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 Table of Contents  
Year : 2017  |  Volume : 4  |  Issue : 4  |  Page : 286-287

Imaging in neurosarcoidosis

Department of Radiology, St. John's Medical College, Bengaluru, Karnataka, India

Date of Web Publication11-Oct-2017

Correspondence Address:
Reddy Ravikanth
St. Johnís Medical College, Bengaluru - 560 034, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cjhr.cjhr_127_16

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How to cite this article:
Ravikanth R. Imaging in neurosarcoidosis. CHRISMED J Health Res 2017;4:286-7

How to cite this URL:
Ravikanth R. Imaging in neurosarcoidosis. CHRISMED J Health Res [serial online] 2017 [cited 2023 Jan 30];4:286-7. Available from: https://www.cjhr.org/text.asp?2017/4/4/286/216465

  Description Top

A 32-year-old female patient was admitted for evaluation of a persistent headache for 4 months. Clinical examination showed her Glasgow coma scale to be 15/15, pulse rate 62 bpm, blood pressure 110/80 mmHg and was afebrile. Motor and sensory examinations were unremarkable. Visual-motor coordination and constructional functions were normal. Most prominent failures were detected in the tests of acquiring new verbal content and memory functions. Verbal fluency tested by naming familiar objects, speed of visual content processing, flexibility of thinking and nonverbal memory was subnormal. Psychological examination detected psychomotor deterioration, memory loss, difficulty in learning, and cognitive deterioration. Laboratory investigations showed white cell count of 8800/mm 3 of blood, erythrocyte sedimentation rate 35, angiotensin-converting enzyme (ACE) in serum, and liquor was increased; serum ACE was 127 IU/L (reference range: 8–51 IU/L). Her chest X-ray showed no evidence of hilar adenopathy or prominent pulmonary markings. She underwent magnetic resonance imaging of the brain with gadolinium which revealed abnormally thickened pituitary stalk [Figure 1] and [Figure 2] and enhancing lesion in the right hemipons [Figure 3]. Based on these findings, a differential diagnosis of neurosarcoidosis was considered. Pathology of the central nervous system tissue specimen revealed noncaseating chronic granulomatous inflammation, consistent with neurosarcoidosis. The patient had improvement of her symptoms after treatment with dexamethasone for 18 months. She was discharged from hospital without further complications and was advised to continue regular follow-up.
Figure 1: Coronal postcontrast T1-weighted image demonstrating abnormally thickened pituitary stalk (arrow)

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Figure 2: Sagittal postcontrast T1-weighted image demonstrating abnormally thickened pituitary stalk with very tiny hypophysis pushed caudally and posteriorly by a mild suprasellar cerebrospinal fluid herniation (arrow)

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Figure 3: Axial postcontrast T1-weighted image demonstrating an enhancing lesion in the right hemipons (arrow)

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  Discussion Top

Sarcoidosis can affect patients of all ages and races but is most common in the third and fourth decades of life with female predilection. The etiology of sarcoidosis is unknown. Neurosarcoidosis has been described in 5% of patients with sarcoidosis.[1] It is estimated that <1% of patients have isolated central nervous system involvement, without systemic evidence of disease.[2] Central neurosarcoidosis involves multiple or solitary supratentorial and infratentorial brain lesions, mostly in the hypothalamus and/or pituitary gland, pituitary stalk, basal ganglia, multiple lacunar infarctions, fourth ventricles, inflammatory lesions in the brain and spinal cord, dural and leptomeningeal enhancement, intracranial hemorrhage, pituitary tuberculoma, amygdale, anterior hippocampus, mesial temporal neocortex, medullary involvement, deep white matter, cerebral aqueduct with hydrocephalus, pons, spinal mass lesion, temporodorsal in the hemisphere, and cranial nerves.[3] MRI findings of neurosarcoidosis are not sufficiently specific to render a diagnosis, especially when neurological involvement is the first or only finding with sarcoidosis. Rather, other parameters must also be considered, including cognitive decline, ACE assays, the Kveim test, and biopsy if necessary.[4]

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  References Top

Shah R, Roberson GH, Curé JK. Correlation of MR imaging findings and clinical manifestations in neurosarcoidosis. AJNR Am J Neuroradiol 2009;30:953-61.  Back to cited text no. 1
Smith JK, Matheus MG, Castillo M. Imaging manifestations of neurosarcoidosis. AJR Am J Roentgenol 2004;182:289-95.  Back to cited text no. 2
Lexa FJ, Grossman RI. MR of sarcoidosis in the head and spine: Spectrum of manifestations and radiographic response to steroid therapy. AJNR Am J Neuroradiol 1994;15:973-82.  Back to cited text no. 3
Seltzer S, Mark AS, Atlas SW. CNS sarcoidosis: Evaluation with contrast-enhanced MR imaging. AJNR Am J Neuroradiol 1991;12:1227-33.  Back to cited text no. 4


  [Figure 1], [Figure 2], [Figure 3]


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