Letters to Editor
Ying Chang, Meng‑Chao Zhang1, Huan‑Huan Wan, Hua Xin2 2
Departments of Neurology, 1Radiology and Thoracic Surgery, China‑Japan Union Hospital, Jilin Univetsity, Changchun, China E‑mail: [email protected]
References 1. Lammouchi T, Zoghlami F, Ben Slamia L, Grira M, Harzallah MS, Benammou S. Epileptic seizures in non‑ketotic hyperglycemia. Neurophysiol Clin 2004;34:183‑7. 2. Qi X, Yan YY, Gao Y, Zheng ZS, Chang Y. Hemichorea associated with non‑ketotic hyperglycaemia: A case report. Diabetes Res Clin Pract 2012;95:e1‑3. 3. Scherer C. Seizures and non‑ketotic hyperglycemia. Presse Med 2005;34:1084‑6. 4. Hennis A, Corbin D, Fraser H. Focal seizures and non‑ketotic hyperglycaemia. J Neurol Neurosurg Psychiatry 1992;55:195‑7. 5. Taieb‑Dogui T, Harzallah MS, Khlifa K, Dogui M, Ben Ammou S, Jallon P. Acute repetitive gyratory seizures as a manifestation of nonketotic hyperglycemia. Neurophysiol Clin 2002;32:254‑7. 6. Siddiqi ZA, VanLandingham KE, Husain AM. Reflex seizures and non‑ketotic hyperglycemia: An unresolved issue. Seizure 2002;11:63‑6. 7. Moien‑Afshari F, Téllez‑Zenteno JF. Occipital seizures induced by hiperglycemia: A case report and review of literature. Seizure 2009;18:382‑5. 8. Schwechter EM, Velísková J, Velísek L. Correlation between extracellular glucose and seizure susceptibility in adult rats. Ann Neurol 2003;53:91‑101. 9. Likhodii SS, Serbanescu I, Cortez MA, Murphy P, Snead OC 3rd, Burnham WM. Anticonvulsant properties of acetone, a brain ketone elevated by the ketogenic diet. Ann Neruol 2003;54:219‑26. 10. Freedman KA, Polepalle S. Transient homonymous hemianopia and positive visual phenomena in nonketotic hyperglycemic patients. Am J Ophthalmol 2004;137:1122‑4. 11. Ozer F, Mutlu A, Ozkayran T. Reflex epilepsy and non‑ketotic hyperglycemia. Epileptic Disord 2003;5:165‑8. 12. Lavin PJ. Hyperglycemic hemianopia: A reversible complication of non‑ketotic hyperglycemia. Neurology 2005;65:616‑9. 13. Kang SS, Keasey MP, Cai J, Hagg T. Loss of neuron‑astroglial interaction rapidly induces protective CNTF expression after stroke in mice. J Neurosci 2012;32:9277‑87. 14. Benjelloun N, Renolleau S, Represa A, Ben‑Ari Y, Charriaut‑Marlangue C. Inflammatory responses in the cerebral cortex after ischemia in the P7 neonatal rat. Stroke 1999;30:1916‑23. 15. Guez A, Obadia M, Lafitte F, Tin SN, Héran F, Gout O. Magnetic resonance spectroscopy findings in a case of hyperglycaemic hemianopia. Rev Neurol (Paris) 2010;166:737‑40. 16. Chu K, Kang DW, Kim DE, Park SH, Roh JK. Diffusion‑weighted and gradient echo magnetic resonance findings of hemichorea‑hemiballismus associated with diabetic hyperglycemia: A hyperviscosity syndrome? Arch Neurol 2002;59:448‑52. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121937
Received: 29‑05‑2013 Review completed: 11‑06‑2013 Accepted: 09‑10‑2013 530
Granulomatous amoebic meningoencephalitis Sir, An 18‑year‑old male presented with progressive left parietal headache evolving into severe holocranial headache associated with vomiting of 27 days duration and gradually progressive right hemiparesis since 5 days. There was no history of fever at the onset of symptoms and he had no immunodeficiency state or on immunosuppression treatment. Neurologic examination revealed altered sensorium, mild right hemiparesis with neck rigidity. Cerebrospinal fluid (CSF) examination revealed glucose of 71 mg/dL, protein of 132 mg/dL, and 20 nucleated cells/dL (all lymphocytes). Results of gram and acid‑fast staining were negative. Brain computed tomography (CT) scan revealed an ill‑defined hypoattenuating lesion in the left frontoparietal lobe and right superior frontal gyrus with linear overlying gyriform enhancement and moderate perilesional edema [Figure 1]. Brain magnetic resonance imaging (MRI) revealed multifocal involvement of bilateral cerebral hemisphere and left cerebellar hemisphere [Figure 2]. The largest lesion in the left frontoparietal lobe resembled a mass lesion with interspersed hemorrhages and showed linear gyriform pattern of enhancement [Figure 1d]. A diagnosis of infective process of the brain and meninges was considered and he was stated on parenteral vancomycin and ceftrixone along with parenteral steroids. Subsequently, the child developed signs of increased intracranial tension and lapsed into unresponsive state and died on day‑10 of admission. A partial autopsy and brain examination revealed granulomatous amoebic meningoencephalitis [Figure 3]. Central nervous system amebiasis is a rare condition that is caused by several free‑living amebic organisms and is broadly divided into granulomatous amebic encephalitis (GAE) and primary amebic meningoencephalitis (PAM).[1] GAE is a subacute to chronic infection caused by Acanthamoeba and also Balamuthia mandrillaris organisms, unlike primary amoebic encephalitis caused by Naegleria fowleri which is acute in onset, rapidly progressive, resulting in fatality within 48–72 h. The incubation period of this disease is not known and is postulated to be more than 10 days.[2] The disease occurs in the 2nd and 4th decades and 10 times more in men. Pathologically, the lesions represent focal areas of cerebritis or microabscesses and leptomeningitis of the overlying cortex. The clinical course for GAE is characterized by a long duration of focal neurologic symptoms. A spectrum of radiological findings in the form of multifocal parenchymal lesions, necrosis, Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
Letters to Editor
a
b
c
d
Figure 1: Noncontrast (a and b) and contrast‑enhanced (c and d) computed tomography axial images shows an ill‑defined hypoattenuating lesion in the left frontoparietal lobe and right superior frontal gyrus with linear overlying gyriform enhancement
represents a combination of enhancement in the inflamed meninges and the underlying cortex. Associated microabscesses are caused by infiltration of brain substance, by amoebae along the pial vessels. The multifocal pattern shows T2 hyperintensities and ring enhancement, with a predilection for the diencephalon, brainstem, and posterior fossa structures. Early diagnosis and surgical removal of granulomatous mass lesions, combined with chemotherapy, such as amphotericin B or clotrimazole, provides the best chance of survival. However, the prognosis remains dismal.[1‑3]
Sameer Vyas, Vikash Jain, Manoj Kumar Goyal1, Bishan Dass Radotra2, Niranjan Khandelwal 2
References
a
b
Departments of Radiodiagnosis, 1Neurology, and Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. E‑mail: [email protected]
1. Singh P, Kochhar R, Vashishta RK, Khandelwal N, Prabhakar S, Mohindra S, et al. Amebic meningoencephalitis: Spectrum of imaging findings. AJNR Am J Neuroradiol 2006;27:1217‑21. 2. Reddy R, Vijayasaradhi M, Uppin MS, Challa S, Jabeen A, Borghain R. Acanthamoeba meningoencephalitis in an immunocompetent patient: An autopsy case report. Neuropathology 2011;31:183‑7. 3. Silva RA, Araújo Sde A, Avellar IF, Pittella JE, Oliveira JT, Christo PP. Granulomatous amoebic meningoencephalitis in an immunocompetent patient. Arch Neurol 2010;67:1516‑20. Access this article online Quick Response Code:
c
d
Figure 2: T2 axial (a), T1 axial (b), post contrast T1 axial and coronal (C and D) magnetic resonance images reveal multiple lesions, the largest lesion in the left frontoparietal lobe resembling a mass lesion with interspersed hemorrhages and linear gyriform pattern of enhancement
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121938
Received: 28‑06‑2013 Review completed: 25‑08‑2013 Accepted: 21‑10‑2013
a
b Figure 3: Gross specimen (a) showing bilateral hemorrhagic and necrotic lesions in the frontal lobes. The photomicrograph (b) demonstrating a few trophozoites among neutrophilic infiltrate in the brain parenchyma (hematoxylin and eosin (H and E), original magnification ×40)
intralesional hemorrhage, pseudotumoral lesions, and leptomeningitis has been described. The mass‑like lesion (pseudotumoral pattern) often demonstrates a linear and superficial gyriform pattern of enhancement, which is a useful indicator of the diagnosis. It possibly Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
A case of post varicella cortical venous thrombosis successfully treated with dabigatran Sir, Dabigatran is a novel reversible direct thrombin inhibitor and does not need monitoring.[1] It has been recently approved by the Food and Drug Administration for use in stroke prevention in nonvalvular atrial fibrillation[2,3] and has been proven to be noninferior to warfarin in 531
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Ying Chang, Meng‑Chao Zhang1, Huan‑Huan Wan, Hua Xin2 2
Departments of Neurology, 1Radiology and Thoracic Surgery, China‑Japan Union Hospital, Jilin Univetsity, Changchun, China E‑mail: [email protected]
References 1. Lammouchi T, Zoghlami F, Ben Slamia L, Grira M, Harzallah MS, Benammou S. Epileptic seizures in non‑ketotic hyperglycemia. Neurophysiol Clin 2004;34:183‑7. 2. Qi X, Yan YY, Gao Y, Zheng ZS, Chang Y. Hemichorea associated with non‑ketotic hyperglycaemia: A case report. Diabetes Res Clin Pract 2012;95:e1‑3. 3. Scherer C. Seizures and non‑ketotic hyperglycemia. Presse Med 2005;34:1084‑6. 4. Hennis A, Corbin D, Fraser H. Focal seizures and non‑ketotic hyperglycaemia. J Neurol Neurosurg Psychiatry 1992;55:195‑7. 5. Taieb‑Dogui T, Harzallah MS, Khlifa K, Dogui M, Ben Ammou S, Jallon P. Acute repetitive gyratory seizures as a manifestation of nonketotic hyperglycemia. Neurophysiol Clin 2002;32:254‑7. 6. Siddiqi ZA, VanLandingham KE, Husain AM. Reflex seizures and non‑ketotic hyperglycemia: An unresolved issue. Seizure 2002;11:63‑6. 7. Moien‑Afshari F, Téllez‑Zenteno JF. Occipital seizures induced by hiperglycemia: A case report and review of literature. Seizure 2009;18:382‑5. 8. Schwechter EM, Velísková J, Velísek L. Correlation between extracellular glucose and seizure susceptibility in adult rats. Ann Neurol 2003;53:91‑101. 9. Likhodii SS, Serbanescu I, Cortez MA, Murphy P, Snead OC 3rd, Burnham WM. Anticonvulsant properties of acetone, a brain ketone elevated by the ketogenic diet. Ann Neruol 2003;54:219‑26. 10. Freedman KA, Polepalle S. Transient homonymous hemianopia and positive visual phenomena in nonketotic hyperglycemic patients. Am J Ophthalmol 2004;137:1122‑4. 11. Ozer F, Mutlu A, Ozkayran T. Reflex epilepsy and non‑ketotic hyperglycemia. Epileptic Disord 2003;5:165‑8. 12. Lavin PJ. Hyperglycemic hemianopia: A reversible complication of non‑ketotic hyperglycemia. Neurology 2005;65:616‑9. 13. Kang SS, Keasey MP, Cai J, Hagg T. Loss of neuron‑astroglial interaction rapidly induces protective CNTF expression after stroke in mice. J Neurosci 2012;32:9277‑87. 14. Benjelloun N, Renolleau S, Represa A, Ben‑Ari Y, Charriaut‑Marlangue C. Inflammatory responses in the cerebral cortex after ischemia in the P7 neonatal rat. Stroke 1999;30:1916‑23. 15. Guez A, Obadia M, Lafitte F, Tin SN, Héran F, Gout O. Magnetic resonance spectroscopy findings in a case of hyperglycaemic hemianopia. Rev Neurol (Paris) 2010;166:737‑40. 16. Chu K, Kang DW, Kim DE, Park SH, Roh JK. Diffusion‑weighted and gradient echo magnetic resonance findings of hemichorea‑hemiballismus associated with diabetic hyperglycemia: A hyperviscosity syndrome? Arch Neurol 2002;59:448‑52. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121937
Received: 29‑05‑2013 Review completed: 11‑06‑2013 Accepted: 09‑10‑2013 530
Granulomatous amoebic meningoencephalitis Sir, An 18‑year‑old male presented with progressive left parietal headache evolving into severe holocranial headache associated with vomiting of 27 days duration and gradually progressive right hemiparesis since 5 days. There was no history of fever at the onset of symptoms and he had no immunodeficiency state or on immunosuppression treatment. Neurologic examination revealed altered sensorium, mild right hemiparesis with neck rigidity. Cerebrospinal fluid (CSF) examination revealed glucose of 71 mg/dL, protein of 132 mg/dL, and 20 nucleated cells/dL (all lymphocytes). Results of gram and acid‑fast staining were negative. Brain computed tomography (CT) scan revealed an ill‑defined hypoattenuating lesion in the left frontoparietal lobe and right superior frontal gyrus with linear overlying gyriform enhancement and moderate perilesional edema [Figure 1]. Brain magnetic resonance imaging (MRI) revealed multifocal involvement of bilateral cerebral hemisphere and left cerebellar hemisphere [Figure 2]. The largest lesion in the left frontoparietal lobe resembled a mass lesion with interspersed hemorrhages and showed linear gyriform pattern of enhancement [Figure 1d]. A diagnosis of infective process of the brain and meninges was considered and he was stated on parenteral vancomycin and ceftrixone along with parenteral steroids. Subsequently, the child developed signs of increased intracranial tension and lapsed into unresponsive state and died on day‑10 of admission. A partial autopsy and brain examination revealed granulomatous amoebic meningoencephalitis [Figure 3]. Central nervous system amebiasis is a rare condition that is caused by several free‑living amebic organisms and is broadly divided into granulomatous amebic encephalitis (GAE) and primary amebic meningoencephalitis (PAM).[1] GAE is a subacute to chronic infection caused by Acanthamoeba and also Balamuthia mandrillaris organisms, unlike primary amoebic encephalitis caused by Naegleria fowleri which is acute in onset, rapidly progressive, resulting in fatality within 48–72 h. The incubation period of this disease is not known and is postulated to be more than 10 days.[2] The disease occurs in the 2nd and 4th decades and 10 times more in men. Pathologically, the lesions represent focal areas of cerebritis or microabscesses and leptomeningitis of the overlying cortex. The clinical course for GAE is characterized by a long duration of focal neurologic symptoms. A spectrum of radiological findings in the form of multifocal parenchymal lesions, necrosis, Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
Letters to Editor
a
b
c
d
Figure 1: Noncontrast (a and b) and contrast‑enhanced (c and d) computed tomography axial images shows an ill‑defined hypoattenuating lesion in the left frontoparietal lobe and right superior frontal gyrus with linear overlying gyriform enhancement
represents a combination of enhancement in the inflamed meninges and the underlying cortex. Associated microabscesses are caused by infiltration of brain substance, by amoebae along the pial vessels. The multifocal pattern shows T2 hyperintensities and ring enhancement, with a predilection for the diencephalon, brainstem, and posterior fossa structures. Early diagnosis and surgical removal of granulomatous mass lesions, combined with chemotherapy, such as amphotericin B or clotrimazole, provides the best chance of survival. However, the prognosis remains dismal.[1‑3]
Sameer Vyas, Vikash Jain, Manoj Kumar Goyal1, Bishan Dass Radotra2, Niranjan Khandelwal 2
References
a
b
Departments of Radiodiagnosis, 1Neurology, and Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. E‑mail: [email protected]
1. Singh P, Kochhar R, Vashishta RK, Khandelwal N, Prabhakar S, Mohindra S, et al. Amebic meningoencephalitis: Spectrum of imaging findings. AJNR Am J Neuroradiol 2006;27:1217‑21. 2. Reddy R, Vijayasaradhi M, Uppin MS, Challa S, Jabeen A, Borghain R. Acanthamoeba meningoencephalitis in an immunocompetent patient: An autopsy case report. Neuropathology 2011;31:183‑7. 3. Silva RA, Araújo Sde A, Avellar IF, Pittella JE, Oliveira JT, Christo PP. Granulomatous amoebic meningoencephalitis in an immunocompetent patient. Arch Neurol 2010;67:1516‑20. Access this article online Quick Response Code:
c
d
Figure 2: T2 axial (a), T1 axial (b), post contrast T1 axial and coronal (C and D) magnetic resonance images reveal multiple lesions, the largest lesion in the left frontoparietal lobe resembling a mass lesion with interspersed hemorrhages and linear gyriform pattern of enhancement
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121938
Received: 28‑06‑2013 Review completed: 25‑08‑2013 Accepted: 21‑10‑2013
a
b Figure 3: Gross specimen (a) showing bilateral hemorrhagic and necrotic lesions in the frontal lobes. The photomicrograph (b) demonstrating a few trophozoites among neutrophilic infiltrate in the brain parenchyma (hematoxylin and eosin (H and E), original magnification ×40)
intralesional hemorrhage, pseudotumoral lesions, and leptomeningitis has been described. The mass‑like lesion (pseudotumoral pattern) often demonstrates a linear and superficial gyriform pattern of enhancement, which is a useful indicator of the diagnosis. It possibly Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
A case of post varicella cortical venous thrombosis successfully treated with dabigatran Sir, Dabigatran is a novel reversible direct thrombin inhibitor and does not need monitoring.[1] It has been recently approved by the Food and Drug Administration for use in stroke prevention in nonvalvular atrial fibrillation[2,3] and has been proven to be noninferior to warfarin in 531
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
