Decreased Diameter of the Optic Nerve Sheath Associated with CSF Hypovolemia

Case Reports

Case 1

A 64-year-old man complaining of nonorthostatic persistent headache and plugged ear persisting for 2 weeks was referred to our hospital. Brain MR imaging demonstrated bilateral subdural fluid collections with diffuse pachymeningeal enhancement, descent of the brain, enlargement of the pituitary gland, and intracranial venous enlargement.⁶ Fat-saturated T2-weighted fast spin-echo MR images of the orbit were obtained using a 1.5T MR scanner (GE Medical Systems, Milwaukee, Wis) with TR at 3500 ms, TE at 100 ms, flip angle at 90°, section thickness at 3.5 mm, section gap at 0.3 mm, matrix at 320 × 224, FOV at 16 × 16 cm, echo-train length at 12, and band width at 31.2 kHz. Orbital thin-section fat-saturated MR imaging showed marked reduction of high signal intensity CSF within the SAS surrounding the optic nerves bilaterally (Fig 1A). Radioisotope cisternography revealed rapid excretion of tracer into the urine and CSF leakage at the upper thoracic spine. Opening pressure at lumbar puncture was 100 mm H₂O. The diagnosis of CSF hypovolemia was determined according to the criteria for “headache attributed to spontaneous low CSF pressure” in the International Classification of Headache Disorder, 2nd edition.⁷ Epidural blood patch treatment was performed at the upper thoracic spine, and his headache and plugged ear resolved. Brain MR imaging 1 month after the treatment demonstrated disappearance of the MR findings related to CSF hypovolemia and marked improvement in the visualization of the SAS around the optic nerves. The ONS diameter was 5.5 mm on the right and 5.8 mm on the left (Fig 1B).

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Fig 1.

Coronal fat-saturated T2-weighted orbital MR images of cases 1, 2, and 3. In case 1, MR images showing the subarachnoid space (arrow) had collapsed and the ONS could not be detected before treatment (A) but became visible with diameter of 5.5 mm on the right and 5.8 mm on the left after treatment (B). In case 2, MR images showing the ONS diameter just behind the optic globe before treatment were 5.0 mm on the right and 4.7 mm on the left (C) and became 5.9 mm and 5.3 mm, respectively, after treatment (D). In case 3, MR images showing the subarachnoid space had collapsed, and the ONS could not be detected before treatment (E) but became visible with a diameter of 6.2 mm on the right and 6.2 mm on the left after treatment (F).

Discussion

In our case 1, the SAS of the optic nerve had collapsed even at a CSF opening pressure of 100 mm H₂O, which can be considered as normal. In our case 2, the SAS was visible, though the CSF pressure was negative. In case 3, the SAS had collapsed with a low CSF opening pressure. Such discrepancies may be due to variations between individual subjects. A normally wide SAS may be visible even under negative intracranial pressure, whereas a narrower SAS may easily disappear with a mild decrease in pressure.

The SAS around the optic nerve can be observed by fat-saturated T2-weighted MR imaging in normal subjects. The ONS diameter measured just behind the optic globe has been reported as 5.52 ± 1.11 mm in normal patient volunteers.² The diameter did not change significantly with the eyeball position or patient's position.^1,8

We measured the SAS just behind the eyeball based on the previous method⁴ and confirmed widening of the SAS after successful treatment of spontaneous intracranial hypotension in our 3 patients. This change reflects the increased CSF volume, as well as increased intracranial pressure after occlusion of the CSF fistula. Therefore, changes in the diameter of the SAS of the ONS reflect alterations in the CSF pressure or volume. In contrast to the cranial dura mater, the ONS is surrounded by soft tissue of the orbit and may easily expand or collapse with changes in SAS pressure. Furthermore, the ONS is located in the uppermost part of the CSF space of the body in the supine position, in which MR images are usually obtained. Therefore, we speculate that the SAS of the optic nerve may collapse earlier than other parts of the CSF space in response to CSF volume decreases because of the pressure gradient caused by gravity.

The diagnostic value of the ONS diameter measurement may be limited because of individual variations, but absence or narrowing of the SAS strongly suggests decreased CSF volume or pressure. Therefore, such measurement would be valuable in the diagnosis of CSF hypovolemia. We speculate the diagnostic possibility of this finding, especially in patients with no obvious typical MR findings for CSF hypovolemia, such as diffuse pachymeningeal enhancement or brain sagging, because some patients with CSF hypovolemia do not show classic MR findings, except for typical orthostatic headache and low CSF pressure. Further experience is necessary to establish the diagnostic value of fat-saturated MR imaging in the evaluation of patients with suspected CSF hypovolemia.