Letters to Editor
Symptoms and signs are largely nonspecific mostly as a result of pressure effect leading to headache, papilledema and hemiparesis. It clinically presents usually as brain abscess, rarely as chronic meningitis, encephalitis, myelitis or significant cerebrospinal fluid eosinophilia and very rarely as an intraventricular mass. [5] CT typically show an irregular variably contrast enhancing mass with surrounding hypodense edema, mimicking high grade gliomas or metastatic lesions in brain.[6] On histopathological examination, they usually have a characteristic appearance of irregularly swollen hyphae with yeast‑like structures. Masson‑Fontana stain for melanin is used to confirm the presence of dematiaceous hyphae. Prognosis is very poor without treatment. There is no standard therapy for these often fatal infections, and few studies reported that a combination of amphotericin B, 5‑fluorouracil and itraconazole was associated with improved survival.[7]
Shantha Ravisankar, R. Vimal Chander1 Department of Pathology, Institute of Neurology, Madras Medical College, 1Department of Pathology, Saveetha Medical College, Thandalam, Chennai, Tamil Nadu, India E‑mail: [email protected]
References 1. 2. 3.
4. 5. 6. 7.
Kumar KK, Hallikeri K. Phaeohyphomycosis. Indian J Pathol Microbiol 2008;51:556‑8. Revankar SG, Sutton DA, Rinaldi MG. Primary central nervous system phaeohyphomycosis: A review of 101 cases. Clin Infect Dis 2004;38:206‑16. Sutton DA, Slifkin M, Yakulis R, Rinaldi MG. U.S. case report of cerebral phaeohyphomycosis caused by Ramichloridium obovoideum (R. mackenziei): Criteria for identification, therapy, and review of other known dematiaceous neurotropic taxa. J Clin Microbiol 1998;36:708‑15. Revankar SG, Patterson JE, Sutton DA, Pullen R, Rinaldi MG. Disseminated phaeohyphomycosis: Review of an emerging mycosis. Clin Infect Dis 2002;34:467‑76. Sujit Kumar GS, Dugar M, Chacko G. Cerebral phaeohyphomycosis presenting as an intraventricular mass. Neurol India 2006;54:102‑3. Hauck EF, McGinnis M, Nauta HJ. Cerebral phaeohyphomycosis mimics high‑grade astrocytoma. J Clin Neurosci 2008;15:1061‑6. Sharkey PK, Graybill JR, Rinaldi MG, Stevens DA, Tucker RM, Peterie JD, et al. Itraconazole treatment of phaeohyphomycosis. J Am Acad Dermatol 1990;23:577‑86.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121936
Received: 18‑05‑2013 Review completed: 29‑07‑2013 Accepted: 20‑10‑2013 528
Magnetic resonance imaging features in seizures associated with nonketotic hyperglycemia Sir, A 57‑year‑old female was admitted for episodic clonic jerks affecting her right face and arm, each episode lasting for approximately 2′ of 10 days duration. There was no improvement of jerks with carbamazepine, instead there was increase in the frequency (every 5′) and also developed right upper limb weakness. Past medical history was negative. Neurological examination revealed right hemiparesia. Admission serum glucose was 29.8 mmol/L with no ketone bodies in the urine; serum sodium was 133.8 mmol/L and potassium was 3.5 mmol/L; blood urea nitrogen was 6.0 mmol/L and calculated serum osmolality was 310.4 mmol/L. Admission computed tomography was normal. Electroencephalography (EEG) revealed inter‑ictal epileptiform discharges around the left central sulcus [Figure 1a‑c]. Brain magnetic resonance imaging (MRI) [Figure 2] done on day 2 of admission showed subcortical hypointensity signal changes in the left parietal region on T2-weighted (T2‑W), fluid attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI). Apparent diffusion coefficient (ADC) map showed isointensity in the corresponding region. Overlying cortical showed hyperintensity on FLAIR, DWI sequences and hypointensity on ADC map. The ADC values in cortical and subcortical lesions were lower than contralateral normal regions, especially in cortical lesions. T1‑W sequences were normal. She was diagnosed as epileptia partialis continua (EPC) associated with nonketotic hyperglycemia (NKH). Carbamazepine was stopped and intravenous insulin therapy was started. She had good glycemic control and the jerking remitted completely within 72 h. Follow up MRI at 5 months showed complete resolution of cortical hyperintensity and subcortical hypointensity. Epileptic seizures are common in hyperglycemia and are often presenting features, particularly in NKH with blood glucose levels more than 20 mmol/L. [1‑3] NKH‑related seizures are mostly focal motor, sometimes it can be EPC. In this patient, hyperglycemia was de novo. In patients presenting with EPC, NKH should be considered and ruled out. Seizures associated with NKH are resistant to antiepileptic drugs and remit with correction of hyperglycemic state. [4] The precise pathgenesis of EPC in patients with NKH Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
Letters to Editor
Figure 1: Ictal electroencephalography showing the presence of fast activity over the left central and parietal region with a frequency between 15 and 16 Hz, occasionally spreading to the left hemisphere with more theta waves
Figure 2: The brain MRI at day 2 of admission showed subcortical hypointensity signal changes in the left parietal region on T2‑W, FLAIR and DWI. ADC map showed isointensity in the corresponding region. Overlying cortical hyperintensity on FLAIR, DWI sequences and cortical hypointensity on ADC map were observed simultaneously. The ADC values in cortical and subcortical lesions were lower than contralateral normal regions, especially in cortical lesions (ADC value: The right parietal lobe: 708.1 mm2/s; the left parietal cortex: 336 mm2/s; the left parietal white matter: 369.9 mm2/s)
is not yet clear. The proposed mechanisms include: Hyperglycemia induce vascular lesions;[5,6] a decrease in brain gamma aminobutyric acid (GABA) level leading to a decrease in the seizure threshold.[7,8] Intracellular acidosis may elevate GABA levels and lack of ketosis may be a trigger factor to induce seizures.[9] Conventional computed tomography and MRI in patients with NKH and seizures are largely unremarkable. [10,11] Recent reports have described transient, but typical changes with subcortical h y p o i n t e n s i t y o n T 2 a n d F L A I R i m a g e s . [12,13] Similar were the MRI findings in our patient. The exact mechanism for these transient subcortical hypointensity remains unclear. One possible Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
mechanism could be subcortical free radical accumulation as a result of excitotoxic axonal d a m a g e d u r i n g s e i z u r e s . [14] B u t w e s u g g e s t that hyperosmolar state in NKH may lead to these secondary pathological changes. DWI hyperintensity changes and low ADC values showed restricted diffusion in left parietal cortical region, which suggested “cytotoxic edema” induced by hyperosmolality. Hyperosmolality may also lead to dehydration of white matter. The existence of hyperosmolality was proved by magnetic resonance spectroscopy studies. [15] While hyperviscosity and the decline in carrying oxygen capacity of red blood cells caused hyperglycemia may be responsible for cortical cytotoxic edema. [16] 529
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
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.
Symptoms and signs are largely nonspecific mostly as a result of pressure effect leading to headache, papilledema and hemiparesis. It clinically presents usually as brain abscess, rarely as chronic meningitis, encephalitis, myelitis or significant cerebrospinal fluid eosinophilia and very rarely as an intraventricular mass. [5] CT typically show an irregular variably contrast enhancing mass with surrounding hypodense edema, mimicking high grade gliomas or metastatic lesions in brain.[6] On histopathological examination, they usually have a characteristic appearance of irregularly swollen hyphae with yeast‑like structures. Masson‑Fontana stain for melanin is used to confirm the presence of dematiaceous hyphae. Prognosis is very poor without treatment. There is no standard therapy for these often fatal infections, and few studies reported that a combination of amphotericin B, 5‑fluorouracil and itraconazole was associated with improved survival.[7]
Shantha Ravisankar, R. Vimal Chander1 Department of Pathology, Institute of Neurology, Madras Medical College, 1Department of Pathology, Saveetha Medical College, Thandalam, Chennai, Tamil Nadu, India E‑mail: [email protected]
References 1. 2. 3.
4. 5. 6. 7.
Kumar KK, Hallikeri K. Phaeohyphomycosis. Indian J Pathol Microbiol 2008;51:556‑8. Revankar SG, Sutton DA, Rinaldi MG. Primary central nervous system phaeohyphomycosis: A review of 101 cases. Clin Infect Dis 2004;38:206‑16. Sutton DA, Slifkin M, Yakulis R, Rinaldi MG. U.S. case report of cerebral phaeohyphomycosis caused by Ramichloridium obovoideum (R. mackenziei): Criteria for identification, therapy, and review of other known dematiaceous neurotropic taxa. J Clin Microbiol 1998;36:708‑15. Revankar SG, Patterson JE, Sutton DA, Pullen R, Rinaldi MG. Disseminated phaeohyphomycosis: Review of an emerging mycosis. Clin Infect Dis 2002;34:467‑76. Sujit Kumar GS, Dugar M, Chacko G. Cerebral phaeohyphomycosis presenting as an intraventricular mass. Neurol India 2006;54:102‑3. Hauck EF, McGinnis M, Nauta HJ. Cerebral phaeohyphomycosis mimics high‑grade astrocytoma. J Clin Neurosci 2008;15:1061‑6. Sharkey PK, Graybill JR, Rinaldi MG, Stevens DA, Tucker RM, Peterie JD, et al. Itraconazole treatment of phaeohyphomycosis. J Am Acad Dermatol 1990;23:577‑86.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121936
Received: 18‑05‑2013 Review completed: 29‑07‑2013 Accepted: 20‑10‑2013 528
Magnetic resonance imaging features in seizures associated with nonketotic hyperglycemia Sir, A 57‑year‑old female was admitted for episodic clonic jerks affecting her right face and arm, each episode lasting for approximately 2′ of 10 days duration. There was no improvement of jerks with carbamazepine, instead there was increase in the frequency (every 5′) and also developed right upper limb weakness. Past medical history was negative. Neurological examination revealed right hemiparesia. Admission serum glucose was 29.8 mmol/L with no ketone bodies in the urine; serum sodium was 133.8 mmol/L and potassium was 3.5 mmol/L; blood urea nitrogen was 6.0 mmol/L and calculated serum osmolality was 310.4 mmol/L. Admission computed tomography was normal. Electroencephalography (EEG) revealed inter‑ictal epileptiform discharges around the left central sulcus [Figure 1a‑c]. Brain magnetic resonance imaging (MRI) [Figure 2] done on day 2 of admission showed subcortical hypointensity signal changes in the left parietal region on T2-weighted (T2‑W), fluid attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI). Apparent diffusion coefficient (ADC) map showed isointensity in the corresponding region. Overlying cortical showed hyperintensity on FLAIR, DWI sequences and hypointensity on ADC map. The ADC values in cortical and subcortical lesions were lower than contralateral normal regions, especially in cortical lesions. T1‑W sequences were normal. She was diagnosed as epileptia partialis continua (EPC) associated with nonketotic hyperglycemia (NKH). Carbamazepine was stopped and intravenous insulin therapy was started. She had good glycemic control and the jerking remitted completely within 72 h. Follow up MRI at 5 months showed complete resolution of cortical hyperintensity and subcortical hypointensity. Epileptic seizures are common in hyperglycemia and are often presenting features, particularly in NKH with blood glucose levels more than 20 mmol/L. [1‑3] NKH‑related seizures are mostly focal motor, sometimes it can be EPC. In this patient, hyperglycemia was de novo. In patients presenting with EPC, NKH should be considered and ruled out. Seizures associated with NKH are resistant to antiepileptic drugs and remit with correction of hyperglycemic state. [4] The precise pathgenesis of EPC in patients with NKH Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
Letters to Editor
Figure 1: Ictal electroencephalography showing the presence of fast activity over the left central and parietal region with a frequency between 15 and 16 Hz, occasionally spreading to the left hemisphere with more theta waves
Figure 2: The brain MRI at day 2 of admission showed subcortical hypointensity signal changes in the left parietal region on T2‑W, FLAIR and DWI. ADC map showed isointensity in the corresponding region. Overlying cortical hyperintensity on FLAIR, DWI sequences and cortical hypointensity on ADC map were observed simultaneously. The ADC values in cortical and subcortical lesions were lower than contralateral normal regions, especially in cortical lesions (ADC value: The right parietal lobe: 708.1 mm2/s; the left parietal cortex: 336 mm2/s; the left parietal white matter: 369.9 mm2/s)
is not yet clear. The proposed mechanisms include: Hyperglycemia induce vascular lesions;[5,6] a decrease in brain gamma aminobutyric acid (GABA) level leading to a decrease in the seizure threshold.[7,8] Intracellular acidosis may elevate GABA levels and lack of ketosis may be a trigger factor to induce seizures.[9] Conventional computed tomography and MRI in patients with NKH and seizures are largely unremarkable. [10,11] Recent reports have described transient, but typical changes with subcortical h y p o i n t e n s i t y o n T 2 a n d F L A I R i m a g e s . [12,13] Similar were the MRI findings in our patient. The exact mechanism for these transient subcortical hypointensity remains unclear. One possible Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5
mechanism could be subcortical free radical accumulation as a result of excitotoxic axonal d a m a g e d u r i n g s e i z u r e s . [14] B u t w e s u g g e s t that hyperosmolar state in NKH may lead to these secondary pathological changes. DWI hyperintensity changes and low ADC values showed restricted diffusion in left parietal cortical region, which suggested “cytotoxic edema” induced by hyperosmolality. Hyperosmolality may also lead to dehydration of white matter. The existence of hyperosmolality was proved by magnetic resonance spectroscopy studies. [15] While hyperviscosity and the decline in carrying oxygen capacity of red blood cells caused hyperglycemia may be responsible for cortical cytotoxic edema. [16] 529
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
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.
