Radiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Murphy, J. M.
Right arrow Articles by Lockwood, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Murphy, J. M.
Right arrow Articles by Lockwood, M.
(Radiology. 1999;213:794-799.)
© RSNA, 1999

Neuroradiology

Wegener Granulomatosis: MR Imaging Findings in Brain and Meninges1

Joseph M. Murphy, FRCR, Beatriz Gomez-Anson, MD, PhD, Jonathan H. Gillard, MD, Nagui M. Antoun, FRCP, FRCR, Justin Cross, FRCR, Jane D. Elliott, BSc, RGN and Martin Lockwood, FRCP

1 From the Departments of Radiology (J.M.M., B.G.A., J.H.G., N.M.A., J.C.) and Medicine (J.D.E., M.L.), Addenbrooke's Hospital and University of Cambridge, England. Received December 17, 1998; revision requested January 5, 1999; revision received March 10; accepted July 1. Address reprint requests to J.M.M., Department of Radiology, Sunnybrook Health Science Centre, 2075 Bayview Ave, North York, Toronto, Ontario, Canada M4N 3MS (e-mail: joemmurphy@hotmail.com).


   Abstract
TOP
 Abstract
Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To determine the spectrum of intracranial magnetic resonance (MR) imaging appearances of Wegener granulomatosis.

MATERIALS AND METHODS: MR imaging studies in 19 patients with Wegener granulomatosis and possible central nervous system involvement were reviewed by two neuroradiologists. Intermediate-weighted and T2-weighted fast spin-echo MR images of the brain had been acquired in all patients, and spin-echo T1-weighted nonenhanced and gadolinium-enhanced images had been acquired in 18 patients.

RESULTS: MR imaging findings included diffuse linear dural thickening and enhancement (n = 6); focal dural thickening and enhancement contiguous with orbital, nasal, or paranasal disease (n = 5); infarcts (n = 4); nonspecific white matter areas of high signal intensity on intermediate-weighted and T2-weighted images (n = 10); enlarged pituitary gland with infundibular thickening and enhancement (n = 2); a discrete cerebellar lesion that was probably granulomatous in origin (n = 1); and cerebral (n = 8) and cerebellar atrophy (n = 2).

CONCLUSION: MR imaging demonstrated the wide spectrum of findings of central nervous system involvement in patients with Wegener granulomatosis and was particularly useful for the evaluation of direct intracranial spread from orbital, nasal, or paranasal disease.

Index terms: Brain, atrophy, 13.83, 153.83 • Brain, diseases, 10.622 • Brain, infarction, 13.78 • Brain, MR, 10.121411, 10.121415, 10.12143 • Gadolinium • Meninges, 10.622 • Wegener granulomatosis, 10.622


   Introduction
TOP
 Abstract
 Introduction
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Wegener granulomatosis is a multisystem disorder characterized by necrotizing granulomas in the upper and/or lower respiratory tract, with or without focal necrotizing glomerulonephritis and a systemic vasculitis (1–6). The orbits, heart, skin, and joints also are frequently involved (4). The nervous system is frequently affected (in 22%–54% of cases), with the condition most commonly manifesting as peripheral neuropathy (in 10.6%–21.2% of patients) or mononeuritis multiplex (2,4–6). Cerebral and meningeal involvement are uncommon, however, occurring in only 2%–8% of patients (1,4,6). Previously published studies (7,8) have contained small numbers of patients; thus, the purpose of this study was to determine the spectrum of cerebral and meningeal magnetic resonance (MR) imaging findings in 19 patients with Wegener granulomatosis.


   MATERIALS AND METHODS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Between June 1992 and July 1998, 19 patients (six men, 13 women) with Wegener granulomatosis had abnormalities of the brain or meninges detected on MR images. All patients fulfilled the American College of Rheumatology 1990 criteria (9) for the diagnosis of Wegener granulomatosis. The mean age of the patients was 47 years 4 months (age range, 17 years to 71 years 5 months). The primary reason for referral in each patient is enumerated in the Table.


View this table:
[in this window]
[in a new window]
  		Reasons for Referral and MR Imaging Findings in 19 Patients
 
The examinations were performed with a 0.5-T (Signa Horizon; GE Medical Systems, Milwaukee, Wis) or 1.5-T (Signa Horizon or LX; GE Medical Systems) MR unit. In all patients, transverse intermediate-weighted fast spin-echo (3,000/15 [repetition time msec/effective echo time msec]) and T2-weighted fast spin-echo (3,000/105 [effective]) images were acquired. These images were obtained with a 22 x 22-cm field of view, a 6-mm section thickness, a 1-mm intersection gap, a 256 x 256 matrix, and one signal acquired.

In 18 patients, transverse, coronal, or sagittal T1-weighted spin-echo MR images (500–540/9–14 [repetition time msec/echo time msec]; field of view, 20–22 x 20–22; section thickness, 5 mm; matrix, 256 x 256; two signals acquired) also were obtained before and after intravenous administration of 0.1 mmol/kg gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany). Eleven examinations were performed with and seven were performed without spectral fat suppression.

Two consulting neuroradiologists (B.G.A., N.M.A.) independently reviewed all 19 studies at a workstation and used the standard postprocessing facilities available at the time. Each study was evaluated for the following features, which are recognized (5–8) as occurring in Wegener granulomatosis: meningeal thickening; direct spread from orbital, nasal, or paranasal disease; remote cerebral granulomatous lesions; infarcts; nonspecific white matter lesions; atrophy; pituitary gland enlargement; and infundibular thickening. A consensus was obtained when necessary.

The clinical history of each patient was subsequently reviewed with the consulting physician responsible for the patient's care, with specific reference to the following features: primary reason for referral for cranial MR imaging; extent of orbital, nasal, and paranasal disease; response to treatment; and presence of any other disease processes that may have contributed to the MR imaging appearance.


   RESULTS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
On MR images in 17 of 19 patients, abnormalities were present in the sinuses, nasal cavity, or orbits. In eight patients, orbital masses were present with low signal intensity on T1-weighted, intermediate-weighted, and T2-weighted images and showed contrast enhancement. Similar lesions were seen in the nasal cavity and paranasal sinuses in two patients. Fourteen patients had inflammatory changes in their nasal cavity and paranasal sinuses that manifested as areas of high signal intensity on intermediate-weighted and T2-weighted images. Bone erosion was evident in six patients. The clinical and radiologic features for all patients are summarized in the Table.

Meningeal Enhancement
The meninges were considered to be abnormal if they showed either diffuse or focal thickening on contrast-enhanced MR images. Meningeal thickening and enhancement were found in 11 patients. Two distinct patterns of distribution were noted: (a) diffusely abnormal meninges unrelated to sinus or orbital disease and (b) focal dural thickening and enhancement adjacent to sinus or orbital disease.

Diffuse thickening and enhancement.—Diffuse meningeal thickening and enhancement (Fig 1) were present in six patients (patients 1–6). In these six patients, enhancement was seen in the dura; in one patient, leptomeningeal enhancement also was present. Nodular enhancement was not found in any patient. Involvement of both the tentorium cerebelli and the dura overlying the convexity of the cerebrum was noted in five patients; the tentorium cerebelli was the sole site of involvement in one. One patient had asymmetric enhancement in which the right side of the tentorium cerebelli initially was more severely involved than the left, but the appearances were symmetric on subsequently obtained MR images. In one patient, there also was diffuse dural thickening and enhancement overlying the thoracic cord, with normal dura in the cervical region (Fig 2). In all six patients, severe headache was the reason for referral for MR imaging. No patient had cranial nerve palsy. In four patients, meningeal biopsy was performed, and histologic results were consistent with Wegener granulomatosis.



View larger version (129K):
[in this window]
[in a new window]
  		Figure 1a. (a) Transverse and (b) coronal T1-weighted contrast-enhanced spin-echo MR images (500/9) demonstrate diffuse symmetric linear dural thickening and enhancement (arrowheads).

 


View larger version (127K):
[in this window]
[in a new window]
  		Figure 1b. (a) Transverse and (b) coronal T1-weighted contrast-enhanced spin-echo MR images (500/9) demonstrate diffuse symmetric linear dural thickening and enhancement (arrowheads).

 


View larger version (88K):
[in this window]
[in a new window]
  		Figure 2a. (a) Sagittal and (b) transverse T1-weighted contrast-enhanced spin-echo MR images (500/9) show extensive thickening and enhancement of the dura (arrows) overlying the thoracic spinal cord.

 


View larger version (105K):
[in this window]
[in a new window]
  		Figure 2b. (a) Sagittal and (b) transverse T1-weighted contrast-enhanced spin-echo MR images (500/9) show extensive thickening and enhancement of the dura (arrows) overlying the thoracic spinal cord.

 
Focal thickening and enhancement.—Focal dural thickening and enhancement adjacent to nasal, orbital, or sinus disease consistent with direct spread were present in five patients (patients 11–15). In three patients, the affected dura was overlying the inferior aspect of the frontal lobes. The enhancement was contiguous with ethmoidal sinus disease in one patient and with orbital, nasal, and paranasal sinus disease in two patients. Dural enhancement was bilateral in one patient (Fig 3). In two patients, there was thickening and enhancement of the dura overlying the anterior temporal lobe (Fig 4), which was contiguous with nasal and paranasal sinus disease in both patients and was bilateral in one. The dural thickening and enhancement were linear in all five patients. Further dural thickening remote from the nasal, paranasal, or orbital areas was not seen in any of these five patients.



View larger version (130K):
[in this window]
[in a new window]
  		Figure 3. Coronal fat-suppressed T1-weighted contrast-enhanced spin-echo MR image (500/9) demonstrates focal thickening and enhancement of the dura (arrows) overlying the inferior aspect of both frontal lobes and contiguous with extensive nasal and paranasal disease.

 


View larger version (132K):
[in this window]
[in a new window]
  		Figure 4. Transverse fat-suppressed T1-weighted contrast-enhanced spin-echo MR image (500/9) shows thickening and enhancement of the dura overlying the anterior left temporal lobe (arrows) contiguous with extensive paranasal disease.

 
Infarcts
Four patients (patients 10, 14, 17, and 18) showed areas of high signal intensity on T2-weighted and intermediate-weighted images, which were indicative of nonhemorrhagic infarcts that affected the cortex, white matter, or both, in a typical vascular distribution. In two patients, more than one area of infarct was seen. Two patients had clinical evidence of cerebral vasculitis, and one patient had an infarct may have been secondary to intraarterial infusion of chemotherapy drugs into the ophthalmic artery to treat extensive orbital involvement by Wegener granulomatosis. No patient had hypertension.

Nonspecific White Matter Lesions
Ten patients had nonspecific white matter lesions with high signal intensity on intermediate-weighted and T2-weighted images. These lesions, which were multiple in all cases, were seen in the periventricular and subcortical regions, the basal ganglia, and the mesencephalon and pons (Fig 5). The mean age of these 10 patients was 53 years 6 months (range, 17 years to 71 years 5 months). Three patients had clinical symptoms suggestive of cerebral vasculitis, and two of these patients had symptoms of paraesthesia, loss of vision, and internuclear ophthalmoplegia consistent with cerebral ischemia and infarct. Three of the 10 patients had coexistent hypertension.



View larger version (155K):
[in this window]
[in a new window]
  		Figure 5. Transverse T2-weighted fast spin-echo MR image (3,000/105 [effective]) in a patient suspected of having cerebral vasculitis shows an ill-defined area of high signal intensity in the pons (arrows).

 
Discrete Cerebellar Granuloma
A discrete right cerebellar lesion with high signal intensity on intermediate-weighted and T2-weighted images, low signal intensity on T1-weighted images, and some peripheral enhancement on gadolinium-enhanced images was demonstrated in a 55-year-old patient (patient 19), who presented with a gradual onset of dysarthria and ataxia (Fig 6). After treatment with anti-CD52, the ataxia improved and the lesion was smaller on subsequently obtained MR images.



View larger version (146K):
[in this window]
[in a new window]
  		Figure 6. Transverse T2-weighted fast spin-echo MR image (3,000/105 [effective]) in a patient with gradual onset of ataxia shows a discrete right cerebellar lesion (arrow) with high signal intensity. An intracerebral granulomatous lesion was thought to be the most likely cause because of the location, gradual onset of symptoms, peripheral enhancement, and improvement in ataxia and reduction in the size of the lesion after treatment.

 
Pituitary Abnormalities
Two patients (patients 11 and 18) had an enlarged pituitary gland (craniocaudal dimension > 11 mm) (Fig 7). In both patients, enhancement of the pituitary gland was homogeneous, and there was thickening and enhancement of the infundibulum, especially superiorly. There also was a large, enhanced inflammatory mass in the sphenoid sinus in both patients. One patient had diabetes insipidus, with resolution of polyuria after treatment with anti-CD52.



View larger version (126K):
[in this window]
[in a new window]
  		Figure 7. Coronal T1-weighted contrast-enhanced spin-echo MR image (500/9) in a patient with diabetes insipidus shows diffuse enlargement of the pituitary gland (straight arrows) with thickening and enhancement of the infundibulum (curved arrows). There also is filling and rim enhancement (arrowheads) in the sphenoid sinuses, consistent with inflammatory disease.

 
Atrophy
Eight (42%) of 19 patients had cerebral atrophy that was more marked than expected given their age (mean age, 50 years 11 months; range, 30 years 11 months to 67 years 11 months). Cerebral atrophy was mild in five patients and moderate in three. Two of these eight patients also had mild cerebellar atrophy. Three of the eight patients had symptoms suggestive of cerebral vasculitis, including peculiar intellectual affect, headaches, confusion, and transient neurologic events such as paraesthesia, blackouts, and visual loss. All patients had undergone steroid therapy at some stage during their illness.


   DISCUSSION
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
In a 1963 literature review of 104 patients with Wegener granulomatosis, Drachman (5) identified three processes of nervous system involvement. First, vasculitis occurred in 29 (28%) patients and produced mononeuritis multiplex, polyneuritis, myopathy, intracerebral hemorrhage, subarachnoid hemorrhage, and cerebral arterial or venous thrombosis. Second, granulomatous lesions resulting from contiguous invasion from nasal, paranasal, or orbital disease and involving the optic nerve, optic chiasm, pituitary, nasal vestibule, base of the brain, and meninges were present in 27 (26%) patients. Third, granulomatous lesions remote from nasal granulomas and involving the meninges, cranial nerves, brain, and parietal bone were described in four (4%) patients.

Because cerebral and meningeal involvement by Wegener granulomatosis is rare, with a reported prevalence of 2%–8% (1,4,6), there are few reports of small series (7,8) in which the MR imaging appearances were described. Asmus et al (7) reported the MR imaging findings in seven patients: Six patients had small, sometimes multiple, focal areas of increased signal intensity in the white matter on T2-weighted images, and one had an infarct. Provenzale and Allen (8) reported the computed tomographic (two patients) and MR imaging (five patients) findings in seven patients, which included dural thickening and contrast enhancement in three patients, infarcts in two, areas of high signal intensity in the white matter on T2-weighted MR images in two, and abnormal high signal intensity in the brainstem on T2-weighted MR images in two. Direct intracranial spread from nasal, paranasal, or orbital disease or remote, discrete granulomatous lesions in brain parenchyma were not reported in either series.

Remote granulomatous involvement of the meninges in Wegener granulomatosis is rare (4–6,10). At postmortem examination in one of 104 patients in Drachman's review (5), meningeal involvement by a necrotic and granulomatous process was observed. Nishino et al (6,10) reported that only one of 324 patients with Wegener granulomatosis had thickening and enhancement of the right tentorium cerebelli, which caused multiple cranial neuropathies and severe headaches. None of 85 patients described by Fauci et al (4) had meningeal involvement with Wegener granulomatosis. In our series, the typical MR imaging appearance was that of bilateral diffuse symmetric linear dural thickening and enhancement. Similar findings were described by Provenzale and Allen (8) in three patients, although focal and nodular thickening have also been previously reported (11). Large areas of high signal intensity in the white matter underlying thickened meninges on T2-weighted images have been previously noted (11,12) but were not present in any of the patients in our series.

One patient in our series had diffuse dural thickening and enhancement both intracranially and overlying the thoracic cord. To our knowledge, such MR imaging findings have not previously been reported. There is one previous report (10) of dural thickening overlying the thoracic cord in a case of Wegener granulomatosis, and this resulted in a subacute myelopathy. There was no evidence of myelopathy in the patient in our series.

One patient had leptomeningeal thickening and enhancement overlying the sulci in addition to dural enhancement. To our knowledge, this radiologic finding has not previously been reported, although thickening, fibrosis, and numerous granulomas that often surrounded and involved blood vessels, as seen at histologic examination of the pia-arachnoid, have been reported (11).

The differential diagnosis for diffuse symmetric linear meningeal thickening is broad and includes neurosarcoid, primary dural tumors such as lymphoma and meningioma, metastases, infectious meningitis, neurosyphilis, and hypertrophic cranial pachymeningitis. In neurosarcoid, the pia is involved more frequently than the dura (13). Clinical evaluation and laboratory and radiologic investigations help the radiologist determine the most likely diagnosis, although biopsy may be necessary for confirmation.

Direct intracranial invasion from adjacent extracranial disease has been reported (5,14) to be the most common means by which the central nervous system is involved with Wegener granulomatosis. There was extensive nasal, paranasal, or orbital disease in all five patients in our series who had evidence of direct spread. Two patients showed a poor response to chemotherapy at these sites, and one patient had refused treatment for 4–5 years, which resulted in advanced disease.

The ability to acquire multiplanar images without irradiating the eyes makes MR imaging an excellent modality for demonstration of subtle intracranial spread from nasal, paranasal, or orbital disease. Because thickened dura can be difficult to differentiate from cerebrospinal fluid on T2-weighted images, we advocate the use of fat-suppressed T1-weighted MR imaging with gadolinium enhancement when direct spread is suspected.

Vasculitis most frequently affects the peripheral nervous system, causing mononeuritis multiplex or polyneuritis; it involves the brain or meninges in 0%–6% of patients, causing intracerebral hemorrhage, subarachnoid hemorrhage, and cerebral arterial or venous thrombosis (4–6). These hemorrhagic complications are thought to be secondary to weakening of blood vessel walls by means of an inflammatory vasculitis, resulting in vessel rupture and bleeding. Four patients in our series had symptoms suggestive of vasculitis, such as altered consciousness or altered affect, or symptoms suggestive of ischemic episodes, such as paraesthesia, blackouts, or internuclear ophthalmoplegia. In three of these patients, nonspecific areas of high signal intensity were seen in the white matter on intermediate-weighted and T2-weighted MR images, and two of these patients had infarcts. There are several other possible causes of infarct in cases of Wegener granulomatosis: arterial occlusion secondary to a granulomatous mass that extends from nasal or paranasal sites into the skull base (15), emboli from marantic endocarditis (8), infarct secondary to renal failure–induced hypertension, and other causes unrelated to Wegener granulomatosis.

Remote granulomatous lesions in brain parenchyma are the least common form of central nervous system involvement with Wegener granulomatosis (5), although there have been a few reported cases (16–18). Patients may present with seizures, and the lesions may be single or multiple (17,18). Homogeneous and ring enhancement have been demonstrated, and the lesions have high signal intensity on T2-weighted MR images and have been shown to either decrease in size or disappear with treatment (17). Cerebral granulomas have been found to be dark brown, scarred, indurated, and poorly demarcated at surgery and to contain plasma cells, lymphocytes, histiocytes, and giant cells at histologic examination (18).

Multiple nonspecific lesions with increased signal intensity on intermediate-weighted and T2-weighted MR images are seen in the white matter in many conditions, including postinfectious encephalitis, viral infections, sarcoidosis, multiple sclerosis, Behçet syndrome, and the leukodystrophies, and are commonly seen in the elderly. Although there was possible coexistent vasculitis in three of the 10 patients with such lesions in our series, the exact etiology in relation to Wegener granulomatosis was unclear. Similar white matter lesions in cases of Wegener granulomatosis have also been reported by Provenzale and Allen (8) and Asmus et al (7). Asmus et al reported that these areas represented areas of microinfarct, and Drachman (5) reported the postmortem examination finding of small (<4 x 6-mm) areas of infarct in the thalamus, cortex, mesencephalon, pons, and subcortical white matter in a patient with cerebral vasculitis secondary to Wegener granulomatosis.

The pituitary and infundibulum may be involved in Wegener granulomatosis by means of distant granulomas or direct spread. Four patients in Drachman's series (5) had involvement of the pituitary gland due to direct extension from nasal, paranasal, or orbital disease that caused diabetes insipidus. Czarnecki and Spickler (19) reported a case of diabetes insipidus and hyperprolactinemia; this was probably secondary to remote granulomatous involvement with Wegener granulomatosis because there was no evidence of direct extension from extracranial disease. MR imaging demonstrated a sellar mass, absence of the posterior pituitary high-signal-intensity spot, and thickening and enhancement of the infundibulum, with almost complete resolution of findings at repeat imaging performed 2 months after treatment with high-dose steroid therapy (19). In the two patients in our series with diffuse enlargement of the pituitary gland and infundibular thickening, it is impossible to be certain whether this represented distal granulomatous involvement with Wegener granulomatosis or direct spread from extensive inflammatory changes in the sphenoid sinus, although the floor of the pituitary fossa appeared to be intact in both patients.

Finally, the exact etiology of brain atrophy in cases of Wegener granulomatosis is unclear, but possible explanations include cerebral vasculitis, drugs used in treatment (eg, steroids), and other unrelated causes such as senile atrophy. Yamashita et al (20) reported the development of cerebral atrophy over 6 months in a patient with cerebral vasculitis secondary to Wegener granulomatosis.

In summary, in patients with cerebral and meningeal involvement with Wegener granulomatosis, there is a wide spectrum of MR imaging findings, which reflect the three means by which the central nervous system can be affected in this disease: vasculitis; direct spread from adjacent disease in the nasal, paranasal, or orbital region; and remote granulomatous lesions. MR imaging, with which it is possible to acquire multiplanar images without radiation, is an excellent modality for demonstration of these abnormalities, especially for evaluation for direct spread to the meninges from orbital, nasal, or paranasal disease.


   Footnotes
 
Author contributions: Guarantors of integrity of entire study, J.M.M., B.G.A., J.H.G., N.M.A., J.C., M.L.; study concepts, J.M.M., B.G.A., J.H.G., N.M.A., M.L.; study design, J.M.M., B.G.A., J.H.G., M.L.; definition of intellectual content, J.M.M., B.G.A., J.H.G., N.M.A., J.C., M.L.; literature research, J.M.M., J.H.G.; clinical studies, J.M.M., B.G.A., N.M.A., M.L.; data acquisition, all authors; data analysis, J.M.M., B.G.A., J.H.G., N.M.A., J.C., M.L.; manuscript preparation, editing, and review, J.M.M., B.G.A., J.H.G., N.M.A., J.C., M.L.


   References
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

  1. Hoffman GS, Kerr GS, Leavitt RY, et al. Wegener granulomatosis: an analysis of 158 patients. Ann Intern Med 1992; 116:488-498.
  2. Anderson JM, Jamieson DG, Jefferson JM. Non-healing granuloma and the nervous system. Q J Med 1975; 44:309-323.[Abstract/Free Full Text]
  3. DeRemee RA, McDonald TJ, Harrison EG, Jr, Coles DT. Wegener's granulomatosis: anatomic correlates, a proposed classification. Mayo Clin Proc 1976; 51:777-781.[Medline]
  4. Fauci AS, Haynes BF, Katz P, Wolff SM. Wegener's granulomatosis: prospective clinical and therapeutic experience with 85 patients for 21 years. Ann Intern Med 1983; 98:76-85.
  5. Drachman DA. Neurological complications of Wegener's granulomatosis. Arch Neurol 1963; 8:145-155.[Abstract/Free Full Text]
  6. Nishino H, Rubino FA, DeRemee RA, Swanson JW, Parisi JE. Neurological involvement in Wegener's granulomatosis: an analysis of 324 consecutive patients at the Mayo Clinic. Ann Neurol 1993; 33:4-9.[Medline]
  7. Asmus R, Koltze H, Muhle C, et al. MRI of the head in Wegener's granulomatosis. Adv Exp Med Biol 1993; 336:319-321.[Medline]
  8. Provenzale JM, Allen NB. Wegener granulomatosis: CT and MR findings. AJNR 1996; 17:785-792.[Abstract]
  9. Leavitt RY, Fauci AS, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of Wegener's granulomatosis. Arthritis Rheum 1990; 33:1101-1107.[Medline]
  10. Nishino H, Rubino FA, Parisi JE. The spectrum of neurologic involvement in Wegener's granulomatosis. Neurology 1993; 43:1334-1337.[Abstract/Free Full Text]
  11. Tishler S, Williamson T, Mirra SS, Lichtman JB, Gismondi P, Kibble MB. Wegener granulomatosis with meningeal involvement. AJNR 1993; 14:1248-1252.[Abstract]
  12. Weinberger LM, Cohen ML, Remler BF, Naheedy MH, Leigh RJ. Intracranial Wegener's granulomatosis. Neurology 1993; 43:1831-1834.[Abstract/Free Full Text]
  13. Sherman JL, Stern BJ. Sarcoidosis of the CNS: comparison of unenhanced and enhanced MR images. AJNR 1990; 11:915-923.[Abstract]
  14. Goldberg AL, Tievsky AL, Jamshidi S. Wegener granulomatosis invading the cavernous sinus: a CT demonstration. J Comput Assist Tomogr 1983; 7:701-703.[Medline]
  15. Satoh J, Miyasaka N, Yamada T, et al. Extensive cerebral infarction due to involvement of both anterior cerebral arteries by Wegener's granulomatosis. Ann Rheum Dis 1988; 47:606-611.[Abstract/Free Full Text]
  16. Castleman B, Towne VW. Wegener's granulomatosis. Massachusetts General Hospital Case Records, case 37511. N Engl J Med 1951; 245:978-985.
  17. Miller KS, Miller JM. Wegener's granulomatosis presenting as a primary seizure disorder with brain lesions demonstrated by magnetic resonance imaging. Chest 1993; 103:316-318.[Abstract/Free Full Text]
  18. Oimomi N, Suehiro I, Mizuno N, Baba S, Okada S, Kanazawa Y. Wegener's granulomatosis with intracerebral granuloma and mammary manifestation. Arch Intern Med 1980; 140:853-854.[Abstract/Free Full Text]
  19. Czarnecki EJ, Spickler EM. MR demonstration of Wegener granulomatosis of the infundibulum, a cause of diabetes insipidus. AJNR 1995; 16(suppl 4):968-970.[Abstract]
  20. Yamashita Y, Takahashi M, Bussaka H, Miyawaki M, Tosaka K. Cerebral vasculitis secondary to Wegener's granulomatosis: computed tomography and angiographic findings. J Comput Assist Tomogr 1986; 10:115-120.



This article has been cited by other articles:


Home page
 RadiologyHome page
M. K. Demir, F. V. Aker, O. Akinci, and A. Ozgultekin
Case 134: Primary Leptomeningeal Melanomatosis
Radiology, June 1, 2008; 247(3): 905 - 909.
[Full Text] [PDF]

Home page
 Br. J. Radiol.Home page
S D Allen and C J Harvey
Imaging of Wegener's granulomatosis
Br. J. Radiol., September 1, 2007; 80(957): 757 - 765.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
J. Short, A. M. McKinney, L. T. Lucato, M. Teksam, and C. L. Truwit
Transalar Encephalocele Associated with Wegener Granulomatosis and Meningeal Enhancement: Case Report
AJNR Am. J. Neuroradiol., August 1, 2005; 26(7): 1873 - 1875.
[Abstract] [Full Text] [PDF]

Home page
 Rheumatology (Oxford)Home page
G. Di Comite, E. Bozzolo, S. Bianchi, and M. G. Sabbadini
Two cases of meningeal involvement in Wegener's granulomatosis
Rheumatology, November 1, 2004; 43(11): 1459 - 1460.
[Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
A. Berlis, F. Petschner, I. C. Botefur, and J. Spreer
Wegener Granuloma in the Fourth Ventricle
AJNR Am. J. Neuroradiol., March 1, 2003; 24(3): 523 - 525.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
H.-J. Mentzel, T. Neumann, C. Fitzek, D. Sauner, J. R. Reichenbach, and W. A. Kaiser
MR Imaging in Wegener Granulomatosis of the Spinal Cord
AJNR Am. J. Neuroradiol., January 1, 2003; 24(1): 18 - 21.
[Abstract] [Full Text] [PDF]

Home page
 Ann Rheum DisHome page
K Warnatz, H H Peter, M Schumacher, L Wiese, A Prasse, F Petschner, P Vaith, B Volk, and S M Weiner
Infectious CNS disease as a differential diagnosis in systemic rheumatic diseases: three case reports and a review of the literature
Ann Rheum Dis, January 1, 2003; 62(1): 50 - 57.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
A. M. Tokumaru, T. Obata, S. Kohyama, T. Kaji, H. Okizuka, K. Suzuki, and S. Kusano
Intracranial Meningeal Involvement in Churg-Strauss Syndrome
AJNR Am. J. Neuroradiol., February 1, 2002; 23(2): 221 - 224.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
J. M. Murphy, K. K. Balan, A. Toms, B. Gomez-Anson, and M. Lockwood
Radiolabeled Leucocyte Imaging in Diffuse Granulomatous Involvement of the Meninges in Wegener's Granulomatosis: Scintigraphic Findings and Their Role in Monitoring Treatment Response to Specific Immunotherapy (Humanized Monoclonal Antilymphocyte Antibodies)
AJNR Am. J. Neuroradiol., August 1, 2000; 21(8): 1460 - 1465.
[Abstract] [Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Murphy, J. M.
Right arrow Articles by Lockwood, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Murphy, J. M.
Right arrow Articles by Lockwood, M.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
RADIOLOGY RADIOGRAPHICS RSNA JOURNALS ONLINE