Книги по МРТ КТ на английском языке / Neurosurgery Fundamentals Agarval 1 ed 2019

[22]Fager CA. Posterolateral approach to ruptured median and paramedian cervical disk. Surg Neurol. 1983; 20(6):443–452

[23]Fager CA. Rationale and techniques of posterior approaches to cervical disk lesions and spondylosis. Surg Clin North Am. 1976; 56(3):581–592

[24]Ghogawala Z, Benzel EC, Heary RF, et al. Cervical spondylotic myelopathy surgical trial: randomized, controlled trial design and rationale. Neurosurgery. 2014; 75(4):334–46

[25]Saavedra-Pozo FM, Deusdara RA, Benzel EC. Adjacent segment disease perspective and review of the literature. Ochsner J. 2014; 14(1):78–83

[26]Wilkinson M. The morbid anatomy of cervical spondylosis and myelopathy. Brain. 1960; 83:589–617

[27]Hoff JT, Wilson CB. The pathophysiology of cervical spondylotic radiculopathy and myelopathy. Clin Neurosurg. 1977; 24:474–487

[28]Parke WW. Correlative anatomy of cervical spondylotic myelopathy. Spine. 1988; 13(7):831–837

[29]Rao RD, Gourab K, David KS. Operative treatment of cervical spondylotic myelopathy. J Bone Joint Surg Am. 2006; 88(7):1619–1640

[30]Dodge HJ, Mikkelsen WM, Duff IF. Age-sex specific prevalence of radiographic abnormalities of the joints of the hands, wrists and cervical spine of adult residents of the Tecumseh, Michigan, Community Health Study area, 1962–1965.

J Chronic Dis. 1970; 23(3):151–159

[31]Dunlop RB, Adams MA, Hutton WC. Disc space narrowing and the lumbar facet joints. J Bone Joint Surg Br. 1984; 66(5):706–710

[32]Gellhorn AC, Katz JN, Suri P. Osteoarthritis of the spine: the facet joints. Nat Rev Rheumatol. 2013; 9(4):216–224

[33]Adams MA, Hutton WC. The mechanical function of the lumbar apophyseal joints. Spine. 1983; 8(3):327–330

[34]Kalichman L, Hodges P, Li L, Guermazi A, Hunter DJ. Changes in paraspinal muscles and their association with low back pain and spinal degeneration: CT study. Eur Spine J. 2010; 19(7):1136–1144

[35]Jiang SD, Jiang LS, Dai LY. Degenerative cervical spondylolisthesis: a systematic review. Int Orthop. 2011; 35(6):869–875

[36]Hechelhammer L, Pfirrmann CW, Zanetti M, Hodler J, Boos N, Schmid MR. Imaging findings predicting the outcome of cervical facet joint blocks. Eur Radiol. 2007; 17(4):959–964

[37]Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns. I: A study in normal volunteers. Spine. 1990; 15(6):453–457

[38]Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns. II: A clinical evaluation. Spine. 1990; 15(6):458–461

[39]Inamasu J, Guiot BH, Sachs DC. Ossification of the posterior longitudinal ligament: an update on its biology, epidemiology, and natural history.

Neurosurgery. 2006; 58(6):1027–1039, discussion 1027–1039

[40]Choi BW, Song KJ, Chang H. Ossification of the posterior longitudinal ligament: a review of literature. Asian Spine J. 2011; 5(4):267–276

[41]Kudo H, Yokoyama T, Tsushima E, et al. Interobserver and intraobserver reliability of the classification and diagnosis for ossification of the posterior longitudinal ligament of the cervical spine. Eur Spine J. 2013; 22(1):205–210

[42]Abiola R, Rubery P, Mesfin A. Ossification of the

Posterior Longitudinal Ligament: Etiology, Diagnosis, and Outcomes of Nonoperative and Operative Management. Global Spine J. 2016; 6(2):195–204

[43]Chiba K, Yamamoto I, Hirabayashi H, et al. Multicenter study investigating the postopera- tive progression of ossification of the posterior longitudinal ligament in the cervical spine: a new computer-assisted measurement. J Neurosurg Spine. 2005; 3(1):17–23

[44]Matsunaga S, Sakou T, Taketomi E, Komiya S.

Clinical course of patients with ossification of the posterior longitudinal ligament: a minimum 10-year cohort study. J Neurosurg. 2004; 100

(3, Suppl Spine):245–248

[45]Li H, Dai LY. A systematic review of complications in cervical spine surgery for ossification of the posterior longitudinal ligament. Spine J. 2011; 11(11):1049–1057

[46]Stillerman CB, Chen TC, Couldwell WT, Zhang W, Weiss MH. Experience in the surgical management of 82 symptomatic herniated thoracic discs

and review of the literature. J Neurosurg. 1998; 88(4):623–633

[47]Wood KB, Garvey TA, Gundry C, Heithoff KB.

Magnetic resonance imaging of the thoracic spine. Evaluation of asymptomatic individuals. J Bone Joint Surg Am. 1995; 77(11):1631–1638

[48]Fernandez M, Gidvani SN. Thoracic Disc Herniation. In: Patel VV, Patel A, Harrop JS, Burger E, eds. Spine Surgery Basics. Springer-Verlag Berlin Heidelberg; 2014:193–201

[49]McCormick WE, Will SF, Benzel EC. Surgery for thoracic disc disease. Complication avoidance: overview and management. Neurosurg Focus. 2000; 9(4):e13

[50]Mulier S, Debois V. Thoracic disc herniations: transthoracic, lateral, or posterolateral approach? A review. Surg Neurol. 1998; 49(6):599–606, discussion 606–608

[51]Oskouian RJ, Johnson JP. Endoscopic thoracic microdiscectomy. Neurosurg Focus. 2005; 18(3):e11

[52]Hoy D, Bain C, Williams G, et al. A systematic review of the global prevalence of low back pain. Arthritis Rheum. 2012; 64(6):2028–2037

[53]Freburger JK, Holmes GM, Agans RP, et al. The rising prevalence of chronic low back pain. Arch Intern Med. 2009; 169(3):251–258

[54]From the Centers for Disease Control and Prevention. From the Centers for Disease Control and Prevention. Prevalence of disabilities and associated health conditions among adults—United States, 1999. JAMA. 2001; 285(12):1571–1572

[55]Katz JN. Lumbar disc disorders and low-back pain: socioeconomic factors and consequences. J Bone Joint Surg Am. 2006; 88(Suppl 2):21–24

[56]Duong LM, McCarthy BJ, McLendon RE, et al. Descriptive epidemiology of malignant and nonmalignant primary spinal cord, spinal

189

meninges, and cauda equina tumors, United States, 2004–2007. Cancer. 2012; 118(17):4220–4227

[57]Schellinger KA, Propp JM, Villano JL, McCarthy BJ. Descriptive epidemiology of primary spinal cord tumors. J Neurooncol. 2008; 87(2):173–179

[58]Nambiar M, Kavar B. Clinical presentation and outcome of patients with intradural spinal cord tumours. J Clin Neurosci. 2012; 19(2):262–266

[59]Mechtler LL, Nandigam K. Spinal cord tumors: new views and future directions. Neurol Clin. 2013; 31(1):241–268

[60]Vassiliou V, Papamichael D, Polyviou P, Koukouma A, Andreopoulos D. Intramedullary spinal cord metastasis in a patient with colon cancer: a case report. J Gastrointest Cancer. 2012; 43(2):370–372

[61]Tihan T, Chi JH, McCormick PC, Ames CP, Parsa

AT. Pathologic and epidemiologic findings of intramedullary spinal cord tumors. Neurosurg Clin N Am. 2006; 17(1):7–11

[62]Newton HB, Newton CL, Gatens C, Hebert R, Pack R. Spinal cord tumors: review of etiology, diagnosis, and multidisciplinary approach to treatment. Cancer Pract. 1995; 3(4):207–218

[63]White JB, Miller GM, Layton KF, Krauss WE. Nonenhancing tumors of the spinal cord. J Neurosurg Spine. 2007; 7(4):403–407

[64]Klekamp J. Spinal ependymomas. Part 1: Intramedullary ependymomas. Neurosurg Focus. 2015; 39(2):E6

[65]Wang H, Zhang S, Rehman SK, et al. Clinicopathological features of myxopapillary ependymoma. J Clin Neurosci. 2014; 21(4):569–573

[66]Milano MT, Johnson MD, Sul J, et al. Primary spinal cord glioma: a Surveillance, Epidemiology, and End Results database study. J Neurooncol. 2010; 98(1):83–92

[67]Nadkarni TD, Rekate HL. Pediatric intramedullary spinal cord tumors. Critical review of the literature. Childs Nerv Syst. 1999; 15(1):17–28

[68]Stein BM. Intramedullary spinal cord tumors. Clin Neurosurg. 1983; 30:717–741

[69]Halliday AL, Sobel RA, Martuza RL. Benign spinal nerve sheath tumors: their occurrence sporadically and in neurofibromatosis types 1 and 2.

J Neurosurg. 1991; 74(2):248–253

[70]Varma DG, Moulopoulos A, Sara AS, et al. MR imaging of extracranial nerve sheath tumors. J Comput Assist Tomogr. 1992; 16(3):448–453

[71]Levine E, Huntrakoon M, Wetzel LH. Malignant nerve-sheath neoplasms in neurofibromato- sis: distinction from benign tumors by using imaging techniques. AJR Am J Roentgenol. 1987; 149(5):1059–1064

[72]Safaee M, Parsa AT, Barbaro NM, et al. Association of tumor location, extent of resection, and neurofibromatosis status with clinical outcomes for 221 spinal nerve sheath tumors. Neurosurg Focus. 2015; 39(2):E5

[73]Balachandra SP, Aleem MA, Rajendran P, et al. Spinal meningioma with positive dural tail sign. Neurol India. 2002; 50(4):540

[74]Solero CL, Fornari M, Giombini S, et al. Spinal meningiomas: review of 174 operated cases. Neurosurgery. 1989; 25(2):153–160

190

[75]Raco A, Pesce A, Toccaceli G, Domenicucci M,

Miscusi M, Delfini R. Factors Leading to a Poor

Functional Outcome in Spinal Meningioma Surgery: Remarks on 173 Cases. Neurosurgery. 2017; 80(4):602–609

[76]Barron KD, Hirano A, Araki S, Terry RD. Experiences with metastatic neoplasms involving the spinal cord. Neurology. 1959; 9(2):91–106

[77]Yáñez ML, Miller JJ, Batchelor TT. Diagnosis and treatment of epidural metastases. Cancer. 2017; 123(7):1106–1114

[78]Chamberlain MC. Neoplastic meningitis and meta­ static epidural spinal cord compression. Hematol Oncol Clin North Am. 2012; 26(4):917–931

[79]Cole JS, Patchell RA. Metastatic epidural spinal cord compression. Lancet Neurol. 2008; 7(5):459–466

[80]Greenberg HS, Kim JH, Posner JB. Epidural spinal cord compression from metastatic tumor: results with a new treatment protocol. Ann Neurol. 1980; 8(4):361–366

[81]Ibrahim A, Crockard A, Antonietti P, et al. Does spinal surgery improve the quality of life for those with extradural (spinal) osseous metastases? An international multicenter prospective observational study of 223 patients. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2007. J Neurosurg Spine. 2008; 8(3):271–278

[82]Steinmetz MP, Mekhail A, Benzel EC. Management of metastatic tumors of the spine: strategies and operative indications. Neurosurg Focus. 2001; 11(6):e2

[83]Fisher CG, DiPaola CP, Ryken TC, et al. A novel classification system for spinal instability in neoplastic disease: an evidence-based approach and expert consensus from the Spine Oncology Study Group. Spine. 2010; 35(22):E1221–E1229

[84]Patsalides A, Santillan A, Knopman J, Tsiouris AJ, Riina HA, Gobin YP. Endovascular management of spinal dural arteriovenous fistulas. J Neurointerv

Surg. 2011; 3(1):80–84

[85]Strugar J, Chyatte D. In situ photocoagulation of spinal dural arteriovenous malformations using the Nd:YAG laser. J Neurosurg. 1992; 77(4):

571–574

[86]Rosenblum B, Oldfield EH, Doppman JL, Di

Chiro G. Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM’s in 81 patients. J Neurosurg. 1987; 67(6):795–802

[87]Flores BC, Klinger DR, White JA, Batjer HH. Spinal vascular malformations: treatment strategies and outcome. Neurosurg Rev. 2017; 40(1):15–28

[88]Anson JA, Spetzler RF. Interventional neuroradiology for spinal pathology. Clin Neurosurg. 1992; 39:388–417

[89]Gross BA, Du R, Popp AJ, Day AL. Intramedullary spinal cord cavernous malformations. Neurosurg Focus. 2010; 29(3):E14

[90]McCormick PC, Michelsen WJ, Post KD, Carmel PW, Stein BM. Cavernous malformations of the spinal cord. Neurosurgery. 1988; 23(4):459–463

[91]Sandalcioglu IE, Wiedemayer H, Gasser T, Asgari S, Engelhorn T, Stolke D. Intramedullary spinal

cord cavernous malformations: clinical features and risk of hemorrhage. Neurosurg Rev. 2003; 26(4):253–256

[92]El-Koussy M, Stepper F, Spreng A, et al. Incidence, clinical presentation and imaging findings of cavernous malformations of the CNS. A twentyyear experience. Swiss Med Wkly. 2011; 141: w13172

[93]Ogilvy CS, Louis DN, Ojemann RG. Intramedullary cavernous angiomas of the spinal cord: clinical presentation, pathological features, and surgical management. Neurosurgery. 1992; 31(2):219–229, discussion 229–230

[94]Badhiwala JH, Farrokhyar F, Alhazzani W, et al. Surgical outcomes and natural history of intra­ medullary spinal cord cavernous malformations: a single-center series and meta-analysis of individual patient data: Clinic article. J Neurosurg Spine. 2014; 21(4):662–676

[95]Reitz M, Burkhardt T, Vettorazzi E, et al. Intramedullary spinal cavernoma: clinical presentation, microsurgical approach, and long-term outcome in a cohort of 48 patients. Neurosurg Focus. 2015; 39(2):E19

[96]Choi GH, Kim KN, Lee S, et al. The clinical features and surgical outcomes of patients with intramedullary spinal cord cavernous malformations. Acta Neurochir (Wien). 2011; 153(8):1677–1684, discussion 1685

[97]Schlenk RP, Kowalski RJ, Benzel EC. Biomechanics of spinal deformity. Neurosurg Focus. 2003; 14(1):e2

[98]Bernhardt M, Bridwell KH. Segmental analysis of the sagittal plane alignment of the normal thoracic and lumbar spines and thoracolumbar junction. Spine. 1989; 14(7):717–721

[99]Heary RF, Kumar S, Bono CM. Decision making in adult deformity. Neurosurgery. 2008; 63

(3, Suppl):69–77

[100]Moe JH, Lonstein JE. Moe's textbook of scoliosis and other spinal deformities. 3rd ed. Philadelphia: W.B. Saunders; 1995

[101]Roussouly P, Nnadi C. Sagittal plane deformity: an overview of interpretation and management. Eur Spine J. 2010; 19(11):1824–1836

[102]Kim H, Kim HS, Moon ES, et al. Scoliosis imaging: what radiologists should know. Radiographics. 2010; 30(7):1823–1842

[103]Potter BK, Rosner MK, Lehman RA, Jr, Polly DW, Jr, Schroeder TM, Kuklo TR. Reliability of end, neutral, and stable vertebrae identification in adolescent idiopathic scoliosis. Spine. 2005; 30(14): 1658–1663

[104]Schwab FJ, Blondel B, Bess S, et al; International Spine Study Group (ISSG). Radiographical spinopelvic parameters and disability in the setting of adult spinal deformity: a prospective multicenter analysis. Spine. 2013; 38(13):E803–E812

[105]Palazzo C, Sailhan F, Revel M. Scheuermann’s disease: an update. Joint Bone Spine. 2014; 81(3):209–214

[106]Bradford DS, Moe JH. Scheuermann’s juvenile kyphosis. A histologic study. Clin Orthop Relat Res. 1975(110):45–53

[107]Bradford DS, Ganjavian S, Antonious D, Winter RB, Lonstein JE, Moe JH. Anterior strut-grafting for the treatment of kyphosis. Review of experience with forty-eight patients. J Bone Joint Surg Am. 1982; 64(5):680–690

[108]Bradford DS, Moe JH, Montalvo FJ, Winter RB. Scheuermann’s kyphosis. Results of surgical treatment by posterior spine arthrodesis in twenty-two patients. J Bone Joint Surg Am. 1975; 57(4):439–448

[109]Chun SW, Lim CY, Kim K, Hwang J, Chung SG. The relationships between low back pain and lumbar lordosis: a systematic review and meta-analysis. Spine J. 2017; 17(8):1180–1191

[110]James JI. Idiopathic scoliosis; the prognosis, diagnosis, and operative indications related to curve patterns and the age at onset. J Bone Joint Surg Br. 1954; 36-B(1):36–49

[111]Silva FE, Lenke LG. Adult degenerative scoliosis: evaluation and management. Neurosurg Focus. 2010; 28(3):E1

[112]Cobb JR. Scoliosis; quo vadis. J Bone Joint Surg Am. 1958; 40-A(3):507–510

[113]Stokes IA. Mechanical effects on skeletal growth.

J Musculoskelet Neuronal Interact. 2002; 2(3):277–280

[114]Parent S, Labelle H, Skalli W, de Guise J. Thoracic pedicle morphometry in vertebrae from scoliotic spines. Spine. 2004; 29(3):239–248

[115]Robinson CM, McMaster MJ. Juvenile idiopathic scoliosis. Curve patterns and prognosis in one hundred and nine patients. J Bone Joint Surg Am. 1996; 78(8):1140–1148

[116]Lenke LG, Betz RR, Harms J, et al. Adolescent idiopathic scoliosis: a new classification to determine extent of spinal arthrodesis. J Bone Joint Surg Am. 2001; 83-A(8):1169–1181

[117]Dubousset J, Herring JA, Shufflebarger H. The crankshaft phenomenon. J Pediatr Orthop. 1989; 9(5):541–550

[118]Hamill CL, Bridwell KH, Lenke LG, Chapman MP, Baldus C, Blanke K. Posterior arthrodesis in the skeletally immature patient. Assessing the risk for crankshaft: is an open triradiate cartilage the answer? Spine. 1997; 22(12):1343–1351

[119]Shufflebarger HL, Clark CE. Prevention of the crankshaft phenomenon. Spine. 1991; 16(8, Suppl):S409–S411

[120]Pritchett JW, Bortel DT. Degenerative symptomatic lumbar scoliosis. Spine. 1993; 18(6):700–703

[121]Errico TJ, Lonner BS, Moulton AW. Surgical management of spinal deformities. Philadelphia, PA: Saunders/Elsevier; 2009: https://www. clinicalkey.com/dura/browse/bookChapter/ 3-s2.0-B9781416033721X5001X

[122]Passalent LA, Soever LJ, O’Shea FD, Inman RD. Exercise in ankylosing spondylitis: discrepancies between recommendations and reality.

J Rheumatol. 2010; 37(4):835–841

[123]Jones SD, Koh WH, Steiner A, Garrett SL, Calin A. Fatigue in ankylosing spondylitis: its

prevalence and relationship to disease activity, sleep, and other factors. J Rheumatol. 1996; 23(3):487–490

191

[124]van der Linden S, van der Heijde D. Ankylosing spondylitis. Clinical features. Rheum Dis Clin North Am. 1998; 24(4):663–676, vii

[125]van der Heijde D, Spoorenberg A. Plain radiographs as an outcome measure in ankylosing spondylitis. J Rheumatol. 1999; 26(4):985–987

[126]Vinson EN, Major NM. MR imaging of ankylosing spondylitis. Semin Musculoskelet Radiol. 2003; 7(2):103–113

[127]Geijer M, Göthlin GG, Göthlin JH. The clinical utility of computed tomography compared to conventional radiography in diagnosing sacroiliitis. A retrospective study on 910 patients and literature review. J Rheumatol. 2007; 34(7):1561–1565

[128]Van Royen BJ, De Gast A. Lumbar osteotomy for correction of thoracolumbar kyphotic deformity in ankylosing spondylitis. A structured review of three methods of treatment. Ann Rheum Dis. 1999; 58(7):399–406

[129]Min K, Hahn F, Leonardi M. Lumbar spinal osteotomy for kyphosis in ankylosing spondylitis: the significance of the whole body kyphosis angle.

J Spinal Disord Tech. 2007; 20(2):149–153

[130]Bland JH. Rheumatoid arthritis of the cervical spine. Bull Rheum Dis. 1967; 18(2):471–476

[131]Morizono Y, Sakou T, Kawaida H. Upper cervical involvement in rheumatoid arthritis. Spine. 1987; 12(8):721–725

[132]Menezes AH, VanGilder JC, Clark CR, el-Khoury G. Odontoid upward migration in rheumatoid arthritis. An analysis of 45 patients with “cranial settling”. J Neurosurg. 1985; 63(4):500–509

[133]Rajangam K, Thomas IM. Frequency of cervical spine involvement in rheumatoid arthritis. J Indian Med Assoc. 1995; 93(4):138–139, 137

[134]Ranawat CS, O’Leary P, Pellicci P, Tsairis P, Marchisello P, Dorr L. Cervical spine fusion in rheumatoid arthritis. J Bone Joint Surg Am. 1979; 61(7):1003–1010

[135]Schmitt-Sody M, Kirchhoff C, Buhmann S, et al.

Timing of cervical spine stabilisation and outcome in patients with rheumatoid arthritis. Int Orthop. 2008; 32(4):511–516

[136]Prendergast H, Jerrard D, O’Connell J. Atypical presentations of epidural abscess in intravenous drug abusers. Am J Emerg Med. 1997; 15(2): 158–160

[137]Joshi SM, Hatfield RH, Martin J, Taylor W. Spinal epidural abscess: a diagnostic challenge. Br J Neurosurg. 2003; 17(2):160–163

[138]Darouiche RO. Spinal epidural abscess and subdural empyema. Handb Clin Neurol. 2010; 96:91–99

[139]Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006; 355(19):2012–2020

[140]Arko L, IV, Quach E, Nguyen V, Chang D, Sukul V, Kim BS. Medical and surgical management of spinal epidural abscess: a systematic review. Neurosurg Focus. 2014; 37(2):E4

[141]Siddiq F, Chowfin A, Tight R, Sahmoun AE,

Smego RA, Jr. Medical vs surgical management of spinal epidural abscess. Arch Intern Med. 2004; 164(22):2409–2412

[142]Mylona E, Samarkos M, Kakalou E, Fanourgiakis P, Skoutelis A. Pyogenic vertebral osteomyelitis: a

192

systematic review of clinical characteristics. Semin Arthritis Rheum. 2009; 39(1):10–17

[143]Balériaux DL, Neugroschl C. Spinal and spinal cord infection. Eur Radiol. 2004; 14(Suppl 3):E72–E83

[144]Grados F, Lescure FX, Senneville E, Flipo RM, Schmit JL, Fardellone P. Suggestions for managing pyogenic (non-tuberculous) discitis in adults. Joint Bone Spine. 2007; 74(2):133–139

[145]Watt JP, Davis JH. Percutaneous core needle biopsies: the yield in spinal tuberculosis. S Afr Med

J.2013; 104(1):29–32

[146]Jung NY, Jee WH, Ha KY, Park CK, Byun JY. Discrimination of tuberculous spondylitis from pyogenic spondylitis on MRI. AJR Am J Roentgenol. 2004; 182(6):1405–1410

[147]Zhang X, Ji J, Liu B. Management of spinal tuberculosis: a systematic review and metaanalysis. J Int Med Res. 2013; 41(5):1395–1407

[148]Mauffrey C, Randhawa K, Lewis C, Brewster M,

Dabke H. Cauda equina syndrome: an anatomically driven review. Br J Hosp Med (Lond). 2008; 69(6): 344–347

[149]Rogers WK, Todd M. Acute spinal cord injury. Best Pract Res Clin Anaesthesiol. 2016; 30(1):27–39

[150]Kingwell SP, Curt A, Dvorak MF. Factors affecting neurological outcome in traumatic conus medullaris and cauda equina injuries. Neurosurg Focus. 2008; 25(5):E7

[151]Aly TA, Aboramadan MO. Efficacy of delayed decompression of lumbar disk herniation causing cauda equina syndrome. Orthopedics. 2014; 37(2):e153–e156

[152]Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus. 2004; 16(6):e3

[153]Raj D, Coleman N. Cauda equina syndrome secondary to lumbar disc herniation. Acta Orthop Belg. 2008; 74(4):522–527

[154]Rege SV, Narayan S, Patil H, Songara A. Spinal myxopapillary ependymoma with interval drop metastasis presenting as cauda equina syndrome: case report and review of literature. J Spine Surg. 2016; 2(3):216–221

[155]Wierzbicki V, Pesce A, Marrocco L, Piccione E, Frati A, Caruso R. Ancient Schwannoma of the Cauda Equina: Our Experience and Review of the Literature. Case Rep Surg. 2016; 2016:7930521

[156]Gelabert-González M, Pita-Buezas L, Arán-Echabe

E.Paraganglioma of the cauda equina. Korean J Spine. 2015; 12(1):29

[157]Bell DA, Collie D, Statham PF. Cauda equina syndrome: what is the correlation between clinical assessment and MRI scanning? Br J Neurosurg. 2007; 21(2):201–203

[158]McCarthy MJ, Aylott CE, Grevitt MP, Hegarty J.

Cauda equina syndrome: factors affecting long- term functional and sphincteric outcome. Spine. 2007; 32(2):207–216

[159]Thomson S. Failed back surgery syndrome — definition, epidemiology and demographics.

Br J Pain. 2013; 7(1):56–59

[160]Tharmanathan P, Adamson J, Ashby R, Eldabe S. Diagnosis and treatment of failed back surgery syndrome in the UK: mapping of practice

using a cross-sectional survey. Br J Pain. 2012; 6(4):142–152

[161]Jalai CM, Wang C, Marascalchi BJ, et al. Trends in the presentation, surgical treatment, and outcomes of tethered cord syndrome: A nationwide study from 2001 to 2010. J Clin Neurosci. 2017; 41:92–97

[162]Filippi CG, Andrews T, Gonyea JV, Linnell G, Cauley

KA. Magnetic resonance diffusion tensor imaging and tractography of the lower spinal cord:

application to diastematomyelia and tethered cord. Eur Radiol. 2010; 20(9):2194–2199

[163]Iskandar BJ, Fulmer BB, Hadley MN, Oakes WJ. Congenital tethered spinal cord syndrome in adults. Neurosurg Focus. 2001; 10(1):e7

[164]Kokubun S, Ozawa H, Aizawa T, Ly NM, Tanaka Y. Spine-shortening osteotomy for patients with tethered cord syndrome caused by lipomyelomeningocele. J Neurosurg Spine. 2011; 15(1):21–27

11  Pain

James Mooney, Charles Munyon

11.1  Pathway Anatomy

Nociception is the process by which information about actual or potential tissue damage is relayed to the brain.

11.1.1  Peripheral Nerves

Peripherally, nociception is mediated by specialized free nerve ending receptors known as nociceptors that are attached to thin myelinated (fast) Aδ and unmyelinated

(slow) C fibers. Specific nociceptors respond to noxious stimuli including thermal, mechanical, and chemical. Polymodal neurons respond to multiple types of stimuli.

axons to the spinal cord through the dorsolateral tract of Lissauer and terminate near second-order nerve cells in the substantia gelatinosa of the dorsal horn.1 Second-order neurons give rise to axons that decussate in the ventral white commissure and ascend in one of two contralateral funiculi. Second-or- der wide dynamic range neurons have cell bodies in the dorsal horn of the spinal cord and respond to all somatosensory modalities in a broad range of intensity of stimulation. All second-order pain neurons ultimately ascend in the anterolateral quadrant of the spinal cord either in the direct lateral spinothalamic pathway or the indirect medial spinoreticulothalamic pathway ( Fig. 11.2).

11.1.2  Spinal Cord

The gray matter of the spinal cord is divided into Rexed’s laminae, which progress from posterior to anterior ( Fig. 11.1). Lamina I–III are known as the “substantia gelatinosa.” Laminae IV and V include the neurons that give rise to the spinothalamic tract. In the spinal cord, primary afferent nociceptors project

11.1.3  Thalamic and Cortical

Neurons in the ventrocaudal thalamus receive nociceptive inputs directly from projecting spinal neurons, and project directly to the somatosensory cortex. Neurons in the medial thalamus receive some indirect input from the spinal cord, but the major input is from the region of the

brainstem reticular formation to which the spinoreticular neurons project. The medial thalamus projects to widespread areas of the forebrain, including the anterior cingulate and somatosensory cortices.2

The lateral pathway is likely responsible primarily for localization and characterization of noxious stimuli while the medial spinoreticulothalamic pathway may modulate the affective and motivational aspects of pain.

11.1.4  Gate Control Theory

The gate control theory of pain, proposed in 1965 by Melzack and Wall,3 asserts that

benign stimuli close the “gates” to painful stimuli, preventing pain from traveling to the brain. The theory requires that the passage of painful impulses via unmyelinated

(C) and small myelinated (δ) fibers should be slowed or abolished by simultaneous input into the larger myelinated Aβ nerve fibers (responding to touch, pressure, and vibration).

Therefore, stimulation by non-noxious input is able to suppress pain.

This theory reconciled earlier specificity and pattern theories of pain ( Fig. 11.3).

Fig. 11.3  Gate control theory of pain. (a) The firing of the projection neuron determines pain. The inhibitory interneuron decreases the chances that the projection neuron will fire. Firing of C fibers inhibits the inhibitory interneuron (indirectly), increasing the chances that the projection neuron will fire. Inhibition is represented in blue, and excitation in yellow. A green circle signifies increased neuron activation, while a red crossed-out circle signifies weakened or reduced activation. (b) Firing of the Aβ fibers activates the inhibitory interneuron, reducing the chances that the projection neuron will fire, even in the presence of a firing nociceptive fiber. (Illustration by Zhu Xiao.)

11.2  Major Types of Pain

11.2.1  Nociceptive

This most common type of pain transmits information about injury or inflammation via small diameter afferent nerve fibers (δ or “pain” fibers).

It corresponds to an actual stimulus, and generally lessens with time and healing.

•Somatic: Well localized. Results from tissue injury, inflammation, or nerve/ plexus compression. Responds to treatment of underlying pathology or inhibition of nociceptive transmission by analgesic or anesthetic medications.

•Visceral: Poorly localized. Arises due to direct stimulation of afferent nerves due to tissue injury, inflammation, or

compression of the soft tissue or viscera. Lesser response to analgesic medications.

•“Sympathetically maintained”/Causalgia/Complex regional pain syndrome (CRPS): All categorized by irregularities in autonomic nervous system function. See section 11.3.5 for further details.

•Neuromas: A neuroma is a disorganized growth of nerve cells at the site of a nerve injury (secondary to trauma or surgery). It can be a ball-shaped terminal stump in the case of nerve transection, or a neuroma “in continuity” in case of injury that has disrupted the axons but not the perineurium. It will typically cause pain or paresthesias when palpated or percussed.

•Other: Etiologies may also include alcoholic and chemotherapy induced polyneuropathies, entrapment neuropathies, HIV sensory neuropathy, neoplastic nerve compression, nutritional deficiency, postradiation, toxic exposure, post-traumatic, cervical spondylotic, multiple sclerosis/Parkinson disease, and post-stroke etiologies.

11.2.2  Neuropathic

Neuropathic pain is caused by a lesion of the peripheral and/or central nervous system, resulting in a sensation of pain that does not correspond to an actual stimulus.

Examples include painful diabetic neuropathy (PDN) and postherpetic neuralgia (PHN). It is typically burning, aching, continuous and frequently refractory to medical and surgical treatment. It is often chronic and can worsen with time.

•Deafferentation: Interruption of sensory conduction via damage to large diameter sensory nerve fibers (mediating touch and pressure sense) can alter upstream firing patterns, leading to pain in an area that is otherwise insensate. This pain is often described as crushing, tearing, or tingling.

Medical Treatment

In contrast to nociceptive pain that primarily involves non-narcotic and opioid analgesia, the initial treatment for neuropathic pain typically involves either antidepressants (tricyclics,­ selective serotonin reuptake ­inhibitors/serotonin and norepinephrine reuptake inhibitors) or calcium channel ligands (gabapentin/pregabalin)­

with adjunctive topical therapy (lidocaine). Opioids should be considered as a second-line option.4

11.3  Craniofacial Pain Syndromes

11.3.1  Trigeminal Neuralgia

This is also known as tic douloureux. A pain disorder that affects the trigeminal nerve.

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There are two main types:

•Typical: Results in episodes of severe, sudden, shock-like pain in one side of the face that lasts for seconds to a few minutes. Groups of episodes can occur over a few hours.

•Atypical: Results in a constant burning pain that is less severe. Episodes may be triggered by any sensory stimulus to the face.

More recently, attempts have been made to classify trigeminal neuralgia (TN) primarily based on patient history5:

•Type 1: Spontaneous onset with more than 50% predominant episodic pain.

•Type 2: Spontaneous onset with more than 50% constant pain.

Pathophysiology

The most common causes are vascular compression of the trigeminal nerve at the root entry zone (80% by the superior cerebellar artery, Fig. 11.4),6,​7,​8 a posterior fossa tumor with nerve compression, or a multiple sclerosis (MS) plaque within the brainstem. The common mechanism is demyelination leading to abnormal (ephaptic) transmission of benign sensory stimuli through the poorly myelinated Aδ and C type pain fibers.

Signs and Symptoms

The primary symptom is paroxysmal pain, generally lasting for a few seconds, that is isolated to the distribution of one or more branches of the trigeminal nerve unilaterally. This pain may be triggered by benign sensory stimuli to a specific area of the face, and is often shock-like or stabbing; no neurologic deficit is associated with this pain. When pain occurs as tic-like spasms in rapid succession, it is known as status trigeminus.

Diagnosis

Diagnosis is made by clinical history, after ruling out other major causes of facial pain such as dental disease, disease of the orbit

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Fig. 11.4  MRI axial T1 image with contrast at the level of the mid pons showing an aberrant loop of the superior cerebellar artery (red arrow) impinging on the root of the trigeminal nerve. The patient presented with clinical symptoms of trigeminal neuralgia.(Reproduced from Gasco J, Nader R, The Essential Neurosurgery Companion, 1st edition, ©2012, Thieme Publishers, New York.)

or sinuses, temporal arteritis, tumor, and herpes zoster. The history must include the distribution and character of the pain as well as localizing the involved division(s) of the trigeminal nerve. The pain is characteristically paroxysmal, with pain free intervals; constant pain should prompt consideration of other diagnoses.

The neurologic examination should be normal unless the patient has undergone microvascular decompression or nerve ablation (see below), in which case there may be decreased sensation or even associated dysfunction of cranial nerves VII and VIII. Noniatrogenic neurologic deficit suggests a brain tumor or other lesion (neurosarcoidosis, demyelinating plaque, etc.). Tests of trigeminal nerve function include the corneal reflex, assessment of facial sensation to all modalities in all three divisions of the