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Bilateral amaurosis due to brain aneurysm rupture

Amaurose bilateral devida a ruptura de aneurisma cerebral

CLINICAL/SCIENTIFIC NOTE

Bilateral amaurosis due to brain aneurysm rupture

Amaurose bilateral devida a ruptura de aneurisma cerebral

Leonides Rocha de Oliveira FilhoI; Luiz Afonso Dias MatosII; Matheus Rodrigo LaurentiIII; Antonio Ronaldo SpottiIV; Waldir A. TognolaV; Marcio Luiz Tostes dos SantosVI

IMedical Student at Universidade de Marília, Marília SP, Brazil - Unidade de Neurocirurgia Endovascular do Serviço de Neurocirurgia do Hospital de Base de São José do Rio Preto, São José do Rio Preto SP, Brasil

IIMD, Neurosurgeon of Unit of Endovascular Neurosurgery at Hospital de Base de São José do Rio Preto, São José do Rio PretoSP, Brazil

IIIMD, Fellow of Unit of Endovascular Neurosurgery at Hospital de Base de São José do Rio Preto, São José do Rio Preto SP, Brazil

IVMD, PhD, Head of the Department of Neurological Sciences at Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto SP, Brazil

VMD, PhD, Professor of the Department of Neurological Sciences at Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto SP, Brazil

VIMD, Head of the Unit of Endovascular Neurosurgery at Hospital de Base de São José do Rio Preto, São José do Rio Preto SP, Brazil

Terson's syndrome (TS) is a vitreous hemorrhage associated with subarachnoid hemorrhage (SAH) usually as a consequence of the rupture of a cerebral aneurysm1. Studies showed an incidence of 40% following SAH2. This syndrome may indicate a poorer prognosis compared to patients with only SAH, and may be related to rebleeding or the occurrence of coma after SAH1,3. Vitreous hemorrhage probably is related to the rapid increase in intracranial pressure with compression of the central retinal vein and its choroidal anastomosis4. Conscious patients with SAH almost always report sudden onset of severe headache, which is also related to the rapid increase in intracranial pressure1.

We report a patient with Terson's syndrome which after aneurysm embolization evoluted with a dramatic bilateral blindness.

CASE

A 52-year-old woman came to the hospital with the complain of a intense headache. The relative who accompanied her affirmed that the patient got up in the morning, with intense headache, followed by loss of consciousness for more than 10 minutes. After regarding consciousness she presented vomit and complained that she wasn't able to see the inferior part of visual field. The past medical history showed arterial hypertension and cigarrete smoker.

The patient so was destinated to intensive care unit. In the examination it was detected arterial hypertension. Her mental status was clear with pupils reacting to light, language and memory preserved. She had no other neurological deficit except for a decrease of visual acuity. She had also nuchal stiffness.

MRI showed SAH and arteriography revealed a left communicating posterior artery aneurysm (Figure). The patient was so submitted to an aneurysm embolization. After embolization, the patient was without complains. In spite of 48 hours later she evolved with a complete visual loss, noting only figures. Pupils were reactive to light. Due to this visual loss, an ophthalmological evaluation was performed with diagnosis of a bilateral vitreous hemorrhage. Than a bilateral vitrectomy was carried out without success. On follow-up the patient had a good neurological outcome staying with bilateral amaurosis.


DISCUSSION

Terson's syndrome is a frequent disease4 and it is caused by a vitreous hemorrhage associated with a subarachnoid hemorrhage usually observed in aneurysm rupture1,5,6. Some authors suggest that it may occurs as result of sudden increase of intracranial pressure, taking a effusion of cerebrospinal fluid inside optic nerve sheet7. Due to this, the sheet of posterior nerve region dilates and compress the choroidal anastomosis located next of sclera and optic nerve beyond of retinal central vein. This results in a decrease of venous draining, occurring hemorrhage and estasis. Simultaneously, intracranial hypertension takes to cerebral ischemia, stimulating vasomotor cerebral center elevating arterial pressure, impairing ocular condition8. There was not found a correlation between anatomical localization of the ruptured aneurysm and TS laterality4.

At the presentation of TS, unilateral or bilateral vitreous hemorrhage can be found. Studies show that unilateral must be treated conservatively and bilateral treated surgically with vitrectomia9. During the treatment the method consists in spontaneous resorption in the unilateral hemorrhage and pars plana vitrectomy in bilateral hemorrhage, both revealing successfully results10.

In the evolution of patients after the treatment, we find different levels of visual losses8. We could observe as well that patients who did vitrectomy soon afterward vitreous hemorrhage had a more effective rehabilitation. Some studies show good recovery of patients after surgical treatment2,9. However, we couldn't find an evolution with bilateral blindness suggesting that our patient suffered a rare manifestation even with treatment advised by literature.

ACKNOWLEDGMENTS - We are grateful to Eliane dos Santos Soeiro and Patrícia Kelley de Freitas for valuable technical assistance.

Received 14 August 2008, received in final form 29 September 2008. Accepted 4 October 2008.

Dr. Marcio Luiz Tostes dos Santos - Hospital de Base / Unidade de Neurocirurgia Endovascular - Avenida Brigadeiro Faria Lima 5544 - 15090-000 São José do Rio Preto SP - Brasil. E-mail: neurocirurgiaendovascular@yahoo.com.br

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Publication Dates

  • Publication in this collection
    09 Dec 2008
  • Date of issue
    Dec 2008
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