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|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 5 | Page : 563-565
Corpus callosal hemorrhage due to deep cerebral venous sinus thrombosis
Girish Baburao Kulkarni, Hima Pendarkar, Masoom Abbas Mirza, Veerendrakumar Mustare
Department of Neurology; Department of Neuroradiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
|Date of Submission||02-Jul-2014|
|Date of Decision||23-Aug-2014|
|Date of Acceptance||28-Sep-2014|
|Date of Web Publication||12-Nov-2014|
Girish Baburao Kulkarni
Department of Neurology; Department of Neuroradiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kulkarni GB, Pendarkar H, Mirza MA, Mustare V. Corpus callosal hemorrhage due to deep cerebral venous sinus thrombosis. Neurol India 2014;62:563-5
Hemorrhage in corpus callosum (CCH) (largest association fiber) is rare and is it is usually due to trauma, hypertension arteriovenous malformation and neoplasm. , Deep cerebral venous thrombosis (DCVT) producing CCH is a rare entity with only one case noted so far.  We report two patients of CCH seen in study of 63 DCVT patients admitted at stroke ward of our institute from January 2008 till December 2013. The institute ethical board approved the study protocol and informed consent was taken.
Case 1: A 33 year old female presented with ten days history of progressively increasing holocranial headache and two episodes of generalized seizures with no other significant history. Her general physical examination and neurological examination including fundus were normal. Computerized tomographic (CT) scan of the brain showed hemorrhage in the genu of corpus callosum [Figure 1]a; with contrast scan showing filling defects in internal cerebral veins, vein of Galen and straight sinus [Figure 1]b. Her Magnetic Resonance Imaging (MRI) of the brain done four days later [Figure 2]a-f showed additional parenchymal lesions with better visualisation of the hemorrhage. Re-examination for the presence of any disconnection syndrome and parietal lobe dysfunction was noncontributory. She was also evaluated for risk factors for venous thrombosis including procagulant work up, which were negetive. She was managed with subcutaneous heparin, antiedema measures and later oral anticoagulants for two years. She is asymptomatic from last three years.
|Figure 1: In Patient No. 1: CT scan of brain plain shows hemorrhage in the genu of corpus callosum (a), contrast scan showing filling defect in vein of Galen (b). Arrows pointing to the abnormalities.: In Patient No. 2: (c) - Hemorrhage in the genu of corpus callosum (white arrow), hyperdense bilateral internal cerebral veins (Black arrow) (d)- Filling defect in Vein of Galen (white arrow)|
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|Figure 2: (a)- T1 axial showing corpus colossal hemorrhage (white arrow) and subacute thrombus in vein of Galen and straight sinus. (b)- T2 Sagital showing hemorrhage in genus corpus callosum, (c)- T2 Axial showing hyperintensities in bilateral thalamus, right parietal cortex (red arrow). (d) - SWI image showing hemorrhage in genu of corpus callosum and thrombosis of straight sinus. (e and f)- MRV showing non visualization (arrow) of deep venous system and right transverse sinus|
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Case 2: A 50 year old female was brought with five days history of generalized headache and two days history of drowsiness with no other significant history. Examination showed pallor; neurologically she was in altered sensorium with left hemiparesis. Investigations showed microcytic hypochromic anemia (Hb 7.5 gm%), with other work up being negative. Her CT brain showed hypodensities in the bilateral thalami, internal capsule and left basal ganglia and hemorrhage in the genu of the corpus callosum [Figure 1]c hyperdense bilateral internal cerebral veins with filling defect in contrast [Figure 1]d. MRI Brain showed thrombosis of deep venous system and left transverse sinus along with corpus colossal hemorrhage which was well appreciated on sequential weighted images [Figure 3]. She was managed with subcutaneous heparin followed by oral anticoagulation, antiedema measures and anemia was corrected. She improved subsequently and two years in to her follow up she is asymptomatic.
|Figure 3: (a)- T1 axial showing corpus callosum hemorrhage, (b)- T1 contrast showing filling defect in internal cerebral veins. (c)- T2 Axial showing hyperintense lesions in bilateral thalamus, right basal ganglia and internal capsule. (d)- T2 Sagital showing corpus callosum (genu) hemorrhage. (e)- SWI sequence showing corpus callosum hemorrhage (white arrow) with thrombosis of straight sinus, vein of Galen and bilateral internal cerebral veins (black arrow). (f)- MRV showing non visualisation of deep cerebral venous system|
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In the present study of 63 DCVT patients, we had two patients (3.2%) with CCH. These patients presented with either headache, seizures due to associated cortical lesions or encephalopathy resulting from the diencephalon involvement. Anemia was found in one while the cause of thrombosis remained uncertain in another patient. Imaging showed involvement of internal cerebral veins in both the cases with other proximal veins and sinuses. Interestingly neither of the patients had clinical features to suggest corpus callosal involvement. Both patients made uneventful recovery and are asymptomatic at follow up.
Clinical manifestations of the corpus callosal involvement are varied; many of the symptoms are also due to involvement of the surrounding structures. The common symptoms due to anterior corpus callosum lesion are alien hand syndrome, ideomotor apraxia, agraphia and tactile anomia restricted to left hand. 
Hemorrhage in corpus callosum is a rare scenario usually described with head injury, neoplasm and arteriovenous malformations.  Venous thrombosis is rarely implicated as causal factor in corpus collosal hemorrhage. There has been one case report with thrombosis of inferior sagital sinus producing such changes.  There is also a case report of splenial infarcts due to deep cerebral venous thrombosis. 
Involvement of corpus callosum in cases of deep cerebral venous thrombosis can be explained by the anatomical factors. Venous drainage of genu of corpus callosum is by anterior septal veins which are formed by a number of small veins in front of frontal horn of lateral ventricle; the two anterior septal veins from both the sides unite near foramen of monro and drain into internal cerebral veins; Posterior septal veins draining splenium of corpus callosum also joins the internal cerebral veins. The internal cerebral veins along with vein of Galen culminate in the straight sinus.  Both our patients had internal cerebral vein involvement which will explain the location of hemorrhage. The low incidence is probably due to alternate drainage of anterior and posterior collosal veins into basal vein and vein of Galen, circumventing the internal cerebral veins.  In conclusion, corpus callosal hemorrhage is a rare feature of deep cerebral venous thrombosis; however this possibility should be entertained as the treatment is significantly different from other etiologies. Imaging with CT and MRI will help in the diagnosis of the etiology.
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[Figure 1], [Figure 2], [Figure 3]