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ARTICLES
Year : 1979  |  Volume : 27  |  Issue : 4  |  Page : 198-199

Etiopathogenesis of fundus changes in hydrocephalus (in children)


K. G's Medical College, Lucknow, India

Correspondence Address:
V B Pratap
K. G's Medical College, Lucknow
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Pratap V B, Misra K K, Mehra K K, Kapoor R. Etiopathogenesis of fundus changes in hydrocephalus (in children). Indian J Ophthalmol 1979;27:198-9

How to cite this URL:
Pratap V B, Misra K K, Mehra K K, Kapoor R. Etiopathogenesis of fundus changes in hydrocephalus (in children). Indian J Ophthalmol [serial online] 1979 [cited 2020 Jun 3];27:198-9. Available from: http://www.ijo.in/text.asp?1979/27/4/198/32627

Table 1

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Table 1

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A rise in intracranial tension due to any cause, not only gives a awkward look due to disproportionately enlarged head, but also pro­duces such serious ocular complications like visual and field changes due to optic nerve involvement.

In the present study we have tried to explore the various factors responsible for fundus changes.


  Materials and Methods Top


In this study 42 cases of congenital (primary) hydrocephalus, upto the age of 12 years were investiga­ted. These cases were subjected to detailed history, physical and ocular examination. In all cases, detailed fundus examination was done, and fundus photography where it was possible. Plain ventriculography, x-ray skull, ventriculography and carotid angiography was done in most of the cases.

Observations

Out of the 42 cases, 25 (59.5%) were males and 17 (40.5%) females.

In this study out of the 42, 30 cases (71.4%) were in the age group of 0-12 months and the next common age group was 13-24 months, i.e. 7 (16.6%), while in Rabinowiez series maximum cases were recorded in 8-18, and 36.96 months age groups, our datas clearly indicate that the disease process starts in intrauterine life in most of the cases.

Fundus changes in 42 congenital cases

Normal:-20 (47.6%), primary optic atrophy-l9 (45.2%), temporal pallor of the disc-3 (7.2%).

Fundus changes in the form of primary optic ; atrophy and temporal pallor were found in 52.4% of the cases, which were significantly higher than the raport of Rabinowiez3 i.e. 31%. It may be due to early onset of the disease in our series.[Table - 1]

The above table shows that head- circumference in 60% of cases of normal fundus group was within normal range of very slightly enlarged and markedly enlarged in 40% cases. Among cases with optic atrophy it was normal only in 31.6 % and enlarged in 68.4%. This explains the theory of stretching of visual pathway as a cause of optic atrophy in congenital hydrocephalus. But normal fundus in 8 cases of markedly enlarged head, and optic atrophy in 6 cases of midly enlarged head contradicts the theory of stretching.

X-Ray Skull-In all the cases showed signs of mild to marked raised intracranial pressure in the form of separation of suture.

Vent riculographv-Showed mild to marked dilated communicated ventricular system.

In this study, it was observed that the cases who had a markedly enlarged head, dilated ventricles but normal retinal vessels and disc capillaries more than 10 and of normal caliber[1] had normal fundus; while the cases who had moderately enlarged or normal head and moderately dilated ventricles but markedly narrow, and less than 7 disc capillaries and slightly narrow retinal vessels, had optic atrophy.


  Discussion Top


Our impression, regarding the development of optic atrophy, congenital hydrocephalus is this: the cases who have normal and good retinal Vasculature do not develop optic atrophy irrespective of dilated ventricles and enlarged head, while cases with poor retinal vasculature developed optic atrophy irrespective of the moderately dilated ventricles and moderately enlarged or normal head circumference. Paton[2] had also mentioned vascular changes responsible for optic atrophy.[4]

 
  References Top

1.
Kestenbaum, A., 1948, Clinical methods of Neuro-Ophthalmological Examination, William. Heinmann, London.  Back to cited text no. 1
    
2.
Paton, L., 1942, Brain, 32, 65.  Back to cited text no. 2
    
3.
Rabinowiez, I.M., 1974, Trans. Ophth. Soc. U.K., 94, 353.  Back to cited text no. 3
    
4.
Walsh, F.B., 2 Hoyt W.F., 1969, Clinical Neuro­ophthal. 3rd Ed. 736. Baltimore, Williams and Wilkinson.  Back to cited text no. 4
    



 
 
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