Case Reports / Journal of Clinical Neuroscience 21 (2014) 517–520
References [1] Franzini A, Marras C, Ferroli P, et al. Long-term high-frequency bilateral pallidal stimulation for neuroleptic-induced tardive dystonia. Report of two cases. J Neurosurg 2005;102:721–5. [2] Kiriakakis V, Bhatia KP, Quinn NP, et al. The natural history of tardive dystonia. A long-term follow-up study of 107 cases. Brain 1998;121:2053–66. [3] Cohen OS, Hassin-Baer S, Spiegelmann R. Deep brain stimulation of the internal globus pallidus for refractory tardive dystonia. Parkinsonism Relat Disord 2007;13:541–4. [4] Magarinos-Ascone CM, Regidor I, Gomez-Galan M, et al. Deep brain stimulation in the globus pallidus to treat dystonia: electrophysiological characteristics and 2 years’ follow-up in 10 patients. Neuroscience 2008;152:558–71. [5] Eltahawy HA, Feinstein A, Khan F, et al. Bilateral globus pallidus internus deep brain stimulation in tardive dyskinesia: a case report. Mov Disord 2004;19:969–72.
517
[6] Zhang J-G, Zhang K, Wang Z-C. Deep brain stimulation in the treatment of tardive dystonia. Chin Med J (Engl) 2006;119:789–92. [7] Sako W, Goto S, Shimazu H, et al. Bilateral deep brain stimulation of the globus pallidus internus in tardive dystonia. Mov Disord 2008;23:1929–31. [8] Damier P, Thobois S, Witjas T, et al. Bilateral deep brain stimulation of the globus pallidus to treat tardive dyskinesia. Arch Gen Psychiatry 2007;64:170–6. [9] Gruber D, Trottenberg T, Kivi A, et al. Long-term effects of pallidal deep brain stimulation in tardive dystonia. Neurology 2009;73:53–8. [10] Halbig TD, Gruber D, Kopp UA, et al. Pallidal stimulation in dystonia: effects on cognition, mood, and quality of life. J Neurol Neurosurg Psychiatry 2005;76:1713–6. [11] Lalli S, Albanese A. The diagnostic challenge of primary dystonia: evidence from misdiagnosis. Mov Disord 2010;25:1619–26.
http://dx.doi.org/10.1016/j.jocn.2013.05.001
Holospinal epidural abscess Darryl Lau a, John Maa b, Praveen V. Mummaneni a, Dean Chou a,⇑ a b
Department of Neurological Surgery, University of California, San Francisco, 505 Parnassus Avenue, Box 0112, San Francisco, CA 94143-0112, USA Department of Surgery, Division of General Surgery, University of California, San Francisco, CA, USA
a r t i c l e
i n f o
Article history: Received 26 April 2013 Accepted 2 May 2013
Keywords: Decompression Epidural abscess Holospinal Laminectomy Spine
a b s t r a c t Holospinal epidural abscess (HEA) is an extremely rare condition in which spinal epidural abscesses extend from the cervical to the sacral spine. We report two patients who presented with myelopathy secondary to HEA. Both patients underwent urgent surgical decompression and abscess drainage, and had significant improvement in neurological function. We discuss the surgical management strategies and briefly review the literature regarding HEA. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction In rare circumstances, a spinal epidural abscess can form throughout the entire spinal canal, an entity known as a holospinal epidural abscess (HEA). HEA can lead to extensive spinal cord compression and devastating neurological consequences if prompt therapies are not provided [1]. Only a limited number of patients with HEA extending from the cervical to the lumbar spine have been reported [2–14]. We describe two patients with HEA that highlight the importance of urgent surgical decompression and discuss the rationale for extent of laminectomy and use of spinal instrumentation.
severe from C2–C3, and L3–L4 discitis and osteomyelitis with epidural extension was present. The patient was started on broad spectrum antibiotics and underwent urgent surgical decompression with abscess drainage through a transoral odontoidectomy, removal of the anterior arch of C1, and partial corpectomy of C2. Six days postoperatively, the patient underwent laminectomy of C3– C6 and C1–C2 posterior cervical fusion. A transoral approach was performed because of the extensive amount of ventral disease. Intraoperative cultures were positive methicillin-sensitive Staphylococcus aureus (MSSA). There were no complications. At 13 month follow-up, the patient was doing well, recovering a significant portion of his upper extremity strength (4 out of 5 bilaterally throughout).
2. Case reports
2.2. Patient 2
2.1. Patient 1
A 46-year-old man presented with a 10 day history of fever and back pain. He also had a 2 day history of paraparesis and an episode of incontinence. Physical examination revealed full strength in the upper extremities but only minimal strength in the lower extremity (2 out of 5 in the right hamstring and 0 out of 5 in all other lower extremity muscle groups). MRI showed a large dorsal epidural abscess spanning the entire spinal axis (C1–L5) with significant compression and ventral displacement of the spinal cord and cauda equina (Fig. 2). There was also a paraspinous abscess at the L3–4 level. The patient was started on broad spectrum antibiotics and underwent urgent decompression and epidural abscess drainage via L2–L3 laminectomy. Two days later, the patient developed
A 50-year-old man with a history of diabetes presented with fever, leukocytosis, and upper extremity weakness. Physical examination showed weakness throughout his upper extremities. Strength in the deltoids was 1 out of 5, and strength was 2 out of 5 in the biceps, triceps, and handgrip bilaterally. MRI revealed an HEA extending from the base of the skull to T5, ventrally and from T1 down to L5, dorsally (Fig. 1). Spinal cord compression was most ⇑ Corresponding author. Tel.: +1 415 353 9095; fax: +1 415 353 3907. E-mail address: [email protected] (D. Chou).
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Case Reports / Journal of Clinical Neuroscience 21 (2014) 517–520
Fig. 1. Patient 1. (A) Preoperative sagittal T2-weighted MRI of the cervical spine demonstrating epidural abscess dorsal to the spinal cord. Preoperative sagittal T1-weighted MRI with gadolinium contrast showing (B) the cervical spine revealing enhancing abscess, (C) the thoracic spine showing continuation of the abscess posteriorly, and (D) the lumbar spine showing continuation of the abscess posteriorly.
upper extremity weakness and underwent additional segmental laminectomies at C3–C6 and T6–T9 for further decompression and abscess drainage. A red rubber catheter was used to irrigate the epidural spaces where no laminectomy was performed. No instrumentation was used because of the intraoperative findings of gross purulent material. Intraoperative cultures isolated MSSA. At discharge, the patient recovered function of upper extremities, and the ability to raise his legs bilaterally. Postoperative MRI showed significant resolution of his HEA (Fig. 3). At 1 month follow-up, he had 3 out of 5 strength throughout his lower extremities. Despite extensive efforts to contact the patient, he was lost to follow-up. 3. Discussion To our knowledge, there are only 13 patients with HEA reported in the literature [2–14]. HEA affects patients of all ages [3,7,8] and should be suspected in high risk patients with back pain, fever, and/or neurological deficit emanating from the spine [12]. Both of our patients had underlying risk factors for HEA (diabetes and a psoas abscess). Reports of HEA have been associated with intraabdominal complications from Crohn’s disease [11], immunosuppression from chemotherapy [3], psoas abscess [4], and a neonatal sacral teratoma [7]. Timely diagnosis and proper treatment of HEA are critical in preventing catastrophic neurological consequences from spinal cord compression. Whole spine MRI with contrast should be obtained if HEA is suspected; CT imaging is unreliable [11,13]. Broad
spectrum intravenous antibiotic is the standard treatment for spinal epidural abscesses, but in the setting of a deteriorating neurological examination surgical intervention is warranted. All but three patients with HEA underwent surgical intervention [2–14]. The three patients who were managed conservatively had minimal neurological deficit [13], rapidly regained neurologic function in response to antibiotic therapy [8], and had a HEA deemed too extensive for surgery (according to the authors) [3]. The effectiveness of antibiotic therapy was monitored with serial MRI and C-reactive protein values [13]. All patients maintained or regained neurological function [3,8,13]. The two principal decompressive methods to treat HEA are segmental laminectomies with catheter irrigation [2,7,11,12] or radical laminectomy of the entire spinal column [9]. We performed segmental laminectomy for both patients. In Patient 2, laminectomy of the whole spine would have been ideal to clear the abscess and obtain maximal decompression, but this would greatly destabilize him without instrumentation, putting him at risk for post-laminectomy kyphosis. Also, the morbidity of a C2 to L5 fusion cannot be underestimated. Therefore ‘‘skip’’ laminectomies were performed to preserve the posterior tension band over the cervicothoracic and thoracolumbar junction at C7–T2 and T10– L1, respectively. This allowed adequate decompression and debridement of the HEA. There are no clear data regarding whether or not implants should be used in the setting of active infections. In the event a patient needed instrumentation, we based our principles on the following guidelines. Implants were placed in the absence of
Case Reports / Journal of Clinical Neuroscience 21 (2014) 517–520
519
Fig. 2. Patient 2. (A) Preoperative sagittal T2-weighted MRI of the cervical spine showing holospinal epidural abscess extending from the base of the foramen magnum with spinal cord compression. Preoperative sagittal T1-weighted MRI with gadolinium contrast showing (B) the cervical spine revealing enhancing abscess, (C) the thoracic spine showing continuation of the abscess, and (D) the lumbar spine showing continuation of the abscess and focal abscess anterior to the lumbar vertebral body.
Fig. 3. Patient 2. Postoperative sagittal T1-weighted MRI with gadolinium contrast of the (A) cervical, (B) thoracic, and (C) lumbar spine demonstrating decreased epidural abscess collection and markedly decreased spinal cord compression.
obvious liquid purulent material at the same setting of decompression. If there was gross purulent material, they would undergo a second staged surgery for instrumentation after 2 weeks of antibiotic therapy to help clear pus and sterilize the operative bed. Titanium implants are preferred because of their lack of a bacteriaharboring biofilm that is seen with stainless steel implants [15]. HEA can result in rapid neurological decline (as demonstrated in Patient 2) and even death. Simpson et al. describe a patient in which a C2–S2 HEA resulted in death; as the patient was being pre-
pared for surgery, he rapidly became quadriplegic, deteriorated, and died of cardiopulmonary arrest [10]. However, most patients with significant preoperative neurological deficits have good outcomes with proper management [2,4,5,7,8,11,12]. 4. Conclusion HEA can result in rapid permanent neurological injury and even death. Timely diagnosis and treatment is essential. In the presence
520
Case Reports / Journal of Clinical Neuroscience 21 (2014) 520–521
of a deteriorating neurological exam, surgical decompression via segmental laminectomies is warranted as outcomes are promising. Conflict of interest/disclosure The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Rigamonti D, Liem L, Sampath P, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol 1999;52:189–96. [2] Elsamaloty H, Elzawawi M, Abduljabar A. A rare case of extensive spinal epidural abscess in a diabetic patient. Spine (Phila Pa 1976) 2010;35:E53–6. [3] Duc C, Grange L, Gaudin P, et al. Extensive primary epidural abscess. Report of a case. Joint Bone Spine 2002;69:312–5. [4] Ghosh PS, Loddenkemper T, Blanco MB, et al. Holocord spinal epidural abscess. J Child Neurol 2009;24:768–71. [5] Gorchynski J, Hwang J, McLaughlin T. A methicillin-resistant Staphylococcus aureus-positive holospinal epidural abscess. Am J Emerg Med 2009;27 [514e7–9].
[6] Jackson F, Assam S. Extensive spinal epidural abscess treated by laminectomy and hypothermia. Case Report. J Neurosurg 1964;21:237–9. [7] Leonard J, Kaufman B. Treatment of a holocord epidural abscess. Case illustration. J Neurosurg 2001;94:179. [8] O’Brien C, Lenehan B, Street J. Non-operative management of an extensive anteriorly located epidural abscess. J Clin Neurosci 2011;18:1401–2. [9] Richmond BK, Schmidt 3rd JH. Seventeen level laminectomy for extensive spinal epidural abscess: case report and review. W V Med J 1994;90:468–71. [10] Simpson Jr RK, Azordegan PA, Sirbasku DM, et al. Rapid onset of quadriplegia from a panspinal epidural abscess. Spine (Phila Pa 1976) 1991;16:1002–5. [11] Smith C, Kavar B. Extensive spinal epidural abscess as a complication of Crohn’s disease. J Clin Neurosci 2010;17:144–6. [12] Tahir MZ, Hassan RU, Enam SA. Management of an extensive spinal epidural abscess from C-1 to the sacrum. Case report. J Neurosurg Spine 2010;13:780–3. [13] Van Bergen J, Plazier M, Baets J, et al. An extensive spinal epidural abscess successfully treated conservatively. J Neurol Neurosurg Psychiatry 2009;80:351–3. [14] Vaught KA. Spinal surgery: an unusual case of spinal epidural abscess. Mo Med 2009;106:297–300. [15] Arens S, Schlegel U, Printzen G, et al. Influence of materials for fixation implants on local infection. An experimental study of steel versus titanium DCP in rabbits. J Bone Joint Surg Br 1996;78:647–51.
http://dx.doi.org/10.1016/j.jocn.2013.05.001
Popliteus muscle hemorrhage as a rare cause of a proximal tibial neuropathy Elliot L. Dimberg a,⇑, Devon I. Rubin a, Cedric J. Ortiguera b, Kathleen D. Kennelly a a b
Mayo Clinic Florida, Department of Neurology, 4500 San Pablo Road, Jacksonville, FL 32082, USA Mayo Clinic Florida, Department of Orthopedics, Jacksonville, FL, USA
a r t i c l e
i n f o
Article history: Received 10 May 2013 Accepted 21 May 2013
Keywords: Electromyography Mononeuropathy Nerve conduction studies Popliteus muscle Tibial neuropathy
a b s t r a c t Proximal tibial neuropathy is an uncommon focal mononeuropathy that is most often caused by trauma, ischemia, or neoplastic infiltration or compression of the tibial nerve. We report a patient who presented with a tibial neuropathy following a leg injury, which initially mimicked a lumbosacral radiculopathy but which was the result of a proximal tibial neuropathy. Electrophysiologic studies confirmed a proximal tibial neuropathy and MRI revealed a popliteus muscle hemorrhage with mass effect on the tibial nerve. Following conservative management the patient had little recovery of function after 15 months. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction
2. Case report
Proximal tibial neuropathy is an uncommon lower extremity mononeuropathy, usually resulting from blunt or penetrating trauma or ischemia to the nerve [1,2]. Popliteus muscle rupture is a rarely reported cause of a proximal tibial neuropathy, and patients often present to orthopedic or sports medicine specialists with knee or calf pain, rather than to neurologists [3–6]. Recognition of a proximal tibial neuropathy due to popliteus muscle rupture and distinguishing this disorder from more common causes of foot and leg symptoms, such as lumbosacral radiculopathies or sciatic neuropathies, is essential for appropriate management. We describe the clinical, electrodiagnostic and imaging features of a patient with a tibial neuropathy due to popliteus intramuscular hemorrhage.
A 54-year-old man with a history of a right L5 radiculopathy jumped a few feet onto a dock, hyperextending his right knee. He experienced immediate posterior knee and calf pain and the next day experienced sensory loss and weakness of his right foot. Neurologic examination 3 weeks later demonstrated severe weakness of flexion of his right toes with mild weakness of foot dorsiflexion, eversion, inversion, and plantar flexion, and an absent right Achilles reflex. Light touch and pinprick sensation were severely reduced at the bottom of the right foot and mildly decreased over the first and second toes. The right calf was mildly swollen. Electrodiagnostic studies demonstrated absent tibial motor and medial plantar sensory responses on the right and a large degree of fibrillation potentials with either no voluntary activation or severely reduced recruitment in right tibial innervated muscles distal to the medial gastrocnemius, consistent with a severe, subacute proximal right tibial neuropathy. There were also findings of a chronic right L5 radiculopathy. MRI of the right lower extremity showed a thickened popliteus muscle with signal abnormality rep-
⇑ Corresponding author. Tel.: +1 904 953 7104; fax: +1 904 953 0757. E-mail address: [email protected] (E.L. Dimberg).
References [1] Franzini A, Marras C, Ferroli P, et al. Long-term high-frequency bilateral pallidal stimulation for neuroleptic-induced tardive dystonia. Report of two cases. J Neurosurg 2005;102:721–5. [2] Kiriakakis V, Bhatia KP, Quinn NP, et al. The natural history of tardive dystonia. A long-term follow-up study of 107 cases. Brain 1998;121:2053–66. [3] Cohen OS, Hassin-Baer S, Spiegelmann R. Deep brain stimulation of the internal globus pallidus for refractory tardive dystonia. Parkinsonism Relat Disord 2007;13:541–4. [4] Magarinos-Ascone CM, Regidor I, Gomez-Galan M, et al. Deep brain stimulation in the globus pallidus to treat dystonia: electrophysiological characteristics and 2 years’ follow-up in 10 patients. Neuroscience 2008;152:558–71. [5] Eltahawy HA, Feinstein A, Khan F, et al. Bilateral globus pallidus internus deep brain stimulation in tardive dyskinesia: a case report. Mov Disord 2004;19:969–72.
517
[6] Zhang J-G, Zhang K, Wang Z-C. Deep brain stimulation in the treatment of tardive dystonia. Chin Med J (Engl) 2006;119:789–92. [7] Sako W, Goto S, Shimazu H, et al. Bilateral deep brain stimulation of the globus pallidus internus in tardive dystonia. Mov Disord 2008;23:1929–31. [8] Damier P, Thobois S, Witjas T, et al. Bilateral deep brain stimulation of the globus pallidus to treat tardive dyskinesia. Arch Gen Psychiatry 2007;64:170–6. [9] Gruber D, Trottenberg T, Kivi A, et al. Long-term effects of pallidal deep brain stimulation in tardive dystonia. Neurology 2009;73:53–8. [10] Halbig TD, Gruber D, Kopp UA, et al. Pallidal stimulation in dystonia: effects on cognition, mood, and quality of life. J Neurol Neurosurg Psychiatry 2005;76:1713–6. [11] Lalli S, Albanese A. The diagnostic challenge of primary dystonia: evidence from misdiagnosis. Mov Disord 2010;25:1619–26.
http://dx.doi.org/10.1016/j.jocn.2013.05.001
Holospinal epidural abscess Darryl Lau a, John Maa b, Praveen V. Mummaneni a, Dean Chou a,⇑ a b
Department of Neurological Surgery, University of California, San Francisco, 505 Parnassus Avenue, Box 0112, San Francisco, CA 94143-0112, USA Department of Surgery, Division of General Surgery, University of California, San Francisco, CA, USA
a r t i c l e
i n f o
Article history: Received 26 April 2013 Accepted 2 May 2013
Keywords: Decompression Epidural abscess Holospinal Laminectomy Spine
a b s t r a c t Holospinal epidural abscess (HEA) is an extremely rare condition in which spinal epidural abscesses extend from the cervical to the sacral spine. We report two patients who presented with myelopathy secondary to HEA. Both patients underwent urgent surgical decompression and abscess drainage, and had significant improvement in neurological function. We discuss the surgical management strategies and briefly review the literature regarding HEA. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction In rare circumstances, a spinal epidural abscess can form throughout the entire spinal canal, an entity known as a holospinal epidural abscess (HEA). HEA can lead to extensive spinal cord compression and devastating neurological consequences if prompt therapies are not provided [1]. Only a limited number of patients with HEA extending from the cervical to the lumbar spine have been reported [2–14]. We describe two patients with HEA that highlight the importance of urgent surgical decompression and discuss the rationale for extent of laminectomy and use of spinal instrumentation.
severe from C2–C3, and L3–L4 discitis and osteomyelitis with epidural extension was present. The patient was started on broad spectrum antibiotics and underwent urgent surgical decompression with abscess drainage through a transoral odontoidectomy, removal of the anterior arch of C1, and partial corpectomy of C2. Six days postoperatively, the patient underwent laminectomy of C3– C6 and C1–C2 posterior cervical fusion. A transoral approach was performed because of the extensive amount of ventral disease. Intraoperative cultures were positive methicillin-sensitive Staphylococcus aureus (MSSA). There were no complications. At 13 month follow-up, the patient was doing well, recovering a significant portion of his upper extremity strength (4 out of 5 bilaterally throughout).
2. Case reports
2.2. Patient 2
2.1. Patient 1
A 46-year-old man presented with a 10 day history of fever and back pain. He also had a 2 day history of paraparesis and an episode of incontinence. Physical examination revealed full strength in the upper extremities but only minimal strength in the lower extremity (2 out of 5 in the right hamstring and 0 out of 5 in all other lower extremity muscle groups). MRI showed a large dorsal epidural abscess spanning the entire spinal axis (C1–L5) with significant compression and ventral displacement of the spinal cord and cauda equina (Fig. 2). There was also a paraspinous abscess at the L3–4 level. The patient was started on broad spectrum antibiotics and underwent urgent decompression and epidural abscess drainage via L2–L3 laminectomy. Two days later, the patient developed
A 50-year-old man with a history of diabetes presented with fever, leukocytosis, and upper extremity weakness. Physical examination showed weakness throughout his upper extremities. Strength in the deltoids was 1 out of 5, and strength was 2 out of 5 in the biceps, triceps, and handgrip bilaterally. MRI revealed an HEA extending from the base of the skull to T5, ventrally and from T1 down to L5, dorsally (Fig. 1). Spinal cord compression was most ⇑ Corresponding author. Tel.: +1 415 353 9095; fax: +1 415 353 3907. E-mail address: [email protected] (D. Chou).
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Case Reports / Journal of Clinical Neuroscience 21 (2014) 517–520
Fig. 1. Patient 1. (A) Preoperative sagittal T2-weighted MRI of the cervical spine demonstrating epidural abscess dorsal to the spinal cord. Preoperative sagittal T1-weighted MRI with gadolinium contrast showing (B) the cervical spine revealing enhancing abscess, (C) the thoracic spine showing continuation of the abscess posteriorly, and (D) the lumbar spine showing continuation of the abscess posteriorly.
upper extremity weakness and underwent additional segmental laminectomies at C3–C6 and T6–T9 for further decompression and abscess drainage. A red rubber catheter was used to irrigate the epidural spaces where no laminectomy was performed. No instrumentation was used because of the intraoperative findings of gross purulent material. Intraoperative cultures isolated MSSA. At discharge, the patient recovered function of upper extremities, and the ability to raise his legs bilaterally. Postoperative MRI showed significant resolution of his HEA (Fig. 3). At 1 month follow-up, he had 3 out of 5 strength throughout his lower extremities. Despite extensive efforts to contact the patient, he was lost to follow-up. 3. Discussion To our knowledge, there are only 13 patients with HEA reported in the literature [2–14]. HEA affects patients of all ages [3,7,8] and should be suspected in high risk patients with back pain, fever, and/or neurological deficit emanating from the spine [12]. Both of our patients had underlying risk factors for HEA (diabetes and a psoas abscess). Reports of HEA have been associated with intraabdominal complications from Crohn’s disease [11], immunosuppression from chemotherapy [3], psoas abscess [4], and a neonatal sacral teratoma [7]. Timely diagnosis and proper treatment of HEA are critical in preventing catastrophic neurological consequences from spinal cord compression. Whole spine MRI with contrast should be obtained if HEA is suspected; CT imaging is unreliable [11,13]. Broad
spectrum intravenous antibiotic is the standard treatment for spinal epidural abscesses, but in the setting of a deteriorating neurological examination surgical intervention is warranted. All but three patients with HEA underwent surgical intervention [2–14]. The three patients who were managed conservatively had minimal neurological deficit [13], rapidly regained neurologic function in response to antibiotic therapy [8], and had a HEA deemed too extensive for surgery (according to the authors) [3]. The effectiveness of antibiotic therapy was monitored with serial MRI and C-reactive protein values [13]. All patients maintained or regained neurological function [3,8,13]. The two principal decompressive methods to treat HEA are segmental laminectomies with catheter irrigation [2,7,11,12] or radical laminectomy of the entire spinal column [9]. We performed segmental laminectomy for both patients. In Patient 2, laminectomy of the whole spine would have been ideal to clear the abscess and obtain maximal decompression, but this would greatly destabilize him without instrumentation, putting him at risk for post-laminectomy kyphosis. Also, the morbidity of a C2 to L5 fusion cannot be underestimated. Therefore ‘‘skip’’ laminectomies were performed to preserve the posterior tension band over the cervicothoracic and thoracolumbar junction at C7–T2 and T10– L1, respectively. This allowed adequate decompression and debridement of the HEA. There are no clear data regarding whether or not implants should be used in the setting of active infections. In the event a patient needed instrumentation, we based our principles on the following guidelines. Implants were placed in the absence of
Case Reports / Journal of Clinical Neuroscience 21 (2014) 517–520
519
Fig. 2. Patient 2. (A) Preoperative sagittal T2-weighted MRI of the cervical spine showing holospinal epidural abscess extending from the base of the foramen magnum with spinal cord compression. Preoperative sagittal T1-weighted MRI with gadolinium contrast showing (B) the cervical spine revealing enhancing abscess, (C) the thoracic spine showing continuation of the abscess, and (D) the lumbar spine showing continuation of the abscess and focal abscess anterior to the lumbar vertebral body.
Fig. 3. Patient 2. Postoperative sagittal T1-weighted MRI with gadolinium contrast of the (A) cervical, (B) thoracic, and (C) lumbar spine demonstrating decreased epidural abscess collection and markedly decreased spinal cord compression.
obvious liquid purulent material at the same setting of decompression. If there was gross purulent material, they would undergo a second staged surgery for instrumentation after 2 weeks of antibiotic therapy to help clear pus and sterilize the operative bed. Titanium implants are preferred because of their lack of a bacteriaharboring biofilm that is seen with stainless steel implants [15]. HEA can result in rapid neurological decline (as demonstrated in Patient 2) and even death. Simpson et al. describe a patient in which a C2–S2 HEA resulted in death; as the patient was being pre-
pared for surgery, he rapidly became quadriplegic, deteriorated, and died of cardiopulmonary arrest [10]. However, most patients with significant preoperative neurological deficits have good outcomes with proper management [2,4,5,7,8,11,12]. 4. Conclusion HEA can result in rapid permanent neurological injury and even death. Timely diagnosis and treatment is essential. In the presence
520
Case Reports / Journal of Clinical Neuroscience 21 (2014) 520–521
of a deteriorating neurological exam, surgical decompression via segmental laminectomies is warranted as outcomes are promising. Conflict of interest/disclosure The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Rigamonti D, Liem L, Sampath P, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol 1999;52:189–96. [2] Elsamaloty H, Elzawawi M, Abduljabar A. A rare case of extensive spinal epidural abscess in a diabetic patient. Spine (Phila Pa 1976) 2010;35:E53–6. [3] Duc C, Grange L, Gaudin P, et al. Extensive primary epidural abscess. Report of a case. Joint Bone Spine 2002;69:312–5. [4] Ghosh PS, Loddenkemper T, Blanco MB, et al. Holocord spinal epidural abscess. J Child Neurol 2009;24:768–71. [5] Gorchynski J, Hwang J, McLaughlin T. A methicillin-resistant Staphylococcus aureus-positive holospinal epidural abscess. Am J Emerg Med 2009;27 [514e7–9].
[6] Jackson F, Assam S. Extensive spinal epidural abscess treated by laminectomy and hypothermia. Case Report. J Neurosurg 1964;21:237–9. [7] Leonard J, Kaufman B. Treatment of a holocord epidural abscess. Case illustration. J Neurosurg 2001;94:179. [8] O’Brien C, Lenehan B, Street J. Non-operative management of an extensive anteriorly located epidural abscess. J Clin Neurosci 2011;18:1401–2. [9] Richmond BK, Schmidt 3rd JH. Seventeen level laminectomy for extensive spinal epidural abscess: case report and review. W V Med J 1994;90:468–71. [10] Simpson Jr RK, Azordegan PA, Sirbasku DM, et al. Rapid onset of quadriplegia from a panspinal epidural abscess. Spine (Phila Pa 1976) 1991;16:1002–5. [11] Smith C, Kavar B. Extensive spinal epidural abscess as a complication of Crohn’s disease. J Clin Neurosci 2010;17:144–6. [12] Tahir MZ, Hassan RU, Enam SA. Management of an extensive spinal epidural abscess from C-1 to the sacrum. Case report. J Neurosurg Spine 2010;13:780–3. [13] Van Bergen J, Plazier M, Baets J, et al. An extensive spinal epidural abscess successfully treated conservatively. J Neurol Neurosurg Psychiatry 2009;80:351–3. [14] Vaught KA. Spinal surgery: an unusual case of spinal epidural abscess. Mo Med 2009;106:297–300. [15] Arens S, Schlegel U, Printzen G, et al. Influence of materials for fixation implants on local infection. An experimental study of steel versus titanium DCP in rabbits. J Bone Joint Surg Br 1996;78:647–51.
http://dx.doi.org/10.1016/j.jocn.2013.05.001
Popliteus muscle hemorrhage as a rare cause of a proximal tibial neuropathy Elliot L. Dimberg a,⇑, Devon I. Rubin a, Cedric J. Ortiguera b, Kathleen D. Kennelly a a b
Mayo Clinic Florida, Department of Neurology, 4500 San Pablo Road, Jacksonville, FL 32082, USA Mayo Clinic Florida, Department of Orthopedics, Jacksonville, FL, USA
a r t i c l e
i n f o
Article history: Received 10 May 2013 Accepted 21 May 2013
Keywords: Electromyography Mononeuropathy Nerve conduction studies Popliteus muscle Tibial neuropathy
a b s t r a c t Proximal tibial neuropathy is an uncommon focal mononeuropathy that is most often caused by trauma, ischemia, or neoplastic infiltration or compression of the tibial nerve. We report a patient who presented with a tibial neuropathy following a leg injury, which initially mimicked a lumbosacral radiculopathy but which was the result of a proximal tibial neuropathy. Electrophysiologic studies confirmed a proximal tibial neuropathy and MRI revealed a popliteus muscle hemorrhage with mass effect on the tibial nerve. Following conservative management the patient had little recovery of function after 15 months. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction
2. Case report
Proximal tibial neuropathy is an uncommon lower extremity mononeuropathy, usually resulting from blunt or penetrating trauma or ischemia to the nerve [1,2]. Popliteus muscle rupture is a rarely reported cause of a proximal tibial neuropathy, and patients often present to orthopedic or sports medicine specialists with knee or calf pain, rather than to neurologists [3–6]. Recognition of a proximal tibial neuropathy due to popliteus muscle rupture and distinguishing this disorder from more common causes of foot and leg symptoms, such as lumbosacral radiculopathies or sciatic neuropathies, is essential for appropriate management. We describe the clinical, electrodiagnostic and imaging features of a patient with a tibial neuropathy due to popliteus intramuscular hemorrhage.
A 54-year-old man with a history of a right L5 radiculopathy jumped a few feet onto a dock, hyperextending his right knee. He experienced immediate posterior knee and calf pain and the next day experienced sensory loss and weakness of his right foot. Neurologic examination 3 weeks later demonstrated severe weakness of flexion of his right toes with mild weakness of foot dorsiflexion, eversion, inversion, and plantar flexion, and an absent right Achilles reflex. Light touch and pinprick sensation were severely reduced at the bottom of the right foot and mildly decreased over the first and second toes. The right calf was mildly swollen. Electrodiagnostic studies demonstrated absent tibial motor and medial plantar sensory responses on the right and a large degree of fibrillation potentials with either no voluntary activation or severely reduced recruitment in right tibial innervated muscles distal to the medial gastrocnemius, consistent with a severe, subacute proximal right tibial neuropathy. There were also findings of a chronic right L5 radiculopathy. MRI of the right lower extremity showed a thickened popliteus muscle with signal abnormality rep-
⇑ Corresponding author. Tel.: +1 904 953 7104; fax: +1 904 953 0757. E-mail address: [email protected] (E.L. Dimberg).
