Letters to Editor
2. 3. 4. a
b
Figure 2: Intra-operative photography. After dissecting gluteus maximus muscle, dark-colored and swelled piriformis muscle (a, arrow) entrapped the sciatic nerve. After dissection of the piriformis muscle (b, arrow), sciatic nerve was released (b, arrowheads)
position, a skin incision from just posterior to the greater trochanter to the middle of the buttock was made. The piriformis muscle was exposed by the blunt dissection of the gluteus maximus muscle. The sciatic nerve was then exposed under the piriformis muscle [Figure 2a]. The piriformis muscle was tight and tense especially on internal rotation of the hip joint. The piriformis muscle was incised at the tendinons portion with which the tension of the piriformis muscle decreased and compression over the sciatic nerve got relieved [Figure 2b]. There was no apparent pus discharge intraoperatively. After the surgery, she had dramatic relief of pain. She returned to her work as a nurse 2 months after the surgery. Follow‑up MR and CT images showed normalized right piriformis muscle [Figure 1c and d]. Chiedozi divided pyomyositis into three stages according depending on the progression of the disease: invasive stage showing myositis without abscess formation, suppurative stage with abscess formation and late stage with sepsis.[4] Pyomyositis in suppurative stage, requires aspiration by the percutaneous route or open drainage. This case illustrates that the possibility of piriformis pyomyositis should be considered in patients with sciatica of undetermined causes, more so when signs of inflammation are present. Masao Koda1,2, Chikato Mannoji1, Hitoshi Watanabe1, Arata Nakajima3, Toshiyuki Yamada1, Tomoyuki Rokkaku1, Ken‑Ichi Murakami2, Masazumi Murakami1, Osamu Ikeda2, Masashi Yamazaki4, Takeo Furuya2, Departments of Orthopedic Surgery, 1Chiba Aoba Municipal Hospital, 2Chiba University Graduate School of Medicine, Chiba, 3Toho University Sakura Medical Center, Sakura, 4 University of Tsukuba, Tsukuba, Japan E‑mail: [email protected]
References 1.
Filler AG, Haynes J, Jordan SE, Prager J, Villablanca JP, Farahani K, et al. Sciatica of nondisc origin and piriformis syndrome: Diagnosis by magnetic resonance neurography and interventional magnetic resonance
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
imaging with outcome study of resulting treatment. J Neurosurg Spine 2005;2:99‑115. Chen WS. Sciatica due to piriformis pyomyositis. Report of a case. J Bone Joint Surg Am 1992;74:1546‑8. Nakai I, Yano Y, Naramatsu M, Hashimoto N. Piriformis syndrome due to piriformis pyomyositis: report of a case. Seikeigeka 2012;63:949‑51. Chiedozi LC. Pyomyositis. Review of 205 cases in 112 patients. Am J Surg 1979;137:255‑9. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125291
Received: 30‑10‑2013 Review completed: 30‑10‑2013 Accepted: 05‑12‑2013
A rare cause of dural venous sinus thrombosis Sir, Poisoning resulting from ingestion of crushed seeds of the plant Abrus precatorius (AP) can occasionally cause neurological manifestations. However, dural venous sinus thrombosis is a rare and hitherto unreported complication of AP poisoning. A 22‑year‑old unmarried lady was admitted after suicidal ingestion of about 20 crushed seeds of AP. She developed abdominal pain, recurrent vomiting, profuse watery diarrhea and subsequently bloody diarrhea from second till seventh day of ingestion. Laboratory evaluation on day‑3 revealed hypernatremia (serum sodium: 154 mEq/l), hypokalemia (serum potassium: 3.1 mEq/l), neutrophilic leucocytosis (leucocyte count: 16.2 × 109/l, neutrophils: 83%), normal hematocrit, platelet count, coagulation tests, hepatic and renal function. On day‑7, she suffered multiple episodes of generalized tonic clonic seizures and developed altered sensorium. Examination revealed right sided hemiplegia and papilledema in both eyes. Unenhanced computerized tomography (CT) of the brain revealed thrombosis of the superior sagittal sinus (SSS), left parieto‑occipital hemorrhagic infarct with midline shift [Figure 1]. She was started on antiepileptic drugs, osmotic therapy and subcutaneous enoxaparin. Magnetic resonance imaging (MRI) and MR‑venography confirmed the thrombosis of SSS and left transverse sinuses [Figure 1]. Subsequently she underwent left parieto‑occipitotemporal craniotomy for cerebral decompression [Figure 1]. Urine pregnancy test was negative. Work‑up for pro‑coagulant states and 669
Letters to Editor
a
b
contributed to CVT. Pregnancy was excluded and work‑up for other thrombophilic states such as protein C and S deficiency, antithrombin III deficiency, factor V Leiden and prothrombin gene mutation was negative in the index patient. Prior personal or family history of deep venous or CVT and intake of hormonal contraceptives were lacking in the index case. Thus, apart from metabolic causes such as hyponatremia or hypernatremia, acute demyelinating encephalitis and toxic encephalitis, CVT has to be considered in the differential diagnosis of a patient with AP poisoning who develops altered sensorium and convulsions, with or without focal neurological deficits. Timely diagnosis and prompt treatment of this thrombotic complication with heparin and oral anticoagulation can be lifesaving.
Kolar Vishwanath Vinod, Molly Mary Thabah, Thammishetty Venkatesh, Gnanavel Thiruvikramaprakash, Shravan R. Kumar, Tarun Kumar Dutta Department of General Medicine, JIPMER, Dhanvantri Nagar, Puducherry, India E‑mail: [email protected] c
d
Figure 1: Unenhanced CT images of the brain (a-c), showing hyperdense thrombus in the posterior part of the superior sagittal sinus (indicated by arrows in a and b), with a hemorrhagic infarct in the left parieto‑occipital region and midline shift to right (b) and CT scan done following left parieto‑occipitotemporal craniotomy (c) Sagittal T1‑weighted magnetic resonance image of the brain (d), showing hyperintense thrombus in the SSS (indicated by arrows)
homocysteinemia was negative. Her condition improved gradually and she was discharged on oral warfarin. Abrin, the toxalbumin present in AP is highly toxic to humans. The manifestations of poisoning predominantly pertain to the gastrointestinal tract, but uncommonly hepatitis, pulmonary edema, central nervous system (CNS) toxicity, hemolysis and acute kidney injury have also been reported.[1,2] CNS manifestations such as drowsiness, confusion, hallucinations, convulsions, coma, papilledema and focal neurological deficits resulting from toxic encephalitis, acute demyelinating encephalitis, cerebral edema and consequent raised intracranial pressure have been reported earlier.[3‑5] As abrin is a known immunomodulator, CNS demyelination is thought to be immune mediated.[4] Systemic steroids are useful for treating acute demyelinating encephalitis.[5] Dehydration has been reported as a risk factor for cerebral venous thrombosis (CVT). Fluid losses from vomiting and diarrhea and consequent dehydration might have contributed to CVT in the index case. Endothelial injury from abrin,[2] apart from causing cerebral edema[3] and intravascular volume depletion from “capillary leak” phenomenon, might have 670
References 1. 2. 3. 4. 5.
Fernando C. Poisoning due to Abrus precatorius (jequirity bean). Anaesthesia 2001;56:1178‑80. Dickers KJ, Bradberry SM, Rice P, Griffiths GD, Vale JA. Abrin poisoning. Toxicol Rev 2003;22:137‑42. Subrahmanyan D, Mathew J, Raj M. An unusual manifestation of Abrus precatorius poisoning: A report of two cases. Clin Toxicol (Phila) 2008;46:173‑5. Sahni V, Agarwal SK, Singh NP, Sikdar S. Acute demyelinating encephalitis after jequirity pea ingestion (Abrus precatorius). Clin Toxicol (Phila) 2007;45:77‑9. Sahoo R, Hamide A, Amalnath SD, Narayana BS. Acute demyelinating encephalitis due to Abrus precatorius poisoning – Complete recovery after steroid therapy. Clin Toxicol (Phila) 2008;46:1071‑3. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125292
Received: 05‑11‑2013 Review completed: 25‑11‑2013 Accepted: 21‑12‑2013
Brucella melitensis shunt infection Sir, Shunt infection is a serious complication of shunt operations Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
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.
2. 3. 4. a
b
Figure 2: Intra-operative photography. After dissecting gluteus maximus muscle, dark-colored and swelled piriformis muscle (a, arrow) entrapped the sciatic nerve. After dissection of the piriformis muscle (b, arrow), sciatic nerve was released (b, arrowheads)
position, a skin incision from just posterior to the greater trochanter to the middle of the buttock was made. The piriformis muscle was exposed by the blunt dissection of the gluteus maximus muscle. The sciatic nerve was then exposed under the piriformis muscle [Figure 2a]. The piriformis muscle was tight and tense especially on internal rotation of the hip joint. The piriformis muscle was incised at the tendinons portion with which the tension of the piriformis muscle decreased and compression over the sciatic nerve got relieved [Figure 2b]. There was no apparent pus discharge intraoperatively. After the surgery, she had dramatic relief of pain. She returned to her work as a nurse 2 months after the surgery. Follow‑up MR and CT images showed normalized right piriformis muscle [Figure 1c and d]. Chiedozi divided pyomyositis into three stages according depending on the progression of the disease: invasive stage showing myositis without abscess formation, suppurative stage with abscess formation and late stage with sepsis.[4] Pyomyositis in suppurative stage, requires aspiration by the percutaneous route or open drainage. This case illustrates that the possibility of piriformis pyomyositis should be considered in patients with sciatica of undetermined causes, more so when signs of inflammation are present. Masao Koda1,2, Chikato Mannoji1, Hitoshi Watanabe1, Arata Nakajima3, Toshiyuki Yamada1, Tomoyuki Rokkaku1, Ken‑Ichi Murakami2, Masazumi Murakami1, Osamu Ikeda2, Masashi Yamazaki4, Takeo Furuya2, Departments of Orthopedic Surgery, 1Chiba Aoba Municipal Hospital, 2Chiba University Graduate School of Medicine, Chiba, 3Toho University Sakura Medical Center, Sakura, 4 University of Tsukuba, Tsukuba, Japan E‑mail: [email protected]
References 1.
Filler AG, Haynes J, Jordan SE, Prager J, Villablanca JP, Farahani K, et al. Sciatica of nondisc origin and piriformis syndrome: Diagnosis by magnetic resonance neurography and interventional magnetic resonance
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
imaging with outcome study of resulting treatment. J Neurosurg Spine 2005;2:99‑115. Chen WS. Sciatica due to piriformis pyomyositis. Report of a case. J Bone Joint Surg Am 1992;74:1546‑8. Nakai I, Yano Y, Naramatsu M, Hashimoto N. Piriformis syndrome due to piriformis pyomyositis: report of a case. Seikeigeka 2012;63:949‑51. Chiedozi LC. Pyomyositis. Review of 205 cases in 112 patients. Am J Surg 1979;137:255‑9. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125291
Received: 30‑10‑2013 Review completed: 30‑10‑2013 Accepted: 05‑12‑2013
A rare cause of dural venous sinus thrombosis Sir, Poisoning resulting from ingestion of crushed seeds of the plant Abrus precatorius (AP) can occasionally cause neurological manifestations. However, dural venous sinus thrombosis is a rare and hitherto unreported complication of AP poisoning. A 22‑year‑old unmarried lady was admitted after suicidal ingestion of about 20 crushed seeds of AP. She developed abdominal pain, recurrent vomiting, profuse watery diarrhea and subsequently bloody diarrhea from second till seventh day of ingestion. Laboratory evaluation on day‑3 revealed hypernatremia (serum sodium: 154 mEq/l), hypokalemia (serum potassium: 3.1 mEq/l), neutrophilic leucocytosis (leucocyte count: 16.2 × 109/l, neutrophils: 83%), normal hematocrit, platelet count, coagulation tests, hepatic and renal function. On day‑7, she suffered multiple episodes of generalized tonic clonic seizures and developed altered sensorium. Examination revealed right sided hemiplegia and papilledema in both eyes. Unenhanced computerized tomography (CT) of the brain revealed thrombosis of the superior sagittal sinus (SSS), left parieto‑occipital hemorrhagic infarct with midline shift [Figure 1]. She was started on antiepileptic drugs, osmotic therapy and subcutaneous enoxaparin. Magnetic resonance imaging (MRI) and MR‑venography confirmed the thrombosis of SSS and left transverse sinuses [Figure 1]. Subsequently she underwent left parieto‑occipitotemporal craniotomy for cerebral decompression [Figure 1]. Urine pregnancy test was negative. Work‑up for pro‑coagulant states and 669
Letters to Editor
a
b
contributed to CVT. Pregnancy was excluded and work‑up for other thrombophilic states such as protein C and S deficiency, antithrombin III deficiency, factor V Leiden and prothrombin gene mutation was negative in the index patient. Prior personal or family history of deep venous or CVT and intake of hormonal contraceptives were lacking in the index case. Thus, apart from metabolic causes such as hyponatremia or hypernatremia, acute demyelinating encephalitis and toxic encephalitis, CVT has to be considered in the differential diagnosis of a patient with AP poisoning who develops altered sensorium and convulsions, with or without focal neurological deficits. Timely diagnosis and prompt treatment of this thrombotic complication with heparin and oral anticoagulation can be lifesaving.
Kolar Vishwanath Vinod, Molly Mary Thabah, Thammishetty Venkatesh, Gnanavel Thiruvikramaprakash, Shravan R. Kumar, Tarun Kumar Dutta Department of General Medicine, JIPMER, Dhanvantri Nagar, Puducherry, India E‑mail: [email protected] c
d
Figure 1: Unenhanced CT images of the brain (a-c), showing hyperdense thrombus in the posterior part of the superior sagittal sinus (indicated by arrows in a and b), with a hemorrhagic infarct in the left parieto‑occipital region and midline shift to right (b) and CT scan done following left parieto‑occipitotemporal craniotomy (c) Sagittal T1‑weighted magnetic resonance image of the brain (d), showing hyperintense thrombus in the SSS (indicated by arrows)
homocysteinemia was negative. Her condition improved gradually and she was discharged on oral warfarin. Abrin, the toxalbumin present in AP is highly toxic to humans. The manifestations of poisoning predominantly pertain to the gastrointestinal tract, but uncommonly hepatitis, pulmonary edema, central nervous system (CNS) toxicity, hemolysis and acute kidney injury have also been reported.[1,2] CNS manifestations such as drowsiness, confusion, hallucinations, convulsions, coma, papilledema and focal neurological deficits resulting from toxic encephalitis, acute demyelinating encephalitis, cerebral edema and consequent raised intracranial pressure have been reported earlier.[3‑5] As abrin is a known immunomodulator, CNS demyelination is thought to be immune mediated.[4] Systemic steroids are useful for treating acute demyelinating encephalitis.[5] Dehydration has been reported as a risk factor for cerebral venous thrombosis (CVT). Fluid losses from vomiting and diarrhea and consequent dehydration might have contributed to CVT in the index case. Endothelial injury from abrin,[2] apart from causing cerebral edema[3] and intravascular volume depletion from “capillary leak” phenomenon, might have 670
References 1. 2. 3. 4. 5.
Fernando C. Poisoning due to Abrus precatorius (jequirity bean). Anaesthesia 2001;56:1178‑80. Dickers KJ, Bradberry SM, Rice P, Griffiths GD, Vale JA. Abrin poisoning. Toxicol Rev 2003;22:137‑42. Subrahmanyan D, Mathew J, Raj M. An unusual manifestation of Abrus precatorius poisoning: A report of two cases. Clin Toxicol (Phila) 2008;46:173‑5. Sahni V, Agarwal SK, Singh NP, Sikdar S. Acute demyelinating encephalitis after jequirity pea ingestion (Abrus precatorius). Clin Toxicol (Phila) 2007;45:77‑9. Sahoo R, Hamide A, Amalnath SD, Narayana BS. Acute demyelinating encephalitis due to Abrus precatorius poisoning – Complete recovery after steroid therapy. Clin Toxicol (Phila) 2008;46:1071‑3. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125292
Received: 05‑11‑2013 Review completed: 25‑11‑2013 Accepted: 21‑12‑2013
Brucella melitensis shunt infection Sir, Shunt infection is a serious complication of shunt operations Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
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.
