pénal : mise en œuvre des recommandations de la Haute Autorité de santé en pratique clinique. Presse Med 2013;42:e1300–09. [5] Lefèvre T, Briffa H, Thomas G, Chariot P. Evaluating the functional impairment of assault survivors in a judicial context: a retrospective study. J Forensic Legal Med 2012;19:215–8. [6] Lefèvre T, Lepresle A, Chariot P. Detangling complex relationships in forensic data: principles and use of causal networks and their application to clinical forensic medicine. Int J Legal Med 2015. http://dx.doi.org/ 10.1007/s00414-015-1164-8 [Epub ahead of print]. [7] Chariot P, Tedlaouti M, Debout M. L'incapacité totale de travail et la victime de violences. Actualité Juridique Pénal (Dalloz) 2006;7–8:300–3. [8] Niort F, Delteil C, Bartoli C, Leonetti G, Piercecchi-Marti MD. Attente de la justice en matière d'incapacité totale de travail : opinions sur cet outil médico-légal d'évaluation. Enquête qualitative réalisée auprès de 21 magistrats, 46 officiers de police judiciaire (police et gendarmerie) et 15 avocats pénalistes. Med Droit 2014;2014:74–8. [9] Rougé D, Bras PM, Alengrin D, Brouchet A, Arbus L. ITT ; application variable selon le médecin et sa fonction. J Med Leg Droit Med 1987;30:287–91. [10] Niort F, Delteil C, Bartoli C, Leonetti G, Piercecchi-Marti MD. Inhomogénéité des évaluations de durée d'incapacité totale de travail : comparaisons d'évaluations des durées d'incapacité totale de travail entre les médecins légistes, les médecins généralistes et les urgentistes. Med Droit 2014;2014:120–3.
Patrick Chariot1,2, Thomas Lefèvre1,2, Céline Denis1, Aude Lepresle1 1
AP–HP, hôpital Jean-Verdier, service de médecine légale, 93140 Bondy, France 2 Sorbonne Paris Cité, université Paris 13, Institut de recherche interdisciplinaire sur les enjeux sociaux (IRIS), UMR 8156-997, UFR SMBH, 74, rue Marcel-Cachin, 93017 Bobigny, France Correspondance : Patrick Chariot, AP–HP, hôpital Jean-Verdier, service de médecine légale, avenue du 14-Juillet, 93140 Bondy, France. [email protected] Reçu le 9 avril 2015 Accepté le 16 avril 2015 Disponible sur internet le : 3 juin 2015 http://dx.doi.org/10.1016/j.lpm.2015.04.022 © 2015 Elsevier Masson SAS. Tous droits réservés.
Giant cell arteritis: A reversible cause of oculomotor nerve palsy Artérite à cellule géante (maladie de Horton) : une cause réversible de paralysie oculomotrice
Letter to the Editor
Giant cell arteritis: A reversible cause of oculomotor nerve palsy
Case report A 83-year-old female patient was hospitalized in November 2012 because of headaches, unilateral red eye and decreased visual acuity. She had previously experienced for 10 months asthenia, anorexia and 9 kg weight loss. Her past medical history was significant for hypertension, Raynaud's phenomenon and Alzheimer disease. Clinical examination revealed an afebrile patient with stable hemodynamic parameters and normal cardiovascular auscultation. She had pupil-sparing unilateral third nerve palsy, with ptosis and adduction palsy of the right eye (figure 1). Testing of other cranial nerve was normal. Temporal and mandibular arteries were pulsatile but hardened. No murmur was found on subclavian or humeral arteries. Biological revealed hypochromic microcytic anemia (10.5 g/dl), with elevated C-reactive protein level (46.2 mg/l), erythrocyte sedimentation rate (56 mm/h) and platelet count (513,000/ ml). A cerebral angiography was performed and revealed a 5.1mm wide and 5.8-mm long saccular aneurysm of the right T carotid (figure 1). There were no sign of complication of this aneurysm. The ophthalmologic examination confirmed the presence of partial right third nerve palsy with binocular diplopia and pupillary sparing. Hess screen test demonstrated partial impairment of the right third nerve with paresis of the right medial rectus and inferior rectus muscles. Finally, a temporal artery biopsy confirmed the diagnosis of giant cell arteritis (GCA).
Figure 1
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859
(A) Clinical observation of third nerve palsy, with right eye ptosis and right eye adduction palsy. Initial (November 2012) brain computed tomography (B) and cerebrovascular three dimensional computed tomographic angiography (C) showing saccular aneurysm of the right T carotid. (D) Follow up brain computed angiography (January 2014) showing a stability of the aneurysm (black arrow)
Letters to the editor
Letters to the editor
The patient was treated with systemic corticosteroid therapy at 0.7 mg per kg per day dosage. After discussion with neuroradiology team, we decided to defer intravascular treatment of the aneurysm, because of its probable inflammatory etiology. Patient outcome improved rapidly after a few days. The oculomotor third nerve palsy recovered completely and biological parameters began to normalize. At 3 months, general examination noticed a significant improvement, with a 4-kg weight gain and the absence of any ophthalmological or neurological symptoms. Laboratory tests returned to normal. Cerebral angiographies were performed in April 2013 and January 2014, and showed stabilization of the aneurysm of the right T. Discussion Ophthalmologic symptoms usually occur in 20–30% of patients [1]. Arteritic anterior ischemic optic neuropathy is the most common ocular finding in GCA. Third nerve palsy is an extremely rare manifestation of CGA [2,3]. GCA can cause a third nerve palsy by a muscular necrosis of extraocular muscles [3], but also through an inflammatory aneurysm of the carotid [4]. In our case, the clinical and biological improvements after treatment with corticosteroids suggest that the intracranial aneurysm was, in part, inflammatory. GCA may appear with highly variable clinical forms, making diagnosis difficult. We report here a case of unilateral third nerve palsy secondary to intracranial aneurysm explained by GCA that was reversible after corticosteroid therapy. In front of an intracranial aneurysm, clinician should evoke GCA and look for the presence of elevated inflammatory markers on biological feature. Disclosure of interest: the authors declare that they have no conflicts of interest concerning this article.
References [1]
[2] [3] [4]
Mari B, Monteagudo M, Bustamante E, Perez J, Casanovas A, Jordana R, et al. Analysis of temporal artery biopsies in an 18-year period at a community hospital. Eur J Intern Med 2009;20:533–6. Sibony PA, Lessell S. Transient oculomotor synkinesis in temporal arteritis. Arch Neurol 1984;41:87–8. Mehler MF, Rabinowich L. The clinical neuro-ophthalmologic spectrum of temporal arteritis. Am J Med 1988;85:839–44. Kozuka S, Iguchi I, Furuse M, Nakaya T, Taki T. Cerebral aneurysm induced by giant cell arteritis: a case report. Angiology 1979;30:131–7. Noémie Gaudre1, Martin Michaud1, Vincent Soler2, Stéphanie Lozano1, Clément Gaudin1, Laurent Balardy1
860
1 CHU de Toulouse, service de médecine interne et gérontologie clinique, pavillon Junod-Casselardit, 170, avenue de Casselardit, TSA 40031, 31059 Toulouse cedex 9, France 2 CHU de Toulouse, hôpital Pierre-Paul-Riquet, service d'ophtalmologie, 330, avenue de Grande-Bretagne, 31059 Toulouse cedex 9, France
Correspondence: Martin Michaud, service de médecine interne et gérontologie clinique, pavillon Junod-Casselardit, 170, avenue de Casselardit, TSA 40031, 31059 Toulouse cedex 9, France [email protected] Received 19 January 2015 Accepted 25 March 2015 Available online: 3 June 2015 http://dx.doi.org/10.1016/j.lpm.2015.03.013 © 2015 Elsevier Masson SAS. Tous droits réservés.
Brown tumors mimicking bone and lung metastases: Key role of radionuclide imaging Tumeurs brunes mimant des métastases osseuses et pulmonaires : rôle clé de l'imagerie isotopique Hypercalcemia is frequently observed in cancerology and leads to suspecting bone metastases [1]. However, a clinician must not forget a common cause of benign hypercalcemia: hyperparathyroidism [2]. Hyperparathyroidism rarely complicates by brown tumors. These may mimic metastatic lesions leading to an inappropriate therapeutic management [3]. We report the case of a patient followed for breast carcinoma with suspected bone, lung and liver metastasis. She had hypercalcemia and lytic bone lesions motivating a bone scintigraphy to search bone metastases. The bone scan showed focal uptake abnormalities consistent with metastatic lesions. However, further radionuclide investigations confirmed the diagnosis of brown tumors complicating a parathyroid adenoma and mimicking lung and bone metastases. Case report Our case is a 53-year-old woman, followed for left breast carcinoma. She had undergone left mastectomy and axillary lymph node dissection. The histopathologic examination showed a 1.3 cm infiltrating ductual carcinoma staged T1N0M0 and SBR2 with positive estrogen receptors. She had anti-estrogen hormonotherapy for 5 years. Three years after the end of this treatment, an abdominal ultrasound examination suspected liver metastases and computed tomography (CT) was indicated. In addition to the liver masses, CT scan showed lytic bone lesions within the 9th dorsal vertebra, the sacrum and both iliac bones evoking bone metastases. A right lung metastasis was suspected on the lung window of the CT scan and on the planar thoracic radiography. The patient also presented hypercalcemia reaching 3 mmol/l suggesting bone metastases and
tome 44 > n87–8 > juillet–août 2015
Patrick Chariot1,2, Thomas Lefèvre1,2, Céline Denis1, Aude Lepresle1 1
AP–HP, hôpital Jean-Verdier, service de médecine légale, 93140 Bondy, France 2 Sorbonne Paris Cité, université Paris 13, Institut de recherche interdisciplinaire sur les enjeux sociaux (IRIS), UMR 8156-997, UFR SMBH, 74, rue Marcel-Cachin, 93017 Bobigny, France Correspondance : Patrick Chariot, AP–HP, hôpital Jean-Verdier, service de médecine légale, avenue du 14-Juillet, 93140 Bondy, France. [email protected] Reçu le 9 avril 2015 Accepté le 16 avril 2015 Disponible sur internet le : 3 juin 2015 http://dx.doi.org/10.1016/j.lpm.2015.04.022 © 2015 Elsevier Masson SAS. Tous droits réservés.
Giant cell arteritis: A reversible cause of oculomotor nerve palsy Artérite à cellule géante (maladie de Horton) : une cause réversible de paralysie oculomotrice
Letter to the Editor
Giant cell arteritis: A reversible cause of oculomotor nerve palsy
Case report A 83-year-old female patient was hospitalized in November 2012 because of headaches, unilateral red eye and decreased visual acuity. She had previously experienced for 10 months asthenia, anorexia and 9 kg weight loss. Her past medical history was significant for hypertension, Raynaud's phenomenon and Alzheimer disease. Clinical examination revealed an afebrile patient with stable hemodynamic parameters and normal cardiovascular auscultation. She had pupil-sparing unilateral third nerve palsy, with ptosis and adduction palsy of the right eye (figure 1). Testing of other cranial nerve was normal. Temporal and mandibular arteries were pulsatile but hardened. No murmur was found on subclavian or humeral arteries. Biological revealed hypochromic microcytic anemia (10.5 g/dl), with elevated C-reactive protein level (46.2 mg/l), erythrocyte sedimentation rate (56 mm/h) and platelet count (513,000/ ml). A cerebral angiography was performed and revealed a 5.1mm wide and 5.8-mm long saccular aneurysm of the right T carotid (figure 1). There were no sign of complication of this aneurysm. The ophthalmologic examination confirmed the presence of partial right third nerve palsy with binocular diplopia and pupillary sparing. Hess screen test demonstrated partial impairment of the right third nerve with paresis of the right medial rectus and inferior rectus muscles. Finally, a temporal artery biopsy confirmed the diagnosis of giant cell arteritis (GCA).
Figure 1
tome 44 > n87–8 > juillet–août 2015
859
(A) Clinical observation of third nerve palsy, with right eye ptosis and right eye adduction palsy. Initial (November 2012) brain computed tomography (B) and cerebrovascular three dimensional computed tomographic angiography (C) showing saccular aneurysm of the right T carotid. (D) Follow up brain computed angiography (January 2014) showing a stability of the aneurysm (black arrow)
Letters to the editor
Letters to the editor
The patient was treated with systemic corticosteroid therapy at 0.7 mg per kg per day dosage. After discussion with neuroradiology team, we decided to defer intravascular treatment of the aneurysm, because of its probable inflammatory etiology. Patient outcome improved rapidly after a few days. The oculomotor third nerve palsy recovered completely and biological parameters began to normalize. At 3 months, general examination noticed a significant improvement, with a 4-kg weight gain and the absence of any ophthalmological or neurological symptoms. Laboratory tests returned to normal. Cerebral angiographies were performed in April 2013 and January 2014, and showed stabilization of the aneurysm of the right T. Discussion Ophthalmologic symptoms usually occur in 20–30% of patients [1]. Arteritic anterior ischemic optic neuropathy is the most common ocular finding in GCA. Third nerve palsy is an extremely rare manifestation of CGA [2,3]. GCA can cause a third nerve palsy by a muscular necrosis of extraocular muscles [3], but also through an inflammatory aneurysm of the carotid [4]. In our case, the clinical and biological improvements after treatment with corticosteroids suggest that the intracranial aneurysm was, in part, inflammatory. GCA may appear with highly variable clinical forms, making diagnosis difficult. We report here a case of unilateral third nerve palsy secondary to intracranial aneurysm explained by GCA that was reversible after corticosteroid therapy. In front of an intracranial aneurysm, clinician should evoke GCA and look for the presence of elevated inflammatory markers on biological feature. Disclosure of interest: the authors declare that they have no conflicts of interest concerning this article.
References [1]
[2] [3] [4]
Mari B, Monteagudo M, Bustamante E, Perez J, Casanovas A, Jordana R, et al. Analysis of temporal artery biopsies in an 18-year period at a community hospital. Eur J Intern Med 2009;20:533–6. Sibony PA, Lessell S. Transient oculomotor synkinesis in temporal arteritis. Arch Neurol 1984;41:87–8. Mehler MF, Rabinowich L. The clinical neuro-ophthalmologic spectrum of temporal arteritis. Am J Med 1988;85:839–44. Kozuka S, Iguchi I, Furuse M, Nakaya T, Taki T. Cerebral aneurysm induced by giant cell arteritis: a case report. Angiology 1979;30:131–7. Noémie Gaudre1, Martin Michaud1, Vincent Soler2, Stéphanie Lozano1, Clément Gaudin1, Laurent Balardy1
860
1 CHU de Toulouse, service de médecine interne et gérontologie clinique, pavillon Junod-Casselardit, 170, avenue de Casselardit, TSA 40031, 31059 Toulouse cedex 9, France 2 CHU de Toulouse, hôpital Pierre-Paul-Riquet, service d'ophtalmologie, 330, avenue de Grande-Bretagne, 31059 Toulouse cedex 9, France
Correspondence: Martin Michaud, service de médecine interne et gérontologie clinique, pavillon Junod-Casselardit, 170, avenue de Casselardit, TSA 40031, 31059 Toulouse cedex 9, France [email protected] Received 19 January 2015 Accepted 25 March 2015 Available online: 3 June 2015 http://dx.doi.org/10.1016/j.lpm.2015.03.013 © 2015 Elsevier Masson SAS. Tous droits réservés.
Brown tumors mimicking bone and lung metastases: Key role of radionuclide imaging Tumeurs brunes mimant des métastases osseuses et pulmonaires : rôle clé de l'imagerie isotopique Hypercalcemia is frequently observed in cancerology and leads to suspecting bone metastases [1]. However, a clinician must not forget a common cause of benign hypercalcemia: hyperparathyroidism [2]. Hyperparathyroidism rarely complicates by brown tumors. These may mimic metastatic lesions leading to an inappropriate therapeutic management [3]. We report the case of a patient followed for breast carcinoma with suspected bone, lung and liver metastasis. She had hypercalcemia and lytic bone lesions motivating a bone scintigraphy to search bone metastases. The bone scan showed focal uptake abnormalities consistent with metastatic lesions. However, further radionuclide investigations confirmed the diagnosis of brown tumors complicating a parathyroid adenoma and mimicking lung and bone metastases. Case report Our case is a 53-year-old woman, followed for left breast carcinoma. She had undergone left mastectomy and axillary lymph node dissection. The histopathologic examination showed a 1.3 cm infiltrating ductual carcinoma staged T1N0M0 and SBR2 with positive estrogen receptors. She had anti-estrogen hormonotherapy for 5 years. Three years after the end of this treatment, an abdominal ultrasound examination suspected liver metastases and computed tomography (CT) was indicated. In addition to the liver masses, CT scan showed lytic bone lesions within the 9th dorsal vertebra, the sacrum and both iliac bones evoking bone metastases. A right lung metastasis was suspected on the lung window of the CT scan and on the planar thoracic radiography. The patient also presented hypercalcemia reaching 3 mmol/l suggesting bone metastases and
tome 44 > n87–8 > juillet–août 2015
