- Email: [email protected]
Cerebral vasculitis in a patient with rheumatoid arthritis
Joint Bone Spine 74 (2007) 201e204 http://france.elsevier.com/direct/BONSOI/
Case report
Cerebral vasculitis in a patient with rheumatoid arthritis Dalila Mrabet*, Nihel Meddeb, Houda Ajlani, Hela Sahli, Slaheddine Sellami Rheumatology Department, La Rabta Hospital, Tunis 1006, Tunisia Received 23 May 2006; accepted 2 August 2006 Available online 6 February 2007
Abstract Inflammatory vasculitis of the central nervous system is exceedingly rare in patients with rheumatoid arthritis (RA). The symptoms may be misleading. Most of the reported cases occurred in males with long-standing, nodular, destructive, rheumatoid factor-positive disease. Severe constitutional symptoms and prominent extraarticular manifestations of vasculitis were usually present. We report a case of cerebral vasculitis in a 59-year-old woman with a 20-year history of destructive rheumatoid factor-positive RA that was well controlled by methotrexate. Headache that was unresponsive to symptomatic treatment developed abruptly, together with gait disorders. Magnetic resonance imaging of the brain showed dot-like areas of high-signal in a periventricular subcortical distribution on both sides. Magnetic resonance angiography visualized a long tight stenosis of the right internal carotid artery and a string-of-beads stenosis of the left internal carotid artery suggesting vasculitis. Pulse therapy with methylprednisolone (1 g/d for 3 days) and cyclophosphamide (1 g) once a month ensured resolution of the neurological symptoms and laboratory evidence of inflammation. There was no evidence of a relapse at last follow-up after 5 months. Cerebral vasculitis is usually treated with monthly glucocorticoid and cyclophosphamide boluses separated by continuous glucocorticoid therapy. TNFa antagonists may be effective in patients who fail to respond to conventional treatment. However, other vasculitides such as giant cell arteritis and Wegener’s granulomatosis must be ruled out, as they are refractory to TNFa antagonist therapy. Ó 2007 Elsevier Masson SAS. All rights reserved. Keywords: Cerebral vasculitis; Rheumatoid arthritis; Cerebral magnetic resonance imaging; Corticosteroids; Cyclophosphamide
1. Introduction
2. Case-report
Vasculitis is defined as vessel wall inflammation with or without necrosis. Primary cerebral vasculitis is exceedingly rare. Although cerebral vasculitis is usually a manifestation of systemic vasculitis, it may develop in association with a systemic inflammatory disease such as systemic lupus erythematosus, Sjo¨gren’s syndrome, Behc¸et’s disease, and more rarely rheumatoid arthritis (RA). We report a case of cerebral vasculitis in a 59-year-old woman with a 20-year history of destructive rheumatoid factor-positive RA treated with methotrexate. The abrupt onset of refractory headaches and gait disorders led to a diagnosis of cerebral vasculitis.
This 59-year-old woman with hypertension and wellcontrolled type 2 diabetes mellitus had a 20-year history of destructive RA with rheumatoid factors that was controlled by methotrexate (15 mg/week) and prednisone (5 mg/d) therapy, together with antiinflammatory drugs as needed. She presented with a 2-week history of bilateral temporal headaches, diplopia, and gait disorders. There was no fever or vomiting. At admission, her body temperature was normal and her blood pressure was 130/80 mmHg. Synovitis was noted at the left wrist and second and third metacarpophalangeal joints of both hands, as well as 30 flexion contracture of both elbows. The deep tendon reflexes and plantar reflexes were normal. No evidence of meningitis or focal neurological signs were found. The temporal pulses were brisk and symmetric. Funduscopy showed bilateral cataract formation with no evidence of intracranial hypertension. We were unable to examine the
* Corresponding author. Tel.: þ216 9 824 4261; fax: þ216 7 156 2834. E-mail address: [email protected] (D. Mrabet).
1297-319X/$ - see front matter Ó 2007 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.jbspin.2006.08.004
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D. Mrabet et al. / Joint Bone Spine 74 (2007) 201e204
cerebrospinal fluid. Laboratory tests revealed inflammation (erythrocyte sedimentation rate, 135 mm/h and C-reactive protein, 57 mg/L), normochromic normocytic anemia (hemoglobin, 8.3 g/dl), 6800/mm3 leukocytes, and 165,000/mm3 platelets. Liver and kidney function tests were normal, as well as blood glucose levels. Tests were positive for rheumatoid factors and negative for antinuclear antibodies, antibodies to extractable nuclear antigens (including anti-Ro and anti-La), and antineutrophil cytoplasmic antibodies. The headaches, visual symptoms, and laboratory evidence of inflammation prompted a temporal artery biopsy, which disclosed arteriosclerosis but no granuloma or other evidence suggesting giant cell arteritis. Magnetic resonance imaging (MRI) of the brain with the FLAIR sequence showed a dot-like pattern of high signal in a bilateral periventricular subcortical distribution suggesting hemispheric vasculitis (Figs. 1 and 2). Magnetic resonance (MR) angiography disclosed a long tight stenosis of the right internal carotid artery and a string-of-beads stenosis of the left internal carotid artery consistent with cerebral vasculitis (Fig. 3). Monthly boluses of methylprednisolone (1 g/d for 3 consecutive days) and cyclophosphamide (1 g) were given. The symptoms resolved and the inflammation abated (erythrocyte sedimentation rate, 22 mm/h; and C-reactive protein, 8 mg/L). Follow-up is 5 months at the time of this writing. An additional monthly bolus is planned, after which the methylprednisolone dosage will be tapered and the interval between cyclophosphamide injections increased to 2 then 3 months.
Fig. 2. Cerebral magnetic resonance imaging, FLAIR sequence, axial section: high signal in the subcortical area of the left frontal and right parietal lobes.
3. Discussion
Fig. 1. Cerebral magnetic resonance imaging, FLAIR sequence, axial section: high signal in the subcortical area of the right frontal lobe.
A few cases of cerebral vasculitis have been reported in patients with RA. The rate of occurrence of cerebral vasculitis in patients with RA has ranged from 1% to 8% [1]. Most of the patients were men who had long-standing, nodular, destructive RA with high levels of rheumatoid factors. Cerebral vasculitis usually developed after inappropriate discontinuation of glucocorticoid therapy. Severe constitutional symptoms were usually present, as well as prominent extraarticular manifestations of vasculitis affecting the skin, eyes, heart, and/or lungs. The joint manifestations, in contrast, were minimal. Our patient had long-standing RAwith joint destruction and rheumatoid factors. However, her disease was well controlled, she adhered to her glucocorticoid therapy regimen, and she had no extraarticular manifestations other than those related to cerebral vasculitis. The neurological manifestations of rheumatoid cerebral vasculitis are usually described as polymorphic [2]. Patients may have focal signs such as hemiplegia, partial epilepsy, cranial nerve involvement, or visual field loss. Diffuse manifestations denoting encephalitis may occur, such as altered consciousness, confusion, and cognitive impairment or dementia. These manifestations may exist in combination. A case of leptomeningeal involvement due to rheumatoid cerebral vasculitis has been reported [3]. Headache is a common symptom and may suggest giant cell arteritis, particularly as this condition can occur in patients with RA [4]. The negative temporal biopsy in our patient militated against giant cell arteritis, and the positive tests for rheumatoid factor supported the diagnosis of rheumatoid
D. Mrabet et al. / Joint Bone Spine 74 (2007) 201e204
Fig. 3. Magnetic resonance angiography: long narrow stenosis of the right internal carotid artery and string-of-beads stenosis of the left internal carotid artery.
vasculitis [4]. Systemic non-neurological manifestations usually antedate the cerebral symptoms. In the rare instances when central nervous system symptoms are inaugural, they indicate an increase in disease severity. Rheumatoid cerebral vasculitis can be diagnosed based on cerebrospinal fluid examination and on imaging studies. Funduscopy should be performed to rule out papilledema before performing the lumbar tap. Moderate lymphocytosis and protein elevation (1.7 g/L on average) indicate non-specific inflammation. Less often, the gammaglobulin level is elevated and electrophoresis shows oligoclonal bands. Cerebral MRI visualizes high signal in the white matter and may show signal abnormalities in the cortical regions or focal cortical atrophy [2]. Although a definitive diagnosis would require a cerebral and leptomeningeal biopsy, this procedure is rarely performed and its indications are poorly standardized [3]. The finding in our patient of high signal from the periventricular white matter was consistent with data in the literature [5]. However, in a study of 33 patients who had RA, high-signal white-matter lesions were not more common than in controls without RA [6]. Several histological patterns of vasculitis have been reported, including non-necrotizing lymphocytic vasculitis, leukocytoclastic vasculitis with immune complex deposition, necrotizing vasculitis, vasculitis associated with cryoglobulinemia, and vasculitis associated with hypergammaglobulinemia. Factors that have been incriminated in the pathophysiology of cerebral vasculitis include antibodies to endothelial cells, TNF, and antiphospholipid antibodies [7,8].
203
Perinuclear antineutrophil cytoplasmic antibodies were found in 29% of patients with rheumatoid cerebral vasculitis, suggesting a pathogenic role. HLA DRB1 has also been incriminated. In an uncontrolled study in 5 patients with rheumatoid cerebral vasculitis, aggressive glucocorticoid and cyclophosphamide therapy was effective, suggesting a role for this combination in patients with highly progressive disease refractory to glucocorticoid therapy [9]. Many treatment regimens have been used in patients with systemic vasculitis. Nevertheless, all of them included monthly boluses of glucocorticoids and cyclophosphamide with continuous glucocorticoid therapy in the intervals. Our patient was given monthly methylprednisolone (1 g/d for 3 days) and cyclophosphamide (1 g on day 4) for 5 consecutive months. After the sixth monthly bolus, the glucocorticoid dose will be tapered and the interval between cyclophosphamide injections increased to 2 then 3 months. Several alternatives are available for patients who fail to respond to conventional therapy. Azathioprine (ImurelÒ) [10], mycophenolate mofetil (CellceptÒ), and intravenous immunoglobulins have been used to good effect in patients with severe central nervous system diseases, usually related to lupus [11,12]. TNFa antagonists [13,14] hold promise for the treatment of rheumatoid cerebral vasculitis, since TNF has been incriminated in the pathogenesis of the lesions. However, other vasculitides such as giant cell arteritis and Wegener’s granulomatosis must be ruled out, as TNFa antagonists are not effective in these conditions. A few cases of sensory neuropathy revealing rheumatoid vasculitis associated with infliximab therapy have been reported [15].
References [1] Watts RA, Mooney J, Lane SE, Scott DG. Rheumatoid vasculitis: becoming extinct? Rheumatology 2004;43:920e3. [2] Zuber M, Mas JL. Ange´ites inflammatoires non-infectieuses du syste`me nerveux central. Encycl Me´d Chir (Elsevier, Paris), Neurologie 17-046A-95, 1997. [3] Chowdhry V, Kumar N, Lachance DH, Salomao DR, Luthra HS. An unusual presentation of rheumatoid meningitis. J Neuroimaging 2005; 15:286e8. [4] Pease CT, Haugeberg G, Morgan AW, Montague B, Hensor EM, Bhakta BB. Diagnosing late onset rheumatoid arthritis, polymyalgia rheumatica, and temporal arteritis in patients presenting with polymyalgic symptoms. A prospective long-term evaluation. J Rheumatol 2005;32:1043e6. Erratum in: J Rheumatol 2005; 32:1852. [5] Ando Y, Kai S, Uyama E, Iyonaga K, Hashimoto Y, Uchino M, et al. Involvement of the central nervous system in rheumatoid arthritis: its clinical manifestations and analysis by magnetic resonance imaging. Intern Med 1995;34:188e91. [6] Bekkelund SL, Pierre-Jerome C, Husby G, Mellgren SL. Quantitative cerebral MR in rheumatoid arthritis. AJNR 1995;16:767e72. [7] Nadeau SE. Neurologic manifestations of connective tissue disease. Neurol Clin 2002;20:151e78. [8] Zuber M, Blustajn J, Arquizan C, Trystram D, Mas JL, Meder JF. Angiitis of the central nervous system. J Neuroradiol 1999;26:101e17. [9] Cupps TR, Moore PM, Fauci AS. Isolated angeitis of the central nervous system. Am J Med 1983;74:97e106. [10] Singleton JD, West SG, Reddy VV, Rak KM. Cerebral vasculitis complicating rheumatoid arthritis. South Med J 1995;88:470e4.
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D. Mrabet et al. / Joint Bone Spine 74 (2007) 201e204
[11] Jose J, Paulose BK, Vasuki Z, Danda D. Mycophenolate mofetil in neuropsychiatric systemic lupus erythematosus. Indian J Med Sci 2005;59:353e6. [12] Milstone AM, Meyers K, Elia J. Treatment of acute neuropsychiatric lupus with intravenous immunoglobulin (IVIG): a case report and review of the literature. Clin Rheumatol 2005;24:394e7. [13] Bartolucci P, Ramanoelina J, Cohen P, Mahr A, Godmer P, Le Hello C, et al. Efficacy of the anti-TNF-alpha antibody infliximab against
refractory systemic vasculitides: an open pilot study on 10 patients. Rheumatology Oxford 2002;41:1126e32. [14] Chin RL, Latov N. Central nervous system manifestations of rheumatologic diseases. Curr Opin Rheumatol 2005;17:91e9. [15] Richette P, Dieude P, Damiano J, Liote F, Orcel P, Bardin T. Sensory neuropathy revealing necrotizing vasculitis during infliximab therapy for rheumatoid arthritis. J Rheumatol 2004;31:2079e81.
Case report
Cerebral vasculitis in a patient with rheumatoid arthritis Dalila Mrabet*, Nihel Meddeb, Houda Ajlani, Hela Sahli, Slaheddine Sellami Rheumatology Department, La Rabta Hospital, Tunis 1006, Tunisia Received 23 May 2006; accepted 2 August 2006 Available online 6 February 2007
Abstract Inflammatory vasculitis of the central nervous system is exceedingly rare in patients with rheumatoid arthritis (RA). The symptoms may be misleading. Most of the reported cases occurred in males with long-standing, nodular, destructive, rheumatoid factor-positive disease. Severe constitutional symptoms and prominent extraarticular manifestations of vasculitis were usually present. We report a case of cerebral vasculitis in a 59-year-old woman with a 20-year history of destructive rheumatoid factor-positive RA that was well controlled by methotrexate. Headache that was unresponsive to symptomatic treatment developed abruptly, together with gait disorders. Magnetic resonance imaging of the brain showed dot-like areas of high-signal in a periventricular subcortical distribution on both sides. Magnetic resonance angiography visualized a long tight stenosis of the right internal carotid artery and a string-of-beads stenosis of the left internal carotid artery suggesting vasculitis. Pulse therapy with methylprednisolone (1 g/d for 3 days) and cyclophosphamide (1 g) once a month ensured resolution of the neurological symptoms and laboratory evidence of inflammation. There was no evidence of a relapse at last follow-up after 5 months. Cerebral vasculitis is usually treated with monthly glucocorticoid and cyclophosphamide boluses separated by continuous glucocorticoid therapy. TNFa antagonists may be effective in patients who fail to respond to conventional treatment. However, other vasculitides such as giant cell arteritis and Wegener’s granulomatosis must be ruled out, as they are refractory to TNFa antagonist therapy. Ó 2007 Elsevier Masson SAS. All rights reserved. Keywords: Cerebral vasculitis; Rheumatoid arthritis; Cerebral magnetic resonance imaging; Corticosteroids; Cyclophosphamide
1. Introduction
2. Case-report
Vasculitis is defined as vessel wall inflammation with or without necrosis. Primary cerebral vasculitis is exceedingly rare. Although cerebral vasculitis is usually a manifestation of systemic vasculitis, it may develop in association with a systemic inflammatory disease such as systemic lupus erythematosus, Sjo¨gren’s syndrome, Behc¸et’s disease, and more rarely rheumatoid arthritis (RA). We report a case of cerebral vasculitis in a 59-year-old woman with a 20-year history of destructive rheumatoid factor-positive RA treated with methotrexate. The abrupt onset of refractory headaches and gait disorders led to a diagnosis of cerebral vasculitis.
This 59-year-old woman with hypertension and wellcontrolled type 2 diabetes mellitus had a 20-year history of destructive RA with rheumatoid factors that was controlled by methotrexate (15 mg/week) and prednisone (5 mg/d) therapy, together with antiinflammatory drugs as needed. She presented with a 2-week history of bilateral temporal headaches, diplopia, and gait disorders. There was no fever or vomiting. At admission, her body temperature was normal and her blood pressure was 130/80 mmHg. Synovitis was noted at the left wrist and second and third metacarpophalangeal joints of both hands, as well as 30 flexion contracture of both elbows. The deep tendon reflexes and plantar reflexes were normal. No evidence of meningitis or focal neurological signs were found. The temporal pulses were brisk and symmetric. Funduscopy showed bilateral cataract formation with no evidence of intracranial hypertension. We were unable to examine the
* Corresponding author. Tel.: þ216 9 824 4261; fax: þ216 7 156 2834. E-mail address: [email protected] (D. Mrabet).
1297-319X/$ - see front matter Ó 2007 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.jbspin.2006.08.004
202
D. Mrabet et al. / Joint Bone Spine 74 (2007) 201e204
cerebrospinal fluid. Laboratory tests revealed inflammation (erythrocyte sedimentation rate, 135 mm/h and C-reactive protein, 57 mg/L), normochromic normocytic anemia (hemoglobin, 8.3 g/dl), 6800/mm3 leukocytes, and 165,000/mm3 platelets. Liver and kidney function tests were normal, as well as blood glucose levels. Tests were positive for rheumatoid factors and negative for antinuclear antibodies, antibodies to extractable nuclear antigens (including anti-Ro and anti-La), and antineutrophil cytoplasmic antibodies. The headaches, visual symptoms, and laboratory evidence of inflammation prompted a temporal artery biopsy, which disclosed arteriosclerosis but no granuloma or other evidence suggesting giant cell arteritis. Magnetic resonance imaging (MRI) of the brain with the FLAIR sequence showed a dot-like pattern of high signal in a bilateral periventricular subcortical distribution suggesting hemispheric vasculitis (Figs. 1 and 2). Magnetic resonance (MR) angiography disclosed a long tight stenosis of the right internal carotid artery and a string-of-beads stenosis of the left internal carotid artery consistent with cerebral vasculitis (Fig. 3). Monthly boluses of methylprednisolone (1 g/d for 3 consecutive days) and cyclophosphamide (1 g) were given. The symptoms resolved and the inflammation abated (erythrocyte sedimentation rate, 22 mm/h; and C-reactive protein, 8 mg/L). Follow-up is 5 months at the time of this writing. An additional monthly bolus is planned, after which the methylprednisolone dosage will be tapered and the interval between cyclophosphamide injections increased to 2 then 3 months.
Fig. 2. Cerebral magnetic resonance imaging, FLAIR sequence, axial section: high signal in the subcortical area of the left frontal and right parietal lobes.
3. Discussion
Fig. 1. Cerebral magnetic resonance imaging, FLAIR sequence, axial section: high signal in the subcortical area of the right frontal lobe.
A few cases of cerebral vasculitis have been reported in patients with RA. The rate of occurrence of cerebral vasculitis in patients with RA has ranged from 1% to 8% [1]. Most of the patients were men who had long-standing, nodular, destructive RA with high levels of rheumatoid factors. Cerebral vasculitis usually developed after inappropriate discontinuation of glucocorticoid therapy. Severe constitutional symptoms were usually present, as well as prominent extraarticular manifestations of vasculitis affecting the skin, eyes, heart, and/or lungs. The joint manifestations, in contrast, were minimal. Our patient had long-standing RAwith joint destruction and rheumatoid factors. However, her disease was well controlled, she adhered to her glucocorticoid therapy regimen, and she had no extraarticular manifestations other than those related to cerebral vasculitis. The neurological manifestations of rheumatoid cerebral vasculitis are usually described as polymorphic [2]. Patients may have focal signs such as hemiplegia, partial epilepsy, cranial nerve involvement, or visual field loss. Diffuse manifestations denoting encephalitis may occur, such as altered consciousness, confusion, and cognitive impairment or dementia. These manifestations may exist in combination. A case of leptomeningeal involvement due to rheumatoid cerebral vasculitis has been reported [3]. Headache is a common symptom and may suggest giant cell arteritis, particularly as this condition can occur in patients with RA [4]. The negative temporal biopsy in our patient militated against giant cell arteritis, and the positive tests for rheumatoid factor supported the diagnosis of rheumatoid
D. Mrabet et al. / Joint Bone Spine 74 (2007) 201e204
Fig. 3. Magnetic resonance angiography: long narrow stenosis of the right internal carotid artery and string-of-beads stenosis of the left internal carotid artery.
vasculitis [4]. Systemic non-neurological manifestations usually antedate the cerebral symptoms. In the rare instances when central nervous system symptoms are inaugural, they indicate an increase in disease severity. Rheumatoid cerebral vasculitis can be diagnosed based on cerebrospinal fluid examination and on imaging studies. Funduscopy should be performed to rule out papilledema before performing the lumbar tap. Moderate lymphocytosis and protein elevation (1.7 g/L on average) indicate non-specific inflammation. Less often, the gammaglobulin level is elevated and electrophoresis shows oligoclonal bands. Cerebral MRI visualizes high signal in the white matter and may show signal abnormalities in the cortical regions or focal cortical atrophy [2]. Although a definitive diagnosis would require a cerebral and leptomeningeal biopsy, this procedure is rarely performed and its indications are poorly standardized [3]. The finding in our patient of high signal from the periventricular white matter was consistent with data in the literature [5]. However, in a study of 33 patients who had RA, high-signal white-matter lesions were not more common than in controls without RA [6]. Several histological patterns of vasculitis have been reported, including non-necrotizing lymphocytic vasculitis, leukocytoclastic vasculitis with immune complex deposition, necrotizing vasculitis, vasculitis associated with cryoglobulinemia, and vasculitis associated with hypergammaglobulinemia. Factors that have been incriminated in the pathophysiology of cerebral vasculitis include antibodies to endothelial cells, TNF, and antiphospholipid antibodies [7,8].
203
Perinuclear antineutrophil cytoplasmic antibodies were found in 29% of patients with rheumatoid cerebral vasculitis, suggesting a pathogenic role. HLA DRB1 has also been incriminated. In an uncontrolled study in 5 patients with rheumatoid cerebral vasculitis, aggressive glucocorticoid and cyclophosphamide therapy was effective, suggesting a role for this combination in patients with highly progressive disease refractory to glucocorticoid therapy [9]. Many treatment regimens have been used in patients with systemic vasculitis. Nevertheless, all of them included monthly boluses of glucocorticoids and cyclophosphamide with continuous glucocorticoid therapy in the intervals. Our patient was given monthly methylprednisolone (1 g/d for 3 days) and cyclophosphamide (1 g on day 4) for 5 consecutive months. After the sixth monthly bolus, the glucocorticoid dose will be tapered and the interval between cyclophosphamide injections increased to 2 then 3 months. Several alternatives are available for patients who fail to respond to conventional therapy. Azathioprine (ImurelÒ) [10], mycophenolate mofetil (CellceptÒ), and intravenous immunoglobulins have been used to good effect in patients with severe central nervous system diseases, usually related to lupus [11,12]. TNFa antagonists [13,14] hold promise for the treatment of rheumatoid cerebral vasculitis, since TNF has been incriminated in the pathogenesis of the lesions. However, other vasculitides such as giant cell arteritis and Wegener’s granulomatosis must be ruled out, as TNFa antagonists are not effective in these conditions. A few cases of sensory neuropathy revealing rheumatoid vasculitis associated with infliximab therapy have been reported [15].
References [1] Watts RA, Mooney J, Lane SE, Scott DG. Rheumatoid vasculitis: becoming extinct? Rheumatology 2004;43:920e3. [2] Zuber M, Mas JL. Ange´ites inflammatoires non-infectieuses du syste`me nerveux central. Encycl Me´d Chir (Elsevier, Paris), Neurologie 17-046A-95, 1997. [3] Chowdhry V, Kumar N, Lachance DH, Salomao DR, Luthra HS. An unusual presentation of rheumatoid meningitis. J Neuroimaging 2005; 15:286e8. [4] Pease CT, Haugeberg G, Morgan AW, Montague B, Hensor EM, Bhakta BB. Diagnosing late onset rheumatoid arthritis, polymyalgia rheumatica, and temporal arteritis in patients presenting with polymyalgic symptoms. A prospective long-term evaluation. J Rheumatol 2005;32:1043e6. Erratum in: J Rheumatol 2005; 32:1852. [5] Ando Y, Kai S, Uyama E, Iyonaga K, Hashimoto Y, Uchino M, et al. Involvement of the central nervous system in rheumatoid arthritis: its clinical manifestations and analysis by magnetic resonance imaging. Intern Med 1995;34:188e91. [6] Bekkelund SL, Pierre-Jerome C, Husby G, Mellgren SL. Quantitative cerebral MR in rheumatoid arthritis. AJNR 1995;16:767e72. [7] Nadeau SE. Neurologic manifestations of connective tissue disease. Neurol Clin 2002;20:151e78. [8] Zuber M, Blustajn J, Arquizan C, Trystram D, Mas JL, Meder JF. Angiitis of the central nervous system. J Neuroradiol 1999;26:101e17. [9] Cupps TR, Moore PM, Fauci AS. Isolated angeitis of the central nervous system. Am J Med 1983;74:97e106. [10] Singleton JD, West SG, Reddy VV, Rak KM. Cerebral vasculitis complicating rheumatoid arthritis. South Med J 1995;88:470e4.
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D. Mrabet et al. / Joint Bone Spine 74 (2007) 201e204
[11] Jose J, Paulose BK, Vasuki Z, Danda D. Mycophenolate mofetil in neuropsychiatric systemic lupus erythematosus. Indian J Med Sci 2005;59:353e6. [12] Milstone AM, Meyers K, Elia J. Treatment of acute neuropsychiatric lupus with intravenous immunoglobulin (IVIG): a case report and review of the literature. Clin Rheumatol 2005;24:394e7. [13] Bartolucci P, Ramanoelina J, Cohen P, Mahr A, Godmer P, Le Hello C, et al. Efficacy of the anti-TNF-alpha antibody infliximab against
refractory systemic vasculitides: an open pilot study on 10 patients. Rheumatology Oxford 2002;41:1126e32. [14] Chin RL, Latov N. Central nervous system manifestations of rheumatologic diseases. Curr Opin Rheumatol 2005;17:91e9. [15] Richette P, Dieude P, Damiano J, Liote F, Orcel P, Bardin T. Sensory neuropathy revealing necrotizing vasculitis during infliximab therapy for rheumatoid arthritis. J Rheumatol 2004;31:2079e81.