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systems provide valuable localization information for the performance of neurosurgical procedures.[4] Marking of the skull prior to craniotomy on the basis of CT images can prove to be a difficult problem. [5] Conventional methods of preoperative localization include measurement and calculation from the baseline, such as orbito–meatal line, or obtaining a CT scan with a marker on the scalp.[6] However, easy and less‑technical localization is mandatory in emergency surgery and small lesion in routine surgery, where such facilities are not available. A similar rapid, simple and inexpensive CT technique has been developed for marking the scalp and lateral skull radiograph of patients with small cerebral convexity lesions.[1] It is safe to use the frame and needs no special training. It is also not costly and can address the issue, where image guidance/stereotactic systems are not available. We need to try it with other small lesions like brain tumor and in a number of cases prior to judging its efficacy. It is helpful in localization of brain lesions in developing countries without high technical facilities. Pralaya Kishore Nayak, Jawhar Dutta Departments of Neurosurgery and Radiology, NeotiaGetwel Healthcare Centre, Siliguri, West Bengal, India Address for correspondence: Dr. Pralaya Kishore Nayak, Department of Neurosurgery, NeotiaGetwel Healthcare Centre, Siliguri - 734 010, West Bengal, India. E‑mail: [email protected]

References 1.

Hayman LA, Evans RA, Hinck VC. Scalp markers for precise craniotomy siting, using computed tomography. J Comput Assist Tomogr 1979;3:701‑2. 2. Azzam NI. Intracranial lesion localisation: A simple method using CT scanning. J Neurol Neurosurg Psychiatry 1982;45:752‑3. 3. Alker G, Kelly PJ. An overview of CT based stereotactic systems for the localization of intracranial lesions. Comput Radiol 1984;8:193‑6. 4. Guthrie BL, Adler JR Jr. Computer‑assisted preoperative planning, interactive surgery, and frameless stereotaxy. Clin Neurosurg 1992;38: 112‑31. 5. Spincemaille GH, Versteege CW, Blaauw G. Computed tomographyguided scalp marking of cerebral surface lesions; an alternative to stereotaxis for small convexity lesions. Eur J Radiol 1990;11:143‑4. 6. Ikeda A, Ito K, Matsuzawa K, Tanaka Y, Miyazaki Y, Yamamoto I, et al. Craniotomy for lesions in the cerebral convexity; how to precisely localize the lesions with conventional CT slices. No Shinkei Geka. Neurological surgery 1992;20:875‑81.

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DOI: 10.4103/0976-3147.131692

Atypical meningioma and acute subdural hemorrhage Sir, A 65‑year‑old woman presented with a sudden onset of vomiting and altered sensorium of a one‑day duration. Her Glasgow coma score at admission was 7  (not opening eyes, localizing to pain, and on an endotracheal tube). There was right hemiplegia. She did not have prior neurological symptoms, including headache. There was no history of trauma. The computed tomography (CT) scan showed a well‑defined, left parietal‑occipital mass lesion, based on cerebral convexity, with left fronto‑tempo‑parietal acute subdural hematoma (SDH) causing a midline shift of 12  mm  [Figure  1a]. The coagulation profile was normal. She immediately u n d e r we n t f r o n t o ‑ t e m p o r o ‑ p a r i e t o ‑ o c c i p i t a l craniotomy, evacuation of the acute SDH, and total excision of the parietal mass lesion. The tumor was arising from the dura, with a broad attachment. There was bleeding inside the tumor that communicated with the SDH. The postoperative CT scan showed total excision of the tumor and complete evacuation of the SDH  [Figure  1b]. The histopathology report revealed atypical meningioma (WHO grade II), with intratumoral hemorrhage. At the one‑month follow up, the right hemiplegia had significantly improved and she was able to walk without any support. The association between meningioma and intracranial bleeding is rare. Meningiomas with bleed are found more often in patients who are older than 70  years or younger than 30  years of age.[1] The most common sites of meningioma, associated with bleeding, are intraventricular and convexity.[1,2] The most common bleeding locations are intracerebral/intratumoral and subarachnoid space, followed by subdural space.[1,3] Convexity meningiomas are more likely to produce SDH. Parasagittal and falcine meningiomas are more likely to produce intracerebral and intratumoral bleeding. Sphenoidal and intraventricular meningiomas are more likely to produce subarachnoid hemorrhage.[1] Among the histological subtypes, increased tendency for bleeding was found in malignant, followed by fibrous and angioblastic meningiomas.[1] The mortality rate associated with SDH is the lowest, and that with intracerebral hemorrhage  (ICH) is the highest[1] The mechanism of bleeding related to meningioma is unclear.

Journal of Neurosciences in Rural Practice | April ‑ June 2014 | Vol 5 | Issue 2

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DOI: 10.4103/0976-3147.131693

a

b

Figures 1: (a) Preoperative plain CT scan axial section showing a well‑defined left parieto‑occipital lesion with left fronto‑parietal acute subdural hemorrhage and midline shift. (b) Postoperative plain CT scan axial section showing total excision of the tumor and evacuation of the SDH

The following are the proposed mechanisms for SDH associated with meningiomas:[1] • Compensatory enlargement and weakening of blood vessels supplying or draining from the tumor • Bleeding from a neo‑membrane on the inner surface of the dura in proximity to the tumor • Meningeal invasion of the vessel wall resulting in vessel disruption • Minor head trauma. In our case none of the above was found. The cause of bleeding in our case could have been thinned and friable vessel walls leading to intratumoral bleeding, with massive spillage into the subdural space. In a patient presenting with acute SDH and a convexity‑based tumor, the possibility of meningioma with bleed should be considered. Prompt evacuation of the SDH should be done, as it is life‑saving. The meningioma should also be removed, if feasible. Ashok Munivenkatappa, Dhaval P. Shukla1 Departments of Clinical Neurosciences and 1Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore, India Address for correspondence: Dr. Dhaval P. Shukla, Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore, India. E‑mail: [email protected]

References 1. 2. 3.

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Bosnjak  R, Derham  C, Popović M, Ravnik  J. Spontaneous intracranial meningioma bleeding: Clinicopathological features and outcome. J Neurosurg 2005;103:473‑84. Lefranc F, Nagy N, Dewitte O, Balériaux D, Brotchi J. Intracranial meningiomas revealed by non‑traumatic subdural haematomas: A series of four cases. Acta Neurochir (Wien) 2001;143:977‑82. Di Rocco F, Mannino S, Puca A, Lauriola L, Pompucci A. Intracranial meningiomas associated with non‑traumatic chronic subdural hematoma. Acta Neurochir (Wien) 2006;148:1097‑102.

Guillain-Barré syndrome following acute viral hepatitis A Sir, A 28‑year‑old male patient presented with progressive symmetric ascending distal followed by proximal weakness over two days, preceded by low grade fever, malaise, nausea and vomiting along with anorexia of two week duration. His initial evaluation at local hospital revealed features of acute hepatitis with rising levels of serum bilirubin (5.6  mg/dl), transaminitis  (SGOT/SGPT  ‑  1877/3058) without any features of hepatic decompensation. He was conscious, alert with jaundice and hepatomegaly without features of hepatic failure. His neurological examination revealed bifacial lower motor neuron weakness, generalized hypotonia with areflexia, neck muscle weakness, and upper and lower limb power of medical research council grade (MRC) 2 with distal more than proximal weakness. In view of rapidly progressive ascending flaccid areflexic quadriparesis along with bifacial weakness, the diagnosis of Guillain‑Barré syndrome (GBS) was considered. His motor nerve conduction study showed significantly reduced or inelicitable CMAP from bilateral tibial and peroneal nerves without any improvement on proximal stimulation with mild prolongation of distal latencies and conduction velocities but not amounting to a coexisting demyelinating process. The F waves were either inelicitable or prolonged from all four limbs. Sensory nerve conduction study showed inelicitable SNAP amplitudes from all tested nerves except from bilateral median nerves, consistent with acute motor and sensory axonal neuropathy (AMSAN) [Table 1]. He was treated with IV IgG of 400 mg/kg/day. His biochemical evaluation showed high IgM hepatitis A antibody titer by ELISA in serum and negative serological investigations for hepatitis B, hepatitis C, hepatitis E and negative anti‑ganglioside antibody. His CSF showed albuminocytological dissociation with protein of 90 mg%. After admission, he developed respiratory weakness requiring prolonged mechanical

Journal of Neurosciences in Rural Practice | April ‑ June 2014 | Vol 5 | Issue 2

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Atypical meningioma and acute subdural hemorrhage.

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