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Retrolaminar Migration of Intraocular Silicone Oil

Boren, Rance A. MD; Cloy, Carson D.; Gupta, Ankur S. MD; Dewan, Vinay N. MD; Hogan, R. Nick MD, PhD

Section Editor(s): Biousse, Valérie MD; Galetta, Steven MD

doi: 10.1097/WNO.0000000000000440
State-of-the-Art Review

Background: Migration of intravitreal silicone to the retrolaminar optic nerve was detected pathologically in 1983, symptomatic migration to the subarachnoid space of the optic nerve was reported in 1994, and asymptomatic intraventricular silicone was first seen radiographically in 1999. Since then, little advance has been made in understanding this phenomenon despite numerous case reports. Although some authors have restricted their attention to cases of intraventricular silicone, we believe that these represent part of a clinical spectrum and that all cases with retrolaminar silicone should be considered. The pathophysiology of silicone migration may have significant implications for the management of patients after vitrectomy.

Evidence Acquisition: Two patients were evaluated by the authors. An internet-based literature review was conducted, beginning with the key search terms “intraventricular, intracranial, subarachnoid, or optic nerve silicone,” and “complications of vitrectomy or intravitreal silicone.” Further searches cascaded from the initial search results. An additional 24 cases of retrolaminar migration of silicone oil were found and summarized. The relevant anatomy and pathophysiology were reviewed, with attention to additional information from enucleation studies, as well as to gaps in the current understanding of this process.

Results: Retrolaminar migration of silicone oil may be more common than previously thought, especially in at-risk patient groups, and may be associated with visual and neurologic symptoms. Some impressions regarding the cause and significance of this syndrome seem incorrect. Although this process is likely linked to postoperative elevations of intraocular pressure, the exact mechanisms of silicone entry into the subarachnoid space remain undefined. A number of anatomic factors may influence the movement of silicone from the orbit and in the various compartments of the subarachnoid space and ventricular system, resulting in variability of clinical presentations and radiologic findings. Implications for clinical decision making and directions for further research are discussed.

Conclusion: Greater awareness on the part of treating physicians, systematic study of at-risk populations, and advances in imaging technology will allow further insight into this phenomenon.

Brownwood Regional Medical Center (RB, CC), Brownwood, Texas; and Department of Ophthalmology (AG, VD, RNH), University of Texas Southwestern Medical Center, Dallas, Texas.

Address correspondence to Rance Boren, MD, PO Box 610, Brownwood, TX 78604; E-mail:

The authors report no conflicts of interest.

Retrolaminar migration of silicone oil is a recognized complication of intravitreal silicone injection, with at least 24 patients reported since 1983 (1–25) (Table 1). A 2014 review of the neuronal complications of silicone oil, including 8 cases of intracranial silicone, concluded that the phenomenon was benign, that preexisting glaucoma and congenital abnormalities (optic disc pits) were the main risk factors for its development, and that in their absence no special preoperative consideration was needed. There was little discussion of postoperative management (26). In addition to an extensive literature review, we report 2 additional cases.



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Patient One

An 82-year-old woman with Type II diabetes mellitus on aspirin and clopidogrel for coronary artery disease was hospitalized with a large pretibial hematoma. Her hemoglobin dropped from 13.6 to 9.7 mg/dL. She became confused and brain computed tomography (CT) showed hyperdense areas in the frontal horns of both lateral ventricles, as well as in the right eye and the nondependent portion of the right temporal horn (Fig. 1). Hounsfield units (HU) were 95 in the right eye and 75 in the intraventricular lesions. The initial radiologic diagnosis for the intracranial abnormalities was one of residual Pantopaque vs atypical intraventricular hemorrhage.

FIG. 1

FIG. 1

Consultation with the patient's ophthalmologist confirmed a history of multiple previous retinal detachments in the right eye because of proliferative retinopathy, with silicone oil placed after a vitrectomy 9 years earlier. There was no history of myelography. The diagnosis of asymptomatic intraventricular silicone oil was made. The patient's mental status changes were attributed to hospital-acquired delirium and gradually resolved.

At follow-up after hospitalization her intraocular pressure (IOP) was 42 mm Hg in the right eye. Further review showed that her IOP in the right eye had been intermittently elevated since her retinal surgery and that she had been blind in that eye for several years.

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Patient Two

A 42-year-old man with Type II diabetes mellitus presented to the emergency department with 3 days of painless vision loss in the right eye because of vitreous hemorrhage. Visual acuity was 20/400, right eye and no light perception, left eye. Brain magnetic resonance imaging (MRI) revealed silicone along the left optic nerve as far as the chiasm (Fig. 2), and small amounts in both lateral ventricles. Sixteen months previously, the patient underwent vitrectomy with silicone tamponade in the left eye for total retinal detachment secondary to proliferative diabetic retinopathy. Over the first postoperative year, he had IOPs of 36, 50, and 65 mm Hg associated with progression to total visual loss in the left eye.

FIG. 2

FIG. 2

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Infiltration of silicone into the retrolaminar optic nerve was first demonstrated pathologically by Ni et al in 1983 (1). Involvement of the optic nerve may or may not be a precondition for further movement into the subarachnoid space, but the 2 may coexist. The frequencies of both these complications are unknown, as are the time course of the migration and the underlying mechanisms. Silicone oil has been documented in the optic nerve sheath 24 hours after intravitreal injection, within the optic nerve by 1 month, and in the lateral ventricle by 8 months (3,9,27). Conversely, a prospective MRI study of 19 patients undergoing silicone extraction after successful treatment of retinal detachment (mean duration of tamponade: 3 months) failed to demonstrate extraocular silicone, despite the use of silicone-sensitive sequences (28).

Based on pathologic studies of silicone optic neuropathy, it seems likely that there is a correlation with both the length of tamponade and the presence of ocular hypertension. A retrospective assessment of 74 enucleated eyes by Budde et al (29) showed presumed silicone vacuoles in 19% of optic nerve specimens. Duration of tamponade was greater in the affected eyes (3.5 vs 1.5 years). Clinical information was available for 10/14 affected eyes; all had postoperative glaucoma. A study of 8 enucleated eyes found similar vacuoles only in the 2 patients with postoperative glaucoma (30) In a series of 36 enucleated eyes, 2 patients with significantly IOP developed presumed optic nerve infiltration within 1 month (27). The status of the other affected patients cannot be determined from the article, although glaucomatous pathology was reported in 56% of eyes and only 25% of nerves demonstrated apparent silicone infiltration. Another series of 9 eyes revealed silicone in the optic nerve of 1 patient (11%) (31). The overall rate of presumed silicone infiltration in these studies was 20%. For comparison, the incidence of Schnabel cavernous degeneration (see below) in a series of 155 enucleated glaucomatous eyes was 1.3%, and in eyes with both glaucoma and uveal melanoma the rate was 11.6%. (32).

Enucleation studies introduce obvious selection bias that may magnify the effect of glaucoma. There are no estimates of the frequency of silicone infiltration in patients who do not come to enucleation, nor are there pathologic studies of patients in whom intracranial silicone has been documented. Subarachnoid (perineural) silicone has only been demonstrated pathologically in 1 eye with optic nerve infiltration (7).

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From a neurologic standpoint, the natural history of migration of silicone seems benign in most cases; many were detected incidentally during evaluation of nonspecific symptoms such as headaches or dizziness. However, a patient with chronic headaches, intraventricular silicone, and elevated cerebrospinal fluid (CSF) pressure (27 cm H2O) has been reported (19). This patient lost sight despite normal postoperative IOPs and eventually underwent enucleation after developing painful neovascular glaucoma (maximum IOP = 52 mm Hg) several months later. He developed headaches 5 years after his initial surgery and failed conservative treatment before obtaining symptomatic relief after ventriculoperitoneal shunting.

Associated visual problems are more common. Tang et al (3) reported a case of immediate postoperative visual loss and perineural subarachnoid silicone oil. The patient was treated with optic nerve decompression within 24 hours but had no significant visual improvement over several months. Another patient with sudden postoperative (1 week) visual loss was found to have an optic nerve sheath that was “distended with silicone oil” on MRI but due to a delayed presentation no treatment was proposed (8). Eckle et al (11) reported a patient who had undergone repair of a retinal detachment in his left eye. One year later, with acuity of 20/20, right eye and light perception, left eye, he suddenly developed temporal visual field loss in the right eye. This was attributed to silicone oil pooling in the “optic nerve sheath” at the chiasm. The patient underwent craniotomy with chiasmal decompression and improvement in the right visual field. Acuity in the left eye remained light perception. The left optic nerve was described as “hollowed out” (11). In another case of monocular temporal field defect of the untreated eye, the field loss resolved over a month in association with radiographically documented migration of silicone from the suprasellar region to lateral ventricle (15).

A patient with immediate postoperative periorbital pain, ptosis, orbital, and meningeal enhancement, inflammatory spinal fluid, and presumed silicone oil in the left lateral ventricle was described by Espinoza et al (33). In this case, the intraventricular abnormality was in the mid-portion of the left lateral ventricle near the foramen of Monro, and, on the basis of the single image provided, may reflect CSF pulsation artifact rather than intraventricular silicone (34). This patient was excluded from our review of cases.

Most of the other patients with a detailed ophthalmologic history described a progressive loss of vision in the treated eye before the discovery of intracranial silicone oil. In some cases this could have been due to glaucoma or retinal disease. However, in 3 patients the authors specifically commented on the loss of vision despite normal or minimally elevated IOPs (1,12,19). A report of visual outcomes after silicone injection has suggested that a significant number of patients with good visual potential may have decline in vision related to the oil itself (35).

Microcystic macular changes detected by optical coherence tomography (OCT) have been described in eyes after silicone oil injection. These retinal changes are similar to those reported from other causes, including Leber hereditary optic neuropathy and multiple sclerosis (36). These macular changes may be secondary to a silicone-related optic neuropathy. However, in a rabbit model, loss of retinal neurons with optic atrophy has been described in the absence of elevated IOP, silicone infiltration of the optic nerve, or subarachnoid silicone (37).

The diagnosis of intraventricular silicone may be made on the basis of an unenhanced CT, with the findings being the globular and nondependent nature of the radiologically hyperdense abnormalities, features that are due to the low specific gravity and high viscosity and interfacial tension of silicone oil (38). Numerous patients have been scanned in the prone position to document buoyancy of silicone (5,9,12,17–19,22). Asymptomatic movement of silicone from the optic nerve/chiasm to the lateral ventricles, and between lateral ventricles, has been noted on serial scans (13,17). Movement of silicone between the third and lateral ventricles has been demonstrated over 48 hours (24). Therefore, it should be remembered that imaging findings reflect only a snapshot of a dynamic process.

Silicone in the optic nerve or sheath appears as a tubular hyperdensity but may be difficult to appreciate without dedicated orbital views, fortuitous slice alignment, or silicone-sensitive sequences (14,25). The main differential diagnosis on CT is hemorrhage, although an isolated globule in the third ventricle mimicked a colloid cyst (24). Silicone oil near the chiasm may resemble an aneurysm or subarachnoid blood in the basal cisterns (23). Several patients underwent additional testing or were referred to neurosurgical centers for these findings (13,16,18,23).

Intraocular silicone was originally found to have a density of 110–130 HU (39). Including our first patient, the average of reported intraventricular lesions was 82 HU (range 55–98 HU) (10,13,14,17,18,24,25). This is still higher than typically seen with hemorrhage (30–60 HU), which tends to be dependent and form fluid levels. Pantopaque has a higher specific gravity than CSF and when seen intracranially, it classically forms multiple lesions near the skull base (40).

The MRI findings with ocular silicone have been well characterized and intraventricular silicone has been found to follow the ocular silicone on all sequences (39,41). In addition, a characteristic chemical shift artifact may be detected (5,39). Two of the reported patients were found to have intracranial silicone after silicone removal from the eye or after enucleation (9,19).

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Both pathology and advanced imaging techniques have revealed the presence of silicone inclusions in all retinal layers, the choroid, and optic nerve (1,2,42–44). This suggests the possibility that infiltration of silicone into the retina could be followed by movement along the retinal nerve fiber layer into the optic nerve. However, it is generally assumed that the silicone infiltrates the optic nerve directly through the lamina cribrosa (along the axis of the entering axons) facilitated by postoperative pressure elevations.

Hyaluronic acid–filled cavities in the optic nerve (Schnabel cavernous degeneration) were initially associated with glaucoma, and the classical paradigm is that the mucopolysaccharide in the optic nerves reflects infiltration by vitreous (45). Shields and Eagle (2) found “optically empty” vacuoles in the optic nerve of a silicone-treated eye and postulated that migrating silicone replaced vitreous in such cases, using the term “pseudo-Schnabel” degeneration to describe this process. Subsequent studies using energy dispersive X-ray analysis confirmed the presence of silicone in these vacuoles (7,46).

Although intraneural silicone oil originates in the vitreous cavity, it has been suggested based on histochemical studies that the hyaluronic acid seen in Schnabel degeneration may be produced in situ by Type II astrocytes as a response to tissue damage (47). Similar pathologic findings have been observed in cases of ischemic optic neuropathy without glaucoma, and a large autopsy study suggested that cavernous degeneration may develop because of chronic ischemia independent of IOP (48,49). Therefore, the exact relationship between these 2 syndromes remains unclear.

Williams et al (5) postulated that infiltration of the optic nerve by silicone was followed by coalescence into larger vacuoles, posterior migration, and eventual entry of silicone into the subarachnoid space of the optic nerve. Although it seems unlikely that this mechanism could be a major factor in patients who present in the immediate postoperative period, it has been shown that Schnabel pathology may develop within 4 days in an animal model of acute glaucoma, even without structural changes in the lamina cribrosa (50).

Rupture through the periphery of the lamina cribrosa with direct passage of silicone to the subarachnoid space was proposed by Fangtian et al (9) whose patient had significant optic disc cupping. (9) Detailed assessments of the anatomic changes in the lamina cribrosa in glaucomatous eyes have shown that thinning and cupping of this structure may combine to bring the posterior lamina into direct contact with the pia (51,52). Laminar holes and dehiscences have been demonstrated in glaucomatous eyes by OCT (53). These defects may provide a route for silicone movement.

Congenital optic nerve pits also have been implicated in migration of silicone into the subarachnoid space. Kuhn et al (12) reported a 15-year-old girl with bilateral optic pits who lost vision 2–3 years after silicone placement in her left eye despite only minimally elevated IOP (26 mm Hg). Three years later she developed “strong persistent headaches,” and was found to have an IOP of 36 mm Hg in the left eye and silicone in the ventricular system on MRI. Optic nerve pits are rare, and are commonly associated with serous retinal detachments (54). Therefore, it is unclear whether the case reported by Kuhn et al represents a chance association or an additional route of silicone migration. To our knowledge, silicone migration has not been reported in patients with retinal detachment related to coloboma or morning glory syndrome (55).

Movement of silicone through the perivascular space could be involved in passage from the retina to the optic nerve or from the nerve to the subarachnoid space. Pathologic studies typically include no more than 1 cm of optic nerve and infiltration of oil has been noted up to the surgical margins (2,4,29). The central retinal artery and vein pierce the optic nerve just beyond this point and may provide the most direct conduit from the optic nerve to the subarachnoid space (Fig. 3). This route has been proposed as an explanation for some cases of Terson syndrome (56). Transpial penetrating vessels supplying the chiasm or optic tract could conceivably play a similar role intracranially.

FIG. 3

FIG. 3

Chiao et al (22) noted that these mechanisms of silicone movement are not mutually exclusive, and there is insufficient evidence to support one over the other. It is possible that rupture through the periphery of the lamina cribrosa or dissection along the central retinal vessels explains cases with rapid subarachnoid spread of silicone oil, but that gradual infiltration of the optic nerve followed by posterior migration (with or without slow leakage into the CSF) also could occur (Fig. 4).

FIG. 4

FIG. 4

Alternatively, owing to the lack of a physiologic communication between the posterior chamber and the subarachnoid space, an “active transport” system has been postulated to explain silicone migration. Knect et al (57) reported a negative study of silicone maintained under pressure in cadaveric eyes in support of this theory. However, a short-duration study in biologically inert eyes is of limited application. Although the term “active transport” was attributed to Budde and Papp, both authors stated that postoperative ocular hypertension was the driving force behind silicone movement (7,29,58).

Because silicone-containing macrophages have been observed throughout the orbit and in some cases of optic nerve infiltration their involvement in the “active transport” of silicone has been proposed (7,59). Macrophages have been noted in inflammatory tissue surrounding breast implants and silicone has been noted in macrophages in lymph nodes after both arthroplasty and mammoplasty (60). However, in the study by Budde et al (29), silicone-laden macrophages were seen in only 3/14 cases (21%) (29). Therefore, it seems more likely that the presence of macrophages/microglia is a response to silicone infiltration of the optic nerve, rather than the cause, and that their role in role in silicone movement is negligible.

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Once silicone gains access to the subarachnoid space of the optic nerve, several factors may influence further movement. The compartmentalized nature of the optic nerve subarachnoid space surrounding the orbital segment of the optic nerve and the choke point at the canalicular segment (Fig. 5) could lead to arrest of silicone migration (61). Owing to the buoyancy of silicone, movement away from the eye may even have a tendency to reverse during supine sleep. Also, dural lymphatics have been proposed as a significant route of CSF reabsorption in the optic nerve (62,63). These might be expected to clear small quantities of silicone from this segment. Owing to a combination of these factors, there may be cases in which subarachnoid silicone never reaches the intracranial compartment.

FIG. 5

FIG. 5

The optic nerve enters the cranial cavity through the optic canal. There the subarachnoid space of the optic nerve is in direct communication with the subarachnoid space of the brain, and ultimately with the ventricular system. Eller et al (6) postulated that individual microbubbles of silicone are carried to the ventricles and coalesce there (6). However, in at least 1 case there was apparent collection of silicone in the suprasellar cistern (15). This, along with the other clinical and radiologic observations described above, suggests that the high viscosity of silicone favors its migration as a large bolus in some cases.

There are numerous trabecula in the cerebral subarachnoid space, and the individual basal cisterns are separated by sheets of arachnoid, which must be circumvented before subarachnoid silicone can reach the fourth ventricle. Historically, delays in migration of air attributable to these structures were seen during the performance of air cisternography (64). Even the foramina of Luschka and Magendie have been found to be obstructed by a membrane in some patients (64,65). Taken together, these factors suggest that anatomic barriers to silicone migration may account for variability between patients. Finally, as it goes against both gravity and the classic model of CSF flow, the entry of silicone into the ventricular system adds additional support to the emerging understanding of CSF flow as a pulsatile bidirectional process (66,67).

In many cases, intracranial silicone lies within the substance of the optic nerve and chiasm. Our second patient (Fig. 2) and others (Table 1) illustrate this. In the case reported by Eckle et al (11), silicone at the chiasm was surgically proven to be subpial. This indicated that silicone can travel long distances along the anterior visual pathway. In 2 patients, silicone extended the length of the optic tract (16,22). Therefore, the pia may be a partial to barrier silicone movement into the subarachnoid space. Both patients had intraventricular silicone; whether it entered the subarachnoid space in the orbit or intracranially is unknown. These 2 cases also suggest a tendency for silicone to be reflected ipsilaterally at the chiasm, either following the nondecussating fibers or possibly filling space created by axonal degeneration.

The possibility of blockage of CSF outflow is supported by the case described by Hruby et al (19). The presence of communicating hydrocephalus would seem to imply widespread diffusion of silicone in the CSF. Further support for this theory exists in the eye, where emulsified silicone in the trabecular meshwork can cause glaucoma (68,69). One experimental animal model for obstructive hydrocephalus involves intraventricular injection of silicone into the cisterna magna and basal cisterns (70). This raises the possibility that transient “nonspecific” symptoms, such as headache, could occur as silicone moves through the ventricular system.

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Optic nerve and intracranial complications of silicone injections may arise more frequently in the future because of an aging population and an increase in the number of indications for silicone usage (71,72). Awareness of the radiographic appearance of intracranial silicone may avoid unnecessary testing.

Although the migration of silicone intracranially is rare in proportion to all ocular silicone injections, the more important issue may be the cases in which silicone remains over the long-term, especially in association with postoperative glaucoma. This patient population is poorly characterized (72) and likely the true prevalence is under-appreciated. Furthermore, it is possible that cases of progressive visual loss associated with intraneural or subarachnoid silicone are incompletely evaluated or simply attributed to glaucoma. The contribution of these processes to long-term visual outcomes in retinal detachment remains unknown, but may be significant. The case reported by Eckle et al (11) suggested that optic nerve fenestration or neurosurgical drainage may have a role in some cases of postoperative visual loss.

Numerous authors have called for more aggressive management of postoperative glaucoma, imaging of patients with postoperative visual loss, and removal of silicone whenever possible (3,7,10,19). It also seems prudent to consider the possibility of silicone migration during discussions with patients regarding silicone implantation and removal. The absence of preoperative glaucoma or optic pits is not protective. Clearly, much more needs to be learned about the routes of dissemination of intraocular silicone and the clinical implications of its spread along the anterior visual pathway and to the subarachnoid space and the ventricular system.

Conclusions regarding the prevalence and natural history of this phenomenon are hampered by the lack of awareness, absence of a convenient, validated, in vivo diagnostic tool, and by fragmentation of care. Additional detailed case reports would be useful. Studies using OCT or other advanced imaging modalities on a larger population of patients with long-term silicone tamponade, especially those with elevated IOPs, would provide additional information regarding the prevalence and natural history of this disorder and the contribution of silicone neuropathy to visual outcomes after retinal detachment (73–75). An animal model incorporating silicone injection and induced glaucoma could yield pathologic confirmation of the theories discussed in this review (76).


Category 1: a. Conception and design: R. Boren, C. Cloy; b. Acquisition of data: R. Boren, A. Gupta, V. Dewan; c. Analysis and interpretation of data: R. Boren, A. Gupta, V. Dewan, R. N. Hogan. Category 2: a. Drafting the manuscript: R. Boren, C. Cloy; b. Revising it for intellectual content: R. Boren, C. Cloy, A. Gupta, V. Dewan, R. N. Hogan. Category 3: a. Final approval of the completed manuscript: R. Boren, C. Cloy, A. Gupta, V. Dewan, R. N. Hogan.

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