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Show Journal of Clinical NeuTo-ophthalmology 13(2); 127-134, 1993. Idiopathic Hypertrophic Cranial Pachymeningitis Steven R. Hamilton, M.D., Craig H. Smith, M.D., and Simmons Lessell, M.D. © 1993 Raven Press, Ltd., New York We evaluated 3 patients with biopsy-proven hypertrophic cranial pachymeningitis apparently unrelated to any systemic disease. Each patient had chronic headache, cranial neuropathy, an elevated ESR, and a mild CSF pleocytosis. Neuro-ophthalmic findings included bilateral sixth nerve palsies in two patients and the third had bilateral optic neuropathies. MR imaging revealed thickened dura that enhanced with Cd-DTPA administration. Histologic examination showed thickened, fibrotic dura with a sterile, chronic, nongranulomatous inflammation. The response to treatment was variable with corticosteroids, immunosuppressive drugs, or radiation. The distinctive MR appearance should help physicians recognize this rarely reported disease. Key Words: Pachymeningitis-Dura-Magnetic resonance imaging. From NW Neuro-Ophthalmic Associates and the Division of Neurology, the Department of Medicine (S.R.H., C.H.S.), Umversity of Washington, Seattle, Washington; and the NeuroOphthalmology Unit, Massachusetts Eye and Ear Infirmary, and the Department of Ophthalmology (S. L.), Harvard Medical School, Boston, Massachusetts, U.S.A. Address correspondence and reprint requests to Dr. Steven R. Hamilton, NW Neuro-Ophthalmic Associates, 1229 MadIson, Suite 1490, Seattle, WA 98104, U.S.A. 127 Dural thickening may be caused by syphilis, tuberculosis, sarcoidosis, rheumatoid arthritis, metastatic carcinoma, meningioma, fibroma, and extension of inflammatory orbital pseudotumor (1,2), We present the findings in three cases of a rare disorder termed idiopathic hypertrophic cranial pachymeningitis in which magnetic resonance (MR) imaging uniformly revealed thickened dura that enhanced strikingly after Gd-DTPA (gadolinium- diethylenetriamine pentaacetic acid) administration. In all cases biopsy demonstrated a sterile, chronic, nongranulomatous inflammation of thickened, fibrotic dura. CASE STUDIES Case 1 A previously healthy 55-year-old white woman developed intermittent headaches in 1980. By 1984 the headaches had become more frequent and were predominantly right-sided, An evaluation at that time revealed an erythrocyte sedimentation rate (ESR) of 90 mmlh, which prompted a temporal artery biopsy, Although the biopsy was negative, oral prednisone therapy was initiated, and she required 60 mg/day of prednisone during the next 3 years to control the headache. In 1986 she developed tongue spasms precipitated by head turning, which responded to Dilantin therapy, Prednisone was gradually tapered off in 1987-1988 with only occasional headaches, but she remained on Dilantin until 1990, In July 1990 the patient developed diplopia on right gaze with brief episodes of paroxysmal headache. An ophthalmologist found limitation of ab- 128 S. R. HAMILTON ET AL. duction of the right eye. General medical and pulmonary evaluations were unrevealing despite an ESR of 85 mmlh. Serum RPR and FTA-ABS tests were nonreactive, while her chest radiograph and serum angiotensin-converting enzyme (ACE) level were normal. Computed tomography (CT) of the brain and orbits showed marked enhancement of the tentorium. The cerebrospinal fluid (CSF) opening pressure was 225 mm CSF with 6 white blood cells/mm3 (3 polymorphonuclear cells and 3 monocytes), 86 mg% protein, and 55 mg% glucose. She was treated with oral dexamethasone (Decadron) which improved, but failed to eliminate, her symptoms. An MR scan of the brain (Fig. 1) demonstrated diffuse meningeal thickening, which enhanced after the administration of Gd-DTPA. No abnormalities were noted on a 4-vessel cerebral angiogram. In November 1990 the brain and meninges were biopsied via a right frontal craniotomy. Fibrous thickening of the dura exceeded 2 mm in several areas. The dura contained a patchy nongranulomatous inflammatory infiltrate consisting of lymphocytes and occasional plasma cells (Fig. 2). The cerebral cortex and all blood vessels appeared normal. Stains for bacteria, fungi, mycobacteria, nocardia, spirochetes, and protozoa were negative. Despite high-dose corticosteroid treatment, she continued to have severe headaches. When the corticosteroid dose was reduced she developed a left sixth nerve palsy. Azathioprine was substituted for prednisone in July 1991, and within 6 months her headache and tongue spasms had ceased, normal motility was restored to the left eye, and there was improved abduction of the right eye. Case 2 A 68-year-old previously healthy white woman presented in July 1989 with fever, lethargy, bilateral hearing loss, nonproductive cough, sore throat, and mandibular pain. There was neither headache nor visual impairment, but she had one brief episode of binocular diplopia. Ophthalmologic, general physical, and neurological examinations gave unremarkable results. The total white blood count was 15,000/mm3 , hematocrit 30%, platelet count 715,000/mm3 , and ESR 95 mmlh. Temporal artery biopsy showed granulomatous inflammation. Oral corticosteroid treatment rapidly relieved all of her symptoms. Several months later the patient complained of blurred vision in the left eye. However, neuroophthalmic examination in December 1989 showed only slight posterior subcapsular cataracts, and fluorescein fundus angiography was unrevealing. Over the next month vision failed to 20/70 in her left eye with dyschromatopsia and an upper altitudinal visual field defect. The fundi were unremarkable, and her ESR was 3 mmlh. Visual function promptly recovered when her prednisone dose was increased to 80 mg/day. However, when the dose was reduced to 60 mg/day, vision again declined. CT of the brain and orbits with contrast was normal. Over the succeeding months she continued to manifest visual loss in the left eye that could only be reversed with 60 to 100 mg/day of (A) (Bl FIG. 1. MR imaging of case 1. T1-weighted (TR = 600 ms, TE = 15 ms) right parasagittal images (A) before and (B) after Gd-DTPA. There IS prominent thickening and enhancement of the tentorium cerebelli as well as the occipita-parietal dura. 10111 Nellro·ophthalmo{. Vol. 13. No.2, 1993 (8) IDIOPATHIC HYPERTROPHIC CRANIAL PACHYMENINGITIS /29 FIG. 2. Sections from the dural biopsy in Case 1. (A) At low magnification the dura is thickened and fibrotic. while (B) higher magnification reveals a chronic inflammatory infiltrate consisting of lymphocytes and plasma cells. Hematoxylin and eosin. Bar = 200 IJ.m at low magnification. and 40 IJ.m at high magnification. prednisone. Even on this dose there was dyschromatopsia and a left relative afferent pupillary defect. Her left optic disc became pale. Throughout this period, the ESR remained in the single digits and fibrinogen levels were normal. By May 1990 vision in the left eye was 20/25 and declined to 10/200 over the next month. Evaluation by a retinal consultant, fluorescein fundus angiography, and CT of the orbits in June 1990 failed to explain her progressive visual failure. In November 1990 the visual acuity in the right eye had declined to 20/30 because of a cataract. An MR scan with Gd-DTPA and a contrast-enhanced CT scan now demonstrated a lesion in the apex of the left orbit. The appearance was considered most compatible with a meningioma. Uncomplicated extracapsular cataract surgery was performed on the right eye in April 1991, but I ClIII Nellro-ol,lrtllallllol, Vol. 13, No.2, 1993 130 S. R. HAMILTON ET AL. vision in the right eye declined to hand motions perception during the immediate postoperative period. Her right fundus was unremarkable. The ESR was normal, but C-reactive protein was positive and fibrinogen was mildly elevated at 418 mg% (normal 200-400 mg%). With the institution of 120 mg/day of prednisone vision rapidly improved to 20/40 and color vision (Ishihara) returned to normal, but there was a temporal visual field defect. An MR scan demonstrated enlargement and enhancement of the apical end of the intraorbital segment of the left optic nerve. Other orbital structures, the optic chiasm, and right optic nerve appeared normal. Coronal images revealed marked Gd-OTPA enhancement of the meninges of the left anterior cranial fossa crossing the midline to the right side (Fig. 3). The CSF opening pressure was 120 mm and contained 9 white blood cells/mm3 (3 polymorphonuclear cells and 6 monocytes), 61 mg% glucose, and 49 mg% protein. Cytological examination for malignant cells, routine bacterial, fungal, and acid fast bacillus (AFB) cultures, and CSF VORL were all negative. Apical scarring and calcified hilar lymph nodes were seen on chest radiographs but there was no evidence of active pulmonary disease. Serum RPR, FTA-ABS, rheumatoid factor, antinuclear cytoplasmic antibody (ANCA) level, ACE level, and lysozyme all gave normal results. FIG. 3. MR imaging of Case 2. T1-weighted (TR = 500 ms, TE = 20 ms) coronal image after Gd-DTPA. There is diffuse thickening and enhancement of the inferior frontal dura as well as the left orbital apex. f Clilf Ncuro-ophthallflOl, Vol. J3, No.2, J993 In May 1991 the meninges were biopsied via a left frontal craniotomy. The dura over the floor of the anterior cranial fossa was markedly thickened. Microscopic examination of the meninges and cerebral cortex demonstrated a multifocal, nongranulomatous, chronic inflammatory infiltrate of the dura consisting of lymphocytes with occasional plasma cells. Blood vessels were not involved. Stains for bacteria (including AFB), fungi, nocardia, spirochetes, and protozoa were negative. The patient has subsequently been maintained on oral prednisone and azathioprine. Visual acuity in November 1992 was 20/15 right eye with normal color vision and a temporal paracentral scotoma. Case 3 A 31-year-old, previously healthy, white man developed paroxysmal, holocephalic nonthrobbing headaches unresponSive to aspirin in 1987. These continued, and 2 years later he noticed binocular horizontal diplopia. Neuro-ophthalmic examination in October 1989 showed partial limitation of abduction of the left eye. A complete blood count, blood glucose determination, thyroid function tests, acetylcholine receptor antibody test, Lyme antibody titer, RPR and FTA-ABS, and antinuclear antibody titer were all within normal limits. The ESR was 4 mrn/h. A nonenhanced MR scan of the brain was unremarkable. His headaches and the abduction deficit cleared spontaneously in 6 weeks. In October 1990 the horizontal diplopia returned accompanied by left hemicranial pain. Neurological examination showed an impaired tandem gait and a right lateral rectus muscle paresis. MR imaging with Gd-OTPA (Fig. 4) revealed diffuse enhancement of the basal meninges, including the cavernous sinuses and suprasellar region. Endocrinological evaluation documented hypothyroidism and a low serum testosterone level. His ESR was 27 mm/h. An ACE level was within normal limits, and a test for HIV was negative. His CSF openin3 pressure was normal with 9 white blood cells/mm (2% polymorphonuclear cells, 85% lymphocytes, 13% histiocytes and monocytes), 55 mg% glucose, and 71 mg% protein. Cytological examination showed no malignant cells and stains and cultures for AFB were negative. An extensive pulmonary evaluation with two transbronchial biopsies and biopsies of an axillary lymph node, the lip, tongue, and conjunctiva failed to show evidence of disease. He was treated for 1 year with daily prednisone doses of 20-60 mg. When depression and obesity IDIOPATHIC HYPERTROPHIC CRANIAL PACHYMENINGITIS 131 FIG. 4. MR imaging of Case 3. A T1-weighted (TR 700 ms, TE = 20 ms) coronal image after Gd-DTPA shows regional enhancement of the basal meninges, as well as the cavernous sinuses and suprasellar region. necessitated tapering of the prednisone, he suffered increased diplopia and left orbital pain. An MR scan with Gd-DTPA showed further thickening of the meninges. The left internal carotid artery, encased by the process in the cavernous sinus, appeared occluded. Cerebral angiography confirmed the MR findings and suggested encasement of the right intracavernous carotid artery as well, but there were no other lesions. A trial of methotrexate was aborted after 6 weeks because he developed tongue ulcers and there had been no beneficial response. Biopsy of the brain, meninges, and cavernous sinus in December 1991 revealed thickened dura with multiple foci of chronic, nongranulomatous inflammation. Cultures for fungi, bacteria, and AFB were negative. Chloroquine therapy was started, and the patient also received 4,500 cGy of whole-brain radiation. Two months later his pain was much improved, and ocular motility was normal. However, he had several IS-minute episodes of right arm and leg weakness with numbness accompanied by mild left hemicranial headache. The transient ischemic attacks subsequently resolved within 4 months on chloroquine therapy. DISCUSSION In 1989 Martin et al. (1) called attention to the existence of cases of idiopathic hypertrophic cranial pachymeningitis. The three patients in their series presented with chronic headaches with an elevated ESR accompanied by ataxia or palsies involving cranial nerves 7, 8, 10, or 11. Contrastenhanced CT or MR imaging (without Gd-DTPA) demonstrated tentorial thickening, which enhanced with contrast. A common pathology consisted of a thickened, fibrotic dura with a chronic inflammatory infiltrate with no evidence of arteritis. All patients eventually received both corticosteroid and azathioprine therapy, but only one enjoyed resolution of symptoms. One patient received whole-brain radiation without improvement. The same three cases were presented in the same year in the French literature by Masson et a1. (3). Willing and Broghamer (4) recently reported a 35-year-old man with headaches, a right abducens nerve palsy, and an enhancing mass seen with cranial MR imaging in the sella and cavernous sinuses that encased the carotid arteries similar to our third case. Transsphenoidal biopsy revealed dense collagen with focal fibroplasia and inflammatory cells consistent with idiopathic cranial pachymeningitis. Our cases of idiopathic hypertrophic cranial pachymeningitis corroborate many of the findings described by Martin et al. (1), while further defining the clinical profile, MR appearance, and response to therapeutic intervention. Table 1 summarizes the features in our cases as well as in the other cases reported in the English literature. Patients commonly present with chronic headache accompanied by symptoms that include either ataxia, blindness, or palsies involving cranial nerves V through XII. Neuro-ophthalmic complications include papilledema, optic neuropathy secondary to inflammation or compression, and sixth nerve palsies. While the disorder does not appear to be systemic, with clinical and imaging abnormalities limited to the nervous system, an elevated ESR is often present. The significance of the association with chronic renal failure in two cases and temporal arteritis in another remains uncertain given the limited number of reported cases. MR imaging with Gd-DTPA, as seen in our three patients, demonstrates a very characteristic pattern of either regional or diffuse dural thickening with enhancement. Our patients showed a more widespread pattern of dural thickening than the cases presented by Martin et al. (1) in which the falx and tentorium were involved. Biopsy of the involved dura revealed thickened, fibrotic dura with a sterile, multifocal, chronic inflammatory infiltrate without evidence of either vasculitis or malignancy. Both our cases and those reported by Martin et al. (1) have been nongranulomatous, although in Table 1 the cases described by Feringa JClill Neuro-ophthalmol. Vol. 13, No.2. 1993 132 S. R. HAMILTON ET AL. TABLE 1. Cases of idiopathic hypertrophic cranial pachymeningitis in the English literature Author (ref.) Feringa & Weatherbee. 1975 (5) Kobayashi et al.. 1985 (6) Martin et al .. 1989 (1) Willing & Broghamer. 1992 (4) Hamilton. Smith. and Lessell, 1993 PI. no. (age/sex) 1 (50/M) 1 (40/M) 2 (68/M) 1 (20/F) 2 (58/F) 3 (58/M) 1 (35/F) 1 (65/F) 2 (68/F) 3 (331M) Clinical findings Bilateral optic neuropathy Headache. papilledema. deafness, right 5th. 6th CN palsies, ataxia Headache. papilledema. deafness. right 7th, 9th, 12th CN palsies Headache Headache. papilledema. ataxia Headache. left 7th, bilateral 8th. and right 10th and 11th CN palsies. ataxia Headache. 6th CN palsy Headache, bilateral 6th CN palsies Bilateral optic neuropathy Headache. bilateral 6th CN palsies. orbital pain MRI/CT findings None Tentorial thickening, enhancement (CT scan) Tentorial thickening. enhancement (CT scan) Tentorial thickening. enhancement (MRI/CT scan) Tentorial enhancement (CT scan) Tentorial thickening (MRl/eT scan) Enhancing mass in the sella/cavernous sinuses (MRI) Diffuse dural thickening, enhancement (MRI) Frontal dural thickening. enhancement (MRI) Basilar dural thickening, enhancement (MRI) ESRJ temporal artery biopsy 64/none None/none 24/none 78/none 67/none 51/none 45/none 85/negative 95/positive 27/none Pathology Thick dura with chronic inflammatory infiltrate. granulomas Thick ten tori u m wit h granulomas Fibrotic thickening of the dura. mild inflammatory infiltrate Thick dura with chronic inflammatory infiltrate Thick dura with chronic inflammatory infiltrate Thick dura with chronic inflammatory infiltrate Dense collagen with scant inflammation Thick dura with chronic inflammatory infiltrate Thick dura with chronic inflammatory infiltrate Thick dura with chronic inflammatory infiltrate Medical therapy None Steroids. antibiotics Steroids Steroids. azathioprine Steroids. azathioprine. radiation Steroids, azathioprine, radiation Steroids Steroids. azathioprine Steroids, azathioprine Steroids. chloroquine. radiation Clinical response Progression Progression Headache relief Asymptomatic Progression Stabilization Resolution of 6th CN palsy Stabilization Stabilization Stabilization Systemic conditions Chronic renal failure. intracerebral hematoma Chronic renal failure Acute pneumonia None Migraine None None Chronic cho' lecystitis Temporal arteritis Hypopituitarism CN. cranial nerve. and Weatherbee (5) and Kobayashi et al. (6) did contain granulomas. Attempts at therapeutic intervention in these small numbers of patients have yielded highly variable responses to corticosteroids, immunosuppression, and whole-brain radiation. Pachymeningitis cases have previously been attributed to syphilitic, mycobacterial, and fungal infections of the central nervous system. In the era , CIIII .\'ellro-0l'hthalmol. Vol. 13, No.2, 1993 before computed tomography, syphilis and tuberculosis were the infectious agents most frequently cited (7,8). The diagnosis rested almost entirely upon the pathologic findings, which often included gumma formation and evidence of an endarteritis, as in the case reported by Hassin and Zeitlin (7). Nevertheless, 2 of the 4 cases described in the French literature by Michel et al. (8) in 1969 were assumed to be noninfectious or of idiopathic IDIOPATHIC HYPERTROPHIC CRANIAL PACHYMENINGITIS 133 origin. Moore et al. (9) published another case in 1985, attributed to syphilis with similar pathology and a late positive serum fluorescein treponemaI antibody titer. A case of biopsy-confirmed tuberculous cranial pachymeningitis was reported by Callebaut et al. (10) with evidence of resolution by MR imaging with Gd-DTPA after antituberculous therapy. Gorell et al. (11) utilized positive fungal stains and fluorescent antibody titers of the involved dura to link another case to systemic candidiasis. Neurosarcoidosis is a potential noninfectious cause of dural thickening and enhancement on imaging studies. CT has revealed contrast-enhancing densities involving the falx, tentorium, and leptomeninges in patients with sarcoidosis (12,13). A more extensive review (14) of 21 patients with neurosarcoidosis studied with CT and MR imaging concluded that MR scanning is the best means of detecting parenchymal lesions, whereas CT is useful for detecting diffuse meningeal involvement. None of the MR scans in that study were performed with Gd-DTPA, and Phillips et al. (15) have subsequently stated that MR imaging with Gd-DTPA is the optimal means of detecting meningeal lesions, although it is nonspecific for inflammatory versus neoplastic etiology. Khaw et al. (16) reported two cases of neurosarcoidosis with enhancement of the tentorium cerebelli or meninges with Gd-DTPA-enhanced MR imaging. No intracranial dural biopsies were obtained, and the diagnoses were based upon other clinical signs compatible with sarcoidosis. Rheumatoid arthritis has also been associated with cranial pachymeningitis, in addition to its more common involvement of the cervical spine. Bathon et al. (17) described a patient with rheumatoid arthritis who developed headaches and an optic neuropathy. A brain CT demonstrated diffuse tentorial enhancement and involvement of the optic chiasm. Biopsy revealed fibrosis of the dura with a chronic inflammatory infiltrate without giant cells or rheumatoid nodules. Weinstein et al. (18) had presented a similar patient with rheumatoid arthritis who had a junctional scotoma from a chiasmal neuropathy with very similar CT and biopsy findings. Yuh et al. (19) reported another rheumatoid arthritis patient with headache, diffuse meningeal enhancement with Gd-DTPAenhanced MR imaging, and similar dural pathology on biopsy. Intracranial hypertrophic pachymeningitis has been reported in a single case of multifocal fibrosclerosis (20). This rare disorder is characterized by clinical findings that may include mediastinal fi-brosis, retroperitoneal fibrosis, orbital pseudotumor, Reidel's thyroiditis, and sclerosing cholangitis. The patient presented was a 34-year-old man with episcleritis, orbital pseudotumor, and sclerosing cholangitis with tentorial thickening on MR imaging. Intracranial biopsy revealed chronic inflammatory cells in a fibrotic dura. Rarely, cases of orbital pseudotumor have been described with intracranial extension (2,21-23). Clifton et al. (2) recently retrospectively reviewed 90 cases of orbital pseudotumor, and found 8.8% had CT evidence of intracranial extension. Most of these cases had localized extension into the adjacent superior orbital fissure or ipsilateral cavernous sinus, but two patients had more extensive intracranial involvement. The pathology in these cases is identical to that seen in pachymeningitis, and an overlap of the two syndromes may be present in those cases with both orbital and intracranial dural involvement. Given the difficulty in distinguishing idiopathic cases of cranial pachymeningitis from those secondary to other disease processes, such as syphilis, tuberculosis, rheumatoid arthritis, or sarcoidosis, extensive systemic evaluations are necessary in symptomatic patients with an elevated ESR and dural thickening on neuroimaging studies. An appropriate evaluation would include a general physical examination; a brain MR scan with GdDTPA; a chest radiograph; an ACE level, rheumatoid factor, and FTA-ABS; CSF examination; and a dural biopsy. So few cases have been reported that it is difficult to offer guidelines for treatment. At present it would seem most appropriate to initiate therapy with prednisone in the range of 40-80 mgl day. Another immunosuppressive drug such as azathioprine could subsequently be introduced if desired to achieve tapering off prednisone and reduction of the risk of systemic side effects from chronic corticosteroid therapy. REFERENCES 1. Martin N, Masson C. 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