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6. Chelly I, Mekni A, Kchir N, Karim BH, Khadija B, Selma B, et al. Intracerebellar granulocytic sarcoma. A case report. Pathologica 2005;97:335‑7. 7. Widhalm G, Dietrich W, Müllauer L, Streubel B, Rabitsch W, Kotter MR, et al. Myeloid sarcoma with multiple lesions of the central nervous system in a patient without leukemia. J Neurosurg 2006;105:916‑9. 8. Grier DD, Al‑Quran SZ, Gray B, Li Y, Braylan R. Intracranial myeloid sarcoma. Br J Haematol 2008;142:681. 9. Balleari E, Panarello S, Capello E, Grosso M, Passalia C, Pitto P, et al. Granulocytic sarcoma: An unusual cause of spinal cord compression. Int J Clin Oncol 2007;12:234‑7.

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Figure 2: Histopathological examination of granulocytic sarcoma (GS) in the presented case. Histopathological examination (hematoxylin and eosin (H and E) staining) showed that the tumor is composed of uniform population of malignant round cells with a high nuclearcytoplasmic ratio, irregular nuclei, and prominent nucleoli (a). Immunohistochemically, most tumor cells were positive for myeloperoxidase (MPO) (b), negative for CD3 (c) and CD20 (d). Original magnification: x200

sampling is imperative to assess the absence of AML if a final diagnosis of GS is made. There is no standard treatment protocol that has been established. The prevailing opinion is that GS with or without bone marrow involvement should be treated as AML because of the high risk of metachronous AML occurrence. Systemic chemotherapy is significantly useful for these patients to have a good long‑term survival. Surgical therapy is the only reserved presenting clinical symptom due to mass effect. The long‑term prognosis of non‑leukemia GS is still despondent.

Jing‑Feng Wang, Peng Sun, Dong‑Liang Lin1, Ming‑Chao Fan Departments of Neurosurgery, and 1Pathology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China E‑mail: [email protected]

References 1.

Llena JF, Kawamoto K, Hirano A, Feiring E. Granulocytic sarcoma of the central nervous system: Initial presentation of leukemia. Acta Neuropathol 1978;42:145‑7. 2. Nickels J, Koivuniemi A, Heiskanen O. Granulocytic sarcoma (chloroma) of the cerebellum and meninges a case report. Acta Neurochir (Wien) 1979;46:297‑301. 3. Yoon DH, Cho KJ, Suh YL, Kim CW, Chi JG, Han DH, et al. Intracranial granulocytic sarcoma (chloroma) in a nonleukemic patient. J Korean Med Sci 1987;2:173‑8. 4. Levy R, Shvero J, Sandbank J. Granulocytic sarcoma (chloroma) of the temporal bone. Int J Pediatr Otorhinolarygol 1989;18:163‑9. 5. Vohra AH, Khawaja MA, Raja IA. Chloroma of the cranium with dural involvement. J Clin Neurosci 1997;4:268‑70. Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149415

Received: 08-10-2014 Review completed: 21-10-2014 Accepted: 06-12-2014

Cerebral venous sinus thrombosis: An unusual initial presentation of mucinous adenocarcinoma of stomach Sir, Thrombotic events in cancer patient manifest commonly as deep venous thrombosis or pulmonary embolism and in less common sites, like veins of cerebral circulation.[1] Thrombosis can represent the earliest clinical manifestation of an occult malignancy, as revealed by study demonstrating idiopathic venous thrombosis have a 4–7 fold increased risk of being diagnosed with cancer in the first year, as compared with secondary causes.[2] Here we describe a case of carcinoma stomach initially presented as cerebral venous thrombosis (CVT), hitherto unreported in the literature. A 56‑year‑old lady presented with headache and intermittent projectile vomiting for 10  days. She developed right side focal motor seizures with secondary generalisation  (six episodes in last 2  days) and altered sensorium for 2 days. She was not taking any hormonal preparation. There was no prior history of spontaneous abortion or history suggestive of collagen vascular disease. At admission, Glasgow coma scale  (GCS) was 13/15  (E4V4M5). She had bilateral papilloedema. There was right sided hemiparesis. There was no pallor, jaundice or lymphadenopathy. On per abdominal examination a firm epigastium mass 695

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of 3 × 5 cm dimension was felt. There was no hepatospleenomegaly. Magnetic resonance imaging  (MRI) brain showed acute venous hemorrhagic infarction and swelling over left tempero‑parieto‑occipital lobe with mild mass effect. The MR‑venography demonstrated left sided sigmoid and left transverse sinus thrombosis. Post contrast study shows patchy enhancement of the abnormal area [Figure 1]. Laboratory findings revealed haemoglobin 13.1 gm%. Liver and renal function test were within normal range. Anti nuclear antibody (ANA), Anti double stranded DNA (DsDNA), Complements, anti cardiolipin antibody were normal. Prothrombin time (PT), Activated partial thromboplastin time (APTT), Platelet count were normal. Sickling test was negative. A full thrombotic workup showed normal prothrombin, activated partial thromboplastin and thrombin time. Factor VIII, fibrinogen, antithrombin III level and activated protein C resistance ratio were normal. The lupus anticoagulant was negative. The protein C and protein S functional assay were within the normal range. Genetic markers for thrombosis like factor V Leiden mutation, methylene tetra hydro folate reductase and prothrombin gene polymorphism were not detected. For the evaluation of epigastric mass, ultrasound abdomen was done, which showed asymmetrical mural thickening of antropyloric region. Computer tomography  (CT) abdomen demonstrated segmental enhancing wall thickening involving antropyloric region of stomach and few subcentimeter perigastric nodes. Upper gastrointestinal (GI) endoscopy showed a ulcero‑nodular growth involving incisura [Figure 2]. The biopsy of the lesion suggested gastric mucosa along with tumor tissue. The tumor cells are seen arranged in acini, cord and sheets showing moderate nuclear pleomorphisim, increased N: C ratio, hyperchromatism, increased mitosis along with few signet ring cells. The tumor is infiltrating the muscularis mucosa [Figure 3]. So diagnosis of mucinous infiltrating adenocarcinoma of stomach was made.

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Figure 1: (a) T2W (b) SWI (c)MRV (d) T1W contrast images reveals acute hemorrhagic venous infarct and swelling in the left temperoparietooccipital lobe with mild mass effect. MRV demonstrates thrombosis in left sided sigmoid and left transverse sinus

Figure 2: Upper GI Endoscopy showed a ulcero-nodular growth involving incisura

She was treated with low molecular weight heparin, antiepileptics and anti edema measures. After 1 month of neurological stabilisation; she underwent subtotal gastrectomy with lymphnode resection. The omental nodes did not reveal any metastatic deposists. Post operation she did not have any complications. At 3 months of follow-up she improved to a modified Rankin scale of 2. In one series, cancer accounted for 7.4% of all CVT and 2.2% were associated with central nervous system (CNS) malignancy, 3.2% with solid tumors outside the CNS and 2.9% with hematological disorders.[3] A study in Chinese population, revealed, of the 376 deep venous

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Figure 3: The histopathology of the lesion at high power view highlighting tumor cells arranged in acini, cord and sheets showing moderate nuclear pleomorphisim, hyperchromatism, increased mitosis (a) along with few signet ring cells (b) There are mucin pools (c) suggesting mucinous infiltrating adenocarcinomas

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thrombosis  (DVT) cases, 4  cases were associated with carcinoma stomach.[4] CVT in association with malignancy was observed in 4 (0.9%) cases like acute lymphoid leukemia and carcinoma tongue in a study from India.[5] Usually the venous thrombosis is seen during the course of malignancy. DVT sometimes may antedated the diagnosis of bronchogenic carcinoma.[4] But the CVT antedating carcinoma stomach has not been reported in the literature. The association of cancer with CVT may be due to various possible mechanisims like, direct tumor compression, tumor invasion of cerebral sinuses, hypercoagulable state, chemotherapeutic side effects or paraneoplastic effects.[6] In our case probable etiology may be hypercoagulable state or paraneoplastic effects of mucinous adenocarcinoma. Mucin‑producing adenocarcinomas are particularly notorious for venous thrmbosis. The cell surface compositions like saccharide and mucin content is altered producing more adhesiveness and coagulation abnormalities.[7] Mucin circulates and stimulates platelet aggregation in response to L‑selectin in thrombocytes and P‑selectin in leukocytes.[7] Heparin inhibits platelet aggregation by inhibiting the ligand of selectin and binding of mucin and selectin.[7] Clinicians should be aware of the potential of carcinoma stomach for causation of CVT. The early diagnosis of carcinoma stomach has definite prognostic role as, appropriate medical and timely surgical interventions are crucial. The CVT can be the first manifestation of an occult malignancy, and patients presenting with idiopathic CVT are more likely to have underlying cancer than those in whom a secondary cause of thrombosis is apparent.

Subhransu Sekhar Jena, Soumyadarshan Nayak, Ishwar Chandra Behera1, Debahuti Mohapatra2, Subrat Kumar Tripathy3

Mridula KR, et al. Risk factors, clinical profile, and long‑term outcome of 428 patients of cerebral sinus venous thrombosis: Insights from Nizam’s Institute Venous Stroke Registry, Hyderabad (India). Neurol India 2012;60:154‑9. 6. Rogers LR. Cerebrovascular complications in patients with cancer. Semin Neurol 2004;24:453‑60. 7. Wahrenbrock M, Borsig L, Le D, Varki N, Varki A. Selectin‑mucin interactions as a probable molecular explanation for the association of Trousseau syndrome with mucinous adenocarcinomas. J Clin Invest 2003;112:853‑62. Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149416

Received: 10-10-2014 Review completed: 11-10-2014 Accepted: 05-12-2014

Giant extra-axial en-plaque tuberculoma with gyriform enhancement: Unusual presentation of a common disease Sir, Though first described in 1927, en‑plaque tuberculoma still remains a diagnostic dilemma because of its rare occurrence.[1] This report presents an unusual case of en‑plaque tuberculoma mimicking en‑plaque meningioma.

Departments of Neurology, 1Critical Care, 2Pathology, Biochemistry, Institute of Medical Sciences and Sum Hospital, Siksha ‘O’ Anusandhan University, Bhubaneswar, Odisha, India E‑mail: [email protected] 3

References Lee AY, Levine MN. The thrombophilic state induced by therapeutic agents in the cancer patient. Semin Thromb Hemost 1999;25:137‑45. 2. Prandoni P, Lensing AW, Büller HR, Cogo A, Prins MH, Cattelan AM, et al. Deep‑vein thrombosis and the incidence of subsequent symptomatic cancer. N Engl J Med 1992;327:1128‑33. 3. Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F. ISCVT Investigators. Prognosis of cerebral vein and dural sinus thrombosis: Results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke 2004;35:664‑70. 4. Liu HS, Kho BC, Chan JC, Cheung FM, Lau KY, Choi FP, et al. Venous thromboembolism in the Chinese population‑‑experience in a regional hospital in Hong Kong. Hong Kong Med J 2002;8:400‑5. 5. Narayan D, Kaul S, Ravishankar K, Suryaprabha T, Bandaru VC,

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c Figure 1: Axial (a), Coronal (b), and Saggital (c) T2 weighted magnetic resonance imaging (MRI) brain revealing mildly hyperintense left frontal, dural-based, extra-axial, enplaque lesion with gyriform pattern and sulcal extensions (marked as asterisk). Note is made of hyperintense massive white matter edema, mass effect, and midline shift of 15 mm to right side

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Cerebral venous sinus thrombosis: an unusual initial presentation of mucinous adenocarcinoma of stomach.

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