Cortical Blindness

Cortical Blindness in Children: A Study of Etiology and Prognosis

Virginia C.N. Wong, MBBS, MRCP

Thirty-four children (20 boys, 14 girls) with congenital and acquired cortical blindness were analyzed for visual outcome in relation to etiology, visual evoked potentials, electroencephalography, and cranial computed tomography. All 7 children with congenital cortical blindness remained blind on subsequent examination. Of the 27 children with acquired blindness, 16 (59%) had poor visual outcome. Poor visual outcome occurred in those with cardiac arrest, hypoxia, status epilepticus, intracranial hemorrhage, cerebral thrombosis, and head trauma. Good visual outcome occurred in children with hypotensive episodes after cardiac surgery. Of the 12 children with recovery of vision, the interval from acute loss of vision to partial or total recovery was 2 weeks to 5 months. Seven children had complete recovery of vision with no residual visual field defect. The majority of children (87%) had focal or multifocal spike-and-waves and slow sharp-wave discharges on electroencephalography. None had photic recruitment response or occipital spike-and-wave discharges. Flash visual evoked potential studies performed during acute episodes of cortical blindness documented 11 with absent response, 10 with bilateral increases in latency, and 6 with normal responses. There was no corre lat ion between normal visual evoked potentials and a good visual outcome. Only 2 of 6 children with normal responses had normal vision. Abnormal or absent responses are more predictive of a poor recovery of vision because only 3 of 21 (14%) had normal vision on subsequent examination. Abnor- mal electroencephalographic findings with focal or multifocal spike-and-wave discharges or cerebral atrophy on cranial computed tomography are also poor prognostic signs.

Wong VCN. Cortical blindness in children: A study of etiology and prognosis. Pediatr Neurol 1991 ;7:178-85.

Introduction

Cortical blindness (CB) has been defined as complete loss of all visual sensation and loss of optokinetic nystag-

mus with preservation of pupillary response, normal eye motility, and normal retina [ 1 ]. Cortical visual impairment (CVI) has been recommended as a better term because it encompasses a spectrum of visual loss ranging from absent to some residual vision [2,3].

Various causes of CB have been reported in children, including cardiac arrest [4,5], status epilepticus [6,7], hypoxia or perinatal asphyxia [8], cerebral infarction [9], meningitis, encephalitis [ 10-13], subacute sclerosing leukoencephalitis [14], hypoglycemia [15,16], uremia [17. 18 ], hydrocephalus, shunt malfunction [19,20], head trauma [21-25], cardiac surgery [26,27], cerebral or vertebral angiography [28-35], drugs (i.e., cyclosporin A and steroids) [36,37], acute carbon monoxide poisoning 138], and the ictal state in occipital lobe epilepsy [39,401 or postictal phenomenon [41 ]. Other causes reported in adults include subclavian vein catheterization [42], pre-eclampsia [43, 44], postpartum pulmonary embolus [45], acupuncture [46], Wegener's granulomatosis [47], sarcoidosis [48 l, and posterior fossa tumor [49],

In this study, the clinical features and laboratory investigations of 34 children with cortical blindness are analyzed to determine the prognosis of visual outcome in relation to etiology, visual evoked potential (VEP), electroencephalographic (EEG), and computed tomographic (CT) findings.

Methods

Thirty-lour CB children (20 boys, 14 girls), ages I month to 14 years, admitted to the Department of Paediatrics, University of Hong Kong at the Queen Mary Hospital from 1985 to 1990. were analyzed. Patients were included when severe visual loss occurred in the presence of normal pupillary response and normal fundi. Patients were excluded when the duration of visual loss lasted less than 48 hours.

All children had multidisciplinary evaluations, including clinical assessment by ophthalmologists, a developmental pediatrician, and a child neurologist. Investigations, including flash VEP, EEG, photic stimulation, and cranial CT, were performed for most children. They were examined subsequently at the Child Assessment Centre of the Duchess of Kent Children's Hospital for I-5 years.

~)'sual Z?sting. The test of visual acuity was difficult in yotmger patients. Therefore, visual acuity was graded as "blind" when no appar- ent vision was present, including light perception or protective blink- ing; "'poor" when only light perception was evident; "l'~.6r" when there was ~m ability to see a 1 inch red woolen ball or I cm chocolate candy

From the Department of Pediatrics; University of Hong Kong; Queen Mary Hospital; Pokfulam, Hong Kong.

Communications should be addressed to: Dr. Wong; Department of Pediatrics; University of Hong Kong; Queen Mary Hospital; Pokfulam, Hong Kong. Received September 11, 1990; accepted October 30, 1990.

178 PEDIATRIC NEUROLOGY Vol. 7 No. 3

at 1 foot; and "good" when there was an ability to see 1 mm chocolate candy at a 1 foot distance.

Visual Evoked Potentials. Flash VEPs were obtained using flash stimuli through LED goggles at a rate of 1 Hz and recorded over the inion (Oz) referenced to the frontal region (Fz) according to the Inter- national 10-20 System using the Medelac MS92a machine. The latency to the peak of the positive response (PI00) was measured.

Electroencephalagraphy. EEG was performed with scalp electrodes according to the International 10-20 System. The latest EEG finding taken with the scoring of the visual outcome was analyzed for any spike-and-wave or sharp-wave activities, the localization of abnormal- ity, and the response to photic stimulation.

Results

(I) Congenital Cortical Blindness (Patients 1-7). The clinical features, etiology, and investigation are recorded in Table 1. Of the 7 children (3 boys, 4 girls) with congenital CB, 3 had lissencephaly and I had mitochondrial myopathy. These children had no visual fixation or visual following at 1-4 months of age. All had associated neurologic deficit, including severe mental retardation and myoclonic epilepsy in all children and cerebral palsy (spastic tetraplegic type) in 4. All remained blind except for some degree of light perception in 3. Six had abnormal VEPs (i.e., 2 absent and 4 bilateral prolonged latencies). All had abnormal EEGs with focal or multifocal spike- and-wave or sharp-wave discharges. None had photic recruitment responses. CT scans demonstrated cerebral atrophy in 5 and pachygyria-agyria pattern in 2.

(II) Acquired Cortical Blindness (Patients 8-34). The most common cause among these 27 patients (17 boys, 10 girls) was hypoxia (N = 14; 58%) with severe perinatal asphyxia in 1, cardiac arrest in 2, severe hypotensive episodes following cardiac surgery in 5, and status epilepticus in 6. Six had encephalitis or meningitis. Hydrocephalus with shunt malfunction occurred in 1, hydrocephalus with subdural hematoma, cerebral thrombosis, intracranial hemorrhage, and head trauma occurred in 1 each. Of the 6 children with status epilepticus, 3 (Patients 21,24,26) subsequently proved to be suffering from metabolic or degenerative diseases. The vision of these 3 children was normal prior to status epilepticus. In the other 3 children, all investigations failed to reveal an underlying etiology. Hypoxia related to prolonged seizure is the most likely cause of the visual damage.

The majority (88%) had associated neurologic deficit with cerebral palsy in 19, mental retardation in 22, myoclonic epilepsy in 7, generalized tonic-clonic epilepsy in 6, complex partial seizure in 1, and deafness in 1. Good recovery of vision occurred in 7 children and partial recovery occurred in 5. Recovery of vision occurred from 2 weeks to 5 months after the insult.

VEP. Of the 23 children with acquired CB who had VEPs performed, only 6 had normal responses. Eleven children had absent VEPs and 10 had bilateral increases in P I00 latencies.

In the congenital CB group, only 1 had normal VEPs. EEG. EEG was performed in 24 children in the ac-

quired CB group. Focal or multifocal spike-and-wave dis-

charges occurred in 12, focal slow-and-sharp-wave discharges in 3, focal or diffuse slowing in 4, and was normal in 5. None had photic recruitment responses. None had occipital spike-and-waves.

In the congenital group, all had abnormal EEGs with focal or multifocal spike-and-wave or sharp-wave discharges and 2 children had additional burst suppression patterns.

Cranial Computed Tomography. The majority of children had cerebral atrophy (11 of 27, 41%). Only 1 had bioccipital infarction.

Prognoses

Prognoses are listed in Table 2. Visual recovery was poor. Of the 7 congenital patients, 4 were completely blind and 3 had only light perception. In the acquired group, 59% had poor visual outcomes; in the majority of them, hypoxia, cardiac arrest, or status epilepticus was impli- cated. Normal visual outcomes occurred in 26%; 3 had had hypotensive episodes after cardiac surgery and 3 had had encephalitis or meningitis. All 5 children with fair visual ou tcomes (Patients 9,12,17,21,34) at tended special schools for the physically and/or mentally handicapped.

VEP. Of the 6 children with normal VEPs in the acquired group, only 2 had good recovery of vision, whereas only 3 of 21 (14%) of those with bilateral increases in latency or absent responses had good visual recovery.

EEG. Children with focal or multifocal spike-and- waves usually had poor visual outcomes. Children with normal EEGs had good visual recovery.

CT. The majority had cerebral atrophy and the visual outcomes were poor (13 of 16, 81%).

Discussion

The outcome of CB was poor in the present study. Of the children with CB due to congenital and acquired causes, 68% had poor visual recovery. The prognosis was particularly poor when the cause of CB was hypoxia, cardiac arrest, status epilepticus, or cerebrovascular diseases. Those sustaining hypotensive episodes after cardiac surgery had much better prognoses; 60% had normal vision. In general, the prognoses of CB children are good in other reports [5,8,19,20,22,23]. Of children with CB, 25-50% recovered useful vision, although they may be left with a complex disorder of visual perceptions. This difference may be due to varying CB etiologies and the different duration of hypoxia in our study [5,8,11 ].

Some degree of visual recovery will occur in CB children. Hoyt [50] and Hoyt and Walsh [51] reported recovery of vision in all 43 infants with CB but the rate of recovery was variable; visual recovery continued to occur for more than 2 years after the original insult in some children. There was no correlation between the duration of CB and the extent of visual recovery. Poor prognostic signs were uncontrolled seizures more than 3 months after insult and the development of microcephaly. The mech- anism of vision recovery is unknown. It may be due to

Wong: CorticalBlindness 179

Table 1. Clinical features and investigations of cortical blindness

Patient Age (yrs) No./Sex/ at Loss Age (yrs) of Vision Cause

G r oup I - Congen i ta l

1/M/6.2 0.1 Congenital

2/M/8 0.3 Congenital

3/F/5.7 0.8 Congenital

4/M/9.6 0.3 Mitochondrial myopathy

5/F/6.8 0. I Lissencephaly

6/F/2.9 0.3 Lissencephaly

7/F/1.9 0.4 Lissencephaly

G roup 2 - A c q u i r e d

8/F/8.9 0.6 Perinatal asphyxia

9/M/5.3 0.4 Cardiac arrest

10/F/4.6 0.6 Cardiac arrest (PCS; TOF)

t 1/M/17.6 14 PCS (DORV)

12/M/5. I 3 PCS (TOF)

13/M/2.3 0.9 PCS (TGA)

14/F/9.4 4.4 PCS (Pul S)

15/F/4.4 0.6 PCS (TAPVD)

16/M/3.9 1.3

17/F/3.6 0.1

18/F/2.2 0.8

Perinatal asphyxia, poren- cephalic cyst

Hydrocephalus with shunt malfunction

Hydrocephalus, subdural hematoma

Associated Neurologic

Deficit

CP (ST), severe MR, Myo Epi

Severe MR, Myo Epi

Severe MR, Myo Epi, deafness

Severe MR, Myo Epi


CP (ST), severe MR. Myo Epi

CP (ST), severe MR, Myo Epi, deafness


CP (H), mild MR, Myo Epi


Low average intelligence


CP (ST), severe MR

CP (ST), severe MR

CP (H)

CP (ST), severe MR

Visual Out- come

B lin d

Blind

Blind

Blind

Blind

Blind

Blind

Blind

Fair

Blind

Normal

Fair, visual field defect

Blind

Normal

Normal

Blind

Fair, visual field defect

Blind

Inter- val of ROV

3 mos

2 wks

5 mos

4 wks

5 mos

5 InOS

F VEP EEG CT

BL 1" latency

Normal

BL $ latency

BL $ latency

BL T latency

Absent

Absent

Absent

S-W (both frontal), Cerebral PS-NR atrophy

Sharp-wave (R Cerebral parieto-temporal ), atrophy PS-NR

S-W (multifocal), Cerebral PS-S-W atrophy

S-W and poly S-W Cerebral (multifocal), PS-NR atrophy

S-W (multifocal) Pachygyria- burst suppression agyria protein, PS-NR

Spike]poly S-W Pachygyria- (multifocal), PS-NR agyria

ttypsarrhythmia, Pachygyria- burst suppression agyria, L pattern, PS-NR cerebral

hemiatrophy

Spike/sharp-wave Cerebral (central, posterior) atrophy PS-NR

BL $ S-W (multifocal) Cerebral latency PS-NR atrophy

Absent

BL ? latency

S-W 0nultifocal Cerebral especially frontal, alrophy temporal) PS-NR

Normal Norlna I

BL $ Normal BL occipital latency infarction

Absent

Absent

Absent

S-W (muhitocal) Cerebral PS-NR atrophy

Normal Nomml

Slow/sharp-wave Cerebral Icentral) PS-NR atrophy

Porenceph- alic cyst

Hydroceph alus

Hydroceph- alus


Table 1. (Continued)

Patient Age (yrs) No./Sex/ at Loss Age (yrs) of Vision

19/M/1 0.3

Cause

Intracranial hemorrhage

20/1=/10 8 Cerebral thrombosis

21/M/4 0.1 Urea cycle defect, SE

22/M/3 1 SE

23/F/5 3.1 SE

24/F/1.1 0.6 Ceroid-lipofus- cinosis, SE

25/M/6.4 3.9 SE

26/M/6.3 2 SE, Reye syn

27/M/6.2 3 Encephalitis

28/M/4.6 2 Encephalitis

29/M/11 6 Encephalitis (influenza)

30/F/5.6 0.9 Encephalitis (herpes simplex)

3 l/M/3 0.6 Meningoen- cephalitis

32/M/4 1

33/M/5 0.4

Meningitis (pneumococ- cal), PPE

Meningitis (pneumococ- cal)

34/M/11.6 8 Head trauma

Associated Visual Inter- Neurologic Out- val of

Deficit come ROV F VEP

CP (ST), severe Blind MR


CP (ST), severe Fair MR, Epi

Severe MR, Epi Blind

CP (SD), moderate MR, Epi

- - Absent

- - Absent

5 mos Normal

- - BL $ latency

Normal 3 mos Absent

CP (ST), severe Blind MR, Epi

Moderate MR, Blind deafness


Moderate MR Normal

- - Normal

- - Normal

- - BL 1" latency

1 mo BL $ latency

- - Normal 2 wks Normal

MR (mild), Epi Normal 1 mo Normal (TLE)



CP (ST), severe Blind MR, Myo Epi

CP (ST), severe Blind MR, Myo Epi

CP (dys), severe Fair MR, Myo Epi

Abbreviations: BL = Bilateral H = Hemiplegia CP = Cerebral palsy MR = Mental retardation DORV = Double outlet right ventricle Myo = Myoclonic Dys = Dyskinetic NR = No response Epi = Epilepsy PCS = Post cardiac surgery F VEP = Flash visual evoked potential PPE = Post pertussis enceph.

- - Absent

EEG

Low-voltage slow background, PS-NR

Slow waves (R parietal, L frontal), PS-NR

S-W (both parietal), sharp slow wave (both posterior), PS-NR

S-W(diffuse)

Slow-sharp-wave (posterior), PS-normal

S-W(diffuse), PS-NR

Diffuse slowing PS-NR

Normal

CT

Subarachnoid, intracranial hemorrhage

BL parietal infarction

Normal

Cerebral atrophy

Cerebral atrophy

Cerebral atrophy

Cerebral atrophy

Normal

Normal Normal

Diffuse slowing

Diffuse slowing, slow-wave (R temporopari- etal), PS-NR

Normal

Normal

Spike/sharp-wave Hypodensity (L temporal) PS- over L tem- slow/sharp-wave, poral region S-W discharges

S-W (multifocal), Cerebral PS-NR atrophy

- - BL $ S-W (multifocal), Cerebral latency PS-NR atrophy

- - Absent S-W (multifocal), Cerebral PS-NR atrophy

Spike/sharp-waves R epidural (R frontal), PS-NR hematoma

3 mos Normal

PS = Photic stimulation S-W = Spike-and-wave Pul S = Pulmonary stenosis TAPVD = Total anomalous pulmonary ROV = Recovery of vision venous drainage SD = Spastic diplegia TGA = Transposition of great arteries SE = Status epilepticus TLE = Temporal lobe epilepsy ST = Spastic tetraplegia TOF = Tetralogy of Fallot

Wong: Conical Blindness 181

Table 2. Relation of visual outcome and etiology, VEP, EEG, and CT

Visual Outcome Blind/ Poor Fa i r Good 'l?otal

Etiology

(1) Congenital 7 0 tt 7

(11) Acquired 16 4 7 27

- Cardiac arrest/hypoxia/status 7 2 1 I0 epilepticus

- Cardiac surgery I I 3 5

Hydrocephalus 1 I 0 2

-- lntracranial hemorrhage/cerebral 3 0 (I 3 thrombosis/head trauma

Encephalit is/meningitis 4 0 3 7

VEP*

Bilaterally $ latency 6 2 2 10

Absent response 9 1 1 I I

Normal 3 1 2 6

EEG

Focal/multifocal spike waves 15 3 0 18

Focal slow/sharp waves 2 0 2 4

Focal/diffuse slowing 3 0 2 5

Normal 0 I 3 4

CT

Cerebral atrophy 13 1 2 16

Infarction I I 0 2

Others 7 2 l) 9

Normal [ I 0 2

* For acquired causes.

resolution of edema, restitution of axonal connections, the use of minute parts of preserved field, or "non-striate vision" [52,53].

The general pattern of recovery from CB was described as denial of the inability to see in some patients followed by perceiving and following light, then perceiving moving objects close to the eyes, and later perceiving large, bright- ly colored objects. Later, visual acuity improved but visual cognitive and visual-perceptual deficits may persist for a long time or may remain permanently. Some may have residual visual field defects [8,51 ]. The pattern of visual recovery in this study also followed a similar trend. Those who were partially sighted needed special education and 2 patients had residual visual field defects on gross examination. The longest recovery time was 5 months and there was no improvement in visual function during a follow-up period of 9 months to 5 years in others with acquired causes.

The pathogenesis of CB was suggested by Barnet et al. [8] as related to the "border-zone hypothesis" [54] with transient cerebral hypotensive episodes causing more severe tissue hypoxia in the border zones among the 3 major cerebral arteries (i.e., the primary visual, sensory, and motor cortices with their association areas). Speech functions, in the distribution of the middle cerebral artery, are relatively spared. Other hypotheses include cerebral edema with herniation of the medial portions of the temporal lobes into the tentorial opening, thus compressing the posterior cerebral arteries; focal edema of the white matter in uremia [18]; thrombosis of superficial cortical veins in meningitis; and transient alteration of the blood-brain barrier in causing transient edema of the striatal cortex [29].

Many patients suffering from shock or hypoxia will have damage to the optic radiations; therefore, it affects not only the geniculocalcarine system to the striatal cortex which is responsible lot precise macular and peripheral


vision and the identification of objects but also the parietal border zones, thus affecting the colliculo-pulvinar-parietal projection which is responsible for the detection of events and the direction of gaze [52,53].

Children with CB behaved differently from those with peripheral blindness. Nystagmus and roving eye move- ments are unusual; patients do not appear to be blind and they exhibit inertia, inattention, and variability in visual performance from moment to moment [52,53].

The use of VEP in predicting the prognosis of CB is controversial [3,50,54-63]. Hess et al. [62] investigated the validity of flash-VEP and pattern-reversal VEP in CB and concluded that flash VEP was not useful for differentiation of CB from psychogenic visual disorders and preserved flash VEP in the acute stage of CB was not reliably prognostic of visual recovery [62]. Abolished flash VEPs probably indicate a poor prognosis, whereas preserved flash VEPs do not allow prediction of good visual recovery. Pattern-reversal VEP, however, is more useful for diagnosis because a normal response is unlikely in acute and complete CB. The only possible exception was a small lesion restricted to the striate area 17 with preservation of areas 18 and 19 [59].

Preserved flash and pattern-reversal VEPs were observed in complete CB of a 6-year-old boy where CT revealed bilateral destruction of the occipital lobes (i.e., areas 18,19), the visual association cortex with sparing of the striatal cortex (i.e., area 17), or the primary receiving area of the geniculocortical visual pathway [58]. Preserved flash VEPs were also reported in complete CB with postmortem findings of extensive bilateral posterior cerebral infarcts. The VEP was probably mediated by extra geniculocalcarine connections between the optic nerve and the secondary visual cortex of the occipital convexity [63]. Celesia et al. reported the complete destruction of bilateral areas 17 with relative preservation of areas 18 and 19 in a woman with CB for more than 2 years and normal VEPs; they proposed the origin of VEP as mediated by extra- geniculocalcarine pathways to the secondary visual cortices which are not capable of providing conscious visual perceptions in humans [59].

In a study of VEPs in 6 children with CB following meningitis and head trauma, changes in short-latency VEPs were correlated with visual ability and changes in longer latency VEPs correlated with levels of psychomotor function on subsequent examination [64].

It has been demonstrated that diffuse light and coarse moving stimuli can activate a "second visual system" which generates flash VEPs [62]. This system originates in cells in the periphery of the retina and projects along the geniculostriatal pathway and the structures of the extrastriatal visual pathway, such as the midbrain (primary superior colliculus), with indirect mediation to the thal- amus or parietal cortex. Cells of the center of the retina are responsible for shape and pattern recognition. Respon- ses are projected through the lateral geniculate nucleus to the striatal cortex and generate the pattern VEP. Thus,

preserved flash VEPs in CB could indicate a certain ad- vantage over absent responses because the ability to have some rough spatial orientation could be achieved through the extrastriatal visual system. In our study, however, absent flash VEPs during acute episodes of CB usually had poor visual recovery and only 3 (20%) regained partial to normal vision.

A study of EEG in 40 children with CB revealed multifocal disturbances because of diffuse cerebral involvement [2]. Isolated occipital spikes were rare and photic stimulation was of little use in diagnosis. Children with some residual vision usually had alpha rhythms, while multi- handicapped children had multifocal abnormalities and suppressed posterior waking backgrounds, but no alpha rhythms. The presence or absence of alpha rhythms ap- peared to reflect the residual activity of the striatal cortex. Absent alpha rhythm in CB was observed in children and adults [55,65].

The majority of children (65%) in our study had spike- and-wave or sharp-wave abnormalities on EEG. Most of these patients have multiple handicaps due to diffuse cerebral involvement and poor visual function. None of the children had occipital spikes or photic recruitment responses. Alpha rhythm was also rarely observed except in those patients with ultimate recovery of vision.

CT and magnetic response imaging (MRI) were helpful in evaluating 30 children with hypoxic CB [66]. Only 2 children had normal scans of the posterior visual pathway and both had favorable visual outcomes. Visual recovery differed significantly with respect to the age at which the hypoxic insult occurred and the CT and MRI abnormalities in the areas of the optic radiations, but not with abnormalities in the striatal or parastriatal cortices. Bioccipital abnormalities on CT were also reported to be associated with poor prognoses [54]. The majority of our patients had cerebral atrophy on CT and visual recovery was poor. Even the 2 children with normal CT scans did not have good outcomes.

In general, this study demonstrated that the prognosis of visual recovery in children with cortical blindness, both congenital and acquired, is poor. Those with absent or abnormal VEPs or abnormal EEG and CT had poorer prognoses probably due to more diffuse cerebral damage.

The author acknowledges Teresa Wong for secretarial assistance.

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Cortical Blindness