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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
[Downloaded free from http://www.neurologyindia.com on Thursday, November 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for journal Letters to Editor
superior sagittal sinus was noted. She was scheduled for a digital subtraction angiogram (DSA) after 6 weeks, to be followed by definitive management. Four‑vessel DSA done (7 weeks after ictus) revealed no opacification of the nidus of the AVM; the arterial feeder ended abruptly. [Figure 2a, b] CT angiogram confirmed these findings and demonstrated a filling
a
b
c
d
Figure 1: Initial imaging study. (a) Sagittal reconstruction of a CT image showing the frontal lobe hematoma. (b) Sagittal reconstruction of a CT angiogram image, showing the nidus of the AVM and a venous varix near the sagittal sinus. (c) Coronal view of the AVM nidus. (d) Magnified view of the single large draining vein with a venous varix
a
b
c
d
e
f
Figure 2: Follow-up imaging studies. (a) DSA, AP view showing no opacification of the nidus on right ICA injection. (b) DSA, lateral view. The nidus is not seen. (c) Sagittal and (d) Coronal views on a CT angiogram. Neither the nidus nor the large venous varix is seen. (e) Axial T1 and f – T2 sagittal MRI images showing gliosis in the region of the nidus
566
defect in the dilated draining vein. [Figure 2c, d] MRI brain showed gliosis in the region of the nidus and T1 hyperintense signals within the draining vein [Figure 2e, f]. These features were confirmative of spontaneous thrombosis of the AVM. She underwent further evaluation to look for a hypercoagulable state. She was not on oral contraceptives. Protein C, protein S, antithrombin III, antiphospholipid antibodies and homocysteine levels were all within normal limits, and anti‑DNA antibodies were negative. She was discharged on anti‑epileptic drug and advised follow up DSA after 6 months. Spontaneous thrombosis of an AVM is a very rare event and occurs in
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
[Downloaded free from http://www.neurologyindia.com on Thursday, November 13, 2014, IP: 202.177.173.189] || Click here to download free Android application for journal Letters to Editor
superior sagittal sinus was noted. She was scheduled for a digital subtraction angiogram (DSA) after 6 weeks, to be followed by definitive management. Four‑vessel DSA done (7 weeks after ictus) revealed no opacification of the nidus of the AVM; the arterial feeder ended abruptly. [Figure 2a, b] CT angiogram confirmed these findings and demonstrated a filling
a
b
c
d
Figure 1: Initial imaging study. (a) Sagittal reconstruction of a CT image showing the frontal lobe hematoma. (b) Sagittal reconstruction of a CT angiogram image, showing the nidus of the AVM and a venous varix near the sagittal sinus. (c) Coronal view of the AVM nidus. (d) Magnified view of the single large draining vein with a venous varix
a
b
c
d
e
f
Figure 2: Follow-up imaging studies. (a) DSA, AP view showing no opacification of the nidus on right ICA injection. (b) DSA, lateral view. The nidus is not seen. (c) Sagittal and (d) Coronal views on a CT angiogram. Neither the nidus nor the large venous varix is seen. (e) Axial T1 and f – T2 sagittal MRI images showing gliosis in the region of the nidus
566
defect in the dilated draining vein. [Figure 2c, d] MRI brain showed gliosis in the region of the nidus and T1 hyperintense signals within the draining vein [Figure 2e, f]. These features were confirmative of spontaneous thrombosis of the AVM. She underwent further evaluation to look for a hypercoagulable state. She was not on oral contraceptives. Protein C, protein S, antithrombin III, antiphospholipid antibodies and homocysteine levels were all within normal limits, and anti‑DNA antibodies were negative. She was discharged on anti‑epileptic drug and advised follow up DSA after 6 months. Spontaneous thrombosis of an AVM is a very rare event and occurs in
