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to diagnose DCS. Early diagnosis and treatment with steroids and hyperbaric oxygen is essential to prevent complications.

Balakrishnan Kannan, Aarathy Kannan1, Chelladurai Saravanan2, Eswaradass Prasanna Venkatesan3 Departments of Neurology, 1Physician, 2Radiologist, Sundaram Arulrhaj Hospitals, Tuticorin, 3 Department of Neurologist, Appusami Hospital, Salem, Tamil Nadu, India E‑mail: [email protected]

References Figure 4: MRI spine shows hyperintense signal involving central portion of spinal cord extending from C2 to C5

was able to take orally and his power was 4/5 in upper limb and 2/5 in lower limb. Tuticorin is a town situated in southern coastal Tamil Nadu. One of the occupations of people here is deep sea diving for collecting sea shells. SCUBA diving has become widely available for occupational and recreational activity. SCUBA enables the diver to breathe high pressure gas from a cylinder through a regulator which allows the diver to stay underwater for about 2 to 3 hours.[1] Acute DCS is rarely reported in India, the first case report was by Tripathy et al. in 1964.[2] When the diver ascends, the sum of the gas tensions in the tissue exceeds the ambient pressure causing inert gases  (nitrogen), which were dissolved under higher pressure, to come out of physical solution and form gas bubbles which leads to multiorgan dysfunction.[3,4] The central nervous system (CNS) involvement in DCS has been studied in detail by Koshi et al. It is believed that arterialized bubbles passing through the lungs and heart involve the brain. MRI commonly shows multiple border zone infarcts.[5] Involvement of cortical gray matter and cerebellum are characteristic due to cerebral arterial gas embolism. Pneumobilia is accumulation of air in biliary tree. To best of our knowledge, pneumobilia in DCS has not been reported in literature. We propose that nitrogen air bubbles probably have accumulated in biliary tree producing pneumobilia. Our divers need to be educated about DCS and its preventive measures. It can be prevented by formal training of divers and following safety measures like slow ascent of 9–10 meters/minute and ear plugs to prevent barotrauma. In our country where there is no formal training, incidence of DCS is likely to increase in future. Physician must have a strong clinical suspicion Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6

1.

Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med 1992;326:30‑5. 2. Tripathy BB, Satpathy SN, Misra KC. Decompression sickness (caisson disease). J Indian Med Assoc 1964;42:130‑1. 3. P h a t a k   UA , D a v i d   E J , K u l k a r n i   P M . D e c o m p r e s s i o n syndrome (Caisson disease) in an Indian diver. Ann Indian Acad Neurol 2010;13:202‑3. 4. Carturan D, Boussuges A, Vanuxem P, Bar‑Hen A, Burnet H, Gardette B. Ascent rate, age, maximal oxygen uptake, adiposity, and circulating venous bubbles after diving. J Appl Physiol (1985) 2002;93:1349‑56. 5. Kohshi K, Katoh T, Abe H, Wong RM. Central nervous system involvement in patients with decompression illness. Sangyo Eiseigaku Zasshi 2003;45:97‑104. Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149413

Received: 27-11-2014 Review completed: 06-12-2014 Accepted: 09-12-2014

Intraventricular hemorrhage – unusual presentation of central neurocytoma Sir, Central neurocytoma is well‑differentiated tumor of neuronal origin, first described in 1982.[1] World Health Organization (WHO) classification of tumors of central nervous system, fourth edition 2007, classifies neurocytoma as a low‑grade neoplasm (WHO grade II) of neuronal differentiation. Neurocytoma accounts for 0.1 to 0.5% of all intracranial tumors.[2] Typical location of central neurocytoma is frontal horn of lateral ventricle. Clinical presentation of central neurocytoma varies from 691

Letters to Editor

being diagnosed incidentally to signs and symptoms suggestive of raised intracranial pressure. A 53‑year‑old female brought to emergency room with an episode of acute onset headache with vomiting and rapidly deteriorating level of consciousness along with weakness of right half of body. Physical examination showed sluggish reactive pupils and Glasgow coma scale  (GCS) score of 10. Computed tomography  (CT) scan showed massive intraventricular hemorrhage along with hyperdense lesion in left lateral ventricle [Figure 1]. Contrast magnetic resonance imaging  (MRI) done at our institution showed large lobulated predominantly hemorrhagic mass in left frontal horn and body of lateral ventricle which appeared to be attached to septum pellucidum along with intraventricular hemorrhage and moderate dilatation of ventricles [Figure 2]. Patient underwent left frontal craniotomy and excision of tumor by transcortical approach. Intraoperatively, tumor was surrounded by blood clots. Tumor was

Figure 1: Non contrast CT brain shows hyperdense mass on left side of septum pellucidum with intraventricular hemorrhage. It is difficult to define lateral border of tumor and its extension or invasion in lateral wall of ventricle

Figure 3: Post operative CT scan shows minimal IVH with Ommaya reservoir tip in situ. No residual lesion seen. Bilateral frontal pneumocephalus is seen

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firm in consistency, completely intraventricular with attachment to septum pellucidum and entering foramen of Monroe on left side. Complete excision of tumor was done. Ommaya reservoir was placed in situ. Frozen section of lesion was suggestive of neurocytoma. Patient electively ventilated for a day and gradually weaned off from ventilator. Postoperatively the patient regained consciousness fully along with power in left upper and lower limb. Patient made good recovery during hospital stay. Histopathological examination showed sheets of tumor cells with uniform stippled round nuclei and perinuclear cytoplasmic clearing and fibrillary matrix seen at places [Figure 3]. To differentiate it from oligodendroglioma, immunohistochemistry was performed. Immunohistochemistry showed positivity for synaptophysin and negative for glial fibrillary acidic protein (GFAP), confirming its neuronal origin [Figure 4]. In our experience of treating neurocytoma in the last 12 years, at our institute we had another patient with neurocytoma

Figure 2: Contrast MRI brain shows mass in left frontal horn body of lateral ventricle with no gross enhancement of contrast. Tumor is arising from septum pellucidum and not invading lateral wall of ventricle

Figure 4: H and E preparation showed well rounded nuclei with perinuclear cytoplasmic clearing. On H and E staining it’s difficult to differentiate between oligodendroglioma and neurocytoma so immunohistochemistry is mandatory

Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6

Letters to Editor

with intraventricular bleed. However in this patient, symptoms were not life‑threatening and he presented with headache and vomiting in outpatient department. CT scan showed intraventricular hemorrhage [Figure 5] and MRI showed tumor in right lateral ventricle with no significant contrast enhancement [Figure 6]. The patient underwent surgery, and biopsy report confirmed the neurocytoma as a pathological diagnosis.

vessel as a cause of intraventricular hemorrhage has been reported as well.[6] To summarize, central neurocytoma is a low‑grade tumor with clinically indolent course but it can lead to rapid deterioration of clinical condition secondary to intraventricular hemorrhage. Early surgery is beneficial in such event. Complete surgical excision is treatment of choice for central neurocytoma.

Central neurocytoma usually presents with symptoms like headache, vomiting, and visual changes. Most of these symptoms are attributed to raised intracranial pressure secondary to obstructive hydrocephalus. Acute presentation secondary to intraventricular hemorrhage is uncommon event. Our first patient did not complain of any of such symptoms; so intraventricular hemorrhage in previously undiagnosed central neurocytoma is rare event. Intratumoral hemorrhage is a well‑described entity in literature. Glioblastoma, anaplastic glioma, metastatic tumor, pituitary adenoma are few common culprits. Rate of hemorrhage in intracranial neoplasm is 2−5%.[3] Intratumoral hemorrhage in intracranial tumor without prior symptoms is even uncommon. High growth rate, high vascularity, fragile new vessels, arteriovenous shunting and venous occlusion due to tumor growth were proposed causes of intratumoral hemorrhage in gliomas.[4,5] An aneurysm on feeding

Prashant V. Gunawat, Subodh Shantaram Patil, Vikram S. Karmarkar, Chandrashekhar E. Deopujari Department of Neurosurgery,Bombay Hospital Instititute of Medical Sciences, Mumbai, Maharashtra, India E‑mail: [email protected]

References 1. 2. 3. 4. 5. 6.

Hassoun J, Gambarelli D, Grisoli F, Pellet W, Salamon G, Pellissier JF, et al. Central neurocytoma. An electron‑microscopic study of two cases. Acta Neuropathol 1982;56:151‑6. Patel DM, Schmidt RF, Liu JK. Update on the diagnosis, pathogenesis, and treatment strategies for central neurocytoma. J Clin Neurosci 2013;20:1193‑9. Licata B, Turazzi S. Bleeding cerebral neoplasms with symptomatic hematoma. J Neurosurg Sci 2003;47:201‑10. Liwnicz BH, Wu SZ, Tew JM Jr. The relationship between the capillary structure and hemorrhage in gliomas. J Neurosurg 1987;66:536‑41. Yuguang L, Meng L, Shugan Z, Yuquan J, Gang L, Xingang L, et al. Intracranial tumoural haemorrhage‑A report of 58 cases. J Clin Neurosci 2002;9:637‑9. Vates GE, Arthur KA, Ojemann SG, Williams F, Lawton MT. A neurocytoma and an associated lenticulostriate artery aneurysm presenting with intraventricular hemorrhage: Case report. Neurosurgery 2001;49:721‑5. Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.149414

Received: 14-09-2014 Review completed: 25-10-2014 Accepted: 05-12-2014 Figure 5: Immunohistochemistry showing positivity for synaptophysin and was negative for GFAP, confirming its neuronal origin

Figure 6: CT scan showed intraventricular hemorrhage with ill defined tumor

Neurology India | Nov-Dec 2014 | Vol 62 | Issue 6

Intracranial granulocytic sarcomaina in a non-leukemia patient Sir, Granulocytic sarcoma  (GS), also known as chloroma, is a solid tumor composed of immature myeloid cells at extramedullary sites. [1] The most common sites of GS includes visceral organs, soft tissue, lymph 693

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Intraventricular hemorrhage--unusual presentation of central neurocytoma.

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