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Year : 2007  |  Volume : 55  |  Issue : 2  |  Page : 154-156

Ocular defects in cerebral palsy

Department of Ophthalmology, Kasturba Medical College Hospital, Manipal - 576 104, Karnataka, India

Date of Submission13-Jun-2005
Date of Acceptance30-Apr-2006

Correspondence Address:
Sabita Katoch
Department of Ophthalmology, Kasturba Medical College Hospital, Manipal - 576 104, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0301-4738.30717

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There is a high prevalence of ocular defects in children with developmental disabilities. This study evaluated visual disability in a group of 200 cerebral palsy (CP) patients and found that 68% of the children had significant visual morbidity. These findings emphasize the need for an early ocular examination in patients with CP.

Keywords: Cerebral palsy, cortical visual impairment, refractive errors, strabismus, visual disability.

How to cite this article:
Katoch S, Devi A, Kulkarni P. Ocular defects in cerebral palsy. Indian J Ophthalmol 2007;55:154-6

How to cite this URL:
Katoch S, Devi A, Kulkarni P. Ocular defects in cerebral palsy. Indian J Ophthalmol [serial online] 2007 [cited 2023 Jan 29];55:154-6. Available from: https://www.ijo.in/text.asp?2007/55/2/154/30717

Refractory errors in 200 cerebral palsy patients

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Refractory errors in 200 cerebral palsy patients

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Strabismic errors in cerebral palsy

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Strabismic errors in cerebral palsy

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Visual acuity in 200 patients with cerebral palsy

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Visual acuity in 200 patients with cerebral palsy

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Cerebral palsy (CP) occurs in 1-2/1000 population and has a variable etiology which results from any disorder that causes perinatal brain damage.[1] It can be subdivided into three clinical types:[2]

  1. Spastics (about 60% of the CP population) presumably have involvement of the pyramidal tracts.
  2. Dyskinetics (about 35%) presumably have lesions in the extrapyramidal system.
  3. Ataxics (about 5%) have the signs and symptoms of cerebellar involvement.

The majority of these children have ocular problems as well.[1] This study was done to assess the extent of ocular problem and evaluate the nature of the treatment required.

  Materials and Methods Top

Two hundred consecutive patients diagnosed with CP from June 2004 to Jan 2005, underwent ophthalmologic evaluation. Vision was assessed by: (a) asking the parents about visual behavior, (b) Snellen's visual acuity, (c) does the child fixate and follow light, (d) visual axis, (e) presence of nystagmus, (f) does the child allow occlusion of either eye, (g) follows a moving object 33 cm away.

This was followed by a complete ocular examination. Cycloplegic refraction was done under atropine ointment in children less than seven years and in those with esotropia. In others 1% cyclopentolate drops were used for cycloplegia.

The age of the patients varied from eight months to 21 years. There were 110 males and 90 females. One hundred and eighty-five patients (91.5%) had spastic diplegia. There were five patients of spastic quadriplegia, two patients each with spastic hemiplegia, paraplegia and mixed CP. There was one patient each with spastic monoplegia, triplegia, athetoid and dystonic CP.

Snellen's visual acuity (VA) could be recorded in 44 patients (22%) [Table - 1]. Visual axis were parallel in 122 patients (61%). Seventy eight patients had strabismus [Table - 2].

Myopic refractive error was seen in 27 (13.5%) children where as 40 (20%) had hypermetropia [Table - 3]. Glasses were prescribed for more than 2 diopter (D) of refractive error and for more than 1D of astigmatism.

One hundred and eighty-eight patients (94%) had normal pupillary reactions. Eleven patients with diffuse disc pallor had sluggish pupillary reactions. One patient with congenital glaucoma had dilated and nonreacting pupils. Five patients (2.5%) had developmental cataract. Sixty-two patients (81%) had normal fundii. Temporal disc pallor was present in 22 patients (11%). Diffuse disc pallor was present in 11 patients (5.5%). One patient had advanced glaucomatous cupping in both eyes. Myopic fundus was present in one patient. Macular choroiditis, fundal coloboma and a salt and pepper fundus associated with deafness was present in one patient each.

Horizontal, jerky nystagmus was found in 11 patients (5.5%). Of these one had bilateral cataract, two had disc pallor, one had fundal coloboma and one had more than -5D of myopia.

Intraocular pressure (IOP) more than 21 mmHg was present in three patients; one had advanced glaucomatous cupping and two had a cup/disc ratio of 0.5: 1. Horizontal corneal diameters > 13 mm were found in eight patients (4%). Only one of these had congenital glaucoma. In the rest, IOP and fundii were normal. Less than 10 mm horizontal corneal diameter was present in one patient who had a fundal coloboma with nystagmus.

Three out of five patients with cataract underwent surgery. Postoperatively one child could only follow light (with nystagmus), one had 20/30 vision and one could see objects at intermediate distance. Squint surgery was done in five patients; three for unilateral exotropia and two for alternating esotropia. One patient underwent bilateral trabeculectomy. However, the vision remained poor and there was advanced glaucomatous cupping in both eyes. Two patients with a cup/disc ratio of 0.5:1 were kept under observation. Two patients with unilateral esotropia underwent occlusion therapy for amblyopia. The vision improved by two lines.

  Discussion Top

In India, vast majority of CP patients have spastic CP (91.4%).[3] It was 98% in our study. Of the 200 patients, 80 patients (40%) had an ocular cause for poor vision while 56 patients (28%) were diagnosed to have cortical visual impairment (CVI). In earlier studies from India, it has been estimated that 9-54%[3],[4] of children with CP have visual disability. Spasticity and blindness are a bad combination, since through touch, the "hands of the blind become their eyes".[1]

The overall incidence of strabismus was 39%. Pigassou-Albouy had reported a 50% incidence of strabismus in a group of CP patients, while the incidence in the general population is only 3%.[5] Dyskinetic srabismus seen exclusively in CP with an athetoid component[6] was not seen. The high incidence of strabismus in the CP population is probably related to lesions in the subcortical oculomotor centers or cerebellar lesions which disrupt binocular vision. Occlusion therapy in two children with unilateral esotropia met with limited success; amblyopia in these children is partly functional and partly neurological and carries a poor prognosis.[5] The association of refractive errors with CP was confirmed in this study. Myopia is reportedly more frequent in spastics while hypemetropia predominates in the dyskinetics.[2] This study as well as others demonstrates that the refractive errors are more evenly distributed.[7]

Other causes of visual disability include optic atrophy found in 16.5%, similar to the figure reported by Lossef in 88 children.[7] CVI was diagnosed in 56 patients where despite a normal ocular examination the vision was judged to be poor. CVI refers to lesions in the posterior visual pathway (from lateral geniculate body to the visual cortex) and represents difficulty in processing and interpreting visual information in the visual cortex.[8] Neuroimaging in this group of children often shows lesions in the visual cortex called periventricular leukomalacia (PVL). PVL affecting the visual radiation is thought to be the end result of hypoxic-ischemic insult to the developing brain. CVI due to PVL is characterized by delayed visual maturation, subnormal VA, crowding, visual field defects and visual perceptual-cognitive problems.[8] The presence of CVI typically worsens the functional outcome in patients with CP.[9]

In conclusion, visual handicap plays a significant role in the overall disability of CP children. All pediatricians engaged in the care of these children must be encouraged to seek ophthalmologic assessment as a part of a broad multidisciplinary approach to the management of these children.

  References Top

Jan JE, Freeman RD, Scott EP. The multihandicapped visually impaired children. In : Visual impairment in children and adolescents. Grune and Stratton: New York; 1977. p. 75-81.  Back to cited text no. 1
Fantl EW, Perlstein MA. Refractive errors in cerebral palsy. Am J Ophthalmol 1967;63:857-63.  Back to cited text no. 2
Srivastava VK, Laisram N, Srivastava RK. Cerebral Palsy. Indian Pediatr 1992;29:993-6.  Back to cited text no. 3
Bhatia M, Joseph B. Rehabilitation of cerebral palsy in a developing country: The need for comprehensive assessment. Pediatr Rehabil 2000;4:83-6.  Back to cited text no. 4
Pigassou-Albouy R, Fleming A. Amblyopia and strabismus in patients with cerebral palsy. Ann Ophthalmol 1975;7:382-4,386-7.  Back to cited text no. 5
Buckley E, Seaber JH. Dyskinetic strabismus as a sign of cerebral palsy. Am J Ophthalmol 1981;91:652-7.  Back to cited text no. 6
Lossef S. Ocular findings in cerebral palsy. Am J Ophthalmol 1962;54:1114-8.  Back to cited text no. 7
Jacobson L, Ygge J, Flodmark O, Ek U. Visual and perceptual characteristics, ocular motility and strabismus in children with periventricular leukomalacia. Strabismus 2002;10:179-83.  Back to cited text no. 8
Schenk-Rootleib AJ, Van Nieuwenhuizen O, Schiemanck N, Van der Graaf Y, Willemse J. Impact of cerebral visual impairment on the everyday life of cerebral palsied children. Child Care Health Dev 1993;19:411-23.  Back to cited text no. 9


  [Table - 1], [Table - 2], [Table - 3]

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