Year : 1964 | Volume
: 12 | Issue : 1 | Page : 19--22
Optic atrophy in internal carotid artery occlusion
IS Jain1, DR Gulati2,
1 Department of Ophthalmology, Institute of Post-graduate Medical Education and Research, Chandigarh, India
2 Department of Neuro-surgery, Institute of Post-graduate Medical Education and Research, Chandigarh, India
I S Jain
Department of Ophthalmology, Institute of Post-graduate Medical Education and Research, Chandigarh
|How to cite this article:|
Jain I S, Gulati D R. Optic atrophy in internal carotid artery occlusion.Indian J Ophthalmol 1964;12:19-22
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Jain I S, Gulati D R. Optic atrophy in internal carotid artery occlusion. Indian J Ophthalmol [serial online] 1964 [cited 2020 Jun 5 ];12:19-22
Available from: http://www.ijo.in/text.asp?1964/12/1/19/39067
Carotid artery thrombosis is a condition in which Ophthalmologists have begun to take an increasing interest through the past ten years or so. The responsibility of the ophthalmologist is great, in suspecting and diagnosing this condition as many patients complaining of ocular symptoms may present themselves for the first time to him, and indeed this may be the only symptom.
Guthrie and Mayou (1908) reported a patient with internal carotid artery thrombosis who had optic atrophy associated with crossed hemiplegia, but it was Hunt (1914) who established the syndrome of carotid hemiplegia and drew attention that the condition was more common than was usually realised.
Prior to the advent of cerebral angiography (as most of the cases are diagnosed by cerebral angiography) there were only scattered reports of spontaneous thrombosis of the carotid artery and the diagnosis was rarely made before death.
Fisher in 1951, called emphatic attention to the incidence of carotid artery disease by finding that in a consecutive series of 432 autopsy cases, in which there was cerebral disease and in which the brains were removed and carotid arteries studied, 6.5 per cent had complete occlusion of one or both carotids and three per cent had severe stenosis of the carotids. Since this report, increasing numbers of pathologic studies have appeared in the literature on neurology, as the carotids are more carefully studied post-mortem and the diagnosis is being more actively considered clinically in the differential diagnosis of cerebal disease.
A typical illustrative case of internal carotid artery thrombosis is summarised below: -
B.D. 30 years old, male, farmer by profession was admitted in the neurosurgical unit of the Post-Graduate Institute of Research and Medical Education on 20-11-1962.
His present trouble started three months ago, when he started complaining of numbness or paresthesias sometimes involving the fingers of the right hand, and at others the whole right upper extremity. These used to occur every 5 - 7 days and lasted for only a few minutes. In addition, he used to get episodes while working, when his right arm would just stop moving. This would occur every 3 - 4 days and last for 5 - 10 minutes. In addition he found that on assuming the upright posture he felt giddy. This state of affairs continued till 1-11-1962 when he had generalised tremor affecting the whole body for about half an hour, followed by fever. He was unconscious for two days, and then was noticed to be hemiplegic on the right side, and completely aphasic. He was brought to the hospital and admitted on 20-11-1962.
On examination the patient was found to have hemiplegia on the right side affecting the face, arm and leg. No movement could be performed on the right side. The patient was unable to speak. On application of painful stimuli he could withdraw the left upper and lower extremeties, but no such response was obtainable on the right side. He did not try to put away the painful stimulus with his right extremities when the stimulus was beine applied on left side.
Laboratory Investigations. The Wassermann & Kahn's test, were negative : E.C.G. was normal: blood pressure 120/70.
Eye Examination. Both the pupils were equal and reacting to light. The right eye fundus did not reveal any abnormality. Left eye fundus examination, revealed that the optic disc was pale white, the arteries were markedly attenuated over the surface of the disc, all the branches could be traced peripherally but were very narrow. There was oedema in the macular area which was subsiding. A few small superficial hemorrhages were present near the optic disc. A diagnosis of central retinal artery occlusion was made.
In view of the clinical picture and ocular findings, a tentative diagnosis of internal carotid artery thrombosis was made; and to confirm this a left arteriogram was done, which demonstrates a very clear picture of complete occlusion of the internal carotid artery [Figure 1] in the neck about one centimeter distal to the bifurcation.
After the study, the patient was advised physiotherapeutic exercises. It was felt that surgery or anti-coagulant therapy was not indicated at this stage.
The etiology in the majority of cases of extracranial carotid artery occlusion is atherosclerosis and only a few cases of non-specific giant-cell and syphlitic arteritis are reported. The usual age range is from 40 to 70 years, although spontaneous thrombosis has been reported in the first, second and third. decades, but this is less common.
The site of occlusion in about 80 per cent of the cases reported is just at or beyond the bifurcation of the common carotid artery in the neck, the remainder of the cases having the occlusion in the intracerebral portions of the carotid, usually at the siphon.
According to Spalter (1959) the symptomatology of the disease varies according to whether the occlusion is slow and progressive or there is an acute thrombosis. He classifies the cases into three groups.
The acute attacks occur in about 35 per cent of the cases and present suddenly without warning. The clinical picture is essentially indistinguishable from that of a cerebrovascular accident with hemiparesis, aphasia, loss of consciousness and homonymous field-defects. About one third of this group die as a consequence of the initial insult. These cases may rarely be associated with simultaneous loss of vision in the eye on the same side as the thrombosis. This finding helps to implicate the carotid artery as the site of main pathology.
The second group consists of about 40 per cent of the cases, and is characterised by intermittent episodes of hemiparesis or monoparesis, transient sensory defects and intermittent amaurosis on the ipsilateral side in about 20 to 30 per cent of cases. The attacks may occur several times in a day, week, month or few in a year. They may last from a few minutes to several hours, with the visual loss rarely lasting more than five minutes.
Between these attacks of carotid insufficiency the patients are asymptomatic and usually have no demonstrable neurologic or opthalmologic abnormalities.
The third group has a progressive course, closely mimicking the clinical picture of an expanding intracranial lesion. This form of carotid disease occurs in approximately 25 per cent of cases and presents a particularly difficult diagnostic problem to the clinician.
Visual lesions need more elaboration, as it is these which are the sole responsibility of the ophthalmologist.
The two commonest ocular lesions are homonymous hemianopia and uniocular blindness or optic atrophy, although diplopia, ptosis, papilloedema, and pupillary changes may occur. Uniocular blindness may be transient (amaurosis fugax) or permanent. Attacks of transient amaurosis could come on quite unassociated with hemiplegic symptoms. They usually stop completely when the hemiplegic symptoms become permanent. Contrarily, transient attacks of blindness associated with hemiplegia progress to permanent optic atrophy, as the attacks of hemiplegia stop. Homolateral blindness, either permanent or temporary may be the only symptom of carotid occlusion. Its incidence is put somewhere about 10 per cent.
Optic atrophy is the most common ophthalmoscopic finding, but in many instances the disc may appear quite normal, yet the patient is blind in that eye. Retina is supplied by the central retinal artery and the optic nerve by pial vessels and the central artery of optic nerve. Therefore when insufficiency of the carotid or ophthalmic artery occurs, either of these two branches may appear clinically to be responsible for loss of vision. As a rule when visual loss is complete the picture of central retinal artery occlusion occurs.
In those patients with no retinal findings of central retinal artery occlusion, it is assumed that the central artery of the optic nerve might be affected. In such patients the disc appears normal or shows signs of mild ischaemic papillitis.
Varying degrees of optic atrophy are, therefore, not uncommon, in cases of carotid artery insufficiency, or occlusion.
The various theories put forward, to explain the transient amaurosis and optic atrophy are (1) extension of thrombosis right upto the central retinal artery, (2) embolism from the thrombosed internal carotid artery, (3) vasospasm and (4) haemodynamic crisis.
Smith (1961) believes that it could be explained on simple pressure basis. He states that uniocular visual lesions occur because the pressure in central retinal artery falls so low, that it is either less than the intraocular pressure or not great enough to satisfy the metabolic equilibrium of retina. Provided that this ischaemic period is short, the result will be transient amaurosis. If, however, it is so prolonged as to produce permanent damage to the retinal neurones then the result will be optic atrophy.
A typical case of proved internal carotid artery occlusion, in a young man, thirty years old is described which had an acute onset with hemiplegia, unconsciousness and aphasia as the involvement was on left side. The associated finding of optic atrophy with the fundus picture of central retinal artery occlusion was a clinching feature for the diagnosis of this condition which was subsequently confirmed by arteriography.
A short resume of the clinical picture, various forms of manifestation and pathogenesis of the visual lesions are discussed.
|1||Fisher G. (1951) AMA Arch. Neuno. & Psychiat. 65, 346-377.|
|2||Fisher G. (1952) Arch. Neurog. & Psychiat. 72: 187-204.|
|3||Guthrie L. G. & Mayou S. (1908) Proceedings of Roy, Soc. Med. 1 Sect. Glin, 180.|
|4||Hunt J. R., Amer. J. Med. Sci. n.s. 147, 704, 1914.|
|5||Splater F. H. (1959) 47: 453-467.|
|6||Smith H. V. (1961) British Journal of Ophthalmology, 45, 1-26.|