To:
Journal of PRACTICAL NEUROLOGY Letters
Electronic Letters to:
|
|
Electronic letters published:
|
|
|||
|
Seyed F. Amlashi, Neurosurgeon CHU Pontchaillou, rennes FRANS, L.Riffaud, X.Morandi
Send letter to journal:
amlashi{at}yahoo.com Seyed F. Amlashi, et al.
|
Dear Editor, We read with great interest the review article by McCarron et al. [1] concerning Terson’s syndrome. Having recently realised a prospective study in the subject, we feel interested to share our experience and to add some information. 1- Although the original description of the syndrome by Dr Terson in 1900 concerned only intravitreous haemorrhages in association with subarachnoid haemorrhage, in our opinion limiting the definition to the original description could be misleading today. The association of the intraocular haemorrhage with other situations with increased ICP such as head trauma is well documented. Thus we suppose that Terson’s syndrome definition should be enlarged to all the intraocular haemorrhages occurred in association with acute intracranial hypertension. 2- The authors stated that “the greater proportion of patients developing Terson’s syndrome in the prospective studies may partly have resulted from delay in the appearance of vitreous haemorrhage”. In our experience with a prospective study of 100 patients with subarachnoid haemorrhage (non published data), all patients who demonstrated an intraocular haemorrhage during hospitalisation had an abnormal fundoscopic examination just after the acute episode and any tardive development of intraocular haemorrhage has not found. The only exception to this finding was the patients who had re-bleeding during hospitalisation period. This observation may lend in part some insight into our understanding of the pathophysiological mechanisms of intraocular haemorrhage and also has clinical importance. It has been demonstrated that the intraocular venous pressure has a linear relationship with intracranial pressure, so that intraocular venous system is the equivalent of the intracranial bridging veins. This concept is the principle of venous ophthalmo-dynamometry which has been showed to be a reliable method for estimation of intracranial pressure[2]. With regard to these explanations, we agree with the authors that a sudden intracranial pressure increase due to aneurismal rupture seems to be the leading cause of the intraocular haemorrhage, however this explanation remains controversial. 3- Another importance of the Terson’s syndrome that had not been discussed by the authors is the diagnostic value of the intraocular haemorrhage in diagnosis of intracranial vascular malformations. In general, between 15% to 20% of patients with a spontaneous subarachnoid haemorrhage have no aneurysm on the initial cerebral angiogram.[3] This may lead to difficulties of the diagnosis and necessity of repeating angiographies. In our experience, all patients with intraocular haemorrhage had an aneurismal subarachnoid haemorrhage, and any patient with non-aneurismal subarachnoid haemorrhage developed intraocular haemorrhage. This means that in a patient with subarachnoid haemorrhage, the presence of intraocular haemorrhage is an important indicator of aneurismal origin. In these cases, if initial angiograms are normal, repeated angiographies could be justified.
References: 1. McCarron M O, Alberts M J, McCarron P. A systematic review of Terson’s syndrome: frequency and prognosis after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2004; 75: 491-493. 2. Firsching R, Schutze M, Motschmann M, Behrens-Baumann W. Venous opthalmodynamometry: a noninvasive method for assessment of intracranial pressure. J Neurosurg. 2000 ;93:33-36. 3. Rinkel GJ, Van Gijn J, Wijdicks EF. Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke 1993;24:1403-1409 |
|||
