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|LETTERS TO EDITOR
|Year : 2016 | Volume
| Issue : 1 | Page : 160-162
Bilateral lateral geniculate body hemorrhagic infarction: A rare cause of acute bilateral painless vision loss in female patients
Thomas Mathew, Delon D'Souza, Raghunandan Nadig, Gosala R. K Sarma
Department of Neurology, St. John's Medical College Hospital, Bengaluru, Karnataka, India
|Date of Web Publication||11-Jan-2016|
Department of Neurology, St. John's Medical College Hospital, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mathew T, D'Souza D, Nadig R, Sarma GR. Bilateral lateral geniculate body hemorrhagic infarction: A rare cause of acute bilateral painless vision loss in female patients. Neurol India 2016;64:160-2
|How to cite this URL:|
Mathew T, D'Souza D, Nadig R, Sarma GR. Bilateral lateral geniculate body hemorrhagic infarction: A rare cause of acute bilateral painless vision loss in female patients. Neurol India [serial online] 2016 [cited 2019 Dec 15];64:160-2. Available from: http://www.neurologyindia.com/text.asp?2016/64/1/160/173671
A 42-year-old woman was admitted with a history of epigastric pain and four episodes of bilious vomiting, which developed in the morning when the patient woke up. In the course of the day, the patient had two to three episodes of loose stools. In the evening, the patient complained of sudden-onset painless loss of vision in both eyes. There was no history of fever. The patient had chronic psoriasis for 16 years and was taking native medications until 2 years ago. At the time of admission, she was on 7.5 of mg methotrexate and hydroxyzine which she had been taking for the past two months. She was detected to be hypertensive 6 months ago and was on beta blockers. On admission, the patient had a blood pressure of 140/90 mmHg and was afebrile. She could only perceive hand movements with both eyes. Visual fields could not be assessed. Her pupils were dilated: Right, 5 mm; and left, 4 mm. Both pupils reacted sluggishly to light. The fundus examination was normal. Extraocular movements were normal and full in range, and there was no associated nystagmus. Rest of the central nervous system examination was normal.
On investigation, she had an increased white blood cell (WBC) count of 22,180 cells/µL, with neutrophilic leukocytosis and normocytic normochromic blood picture. She had a mild anemia with the hemoglobin levels being 10.8 g/dL, and the platelet counts were normal. Her creatinine was 3.1 mg/dL, and she had deranged liver functions. The total bilirubin was 2.7 mg/dL, aspartate transaminase (AST) was 113 U/L, and alanine transaminase (ALT) 115 U/L; and, alkaline phosphatase and gamma-glutamyl levels were normal. Rest of the blood investigations were within normal limits. A diagnosis of acute infective systemic illness with renal and hepatic dysfunction was considered, and the patient was empirically started on ceftriaxone and doxycycline. MRI of the brain was done, which showed T2 fluid attenuated inversion recovery (FLAIR) hyperintensity in the posterior thalamus in the region corresponding to the lateral geniculate bodies (LGBs) [Figure 1]. There was restricted diffusion in the same areas [Figure 2] as well as hyperintensity on T1-weighted images [Figure 3], suggestive of a hemorrhagic lesion. A cerebrospinal fluid study was done, which showed no cells and normal protein and glucose levels.
|Figure 1: Axial T2 FLAIR MRI showing hyperintensity of bilateral lateral geniculate bodies|
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|Figure 2: Diffusion-weighted MRI showing restricted diffusion suggestive of infarction of the lateral geniculate body|
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|Figure 3: T1-weighted MRI axial image showing hyperintensity of bilateral lateral geniculate bodies suggestive of hemorrhagic infarction|
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Investigation for an infectious etiology showed no positive results. Blood and urine cultures were sterile, smear for malarial parasite was negative, and serology for dengue, leptospirosis, and rickettsial fever as well as Widal test for typhoid were negative. Human immunodeficiency virus (HIV) and venereal disease research laboratory (VDRL) tests were negative. The antinuclear antibody (ANA), antiphospholipid antibody (APLA) and immunoline tests were negative as well. The patient was given a complete course of antibiotics as well as 5 days of methylprednisolone injection, 1 g/day. Patient had no improvement in vision. However, the renal and liver functions normalized within a week. The blood count improved to 19,120 cells/µL. At a follow up after two weeks, the WBC count normalized, but there was no improvement in vision. After a year of follow-up, the patient had minimal improvement in vision.
Acute bilateral visual loss is usually caused by post-geniculate optic pathway lesions. These sites include the optic radiations, primary visual cortex, and associated visual cortices. The most common etiology for a lesion in these areas is posterior circulation stroke and head trauma. Another rare and unusual cause can be bilateral isolated lesions of the LGBs. Since 1930s, there are only seven case reports in literature of lesions of LGBs resulting in bilateral acute painless vision loss [Table 1].
|Table 1: The causes of lateral geniculate body lesions reported in literature|
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The reasons why the LGBs were involved in isolation have not been understood. The postulated mechanisms for LGB lesions are hemorrhagic infarction ,,, and osmotic demyelination. The LGBs have a very high metabolic rate and a dual blood supply. The anterior choroidal artery, a branch of the internal carotid artery, supplies the anterior part; while rest of the LGB is supplied by the posterior choroidal artery, a branch of the posterior cerebral artery. Vascular occlusion due to microangiopathic disorders or arteritis have been proposed as a mechanism for the vascular compromise in the LGB. The hemorrhagic infarcts seen in these lesions are thought to be due to the disruption of the blood–brain barrier in the distribution of anterior and posterior choroidal arteries. The LGB is also considered as a site for extrapontine myelinolysis because it has a similar grid arrangement of gray and white matter as the pons. The tight mesh between neurons and oligodendroglia makes it difficult for the latter cells to expand when there is rapid increase in sodium levels. The cells extrude osmolytes leading to cell shrinkage.
It is interesting to note that till date (since 1933), all the seven patients reported in literature with bilateral LGB infarctions are females patients. The reason for this predilection is not known. Whether this association is by chance or they are predisposed to such a complication is not known at present. In our patient, there was no documented hypo- or hyponatremia. We, therefore, postulate a vascular pathology, possibly arteritis of bilateral LGBs. In view of the renal and liver derangement with leukocytosis and a negative autoimmune test, an infectious etiology is a strong possibility; however, it could not be conclusively proven. Some patients have improved slowly over 1–2 years to have a normal vision, while others have had residual visual defects. At a 1-year follow-up, our patient still had significant visual loss, with only hand movement perception in both eyes.
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[Figure 1], [Figure 2], [Figure 3]