Neuroradiology Image Teaching Files - Case Twenty Three - Granulomatous Meningitis

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Clinical History: Septagenarian female with transient left leg weakness, and dysphasia which resolved without residual deficit. A vascular workup found no apparent cause. This was followed several weeks later by an acute episode of right leg weakness and right numbness. This resolved after several hours following admission. Past medical history included hypertension. Review of systems was significant for recent increased fatigue, occasional night sweats and arthralgias. Fever, chills, nor weight loss were reported. Physical exam following episodes was unremarkable. While in the hospital the transient right sided symptoms and an aphasia recurred. Analysis of CSF showed no abnormality and all CSF and blood cultures were negative.

Findings: A non-contrasted CT of the head was remarkable for unilateral left hemispheric sulcal effacement. This is seen in figure 1 and can be best appreciated by comparing the Sylvian fissure from side to side. Note additionally the lack of other mass effects. The ventricular system is normal, there is no midline shift, and visualized gray-white matter differentiation remains intact.

Non-contrast double echo MR images demonstrate a small rectangular area of increased signal intensity in a right paramedian distribution along the gray-white border on a spin density image shown (figure 2). The second echo image shows a wider and bilateral region of abnormal signal (figure 3). Again note the relative lack of signal from CSF in the subarachnoid spaces on the left. The pre-contrast T1-weighted image presented shows scattered increased signal on the right likely representing petechial hemorrhage (figure 4).

Gadolinium enhanced MR images (figures 5 & 6) reveal diffuse abnormal enhancing meninges largely in a pia-arachnoid pattern, and more severe over the left hemisphere. Note the abnormal enhancement flowing into the CSF interstices. The right cingulate sulcus contains a plaque of enhancing tissue corresponding to the rectangular area of signal change seen prior to contrast.

Diagnosis: Granulomatous Meningitis

Discussion: Thickened and abnormal enhancement of the pial and arachnoid components of the meninges has a wide differential. This can include infections (parasitic, bacterial, fungal, or viral), inflammations (vasculitic, auto-immune, granulomatous), neoplasms (usually secondary), or following surgical or traumatic manipulation. As such the patient agreed to undergo an open meningeal biopsy. This provided a sample showing diffusely inflamed meninges with intact normal cortex beneath as presented in figure 7. High power inspection (figure 8) revealed numerous multi-nucleated giant cells of the variety shown. No caseation was apparent. All cultures and pathologic screening for infectious etiologies have been negative. A CT of the chest showed no hilar adenopathy. A gallium scan did reveal diffuse lung uptake (as well as right frontal brain cortex and parotid uptake) but again no mediastinal abnormality.

Given the pathologic results (non-caseating granulomatous meningitis), gallium scan and lack of infectious agent, but despite the patient’s age, race (caucasian) and relatively normal basal meninges a presumptive diagnosis of exclusion, neurosarcoid has been given and the patient is undergoing treatment with steroids. An idiopathic granulomatous meningitis remains an alternate possibility.

References:
Meltzer, C C, et al., MR Imaging of the Meninges. Part I. Normal Anatomic
Features and Nonneoplastic Disease, Radiology, 210:297, 1996

Ranoux, D, et al., Meningeal sarcoidosis, pseudo-meningioma, and
pachymeningitis of the convexity, J Neurol., Neurosurg., and Psychiatry,
55:300, 1992

Bakheit, A M, et al., Idiopathic Granulomatous Meningitis, J Neurol., Neurosurg.,
and Psychiatry, 52:1286, 1989

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Submitted by:
J. L. Sunshine, M.D., Ph.D.