- Email: [email protected]
Mural aortic thrombi, what else?
revue neurologique 167 (2011) 856–865
non-re´ponse, de bolus d’immunoglobulines intraveineuses (Ulmer et al., 2002). Paralle`lement, un traitement symptomatique avec les anticonvulsivants, les antide´presseurs et les antipsychotiques doivent eˆtre largement utilise´s. Dans la se´rie de Bennett et al., 1978, un seul patient psychotique n’a pas re´pondu a` la corticothe´rapie, les deux autres ont bien re´pondu. Il n’y avait pas de re´e´valuation neuropsychologique chez notre patiente.
4.
Conclusion
La CM, rare chez le sujet aˆge´, est d’expression clinique polymorphe. Elle peut eˆtre rarement re´ve´le´e par une psychose conduisant a` un retard diagnostique, parfois important. Ne´anmoins, cette affection ne´cessite bien plus qu’une psychose pour eˆtre e´voque´e : en fait, le diagnostic repose sur la mise en e´vidence des anomalies cliniques et biologiques caracte´ristiques de cette maladie.
De´claration d’inte´reˆts Les auteurs de´clarent ne pas avoir de conflits d’inte´reˆts en relation avec cet article.
r e´ f e´ r e n c e s
Alpert MA, Pressly TA, Mukerji V, Lambert CR, Mukerji B, Panayiotou H, et al. Acute and long-term effects of nifedipine on pulmonary and systemic hemodynamics in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease. Am J Cardiol 1991;68(17):1687–91. Bennett RM, Bong DM, Spargo BH. Neuropsychiatric problems in mixed connective tissue disease. Am J Med 1978;65: 955–62. Bennett RM, O’Connell DJ. Mixed connective tissue disease: a clinicopathologic study of 20 cases. Semin Arthritis Rheum 1980;10(1):25–51. Creange A, Laplane D, Habib K, Attal N, Assue´rus V. De´mence re´ve´latrice du syndrome de Gougerot Sjo¨gren. Rev Neurol 1992;148:376–80. Delalande S, de Seze J, Fauchais AL, Hachulla E, Stojkovic T, Ferriby D, et al. Neurological manifestations in primary Sjo¨gren syndrome: a study of 82 patients. Medicine 2004;83:280–371. Hoffman M, Gray RG. Ibuprofen-induced meningitis in mixed connective tissue disease. Clin Rheumatol 1982;1(2):128–30. Kahn MF, Appelbom T. Syndrome de Sharp et connectivite mixte., In: Kahn MF, Peltier AP, editors. 3e ed, Maladies syste´miques, Paris: Flammarion; 1991. p. 545–6. Matsui H, Udaka F, Oda M, Kubori T, Nishinaka K, Kameyama M. Encephalopathy and severe neuropathy due to probable systemic vasculitis as an initial manifestation of mixed connective tissue disease. Neurol India 2006;54(1):83–5. Mok CC, Lau CS. Transverse myelopathy complicating mixed connective tissue disease. Clin Neurol Neurosurg 1995;97(3):259–60. Lafitte C, Amoura Z, Cacoub P, Pradat-Diehl P, Picq C, Salachas F, et al. Neurological complications of primary Sjo¨gren syndrome. J Neurol 2001;248:577–84.
859
Pedersen C, Bonen H, Boesen F. Transverse myelitis in mixed connective tissue disease. Clin Rheummatol 1987;6:290–2. Sato M, Yanagisawa K, Matsubara N, Kondo H, Miyatake T. Mixed connective tissue disease – various neuromuscular complications prior to the elevation of antibody to RNP. Rinsho Shinkeigaku 1991;31(10):1143–6. Sharp GC, Irvin WS, Tan EM, Gould RG, Holman HR. Mixed connective tissue disease: an apparently distinct rheumatic disease syndrome associated with specific antibody to an extractable nuclear antigen (ENA). Am J Med 1972;52: 148–59. Ulmer A, Kotter I, Pfaff A, Fierlbeck G. Efficacy of pulsed intravenous immunoglobulin therapy in mixed connective tissue disease. J Am Acad Dermatol 2002;46:123–7. Yasuda Y, Akiguchi I, Kameyama M. Sulindac-induced aseptic meningitis in mixed connective tissue disease. Clin Neurol Neurosurg 1989;91(3):257–60.
N. Khammassia,* A. Gargourib R. Gouiderb M. Hamzaa O. Cherif a a Service de me´decine interne, hoˆpital Razi, 2010 La-Manouba, Tunisie b Service de neurologie, hoˆpital Razi, 2010 La-Manouba, Tunisie *Auteur correspondant Adresse e-mail : [email protected] (N. Khammassi) Rec¸u le 2 juillet Rec¸u sous la forme re´vise´e le 8 fe´vrier Accepte´ le 1 mars Disponible sur Internet le 6 mai
2010 2011 2011 2011
0035-3787/$ – see front matter # 2011 Elsevier Masson SAS. Tous droits re´serve´s. doi:10.1016/j.neurol.2011.03.004
Mural aortic thrombi, what else? Thrombi aortiques mobiles, mais quoi d’autre ? Here, we report a patient with ischemic stroke and mobile aortic arch thrombi on transesophageal echocardiography (TEE) in whom the diagnosis of pulmonary cancer was made. A 59-year-old woman was referred to our stroke unit for sudden aphasia and right hemiparesis. Her NIH stroke scale was 16. Brain MRI was performed. Diffusion-weighted imaging showed a left MCA stroke associated with a left cerebellar stroke. Her EKG was in sinus rhythm. Blood pressure was 128/83 mmHg and heart rate was 76/min. Biology: WBC count 13,500 per millimetre cube, fibrinogen 10.95 g/l, CRP 402 mg/l, LDL-C 0.69 g/l. TEE was performed. It revealed three mobile thrombi in the ascending aorta (Fig. 1A and B). Thrombi were inserted on an atherosclerotic plaque of 2.9 to 3.3 mm (Fig. 1A and B). Anticoagulation therapy was started. On the control TEE 2 months later, only a small residual thrombus was present. The TEE at 10 months showed
860
revue neurologique 167 (2011) 856–865
[()TD$FIG]
Fig. 1 – A and B. Three mobile thrombi in the aortic arch on TEE. C. Protruding mass in the aortic arch on CT scan. D. Mass of the right lung base on CT scan, diagnosed as a cancer. A et B. Trois thrombi mobiles dans la crosse aortique en ETO. C. Masse saillante dans la crosse aortique en scanner. D. Masse de la base pulmonaire droite en scanner, il s’agissait d’un cancer.
a complete disappearance of the thrombi, without recurrent embolic event. As floating thrombi are a rare cause of stroke, a thoracic CT was performed at 2 months. It showed a protruding mass in the ascending aorta (Fig. 1C, arrow) and a mass of the right lung base, diagnosed as a cancer (Fig. 1D, arrow).
Our patient had a cardioembolic stroke, with three mobile thrombi in the aortic arch. Aortic atherosclerotic plaques are known to be associated with ischemic stroke (Di Tullio et al., 2008). However, mobile thrombi in the aorta are a rare finding. They were described in a series of young adults with ischemic stroke of unknown cause, some of whom have been operated
861
revue neurologique 167 (2011) 856–865
(Laperche et al., 1997). Since there is no consensus regarding the management of aortic thrombi, the decision to treat with anticoagulants or to send to surgery is made on an individual basis. No specific recommendations are contained in American Heart Association/American Stroke association guidelines (Sacco et al., 2006). In the American College of Chest Physicians guidelines, it is stated: for patients with cryptogenic stroke associated with mobile aortic arch thrombi, we suggest either oral anticoagulation or antiplatelet agents (Albers et al., 2008). In older patients, as in our patient, they are often associated with blood hypercoagulability. It has recently been shown that hypercoagulability was associated with aortic arch plaques of 4 mm and more in stroke patients but not in control subjects (Di Tullio et al., 2008). In our patient, thrombi disappeared under anticoagulant therapy. A similar case was reported by Farah. In the presence of an aortic thrombus in a 74-year-old stroke woman, the colonoscopy showed a cancer of the colon (Farah and Hawawini, 1993). In conclusion, cancer is known to cause hypercoagulability. In the presence of aortic thrombi in a stroke patient, especially in aged patients, a cancer should be evoked. TEE is mandatory in the setting of ischemic stokes of unknown cause.
M. Obadia O. Gout Department of neurology, fondation ophtalmologique Adolphe-de-Rothschild, 25-29, rue Manin, 75940 Paris cedex 19, France *Corresponding author. E-mail address: [email protected] (N. Benyounes) Received 27 January Revised 31 January Accepted 8 February Available online 22 April
2011 2011 2011 2011
0035-3787/$ – see front matter # 2011 Elsevier Masson SAS. Tous droits re´serve´s. doi:10.1016/j.neurol.2011.02.041
Compression me´dullaire par de multiples foyers d’e´rythropoı¨e`se extrame´dullaire au cours d’une dre´panothalasse´mie
Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.
Spinal cord compression due to multiple extramedullary haematopoiesis in a patient with drepanothalassaemia
references
Albers GW, Amarenco P, Easton JD, Sacco RL, Teal P, American College of Chest Physicians. Antithrombotic and thrombolytic therapy for ischemic stroke: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest 2008;133:630S–69S. Di Tullio MR, Homma S, Jin Z, Sacco RL. Aortic atherosclerosis, hypercoagulability, and stroke the Aortic Plaque and Risk of Ischemic Stroke (APRIS) study. J Am Coll Cardiol 2008;52: 855–61. Farah MG, Hawawini H. Thrombus of the ascending aorta as a source of cerebral embolism. Chest 1993;104:1604–5. Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. The filiale echocardiographie de la Socie´te´ franc¸aise de cardiologie. Circulation 1997;96:288–94. Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on stroke: co-sponsored by the Council on cardiovascular radiology and intervention: the American Academy of neurology affirms the value of this guideline. Circulation 2006;113:e409–49.
N. Benyounes* Departments of internal medicine, fondation ophtalmologique Adolphe-de-Rothschild, 25-29, rue Manin, 75940 Paris cedex 19, France
Une femme de 62 ans, aux ante´ce´dents de dre´panothalasse´mie mineure, a e´te´ hospitalise´e pour une compression me´dullaire subaigue¨. Elle a pre´sente´ deux mois avant son admission des troubles progressifs de la marche et des fourmillements des deux membres infe´rieurs. L’examen neurologique trouvait aux membres infe´rieurs un syndrome pyramidal, un syndrome cordonal poste´rieur et une hypoesthe´sie superficielle sans niveau sensitif. L’examen somatique notait une paˆleur cutane´omuqueuse. Le bilan biologique a re´ve´le´ une ane´mie hypochrome microcytaire (he´moglobine a` 8,6 g/dL, volume globulaire moyen a` 73 m3). Devant ce syndrome de scle´rose combine´e de la moelle, un de´ficit vitaminique a e´te´ e´limine´ par le dosage normal de la vitamine B12 et des folates. L’IRM spinome´dullaire montrait un hyposignal T2 diffus du rachis et de multiples le´sions, expansives intracanalaires dorsales poste´rieures e´tage´es de D4 a` D10, effac¸ant la graisse e´pidurale et refoulant le cordon me´dullaire vers l’avant. Ces le´sions e´taient hypo-intenses en T2 (Fig. 1a), iso-intenses en T1 (Fig. 1b) et discre`tement rehausse´es par le gadolinium (Fig. 1c). Il existait de D8 jusqu’au niveau lombosacre´ des le´sions similaires intracanalaires ante´rieures et une masse pre´sacre´e centre´e sur S3 et S4 (Fig. 2). Au niveau des gouttie`res costodiaphragmatiques, il existait des masses thoraciques poste´rieures bilate´rales de T2 a` T8, dont la plus volumineuse se situait en T4-T5 (Fig. 3). Le diagnostic de compression me´dullaire e´tage´e a e´te´ retenu. L’aspect IRM des le´sions et leur confrontation avec le contexte clinique nous ont permis d’e´carter le diagnostic de me´tastases verte´brales et e´pidurales ainsi que des localisations verte´-
non-re´ponse, de bolus d’immunoglobulines intraveineuses (Ulmer et al., 2002). Paralle`lement, un traitement symptomatique avec les anticonvulsivants, les antide´presseurs et les antipsychotiques doivent eˆtre largement utilise´s. Dans la se´rie de Bennett et al., 1978, un seul patient psychotique n’a pas re´pondu a` la corticothe´rapie, les deux autres ont bien re´pondu. Il n’y avait pas de re´e´valuation neuropsychologique chez notre patiente.
4.
Conclusion
La CM, rare chez le sujet aˆge´, est d’expression clinique polymorphe. Elle peut eˆtre rarement re´ve´le´e par une psychose conduisant a` un retard diagnostique, parfois important. Ne´anmoins, cette affection ne´cessite bien plus qu’une psychose pour eˆtre e´voque´e : en fait, le diagnostic repose sur la mise en e´vidence des anomalies cliniques et biologiques caracte´ristiques de cette maladie.
De´claration d’inte´reˆts Les auteurs de´clarent ne pas avoir de conflits d’inte´reˆts en relation avec cet article.
r e´ f e´ r e n c e s
Alpert MA, Pressly TA, Mukerji V, Lambert CR, Mukerji B, Panayiotou H, et al. Acute and long-term effects of nifedipine on pulmonary and systemic hemodynamics in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease. Am J Cardiol 1991;68(17):1687–91. Bennett RM, Bong DM, Spargo BH. Neuropsychiatric problems in mixed connective tissue disease. Am J Med 1978;65: 955–62. Bennett RM, O’Connell DJ. Mixed connective tissue disease: a clinicopathologic study of 20 cases. Semin Arthritis Rheum 1980;10(1):25–51. Creange A, Laplane D, Habib K, Attal N, Assue´rus V. De´mence re´ve´latrice du syndrome de Gougerot Sjo¨gren. Rev Neurol 1992;148:376–80. Delalande S, de Seze J, Fauchais AL, Hachulla E, Stojkovic T, Ferriby D, et al. Neurological manifestations in primary Sjo¨gren syndrome: a study of 82 patients. Medicine 2004;83:280–371. Hoffman M, Gray RG. Ibuprofen-induced meningitis in mixed connective tissue disease. Clin Rheumatol 1982;1(2):128–30. Kahn MF, Appelbom T. Syndrome de Sharp et connectivite mixte., In: Kahn MF, Peltier AP, editors. 3e ed, Maladies syste´miques, Paris: Flammarion; 1991. p. 545–6. Matsui H, Udaka F, Oda M, Kubori T, Nishinaka K, Kameyama M. Encephalopathy and severe neuropathy due to probable systemic vasculitis as an initial manifestation of mixed connective tissue disease. Neurol India 2006;54(1):83–5. Mok CC, Lau CS. Transverse myelopathy complicating mixed connective tissue disease. Clin Neurol Neurosurg 1995;97(3):259–60. Lafitte C, Amoura Z, Cacoub P, Pradat-Diehl P, Picq C, Salachas F, et al. Neurological complications of primary Sjo¨gren syndrome. J Neurol 2001;248:577–84.
859
Pedersen C, Bonen H, Boesen F. Transverse myelitis in mixed connective tissue disease. Clin Rheummatol 1987;6:290–2. Sato M, Yanagisawa K, Matsubara N, Kondo H, Miyatake T. Mixed connective tissue disease – various neuromuscular complications prior to the elevation of antibody to RNP. Rinsho Shinkeigaku 1991;31(10):1143–6. Sharp GC, Irvin WS, Tan EM, Gould RG, Holman HR. Mixed connective tissue disease: an apparently distinct rheumatic disease syndrome associated with specific antibody to an extractable nuclear antigen (ENA). Am J Med 1972;52: 148–59. Ulmer A, Kotter I, Pfaff A, Fierlbeck G. Efficacy of pulsed intravenous immunoglobulin therapy in mixed connective tissue disease. J Am Acad Dermatol 2002;46:123–7. Yasuda Y, Akiguchi I, Kameyama M. Sulindac-induced aseptic meningitis in mixed connective tissue disease. Clin Neurol Neurosurg 1989;91(3):257–60.
N. Khammassia,* A. Gargourib R. Gouiderb M. Hamzaa O. Cherif a a Service de me´decine interne, hoˆpital Razi, 2010 La-Manouba, Tunisie b Service de neurologie, hoˆpital Razi, 2010 La-Manouba, Tunisie *Auteur correspondant Adresse e-mail : [email protected] (N. Khammassi) Rec¸u le 2 juillet Rec¸u sous la forme re´vise´e le 8 fe´vrier Accepte´ le 1 mars Disponible sur Internet le 6 mai
2010 2011 2011 2011
0035-3787/$ – see front matter # 2011 Elsevier Masson SAS. Tous droits re´serve´s. doi:10.1016/j.neurol.2011.03.004
Mural aortic thrombi, what else? Thrombi aortiques mobiles, mais quoi d’autre ? Here, we report a patient with ischemic stroke and mobile aortic arch thrombi on transesophageal echocardiography (TEE) in whom the diagnosis of pulmonary cancer was made. A 59-year-old woman was referred to our stroke unit for sudden aphasia and right hemiparesis. Her NIH stroke scale was 16. Brain MRI was performed. Diffusion-weighted imaging showed a left MCA stroke associated with a left cerebellar stroke. Her EKG was in sinus rhythm. Blood pressure was 128/83 mmHg and heart rate was 76/min. Biology: WBC count 13,500 per millimetre cube, fibrinogen 10.95 g/l, CRP 402 mg/l, LDL-C 0.69 g/l. TEE was performed. It revealed three mobile thrombi in the ascending aorta (Fig. 1A and B). Thrombi were inserted on an atherosclerotic plaque of 2.9 to 3.3 mm (Fig. 1A and B). Anticoagulation therapy was started. On the control TEE 2 months later, only a small residual thrombus was present. The TEE at 10 months showed
860
revue neurologique 167 (2011) 856–865
[()TD$FIG]
Fig. 1 – A and B. Three mobile thrombi in the aortic arch on TEE. C. Protruding mass in the aortic arch on CT scan. D. Mass of the right lung base on CT scan, diagnosed as a cancer. A et B. Trois thrombi mobiles dans la crosse aortique en ETO. C. Masse saillante dans la crosse aortique en scanner. D. Masse de la base pulmonaire droite en scanner, il s’agissait d’un cancer.
a complete disappearance of the thrombi, without recurrent embolic event. As floating thrombi are a rare cause of stroke, a thoracic CT was performed at 2 months. It showed a protruding mass in the ascending aorta (Fig. 1C, arrow) and a mass of the right lung base, diagnosed as a cancer (Fig. 1D, arrow).
Our patient had a cardioembolic stroke, with three mobile thrombi in the aortic arch. Aortic atherosclerotic plaques are known to be associated with ischemic stroke (Di Tullio et al., 2008). However, mobile thrombi in the aorta are a rare finding. They were described in a series of young adults with ischemic stroke of unknown cause, some of whom have been operated
861
revue neurologique 167 (2011) 856–865
(Laperche et al., 1997). Since there is no consensus regarding the management of aortic thrombi, the decision to treat with anticoagulants or to send to surgery is made on an individual basis. No specific recommendations are contained in American Heart Association/American Stroke association guidelines (Sacco et al., 2006). In the American College of Chest Physicians guidelines, it is stated: for patients with cryptogenic stroke associated with mobile aortic arch thrombi, we suggest either oral anticoagulation or antiplatelet agents (Albers et al., 2008). In older patients, as in our patient, they are often associated with blood hypercoagulability. It has recently been shown that hypercoagulability was associated with aortic arch plaques of 4 mm and more in stroke patients but not in control subjects (Di Tullio et al., 2008). In our patient, thrombi disappeared under anticoagulant therapy. A similar case was reported by Farah. In the presence of an aortic thrombus in a 74-year-old stroke woman, the colonoscopy showed a cancer of the colon (Farah and Hawawini, 1993). In conclusion, cancer is known to cause hypercoagulability. In the presence of aortic thrombi in a stroke patient, especially in aged patients, a cancer should be evoked. TEE is mandatory in the setting of ischemic stokes of unknown cause.
M. Obadia O. Gout Department of neurology, fondation ophtalmologique Adolphe-de-Rothschild, 25-29, rue Manin, 75940 Paris cedex 19, France *Corresponding author. E-mail address: [email protected] (N. Benyounes) Received 27 January Revised 31 January Accepted 8 February Available online 22 April
2011 2011 2011 2011
0035-3787/$ – see front matter # 2011 Elsevier Masson SAS. Tous droits re´serve´s. doi:10.1016/j.neurol.2011.02.041
Compression me´dullaire par de multiples foyers d’e´rythropoı¨e`se extrame´dullaire au cours d’une dre´panothalasse´mie
Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.
Spinal cord compression due to multiple extramedullary haematopoiesis in a patient with drepanothalassaemia
references
Albers GW, Amarenco P, Easton JD, Sacco RL, Teal P, American College of Chest Physicians. Antithrombotic and thrombolytic therapy for ischemic stroke: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest 2008;133:630S–69S. Di Tullio MR, Homma S, Jin Z, Sacco RL. Aortic atherosclerosis, hypercoagulability, and stroke the Aortic Plaque and Risk of Ischemic Stroke (APRIS) study. J Am Coll Cardiol 2008;52: 855–61. Farah MG, Hawawini H. Thrombus of the ascending aorta as a source of cerebral embolism. Chest 1993;104:1604–5. Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. The filiale echocardiographie de la Socie´te´ franc¸aise de cardiologie. Circulation 1997;96:288–94. Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on stroke: co-sponsored by the Council on cardiovascular radiology and intervention: the American Academy of neurology affirms the value of this guideline. Circulation 2006;113:e409–49.
N. Benyounes* Departments of internal medicine, fondation ophtalmologique Adolphe-de-Rothschild, 25-29, rue Manin, 75940 Paris cedex 19, France
Une femme de 62 ans, aux ante´ce´dents de dre´panothalasse´mie mineure, a e´te´ hospitalise´e pour une compression me´dullaire subaigue¨. Elle a pre´sente´ deux mois avant son admission des troubles progressifs de la marche et des fourmillements des deux membres infe´rieurs. L’examen neurologique trouvait aux membres infe´rieurs un syndrome pyramidal, un syndrome cordonal poste´rieur et une hypoesthe´sie superficielle sans niveau sensitif. L’examen somatique notait une paˆleur cutane´omuqueuse. Le bilan biologique a re´ve´le´ une ane´mie hypochrome microcytaire (he´moglobine a` 8,6 g/dL, volume globulaire moyen a` 73 m3). Devant ce syndrome de scle´rose combine´e de la moelle, un de´ficit vitaminique a e´te´ e´limine´ par le dosage normal de la vitamine B12 et des folates. L’IRM spinome´dullaire montrait un hyposignal T2 diffus du rachis et de multiples le´sions, expansives intracanalaires dorsales poste´rieures e´tage´es de D4 a` D10, effac¸ant la graisse e´pidurale et refoulant le cordon me´dullaire vers l’avant. Ces le´sions e´taient hypo-intenses en T2 (Fig. 1a), iso-intenses en T1 (Fig. 1b) et discre`tement rehausse´es par le gadolinium (Fig. 1c). Il existait de D8 jusqu’au niveau lombosacre´ des le´sions similaires intracanalaires ante´rieures et une masse pre´sacre´e centre´e sur S3 et S4 (Fig. 2). Au niveau des gouttie`res costodiaphragmatiques, il existait des masses thoraciques poste´rieures bilate´rales de T2 a` T8, dont la plus volumineuse se situait en T4-T5 (Fig. 3). Le diagnostic de compression me´dullaire e´tage´e a e´te´ retenu. L’aspect IRM des le´sions et leur confrontation avec le contexte clinique nous ont permis d’e´carter le diagnostic de me´tastases verte´brales et e´pidurales ainsi que des localisations verte´-