[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application fo this journal Letters to Editor
To our best of our knowledge, this is the first case of copper deficiency presenting with electrophysiological findings typical for an acquired demyelinating polyneuropathy. This patient represents the importance of work‑up for copper deficiency in patients with history of gastric surgery and acquired demyelinating neuropathy.
Geysu Karlikaya, Dilaver Kaya Department of Neurology, Acibadem University School of Medicine, Istanbul, Turkey E-mail: [email protected]
References 1.
Figure 2: Left median nerve F wave study displaying, min F latency 58 ms
and his nerve conduction studies showed improved distal latencies and conduction velocities. Acquired copper deficiency is quite rare since a normal diet has a daily amount of 1-5 mg copper and is usually sufficient to meet the daily requirement of 0.9 mg/ day.[1,2] Gastric pH is necessary to free copper from ingested food, and then it is absorbed primarily in the duodenum, stomach, and ileum. Therefore, the most common cause of copper deficiency is malabsorbtion, most commonly related to a history of gastric surgery; up to 10-15% have been reported following bariatric surgery. Other rare causes are malabsorbtion syndromes such as celiac disease, prolonged total parenteral nutrition, and excessive zinc ingestion.[2,6] Copper deficiency has been reported to be a relatively late complication of gastric surgery and has even been reported 23 years after a total gastrectomy.[7‑9] In our patient, the symptoms developed after 5 years. Our case demonstrates the importance of recommending not only vitamin B12 and thiamine but also copper to patients following surgery and obtaining periodical blood works. Kumar studied 13 patients with acquired copper deficiency; he reported that only 3 out of 10 patients with a positive Babinski’s sign had increased T2 signal on the spinal cord MRI.[10] Two years later he described 25 patients with copper deficiency myelopathy and neuroimaging was positive in only 11/25 patients.[6] In our patient, the neurological signs were suggestive of a myelopathy. Although there were no signal changes in his spinal cord MRI studies, examination of the upper motor neuron findings (brisk tendon reflexes and clonus) suggests spinal cord involvement. The neuropathy related to copper deficiency was previously described as an axonal type polyneuropathy, as it was in the study by Kumar et al. An axonal peripheral neuropathy was found in 21 out of 24 patients diagnosed with copper deficiency myelopathy.[6] Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
Lazarchick J. Update on anemia and neurtopenia in copper deficiency. Curr Opin Hematol 2012;19:58‑60. 2. Miller NG. Copper deficiency after bariatric surgery. Clin Nutr Insight 2013;39:1‑4. 3. Schleper B, Stuerenburg HJ. Copper deficiency associated myelopathy in a 46 year old women. J Neurol 2001;248:705‑6. 4. Reyes CV. Polyneuropathy and pancytopenia secondary to copper deficiency. Fed Pract 2011;28:23‑6. 5. Tormoehlen LM, Kumar N. Neurotoxicology five new things. Neurol Clin Pract 2012;2:301‑8. 6. Kumar N. Copper deficiency myelopathy (human swayback). Mayo Clin Proc 2006;81:1371‑84. 7. Rudnicki SA. Prevention and treatment of peripheral neuropathy after bariatric surgery. Curr Treat Options Neurol 2010;12:29‑36. 8. Inaba M, Torii T, Shinoda K, Yamasaki R, Ohyagi Y, Kira J. Peripheral neuropathy, myelopathy, cerebellar ataxia, and subclinical optic neuropathy associated with copper deficiency occuring 23 years after total gastrectomy. Rinsho Shinkeigaku 2011;51:412‑6. 9. Wu J, Ricker M, Muench J. Copper deficiency as cause of unexplained hematolologic and neurologic deficits in patient with prior gastrointestinal surgery. J Am Board Fam Med 2006;19:191‑4. 10. Kumar N, Gross JB Jr, Ahlskog JE. Copper deficiency myelopathy produces a clinical picture like subacute combined degeneration. Neurology 2004;63:33‑9. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141219
Received: 25-06-2014 Review completed: 11-07-2014 Accepted: 10-08-2014
Brainstem hemorrhage secondary to evacuation of chronic subdural hematoma Sir, Although surgery on chronic subdural hematomas (CSDH) usually has a rewarding outcome, it is not exempted from complications. We report an extremely rare case where 429
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application fo this journal Letters to Editor
there was remote brainstem hemorrhage following drainage of subdural hematoma. A 58‑year‑old man was admitted to our hospital with history of severe headache and vomiting of 4‑days duration. He was on low‑dose aspirin and clopidogrel for coronary heart disease and a known patient of hypertension and diabetes. There had been no prior head trauma. Preoperative coagulation parameters (prothrombin time, partial thromboplastin time, anti‑thrombin III, bleeding time, platelet count) were within normal limits. Magnetic resonance imaging showed bilateral chronic subdural hematoma (CSDH) [Figure 1]. Surgery was performed under local anesthesia with patient in supine position. One each frontal burr hole were drilled. Hematoma was thin, liquefied, and xanthochromic. The hematoma was evacuated slowly and the region was gently irrigated until clear fluid returned. Approximately 150 ml of blood clot was evacuated from each side. There was no active bleeding point. The procedure was uneventful and during the entire procedure patient said that the headache had improved. However, as he was being wheeled out of operation theater, he complained of severe headache and slurred speech. Within few minutes, he lapsed into unconsciousness. The blood pressure at this time was 270/140 mm of mercury. An emergent computed tomography (CT) scan showed bilateral frontoparietal convexity acute subdural hemorrhage. The patient was rushed to the operation theater and mini‑craniotomies were done around the region of previous burr‑hole and large subdural clots were evacuated from both sides. The time for the burr‑holes and subsequent craniotomies and the time for CT scan were about 3 hours. Following the craniotomy, the patient improved transiently and moved limbs, but remained unconscious. He was electively ventilated. At 3 hours post‑operation, he was deeply comatosed with dilated pupils. A repeat CT scan showed large amount of
Figure 1: T2-weighted axial MRI of the brain showing bilateral chronic subdural hematoma with effacement and mass effect
430
air in the subdural spaces and evidence of brainstem and fourth ventricle hemorrhage [Figure 2]. He continued to be unconscious and subsequently succumbed. CSDHs are common neurosurgical problems and treatment includes evacuation of the hematoma by burr‑hole drainage. [1-4] The results of surgery are gratifying and recurrence of subdural hematoma is low. Postoperative complications though rare, include re‑accumulation, re‑hemorrhage, cerebral edema, infection, seizures, and intracerebral hemorrhage (ICH). ICH is a well‑known complication of supratentorial neurosurgery.[5] However, ICH following evacuation of a subdural hematoma is a rare clinical event. ICH following evacuation of the subdural hematoma may be on the same side of evacuation or on the contralateral side,[6,7] infratentorial,[8‑11] and extremely rarely cerebellar or intraaxial brain stem.[4,12‑14] Our literature search showed reports of only four cases of brainstem hemorrhage after evacuation of CSDH. In all cases, the subdural hematoma was on both sides. Two cases of brainstem hemorrhage were detected at autopsy;[4,13] one patient died during the hospital stay[14] and the fourth patient gradually improved.[12] In general, brainstem hematoma following drainage of subdural hematoma has a high mortality [Table 1]. The site and size of the hematoma that resulted in death has not been clearly specified in the reported cases. The pathogenesis of postoperative hemorrhage after evacuation of CSDH is not clear and can only be speculated. [6‑11,15] Rapid evacuation of hematoma, increase in cerebral blood flow, alteration in vascular autoregulation, damage of small fragile vessel secondary to increased intracranial pressure or damage directly to a vessel following transtentorial herniation may be the possible mechanisms. Altered
Figure 2: Axial plain CT image showing evacuation of bilateral subdural hematoma with air in the cavity. Also seen is hemorrhage in the brainstem and the fourth ventricle
Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application f this journal Letters to Editor
Table 1: Cases reported with brain stem hemorrhage after drainage CSDH
N/Ref 1[13] 2[4] 3[12] 4[14] Our case
Age/Sex Symptoms Diagnosis ND 59/ND 73/M 77/M 58/M
ND Coma Stuporous Coma Severe Headache
ND Bilateral CSDH Bilateral CSDH Bilateral CSDH Bilateral CSDH
Past history Surgery
IVH Treatment brain stem Outcome
ND ND No HT HT DM
ND ND No Yes Yes
Burr hole Burr hole One burr hole on each side Mini Craniotomy on each side One burr hole on each side
Conservative Conservative Conservative Conservative Conservative
Died Died Improved Died Died
N - Number, Ref - Reference, IVH - Intraventricle hemorrhage, M - Male, F - Female, ND - Not described, CSDH - Chronic subdural hematoma, HT - Hypertension, DM - Diabetes mellitus
coagulation parameters and a massive air reflux into the cranial cavity through the drainage hole may pose additional risk. Other mechanism, though less possible, is a traumatic small contusion not detected in CT scan or MRI In all cases it may be mandatory to rule out secondary pathology like arteriovenous malformation, cavernous malformation and neoplasm. Rapid drainage of CSDH increases mobility of the intracranial structures and can lead to remote site hemorrhage. Associated high blood pressure could be an initiating factor. A hypertensive crisis with or without raised intracranial pressure may cause a direct brain stem hematoma unrelated to surgical manipulation. Another unlikely but posible cause of remote site hemorrhagic infarction could be a phenomenon simulating deep venous thrombosis. Okuchi et al.[15] reported a patient with oculomotor nerve paresis and brain stem symptoms following evacuation of bilateral CSDH and speculated that the complication is probably related to rapid decompression. Stefini et al.[5] reported a patient with ruptured intracranial aneurysm after evacuation with craniotomy of left CSDH. Aneurysmal rupture was probably caused by the alterations in the intracranial pressure dynamics following the evacuation of the clot. In our patient, although there were no significant hematological abnormalities, long‑term use low‑dose aspirin and clopidogrel could have altered the coagulation profile that might have led to hemorrhage. The other possible causes include increase in cerebral blood flow, alteration in autoregulation, possible damaged vessel, and supratentorial decompression.
Luis Mariano Rojas‑Medina, Atul Goel Department of Neurosurgery, King Edward Memorial Hospital and Seth Gordhandas Sunderdas Medical College, Parel, Mumbai, Maharashtra, India E‑mail: [email protected]
References 1. Kotwica Z, Brzezinski J. Chronic subdural haematoma treated by by burr holes and closed system drainage: Personal experience in 131 patients. Br J Neurosurg 1991;5:461‑5. Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
2. 3. 4. 5.
6. 7. 8. 9. 10. 11.
12. 13. 14.
15.
Richter HP, Klein HJ, Schafer M. Chronic subdural haematoma treated by enlarge burr hole craniotomy and closed system drainage. Retrospective study of 120 patients. Acta Neurochir (Wien) 1984;71:179‑88. Sambasivan M. An overview of chronic subdural hematoma: Experience with 2300 cases. Surg Neurol 1997;47:418‑22. Robinson RG. Chronic subdural hematoma: Surgical management in 133 patients. J Neurosurg 1984;61:263‑8. Stefini R, Ghitti F, Bergomi R, Catenacci E, Latronico N, Mortini P. Uncommon presentation of ruptured intracranial aneurysm during surgical evacuation of chronic subdural hematoma: Case report. Surg Neurol 2008;69:89‑92. Cohen‑Gadol AA. Remote contralateral intraparenchymal hemorrhage after overdrainage of a chronic subdural hematoma. Int J Surg Case Rep 2013;4:834‑6. Kim JK, Kim SW, Kim SH. Intracerebral hemorrhage following evacuation of a chronic subdural hematoma. J Korean Neurosurg Soc 2013;53:108‑11. Chang SH, Yang SH, Son BC, Lee SW. Cerebellar hemorrhage after burr hole drainage of supratentorial chronic subdural hematoma. J Korean Neurosurg Soc 2009;46:592‑5. Kollatos C, Konstantinou D, Raftopoulos S, Klironomos G, Messinis L, Zampakis P, et al. Cerebellar hemorrhage after supratentorial burr hole drainage of a chronic subdural hematoma. Hippokratia 2011;15:370‑2. Ulivieri S, Oliveri G. Intracerebral haemorrhage following surgical evacuation of chronic subdural haematoma: Case report. G Chir 2008;29:233‑4. Vega Basulto S, Mosqueda Betancourt G, Gutiérrez Muñoz F, Vega Trenado A, Rivero García C. Postoperative intracerebral hematoma. An unusual complication of chronic subdural hematoma. Rev Neurol 2004;38:497‑8. Park KJ, Kang SH, Lee HK, Chung YG. Brain stem hemorrhage following burr hole drainage for chronic subdural hematoma‑case report. Neurol Med Chir (Tokyo) 2009;49:594‑7. McKissock W. Subdural haematoma. A review of 389 cases. Lancet 1960;1:1365‑9. Alcalá‑Cerra G, Gutiérrez‑Paternina JJ, Niño‑Hernández LM, Polo‑Torres C, Romero‑Ramírez H, Sabogal‑Barrios R. Intracerebral hemorrhages following drainage of chronic subdural hematomas. Rev Med Inst Mex Seguro Soc 2011;49:547‑50. Okuchi K, Fujioka M, Maeda Y, Kagoshima T, Sakaki T. Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis an brain stem symptoms after operation. Neurol Med Chir (Tokyo) 1999;39:367‑71.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141222
Received: 26‑04‑2014 Review completed: 12‑05‑2014 Accepted: 29‑06‑2014 431
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.
To our best of our knowledge, this is the first case of copper deficiency presenting with electrophysiological findings typical for an acquired demyelinating polyneuropathy. This patient represents the importance of work‑up for copper deficiency in patients with history of gastric surgery and acquired demyelinating neuropathy.
Geysu Karlikaya, Dilaver Kaya Department of Neurology, Acibadem University School of Medicine, Istanbul, Turkey E-mail: [email protected]
References 1.
Figure 2: Left median nerve F wave study displaying, min F latency 58 ms
and his nerve conduction studies showed improved distal latencies and conduction velocities. Acquired copper deficiency is quite rare since a normal diet has a daily amount of 1-5 mg copper and is usually sufficient to meet the daily requirement of 0.9 mg/ day.[1,2] Gastric pH is necessary to free copper from ingested food, and then it is absorbed primarily in the duodenum, stomach, and ileum. Therefore, the most common cause of copper deficiency is malabsorbtion, most commonly related to a history of gastric surgery; up to 10-15% have been reported following bariatric surgery. Other rare causes are malabsorbtion syndromes such as celiac disease, prolonged total parenteral nutrition, and excessive zinc ingestion.[2,6] Copper deficiency has been reported to be a relatively late complication of gastric surgery and has even been reported 23 years after a total gastrectomy.[7‑9] In our patient, the symptoms developed after 5 years. Our case demonstrates the importance of recommending not only vitamin B12 and thiamine but also copper to patients following surgery and obtaining periodical blood works. Kumar studied 13 patients with acquired copper deficiency; he reported that only 3 out of 10 patients with a positive Babinski’s sign had increased T2 signal on the spinal cord MRI.[10] Two years later he described 25 patients with copper deficiency myelopathy and neuroimaging was positive in only 11/25 patients.[6] In our patient, the neurological signs were suggestive of a myelopathy. Although there were no signal changes in his spinal cord MRI studies, examination of the upper motor neuron findings (brisk tendon reflexes and clonus) suggests spinal cord involvement. The neuropathy related to copper deficiency was previously described as an axonal type polyneuropathy, as it was in the study by Kumar et al. An axonal peripheral neuropathy was found in 21 out of 24 patients diagnosed with copper deficiency myelopathy.[6] Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
Lazarchick J. Update on anemia and neurtopenia in copper deficiency. Curr Opin Hematol 2012;19:58‑60. 2. Miller NG. Copper deficiency after bariatric surgery. Clin Nutr Insight 2013;39:1‑4. 3. Schleper B, Stuerenburg HJ. Copper deficiency associated myelopathy in a 46 year old women. J Neurol 2001;248:705‑6. 4. Reyes CV. Polyneuropathy and pancytopenia secondary to copper deficiency. Fed Pract 2011;28:23‑6. 5. Tormoehlen LM, Kumar N. Neurotoxicology five new things. Neurol Clin Pract 2012;2:301‑8. 6. Kumar N. Copper deficiency myelopathy (human swayback). Mayo Clin Proc 2006;81:1371‑84. 7. Rudnicki SA. Prevention and treatment of peripheral neuropathy after bariatric surgery. Curr Treat Options Neurol 2010;12:29‑36. 8. Inaba M, Torii T, Shinoda K, Yamasaki R, Ohyagi Y, Kira J. Peripheral neuropathy, myelopathy, cerebellar ataxia, and subclinical optic neuropathy associated with copper deficiency occuring 23 years after total gastrectomy. Rinsho Shinkeigaku 2011;51:412‑6. 9. Wu J, Ricker M, Muench J. Copper deficiency as cause of unexplained hematolologic and neurologic deficits in patient with prior gastrointestinal surgery. J Am Board Fam Med 2006;19:191‑4. 10. Kumar N, Gross JB Jr, Ahlskog JE. Copper deficiency myelopathy produces a clinical picture like subacute combined degeneration. Neurology 2004;63:33‑9. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141219
Received: 25-06-2014 Review completed: 11-07-2014 Accepted: 10-08-2014
Brainstem hemorrhage secondary to evacuation of chronic subdural hematoma Sir, Although surgery on chronic subdural hematomas (CSDH) usually has a rewarding outcome, it is not exempted from complications. We report an extremely rare case where 429
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application fo this journal Letters to Editor
there was remote brainstem hemorrhage following drainage of subdural hematoma. A 58‑year‑old man was admitted to our hospital with history of severe headache and vomiting of 4‑days duration. He was on low‑dose aspirin and clopidogrel for coronary heart disease and a known patient of hypertension and diabetes. There had been no prior head trauma. Preoperative coagulation parameters (prothrombin time, partial thromboplastin time, anti‑thrombin III, bleeding time, platelet count) were within normal limits. Magnetic resonance imaging showed bilateral chronic subdural hematoma (CSDH) [Figure 1]. Surgery was performed under local anesthesia with patient in supine position. One each frontal burr hole were drilled. Hematoma was thin, liquefied, and xanthochromic. The hematoma was evacuated slowly and the region was gently irrigated until clear fluid returned. Approximately 150 ml of blood clot was evacuated from each side. There was no active bleeding point. The procedure was uneventful and during the entire procedure patient said that the headache had improved. However, as he was being wheeled out of operation theater, he complained of severe headache and slurred speech. Within few minutes, he lapsed into unconsciousness. The blood pressure at this time was 270/140 mm of mercury. An emergent computed tomography (CT) scan showed bilateral frontoparietal convexity acute subdural hemorrhage. The patient was rushed to the operation theater and mini‑craniotomies were done around the region of previous burr‑hole and large subdural clots were evacuated from both sides. The time for the burr‑holes and subsequent craniotomies and the time for CT scan were about 3 hours. Following the craniotomy, the patient improved transiently and moved limbs, but remained unconscious. He was electively ventilated. At 3 hours post‑operation, he was deeply comatosed with dilated pupils. A repeat CT scan showed large amount of
Figure 1: T2-weighted axial MRI of the brain showing bilateral chronic subdural hematoma with effacement and mass effect
430
air in the subdural spaces and evidence of brainstem and fourth ventricle hemorrhage [Figure 2]. He continued to be unconscious and subsequently succumbed. CSDHs are common neurosurgical problems and treatment includes evacuation of the hematoma by burr‑hole drainage. [1-4] The results of surgery are gratifying and recurrence of subdural hematoma is low. Postoperative complications though rare, include re‑accumulation, re‑hemorrhage, cerebral edema, infection, seizures, and intracerebral hemorrhage (ICH). ICH is a well‑known complication of supratentorial neurosurgery.[5] However, ICH following evacuation of a subdural hematoma is a rare clinical event. ICH following evacuation of the subdural hematoma may be on the same side of evacuation or on the contralateral side,[6,7] infratentorial,[8‑11] and extremely rarely cerebellar or intraaxial brain stem.[4,12‑14] Our literature search showed reports of only four cases of brainstem hemorrhage after evacuation of CSDH. In all cases, the subdural hematoma was on both sides. Two cases of brainstem hemorrhage were detected at autopsy;[4,13] one patient died during the hospital stay[14] and the fourth patient gradually improved.[12] In general, brainstem hematoma following drainage of subdural hematoma has a high mortality [Table 1]. The site and size of the hematoma that resulted in death has not been clearly specified in the reported cases. The pathogenesis of postoperative hemorrhage after evacuation of CSDH is not clear and can only be speculated. [6‑11,15] Rapid evacuation of hematoma, increase in cerebral blood flow, alteration in vascular autoregulation, damage of small fragile vessel secondary to increased intracranial pressure or damage directly to a vessel following transtentorial herniation may be the possible mechanisms. Altered
Figure 2: Axial plain CT image showing evacuation of bilateral subdural hematoma with air in the cavity. Also seen is hemorrhage in the brainstem and the fourth ventricle
Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
[Downloaded free from http://www.neurologyindia.com on Thursday, September 25, 2014, IP: 202.177.173.189] || Click here to download free Android application f this journal Letters to Editor
Table 1: Cases reported with brain stem hemorrhage after drainage CSDH
N/Ref 1[13] 2[4] 3[12] 4[14] Our case
Age/Sex Symptoms Diagnosis ND 59/ND 73/M 77/M 58/M
ND Coma Stuporous Coma Severe Headache
ND Bilateral CSDH Bilateral CSDH Bilateral CSDH Bilateral CSDH
Past history Surgery
IVH Treatment brain stem Outcome
ND ND No HT HT DM
ND ND No Yes Yes
Burr hole Burr hole One burr hole on each side Mini Craniotomy on each side One burr hole on each side
Conservative Conservative Conservative Conservative Conservative
Died Died Improved Died Died
N - Number, Ref - Reference, IVH - Intraventricle hemorrhage, M - Male, F - Female, ND - Not described, CSDH - Chronic subdural hematoma, HT - Hypertension, DM - Diabetes mellitus
coagulation parameters and a massive air reflux into the cranial cavity through the drainage hole may pose additional risk. Other mechanism, though less possible, is a traumatic small contusion not detected in CT scan or MRI In all cases it may be mandatory to rule out secondary pathology like arteriovenous malformation, cavernous malformation and neoplasm. Rapid drainage of CSDH increases mobility of the intracranial structures and can lead to remote site hemorrhage. Associated high blood pressure could be an initiating factor. A hypertensive crisis with or without raised intracranial pressure may cause a direct brain stem hematoma unrelated to surgical manipulation. Another unlikely but posible cause of remote site hemorrhagic infarction could be a phenomenon simulating deep venous thrombosis. Okuchi et al.[15] reported a patient with oculomotor nerve paresis and brain stem symptoms following evacuation of bilateral CSDH and speculated that the complication is probably related to rapid decompression. Stefini et al.[5] reported a patient with ruptured intracranial aneurysm after evacuation with craniotomy of left CSDH. Aneurysmal rupture was probably caused by the alterations in the intracranial pressure dynamics following the evacuation of the clot. In our patient, although there were no significant hematological abnormalities, long‑term use low‑dose aspirin and clopidogrel could have altered the coagulation profile that might have led to hemorrhage. The other possible causes include increase in cerebral blood flow, alteration in autoregulation, possible damaged vessel, and supratentorial decompression.
Luis Mariano Rojas‑Medina, Atul Goel Department of Neurosurgery, King Edward Memorial Hospital and Seth Gordhandas Sunderdas Medical College, Parel, Mumbai, Maharashtra, India E‑mail: [email protected]
References 1. Kotwica Z, Brzezinski J. Chronic subdural haematoma treated by by burr holes and closed system drainage: Personal experience in 131 patients. Br J Neurosurg 1991;5:461‑5. Neurology India | Jul-Aug 2014 | Vol 62 | Issue 4
2. 3. 4. 5.
6. 7. 8. 9. 10. 11.
12. 13. 14.
15.
Richter HP, Klein HJ, Schafer M. Chronic subdural haematoma treated by enlarge burr hole craniotomy and closed system drainage. Retrospective study of 120 patients. Acta Neurochir (Wien) 1984;71:179‑88. Sambasivan M. An overview of chronic subdural hematoma: Experience with 2300 cases. Surg Neurol 1997;47:418‑22. Robinson RG. Chronic subdural hematoma: Surgical management in 133 patients. J Neurosurg 1984;61:263‑8. Stefini R, Ghitti F, Bergomi R, Catenacci E, Latronico N, Mortini P. Uncommon presentation of ruptured intracranial aneurysm during surgical evacuation of chronic subdural hematoma: Case report. Surg Neurol 2008;69:89‑92. Cohen‑Gadol AA. Remote contralateral intraparenchymal hemorrhage after overdrainage of a chronic subdural hematoma. Int J Surg Case Rep 2013;4:834‑6. Kim JK, Kim SW, Kim SH. Intracerebral hemorrhage following evacuation of a chronic subdural hematoma. J Korean Neurosurg Soc 2013;53:108‑11. Chang SH, Yang SH, Son BC, Lee SW. Cerebellar hemorrhage after burr hole drainage of supratentorial chronic subdural hematoma. J Korean Neurosurg Soc 2009;46:592‑5. Kollatos C, Konstantinou D, Raftopoulos S, Klironomos G, Messinis L, Zampakis P, et al. Cerebellar hemorrhage after supratentorial burr hole drainage of a chronic subdural hematoma. Hippokratia 2011;15:370‑2. Ulivieri S, Oliveri G. Intracerebral haemorrhage following surgical evacuation of chronic subdural haematoma: Case report. G Chir 2008;29:233‑4. Vega Basulto S, Mosqueda Betancourt G, Gutiérrez Muñoz F, Vega Trenado A, Rivero García C. Postoperative intracerebral hematoma. An unusual complication of chronic subdural hematoma. Rev Neurol 2004;38:497‑8. Park KJ, Kang SH, Lee HK, Chung YG. Brain stem hemorrhage following burr hole drainage for chronic subdural hematoma‑case report. Neurol Med Chir (Tokyo) 2009;49:594‑7. McKissock W. Subdural haematoma. A review of 389 cases. Lancet 1960;1:1365‑9. Alcalá‑Cerra G, Gutiérrez‑Paternina JJ, Niño‑Hernández LM, Polo‑Torres C, Romero‑Ramírez H, Sabogal‑Barrios R. Intracerebral hemorrhages following drainage of chronic subdural hematomas. Rev Med Inst Mex Seguro Soc 2011;49:547‑50. Okuchi K, Fujioka M, Maeda Y, Kagoshima T, Sakaki T. Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis an brain stem symptoms after operation. Neurol Med Chir (Tokyo) 1999;39:367‑71.
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.141222
Received: 26‑04‑2014 Review completed: 12‑05‑2014 Accepted: 29‑06‑2014 431
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.
