Letters to Editor 4.
5.
6. 7. 8. 9.
Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and Center for disease control and prevention. Available from: http://www.who.int/cardiovascular_diseases/resources/atlas/en/ [Last accessed on 2013 Feb 14]. O’Donnell MJ, Xavier D, Liu L, Zhang H, Chin SL, Rao-Melacini P, et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): A case-control study. Lancet 2010;376:112-23. Sridharan SE, Unnikrishnan JP, Sukumaran S, Sylaja PN, Nayak SD, Sarma PS, et al. Incidence, types, risk factors, and outcome of stroke in a developing country: The Trivandrum stroke registry. Stroke 2009;40:1212-8. Hamer M, Batty GD, Stamatakis E, Kivimaki M. Comparison of risk factors for fatal stroke and ischemic heart disease: A prospective follow up of the health survey for England. Atherosclerosis 2011;219:807-10. Brainin M, Teuschl Y, Kalra L. Acute treatment and long-term management of stroke in developing countries. Lancet Neurol 2007;6:553-61. Mendis S. Prevention and care of stroke in low- and middle-income countries: The need for a public health perspective. Int J Stroke 2010;5:86-91. Access this article online Quick Response Code:
Website: www.ruralneuropractice.com
DOI: 10.4103/0976-3147.120194
Bilateral cystic glioblastoma multiforme Sir, Cystic glioblastoma multiforme (GBM) is a rare disease whose exact prevalence is unknown. Glioblastoma is usually seen as a unilateral solid tumor more commonly in the supratentorial compartment. The presence of cyst in the GBM is rare. Bilateral large cystic GBM is still rarer and we report such a case. An 83‑year‑old female was admitted with right hemiparesis and inability to speak for the last 4 days. There was no history of headache or seizures. On examination, there was increased tone on the right side with hemiparesis and aphasia. Magnetic resonance imaging revealed large enhancing cystic lesions measuring 4 × 2.8 × 3 cm and 4.5 × 4 × 3.5 cm in the right and left frontal regions respectively with surrounding edema [Figure 1]. Radiological possibilities suggested were glioma with differential diagnosis of abscess and metastasis. Burr‑hole aspiration revealed hemorrhagic fluid and biopsy of the cyst wall confirmed the diagnosis of GBM. Attendants were explained the prognosis and did not give consent for definitive surgery. Patient died within 5 months of discharge from the hospital.
476
a
b
Figure 1: (a) Axial T‑2 weighted magnetic resonance image showing cystic glioblastoma multiforme in both frontal regions and (b) axial contrast enhanced T‑1 weighted magnetic resonance image showing ring enhancing bifrontal lesions
GBM is the most malignant form of astrocytoma and associated with a poor prognosis. Cysts are commonly found in low‑grade astrocytoma especially pilocytic astrocytoma. Cyst also develops in high grade tumors, but the presence of large cysts in GBM is extremely rare. [1] Cystic GBM may be primary or secondary. Secondary cystic GBM are due to malignant transformation in primary undiagnosed cystic low‑grade gliomas and usually occur in younger patients whereas primary cystic GBM occur de novo. Other hypothesis put forward regarding cyst formation are necrotic degeneration of the tumor tissue, central hemorrhage and subsequent liquefaction, entrapment of adjacent cerebrospinal fluid space and blood brain disruption.[2] A GBM is said to be multifocal when there are multiple lesions and there is an established route of spread or dissemination between these lesions and multicentric if there is no established route of spread between the two lesions.[3,4] Our patient belongs to the multicentric category. GBM have a relatively narrow pericystic rim of the glioma with limited infiltration of the surrounding neuropils indicating that cystic GBM may be less infiltrative than non‑cystic ones. This fact may be responsible for longer survival and lower recurrence, which could not be corroborated in our patient as she was not subjected to definitive surgery. Maldaun et al. reported median survival time after surgery to be 18.7 months in patients with cystic GBM, whereas it was 14.3 months in patients with non‑cystic GBM, but the difference in overall survival was not statistically significant.[5]
Journal of Neurosciences in Rural Practice | October - December 2013 | Vol 4 | Issue 4
Letters to Editor
The management of GBM remains controversial. The lesion should be surgically removed whenever possible and some authors recommend early aggressive surgical removal of easily accessible tumors with a mass effect. Hassaneen et al. advocated multiple craniotomies in the same sitting for multiple GBM without any added mortality or morbidity.[6] Review of literature suggests that most patients die approximately 6‑8 months after the onset of symptoms, although in some studies the outcome was worse ranging from 2.8 to 4.8 months. Sushil Kumar, Amit Handa, Rohan Sinha, Ravi Tiwari Department of Neurosurgery, St. Stephen’s Hospital, Tis Hazari, Delhi, India Address for correspondence: Dr. Amit Handa, Department of Neurosurgery, St. Stephen’s Hospital, Tis Hazari, Delhi ‑ 110 054, India. E‑mail: [email protected]
References Utsuki S, Oka H, Suzuki S, Shimizu S, Tanizaki Y, Kondo K, et al. Pathological and clinical features of cystic and noncystic glioblastomas. Brain Tumor Pathol 2006;23:29‑34. 2. Kleihues P, Ohgaki H. Primary and secondary glioblastomas: From concept to clinical diagnosis. Neuro Oncol 1999;1:44‑51. 3. Batzdorf U, Malamud N. The problem of multicentric gliomas. J Neurosurg 1963;20:122‑36. 4. Cugati G, Jain PK, Pande A, Symss NP, Chakravarthy V, Ramamurthi R. Pediatric multifocal glioblastoma multiforme with fulminant course. J Neurosci Rural Pract 2012;3:174‑7. 5. Maldaun MV, Suki D, Lang FF, Prabhu S, Shi W, Fuller GN, et al. Cystic glioblastoma multiforme: Survival outcomes in 22 cases. J Neurosurg 2004;100:61‑7. 6. Hassaneen W, Levine NB, Suki D, Salaskar AL, de Moura Lima A, McCutcheon IE, et al. Multiple craniotomies in the management of multifocal and multicentric glioblastoma. Clinical article. J Neurosurg 2011;114:576‑84. 1.
Access this article online Quick Response Code:
Website: www.ruralneuropractice.com
DOI: 10.4103/0976-3147.120196
Ethylene glycol toxic encephalopathy Sir, The neurological clinic is the most frequent and early to appear in the Ethylene Glycol (EG) intoxication. It
is characterized by inebriation symptoms very early (from 30 minutes till 12 hours), from lethargy to coma. Seizures can occur and even status epilepticus. Other neurological signs are papiledema, ophtalmoplegia, nystagmus, ataxia, and tetany. In patients who died at this stage are described cerebral swelling, brain hemorrhage, aseptic meningitis, and encephalitis, and crystal formation in central neurological system (CNS).[1] The diagnosis is based on the suspicion of ingestion, the presence of visual disorders, high anion gap metabolic acidosis and an osmolar gap, and elevated levels of creatine kinase (CK). The confirmation is provided by the determination of plasma levels or in gastric juice of EG. We present a case of a 53‑year‑old man, found by his neighbors at home, with low level of consciousness. He was transferred to the Emergency Department who arrived in coma (GCS 3‑4) and hypotensive. Laboratory studies reveled a severe metabolic acidosis (pH of 6.96, pCO2 of 36 mm Hg, HCO3 of 8.1 mmol/L with a base deficit of ‑23’5), plasma osmolarity of 333 mOsm/L, anion gap of 46 mmol/L, lactate of 9.92 mmol/L, creatinine of 9.37 mg/dl, urea of 258 mg/dl, CK of 5940 U/L, thrombocytopenia of 73.000/µL, and leukocytosis of 13.600/µL. Urine analysis of drugs and blood alcohol was negative. A computed tomography (CT) scan was performed at admission, without pathological findings. For the clinical situation of unknown cause of coma, analytical data of severe high anion gap metabolic acidosis, anuric renal failure and rhabdomyolysis, methanol or EG poisoning was suspected; so, ethanol and dialysis treatment was started. We provide 10% ethanol bolus of 1 g/kg/iv for 30 'and then an infusion of 1.5 ml/kg/h for serum levels of 150 mg dl. The metabolic problem was resolved, but the renal failure persisted requiring dialysis, and also the coma status with a maximum GCS of 9 (4‑1‑4). The determination of toxics was held in a blood sample by gas chromatography technique attached to mass spectrometry (GC/MS), confirming the presence of EG. Estimated concentration EG was 285 mg/dl. Six days after admission, a new CT scan was performed, and it showed multiple areas of hypodensity at the basal ganglia (head of caudate nucleus) and in bordering territories [Figure 1]. After a month, the patient didn’t suffer neurological changes, remained comatose. The 80% of the EG absorbed is metabolized mainly in the liver by the enzyme, alcohol dehydrogenase, and the rest is excreted unchanged by kidneys, such as calcium oxalate. The EG metabolites are glycoaldehyde, glycolic acid, glyoxylic acid, oxalic acid, and calcium oxalate. The blocking of conversion of glycolic acid to
Journal of Neurosciences in Rural Practice | October - December 2013 | Vol 4 | Issue 4
477
Copyright of Journal of Neurosciences in Rural Practice 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.
5.
6. 7. 8. 9.
Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and Center for disease control and prevention. Available from: http://www.who.int/cardiovascular_diseases/resources/atlas/en/ [Last accessed on 2013 Feb 14]. O’Donnell MJ, Xavier D, Liu L, Zhang H, Chin SL, Rao-Melacini P, et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): A case-control study. Lancet 2010;376:112-23. Sridharan SE, Unnikrishnan JP, Sukumaran S, Sylaja PN, Nayak SD, Sarma PS, et al. Incidence, types, risk factors, and outcome of stroke in a developing country: The Trivandrum stroke registry. Stroke 2009;40:1212-8. Hamer M, Batty GD, Stamatakis E, Kivimaki M. Comparison of risk factors for fatal stroke and ischemic heart disease: A prospective follow up of the health survey for England. Atherosclerosis 2011;219:807-10. Brainin M, Teuschl Y, Kalra L. Acute treatment and long-term management of stroke in developing countries. Lancet Neurol 2007;6:553-61. Mendis S. Prevention and care of stroke in low- and middle-income countries: The need for a public health perspective. Int J Stroke 2010;5:86-91. Access this article online Quick Response Code:
Website: www.ruralneuropractice.com
DOI: 10.4103/0976-3147.120194
Bilateral cystic glioblastoma multiforme Sir, Cystic glioblastoma multiforme (GBM) is a rare disease whose exact prevalence is unknown. Glioblastoma is usually seen as a unilateral solid tumor more commonly in the supratentorial compartment. The presence of cyst in the GBM is rare. Bilateral large cystic GBM is still rarer and we report such a case. An 83‑year‑old female was admitted with right hemiparesis and inability to speak for the last 4 days. There was no history of headache or seizures. On examination, there was increased tone on the right side with hemiparesis and aphasia. Magnetic resonance imaging revealed large enhancing cystic lesions measuring 4 × 2.8 × 3 cm and 4.5 × 4 × 3.5 cm in the right and left frontal regions respectively with surrounding edema [Figure 1]. Radiological possibilities suggested were glioma with differential diagnosis of abscess and metastasis. Burr‑hole aspiration revealed hemorrhagic fluid and biopsy of the cyst wall confirmed the diagnosis of GBM. Attendants were explained the prognosis and did not give consent for definitive surgery. Patient died within 5 months of discharge from the hospital.
476
a
b
Figure 1: (a) Axial T‑2 weighted magnetic resonance image showing cystic glioblastoma multiforme in both frontal regions and (b) axial contrast enhanced T‑1 weighted magnetic resonance image showing ring enhancing bifrontal lesions
GBM is the most malignant form of astrocytoma and associated with a poor prognosis. Cysts are commonly found in low‑grade astrocytoma especially pilocytic astrocytoma. Cyst also develops in high grade tumors, but the presence of large cysts in GBM is extremely rare. [1] Cystic GBM may be primary or secondary. Secondary cystic GBM are due to malignant transformation in primary undiagnosed cystic low‑grade gliomas and usually occur in younger patients whereas primary cystic GBM occur de novo. Other hypothesis put forward regarding cyst formation are necrotic degeneration of the tumor tissue, central hemorrhage and subsequent liquefaction, entrapment of adjacent cerebrospinal fluid space and blood brain disruption.[2] A GBM is said to be multifocal when there are multiple lesions and there is an established route of spread or dissemination between these lesions and multicentric if there is no established route of spread between the two lesions.[3,4] Our patient belongs to the multicentric category. GBM have a relatively narrow pericystic rim of the glioma with limited infiltration of the surrounding neuropils indicating that cystic GBM may be less infiltrative than non‑cystic ones. This fact may be responsible for longer survival and lower recurrence, which could not be corroborated in our patient as she was not subjected to definitive surgery. Maldaun et al. reported median survival time after surgery to be 18.7 months in patients with cystic GBM, whereas it was 14.3 months in patients with non‑cystic GBM, but the difference in overall survival was not statistically significant.[5]
Journal of Neurosciences in Rural Practice | October - December 2013 | Vol 4 | Issue 4
Letters to Editor
The management of GBM remains controversial. The lesion should be surgically removed whenever possible and some authors recommend early aggressive surgical removal of easily accessible tumors with a mass effect. Hassaneen et al. advocated multiple craniotomies in the same sitting for multiple GBM without any added mortality or morbidity.[6] Review of literature suggests that most patients die approximately 6‑8 months after the onset of symptoms, although in some studies the outcome was worse ranging from 2.8 to 4.8 months. Sushil Kumar, Amit Handa, Rohan Sinha, Ravi Tiwari Department of Neurosurgery, St. Stephen’s Hospital, Tis Hazari, Delhi, India Address for correspondence: Dr. Amit Handa, Department of Neurosurgery, St. Stephen’s Hospital, Tis Hazari, Delhi ‑ 110 054, India. E‑mail: [email protected]
References Utsuki S, Oka H, Suzuki S, Shimizu S, Tanizaki Y, Kondo K, et al. Pathological and clinical features of cystic and noncystic glioblastomas. Brain Tumor Pathol 2006;23:29‑34. 2. Kleihues P, Ohgaki H. Primary and secondary glioblastomas: From concept to clinical diagnosis. Neuro Oncol 1999;1:44‑51. 3. Batzdorf U, Malamud N. The problem of multicentric gliomas. J Neurosurg 1963;20:122‑36. 4. Cugati G, Jain PK, Pande A, Symss NP, Chakravarthy V, Ramamurthi R. Pediatric multifocal glioblastoma multiforme with fulminant course. J Neurosci Rural Pract 2012;3:174‑7. 5. Maldaun MV, Suki D, Lang FF, Prabhu S, Shi W, Fuller GN, et al. Cystic glioblastoma multiforme: Survival outcomes in 22 cases. J Neurosurg 2004;100:61‑7. 6. Hassaneen W, Levine NB, Suki D, Salaskar AL, de Moura Lima A, McCutcheon IE, et al. Multiple craniotomies in the management of multifocal and multicentric glioblastoma. Clinical article. J Neurosurg 2011;114:576‑84. 1.
Access this article online Quick Response Code:
Website: www.ruralneuropractice.com
DOI: 10.4103/0976-3147.120196
Ethylene glycol toxic encephalopathy Sir, The neurological clinic is the most frequent and early to appear in the Ethylene Glycol (EG) intoxication. It
is characterized by inebriation symptoms very early (from 30 minutes till 12 hours), from lethargy to coma. Seizures can occur and even status epilepticus. Other neurological signs are papiledema, ophtalmoplegia, nystagmus, ataxia, and tetany. In patients who died at this stage are described cerebral swelling, brain hemorrhage, aseptic meningitis, and encephalitis, and crystal formation in central neurological system (CNS).[1] The diagnosis is based on the suspicion of ingestion, the presence of visual disorders, high anion gap metabolic acidosis and an osmolar gap, and elevated levels of creatine kinase (CK). The confirmation is provided by the determination of plasma levels or in gastric juice of EG. We present a case of a 53‑year‑old man, found by his neighbors at home, with low level of consciousness. He was transferred to the Emergency Department who arrived in coma (GCS 3‑4) and hypotensive. Laboratory studies reveled a severe metabolic acidosis (pH of 6.96, pCO2 of 36 mm Hg, HCO3 of 8.1 mmol/L with a base deficit of ‑23’5), plasma osmolarity of 333 mOsm/L, anion gap of 46 mmol/L, lactate of 9.92 mmol/L, creatinine of 9.37 mg/dl, urea of 258 mg/dl, CK of 5940 U/L, thrombocytopenia of 73.000/µL, and leukocytosis of 13.600/µL. Urine analysis of drugs and blood alcohol was negative. A computed tomography (CT) scan was performed at admission, without pathological findings. For the clinical situation of unknown cause of coma, analytical data of severe high anion gap metabolic acidosis, anuric renal failure and rhabdomyolysis, methanol or EG poisoning was suspected; so, ethanol and dialysis treatment was started. We provide 10% ethanol bolus of 1 g/kg/iv for 30 'and then an infusion of 1.5 ml/kg/h for serum levels of 150 mg dl. The metabolic problem was resolved, but the renal failure persisted requiring dialysis, and also the coma status with a maximum GCS of 9 (4‑1‑4). The determination of toxics was held in a blood sample by gas chromatography technique attached to mass spectrometry (GC/MS), confirming the presence of EG. Estimated concentration EG was 285 mg/dl. Six days after admission, a new CT scan was performed, and it showed multiple areas of hypodensity at the basal ganglia (head of caudate nucleus) and in bordering territories [Figure 1]. After a month, the patient didn’t suffer neurological changes, remained comatose. The 80% of the EG absorbed is metabolized mainly in the liver by the enzyme, alcohol dehydrogenase, and the rest is excreted unchanged by kidneys, such as calcium oxalate. The EG metabolites are glycoaldehyde, glycolic acid, glyoxylic acid, oxalic acid, and calcium oxalate. The blocking of conversion of glycolic acid to
Journal of Neurosciences in Rural Practice | October - December 2013 | Vol 4 | Issue 4
477
Copyright of Journal of Neurosciences in Rural Practice 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.
