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References 1. 2. 3.

4. 5.

Dhandapani S, Anirudh S, Garg R, Vasishta RK, Vyas S. Subependymoma causing conus‑cauda syndrome: Cured by total excision. Neurol India 2013;61:675‑7. Grant R, Papadopoulos SM, Greenberg HS. Metastaticepidural spinal cord compression. Neurol Clin 1991;9:825‑41. Dhandapani S, Mehta VS, Sharma BS. "Horseshoe cord terminus" sans filum around a bone spur: a rare composite of faulty gastrulation with agenesis of secondary neurulation: Case report. J Neurosurg Pediatr 2013;12:411-3.. Si Q, Dancer J, Stanton ML, Tamboli P, Ro JY, Czerniak BA, et al. Small cell carcinoma of the kidney: A clinicopathologic study of 14 cases. Hum Pathol 2011;42:1792‑8. Masuda T, Oikawa H, Yashima A, Sugimura J, Okamoto T, Fujioka T. Renal small cell carcinoma (neuroendorine carcinoma) without features of transitional cell carcinoma. Pathol Int 1998;48:412‑5. Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.144494

Received: 11-09-2014 Review completed: 14-09-2014 Accepted: 28-09-2014

Corpus callosal hemorrhage due to deep cerebral venous sinus thrombosis Sir, Hemorrhage in corpus callosum (CCH) (largest association fiber) is rare and is it is usually due to trauma, hypertension arteriovenous malformation and neoplasm.[1,2] Deep cerebral venous thrombosis (DCVT) producing CCH is a rare entity with only one case noted so far.[3] 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 1a]; with contrast scan showing filling defects in internal cerebral veins, vein of Galen and straight sinus [Figure 1b]. Her Magnetic Resonance Imaging (MRI) of the brain Neurology India | Sep-Oct 2014 | Vol 62 | Issue 5

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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)

done four days later [Figure 2a‑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. 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 1c] hyperdense bilateral internal cerebral veins with filling defect in contrast [Figure 1d]. 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. 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 563

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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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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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Neurology India | Sep-Oct 2014 | Vol 62 | Issue 5

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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.[4] Hemorrhage in corpus callosum is a rare scenario usually described with head injury, neoplasm and arteriovenous malformations.[1] 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.[3] There is also a case report of splenial infarcts due to deep cerebral venous thrombosis.[5] 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.[6] 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.[7] 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.

Girish Baburao Kulkarni1,2, Hima Pendarkar1,2, Masoom Abbas Mirza1,2, Veerendrakumar Mustare1,2 1

Departments of Neurology, and 2Neuroradiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India E‑mail: [email protected]

Neurology India | Sep-Oct 2014 | Vol 62 | Issue 5

References 1. Bourekas EC, Varakis K, Bruns D, Christoforidis GA, Baujan M, Slone HW, et al. Lesions of the corpus callosum: MR imaging and differential considerations in adults and children. Am J Roentgenol 2002;179:251‑7. 2. Kasahara T, Toyokura M, Shimoda N, Ishida A. Cerebral hemorrhage restricted to the corpus callosum. Am J Phys Med Rehabil 2005;84:386‑90. 3. Erbaş G, Oner AY, Akpek S, Tokgoz N. Corpus callosum hematoma secondary to isolated inferior sagital sinus thrombosis. Acta Radiol 2006;47:1085‑8. 4. Giroud M, Dumas R. Clinical and topographical range of callosal infarction: A clinical and radiological correlation study. J Neurol Neurosurg Psychiatry 1995;59:238‑42. 5. Lai W, Katirji B. Splenium infarct due to cerebral venous thrombosis. Arch Neurol 2007;64:1540. 6. Ono M, Rhoton AL Jr, Peace D, Rodriguez RJ. Microsurgical anatomy of the deep venous system of the brain. Neurosurgery 1984;15:621‑57. 7. Andeweg J. The anatomy of collateral venous flow from the brain and its value in aetiological interpretation of intracranial pathology. Neuroradiology 1996;38:621‑8. Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.144497

Received: 02-07-2014 Review completed: 23-08-2014 Accepted: 28-09-2014

Spontaneous thrombosis of a cerebral arteriovenous malformation Sir, Spontaneous thrombosis of cerebral arteriovenous malformations (AVM) is exceedingly rare[1] and only 29 such cases have been reported in the literature.[1‑5] We report one such case. A 25‑year‑old female presented with headache, vomiting and generalized tonic‑clonic seizures. She was drowsy but arousable and confused, and had no obvious motor or sensory deficits. Computed tomography (CT) of brain revealed a right frontal lobe hematoma with surrounding edema. [Figure 1a] She was managed conservatively and was referred to our institute after 1 week. CT angiogram (CTA) [Figure 1b-d] revealed a right frontal arteriovenous malformation (AVM) with a compact nidus supplied by an enlarged and tortuous frontopolar branch of the right anterior cerebral artery (ACA). A single large vein draining into the 565

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Corpus callosal hemorrhage due to deep cerebral venous sinus thrombosis.

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