth­0" 1<; nf Heilman et al. ( 23). They evaluated 102 right and 125 left brain- damaged patients by asking them to complete missing parts of a star, a cube, and a house. Patients with right brain damage failed to complete the contralateral side of the pic­ture more frequently than patients with left brain damage, but no difference was found between the two hemispheric groups when ipsilateral visual at­tention was evaluated. Nor did Lavadas's findings ( 26) support the hy­pothesis of Heilman et al. ( 23). She showed that, in patients with right parietal lesions, the essential element characterizing the response to visual stim­uli was the specification of the direction " right," as opposed to " left." She found that, as a result of the increased attention to the right, there was a pro­gressively decreasing attention to the left. This dif­fers from the hypothesis of Heilman et al. that lat­eral attentional differences can exist only between the two half- fields. In contrast, the attentional im­balance found by Lavadas is predicted by Kins­bourne's model ( 27) postulating that, when the right hemisphere is inactivated by a lesion, the left­oriented <' ector is impaired and consequently re­leases the right- oriented one from the inhibition. Visual field defects and visuospatial neglect Visual field defects do not appear to adversely affect performance of patients suffering from visu­ospatial neglect. This finding resulted from a study by Halligan et al. ( 28), involving a series of 51 pa­tients with unilateral right hemisphere stroke. Some patients with neglect and hemianopia even scored slightly better than those without field de­fect. In a number of patients with visual field de­fects, poor functional recovery might be due to the association of sensory loss with neglect. Testing visual half- field for determining cerebral speech dominance Patients with epilepsy who were being consid­ered for surgical treatment were asked to recognize pairs of words shown in each lateral visual half­field. This allowed reliable prediction of cerebral speech hemisphere functioning. The results of this study by Saisa et al. ( 29) might provide an empir­ical basis for replacing the sodium amytal test with a noninvasive technique. However, no test is yet available for replacing memory testing. Cholinergic mechanisms of visual hallucinations in dementia It is well established that anticholinergic drugs such as scopolamine occasionally induce visual RECENT EUROPEAN LITERATURE 195 hallucinations. Similarly, severe degeneration of cholinergic neurons innervating cortical areas in some types of dementia, as in Alzheimer's disease and Parkinson's disease, might give rise to this symptom. Evidence supporting this hypothesis was provided by neurochemical analyses per­formed by Perry et al. ( 30) in 12 cases of senile dementia of Lewy body type, 6 of whom presented with visual hallucinations. Choline acetyl­transferase activities were found to be significantly lower in patients with hallucinations than in those without. The " point of minor resistance" in conversion disorders of childhood The medical histories of 84 children with a diag­nosis of conversion disorder were reviewed in a follow- up study by Spierings et al. ( 31). The mean follow- up period was 50.7 months. In this series, only 4 patients complained of anosmia, deafness, or visual disturbances. The authors emphasized that ( a) a history of organic illness in the patients and their families was frequent ( a personal model for the symptoms was present in 29% of cases), and ( b) when patients viewed a part of their body as a weak point because of a preexisting defect, the conversion symptom occurred in that part of the body. Five of the 84 patients studied received an organic diagnosis during the follow- up period. In psychogenic disorders, depressive syndromes appear to be much commoner than hysterical ones Among the adult patients admitted to the neu­rology department of the Munich University hos­pital between 1985 and 1987, 405 ( 9%) were found to have psychogenic symptoms and 8 presented with visual symptoms. Lempert et al. ( 32) state that, of these 405 patients, 38% suffered from de­pressive symptoms, whereas only 9% were found to be hysterical. Improvement was much better in patients with recent onset of symptoms ( 2 weeks or less), and for motor symptoms than for pain. Improvement was unrelated to sex or age. The im­portance of recognizing masked depression is em­phasized. Neuro- ophthalmological findings in myelomeningocele and Chiari malformations In reviewing the charts of 28 patients ( 4- 34 years of age) treated by neurosurgery for myelomenin­gocele and Chiari malformations, Lennerstrand et al. ( 33) found no case of visual disability resulting from lesions in the intracranial parts of the visual pathways. These findings contrast with those of previous studies. Neither was downbeat nystag­mus observed. The authors related the absence of downbeat nystagmus to the young age of the pa­tients included in the series. Ocular motility disor­ders, however, were frequent, especially sponta­neous and gaze- evoked nystagmus and abnormal optokinetic nystagmus. Strabismus was noted in 11 patients. In another study involving the same patients, Lennerstrand et al. ( 34) reported that the occur­rence of strabismus and spontaneous nystagmus was correlated mainly with the importance of hy­drocephalus. Oblique muscle functions, horizontal and vertical gaze, and saccadic control were re­lated to lower brainstem changes, and conver­gence alteration to upper brainstem lesions. These anatomicoclinical correlations could not, however, be demonstrated in individual cases. Visual field indices: The influence of age and jogging In contrast to the results of previous studies, Autzen and Work ( 35) found a significant correla­tion between age and short- term fluctuation when examining the visual field by means of automated perimetry. On the other hand, jogging appears to cause a significant increase in sensitivity of the visual system. This was suggested in a study by Koskela et al. ( 36) who repeatedly performed au­tomated perimetry in a 55- year- old patient with a - 7.0- diopter myopia in the right eye and a - 8.0­diopter myopia in the left eye, before and after jogging 8 km. Therefore, in some individuals, physical exercise might influence factors determin­ing long- term fluctuation in the visual field. VEP monitoring of the optic nerve during surgery Harding et al. ( 37) reevaluated the value of in­traoperative monitoring of optic nerve function by means of VEP in 57 patients. They found that ab­olition of the VEP occurred under many circum­stances and showed no correlation with the visual outcome of the procedure. However, absence of any measurable response for more than 4 minutes, following previous recording of a normal VEP, was associated with postoperative visual deterioration. REFERENCES 1. Plant GT, Perry VH. The anatomical basis of the caecocen­tral scotoma. New observations and a review. Brain 1990; 113: 1441- 57. [ Reprint requests to Dr. Gordon T. 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Contralateral and ip­SIlateral dl~ orders of VIsual attention in patients with uni­lat. eral braIn da~ age. I Neurol Neurosurg Psychiatry 1990; 53.422- 42. ( Repnnt requests to G. Gainotti Clinica Neuro­logica Policlinico Gemelli, Largo A Gemell, 00168 Roma, Italy). 26. La~ adas E. Selective spatial attention in patients with visual extinction. Bram 1990; 113: 1527- 38. [ Reprint requests to Dr. E~ lsabetta Lavadas, Dipartimento di Psicologia, Viale Berti Plchat 5, Bologna, Italy). 27. Kinsbourne M. Mechanisms of unilateral neglect. In: Jean­nerod M, ed. Neuropsychological and neurophysiological aspects of spallal neglect. Amsterdam: North- Holland/ Elsevier 1987: 69- 86. ' 28. Halligan PW, MarshallJC, Wade DT. Do visual field deficits exacerbate visuo- spatial neglect? I Neurol Neurosurg Psychi- RECENT EUROPEAN LITERATURE 197 atry 1990; 53: 487- 91. [ Reprint requests to P. W. Halligan, Rivermead Rehabilitation Centre, Abingdon Road, Oxford OX1 4XD, UK). 29. 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Psychogenic disorders in neurology: frequency and clinical spectrum. Acta Neurol Scand 1990; 82: 335-- 40. [ Reprint requests to Thomas Lempert, Neurologische Abteilung, Universitatsk­linikum Rudolf Virchow Spandauer Damm 130, 1000 Berlin 19, Germany). 33. Lennerstrand G, Gallo JE. Neuro- ophthalmological evalua-tion of patients with myelomeningocele and Chiari malfor­mations. Dev Med Child Neural 1990; 32: 415- 22. [ Reprint re­quests to Gunnar Lennerstrand, M. D., Ph. D., Karolinska Institute, Huddinge University Hospital, 5- 141 86 Hud­dinge, Sweden]. 34. Lennerstrand G, Gallo JE, Samuelsson L. Neuro- oph­thalmological findings in relation to CNS lesions in patients with myelomenincocele. Dev Med Child NeuroI1990; 32: 423­31. [ Reprint requests to Gunnar Lennerstrand, M. D., Ph. D., Department of Ophthalmology, Karolinska Insti­tute, Huddinge University Hospital, S- 141 86 Huddinge, Sweden). 35. Autzen T, Work K. The effect of learning and age on short­term fluctuation and mean of automated static perimetry. Acta OphthalmaI1990; 68: 327- 30. [ Reprint requests to Torben Autzen, M. D., Department of Ophthalmology, Odense University Hospital, DK- 5000 Odense C, Denmark). 36. Koskela PU, Airaksinen PJ, Tuulonen A. The effect of jog­ging on visual field indices. Acta Ophthalmol 1990; 68: 91- 3. [ Reprint requests to Pentti U. Koskela, M. D., Department of Ophthalmology, University of Oulu, SF- 90220 Oulu, Fin­land]. 37. Harding GFA, Bland JDP, Smith VH. Visual evoked poten­tial monitoring of optic nerve function during surgery. J Neural Neurosurg Psychiatry 1990; 53: 890- 5. [ Reprint requests to G. F. A. Harding, Department of Vision Sciences, Uni­versity of Aston, Birmingham 54 7ET, UK). JClin Neuro- ophthalmol, Vol. 11, No. 3, 1991