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Visual evoked potentials (clinical neurophysiology updates, vol. 3)
books
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IIIII IIIIIII1!
lUlII
Visual Evoked Potentials (Clinical Neurophysiology Updates, Vol. 3) Richard Srebro
TheUniversityof TexasSouthwestern MedicalCenterat Dallas,Deptof Ophthalmology, DaJlas,TX752359O57,USA
260
edited by £ "E. Desmedt, Elsevier, 1990. Dfl. 265.00 (251 pages) 15BN 0 444 81240 7 Visual Evoked Potentials, an update of the celebrated Visual Evoked
Potentials
in
Man
(Desmedt, J. E., ed., Oxford University Press, 1977), is a compendium of chapters by a variety of authors who, for the most part, describe how they practice the art. Let there be no doubt of the diversity. The keynote is sounded by Bodis-Wollner in the first chapter. Since the visual system processes several aspects of a stimulus in parallel, it is necessary to tailor stimuli suitable to the clinical problem at hand in case it escapes the test procedure altogether. One stimulus size definitely does not fit all. However, the diversity of practice reflects more than just this basic reality of visual physiology. Not to be neglected are the research interests of the practitioner and the needs of the local medical community that he or she serves. In their best manifestation, and there are several examples in this book, these two aspects are skilfully merged and presented as first-rate work by any standard. As with any compendium, there is a certain amount of overlap and redundancy but not to the extent of distraction, although the book might have benefited by an overview, perhaps as a final chapter, and by a better chapter devoted to methodological considerations. Nevertheless, the chapters are, by and large, appropriate in subject matter and scope, and reflect a respectful awareness of the complexity of the issues. A possible exception is a seemingly selfserving chapter that describes how dipoles are fitted to the scalp topography of the visual evoked potential. At one end of the spectrum of diversity of practice lies Harding's 'no-nonsense' approach. In this chapter, mundane but essential issues such as the evaluation of badly traumatized eyes, hysterical blindness, and cortical damage
I 31
I IIII IIIIII
are discussed. Normative data for transient visual evoked potentials to simple flashes help establish a useful strategy. Harding's experience parallels my own at Parkland Memorial Hospital, a major trauma center. A flash visual evoked potential and a full field electroretinogram are very useful for predicting the outcome of restorative surgery, not only in severe eye injuries, but in cases of advanced cataract where the surgeon has never seen the fundus. Although, as Harding notes, cortical blindness in adults might be associated with a normal visual evoked potential, (presumably because area 17 remains intact), abnormal potentials are more often recorded from infants and young children where anoxia and trauma are frequent causes and widespread cortical dysfunction is the rule. At the other end of the spectrum is the painstaking work reported by Onofrj, which proposes a resolution to the longstanding confusion concerning the expression of visual field defects in the scalp topography of the pattern visual evoked potential. Careful topographic analysis provides the basis of a viable model for the sources of patternonset and pattern-reversal visual evoked potentials, which takes into account the details of how the visual fields are mapped onto the cortical surfaces within and near the calcarine fissure. This model neatly explains 'paradoxical' ipsilateral peaks in the visual evoked potential topography for some hemifield stimuli and might account for the affect of pattern element size as well. Onofrj's use of a 'grand average' mean scalp topography (over 30 subjects) is a bit disconcerting at first, since variability of cortical anatomy between subjects might have obscured useful topographic. information. Or is this actually a good approach if comparisons to 'average anatomy' are to be made? Future studies using magnetic resonance images in individual subjects should be very useful. Developmental aspects of the visual evoked potential are handled adequately, if somewhat
II
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IIII /I
cryptically, by Sokol. Of particular interest is the discussion of why the development curve for potential acuity rises more quickly than that estimated by the preferentiallooking technique. One suggestion that preferential looking might measure peripheral acuity seems to be a little far-fetched. Spekreijse comes to the rescue in a later chapter, suggesting the much more plausible hypothesis that pattern reversal, the mainstay of the developmental workers, might assess the maturation of visual motion detection. However, while visual motion seems to be important in checkerboard pattern reversal, I am unaware of studies concerning its role in grating contrast reversal, and there are clear differences between the properties of checkerboard and grating visual evoked potentials. Especially noteworthy are wellwritten and scholarly chapters by the group at Mount Sinai and by Celesia and Brigell, which really shine in their use of evoked potentials to pull apart the pathophysiology of multiple sclerosis. These chapters also document a changing view concerning the role of macular degeneration in causing delays in the pattern visual evoked potential. Apkarian and Spekreijse do a first-class job of analysis with regard to the detection of misrouted geniculostriate projections in human albinism. By far the most newsworthy item in this update is the coming of age of the pattern electroretinogram. Originally introduced by the group at Brown University, particularly Riggs, Schick and Armington, to study local electroretinograms without interference from stray light, a landmark experiment by Maffei and Fiorentini has dramatically changed our understanding. When the optic nerve is cut, the pattern electroretinogram is abolished in about six weeks, while the full field electroretinogram continues unabated. Maffei and Fiorentini succinctly review the veritable flood of work that followed their report. Celesia also shows some effective uses of the pattern electroretinogram together with TINS, VoL 14, No. 6, 1991
books the pattern visual evoked potential in the clinical assessment of optic nerve function. While much remains to be done in understanding the human pattern electroretinogram, particularly in dissecting apart contrast and local luminance contributions, its clinical usefulness is already clear. Somewhat surprisingly, the original use of the pattern electroretinogram as a tool to study local retinal function does not seem to have been used to its full potential in clinical application. It is far
Glycine Neurotransmission
more reliable than the currently available focal electroretinogram and I have found it of some use in assessing macular function and in monitoring for toxicity to hydroxychloroquin. No book can hope to cover all topics, but a number of areas that either received only cursory treatment or none at all in this book should have been expanded or included. These are the swept frequency visual evoked potential, advances in non-linear analysis, non-linear binocular inter-
than in other neuronal elements (Ottersen, Storm-Mathisen and edited by O. P. Ottersen and Laake). Of interest are the coJ. Storm-Mathisen, John Wiley & localization of GABA and glycine Sons, 1990. £75.00 (489 pages) ISBN and the presence of glycine in, 0 471 92717 1 and evidence for its uptake and The stated aim of this book is to release from, Golgi cells in the give an up-to-date review of the cerebellar granule cell layer, recent advances in basic research where there is little evidence for on glycine as a neurotransmitter strychnine-sensitive glycine inand to convey to the reader an hibition. This book went to print image of a very dynamic research before evidence for a co-transfield. In this, the book succeeds mitter role for glycine released by admirably. Researchers involved Golgi cells cooperating with gluin one aspect of this field will tamate released from mossy fibres certainly find much to inform and was published (D'Angelo et al., interest them, given the sheer Nature 346, 467-470). Evidence breadth of techniques applied that glycine is a co-transmitter and described. It is beautifully at the N-methyI-D-aspartate presented and illustrated with (NMDA) receptor/channel is remicrographs and with models viewed (Fletcher, Beart and presented as easily decipherable Lodge, Monaghan); this provides cartoons. For those not expert in a role for the high affinity glycinethe field, this book will provide an binding sites that correlate poorly excellent review of the many dif- with strychnine-binding sites ferent ways that central neuro- (Cortes and Palacios), but well transmission can be studied and a with glutamate-binding sites. The useful (if advanced) teaching aid. information provided in the book The price might deter its use as a about the localization, synthesis student text, but its addition to from, for example, serine by the library is to be recommended. serine hyd roxymethyltransferase In 1965, Aprison and Werman (Daly), high and low affinity uppresented the first evidence that take (Wilkin, Dennison-Cavanagh, glycine acts as a postsynaptic Fletcher and Bowery) and release inhibitory transmitter in the mam- of glycine, apply equally to both malian spinal cord. Evidence that its familiar inhibitory and its coglycine is present presynaptically transmitter roles, but much of the comes from immunocytochemical book concentrates on the strychstudies that made use of anti- nine-sensitive, inhibitory recepbodies raised against gluteralde- torlCl- channel. hyde-fixed glycine. These stain The molecular structure of the specific neuronal classes (Pourcho receptor, obtained from studies and Goebel, Wenthold and Hunter, of affinity-purified proteins, Osen, Ottersen and Storm- suggests a pentameric structure Mathisen) and immunogold par- (Langosch, Betz and Becker), ticles are present in quantitatively whose membrane-spanning rehigher concentrations in the nerve gions share structural similarities terminals of inhibitory neurones with other ligand-gated channels. TIN& Vol. 14, No. 6, 1991
actions, and the use of the full field electroretinogram to predict neovascular glaucoma in central retinal vein occlusion. Also, it is a pity that numerous citations from the last chapter somehow missed finding their way into the reference list at the end of the book. Still, the book is an interesting one that is essential reading for anyone working on the clinical neurophysiology of the visual system, as well as for the wellinformed neurologist and ophthalmologist. Positive charges at the presump- Alex M. tive mouth of the pore might Thomson determine the anion selectivity of Deptof Physiology, the channel. Purification of chan- RoyalFreeHospital nel proteins meant that anti- Schoolof Medicine, . bodies could be raised, allowing RowlandHillStreet, LondonNW3 2PF, channel localization at the ultra- UK. structural level (Triller, Cluzeaud and Seitanidou). Evidence that glycine and GABA might activate a similar CI- ionophore, albeit via different receptors, is provided by studies of channel activation and desensitization kinetics that predict a complex scheme including several open and closed states (Bormann), and in which the binding of anions within the channel might occur at two sites. However, glycine- and GABAactivated currents sum, indicating that each ligand acts on its own set of channels. Also, glycineactivated currents are more sensitive to increased intracellular CI-, which also depresses single, quantal inhibitory synaptic currents whose amplitude corresponds to activation of 1500 glycine-activated channels in lamprey neurones (Martin). Glycinergic synapses on Mauthner cells provide a model for quantal transmitter release that might be applicable to other central synapses (Korn and Faber). Ultrastructural localization of receptors and electrophysiological studies of the characteristics of the postsynaptic response to release from a single presynaptic bouton have been correlated. For example, lateral diffusion of transmitter away from subsynaptic receptors is proposed to account for the timecourse of synaptic events and, given the possibility that two glycine molecules might be required 261
IIIII
IIIIIIIII
IIIII IIIIIII1!
lUlII
Visual Evoked Potentials (Clinical Neurophysiology Updates, Vol. 3) Richard Srebro
TheUniversityof TexasSouthwestern MedicalCenterat Dallas,Deptof Ophthalmology, DaJlas,TX752359O57,USA
260
edited by £ "E. Desmedt, Elsevier, 1990. Dfl. 265.00 (251 pages) 15BN 0 444 81240 7 Visual Evoked Potentials, an update of the celebrated Visual Evoked
Potentials
in
Man
(Desmedt, J. E., ed., Oxford University Press, 1977), is a compendium of chapters by a variety of authors who, for the most part, describe how they practice the art. Let there be no doubt of the diversity. The keynote is sounded by Bodis-Wollner in the first chapter. Since the visual system processes several aspects of a stimulus in parallel, it is necessary to tailor stimuli suitable to the clinical problem at hand in case it escapes the test procedure altogether. One stimulus size definitely does not fit all. However, the diversity of practice reflects more than just this basic reality of visual physiology. Not to be neglected are the research interests of the practitioner and the needs of the local medical community that he or she serves. In their best manifestation, and there are several examples in this book, these two aspects are skilfully merged and presented as first-rate work by any standard. As with any compendium, there is a certain amount of overlap and redundancy but not to the extent of distraction, although the book might have benefited by an overview, perhaps as a final chapter, and by a better chapter devoted to methodological considerations. Nevertheless, the chapters are, by and large, appropriate in subject matter and scope, and reflect a respectful awareness of the complexity of the issues. A possible exception is a seemingly selfserving chapter that describes how dipoles are fitted to the scalp topography of the visual evoked potential. At one end of the spectrum of diversity of practice lies Harding's 'no-nonsense' approach. In this chapter, mundane but essential issues such as the evaluation of badly traumatized eyes, hysterical blindness, and cortical damage
I 31
I IIII IIIIII
are discussed. Normative data for transient visual evoked potentials to simple flashes help establish a useful strategy. Harding's experience parallels my own at Parkland Memorial Hospital, a major trauma center. A flash visual evoked potential and a full field electroretinogram are very useful for predicting the outcome of restorative surgery, not only in severe eye injuries, but in cases of advanced cataract where the surgeon has never seen the fundus. Although, as Harding notes, cortical blindness in adults might be associated with a normal visual evoked potential, (presumably because area 17 remains intact), abnormal potentials are more often recorded from infants and young children where anoxia and trauma are frequent causes and widespread cortical dysfunction is the rule. At the other end of the spectrum is the painstaking work reported by Onofrj, which proposes a resolution to the longstanding confusion concerning the expression of visual field defects in the scalp topography of the pattern visual evoked potential. Careful topographic analysis provides the basis of a viable model for the sources of patternonset and pattern-reversal visual evoked potentials, which takes into account the details of how the visual fields are mapped onto the cortical surfaces within and near the calcarine fissure. This model neatly explains 'paradoxical' ipsilateral peaks in the visual evoked potential topography for some hemifield stimuli and might account for the affect of pattern element size as well. Onofrj's use of a 'grand average' mean scalp topography (over 30 subjects) is a bit disconcerting at first, since variability of cortical anatomy between subjects might have obscured useful topographic. information. Or is this actually a good approach if comparisons to 'average anatomy' are to be made? Future studies using magnetic resonance images in individual subjects should be very useful. Developmental aspects of the visual evoked potential are handled adequately, if somewhat
II
IIIII
I IIIIIIIIII
IIII /I
cryptically, by Sokol. Of particular interest is the discussion of why the development curve for potential acuity rises more quickly than that estimated by the preferentiallooking technique. One suggestion that preferential looking might measure peripheral acuity seems to be a little far-fetched. Spekreijse comes to the rescue in a later chapter, suggesting the much more plausible hypothesis that pattern reversal, the mainstay of the developmental workers, might assess the maturation of visual motion detection. However, while visual motion seems to be important in checkerboard pattern reversal, I am unaware of studies concerning its role in grating contrast reversal, and there are clear differences between the properties of checkerboard and grating visual evoked potentials. Especially noteworthy are wellwritten and scholarly chapters by the group at Mount Sinai and by Celesia and Brigell, which really shine in their use of evoked potentials to pull apart the pathophysiology of multiple sclerosis. These chapters also document a changing view concerning the role of macular degeneration in causing delays in the pattern visual evoked potential. Apkarian and Spekreijse do a first-class job of analysis with regard to the detection of misrouted geniculostriate projections in human albinism. By far the most newsworthy item in this update is the coming of age of the pattern electroretinogram. Originally introduced by the group at Brown University, particularly Riggs, Schick and Armington, to study local electroretinograms without interference from stray light, a landmark experiment by Maffei and Fiorentini has dramatically changed our understanding. When the optic nerve is cut, the pattern electroretinogram is abolished in about six weeks, while the full field electroretinogram continues unabated. Maffei and Fiorentini succinctly review the veritable flood of work that followed their report. Celesia also shows some effective uses of the pattern electroretinogram together with TINS, VoL 14, No. 6, 1991
books the pattern visual evoked potential in the clinical assessment of optic nerve function. While much remains to be done in understanding the human pattern electroretinogram, particularly in dissecting apart contrast and local luminance contributions, its clinical usefulness is already clear. Somewhat surprisingly, the original use of the pattern electroretinogram as a tool to study local retinal function does not seem to have been used to its full potential in clinical application. It is far
Glycine Neurotransmission
more reliable than the currently available focal electroretinogram and I have found it of some use in assessing macular function and in monitoring for toxicity to hydroxychloroquin. No book can hope to cover all topics, but a number of areas that either received only cursory treatment or none at all in this book should have been expanded or included. These are the swept frequency visual evoked potential, advances in non-linear analysis, non-linear binocular inter-
than in other neuronal elements (Ottersen, Storm-Mathisen and edited by O. P. Ottersen and Laake). Of interest are the coJ. Storm-Mathisen, John Wiley & localization of GABA and glycine Sons, 1990. £75.00 (489 pages) ISBN and the presence of glycine in, 0 471 92717 1 and evidence for its uptake and The stated aim of this book is to release from, Golgi cells in the give an up-to-date review of the cerebellar granule cell layer, recent advances in basic research where there is little evidence for on glycine as a neurotransmitter strychnine-sensitive glycine inand to convey to the reader an hibition. This book went to print image of a very dynamic research before evidence for a co-transfield. In this, the book succeeds mitter role for glycine released by admirably. Researchers involved Golgi cells cooperating with gluin one aspect of this field will tamate released from mossy fibres certainly find much to inform and was published (D'Angelo et al., interest them, given the sheer Nature 346, 467-470). Evidence breadth of techniques applied that glycine is a co-transmitter and described. It is beautifully at the N-methyI-D-aspartate presented and illustrated with (NMDA) receptor/channel is remicrographs and with models viewed (Fletcher, Beart and presented as easily decipherable Lodge, Monaghan); this provides cartoons. For those not expert in a role for the high affinity glycinethe field, this book will provide an binding sites that correlate poorly excellent review of the many dif- with strychnine-binding sites ferent ways that central neuro- (Cortes and Palacios), but well transmission can be studied and a with glutamate-binding sites. The useful (if advanced) teaching aid. information provided in the book The price might deter its use as a about the localization, synthesis student text, but its addition to from, for example, serine by the library is to be recommended. serine hyd roxymethyltransferase In 1965, Aprison and Werman (Daly), high and low affinity uppresented the first evidence that take (Wilkin, Dennison-Cavanagh, glycine acts as a postsynaptic Fletcher and Bowery) and release inhibitory transmitter in the mam- of glycine, apply equally to both malian spinal cord. Evidence that its familiar inhibitory and its coglycine is present presynaptically transmitter roles, but much of the comes from immunocytochemical book concentrates on the strychstudies that made use of anti- nine-sensitive, inhibitory recepbodies raised against gluteralde- torlCl- channel. hyde-fixed glycine. These stain The molecular structure of the specific neuronal classes (Pourcho receptor, obtained from studies and Goebel, Wenthold and Hunter, of affinity-purified proteins, Osen, Ottersen and Storm- suggests a pentameric structure Mathisen) and immunogold par- (Langosch, Betz and Becker), ticles are present in quantitatively whose membrane-spanning rehigher concentrations in the nerve gions share structural similarities terminals of inhibitory neurones with other ligand-gated channels. TIN& Vol. 14, No. 6, 1991
actions, and the use of the full field electroretinogram to predict neovascular glaucoma in central retinal vein occlusion. Also, it is a pity that numerous citations from the last chapter somehow missed finding their way into the reference list at the end of the book. Still, the book is an interesting one that is essential reading for anyone working on the clinical neurophysiology of the visual system, as well as for the wellinformed neurologist and ophthalmologist. Positive charges at the presump- Alex M. tive mouth of the pore might Thomson determine the anion selectivity of Deptof Physiology, the channel. Purification of chan- RoyalFreeHospital nel proteins meant that anti- Schoolof Medicine, . bodies could be raised, allowing RowlandHillStreet, LondonNW3 2PF, channel localization at the ultra- UK. structural level (Triller, Cluzeaud and Seitanidou). Evidence that glycine and GABA might activate a similar CI- ionophore, albeit via different receptors, is provided by studies of channel activation and desensitization kinetics that predict a complex scheme including several open and closed states (Bormann), and in which the binding of anions within the channel might occur at two sites. However, glycine- and GABAactivated currents sum, indicating that each ligand acts on its own set of channels. Also, glycineactivated currents are more sensitive to increased intracellular CI-, which also depresses single, quantal inhibitory synaptic currents whose amplitude corresponds to activation of 1500 glycine-activated channels in lamprey neurones (Martin). Glycinergic synapses on Mauthner cells provide a model for quantal transmitter release that might be applicable to other central synapses (Korn and Faber). Ultrastructural localization of receptors and electrophysiological studies of the characteristics of the postsynaptic response to release from a single presynaptic bouton have been correlated. For example, lateral diffusion of transmitter away from subsynaptic receptors is proposed to account for the timecourse of synaptic events and, given the possibility that two glycine molecules might be required 261