Transcription
pdf
MR Imaging of Plexopathies Revisited Poster No.: C-0221 Congress: ECR 2011 Type: Educational Exhibit Authors: R. M. S. V. Vadapalli, M. AK; Hyderabad, AP/IN Keywords: Inflammation, Edema, Imaging sequences, Education, MR, Neuroradiology peripheral nerve DOI: 10.1594/ecr2011/C-0221 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. www.myESR.org Page 1 of 67 Learning objectives 1.To discuss cardinal MR Imaging a Plexopathy 2.To illustrate vaious etiologies for brachial and lumbar plexopathies with clinical examples. 3.Immune mediated plexopathies like CIDP,MMN,MADSAM which are plexo neuropathies are hgihlighted with illustrative examples. Background The pathologic basis and histologic changes seen with brachial plexus lesions vary with the underlying cause, which include compression, transection, ischemia, inflammation, metabolic abnormalities, neoplasia, and radiation therapy. Causes of Brachial Plexopathies wide range of disease processes that may cause a brachial plexopathy, radiation fibrosis, primary and metastatic lung cancer, and metastatic breast cancer account for almost three-fourths of the causes. Radiation fibrosis, the common cause, may occur several months to years after the completion of therapy. Findings of radiation fibrosis include (a) thickening and diffuse enhancement of the brachial plexus without a focal mass and (b) soft-tissue changes with low signal intensity on both T1- and T2-weighted images. Superior sullcus tumors at the lung apex may invade the lower portion of the brachial plexus. Many tumors may metastasize to the brachial plexus, causing a brachial plexopathy. Breast cancer is the most likely to metastasize becausemajor lymphatic drainage routes for the breast course through Page 2 of 67 Radiation fibrosis Breast cancer Lung cancer Benign tumors Lymphangioma Desmoid Neurofibroma Lipoma Other malignant tumors Neurofibrosarcoma Ewing sarcoma Eccrine sarcoma Osteosarcoma Auto immune/Immune mediated Plexopathies CIDP(chronic inflammatory demyelinating polyneuropathy) The symptoms and signs of CIDP may be asymmetrical initially and have ascending involvements. progresses slowly to symmetric weakness, loss of deep tendon reflex, and impaired sensation in hands and feet. Antecedent infections can be identified far less regularly in patients with CIDP than those with acute inflammatory demyelinating polyneuropathy (AIDP). Page 3 of 67 Elevated concentration of CSF protein and evidence of demyelination on electrodiagnostic examination are found in most patients with CIDP. The pathophysiology of CIDP is still unclear, but an autoimmune mechanism is proposed due to the likely responsiveness of immune modulating treatments of CIDP.The efficacy of corticosteroids plasma exchange and IVIg MMN (multifocal motor neuropathy) In contrast to CIDP, multifocal motor neuropathy (MMN) shows an asymmetrical weakness and muscle atrophy, typically in the distribution of individual peripheral nerves without sensory involvement. MMN with a clinical picture of mononeuritis multiplex and electrophysiologic evidence of persistent motor conduction block (MCB) is considered an acquired immune-mediated demyelinating motor polyneuropathy. The diagnosis of MMN usually relies on the presence of MCBs. High titers of anti-GM1 antibodies are often detected in the serum of patients with MMN.IVIg and cyclophosphamide are effective treatment for the majority of patients with MMN. The major features that separate MADSAM neuropathy from Page 4 of 67 typical CIDP are the electrophysiological findings and favorable responses to plasma exchange, prednisone, or IVIg. Similar to CIDP, CSF protein content is increased in 60-80% of patients with MADSAM neuropathy. On the other hand, polyclonal IgM antibodies against GM1 may be detected in 40-80% of MMN patients, but difficult to detect in CIDP and MADSAM neuropathy MADSAM Neuropathy Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is characterized by an asymmetric multifocal pattern of motor and sensory loss, and conduction block and other features of demyelination in nerve conduction studies. MADSAM neuropathy needs to be differentiated from chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). In classic CIDP, there are symmetric proximal and distal weakness, sensory deficit in both upper and lower extremities and reduced deep tendon reflex(2). In MMN, limb weakness without sensory loss is asymmetric in the distribution of individual peripheral nerves and the weakness typically begins in the distal upper extremities. It is very important to distinguish between CIDP, MADSAM neuropathy, and MMN by clinical, laboratory, and histological features because of different effective therapeutic strategies. EMNG findings of CIDP,MMN,MADSAM In MADSAM neuropathy, MMN, and CIDP, the nerve conduction studies show features of demyelination, such as conduction block, temporal dispersion, prolonged distal latencies, slow conduction velocities, and Page 5 of 67 absent or prolonged F-wave latencies in one or more motor nerves .MADSAM neuropathy is different from MMN due to sensory nerves are involved and different from CIDP due to conspicuous asymmetric multiple nerves involvement. Lumbar Plexopathies Diabetic Plexopathy Diabetic plexopathy typically affects the lumbosacral plexus more than a brachial. It is distinguished from a peripheral polyneuropathy of long-standing diabetes by its predominantly proximal symptoms. . Diagnosis is therefore based on presentation, presence of diabetes, and the presence of acute electrodiagnostic findings to be discussed later. Traumatic Plexopathy . Fractures or dislocations of the hip joint can produce traction injuries to the lumbosacral plexus. Surgical intervention is imminent and requires initial periods of immobilization post-operatively. The initial lesions can slowly recover during the post-operative rehabilitation. Hemorrhagic Plexopathy Hemorrhagic plexopathy is usually caused in the retroperitoneal region, which can compress on the plexus as it passes through either the iliac or psoas muscles. An expanding hematoma within the more laterally located iliopsoas muscle can cause local compression of the femoral nerve at the point along its course from its origin to the inguinal ligament. A hemorrhagic plexopathy presents with severe groin pain radiating to the anterior medial thigh and saphenous nerve territory. . Neoplastic Plexopathy Neoplastic plexopathy lesions originating in the pubic regions can invade the lumbosacral plexus by direct expansion. The most common is a colorectal carcinoma., uterine, prostatic, and ovarian tumors ,.Metastatic invasions of the retroperitoneum and the lumbosacral plexus by breast, thyroid, testicular cancers, lymphomas, myelomas, and melanomas are also well known. Patients with neurofibromatosis can develop grossly Page 6 of 67 huge tumors involving any compartment of the plexus. Neoplastic plexopathies generally present with unilateral pelvic pain and, when progressive, show lower motor neuron signs. Radiation-Induced Lumbosacral Plexopathy Radiation-induced lumbosacral plexopathy is similar to that affecting the brachial plexus. Onset is difficult to determine, occurring from one to 31 years after radiation. Patients receiving an external beam or internal cavity radiation are equally susceptible. Patients generally present with slowly progressive, bilateral lower extremity weakness that tends to affect the distal muscles more. Paresthesia and numbness are less frequently reported in the initial symptoms. Images for this section: Fig. 1: MADSAM Neuropathy:EMNG In MADSAM neuropathy, MMN, and CIDP, the nerve conduction studies show features of demyelination, such as conduction block, temporal dispersion, prolonged distal latencies, slow conduction velocities, and absent or prolonged F-wave latencies in one or more motor nerves .MADSAM neuropathy is Page 7 of 67 different from MMN due to sensory nerves are involved and different from CIDP due to conspicuous asymmetric multiple nerves involvement. Fig. 2: MADSAM Neuropathy:EMNG Page 8 of 67 Fig. 3: MADSAM Neuropathy:EMNG Page 9 of 67 Fig. 4: MADSAM Neuropathy:EMNG Page 10 of 67 Fig. 5: MADSAM Neuropathy:EMNG Page 11 of 67 Fig. 6: CIDP Neuropathy:EMNG Page 12 of 67 Fig. 7: CIDP Neuropathy:EMNG Page 13 of 67 Fig. 8: CIDP Neuropathy:EMNG Page 14 of 67 Fig. 9: CIDP Neuropathy:EMNG Page 15 of 67 Fig. 10: In MADSAM neuropathy, MMN, and CIDP, the nerve conduction studies show features of demyelination, such as conduction block, temporal dispersion, prolonged distal latencies, slow conduction velocities, and absent or prolonged F-wave latencies in one or more motor nerves .MADSAM neuropathy is different from MMN due to sensory nerves are involved and different from CIDP due to conspicuous asymmetric multiple nerves involvement. Page 16 of 67 Fig. 11: MADSAM Neuropathy:EMNG Page 17 of 67 Fig. 12: MADSAM Neuropathy:EMNG Page 18 of 67 Fig. 13: MADSAM Neuropathy:EMNG Page 19 of 67 Fig. 14: CIDP Neuropathy:EMNG Page 20 of 67 Fig. 15: Nerve Biopsy :Inflammatory neuropathy:Sarcoid Page 21 of 67 Fig. 16: Nerve Biopsy :Inflammatory neuropathy:Sarcoid Page 22 of 67 Fig. 17: Nerve Biopsy :Inflammatory neuropathy:Sarcoid Page 23 of 67 Fig. 18: Nerve Biopsy :Inflammatory neuropathy:Sarcoid Page 24 of 67 Imaging findings OR Procedure details Cardinal MR Imaging features of a Plexopathy .Thickening of plexus .pre ganglionic,ganglionic or post ganglionic segments of the nerve Root, trunks and divisions is Present . can be symmetrical(CIDP),Asymmetrical (MMN,MADSAM) .Inflammation and fibrosis secondary to Radiation can occur .Loss of Normal inter neural bundle fat planes .Clumping and crowdin of roots and trunks .T2 and STIR hyper intensity with nerve edema/Gliosis .Presence of a Mass if the plexus is invaded ,with interruption,compression or splaying .Patchy/heterogenous contrast enhancement . Findings of radiation fibrosis include (a) thickening and diffuse enhancement of the brachial plexus without a focal mass and (b) soft-tissue changes with low signal intensity on both T1- and T2-weighted images. Superior sullcus tumors at the lung apex may invade the lower portion of the brachial plexus. In MADSAM neuropathy, MMN, and CIDP, the nerve conduction studies show features of demyelination, Page 25 of 67 such as conduction block, temporal dispersion, prolonged distal latencies, slow conduction velocities, and absent or prolonged F-wave latencies in one or more motor nerves .MADSAM neuropathy is different from MMN due to sensory nerves are involved and different from CIDP due to conspicuous asymmetric multiple nerves involvement. Images for this section: Fig. 1: Sarcoidosis Inflammatory brachial plexopathy Right Page 26 of 67 Fig. 2: Sarcoidosis Inflammatory brachial plexopathy Right Normal Plexus on left Page 27 of 67 Fig. 3: Sarcoidosis Inflammatory brachial plexopathy Right Normal Plexus on left Page 28 of 67 Fig. 4: Lumbar Plexopathy with thickening of pre,post ganglionic segments of the roots and lumbosacral trunks and sciatic nerves:Sarcoid Page 29 of 67 Fig. 5: Lumbar Plexopathy with thickening of pre,post ganglionic segments of the roots and lumbosacral trunks and sciatic nerves:Sarcoid Page 30 of 67 Fig. 6: Brachial Plexopathy:Thoracic outlet syndrome Page 31 of 67 Fig. 7: Brachial Plexopathy:Thoracic outlet syndrome Page 32 of 67 Fig. 8: Brachial Plexopathy:Thoracic outlet syndrome Page 33 of 67 Fig. 9: Brachial Plexopathy:Thoracic outlet syndrome Page 34 of 67 Fig. 10: CIDP:Brachial Plexopathy symmetrical pattern Page 35 of 67 Fig. 11: CIDP:Brachial Plexopathy symmetrical pattern Page 36 of 67 Fig. 12: Brachial Plexopathy:Thoracic outlet syndrome Page 37 of 67 Fig. 13: DTI with fiber tracking:Metastatic ca prostae with Lymphnodal masses compressing the left lumbar Plexus Page 38 of 67 Fig. 14: Contrast enhancement patterns of Plexopathy Lumbar (sarcoid) Page 39 of 67 Fig. 15: Contrast enhancement patterns of Plexopathy Lumbar (sarcoid) Over view Page 40 of 67 Fig. 16: Contrast enhancement patterns of Plexopathy Lumbar (sarcoid) Page 41 of 67 Fig. 17: Contrast enhancement patterns of Plexo Neuro pathy Lumbar (sarcoid) Page 42 of 67 Fig. 18: Lumbar Plexopathy with thickening of pre,post ganglionic segments of the roots and lumbosacral trunks and sciatic nerves:Sarcoid Post contrast fat sat T1 weighted images showing enhancement of roos and plexus Page 43 of 67 Fig. 19: Lumbar Plexopathy with thickening of pre,post ganglionic segments of the roots and lumbosacral trunks and sciatic nerves:Sarcoid Post contrast fat sat T1 weighted images showing enhancement of roos and plexus Page 44 of 67 Fig. 20: CIDP:Brachial Plexopathy symmetrical pattern 3D MIP Page 45 of 67 Fig. 21: CIDP:Brachial Plexopathy symmetrical pattern 3D MIP Page 46 of 67 Fig. 22: Aggressive Giant cell tumor Sacrum Infiltrating Sacral plexus with GS foraminal extension on right:DTI with fiber tracking Page 47 of 67 Fig. 23: Post Radiotherapy Ca Cervix with Radiation fibrosis,Lumboasacral plexopathy,Pyriformis syndrome Page 48 of 67 Fig. 24: Tracking exudate along scatic nerve and LS plexus Right from para spinal Koch's Edema of pyriformis muscle. Page 49 of 67 Fig. 25: Sacro iliac TB :Tracking exudate along scatic nerve and LS plexus Right Page 50 of 67 Fig. 26: Sacro iliac TB inflammatory plexo neuropathy Right Page 51 of 67 Fig. 27: CIDP:Lumbar Plexopathy symmetrical pattern 3D MIP Page 52 of 67 Fig. 28: CIDP:Lumbar Plexopathy symmetrical pattern 3D MIP Page 53 of 67 Fig. 29: CIDP:Lumbar Plexopathy symmetrical pattern 3D MIP Page 54 of 67 Fig. 30: CIDP:Brachial Plexopathy symmetrical pattern 3D MIP Page 55 of 67 Fig. 31: DTI with fiber tracking Aggressive Giant cell tumor Sacrum Infiltrating Sacral plexus with GS foraminal extension on right:DTI with fiber tracking Page 56 of 67 Fig. 32: POEMS SYNDROMEPolyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome is a rare multisystemic disease that occurs in the setting of a plasma cell dyscrasia. Page 57 of 67 Fig. 33: POEM'S SYNDROME Page 58 of 67 Fig. 34: POEMS SYNDROME Polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome is a rare multisystemic disease that occurs in the setting of a plasma cell dyscrasia. Page 59 of 67 Fig. 35: MADSAM :Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is characterized by an asymmetric multifocal pattern of motor and sensory loss, and conduction block and other features of demyelination in nerve conduction studies. MADSAM neuropathy needs to be differentiated from chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). Page 60 of 67 Fig. 36: MADSAM :Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is characterized by an asymmetric multifocal pattern of motor and sensory loss, and conduction block and other features of demyelination in nerve conduction studies. MADSAM neuropathy needs to be differentiated from chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). Page 61 of 67 Fig. 37: MADSAM :Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is characterized by an asymmetric multifocal pattern of motor and sensory loss, and conduction block and other features of demyelination in nerve conduction studies. MADSAM neuropathy needs to be differentiated from chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). Page 62 of 67 Conclusion MR Imaging features of Plexopathies and the spectrum of Imaging manifestations in various etiologies,sub types involving brachial and lumbar plexuses or both are highlighted in this educational exhibit Personal Information Rammohan Vadapalli MD Vijaya Diagnostics and research Chippendale apartments,202 1-7-12 Musheerabad Hyderabad AP India References References Page 63 of 67 Top 1. 2. 3. 4. 5. 6. 7. Ferrante, MA, Wilbourn, AJ. The utility of various sensory nerve conduction responses in assessing brachial plexopathies. Muscle Nerve 1995; 18:879. Jaeckle, KA. Neurological manifestations of neoplastic and radiation-induced plexopathies. Semin Neurol 2004; 24:385. Dyck, PJ, Windebank, AJ. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: new insights into pathophysiology and treatment. Muscle Nerve 2002; 25:477. Tsairis, P, Dyck, PJ, Mulder, DW. Natural history of brachial plexus neuropathy. Report on 99 patients. Arch Neurol 1972; 27:109. Beghi, E, Kurland, LT, Mulder, DW, Nicolosi, A. Brachial plexus neuropathy in the population of Rochester, Minnesota, 1970-1981. Ann Neurol 1985; 18:320. MacDonald, BK, Cockerell, OC, Sander, JW, Shorvon, SD. The incidence and lifetime prevalence of neurological disorders in a prospective community-based study in the UK. Brain 2000; 123 ( Pt 4):665. van Alfen, N, van Engelen, BG. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain 2006; 129:438. Page 64 of 67 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. Ferrante, MA. Brachial plexopathies: classification, causes, and consequences. Muscle Nerve 2004; 30:547. Zhou, L, Yousem, DM, Chaudhry, V. Role of magnetic resonance neurography in brachial plexus lesions. Muscle Nerve 2004; 30:305. Moore, K. MR imaging of peripheral nerve. In: Handbook of Peripheral Neuropathy, 1st ed, Bromberg, M, Smith, A, (Eds), Taylor & Francis Group, Boca Raton 2005. p.91. Wilbourn, AJ. Plexopathies. Neurol Clin 2007; 25:139. Clancy WG, Jr, Brand, RL, Bergfield, JA. Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 1977; 5:209. Weinberg, J, Rokito, S, Silber, JS. Etiology, treatment, and prevention of athletic "stingers". Clin Sports Med 2003; 22:493. van Alfen, N, Schuuring, J, van Engelen, BG, et al. Idiopathic neuralgic amyotrophy in children. A distinct phenotype compared to the adult form. Neuropediatrics 2000; 31:328. England, JD, Sumner, AJ. Neuralgic amyotrophy: an increasingly diverse entity. Muscle Nerve 1987; 10:60. Malamut, RI, Marques, W, England, JD, Sumner, AJ. Postsurgical idiopathic brachial neuritis. Muscle Nerve 1994; 17:320. Meulemann, J, Kuhlenbäumer, G, Schirmacher, A, et al. Genetic refinement of the hereditary neuralgic amyotrophy (HNA) locus at chromosome 17q25. Eur J Hum Genet 1999; 7:920. Kuhlenbäumer, G, Hannibal, MC, Nelis, E, et al. Mutations in SEPT9 cause hereditary neuralgic amyotrophy. Nat Genet 2005; 37:1044. Hannibal, MC, Ruzzo, EK, Miller, LR, et al. SEPT9 gene sequencing analysis reveals recurrent mutations in hereditary neuralgic amyotrophy. Neurology 2009; 72:1755. Dunn, HG, Daube, JR, Gomez, MR. Heredofamilial branchial plexus neuropathy (hereditary neuralgic amyotrophy with branchial predilection) in childhood. Dev Med Child Neurol 1978; 20:28. van Alfen, N, van Engelen, BG, Reinders, JW, et al. The natural history of hereditary neuralgic amyotrophy in the Dutch population: two distinct types? Brain 2000; 123 ( Pt 4):718. Jeannet, PY, Watts, GD, Bird, TD, Chance, PF. Craniofacial and cutaneous findings expand the phenotype of hereditary neuralgic amyotrophy. Neurology 2001; 57:1963. Arts, WF, Busch, HF, Van den Brand, HJ, et al. Hereditary neuralgic amyotrophy. Clinical, genetic, electrophysiological and histopathological studies. J Neurol Sci 1983; 62:261. van Alfen, N, Gabreëls-Festen, AA, Ter Laak, HJ, et al. Histology of hereditary neuralgic amyotrophy. J Neurol Neurosurg Psychiatry 2005; 76:445. Wilbourn, AJ. Thoracic outlet syndromes. Neurol Clin 1999; 17:477. Wilbourn, AJ. Thoracic outlet syndrome surgery causing severe brachial plexopathy. Muscle Nerve 1988; 11:66. Page 65 of 67 27. Cormier, JM, Amrane, M, Ward, A, et al. Arterial complications of the thoracic outlet syndrome: fifty-five operative cases. J Vasc Surg 1989; 9:778. 28. Hood, DB, Kuehne, J, Yellin, AE, Weaver, FA. Vascular complications of thoracic outlet syndrome. Am Surg 1997; 63:913. 29. Roos, DB. The thoracic outlet syndrome is underrated. Arch Neurol 1990; 47:327. 30. Wilbourn, AJ. The thoracic outlet syndrome is overdiagnosed. Arch Neurol 1990; 47:328. 31. Le Forestier, N, Moulonguet, A, Maisonobe, T, et al. True neurogenic thoracic outlet syndrome: electrophysiological diagnosis in six cases. Muscle Nerve 1998; 21:1129. 32. Dale, WA. Thoracic outlet compression syndrome. Critique in 1982. Arch Surg 1982; 117:1437. 33. Cuetter, AC, Bartoszek, DM. The thoracic outlet syndrome: controversies, overdiagnosis, overtreatment, and recommendations for management. Muscle Nerve 1989; 12:410. 34. Dyck, PJ, Norell, JE, Dyck, PJ. Microvasculitis and ischemia in diabetic lumbosacral radiculoplexus neuropathy. Neurology 1999; 53:2113. 35. Wilbourn, AJ. Iatrogenic nerve injuries. Neurol Clin 1998; 16:55. 36. Smith, DC, Mitchell, DA, Peterson, GW, et al. Medial brachial fascial compartment syndrome: anatomic basis of neuropathy after transaxillary arteriography. Radiology 1989; 173:149. 37. Tsao, BE, Wilbourn, AJ. The medial brachial fascial compartment syndrome following axillary arteriography. Neurology 2003; 61:1037. 38. Tsao, BE, Wilbourn, AJ. Infraclavicular brachial plexus injury following axillary regional block. Muscle Nerve 2004; 30:44. 39. Chitwood, RW, Shepard, AD, Shetty, PC, et al. Surgical complications of transaxillary arteriography: a case-control study. J Vasc Surg 1996; 23:844. 40. Kay, SP. Obstetrical brachial palsy. Br J Plast Surg 1998; 51:43. 41. van Dijk, JG, Pondaag, W, Malessy, MJ. Obstetric lesions of the brachial plexus. Muscle Nerve 2001; 24:1451. 42. Levine, MG, Holroyde, J, Woods JR, Jr, et al. Birth trauma: incidence and predisposing factors. Obstet Gynecol 1984; 63:792. 43. Eng, GD, Binder, H, Getson, P, O'Donnell, R. Obstetrical brachial plexus palsy (OBPP) outcome with conservative management. Muscle Nerve 1996; 19:884. 44. Wolf, H, Hoeksma, AF, Oei, SL, Bleker, OP. Obstetric brachial plexus injury: risk factors related to recovery. Eur J Obstet Gynecol Reprod Biol 2000; 88:133. 45. Spinner, RJ, Kline, DG. Surgery for peripheral nerve and brachial plexus injuries or other nerve lesions. Muscle Nerve 2000; 23:680. 46. Bodensteiner, JB, Rich, KM, Landau, WM. Early infantile surgery for birthrelated brachial plexus injuries: justification requires a prospective controlled study. J Child Neurol 1994; 9:109. Page 66 of 67 47. Shenaq, SM, Berzin, E, Lee, R, et al. Brachial plexus birth injuries and current management. Clin Plast Surg 1998; 25:527. 48. Grossman, JA. Early operative intervention for birth injuries to the brachial plexus. Semin Pediatr Neurol 2000; 7:36. 49. Lumbosacral Plexopathies: Diagnosis and rehabilitationJournal of the American Chiropractic Association, Mar 1999 by Matiscik, R Martin Page 67 of 67
Similar documents
The symptoms and signs of CIDP may be asymmetrical initially and have ascending involvements. progresses slowly to symmetric weakness, loss of deep
More information