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Recent advances in cortical visual impairment

William V Good* MD, Smith-Kettlewell Eye Research Institute, = San=20 Francisco, California, USA;
James E Jan MD, Vancouver = Children's=20 Hospital, British Columbia, Canada;
Susan K Burden BS, = University of=20 Michigan Medical School, Ann Arbor, Michigan;
Ann Skoczenski = PhD,=20 University of Massachusetts Medical School, Massachusetts:
Rowan = Candy=20 PhD, Smith-Kettlewell Eye Research Institute, San Francisco, = California,=20 USA.

*Correspondence to first author at Smith-Kettlewell Eye Research = Institute,=20 2318 Fillmore Street, San Francisco, CA 94115, USA
E-mail:=20 good@skivs.ski.org

Originally appeared in=20 Developmental Medicine & Child Neurology 2001, 43: = 56-60

Cortical visual impairment (CVI) is the leading cause of bilateral = visual=20 impairment in children in western countries^1-3. This=20 finding reflects better methods for identifying visual impairment due to = CNS=20 injury and also advances in perinatal care, which have increased the = survival=20 rate of children with neurological morbidity. This review will describe = advances=20 in the diagnosis and management of CVI. Central to our discussion is a=20 definition of CVI that includes a decrease in visual acuity. New = treatment and=20 rehabilitative measures are badly needed for this disorder. We hope to = stimulate=20 interest in CVI, a disease that has become a significant public health=20 problem.

The incidence of CVI is increasing³. In = a study of=20 five Nordic countries, Rosenberg and coworkers5 noted that brain damage = accounts=20 for a growing number of cases of childhood visual impairment. They = suggested=20 that better medical care has lowered the mortality rate of children with = severe=20 medical problems. Although CVI alone is not life threatening, its = associated=20 neurological disorders may have been fatal in the past. In one study = from Chile,=20 2.1% of children enrolled in schools for the blind, who are either = visually=20 impaired or blind, had visual diagnoses involving CVI, although this may = be an=20 underestimate6. In another study from Liverpool, Rogers7 found that CVI = was the=20 most common cause of visual Impairment in children with associated = neurological=20 disorders (49% of the study population). The Oxford Register of Early = Childhood=20 Impairments8 reports the overall incidence of bilateral vision = impairment at=20 0.14%, with 29.5% of cases due to CVI and 14.1 % due to nystagmus: the = second=20 major cause of impairment in this study population. In Northern = California, CVI=20 was also found to be the leading cause of visual impairment in children = under=20 the age of 5 years⁹.

Visual deficits in cortical visual impairment

CVI is a neurological disorder resulting in bilateral impairment of = visual=20 acuity caused by damage to the CNS, meaning visual acuity is reduced as = a result=20 of non-ocular diseases³. Visual acuity is a = measure=20 of the ability to visually resolve objects of interest in detail. One of = the=20 remarkable aspects of CVI is the near universal retention of residual = vision,=20 (although diminished) which often improves over time1. Children with = pure CVI=20 have a normal pupillary reaction to light, and normal outcome on=20 ophthalmological examination. CVI frequently co-occurs with other ocular = disorders^10,11. In fact, as many as 65% of = patients=20 with CVI may have associated ophthalmological abnormalities11.

Recently, Cioni and colleagues12 proposed that a broader range of = visual=20 impairments should be added to the general CVI category. In CVI, visual = acuity=20 is decreased because the visual pathway subserving the macula has been = damaged.=20 The macula is subserved by as much as two-thirds of the visual = cortex13-15, so loss of visual acuity is very likely = to=20 accompany any injury to this part of the brain. Some children may have=20 associated deficits in visual field, contrast sensitivity, or ocular=20 motility⁴. Other aspects of higher-order = spatial=20 vision (e.g. contour integration) are likely to be affected as well. To = date,=20 there have been few studies to systematically and quantitatively = evaluate these=20 important visual functions in patients with CVI.

Not all types of visual deficits caused by CVI will affect visual = acuity. For=20 example, in cortical visual dysfunction (CVD)¹⁶, the=20 predominant visual deficit is not visual acuity loss, but rather = disturbances in=20 visual perception and integration. In higher-functioning children with = CVI or=20 CVD, specific visual disorders such as agnosias may be diagnosed. These = include=20 cerebral motion blindness or cerebral akinetopsia (the inability to = perceive=20 moving targets), simultanagnosia (the inability to focus on more than = one visual=20 object at a time), central achromatopsia¹⁶ = (color=20 desaturation), prosopagnosia (difficulty in recognizing faces), = topographic=20 agnosia (problems with orientation; see section on rehabilitation), and=20 astereocognosis (difficulty with depth perception)¹⁷.=20 Thus, although not all children with CVD have associated CVI, certain = children=20 with CVI (with loss of visual acuity) may show signs of CVD16,18.

Etiology of CVI

The most common cause of CVI is an hypoxic-ischemic injuryl-3,10,19,20. At least 60% of children with = neonatal=20 hypoxic-ischemic encephalopathy have cerebral visual impairment12. Hypoxia (lack of oxygen) or ischemia (tissue = death due=20 to loss of blood flow, and thus oxygen deprivation) in the preterm baby = leads to=20 a characteristic injury of the brain, namely periventricular = leukomalacia=20 (PVL)^21,22, which can be detected by = MRI.

Head injury is a major cause of CVl, with half the cases of traumatic = injury=20 resulting from child abuse². Trauma-induced = CVI is an=20 acute reaction to a reversible disease process, and is often accompanied = by=20 headaches, confusion, and vomiting23. Cranial injury may induce = transient=20 ischemia or edema^23,24. Visual problems = resulting=20 from traumatic injury may also be chronic and lead to complete = blindness24.

Other causes of CVI include shunt failure¹⁰ (which=20 can lead to ischemia and occipital lobe infarction), infections = (bacterial=20 meningitis1, encephalitis²⁵,=20 meningitis/encephalitis², congenital = toxoplasmosis,=20 and neonatal herpes simplex^l0), antenatal = use of=20 cocaine and amphetamines by the mother¹¹, = metabolic=20 disease (most of the neurodegenerative diseases have the potential to = disrupt=20 cortical vision)^26,27, complications of = cardiac=20 treatment (CVI has been reported after cardiac arrest and open heart=20 surgery)^1,24, twin pregnancy1,28, epilepsy²⁹, = and CNS=20 developmental defect²⁹ (lissencephaly,=20 holoprosencephaly, and schizencephaly). CVI is virtually always = associated with=20 other serious neurological abnormatities^2,7,11,30,31.=20 Whiting and coworkers²⁵ found evidence of = abnormal=20 cognitive development, cerebral palsy (CP), seizures, microcephaly,=20 hydrocephalus, sensorineural hearing loss, myelomeningocoele, and = progressive=20 CNS degeneration in children with CVI.

CVI is also associated with ophthalmological abnormalities including = various=20 types of nystagmus, strabismus, and refractive error11,32 which should be corrected (e.g. with = glasses) to=20 maximize any residual vision². Optic nerve = atrophy,=20 which itself causes vision impairment, has been seen in children with = CVI21. Visual field development may be delayed in = preterm=20 children who have perinatal hypoxia-ischemia. Strabismus with a cerebral = origin=20 may also be present in these children³³.

Prognosis

Most patients with CVI will not regain normal vision34. However, improvement is usually seen over = time2,3,11,34. Visual improvement may be rapid, = particularly=20 in cases of traumatic injury, however, usually visual recovery is = gradual. Very=20 little is known about specific prognostic findings in CVI. In general, = children=20 with CVI and extensive neurological damage have the least favorable = prognosis=20 for recovery of vision. The finding of PVL confers a particularly poor=20 prognosis³⁵, compared to damage to the = visual cortex=20 only.

The prognosis for recovery of vision is probably better when the = injury=20 involves the striate cortex, not the optic radiations35. However, involvement of basal ganglia on = neuroimaging=20 also indicates a poor developmental and visual prognosis36. Basal ganglia disorders are almost = invariably=20 accompanied by generalized involuntary movements of the head, neck, and = eyes=20 which interfere with motor functions and vision21.

Bacterial meningitis is associated with a poorer prognosis than most = other=20 causes of CVI²⁹. Cardiac arrest and status=20 epilepticus are also typically associated with an unfavorable = prognosis30. Fortunately, status epilepticus is now rare. = Chen and=20 colleagues²⁹ have suggested that epilepsy = is also=20 associated with a poor prognosis. CVI is very common in infants with = infantile=20 spasms, especially when the EEG is hypsarhythmic. Abnormal visual = function can=20 result from loss of visual acuity and impaired perception.

Diagnostic Findings

The clinical examination is usually sufficient to establish the = diagnosis of=20 CVI. Children with CVI who have no anterior visual pathway abnormality = will have=20 a normal eye examination but will show poor visual behavior. For = example, they=20 will fail to regard a face or to pay visual attention to their = surroundings. The=20 ophthalmoscopic examination in typical cases of CVI is normal. Some = children=20 will have both anterior visual pathway disease and CVI. In these cases, = clinical=20 judgment is used to determine whether a component of vision impairment = is caused=20 by CVI. Additional physical findings may help to clarify the diagnosis = and must=20 be taken into account in determining the overall management of the child = with=20 CVI.

Children with CVI may experience head- and eye-movement = difficulties37. Abnormalities such as apraxia of eye = movement and gaze=20 palsies are common, as are abnormal pursuit eye movements. In these = ocular motor=20 disturbances, it may be difficult to distinguish the true loss of visual = acuity=20 from a disorder of eye movement that may mimic vision impairment.

Visual field defects are also common in CVI34. Measurement of visual = field=20 defects is difficult, even in normally developing children38,39. One method used effectively to measure = visual=20 fields is the confrontational examination, which relies on the child's = eye or=20 head movement to indicate that a target has been observed.

Children with CVI exhibit slow, inefficient, and highly variable = visual=20 performance. Patients with CVI characteristically have a short visual = attention=20 span^2,25,30,37. They typically see better = in familiar=20 surroundings^4,25 and when they are relaxed = and well=20 rested. Other aspects of behavior associated with vision could account = for this=20 variation in visual behavior (e.g. poor motor control mimicking vision=20 impairment or subclinical seizures interfering with visual = behavior).

Color vision and perception of movement are often preserved in = children with=20 CVI1. Often, these children use peripheral vision to search for objects. = They=20 may turn their heads before reaching for an object (retinal reach)3,25 with the head turned away from the side of = vision=20 loss. Moreover, they often bring objects closer to their eyes to = increase linear=20 magnification of the object of visual interest².

Gazing at lights is a common feature in CVI⁴⁰.=20 Paradoxically, a third of patients with CVI will exhibit photophobia, = but will=20 still gaze at lights from time to time^4l. = Children=20 tend to outgrow their photophobic behavior.

Investigational studies

Quantitative information about a patient's condition can be = clinically useful=20 and reassuring to patients and their families. A variety of techniques = can be=20 used to assess the extent of injury to the posterior visual pathways, = but while=20 a particular technique may be a good predictor of prognosis in = expertmental=20 cohorts, in the case of individuals such predictions are less useful^22,42.

In forced-choice preferential looking (FPL) tests, acuity is = determined by=20 noting the finest grating to which children reliably orient their gaze.=20 Inattention or inability to gaze directly could prevent a child from = following a=20 stimulus above chance levels³². Moreover, = FPL=20 measures may be difficult to interpret in children with head- and = eye-movement=20 difficulties. Thus, failure to reliably direct gaze towards a grating = card may=20 be determined more by motor-coordination problems than by vision = problems alone=20 in the child with CVI. On the other hand, FPL testing may reveal = specific=20 defects in gaze control in conjunction with other tests.

Research on visual evoked potentials (VEPs) has focused on this = method's=20 usefulness in confirming CVI or on its prognostic value for visual = outcome43. Several types of VEPs can be performed, = including the=20 transient, non-patterned flash VEP and the transient pattern reversal = VEP, each=20 of which yields information about the temporal waveform of responses to = single=20 presentations of a visual stimulus. Clarke and colleagues44 found that CVI patients with normal flash = VEPs had a=20 good prognosis for improvement. However, flash VEP may not accurately = assess=20 higher levels of visual processing. Pattern VEPs are more useful for = monitoring=20 visual development and rehabilitation in children⁴⁵.=20 Steady state VEPs show promising potential for quantification of visual = loss in=20 CVI and offer the advantage of testing several types of visual function = (e.g.=20 contrast sensitivity, grating acuity, vernier acuity)46. The VEP provides general information about=20 geniculocalcarine dysfunction and occipital responses to photic = stimuli1; the EEG can be interpreted in association = with VEPs.=20 The presence of normal alpha rhythm, superimposed on a normal = background, rules=20 out cortical visual impairment and homonymous hemianopia due to cortical = lesions³¹.

Clinical assessment can be supported with brain imaging studies. = Neuroimaging=20 of the brain can be used to confirm the clinical diagnosis of CVI4. MRI is often used to detect PVL in the first = days of=20 life, although the child's visual outcome cannot be accurately predicted = based=20 on neuroimaging findings³³. Ultrasound, = which is=20 portable and non-invasive, is also used to detect PVL in the first days = of life=20 and may be more sensitive than MRI during this period. Eken and = coworkers47 found that ultrasound could be used to = correlate=20 structural abnormalities with poor visual outcome.

MRI is also used to assess asphyxia in neonates⁴⁸=20 and may be the best predictor of outcome in the first week following = injury. A=20 normal MRI correlates with normal vision, although an abnormal MRI = finding does=20 not necessarily indicate loss of visual acuity⁴⁹.=20 Finally, MRI may show selective damage to periventricular white matter, = with a=20 less favorable prognosis for visual recovery35,49.

SPECT and PET scans have been used to investigate changes in cerebral = blood=20 flow⁵⁰. These tools may be better at = predicting=20 outcome than MRI but have not been widely used, mainly because PET = requires=20 delivery of a small amount of a radioactive isotope. Functional magnetic = resonance imaging (fMRI) shows promise as a diagnostic tool. The fMRI = measure=20 demonstrates areas of the brain that are metabolically active. However, = fMRI=20 requires an alert, immobile, cooperative patient and, therefore, has = limited use=20 in children.

Clinical management

The identification of other neurological disorders associated with = CVI is an=20 important component of management. Many children with CVI have motor=20 complications, including disturbances of ocular motor function. These = motor=20 control problems complicate the interpretation of behavioral signs of = vision in=20 children with CVI, and pose potential problems in the diagnosis and = management=20 of CVI.

Prompt management of any medical problem that could interfere with = hearing=20 (e.g. otitis media) is essential, since children with CVI may rely = extensively=20 on their other sensory functions. Patients with CVI frequently have = complex=20 epileptic disorders. Anticonvulsant drugs must be carefully selected, = with=20 continuous monitoring of the blood levels, in order to avoid excessive=20 sedation.

Sleep disorders in visually impaired children have complex = etiologies51 and=20 have been associated with painful esophageal reflux and orthopedic = problems.=20 Chronic sleep disturbances in children with CVI who have multiple = disabilities=20 may be treated with hypnotics or melatonin⁵².

Poor feeding skills and recurrent problems with aspiration are common = because=20 of difficulties encountered with foods that require chewing (partly a = visually=20 learned skill) and swallowing. Affected children frequently have CP with = its=20 associated orthopedic problems, such as subluxated or dislocated hips. = These=20 children will benefit from a comfortable and functional seating = arrangement,=20 which may help to promote cooperation during visual rehabilitation.

Many patients with severe developmental delays are readily = overstimulated in=20 an uncontrolled environment. The inability to cope efficiently in this=20 environment may provoke sleep disruptions, which may ultimately trigger=20 self-abusive behavior. The neurological disorder of physical self-abuse = is often=20 overlooked and can only be treated effectively by modifying home and = school=20 environments.

Children with neurodevelopmental disabilities and their families = require the=20 services of a multidisciplinary team specialized in the development of = children=20 with visual impairments. These specialists can provide an accurate = evaluation of=20 the patient's condition and formulate an individual program plan to = monitor the=20 child's progress⁵³. Major medical centers = now have=20 experienced specialists who deal with the needs of children with = disabilities.=20 The effectiveness of the team approach may ultimately provide a better=20 developmental outcome for the child⁵⁴.

Rehabilitation program

The goal of visual rehabilitation is to maximize the use of = functional=20 residual vision. Early assessment is critical². The=20 misdiagnosis of CVI, either as a behavioral difficulty or a learning = disability,=20 can delay remediation and result in significant educational delays that = leave=20 emotional sequelae⁵⁵.

Visual and cognitive development are closely related54. Younger patients, who have not reached = developmental=20 maturity will require special learning environments that promote maximum = stimulation of residual vision. Such environmental stimulation may help = to=20 prevent developmental delays⁵⁶. Research = indicates=20 that developmental milestones that normally require vision ('reaching' = and=20 'walking')⁵⁷ are often delayed in children = with=20 visual impairment, even in the absence of other disabilities.

Although traditional educational settings strive to provide = stimulation and=20 diversity to encourage children's developmental growth, a simplified = visual=20 environment is more beneficial to children with CVI because it forces = them to=20 focus attention on a particular visual stimulus^1,2.=20 In these children, color, high contrast, and the use of motion may = facilitate=20 visual recognition of an object^1,3,37. = Reinforcement=20 with tactile and verbal stimulation is also important. The = 'ritualization' of=20 tasks performed in standardized fashion at the same time every day may = also be=20 helpful². Consistency of the environment = may be=20 particularly helpful for those children with orientation problems, known = as=20 topographical agnosia⁵⁸ which is = characterized by a=20 poor sense of location or direction. This condition may affect children = who are=20 ambulatory or have mobility in a wheelchair.

Children with CVI appear to be at a disadvantage when performing = reading and=20 mathematical tasks, although this may only be partly attributed to = intellectual=20 capacity and visual impairments. Reading difficulties may derive in part = from=20 the 'crowding' effect, which is the child's inability to see a symbol = when it is=20 flanked by other symbols that crowd the visual field2,37. Sliding a finger along a line of text may = facilitate=20 reading in children with CVI who have developed higher functioning = skills.=20 Pointing at distant targets may improve tracking16.

Some studies suggest that children with visual impairments may learn = to=20 express themselves before sighted children⁴, although=20 other studies have reported that language development is initially = delayed59. Children with CVI are usually delayed in = language=20 skills. Learning to write legibly can also be difficult for children = with visual=20 impairment⁶⁰.

Intelligence tests in children with visual impairment may not reveal = their=20 true potential if their scores are compared to those of either sighted = or blind=20 children⁶¹. Therefore, assessment of = children with=20 visual impairment should be performed by experienced specialists = knowledgeable=20 about the development of children with visual impairments. There is a = trend in=20 the USA to integrate children with disabilities into the mainstream = classroom.=20 However, children with CVI will benefit more from the implementation of=20 rehabilitation programs that provide a streamlined, simplified, visual=20 environment.

Conclusion

Central to the diagnosis of CVI is loss of visual acuity. Future = research in=20 CVI will continue to elucidate the various patterns of vision loss that=20 accompany loss of visual acuity. To this effect, better diagnostic tools = are=20 needed to accurately define deficits in pattern vision and vision = processing=20 (higher-order vision). Currently, there is no precise treatment for CVI, = and=20 many rehabilitative measures are unproven. Clearly, there is a great = need for=20 additional research on treatment and management of this common and = complex=20 disorder.

Accepted for publication 15th June 2000.

Acknowledgements

Dr.Good was supported by National Eye Institute grant EY00384.

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