Eales' disease with neurological involvement

Journal of the Neurological Sciences, 27 (1976) 313-321

313

© Elsevier Scientific Publishing Company, Amsterdam - Printed in The Netherlands

EALES' DISEASE W I T H N E U R O L O G I C A L I N V O L V E M E N T Part 1. Clinical Features in 9 Patients

B. S. S I N G H A L and D A R A B K. D A S T U R

Department of Neurology and Neuropathology Unit, Sir J. J. Group of Hospitals, Bombay-8 (India) (Received 18 July, 1975)

SUMMARY

Nine patients with characteristic changes of Eales' disease in the eye in whom there was neurological involvement, have been described. The characteristic neurological picture comprised an acute or subacute myelopathy occurring at an interval of a few weeks to a few years after the eye episode; in only 1 patient was there cerebral involvement without any evidence of myelopathy. Besides the involvement of spinal cord at the dorsal level in the 8 patients, there was evidence of additional lesions in the brain stem in 1 patient and in the cervical cord in another. The neurological disability was severe, affecting pyramidal and sensory pathways with involvement of sphincters in all 8 patients with myelopathy. There was a tendency to slight improvement in 7 of these and in 4 there was further relapse at the same site. On later examination, the patients exhibited slight to moderate disability and 2 died of chronic renal failure. In the acute or subacute phase of the illness, CSF showed elevation of proteins and cells higher than that seen in patients with multiple sclerosis (MS). Although superficially the clinical symptomatology tended to be similar to MS, there were notable differences from MS in the eye signs, neurological picture and CSF changes. Our observations and the existing literature suggest that the neurological manifestations are likely to be due to an expression of Eales' disease which usually affects only the eyes, with periphlebitis, retinal haemorrhages and neovascular formation. The aetiology o f Eales' disease is uncertain but hypersensitivity to a variety of allergens and notably to tuberculosis, needs to be considered.

INTRODUCTION

The ocular findings of periphlebitis, neovascular formation and recurrent retinal and vitreous haemorrhages constitute Eales' disease. The disease has a pre-

314 dilection for young males and its incidence is said to be slightly higher in the tropics (Gupta 1962). Though infrequent, an occasional association of neurological involvement has been described (Silfverskiold 1947; White t961). Since 1966, at the Department of Neurology, J. J. Hospitals, Bombay, we have seen 9 patients who h~d involvement of the central nervous system in association with the characteristic ocular changes of Eales' disease. The purpose o f this report is to study the pattern of neurological involvement and to examine the association between the neurological findings and ocular changes. We were able to study the neuropathological changes in 1 patient who died and these together with a discussion of the pathogenesis are reported in the following paper (Dastur and Singhal 1976). CASE HISTORIES

In view of the rarity of the reported cases, below are set out brief case histories of 8 patients (Cases 2 to 9). Case 1

This case is described in detail in the following paper (Dastur and Singhal 1976). Case 2

I.K., male, 40 years (J.J.H. 4743/70). Seven years ago loss of vision in right eye. One and a half year later, over a few days, retention of urine followed by weakness first in right lower limb and later in left lower limb. The lower limbs became spastic and the condition remained static. On examination (O/E): visual acuity (V.A.) right eye only light perception; left eye 6/6. Right fundus : disc not visible, perivenous sheathing and picture of retinitis proliferans. Lower limbs: Spastic weakness grade Ill-IV. Spinothalamic sensory impairment below T10. Knee and ankle jerks exaggerated. Lower abdominals lost and plantars extensor. ESR 30 mm/hr. VDRL negative. Mantoux test positive, CSF protein 25 mg/100 ml, cells 0/mm 3. He was treated with anti-tuberculous medication without steroids; there was no improvement. Comment. This patient had evidence of Eales' disease in the right eye. One and a half years later he developed a dorsal spinal cord lesion which remained static. Case 3

B.D., male, 37 years (J.J.H.O.P.D.-20-11-69). Twenty-nine years ago (at age 8 years) loss of vision while playing (details not available); total recovery in 2 months. Two years ago sudden dark spot in front of left eye which was diagnosed to be due to "vitreous haemorrhagc" ; since then persistent visual impairment in left eye. Six months later pain in small joints of hands and feet without swelling or fever for 20 days. Two months ago, tingling in both lower limbs which spread to the waist in 2 days; mild weakness of both lower limbs, incontinence of urine and stool Father had pulmonary tuberculosis. O/E: V.A. right eye 6/6, left eye finger counting at 0.5 m. Right fundus showed whitish scars towards the extreme periphery with old perivasculitis. Left fundus showed irregular large areas of old and recent haemorrhages with perivasculitis, yellow round nodules floating in the vitreous. In addition few traction bands over the macula. Lower limbs mild spastic weakness (right more than left) with spinothalamic loss below T12. Knee and ankle jerks exaggerated, abdominals lost and plantars extensor. ESR 50 mm/hr. CSF protein 80 mg/100 ml, cells 110/mm 8 (lymphocytes 95 %). V D R L negative. Lange 1111100000. Mantoux test not done. Treated with A C T H injections without antituberculous drugs. Improved by 50 % over 6 weeks. Comment. This patient had Eales' disease affecting both eyes. In addition he had a dorsal spinal cord lesion from which he made a partial recovery. Case 4

H.B., male, 42 years (J.J.H. 26642/68). Two years ago left lower motor neurone 7th nerve palsy and pain in mastoid region ; palsy persisted. Six months later visual impairment in left eye over

315 a few days; partial improvement only. Few weeks later weakness and numbness in both lower limbs, left more than right; fluctuations in this over 3 months, with final persistent difficulty in walking. One m o n t h before admission sudden weakness right upper limb, worsening in lower limbs with inability to walk and incontinence of bladder and bowel. Upper limb weakness cleared completely, the rest persisted. O/E: Right fundus normal, left fundus showed a patch of old choroiditis, perivenous sheathing and retinitis proliferans. V.A. : right normal, left only perception of light. Residual left facial palsy, upper limbs normal, spastic weakness lower limbs, position sense impaired right foot, vibration sense impaired up to costal margins, right KJ absent, left KJ and both AJ brisk, left abdominal reflex absent, both plantars extensor. ESR varied from 70-90 mm/hr. Mantoux test positive; C.S.F. protein 250 mg/100 ml, Pandy and Nonne-Apelt tests positive, sugar 44 mg/100ml, cells 70/mm 3 (L 74%, P 2 6 ~ ) , CSF W R and colloidal gold curve negative. Myelography mild disc indentation at C6-7 level, otherwise normal. He was treated with antituberculous drugs and prednisolone. Only slight subjective improvement. Ten months later he died at home possibly of urinary infection. Comment. This patient showed clear evidence of Eales' disease in left eye and of involvement of lower dorsal spinal cord; facial palsy may or may not be related; possibly another transient lesion in upper cervical spinal cord. Case 5

S.A., male, 24 years (J.J.H. 38128/67, 8096/68). Seven years ago sudden blindness left eye with improvement over 20 days. Four years ago, total paraplegia with retention of urine and sensory loss below TI0, developing over 24 hr. Partial improvement over the next month and could walk with difficulty. Three years ago recurrence of blindness in left eye with partial improvement over 3 weeks. Two months before admission worsening of the paraparesis. In the hospital 10 spells in 3 days, each lasting a few minutes to 1 hr, of worsening of vision and scotomata in right eye. O/E: right eye, prominent perivenous sheathing with few whitish exudates in upper sector. Left eye, old perivenous haemorrhage and linear whitish perivenous streaks. Lower limbs spastic and slightly weak, left more than right. Superficial sensory loss below T4; position sense impaired left leg. KJ and AJ brisk, plantars both extensor, lower abdominal reflexes lost. Later in hospital two fresh haemorrhages in right fundus. ESR 10 ram/hr. Mantoux positive. CSF protein 20 mg/100 ml, cells 3 lymphocytes/ mm 3, myelogram normal. He was treated with antituberculous medication and steroids. There was partial improvement in both vision and paraplegia. Comment. This patient had clear evidence of Eales' disease in both eyes with three episodes of worsening and improvement in vision over 7 years. In addition he had a dorsal spinal cord involvement which showed partial remission and worsening over 4 years. Case 6

M.B., male, 23 years (.I.J.H. 14968/73). Seven years ago marked impairment of vision in both eyes with partial improvement after 3 months. Six years later, urgency of micturition; a month later, over 2 weeks paraesthesiae and weakness, first in right lower limb and later the left. Treated at Osmanabad Hospital with partial improvement. Three months before admission, recurrence of severe weakness in legs with retention of urine. Admitted with sensory level at Ts; CSF and myelogram reported to be normal. Treated on antituberculous regime with no improvement. The disability persisted and he was referred to us. O/E. : both fundi showed patches of old chorioretinitis and perivenous sheathing; V.A. : right 6/18; left 6/60. Lower limbs spastic paraparesis with power grade 3. Position sense lost in toes; vibration sense lost in left lower limb and impaired in right. Cutaneous sensory loss below Ts. KJ, AJ exaggerated, plantars both extensor. ESR 10 mm/hr. Mantoux test strongly positive. X-ray chest old tuberculous infiltration right apex. Bone marrow normoblastic. Serum folate and BI~ normal. CSF protein 25 rag/100 ml, cells 20 lymphocytes/mm 3. Repeat myelography normal. He was treated with antituberculous medication and corticosteroids without any significant improvement. Comment. This patient had evidence of Eales' disease in both eyes. Six years later he developed spinal cord symptoms at Ts level which showed slight initial improvement followed by worsening at the same level. Case 7

M.S., male, 23 years (J.J.H. 35466/67). Four years ago blurring of vision left eye. Diagnosed as having Eales' disease; photo-coagulation done at Lucknow hospital. Two and a half years ago

316 fever for 2 days, followed 4 weeks later by weakness of right lower limb and 6 weeks later by weakness of left lower limb. Admitted to Lucknow Medical College. After myelography, laminectomy done mid-dorsal region. Operative findings not available, but total paraplegia after operation followed by partial recovery. O/E: right fundus normal with visual acuity 6/6; left fundus retinitis proliferans with the V.A. 6/36. Lower limbs spastic paraparesis with power grade 2-3. Sensory loss to all modalities below T10, Knee and ankle jerks exaggerated. Abdominal reflexes absent, plantars both extensor. ESR/10 mm. Mantoux test positive. CSF proteins 20 rag/100 ml, cells 2 lymphocytes/mm:. myelogram normal. He was treated with antituberculous medication and steroids, without any improvement. Comment. This patient had Eales' disease in left eye. A year and a half later he developed a dorsal spinal cord lesion. Exploration was performed to exclude compression. Repeat myelography did not show any defect suggesting intrinsic spinal cord pathology.

Case 8

R.K., male, 43 years (J.J.H. 4242/71). At age 15 years diminished vision left eye. At age 42 left-sided focal convulsions with unconsciousness for 2 hr. Next day heaviness and weakness on the left side of the body, followed by unconsciousness for 6 hr. On regaining consciousness total left hemiplegia which slowly improved. Five months later recurrence of generalised convulsions followed by increase in left hemiparesis and partial improvement over 2 months. After 3 months of second episode, recurrence of convulsion with increase of weakness, followed by slow partial recovery. O/E: right fundus normal with V.A. 6/18, left fundus showed perivenous sheathing, whitish fluffy exudate near the vein and a patch of old choroiditis. Left mild hemiparesis with supranuclear 7th nerve palsy but no field defect. Also sensory impairment to all modalities on left side. Deep reflexes exaggerated on the left side with absent left abdominals and extensor left plantar. ESR 4 mm. Mantoux test positive. CSF protein 10 mg/100 ml, cells 3 lymphocytes/mm 3. Right carotid angiogram and pneumoencephalogram normal. Patient was treated with antituberculous drugs and anticonvulsants without any significant improvement. Comment. This patient had Eales' disease affecting the left eye. After an interval of 27 years he had a right cerebral episode. He improved and over 8 months he had two further episodes of convulsions, increase in weakness followed by slow partial recovery. Case 9

S.M., male, 18 years (J.J.H. 18000/74). At age 11 years in 1967, sudden visual impairment in right eye. Over 3 weeks almost total recovery. A year later recurrence of visual loss in right eye with improvement over 25 days. In early 1973, sudden visual loss in left eye followed by a near total recovery. During the next few months an episode each in right and left eye and finally in August 1973 both eyes affected simultaneously. On each occasion he improved. In October t973 a relapse in the right eye. In April 1974 feeling of malaise. Nine days later aching in the left gluteal region and weakness of left lower limb over a few hours resulting in dragging of left leg. Over next week, nearly 60% recovery. In June 1974, recurrence of weakness in left lower limb over 2 days with difficulty in passing urine. About 10 days later, weakness in right lower limb. On 15 July, 1974, a lumbar puncture was done. Three hours later, he deteriorated and developed severe weakness and numbness in both lower limbs with incontinence of urine. On admission to J.J. Hospital on 22 July, 1974, V.A. in right eye 6/60 and in the left, finger counting at 1.5 m. Optic discs normal but retina showed pronounced changes of Eales' disease in both eyes with perivenous sheathing, patches of healed chorioretinitis in the left eye, new vascular formation in both eyes and changes of retinitis proliferans in the right eye. There were few fresh haemorrhages in the left eye. Moderately severe weakness in both lower limbs with impairment of position and vibration sense in lower limbs. Subjective impairment of pinprick in the lower limbs distally without any impairment of thermal sensibility. N o sensory level. Left ankle jerk was absent but other deep jerks were present. Abdominal reflexes lost and both plantars extensor. Chest and spine X-rays normal. Blood and CSF VDRL negative. CSF protein 120 mg/100 ml with 60 cells (lymphocytes)/mm 8. Mantoux test negative. He was treated with streptomycin, isonicotinic acid hydrazide and corticosteroids. Partial improvement and when last seen on 1 September, 1974, he was able to walk with support. Comment. This patient had evidence of Eales' disease in both eyes. Despite repeated eye involvement, the optic discs were normal. In addition he developed a spinal cord lesion in the dorsolumbar region.

317

Summary of clinicalfeatures The age at onset ranged from 11 to 40 years and all patients were males. Involvement of the eye was the first manifestation in nearly all patients. The interval between the onset of ocular changes and the neurological involvement varied from a few weeks to 7 years in 8 o f the patients. In 1 patient there was cerebral involvement 27 years after the eye disease. In 2 patients (Cases 5 and 9) the ocular disease was active when the neurological picture evolved. These patients developed fresh haemorrhages in the retina while they were being investigated for the recent neurological disease. There was unilateral eye involvement in 4 patients (right eye in 1 and left eye in 3) and bilateral disease in 5 patients. Perivenous sheathing was evident in all 9 patients. Besides this, 5 patients showed evidence of recent or old haemorrhages in the retina, 3 patients showed neo-vascular formation and 6 showed advanced changes of retinitis proliferans. Optic pallor was seen in only 2 patients. Old patches of choroiditis or chorioretinitis were found in 4 of our cases. Similar patches have been noted in patients with Eales' disease by Silfverskiold (1947), Elliot (1954) and Gupta (1962), although choroiditis is generally not recognised to be a component of Eales' disease. Although retinal and vitreous haemorrhages can occur in diabetic retinopathy, none of our patients had diabetes and none showed microaneurysms on fundoscopy. The neurological illness was acute or subacute in most and the full development of the disability was spread over a few hours to 2 weeks in the majority. Except in 1 patient (Case 8) where the brain was involved and the patient presented with convulsions and hemiparesis, the main brunt of the disease fell on the spinal cord. The mid or lower dorsal spinal cord was predominantly affected. In 2 patients there were additional sites of lesions. Thus in Case I, there was involvement of the brain stem and in Case 4 there was clinical evidence to indicate an additional lesion of the cervical cord. In patients with spinal cord involvement there was moderate to severe loss of power in 8 patients, spinothalamic involvement in 7 patients with a level of sensory loss in 6 and impairment of position sense in 5 patients. Bladder involvement was present in all 8 patients with myelopathy. There was partial improvement in 7 out of 8 patients with the spinal cord lesion. After initial improvement, there was a relapse at the same site in 4 patients. Table 1 gives the CSF findings. It will be noted that there was a significant elevation of protein and cells (mainly lymphocytes) when the patients were seen in the acute or subacute phase of the illness. Excepting for a mild pleocytosis in 1 patient (Case 6), the CSF was normal when the patient presented a year after the onset of neurological disease. Mantoux test was positive in 7 out of 8 patients in whom it was done. Chest X-ray was normal in all except 1 patient (Case 6) where it showed evidence of old tuberculosis. Excepting 1 patient (Case 3) who was treated with ACTH alone, all other patients were given antituberculous therapy which was combined with corticosteroids in 6 patients. The improvement was slight and perhaps unrelated to the therapy. In the longterm follow up, 2 patients who were bed-ridden from paralysis died of chronic renal failure arising from pyelonephritis. The remaining 7 patients were left with mild to moderate disability.

318 TABLE I CSF CHANGES

Protein (mg/100 ml) Cells/mmz

Acute or subacute phase of CNS disorder

Chronic phase of CNS disorder (over 1 year)

Case No.

Case No.

1

3

4

9

2

5

6

7

8

156 80

80 110

250 70

120 60

25 0

20 3

25 20

20 2

10 3

DISCUSSION

The salient clinical picture in most of these patients was that of acute or subacute myelopathy following an ocular episode with characteristic retinal changes of Eales' disease. All the patients were males with age at onset ranging from 1 l to 40 years. Except in 1 patient where only the brain was involved, in all others the spinal cord was affected and the dorsal spinal cord was the site of predilection. There was a partial, albeit slight, improvement after the initial episode in the majority of our patients. In 2 patients there were additional sites of lesions in the nervous system, namely brain stem in 1 patient and cervical cord in another. These features superficially resembled the events seen in demyelinating diseases. Therefore the association of neurological manifestations with the picture of Eales' disease in the eyes raises some pertinent questions: (1) Is the combination of neurological disease and the ocular changes merely fortuitous? (2) Is it a form of multiple sclerosis (MS)? (3) is this a distinct syndrome with the pathological changes in the central nervous system similar to those in the eye? and (4) What is the pathogenesis and aetiotogy? The clinical picture did not point to any known neurological disorder occurring concurrently with the disease of the eye. Various other possibilities like syphilitic myelitis, tuberculous meningomyelitis and spinal cord compression were excluded by appropriate serological tests for syphilis, CSF examination and myelography. In India where tuberculous spinal meningitis is relatively frequent (Wadia and Dastur 1969), and keeping in view the possible relationship of Eales' disease to tuberculosis (Elliot 1954), one may argue that neurological involvement may be the result of tuberculous spinal meningitis. However, in our patients the clinical features were totally different. Radicular pains were absent, the lesion was localised rather than diffuse and myelography failed to show any changes of the type described by Sidhva (1963) to be characteristic of arachnoiditis. Although CSF changes in the acute phase showed elevation of protein and cells, these are non-specific changes and sugar was within normal limits. Partial improvement with relapse at the same site in 4 patients and additional lesions at other levels in 2 patients would also be against the possibility of tuberculous spinal meningitis. There was no evidence to suggest Behc~t's

319 syndrome, collagen disorder, thromboangiitis obliterans or abnormal haemoglobinopathy like sickle cell disease in any of our patients. In 1 patient (Case 8) who developed hemiparesis following a long latent period of 27 years after the initial ocular disease, the association of these two disorders may seem to be far fetched. The reasons for inclusion of this case are: (a) the possible occurrence of Eales' disease with cerebral involvement has been suggested by White (1961). (b) Patients with MS are well known occasionally to have a long latent period after the first episode of illness. This latent period can be over 15 years and is known to extend up to as much as 37 years (McAlpine 1972). More relevant to us is the observation that the patients with optic neuritis as the first episode of MS tend to have a longer latent period. Of the 26 patients with a long latent interval, 17 had optic neuritis initially as against 9 patients with other types of onset. We realise that one should be careful in attempting to associate any neurological manifestation occurring with Eales' disease. One should be wary of accepting conditions like headaches, convulsions, polyneuritis and epilepsy (reviewed by White 1961 and Ashton 1962) as neurological manifestations of the syndrome of Eales' disease. The description of retinal periphlebitis in cases of MS (Rucker 1947; Haarr 1964), the acute or subacute onset of neurological involvement with Eales' disease, remission followed by relapse at the same site in 4 patients and occurrence of lesions at more than one site in 2 patients raise the question of similarity of the syndrome being described to MS. On clinical grounds there are important differences between the two conditions. Optic pallor is a frequent finding in patients with MS but infrequently seen in patients with Eales' disease. Although some workers (Field and Foster 1962) have even questioned the occurrence of retinal periphlebitis in MS, the band of periphlebitis in MS is very thin (Rucker 1975) and unlike the thick band of periphlebitis seen in Eales' disease. Besides, neovascular formation, retinal haemorrhages and retinitis proliferans are seldom seen in patients with MS. McAlpine (1972) concluded that from the clinical standpoint the periphlebitis retinae of MS differs from that observed in conditions such as tuberculosis and sarcoidosis in that both haemorrhages and a proliferating type of retinitis are uncommon in MS. Apart from these differences in the ocular picture, there are differences in the neurological expression of the two diseases. The disability tends to be considerable in the very first neurological episode in patients with Eales' disease. The improvement is only slight which is unlike the very frequent and characteristic remission from the first episode in patients with MS. The CSF changes in the acute phase of the neurological disorder in patients with Eales' disease have been significantly different from those in patients with MS. In MS it is rare to get a protein level beyond I00 mg/100 ml and a cell rise above 40 cells/mma. It was interesting to note the presence of RBCs in the CSF of all the 3 patients described by Silfverskiold (1947), a feature which he does not comment on. However, in none of our patients were RBCs detected in the CSF. A similar clinical presentation, namely ocular disease followed by spinal cord involvement in 8 of our patients, and the description of similar cases by Silfverskiold (1947) and White (1961) from other countries, would favour a relationship between

320 retinal disease and neurological manifestations. Silfverskiold described 3 patients who had paraplegia following Eales' disease. The similarity of the clinical features in all his 3 patients had led him to speak of the possibility of a specific syndrome even though the number was small. In White's series 2 out of 4 patients with neurological involvement had evidence of paraparesis. Two of our patients while under investigation for neurological disease showed fresh changes of haemorrhages in the retina. Such a close association in time between the eye and neurological disorder favours a relationship between the two. Besides, the retina is functionally and anatomically an extension of the brain and patients with ocular manifestations (uveitis and choroiditis) in varied systemic diseases like sarcoid are more likely to have neurological manifestations of that disease than if the eye were not affected (H66k 1954; Gould and K a u f m a n 1961). The occurrence of neurological involvement in patients with Eales' disease of the eye is rare as was suggested by Silfverskiold (1947). In a follow up study of 25 patients over 6 to 15 years he failed to find any evidence of neurological disease developing in them. White (1961) described 3 patients in whom there were no clinical features to indicate neurological involvement but there were CSF changes suggesting it. It is therefore possible that CNS involvement may be more frequent than hitherto believed. To sum up, the characteristic clinical pattern in our patients and in those reported by others, the CSF changes in the acute phase, and the temporal relationship in some cases between the ocular and CNS manifestations, make us feel that we are dealing with a specific association wherein occasionally the neurological involvement follows the ocular episode. The final p r o o f of a link up between the ocular and neurological manifestations could come from the pathological observations and in our next paper we have been able to describe the pathology in the only case where the autopsy findings were available (Dastur and Singhal 1976). ACKNOWLEDGEMENTS

We are grateful to Dr. Anil Desai for referring Case 3 and to Dr. N. H. Wadia for allowing us to study Case 9. We thank our resident staff over the yeals and in particular Dr. R. K. Swamy. Many thanks are due to Dr. Nergish Patel, Dr. R. J. Patel and Dr. P. H. Patel for their ophthalmic opinions.

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321 Gupta, S. P. (1962) Eales' disease - - Its etiology and prognosis. In: Acta 19th Concilium Ophthalmologicum, New Delhi, Vol. 2, pp. 868-871. Haarr, M. (1964) Changes of the retinal veins in multiple sclerosis, Acta neurol, scand., 40: 17-20. H66k, O. (1954) Sarcoidosis with involvement of the nervous system, Arch. NeuroL Psychiat. (Chic.), 71 : 554-575. McAIpine, D. (1972) Clinical studies. In: D. McAlpine, C. E. Lumsden and E. D. Acheson (Eds.), Multiple Sclerosis - - A Reappraisal, Part 2, Churchill Livingstone, London, pp. 83-276. Rucker, C. W. (1947) Retinopathy of multiple sclerosis, Trans. Arner. ophthaL Soc., 45: 564-570. Rucker, C. W. (1975) Personal communication through Prof. L. T. Kurland to D.K.D. Sidhva, J. N. (1963) The radiology of spinal arachnoiditis, Neurology (India), 11: 59-62. Silfverskiold, B. P. (1947) Retinal periphlebitis associated with paraplegia, Arch. Neurol. (Chic.), 57: 351-357. Wadia, N. H. and D. K. Dastur (1969) Spinal meningitides with radiculo-myelopathy, Part 1 (Clinical and radiological features), J. neuroL Sci., 8: 239-260. White, R. H. R. (1961) The aetiology and neurological complications of retinal vasculitis, Brain, 84: 262-273.