Journal of Neuro-Ophthalmology, September 1995, Volume 15, Issue 3

Intracranial Hypertension and the Syndrome of Acquired Hyperopia with Choroidal Folds

An idiopathic syndrome of acquired hyperopia with choroidal folds has been characterized. Orbital imaging correlates of this syndrome include flattening of the posterior globe and distention of the perioptic subarachnoid space. The mechanism responsible for the clinical and radiographic findings of this syndrome is undefined. Two patients with unusual presentations of papilledema are reported whose clinical and radiographic findings were otherwise identical to those described in the idiopathic syndrome of acquired hyperopia with choroidal folds. One patient had unilateral disc edema and bilateral choroidal folds. The other patient had bilateral choroidal folds observed 2 years before he developed papilledema in both eyes. Both patients had intracranial hypertension, idiopathic in the first, and related to severe chronic obstructive pulmonary disease and cor pulmonale in the second. A third patient is also described who had typical clinical and orbital imaging findings of idiopathic unilateral acquired hyperopia with choroidal folds. He was also found to have mild intracranial hypertension. Intracranial hypertension can cause acquired hyperopia and choroidal folds and may be the underlying mechanism in some patients with what appears to be idiopathic acquired hyperopia with choroidal folds.

lourtwl t> j Nntii)- Oi'lilliiilimihyti{ 15( 3): 178- 185, t$!) 5. © 1995 LippincoLt- Raven Publishers, Philadelphia Intracranial Hypertension and the Syndrome of Acquired Hyperopia with Choroidal Folds Daniel M. Jacobson, M. D. An idiopathic syndrome of acquired hyperopia with choroidal folds has been characterized. Orbital imaging correlates of this syndrome include flattening of the pos­terior globe and distention of the perioptic subarachnoid space. The mechanism responsible for the clinical and radiographic findings of this syndrome is undefined. Two patients with unusual presentations of papilledema are reported whose clinical and radiographic findings were otherwise identical to those described jn the idio­pathic syndrome of acquired hyperopia with choroidal folds. One patient had unilateral disc edema and bilat­eral choroidal folds. The other patient had bilateral cho­roidal folds observed 2 years before he developed pap­illedema in both eyes. Both patients had intracranial hy­pertension, idiopathic in the first, and related to severe chronic obstructive pulmonary disease and cor pulmon­ale in the second. A third patient is also described who had typical clinical and orbital imaging findings of idio­pathic unilateral acquired hyperopia with choroidal folds. He was also found to have mild intracranial hy­pertension. Intracranial hypertension can cause ac­quired hyperopia and choroidal folds and may be the underlying mechanism in some patients with what ap­pears to be idiopathic acquired hyperopia with choroidal folds. Key Words: Hyperopia- Choroidal folds- Papille­dema- Idiopathic intracranial hypertension- Pseudo­tumor cerebri. Manuscript received December 19, 1994. From the Departments of Neurology and Ophthalmology, Marshfiold Clinic, Marshfield, Wisconsin, U. S. A. Address correspondence and reprint requests to Dr. D. M. Jacobson, Marsh field Clinic, 1000 N. Oak Ave., Marsh field, Wl 54449, U. S. A. Most large series reporting the causes of choroi­dal folds describe an association with hyperopia, although the mechanism of this association is un­defined ( 1- 5). Norton ( 1) and Bullock and Egbert ( 6) suggested that choroidal folds might develop in this setting on the basis of scleral shrinkage and shortening of the globe. The orbital echographic findings associated with many cases of choroidal folds associated with hyperopia indeed show shortening of the axial length, as well as flatten­ing of the posterior globe, retinochoroidal thick­ening, and distention of the optic nerve sheath ( 4,7). In 1980, Kalina and Mills ( 8) reported six healthy adults who developed symptoms associated with acquired hyperopia who were found to have cho­roidal folds. The similarities of the clinical features of these patients suggested a syndrome. Their re­port ( 8), along with a long- term follow- up study of these patients ( 9), emphasized the benign na­ture of this syndrome because most patients dem­onstrated stable visual acuity, refraction, and pos­terior pole appearance. The same group of inves­tigators further characterized this syndrome by describing the typical computed tomography cor­relates, which included flattening of the posterior globe and enlargement of the subarachnoid space around the optic nerve sheath ( 9,10). Other investigators have since reported cases with similar clinical and neuroimaging findings ( 11,12). However, the underlying mechanism causing this syndrome is unknown. Daily and col­leagues ( 9) suggested similarities between ac­quired hyperopia with choroidal folds and the uveal effusion syndrome. The following case reports and discussion are offered in support of the hypothesis that the syn­drome of acquired hyperopia with choroidal folds in some patients may actually represent unusual presentations of intracranial hypertension. 178 ACQUIRED HYPEROPIA CASE REPORTS Casel A 28- year- old man was referred to evaluate " papilledema of the left eye." For the preceding 6 months, he had noted vague trouble judging dis­tances and a few brief spells of transient dimming of vision in his left eye, after bending over. He also noted an intermittent, mild, dull, left- sided retro-orbital ache for the preceding 18 months. He first sought care from his optometrist, who found that he had developed + 0.75 and + 1.00 diopters of hyperopia in his right and left eye, respectively, since his Last examination 4 years earlier. " Papille­dema" of his left disc was noted. A consulting neu­rologist then obtained normal complete blood counts, serum chemistries, erythrocyte sedimenta­tion rate, antinuclear antibody, and visual evoked potentials. Brain computed tomography was re­portedly " normal." Lumbar puncture, performed with the patient fully relaxed, on his side, and with his legs extended, revealed an opening pressure of 210 mm cerebrospinal fluid, three leukocytes/ microliter, protein 36 mg/ dl, glucose 57 mg/ dl, and negative microbiological and cytological studies. He was otherwise healthy, taking no medications, and had no other neurological or visual symptoms. When evaluated 1 week later, he was not obese ( weight, 177 pounds; height, 71 inches). His best corrected visual acuity was 20/ 20 + 2 in his right eye and 20/ 25 in his left eye. Cycloplegic refraction was piano + 1.50 X 90 in his right eye, and + 2.00 + 1.00 x 65 in his left eye. Color vision, assessed using pseudoisochromatic plates ( Richmond Prod­ucts, Boca Raton, FL, U. S. A.), was normal in both eyes. He had a small afferent pupillary defect in his left eye, neutralized with a 0.3 log unit neutral density filter held before the right eye during the swinging flashlight test. Goldmann perimetry re­vealed mild enlargement of the relative scotoma around the absolute blind spot in the right eye and moderate enlargement of the absolute and relative blind spot in the left eye. The size of the relative blind spot decreased in the left eye when tested with serial addition of plus sphere. Ophthalmos­copy of the right eye revealed a flat, normal-appearing optic disc, and subtle, horizontally ori­ented retinal folds extending from the disc to the fovea ( Fig. 1). Ophthalmoscopy of the left eye re­vealed a peculiar elevation and whitish opacifica­tion of the immediate peripapillary nerve fiber layer, with little swelling of the disc itself ( Fig. 2). Numerous retinal folds were observed extending from the disc in all directions, but mainly in the horizontal plane ( Fig. 2). Mo spontaneous venous rH CHOROIDAL FOLDS 179 FIG. 1. Case 1. Posterior pole of the right eye, show­ing a normal optic disc and subtle retinal folds. pulsations were observed in cither eye. Fluores­cein fundus angiography, performed several weeks later, confirmed that the retinal folds were choroidal in origin in both eyes and demonstrated late leakage and staining of dye at the left disc border and immediate peripapillary retina, but not within the disc itself ( Fig, 3). A- scan echography revealed the following axial measurements in the right and left eye, respectively: cornea to sclera, 23.7 mm, 23.3 mm; cornea to retina, 22.5 mm, 21.8 mm; scleral thickness, 1.2 mm, 1.5 mm. The re­mainder of his ophthalmic and neurologic exami­nations were normal. FIG. 2. Case 1. Posterior pole of the left eye, showing whitish edema of the immediate peripapillary nerve fiber and retinal folds extending peripherally from the optic disc. / Nami- Oitlilhahmil, Vvl. 15, No, .1, 13£ tf 180 D. M. FIG. 3. Case 1. Fluorescein fundus angiogram of the posterior pole of the left eye obtained 5 min after in­jection of dye, showing staining of the immediate peri­papillary retina but not of the optic disc itself. Note that the fluorescein dye appears to be accumulating deep to the retinal vessels, not within the peripapillary nerve fiber layer. Also note the alternating hypofiuo-rescent and hyperfluorescent lines representing cho­roidal folds. Review of his previously performed " normal" computed tomography study suggested thicken­ing and tortuosity of the left optic nerve sheath complex and flattening of the left posterior globe. High- resolution orbital computed tomography and magnetic resonance imaging confirmed that the thickened optic nerve sheath complex was due to dilation of the perioptic cerebrospinal fluid space with expansion of the optic nerve sheaths on both sides ( Figs. 4 and 5). The posterior globes were thickened and flattened in the region of the optic nerve insertion ( Figs. 4 and 5). These findings were present bilaterally but were more apparent on the left. He received acetazolamide, 1,500 mg daily in di­vided doses, and was followed serially over the next 3 years. His transient visual obscurations and retroorbital ache resolved within weeks. His visual acuity gradually improved to 20/ 15 in both eyes. His refraction remained piano in the right eye but gradually changed to 4- 1.25 sphere in his left eye. The peripapillary nerve fiber edema around the left disc slowly improved during the 10- month pe­riod after initiation of treatment, although mild na­sal edema persisted ( Fig. 6). The choroidal folds remained unchanged ( Fig. 6). A- scan echography measurements of axial lengths, serially measured during the first 19 months, did not significantly change. Orbital magnetic resonance imaging, re- FIG. 4. Case 1. Orbital computed tomography image in the axial plane after contrast administration, show­ing widening of the optic nerve sheath on both sides due to distention of the perioptic subarachnoid space. Also note the thickened and flattened appearance of the posterior globes at the site of optic nerve inser­tion. For orientation purposes of this figure, and all subsequent neuroimaging figures, right side is on the reader's left side of the figure, peated 3 years after his initial evaluation, showed similar changes without any significant reduction in optic nerve sheath distention or posterior globe flattening. Case 2. A 48- year- old man was referred to evaluate " papilledema." He had been followed at my insti­tution for routine eye care for the past 10 years FIG. 5. Case 1. Orbital T1- weighted magnetic reso­nance image ( TR = 550 ms, TE = 15 ms) in the axial plane showing distention of the perioptic subarach­noid space and flattening of the posterior globe, es­pecially on the left side. / Naim- OfhlliiiliiMl, Vol. 15, No. . I. 1995 ACQUIRED HYPEROPIA FIG. 6. Case 1. Posterior pole of the left eye, showing resolution of most of the peripapillary nerve fiber edema but persistence of choroidal folds. with previous stable retractive errors of piano + 0.50 x ISO in both eyes. He was evaluated in July 1991 for conjunctivitis. He had no other visual or neurological symptoms but had developed hy­peropia ( + 1.00 + 0.25 x 90) and retinal folds in both eyes ( Fig. 7), His visual acuity was 20/ 30 in both eyes, and his discs were flat ( Fig. 7), Fluores­cein fundus angiography confirmed horizontally oriented choroidal folds extending from both optic discs but no leakage of dye from the discs ( Fig. 8). Computed tomography was reported as " normal" at that time but, in retrospect, suggested disten­tion of the optic nerve sheaths and flattening of both posterior globes at the site of optic nerve in- FIG. 7. Case 2. Posterior pole of the left eye, showing retinal folds extending horizontally from a flat optic disc. CHOROIDAL FOLDS 181 FiG. 8. Case 2. Fluorescein fundus angiogram of the posterior pole of the right eye obtained 1 min after injection of dye, showing alternating hypofluorescent and hyperfluorescent lines representing choroidal folds. Note the absence of staining of the optic disc. sertion. When evaluated 1 year later, he remained asymptomatic and had the same findings. When reevaluated 1 year Later in August 1993, massive bilateral optic disc edema was noted for the first time. He admitted to mild intermittent headaches since the 1960s, which had not changed in charac­ter during the past 3 years. However, he had ex­perienced frequent, daily, posturally induced, transient visual obscurations and subjective pulsa­tile intracranial noises for the preceding 3 months. His past medical history was significant for se­vere tobacco- associated chronic obstructive pulmo­nary disease. A typical arterial blood gas on room air showed pH, 7.32; pco2, 74 mm Hg; and po2, 42 mm Hg. He also had severe right- sided heart fail­ure with pulmonary hypertension and secondary polycythemia, with a typical hemogram showing hematocrit 65% and hemoglobin, 21.8 g/ dl. When evaluated 1 week later, he was not obese ( weight, 185 pounds; height, 67 inches). His best corrected visual acuity was 20/ 20 - 2 in his right eye and 20/ 20 in his left eye. Non- cycloplegic re­fraction was + 1.50 sphere in his right eye and + 1.75 sphere in his left eye. Color vision was nor­mal in both eyes. Goldmann perimetry showed moderate enlargement of the relative blind spot in both eyes. Ophthalmoscopy revealed marked hy-peremic swelling of both optic discs with numer­ous nerve fiber layer hemorrhages ( Fig. 9). The retinal veins were mildly full and tortuous. Fluo­rescein fundus angiography revealed early leakage of dye from the optic discs and persistence of the previously documented choroidal folds in both } Ntura- Oplilhtilimi), Vol. 15, No. 3, 1995 182 D. M. FIG. 9. Case 2. Posterior pole of the right eye, show­ing massive, fully developed papilledema. eyes. There was mild delay in venous filling but no capillary dropout, microaneurysms, or arteriove­nous or retinochoroidal shunt vessels. The remain­der of his ophthalmic and neurologic examinations were normal. Orbital computed tomography revealed promi­nent optic nerve sheath distention and flattening of the globes at the insertion of the optic nerves on both sides { Figs. 10 and 11). Brain sections showed no findings of dural sinus thrombosis but revealed changes consistent with intracranial hypertension, including blunting of cerebral sulci, small ventri­cles, and obliteration of basal cisterns. These brain findings were not present on his original study 2 years earlier. He refused to undergo lumbar punc­ture. He was treated with serial phlebotomies and FIG. 10. Case 2. Orbital computed tomography image in the axial plane after contrast administration, show­ing distention of the optic nerve sheath from dilation of the subarachnoid space on the left. Also note the subtle thickening and flattening of the posterior globe on the left. FIG. 11. Case 2. Sagittal reconstructed computed to­mography image of the right orbit, showing thicken­ing and flattening of the posterior gfobe at the site of optic nerve insertion. received a brief course of oral corticosteroids for exacerbation of his pulmonary disease. His papil­ledema dramatically improved during the next several months, but his choroidal folds persisted. Case 3 An otherwise healthy 46- year- old man was re­ferred to evaluate choroidal folds. During the pre­ceding 9 months, he had noted progressive blur when reading. Removing his spectacles resulted in clear vision. He denied headache, retroorbital pain, scotomatous visual loss, diplopia, or pulsa­tile intracranial noises. His optometrist noted reti­nal folds in his left eye and referred him to a retinal consultant who performed fluorescein angiogra­phy. This confirmed horizontally oriented choroi­dal folds streaming across the posterior pole of the left eye, extending through the optic disc and fovea. No choroidal folds were seen in the right eye. There was no leakage of dye from either optic disc. He was overweight ( weight, 218 pounds; height, 66 inches) but had not experienced any recent weight gain. His 4- year- old spectacle correction was - 2.25 + 0.75 X 149 in his right eye and - 2.50 + 0.25 X 55 in his left eye. Manifest refraction without cycloplegia was - 2.25 + 0.75 x 160 in his right eye and - 0.25 + 0.50 X 78 in his left eye. His best corrected visual acuity was 20/ 20 + 3 in his right eye and 20/ 50 - 2 in the left eye. Color vision was normal and symmetrical between both eyes. Goldmann perimetry showed mild enlargement of the relative blind spot and mild central depression of his left eye and normal findings in his right eye. He had a 0,2 log unit relative afferent pupillary defect on the left. Ophthalmoscopy revealed nor­mal optic discs in both eyes but without spontane­ous venous pulsations. The chorioretinal folds I Neiiro- Oi> l> tliahm> L Vat. 15, No. 3, 1995 ACQUIRED HYPEROPIA WITH CHOROIDAL FOLDS 183 were easily visible in the left eye ( Fig. 12); none was seen on the right. A- scan echography revealed the following measurements in the right and left eye, respectively: cornea to sclera, 26.5 mm, 25.8 mm; cornea to retina, 25.0 mm, 24.7 mm. The re­mainder of his ophthalmic and neurologic exami­nations were normal. Orbital computed tomography revealed optic nerve sheath distention and flattening and thick­ening of the posterior globe on the left ( Fig. 13); the brain appeared normal. Lumbar puncture, per­formed with the patient fully relaxed, on his side, and with his legs extended, revealed an opening pressure of 240 mm cerebrospinal fluid; one leuko-cyte/ microliter; protein, 38 mg/ dl; glucose, 59 mg/ dl; and negative microbiological and cytological studies. DISCUSSION These three patients shared the seminal clinical features common to those patients originally de­scribed by Kalina and Mills ( 8) with the idiopathic syndrome of acquired hyperopia with choroidal folds, including documented hyperopk: shifts and choroidal folds. In addition, the orbital imaging findings demonstrated in my three patients were the same as those described in the idiopathic syn­drome of acquired hyperopia with choroidal folds ( 9,10,12). Optic disc swelling has been observed in other cases of acquired hyperopia with choroidal folds described by Dailey and colleagues ( 9; cases 3- 5) and Garrity and colleagues ( 12; cases 6 and 7). All three patients reported herein had evidence of intracranial hypertension, idiopathic in Cases 1 and 3, and related to severe cor pulmonale, FIG. 12. Case 3. Posterior pole of the left eye, showing retinal folds and flat optic disc. FIG. 13. Case 3. Orbital computed tomography image in the axial plane after contrast administration, show­ing flattening of the posterior globe on the left. chronic obstructive pulmonary disease, and poly­cythemia in Case 2. The cerebrospinal fluid open­ing pressure in Cases 1 and 3, although not dra­matically elevated, were higher than the usual range observed in nonobese, healthy, young adults ( 13) and were in the range often observed in many patients with established pseudotumor cere­bri ( 13,14). Other reported patients with the syn­drome of acquired hyperopia with choroidal folds have also been found to have elevated cerebrospi­nal fluid pressure, including Case 3 reported by Kalina and Mills ( 8) and Dailey and colleagues ( 9), the patient reported by Corbett and colleagues ( 11), and Cases 6 and 7 reported by Garrity and colleagues ( 12). However, none of the investiga­tors reporting this finding discussed the possible significance of intracranial hypertension in their patients ( 8,9,11,12). In fact, an opening pressure of 320 mm during lumbar puncture of one such re­ported patients was dismissed as being unrelated ( 8) or an artifact of technique ( 9), Although Case 2 did not undergo lumbar puncture to document his cerebrospinal fluid pressure, he had medical con­ditions that can cause intracranial hypertension ( 15), he developed ophthalmoscopic and visual sensory findings compatible with papilledema, and his computed tomography changes of the brain were consistent with intracranial hyperten­sion. The orbital imaging changes observed in my three cases are not only the same as those others have described in the idiopathic syndrome of ac­quired hyperopia with choroidal folds ( 9,10,12) but also exactly what is observed in patients with id­iopathic intracranial hypertension ( 16,17). With in- I Nmiv- Ophthulniol, Vol. 15, No. 3-, 1995 184 D. M. JACOBSON tracranial hypertension, the elevated subarachnoid pressure is directly transmitted from the intracra­nial compartment to the intraorbital compartment through the perioptic subarachnoid space ( 18), re­sulting in distention of the optic nerve sheaths ( 16,17). Elevation of optic perineural pressure has two consequences. First, it causes stasis of axoplas-mic flow through the optic nerve head, resulting in axonal swelling and ophthalmoscopically apparent disc edema ( 19). Second, the elevated intrasheath pressure can cause the subarachnoid compartment to act as a mass at the point of contact with the globe, resulting in axia! length shortening and cho­roidal folds ( 20). The anatomical and physiological factors that dictate to what extent either papilledema or axial length shortening and choroidal folds will develop in intracranial hypertension are undefined. Al­though choroidal folds are often observed in pa­tients with idiopathic intracranial hypertension ( 21), the ophthalmoscopic hallmark of this disor­der is papilledema. The right eye of Case 1, the initial presentation of both eyes of Case 2, and the left eye of Case 3 in this report exemplify the un­usual development of choroidal folds as the initial ophthalmoscopic manifestation of intracranial hy­pertension. Given the similar orbital imaging ap­pearance in other cases of acquired hyperopia with choroidal folds ( 9,10,12), I suspect that many of these cases may also represent unusual presenta­tions of idiopathic intracranial hypertension. Certainly Cases 1 and 3 in this report are not typical examples of patients with idiopathic intra­cranial hypertension. Unlike most patients with this disorder ( 21), these two individuals were men without headaches, diplopia, or pulsatile intracra­nial noises. The peculiar- appearing peripapillary disc edema in Case 1 and choroidal folds in Case 3 were strictly unilateral. Unilateral, or highly asym­metric, papilledema has been well described in id­iopathic intracranial hypertension ( 22- 26). In fact, idiopathic intracranial hypertension may rarely oc­cur without papilledema ( 27). It is not known why one optic disc is protected from the effects of in­tracranial hypertension in unilateral cases of pap­illedema, although anatomical and physiological factors of the optic nerve head are believed to be important ( 25,26). The unusual ophthalmoscopic and fluorescein fundus angiographic appearance of the left optic disc in Case 1 deserves further comment. The re­gion of nerve fiber edema and fluorescein dye leak­age was peripapillary, not within the disc itself. The intermediary tissue of Kuhnt lies between the outer retinal layers and the prelaminar region of the optic nerve head, is composed of tight junc­tions, and prevents leakage of materials, such as fluorescein dye and exudates, from the anterior optic nerve head from reaching the peripapillary retina ( 28). Perhaps compression of the posterior globe by the pressure of the distended optic nerve sheath at its insertion somehow mechanically transformed this intermediary tissue into a leaky barrier. The syndrome of acquired hyperopia with cho­roidal folds, just like the syndrome of pseudotu­mor cerebri ( 29), is probably a heterogeneous group of disorders. At least some cases of acquired hyperopia with choroidal folds represent unusual presentations of idiopathic intracranial hyperten­sion or secondary pseudotumor cerebri syn­dromes. Patients with newly diagnosed acquired hyperopia with choroidal folds should undergo brain and orbital imaging to exclude structural in­tracranial and intraorbital causes and to seek the orbital neuroimaging correlates of intracranial hy­pertension. Evaluation of cerebrospinal fluid open­ing pressure and constituents in patients with symptoms or neuroimaging findings of intracrani­al hypertension also seems prudent. Measurement of intracranial pressure in all patients with ac­quired hyperopia with choroidal folds would pro­vide further insight into the frequency of intracra­nial hypertension causing this syndrome. Addendum: Six months after Case 2 was last seen at my institution, he received a second opinion through the courtesy of Leonard A. Levin, M. D., Ph. D. ( Madi­son, WI). He underwent a lumbar puncture which re­vealed an opening pressure of 370 mm cerebrospinal fluid ( with normal constituents) and a normal magnetic resonance imaging study of his brain. 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