76
Partial Visual Recovery in Two Fullterm Infants After Perinatal Hypoxia By F. Groenendaal and]. van Hofvan Duin Department of Physiology, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Abstract Behavioural methods were used to assess the visual development of two infants with a history of severe perinatal hypoxia. Both infants were born fullterm and showed hypoxic-ischaemic encephalopathy and subsequent cerebral palsy. Low visual acuity, small and asymmetrical visual fields, asymmetrical binocular and monocular OKN, and absent visual threat response were demonstrated initially. Ophthalmological examination revealed strabismus, but no further abnormalities. Longitudinal assessments up to the age of two years showed impressive (partial) improvements of visual functions. The mechanism for these improvements is unknown. The present study emphasizes the necessity of repeated testing of visual functions in infants with cerebral damage after perinatal hypoxia.
Keywords Perinatal hypoxia - Visual functions Hypoxic-ischaemic encephalopathy - Delayed development - Visual impairments
Introduction Perinatal hypoxia may have severe effects on the neurodevelopment of infants. Especially infants with signs of hypoxic-ischaemic encephalopathy are at risk for cerebral palsy, psychomotor retardation and epilepsy (1, 3, 4, 11, 12, 13, 18). Delayed visual development has recently been demonstrated after perinatal hypoxia (9, 10) by using behavioural methods which are suitable for visual assessment from birth onwards. So far, no longitudinal studies of visual development beyond the first year of age after perinatal hypoxia have been published. We had the opportunity to study visual development longitudinally in two fullterm infants with a history of severe perinatal hypoxia and hypoxic-ischaemic encephalopathy.
Received lune 30, 1989; accepted luly 14, 1989 Neuropediatrics 21 (1990) 76-78 © Hippokrates Verlag Stuttgart
Both subjects (patient A and patient B) were born at term after an uncomplicated pregnancy. Labour started spontaneously. Foetal heart rate was recorded and indicated tachycardia in patient A. In patient B foetal heart rate was not recorded. After birth, both infants did not breathe spontaneously and resuscitation was started. Apgar scores were low: 1 at one minute, 3 resp. 4 at five minutes. Spontaneous gasping movements were seen at 15 minutes (patient A) and 5 minutes (patient B). Blood gas values indicated severe acidosis in botb (pH 7.00-7.10, base deficit 15.0-20.0 mmol/l). The infants showed signs of hypoxic-ischaemic encephalopathy with apathy, hypotonia and absent reflexes. Patient B showed convulsions which were confirmed by EEG. Cerebral oedema and subarachnoidal haemorrhages were demonstrated by ultrasound and CT-scans in both patients, whereas patient A had periventricular haemorrhages as weIl. Examination of the infants at two months after birth showed spastic quadriplegia. In patient A the left side was more affected, in patient B the right side. Neuromotor improvements were seen in both infants in the second half of the second and of the first year respectively. Visual assessment was performed between six and a half months and two years and two months of age in patient A, and from two months to two years and 8 months in patient B (Table 1). Methods Visual assessment was performed at the Department of Physiology of the Erasmus University Rotterdam. Visual acuity was assessed with forced-choice preferentiallooking (20, 23) or acuity cards (14, 16). Both methods are based on the seemingly innate preference of infants for black-and-white grating patterns above a uniform grey stimulus when both are presented simultaneously. The extent of the binocular and monocular visual fields were assessed with kinetic perimetry (15). Results were compared with normal values from our laboratory (15, 16,23). Binocular and monocular optokinetic nystagmus (OKN) were elicited in a large rotating drum covered with a pattern of random dots of 1 cm2 (21). The infant was held in the drum on the examiner's lap with the head fixated. Spontaneous eye movements, binocular OKN and monocular OKN were recorded electro-oculographically using Ag-AgCI electrodes.
Downloaded by: Universite Laval. Copyrighted material.
Subjects and clinical data
Neuropediatrics 21 (1990)
Partial Visual Recovery After Perinatal Hypoxia
of the second and of the first year respectively, but normal values were never reached.
Visual threat response was tested by moving an object rapidly towards the infant's face, while tactile stimulation was prevented by a large piece of clear plexiglass (24).
Binocular OKN showed a preference for clockwise (CW) stimulation in both infants initially. The directional preference changed in both infants.
Pupillary reflexes, eye-movements and ocular alignment were tested with routine clinical methods.
Monocular OKN was influenced by the nystagmus. Still, in all recordings a preference for temporonasal above naso-temporal stimulation could be seen.
Results
In both infants visual development was abnormal. They did not fixate up to the age of one year and 8 months (patient A) and 10 months (patient B), although pupillary reflexes were normal in both. Following eye movements could be elicited in all directions in patient A. Patient B showed a paresis of the abducens muscle of his right eye. Patient A showed a very small spontaneous horizontal nystagmus at the age of one year and 8 months which had almost disappeared at the age of two years and two months. In patient B a small spontaneous nystagmus was present at three and a half months; its frequency increased up till 10 months of age, then declined again, but never disappeared completely. Both had a latent nystagmus (Table 1). Convergent strabismus was seen in both infants. Ophthalmological examination revealed no further abnormalities.
Discussion
Visual field deficits existed in both (Table 1). The visual fields of patient A could not be tested up to the age of one year and eight months due to roaming eye movements and lack of fixation. In patient B, both binocular and monocular visual field testing demonstrated right-sided hemianopia at three and a half months of age. The extent of the binocular visual field showed partial improvements in both infants in the second half
Severe deficits in visual functions after perinatal and postnatal hypoxia have been demonstrated in other studies (9, 10, 22). In the present study, visual development of both infants has been assessed longitudinally up to the age of two years and two months and two years and eight months respectively with quantitative, behavioural methods. Earlier studies indicated the usefulness of these methods for visual assessments in handicapped infants and children (9, 14, 15, 16,21,24). Both infants of the present study showed a spastic quadriplegia. The lateralization of major neuromotor handicaps coincided with the lateralization of visual field deficits. Partial improvement of the extent of the binocular visual field and neuromotor improvement were demonstrated simultaneously. This suggests dysfunction of one hemisphere followed by partial recovery and/or delayed maturation. Delayed development of visual acuity was clearly demonstrated in both infants. Delayed visual maturation
Patient A 2 2/12 years AC (mins of are) VF (degrees) VT nystagm. OKNb OKNm Strab
3.5
negative lat. CW>CCW TN>NT eso
negative lat. CW>CCW TN>NT roaming eye movements
L: 18 R:42 U:25 0:40 positive spont./lat. CCW>CW TN>NT eso
L: 54 R: 52 U:32 0:40 positive spont./lat. CCW>CW TN>NT eso
Patient B 2 8 /12 years AC (mins of are) VF (degrees) VT nystagm. OKNb OKNm Strab
9
negative
* eso
L: 45 R:O U:30 0:20 negative spant. CW>CCW TN>NT eso
L: 55 R: 27
L: 75 R: 50
L: 75 R: 75
L:84 R: 76
negative spont./lat. CCW>CW TN>NT eso
negative spont./lat. CCW>CW TN>NT eso
negative spont./lat. CCW>CW TN>NT eso
negative spont./lat. CCW>CW TN>NT eso
Downloaded by: Universite Laval. Copyrighted material.
Visual disturbances were demonstrated in both infants with a history of perinatal hypoxia and signs of hypoxicischaemic encephalopathy. Since ophthalmological examinations were normal except for a convergent strabismus, visual deficits resulted from cerebral dysfunction.
Visual acuity was abnormal in both infants, but partial improvements were demonstrated up to the age of two years two months in patient A, who was not tested thereafter and up to the age of 10 months in patient B, whose visual acuity did not improve at further age (Table 1).
Table 1 Visual funetions and testing ages of patients A and B. Abbreviations: AC: visual aeuity; VF: visual field; OKNb: binoeular OKN; OKNm: monoeular OKN; VT: visual threat; Strab: strabismus; mo: months; nystagm.: nystagmus; spant.: spontaneaus; lat.: latent nystagmus; eso: esotropia. Movements in the visual fields in the following direetions: L: left; R: right; U: up; 0: down; CW: eloekwise; CCW: eounter-eloekwise; TN: tempora-nasal; NT: nasa-temporal; //*" indieates "not testable"
77
Neuropediatrics 21 (1990)
has also been demonstrated by others in infants with or without a history of cerebral hypoxia (2, 6, 8, 9, 10, 19, 22, 26). One of the most striking findings was the resolution of hemianopia in patient B. This hemianopia was demonstrated at the age of three and a half months and improved during the first year of life. Normal values of the extent of the binocular visual field were seen at the age of 13 months. In both infants, binocular OKN showed asymmetries, followed by a change in directional preference. The causes of these. changes are unknown. Monocular recordings showed a latent nystagmus and a temporo-nasal preference of the OKN. In earlier studies, a temporo-nasal preference was demonstrated in infants with neurological abnormalities (21). A temporo-nasal preference of monocular OKN is seen in normal visual development up to the age of 20 weeks. Persisting temporo-nasal preferences are not only demonstrated in neurological abnormal infants, but also in infants with delayed visual development and/or strabismus (21, 24). The visual threat response of patient A became positive after the first year of life, much later than in normal infants (24), but remained negative in patient B. Improvements of neuromotor dysfunction and visual dysfunction after perinatal hypoxia were seen in both infants. Although the precise nature of the mechanisms of these improvements is unknown, a number of mechanisms might be suggested. Perinatal hypoxia may cause interruption of protein synthesis in neurones or glial cells, and eventually cell death. Furthermore, delayed dendrite formation and synaptogenesis (17), and abnormal myelination in visual pathways (5) are mentioned as mechanisms of post-hypoxie cerebral dysfunction. Mechanisms which could account for recovery are reactive synaptogenesis (7), rerouting ofaxones, or interruption of axon retraction. The present study shows impressive, though partial improvement of visual functions in two infants with severe perinatal hypoxia and hypoxic-ischaemic encephalopathy even up to the second year of life. Further studies are required to assess the duration and extent of this visual improvement.
Acknowledgment
We would like to thank Dr. Gesine Mohn for her help in testing the infants.
F. Groenendaal andl. van Hofvan Duin Finger, S., C. R. Almli: Brain damage and neuroplasticity: mechanisms of recovery or development? Brain Res. Rev. 10 (1985) 177-186 8 Givner, 1.: Visual loss following cardiac arrest. Arch. Ophthalmol. 51 (1954) 878-879 9 Groenendaal, F., J. Van Hofvan Duin, W. P. F. Fetter: Is delayed visual development caused by perinatal hypoxia? Lancet 11 (1988) 1308-1309 10 Groenendaal, F.,J. VanHofvanDuin, W. Baerts, W. P. F. Fetter: Effects of perinatal hypoxia on visual development during the first year of (corrected) age. Early Hum. Dev., in press. 11 Holden, K. R., E. D. Mellits,J. M. Freeman: Neonatal seizures. I. Correlation of prenatal and perinatal events with outcome. Pediatrics 70 (1982) 165-176 12 Levene, M. 1.,J. Kornberg, T. H. C. Williams: The incidence and severity of post-asphyxial encephalopathy in full-term infants. Early Hum. Dev. 11 (1985) 21-26 13 Levene, M. 1., C. Sands, H. Grindulis, J. R. Moore: Comparison of two methods of predicting outcome in perinatal asphyxia. Lancet I (1986) 67-69 14 McDonald, M., V. Dobson, S. L. Sebris, L. Baitch, D. Varner, D. Y. Teller: The acuity card procedure: a rapid test of infant acuity.. Invest. Ophthalmol. Vis. Sci. 26 (1985) 1158-1162 15 Mohn, G., J. Van Hofvan Duin: Developmeilt of the binocular and monocular visual fields of human infants during the first year of life. Clin. Vision Sei. 1 (1986) 51-64 16 Mohn, G.,J. Van Hofvan Duin, W. P. F. Fetter, L. De Groot-Buskop, M. Hage: Acuity assessment in non-verbal infants and children: Clinical experience with the acuity card procedure. Dev. Med. Child Neurol. 30 (1988) 232-244 17 Purpura, D. P.: Structure-dysfunction relation in the visual cortex of preterm infants. In: Brazier, M. A. B., Coceani, F. (Eds.). Brain Dysfunction in Infantile Febrile Convulsions. New York, Raven Press (1976) 223-240 18 Robertson, C., N. Finer: Term infants with hypoxic-ischemic encephalopathy: outcome at 3-5 years. Dev. Med. Child Neurol. 27 (1985) 473-484 19 Ronen, S., 1. Nawratzki, L. Yanko: Cortical blindness in infancy; a followup study. Ophthalmologica 187 (1983) 217-221 20 Teller, D. Y., R. Morse, R. Borton, D. Regal: Visual acuity for vertical and diagonal gratings in human infants. Vision Res. 14 (1974) 1433-1439 21 Van Hofvan Duin,J., G. Mohn: Optokinetic and spontaneous nystagmus in children with neurological disorders. Behav. Brain Res. 10 (1983) 163-175 22 Van Hofvan Duin,J., G. Mohn: Visual defects in children after cerebral hypoxia. Behav. Brain Res. 14 (1984) 147-155 23 Van Hofvan Duin, J., G. Mohn: The development of visual acuity in normal fullterm and preterm infants. Vision Res. 26 (1986) 909-916 24 Van Hofvan Duin,J., G. Mohn: Visual field measurements, optokinetic nystagmus and the visual threatening response: normal and abnormal development. In: Jay, B. (Ed.). Detection and Measurement of Visual Impairment in Preverbal Children. Doc. Ophthalmol. Proc. Sero 45 (1986) 305-316 25 Van Nieuwenhuizen, O.,J. Willemse: CT-scanning in children with cerebral visual disturbance and its possible relation to hypoxia and ischaemia. Behav. Brain Res. 14 (1984) 143-145 26 Weinberger, H.A., R. VanDer Woude, H. C. Maier: Prognosisofcortical blindness following cardiac arrest in children. JAMA 179 (1962) 126129 7
References Adsett, D. B., C. R. Fitz, A. HilI: Hypoxic-ischaemic cerebral injury in the term newborn: correlation of CT findings with neurological outcome. Dev. Med. Child Neurol. 27 (1985) 155-160 2 Barnet, A. B.,J. 1. Manson, E. Wilner: Acute cerebral blindness in childhood. Neurology 20 (1970) 1147-1156 3 Bergman, 1., M.J. Painter, R. P. Hirsch, P. K. Crumrine, R. David: Outcome in neonates with convulsions treated in an intensive care unit. Ann. Neurol. 14 (1983) 642-647 4 Brown,J. K., R.J. Purvis,J. O. Forfar, F. Cockburn: Neurological aspects ofperinatal asphyxia. Dev. Med. Child Neurol..16 (1974) 567-580 5 Dubowitz, L. M. S., G. M. Bydder,J. Mushin: Developmental sequence of periventricular leukomalaeia. Arch. Dis. Child 60 (1985) 349-355 6 Fielder, A. R., 1. R. Russell-Eggitt, K. L. Dodd, D. H. Mellor: Delayed visual maturation. Trans. Ophthalmol. Soc. UK 104 (1985) 653-661 1
F. Groenendaal, M. D., Ph. D. Dept. of Physiology Erasmus University Rotterdam P.O. Box 1738 3000 DR Rotterdam, The Netherlands Present address: Sophia Children's Hospital Gordelweg 160 3038 GE Rotterdam, The Netherlands
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78
Partial Visual Recovery in Two Fullterm Infants After Perinatal Hypoxia By F. Groenendaal and]. van Hofvan Duin Department of Physiology, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Abstract Behavioural methods were used to assess the visual development of two infants with a history of severe perinatal hypoxia. Both infants were born fullterm and showed hypoxic-ischaemic encephalopathy and subsequent cerebral palsy. Low visual acuity, small and asymmetrical visual fields, asymmetrical binocular and monocular OKN, and absent visual threat response were demonstrated initially. Ophthalmological examination revealed strabismus, but no further abnormalities. Longitudinal assessments up to the age of two years showed impressive (partial) improvements of visual functions. The mechanism for these improvements is unknown. The present study emphasizes the necessity of repeated testing of visual functions in infants with cerebral damage after perinatal hypoxia.
Keywords Perinatal hypoxia - Visual functions Hypoxic-ischaemic encephalopathy - Delayed development - Visual impairments
Introduction Perinatal hypoxia may have severe effects on the neurodevelopment of infants. Especially infants with signs of hypoxic-ischaemic encephalopathy are at risk for cerebral palsy, psychomotor retardation and epilepsy (1, 3, 4, 11, 12, 13, 18). Delayed visual development has recently been demonstrated after perinatal hypoxia (9, 10) by using behavioural methods which are suitable for visual assessment from birth onwards. So far, no longitudinal studies of visual development beyond the first year of age after perinatal hypoxia have been published. We had the opportunity to study visual development longitudinally in two fullterm infants with a history of severe perinatal hypoxia and hypoxic-ischaemic encephalopathy.
Received lune 30, 1989; accepted luly 14, 1989 Neuropediatrics 21 (1990) 76-78 © Hippokrates Verlag Stuttgart
Both subjects (patient A and patient B) were born at term after an uncomplicated pregnancy. Labour started spontaneously. Foetal heart rate was recorded and indicated tachycardia in patient A. In patient B foetal heart rate was not recorded. After birth, both infants did not breathe spontaneously and resuscitation was started. Apgar scores were low: 1 at one minute, 3 resp. 4 at five minutes. Spontaneous gasping movements were seen at 15 minutes (patient A) and 5 minutes (patient B). Blood gas values indicated severe acidosis in botb (pH 7.00-7.10, base deficit 15.0-20.0 mmol/l). The infants showed signs of hypoxic-ischaemic encephalopathy with apathy, hypotonia and absent reflexes. Patient B showed convulsions which were confirmed by EEG. Cerebral oedema and subarachnoidal haemorrhages were demonstrated by ultrasound and CT-scans in both patients, whereas patient A had periventricular haemorrhages as weIl. Examination of the infants at two months after birth showed spastic quadriplegia. In patient A the left side was more affected, in patient B the right side. Neuromotor improvements were seen in both infants in the second half of the second and of the first year respectively. Visual assessment was performed between six and a half months and two years and two months of age in patient A, and from two months to two years and 8 months in patient B (Table 1). Methods Visual assessment was performed at the Department of Physiology of the Erasmus University Rotterdam. Visual acuity was assessed with forced-choice preferentiallooking (20, 23) or acuity cards (14, 16). Both methods are based on the seemingly innate preference of infants for black-and-white grating patterns above a uniform grey stimulus when both are presented simultaneously. The extent of the binocular and monocular visual fields were assessed with kinetic perimetry (15). Results were compared with normal values from our laboratory (15, 16,23). Binocular and monocular optokinetic nystagmus (OKN) were elicited in a large rotating drum covered with a pattern of random dots of 1 cm2 (21). The infant was held in the drum on the examiner's lap with the head fixated. Spontaneous eye movements, binocular OKN and monocular OKN were recorded electro-oculographically using Ag-AgCI electrodes.
Downloaded by: Universite Laval. Copyrighted material.
Subjects and clinical data
Neuropediatrics 21 (1990)
Partial Visual Recovery After Perinatal Hypoxia
of the second and of the first year respectively, but normal values were never reached.
Visual threat response was tested by moving an object rapidly towards the infant's face, while tactile stimulation was prevented by a large piece of clear plexiglass (24).
Binocular OKN showed a preference for clockwise (CW) stimulation in both infants initially. The directional preference changed in both infants.
Pupillary reflexes, eye-movements and ocular alignment were tested with routine clinical methods.
Monocular OKN was influenced by the nystagmus. Still, in all recordings a preference for temporonasal above naso-temporal stimulation could be seen.
Results
In both infants visual development was abnormal. They did not fixate up to the age of one year and 8 months (patient A) and 10 months (patient B), although pupillary reflexes were normal in both. Following eye movements could be elicited in all directions in patient A. Patient B showed a paresis of the abducens muscle of his right eye. Patient A showed a very small spontaneous horizontal nystagmus at the age of one year and 8 months which had almost disappeared at the age of two years and two months. In patient B a small spontaneous nystagmus was present at three and a half months; its frequency increased up till 10 months of age, then declined again, but never disappeared completely. Both had a latent nystagmus (Table 1). Convergent strabismus was seen in both infants. Ophthalmological examination revealed no further abnormalities.
Discussion
Visual field deficits existed in both (Table 1). The visual fields of patient A could not be tested up to the age of one year and eight months due to roaming eye movements and lack of fixation. In patient B, both binocular and monocular visual field testing demonstrated right-sided hemianopia at three and a half months of age. The extent of the binocular visual field showed partial improvements in both infants in the second half
Severe deficits in visual functions after perinatal and postnatal hypoxia have been demonstrated in other studies (9, 10, 22). In the present study, visual development of both infants has been assessed longitudinally up to the age of two years and two months and two years and eight months respectively with quantitative, behavioural methods. Earlier studies indicated the usefulness of these methods for visual assessments in handicapped infants and children (9, 14, 15, 16,21,24). Both infants of the present study showed a spastic quadriplegia. The lateralization of major neuromotor handicaps coincided with the lateralization of visual field deficits. Partial improvement of the extent of the binocular visual field and neuromotor improvement were demonstrated simultaneously. This suggests dysfunction of one hemisphere followed by partial recovery and/or delayed maturation. Delayed development of visual acuity was clearly demonstrated in both infants. Delayed visual maturation
Patient A 2 2/12 years AC (mins of are) VF (degrees) VT nystagm. OKNb OKNm Strab
3.5
negative lat. CW>CCW TN>NT eso
negative lat. CW>CCW TN>NT roaming eye movements
L: 18 R:42 U:25 0:40 positive spont./lat. CCW>CW TN>NT eso
L: 54 R: 52 U:32 0:40 positive spont./lat. CCW>CW TN>NT eso
Patient B 2 8 /12 years AC (mins of are) VF (degrees) VT nystagm. OKNb OKNm Strab
9
negative
* eso
L: 45 R:O U:30 0:20 negative spant. CW>CCW TN>NT eso
L: 55 R: 27
L: 75 R: 50
L: 75 R: 75
L:84 R: 76
negative spont./lat. CCW>CW TN>NT eso
negative spont./lat. CCW>CW TN>NT eso
negative spont./lat. CCW>CW TN>NT eso
negative spont./lat. CCW>CW TN>NT eso
Downloaded by: Universite Laval. Copyrighted material.
Visual disturbances were demonstrated in both infants with a history of perinatal hypoxia and signs of hypoxicischaemic encephalopathy. Since ophthalmological examinations were normal except for a convergent strabismus, visual deficits resulted from cerebral dysfunction.
Visual acuity was abnormal in both infants, but partial improvements were demonstrated up to the age of two years two months in patient A, who was not tested thereafter and up to the age of 10 months in patient B, whose visual acuity did not improve at further age (Table 1).
Table 1 Visual funetions and testing ages of patients A and B. Abbreviations: AC: visual aeuity; VF: visual field; OKNb: binoeular OKN; OKNm: monoeular OKN; VT: visual threat; Strab: strabismus; mo: months; nystagm.: nystagmus; spant.: spontaneaus; lat.: latent nystagmus; eso: esotropia. Movements in the visual fields in the following direetions: L: left; R: right; U: up; 0: down; CW: eloekwise; CCW: eounter-eloekwise; TN: tempora-nasal; NT: nasa-temporal; //*" indieates "not testable"
77
Neuropediatrics 21 (1990)
has also been demonstrated by others in infants with or without a history of cerebral hypoxia (2, 6, 8, 9, 10, 19, 22, 26). One of the most striking findings was the resolution of hemianopia in patient B. This hemianopia was demonstrated at the age of three and a half months and improved during the first year of life. Normal values of the extent of the binocular visual field were seen at the age of 13 months. In both infants, binocular OKN showed asymmetries, followed by a change in directional preference. The causes of these. changes are unknown. Monocular recordings showed a latent nystagmus and a temporo-nasal preference of the OKN. In earlier studies, a temporo-nasal preference was demonstrated in infants with neurological abnormalities (21). A temporo-nasal preference of monocular OKN is seen in normal visual development up to the age of 20 weeks. Persisting temporo-nasal preferences are not only demonstrated in neurological abnormal infants, but also in infants with delayed visual development and/or strabismus (21, 24). The visual threat response of patient A became positive after the first year of life, much later than in normal infants (24), but remained negative in patient B. Improvements of neuromotor dysfunction and visual dysfunction after perinatal hypoxia were seen in both infants. Although the precise nature of the mechanisms of these improvements is unknown, a number of mechanisms might be suggested. Perinatal hypoxia may cause interruption of protein synthesis in neurones or glial cells, and eventually cell death. Furthermore, delayed dendrite formation and synaptogenesis (17), and abnormal myelination in visual pathways (5) are mentioned as mechanisms of post-hypoxie cerebral dysfunction. Mechanisms which could account for recovery are reactive synaptogenesis (7), rerouting ofaxones, or interruption of axon retraction. The present study shows impressive, though partial improvement of visual functions in two infants with severe perinatal hypoxia and hypoxic-ischaemic encephalopathy even up to the second year of life. Further studies are required to assess the duration and extent of this visual improvement.
Acknowledgment
We would like to thank Dr. Gesine Mohn for her help in testing the infants.
F. Groenendaal andl. van Hofvan Duin Finger, S., C. R. Almli: Brain damage and neuroplasticity: mechanisms of recovery or development? Brain Res. Rev. 10 (1985) 177-186 8 Givner, 1.: Visual loss following cardiac arrest. Arch. Ophthalmol. 51 (1954) 878-879 9 Groenendaal, F., J. Van Hofvan Duin, W. P. F. Fetter: Is delayed visual development caused by perinatal hypoxia? Lancet 11 (1988) 1308-1309 10 Groenendaal, F.,J. VanHofvanDuin, W. Baerts, W. P. F. Fetter: Effects of perinatal hypoxia on visual development during the first year of (corrected) age. Early Hum. Dev., in press. 11 Holden, K. R., E. D. Mellits,J. M. Freeman: Neonatal seizures. I. Correlation of prenatal and perinatal events with outcome. Pediatrics 70 (1982) 165-176 12 Levene, M. 1.,J. Kornberg, T. H. C. Williams: The incidence and severity of post-asphyxial encephalopathy in full-term infants. Early Hum. Dev. 11 (1985) 21-26 13 Levene, M. 1., C. Sands, H. Grindulis, J. R. Moore: Comparison of two methods of predicting outcome in perinatal asphyxia. Lancet I (1986) 67-69 14 McDonald, M., V. Dobson, S. L. Sebris, L. Baitch, D. Varner, D. Y. Teller: The acuity card procedure: a rapid test of infant acuity.. Invest. Ophthalmol. Vis. Sci. 26 (1985) 1158-1162 15 Mohn, G., J. Van Hofvan Duin: Developmeilt of the binocular and monocular visual fields of human infants during the first year of life. Clin. Vision Sei. 1 (1986) 51-64 16 Mohn, G.,J. Van Hofvan Duin, W. P. F. Fetter, L. De Groot-Buskop, M. Hage: Acuity assessment in non-verbal infants and children: Clinical experience with the acuity card procedure. Dev. Med. Child Neurol. 30 (1988) 232-244 17 Purpura, D. P.: Structure-dysfunction relation in the visual cortex of preterm infants. In: Brazier, M. A. B., Coceani, F. (Eds.). Brain Dysfunction in Infantile Febrile Convulsions. New York, Raven Press (1976) 223-240 18 Robertson, C., N. Finer: Term infants with hypoxic-ischemic encephalopathy: outcome at 3-5 years. Dev. Med. Child Neurol. 27 (1985) 473-484 19 Ronen, S., 1. Nawratzki, L. Yanko: Cortical blindness in infancy; a followup study. Ophthalmologica 187 (1983) 217-221 20 Teller, D. Y., R. Morse, R. Borton, D. Regal: Visual acuity for vertical and diagonal gratings in human infants. Vision Res. 14 (1974) 1433-1439 21 Van Hofvan Duin,J., G. Mohn: Optokinetic and spontaneous nystagmus in children with neurological disorders. Behav. Brain Res. 10 (1983) 163-175 22 Van Hofvan Duin,J., G. Mohn: Visual defects in children after cerebral hypoxia. Behav. Brain Res. 14 (1984) 147-155 23 Van Hofvan Duin, J., G. Mohn: The development of visual acuity in normal fullterm and preterm infants. Vision Res. 26 (1986) 909-916 24 Van Hofvan Duin,J., G. Mohn: Visual field measurements, optokinetic nystagmus and the visual threatening response: normal and abnormal development. In: Jay, B. (Ed.). Detection and Measurement of Visual Impairment in Preverbal Children. Doc. Ophthalmol. Proc. Sero 45 (1986) 305-316 25 Van Nieuwenhuizen, O.,J. Willemse: CT-scanning in children with cerebral visual disturbance and its possible relation to hypoxia and ischaemia. Behav. Brain Res. 14 (1984) 143-145 26 Weinberger, H.A., R. VanDer Woude, H. C. Maier: Prognosisofcortical blindness following cardiac arrest in children. JAMA 179 (1962) 126129 7
References Adsett, D. B., C. R. Fitz, A. HilI: Hypoxic-ischaemic cerebral injury in the term newborn: correlation of CT findings with neurological outcome. Dev. Med. Child Neurol. 27 (1985) 155-160 2 Barnet, A. B.,J. 1. Manson, E. Wilner: Acute cerebral blindness in childhood. Neurology 20 (1970) 1147-1156 3 Bergman, 1., M.J. Painter, R. P. Hirsch, P. K. Crumrine, R. David: Outcome in neonates with convulsions treated in an intensive care unit. Ann. Neurol. 14 (1983) 642-647 4 Brown,J. K., R.J. Purvis,J. O. Forfar, F. Cockburn: Neurological aspects ofperinatal asphyxia. Dev. Med. Child Neurol..16 (1974) 567-580 5 Dubowitz, L. M. S., G. M. Bydder,J. Mushin: Developmental sequence of periventricular leukomalaeia. Arch. Dis. Child 60 (1985) 349-355 6 Fielder, A. R., 1. R. Russell-Eggitt, K. L. Dodd, D. H. Mellor: Delayed visual maturation. Trans. Ophthalmol. Soc. UK 104 (1985) 653-661 1
F. Groenendaal, M. D., Ph. D. Dept. of Physiology Erasmus University Rotterdam P.O. Box 1738 3000 DR Rotterdam, The Netherlands Present address: Sophia Children's Hospital Gordelweg 160 3038 GE Rotterdam, The Netherlands
Downloaded by: Universite Laval. Copyrighted material.
78
