(Radiology. 1999;212:151-154.)
© RSNA, 1999
MR Imaging of Intraventricular Silicone: Case Report1
Robert L. Williams, MD,
Randall L. Beatty, MD,
Emanuel Kanal, MD and
Jane L. Weissman, MD
1 From the Departments of Radiology (R.L.W., E.K., J.L.W.), Ophthalmology (R.L.B.), and Otolaryngology (J.L.W.), University of Pittsburgh Medical Center, Rm D132PUH, 200 Lothrop St, Pittsburgh, PA 15213. Received March 26, 1998; revision requested June 24;
revision received September 18; accepted December 8. Address reprint requests to R.L.W. (e-mail: williamsrl@radserv.arad.upmc.edu).
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Abstract
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A 42-year-old man with human immunodeficiency viral infection developed cytomegaloviral retinitis that was complicated by retinal detachment and was treated with an intravitreous injection of silicone. Fifteen months later, magnetic resonance imaging revealed intraocular and intraventricular silicone. Signal intensity characteristics and chemical shifts of silicone in the two locations were identical.
Index terms: Brain, MR, 161.121411, 161.121413, 161.121414, 161.121415 • Brain, ventricles, 161.458 • Cytomegalovirus, 2245.2066 • Eye, diseases, 2245.2066, 2245.241, 2245.892 • Eye, MR, 2245.121411, 2245.121413, 2245.121414, 2245.121415 • Retina, 2245.892 • Silicone, 161.458, 2244.126
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Introduction
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Intraocular silicone is an increasingly common finding on magnetic resonance (MR) studies of the brain due to the high success rate of silicone tamponade in treating retinal detachment (1). Intravitreous silicone maintains retinal attachment, primarily because silicone has a higher surface tension than water has. Small retinal tears are functionally closed, which prevents repeated detachment of the retina (2).
The MR imaging appearance of intraocular silicone oil has been well described (3–6). However, to our knowledge, there are no prior reports of the extension of silicone into the ventricles and of the corresponding MR imaging findings. A mechanism of communication between the vitreous body and the cerebrospinal fluid is proposed for this unusual complication that follows the repair of retinal detachment.
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Case Report
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A 42-year-old man with a 13-year history of human immunodeficiency viral infection was examined at an ophthalmologic consultation 2 years prior to MR imaging, when he complained of a 1-week history of a decrease in vision in the left eye. At examination, the visual acuity was 20/20 in the right eye and 20/200 in the left eye. Retinal evaluation revealed cytomegaloviral retinitis with cytomegaloviral optic neuritis. Both of these gradually resolved following treatment with intravenous injection of ganciclovir sodium (Cytovene; Hoffmann-La Roche, Nutley, NJ).
Five months later, the cytomegaloviral retinitis recurred, with an associated retinal detachment. The patient was treated with an intravitreous injection of the antiviral agent foscarnet sodium (Foscavir; AstraZeneca, Wayne, Pa). The patient returned in 3 months, at which time his visual acuity had decreased to only light perception. The patient was treated with a second intravitreous injection of foscarnet sodium. To treat the retinal detachment, he underwent an orbiculus ciliaris vitrectomy, an orbiculus ciliaris lensectomy, a gas and fluid exchange, and the injection of 5,000-centistoke-viscosity (50 cm2/sec) silicone oil.
Intraocular pressure was elevated following the procedure, and medications used to treat glaucoma were administered. Following surgery, visual acuity gradually deteriorated to no light perception. The cytomegalovirus appeared to be completely inactive; only retinal scarring was observed. However, damage to the optic nerve due to glaucoma was considerable and included cupping of the optic disc.
Seven months after retinal detachment surgery, subconjunctival silicone oil was noted during a slit-lamp examination. The patient's health began to deteriorate, and 8 months later, he developed a peripheral neuropathy. Due to the new neurologic deficit, we obtained MR images of the brain and cervical spine.
MR imaging was performed on two occasions over 5 months, with a 1.5-T unit (Signa; GE Medical Systems, Milwaukee, Wis) (Figs 1, 2). Sagittal T1-weighted spin-echo (500–566/14 [repetition time msec/echo time msec], one signal acquired), axial intermediate-weighted fast spin-echo (2,000–2,366/13–39, one signal acquired), axial T2-weighted fat-saturated chemical shift–selective fast spin-echo (2,183–2,500/104–105, one signal acquired), and axial fluid-attenuated inversion-recovery fast spin-echo (9,002–10,002/172–175/2,200 [repetition time msec/echo time msec/inversion time msec], one signal acquired) images were all obtained. A section thickness of 5 mm, an intersection gap of 1 mm, a field of view of 20 x 20 cm, an image matrix of 256 x 160 pixels, and a bandwidth of ±16 kHz (32 kHz) were used.
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Figure 1a. (a, b) Sagittal T1-weighted spin-echo MR images (566/14) demonstrate (a) intraocular silicone (S), which is hyperintense when compared with normal vitreous, and (b) intraventricular silicone (arrow), which is hyperintense when compared with cerebrospinal fluid. (c, d) Axial T2-weighted fat-saturated fast spin-echo MR images (2,500/104) demonstrate hypointense signal in (c) the silicone (S) in the left globe and (d) the silicone (arrow) in the left lateral ventricle.
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Figure 1b. (a, b) Sagittal T1-weighted spin-echo MR images (566/14) demonstrate (a) intraocular silicone (S), which is hyperintense when compared with normal vitreous, and (b) intraventricular silicone (arrow), which is hyperintense when compared with cerebrospinal fluid. (c, d) Axial T2-weighted fat-saturated fast spin-echo MR images (2,500/104) demonstrate hypointense signal in (c) the silicone (S) in the left globe and (d) the silicone (arrow) in the left lateral ventricle.
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Figure 1c. (a, b) Sagittal T1-weighted spin-echo MR images (566/14) demonstrate (a) intraocular silicone (S), which is hyperintense when compared with normal vitreous, and (b) intraventricular silicone (arrow), which is hyperintense when compared with cerebrospinal fluid. (c, d) Axial T2-weighted fat-saturated fast spin-echo MR images (2,500/104) demonstrate hypointense signal in (c) the silicone (S) in the left globe and (d) the silicone (arrow) in the left lateral ventricle.
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Figure 1d. (a, b) Sagittal T1-weighted spin-echo MR images (566/14) demonstrate (a) intraocular silicone (S), which is hyperintense when compared with normal vitreous, and (b) intraventricular silicone (arrow), which is hyperintense when compared with cerebrospinal fluid. (c, d) Axial T2-weighted fat-saturated fast spin-echo MR images (2,500/104) demonstrate hypointense signal in (c) the silicone (S) in the left globe and (d) the silicone (arrow) in the left lateral ventricle.
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Figure 2a. (a, b) Axial intermediate-weighted MR images (2,333/15) demonstrate (a) silicone (S) in the left globe, which is slightly hyperintense when compared with normal vitreous, and (b) similar signal intensity (arrow) and chemical shift artifact (arrowheads) in the silicone in the left lateral ventricle. Only chemical shift artifact is seen from the silicone in the right lateral ventricle. (c, d) Axial intermediate-weighted images (2,366/39) obtained with the low bandwidth technique and with interchanged phase and frequency directions show that (c) the hyper- and hypointense bands of signal (arrows) from chemical shift artifact adjacent to the silicone (S) in the left globe have changed in direction and are more apparent. (d) The chemical shift artifact at the lateral ventricles is identical to the artifact seen in the globe. The magnitude of the chemical shift (arrows) was measured and was used to calculate the frequency shift in Hertz. (e) Sagittal T1-weighted image (500/14) demonstrates silicone within or adjacent to the intracranial left optic nerve and chiasm (arrow).
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Figure 2c. (a, b) Axial intermediate-weighted MR images (2,333/15) demonstrate (a) silicone (S) in the left globe, which is slightly hyperintense when compared with normal vitreous, and (b) similar signal intensity (arrow) and chemical shift artifact (arrowheads) in the silicone in the left lateral ventricle. Only chemical shift artifact is seen from the silicone in the right lateral ventricle. (c, d) Axial intermediate-weighted images (2,366/39) obtained with the low bandwidth technique and with interchanged phase and frequency directions show that (c) the hyper- and hypointense bands of signal (arrows) from chemical shift artifact adjacent to the silicone (S) in the left globe have changed in direction and are more apparent. (d) The chemical shift artifact at the lateral ventricles is identical to the artifact seen in the globe. The magnitude of the chemical shift (arrows) was measured and was used to calculate the frequency shift in Hertz. (e) Sagittal T1-weighted image (500/14) demonstrates silicone within or adjacent to the intracranial left optic nerve and chiasm (arrow).
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Figure 2e. (a, b) Axial intermediate-weighted MR images (2,333/15) demonstrate (a) silicone (S) in the left globe, which is slightly hyperintense when compared with normal vitreous, and (b) similar signal intensity (arrow) and chemical shift artifact (arrowheads) in the silicone in the left lateral ventricle. Only chemical shift artifact is seen from the silicone in the right lateral ventricle. (c, d) Axial intermediate-weighted images (2,366/39) obtained with the low bandwidth technique and with interchanged phase and frequency directions show that (c) the hyper- and hypointense bands of signal (arrows) from chemical shift artifact adjacent to the silicone (S) in the left globe have changed in direction and are more apparent. (d) The chemical shift artifact at the lateral ventricles is identical to the artifact seen in the globe. The magnitude of the chemical shift (arrows) was measured and was used to calculate the frequency shift in Hertz. (e) Sagittal T1-weighted image (500/14) demonstrates silicone within or adjacent to the intracranial left optic nerve and chiasm (arrow).
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Figure 2b. (a, b) Axial intermediate-weighted MR images (2,333/15) demonstrate (a) silicone (S) in the left globe, which is slightly hyperintense when compared with normal vitreous, and (b) similar signal intensity (arrow) and chemical shift artifact (arrowheads) in the silicone in the left lateral ventricle. Only chemical shift artifact is seen from the silicone in the right lateral ventricle. (c, d) Axial intermediate-weighted images (2,366/39) obtained with the low bandwidth technique and with interchanged phase and frequency directions show that (c) the hyper- and hypointense bands of signal (arrows) from chemical shift artifact adjacent to the silicone (S) in the left globe have changed in direction and are more apparent. (d) The chemical shift artifact at the lateral ventricles is identical to the artifact seen in the globe. The magnitude of the chemical shift (arrows) was measured and was used to calculate the frequency shift in Hertz. (e) Sagittal T1-weighted image (500/14) demonstrates silicone within or adjacent to the intracranial left optic nerve and chiasm (arrow).
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Figure 2d. (a, b) Axial intermediate-weighted MR images (2,333/15) demonstrate (a) silicone (S) in the left globe, which is slightly hyperintense when compared with normal vitreous, and (b) similar signal intensity (arrow) and chemical shift artifact (arrowheads) in the silicone in the left lateral ventricle. Only chemical shift artifact is seen from the silicone in the right lateral ventricle. (c, d) Axial intermediate-weighted images (2,366/39) obtained with the low bandwidth technique and with interchanged phase and frequency directions show that (c) the hyper- and hypointense bands of signal (arrows) from chemical shift artifact adjacent to the silicone (S) in the left globe have changed in direction and are more apparent. (d) The chemical shift artifact at the lateral ventricles is identical to the artifact seen in the globe. The magnitude of the chemical shift (arrows) was measured and was used to calculate the frequency shift in Hertz. (e) Sagittal T1-weighted image (500/14) demonstrates silicone within or adjacent to the intracranial left optic nerve and chiasm (arrow).
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The condition was clinically stable when repeat imaging was performed 5 months later. MR imaging was performed as described but with an increase in the matrix to 256 x 192 and with a decrease in the bandwidth of 7.82 kHz before and after interchanging the phase- and frequency-encoding directions (Fig 2c, 2d). An axial T1-weighted series (600/12, one signal acquired) was obtained with the fat-saturated chemical shift–selective technique, and intermediate-weighted images (2,000/16, one signal acquired) were also obtained, with the patient prone, after the field of view was increased to 22 x 22 cm.
Silicone in the left globe was hyperintense when compared with normal vitreous on the T1-weighted and fluid-attenuated inversion-recovery images (Fig 1a). Identical signal intensity on the T1-weighted images was seen in the substance in the lateral ventricle (Fig 1b). Silicone was hypointense when compared with vitreous in the globe (Fig 1c) and with the substance in the ventricle (Fig 1d) on the T2-weighted fat-saturated images. On the intermediate-weighted images, the silicone was slightly hyperintense when compared with normal vitreous (Fig 2a). Similar signal intensity was present in the substance in the ventricle, as seen on images obtained with the same sequence (Fig 2b).
A prominent chemical shift artifact was present along the frequency-encoding direction, which changed appropriately as the phase and frequency directions were interchanged (Fig 2c, 2d). Chemical shift artifact between silicone and water and between fat and water increased as the bandwidth decreased. A substance with a small (7-mm-long), oval shape in the left lateral ventricle and a round 1-mm focus in the right lateral ventricle had, on images obtained from all MR sequences, signal intensities and associated artifact that were identical to the signal intensity and associated artifact of the silicone in the globe. Similar signal intensity was also present along the superior aspect of the intracranial optic nerve on the left (Fig 2e). The substance in the ventricle was nondependent and changed in position as the patient's position changed from supine to prone.
On images obtained with fat-saturation techniques, the substance in the lateral ventricles and superior to the optic nerve had signal intensity loss identical to the signal intensity loss of silicone in the globe. The magnitude and direction of the chemical shift artifact also suggested that the substances in the ventricles and in the globe were identical.
We calculated the frequency shift (in Hertz) between the silicone in the left globe, with surrounding water protons, and the substance in the ventricles, with surrounding water protons, on the basis of the known relationship among the amount of shift in the frequency direction (in millimeters), the field of view (in millimeters), and the bandwidth (in Hertz). This was calculated as follows: FS = (x/FOV) x BW, where FS is the frequency shift in Hertz, x is the frequency direction, FOV is the field of view, and BW is the bandwidth.
The magnitude and direction of the chemical shift were identical between the silicone in the globe and the substance in the ventricles. With bandwidths of 32.00 and 7.82 kHz, the displacements in the frequency-encoding direction were 2 and 7 mm, respectively, which corresponded to calculated frequency differences of 273 and 320 Hz, respectively. The calculated frequency shifts are, in each case, within one frequency column of resolution from the known 290 Hz of shift from the water peak, as seen in some types of silicone (7). The accuracy of this calculation is limited by the bandwidth per pixel and the spatial resolution of the study parameters. These similarities between the material in the globe and the material in the ventricles are compelling evidence that silicone is in the ventricles.
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Discussion
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Intravitreous silicone oil is injected to provide a mechanical tamponade that maintains retinal attachment following retinal detachment repair. The MR imaging appearance of intraocular silicone oil has been well described (Table). Signal intensity characteristics are variable and depend on the sequence parameters, field strength, and viscosity of silicone oil, as measured in stokes (centimeters squared per second) (6).
Typically, in vivo silicone oil is hyperintense on T1-weighted images, when compared with normal vitreous, and variably is iso-, hypo-, or hyperintense on T2-weighted images, when compared with the vitreous. This inconsistent signal intensity is partially related to the different viscosities of silicone oils. In general, the higher the viscosity is (higher resistance to flow), the more efficient T2 relaxation becomes, which leads to faster dephasing of protons and corresponding shorter T2 values that produce a hypointense signal on T2-weighted images (12).
This case is unique since intraventricular silicone, to the best of our knowledge, has not been reported as a complication of the intravitreous injection of silicone. In addition, the MR imaging features of intraventricular silicone, to our knowledge, have never been described. The pathway that allows the transit of silicone from the vitreous to the cerebrospinal fluid is uncertain. There is no normal anatomic communication between the vitreous and the subarachnoid space (13).
Silicone oil has a propensity to leak through very small openings, such as the 1-mm sclerotomy sites, despite tight suturing of these sites. Silicone may even egress through the entrance and exit sites of the needle during suture placement (14). The presence of silicone in the subconjunctival space is, therefore, not unusual in cases in which the vitreous has been replaced with silicone oil for the treatment of retinal detachment (15). Subconjunctival oil, however, has no access to the subarachnoid space that surrounds the intraorbital optic nerve.
We hypothesize that the silicone may have entered the atrophic optic disc due to the raised intraocular pressure (15,16). The intraneural silicone then coalesced and extended posteriorly, eventually migrating into the subarachnoid space that surrounds the optic nerve. Communication of the subarachnoid space that surrounds the optic nerve with the intracranial subarachnoid space would then allow the passage of silicone into the ventricles.
This theory is supported by case reports that demonstrate the extension of intravitreous silicone into the intraorbital optic nerve (15,16). In fact, the potential for the extension of intravitreous silicone into the central nervous system was originally predicted by Shields and Eagle (16). In addition, the clinical histories of patients in whom extravitreous silicone has been identified included severely elevated intraocular pressure (15,16), as seen in our case.
This correlation with severe glaucoma has also been noted in cases of cystic degeneration of the optic nerve. Zimmerman et al (17) theorized that cystic degeneration of the optic nerve is caused by ischemic necrosis of the nerve, which develops secondarily to severe acute glaucoma. The cystic spaces in cystic degeneration were filled with vitreous, which was believed to be "forced into the optic nerve" (17). Similar cystic spaces were filled with silicone in one report (16), a finding that may be present in our case. Damage to the optic nerve due to glaucoma may, therefore, be required to allow oil to enter the optic disc and nerve. Continued elevation of intraocular pressure may also promote extension of silicone through the nerve.
Imaging evidence that supports this theory is present in our case, in which silicone is seen immediately adjacent to the intracranial optic nerve (Fig 2e). This silicone is believed to be intraneural, since the silicone has not changed in position between the two studies. Further imaging evidence is found in another case in which MR imaging demonstrated perfluorocarbon liquid (an intravitreous substance which is also used for mechanical tamponade of retinal detachment) within the intraorbital optic nerve sheath (7). Subarachnoid space involvement confirms our theory that intravitreous substances may enter the perineural subarachnoid space.
In conclusion, MR imaging demonstrated, in a patient who was treated for retinal detachment with intravitreous silicone, intraocular and intraventricular silicone oil, as confirmed by identical signal intensity characteristics and chemical shifts in the two locations. The MR appearance of intraventricular silicone may vary with the field strength, the sequence parameters, and the viscosity of the silicone injected. The proposed pathway for the extension of silicone is through the optic nerve, which migrates into the surrounding subarachnoid space and which communicates with the ventricles. This mechanism may require a necrotic optic nerve and a raised intraocular pressure.
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Acknowledgments
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We express our appreciation to Karol Rosengarth for assistance with manuscript preparation.
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Footnotes
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Author contributions: Guarantor of integrity of entire study, R.L.W.; study concepts and design, R.L.W.; definition of intellectual content, J.L.W.; literature research, R.L.W., R.L.B.; data acquisition and analysis, R.L.W., E.K.; manuscript preparation, R.L.W.; manuscript editing and review, R.L.B., J.L.W., E.K.
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References
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Abstract
Introduction
