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Purpose We chose to compare histologically and ultrastructurally changes in the optic nerve sheath after optic nerve sheath decompression, initially after a second surgery and after treatment with mitomycin-C. The mechanism by which optic nerve sheath decompression alleviates papilledema can be further understood in consideration of the results. Methods Tissue was obtained by biopsy from 3 first-time surgical and 4 reoperative cases with and without mitomycin-C in patients with idiopathic intracranial hypertension. The sheaths were fixed in a mixture of 2% paraformaldehyde and 2% glutaraldehyde, osmicated and dehydrated in a series of ethanol, and finally embedded in epon. Tissue blocks were sectioned at 1 microm and stained with both PPD and toluidine blue. Thin sections were examined by transmission electron microscopy. Results Normal meningeal tissue obtained at the time at optic nerve sheath decompression consisted mainly of collagen, closely packed and roughly parallel to the axis of the optic nerve. Collagen deposition seen in scar tissue after secondary optic nerve sheath decompression was extremely disorganized and irregular, with the individual fibers laid down seemingly at random. There was little sense of layering or of parallel arrays. Mitomycin-C appeared to influence collagen deposition in such a way that the collagen was more regularly packed and more closely resembled unoperated tissue. Conclusions The regular well-organized collagen packing seen in normal sheath tissue is disrupted and replaced by less organized but compact scar tissue after optic nerve sheath decompression. With mitomycin use, more regular collagen packing closely approximating that found in unoperated sheath occurs. This configuration of fibers lends support for the filtration mechanism of optic nerve sheath decompression in treating papilledema.

Absidia are rare causes of rhino-orbital mucormycosis, which is generally associated with Rhizopus infection. A 61 -year-old man sustained ocular trauma to his left eye. His traumatic optic neuropathy was treated with high-dose corticosteroids and with optic nerve sheath and optic nerve canal decompressions. A retinal dialysis was also corrected surgically. Two weeks later, the patient developed an orbital cellulitis with extensive upper eyelid necrosis. Biopsies revealed necrotic tissues on two occasions. Absidia and Peptostreptococcus were isolated from both specimens. Combined intensive amphotericin B and antibacterial therapy and two extensive surgical debridements successfully treated the polymicrobial mucormycosis, allowing eventual skin-graft repair.Intensive corticosteroid use appeared to be the principal inducing factor in this case, compounded by surgery involving the sinuses. The pathogenesis appeared entirely iatrogenic, complicating the management of ocular trauma. The characteristic constell...

Purpose: Optic nerve sheath fenestration has been advocated as an effective treatment for progressive nonarteritic ischemic optic neuropathy (NAION) and anecdotally effective for selected patients with NAION who have not had progressive visual loss. To determine whether optic nerve sheath decompression is of any benefit in patients with NAION, the authors reviewed their experience, surgically treating 23 patients with progressive NAION and 15 patients with static or nonprogressive NAION. Results: Patients with progressive NAION had a significant improvement in visual function as measured by Snellen visual acuity after optic nerve sheath decompression ( P = 0.0005). There was no statistically significant improvement in visual field mean deviation ( P = 0.11). The 15 patients undergoing optic nerve sheath decompression for static NAION failed to demonstrate significant improvement in either visual acuity ( P = 0.90) or visual field mean deviation ( P = 0.87). Preoperative standardized echography was used to measure the optic nerve sheath diameter and ascertain its compressibility (30° test). There was a significant difference in compressibility between eyes with static NAION and eyes with progressive NAION ( P = 0.001). Accumulation of optic nerve sheath fluid was documented in three eyes initially presenting with NAION and then with development of progressive visual dysfunction. Conclusion: Optic nerve sheath decompression improves visual acuity but has little effect on overall visual function in patients with progressive NAION. Optic nerve sheath decompression does not improve visual field or acuity in patients with static NAION. Detection of significant intrasheath fluid by standardized echography helps to objectively differentiate patients with NAION who may benefit from optic nerve sheath decompression.

We compared the automated visual field test results of 24 patients with normal-tension glaucoma and 24 patients with high-tension glaucoma who were closely matched for the amount of visual field loss to determine any differences in the characteristics of visual field defects between the two groups. Patients were matched with a maximum allowable difference in mean deviation of 0.3 dB. Although the normal-tension group had a greater amount of focal visual field loss (pattern standard deviation), the difference was not statistically significant (P = .628). Additionally, there was no statistically significant difference in the amount of diffuse or focal visual field damage in the superior hemifields between the two groups; however, the patients with normal-tension glaucoma had a significantly greater amount of localized visual field loss in the inferior hemifield than the patients with high-tension glaucoma (P = .015). Our data support the hypothesis that a vascular mechanism may have a greater role in the pathogenesis of optic nerve damage and visual field loss in patients with normal-tension glaucoma than in patients with high-tension glaucoma.

We treated 21 patients (22 eyes) with traumatic optic neuropathy by using intravenous megadose methylprednisolone (13 patients) or high-dose dexamethasone (eight patients). Of 13 patients treated with megadose methylprednisolone, 12 had improved visual function, as did seven of nine eyes treated with intravenous dexamethasone. This difference was not significant (P = .3). Initial total blindness, mechanism of injury, or time from injury to treatment did not correlate with visual improvement.

Purpose: To describe a patient with acinic cell carcinoma of the lacrimal gland presenting with atypical manifestations including erosion of the orbital roof and intracranial extension. We compare his clinical manifestations with two previously reported cases. Methods: Case report. Results: A 51-year-old man presented with a firm, tender, palpable mass in the superior temporal portion of his right orbit. CT scan demonstrated a large homogeneously enhancing mass displacing the globe inferiorly and eroding the roof of the orbit. MRI of the orbit showed intracranial extension of tumor. Biopsy revealed an acinic cell carcinoma of the lacrimal gland. Conclusions: Acinic cell carcinoma is a rare neoplasm occurring primarily in the major and minor salivary glands.

Purpose We used subtenon's local anesthesia for optic nerve sheath fenestration as an alternative to either general or retrobulbar anesthesia. Methods Thirty patients with pseudotumor cerebri, who were unresponsive to medical treatment, underwent optic nerve sheath fenestration after administration of topical and subtenon's local anesthesia. Results When topical tetracaine, in conjunction with subtenon's anesthesia, was administered at the beginning of the procedure, excellent anesthesia and maximal patient comfort were achieved. Conclusions The use of local anesthesia allows for a pain-free, expeditious operation with fewer potential anesthetic complications.

Purpose: Up to 35% of patients undergoing optic nerve sheath decompression (ONSD) for pseudotumor cerebri who show initial improvement in visual function later show deterioration in visual field and acuity. Although repeat surgery can result in subsequent visual improvement, these procedures are technically difficult because of scarring and fibrosis. Attempting to improve the long-term success of ONSD, the authors sought to analyze the long-term success of ONSD by pretreating optic nerve sheaths with mitomycin C before incision. Methods: Using a standard transconjunctival medial orbitotomy, optic nerve sheaths were exposed and treated for 5 minutes with mitomycin C (0.5 mg/ml)-soaked neurosurgical cottonoids before incision. Results: Both eyes undergoing repeat ONSD with adjunctive mitomycin C had initial improvement and stable visual function for follow-up of more than 3 years. Four eyes that underwent primary ONSD all initially showed improvement in visual field. Three eyes with large cysts or fistulas remained stable. Another eye had gradual decline in visual function. Repeat ONSD in this eye showed no orbital scarring, and lysis of adhesions between dura-arachnoid and optic nerve resulted in improved, stable visual function for 31 months of follow-up. Conclusion: Mitomycin C appears to be a safe adjunct to ONSD in a series of six patients followed between 20 and 37 months. Fistulization and cyst formation are associated with improved visual function. Closure of cysts and fistulas may result in worsening visual function due to intersheath adhesions. Repeat surgery shows significantly less orbital scarring and allows for easier and successful repeat surgery. Adjunctive mitomycin C leads to less orbital scarring after ONSD, allowing for easier repeat surgery.

• Objective. —To determine the long-term success of optic nerve sheath decompression in preserving visual function in patients with pseudotumor cerebri (PTC). Design. —To define stability of visual fields, we reviewed 32 series of postoperative visual fields in patients who were undergoing optic nerve sheath decompression for PTC who had stable visual acuity and four or more fields during 6 to 60 months of follow-up. The SD of these series was 0.80 dB (±0.39 dB) of mean deviation. Fluctuations within 2 SDs of the 1-month postoperative field were ±−1.60 dB. We therefore defined stability as a mean deviation within 2 dB of the preoperative visual field; improvement, greater than 2-dB mean deviation, and worsening, less than 2-dB mean deviation. We then extended our review to include all patients (54 patients, 75 eyes) who underwent optic nerve sheath decompression for PTC, who were followed up with serial automated perimetry (Humphrey 30-2). Results. —Fifty-one eyes (68%) showed improvement (36%) or stabilization (32%) of visual function. Twenty-four eyes (32%) experienced deterioration of visual function after an initially successful optic nerve sheath decompression. The probability of failure from 3 to 5 years was.35 by life-table analysis. Conclusion. —Optic nerve sheath decompression effectively stabilizes or improves visual function in the majority of patients with PTC and visual loss. However, it may fail at any time after surgery. Patients with PTC need to be followed up routinely with automated perimetry to detect deterioration of visual function.

We quantified optic disc pallor in patients with pseudotumor cerebri with the Rodenstock Optic Nerve Head Analyzer before and after optic nerve sheath decompression. Mean frequency distribution of pallor peaked between the pallor values of 0.10 and 0.20 in four pseudotumor cerebri patients and between 0.50 and 0.60 in five normal subjects. The red dominant pallor reflectance in pseudotumor cerebri patients decreased significantly and shifted toward the reflectance of normal subjects gradually during the 9 weeks after successful optic nerve sheath decompression, coinciding with the ophthalmoscopic resolution of papilledema. The computerized pallor measurement with the Rodenstock Optic Nerve Head Analyzer allows an objective and quantitative assessment of papilledema in pseudotumor cerebri patients.

We performed optic nerve sheath decompression in 53 patients (101 eyes) with pseudotumor cerebri and visual loss. Sixty-nine eyes (85 patients) with acute papilledema uniformly had improved visual function after optic nerve sheath decompression. Of 32 eyes with chronic papilledema (18 patients), only ten had improved visual function after optic nerve sheath decompression. This difference was significant (P = .0001). Thirteen eyes required secondary or tertiary optic nerve sheath decompression after an initial successful result. Eleven of 13 eyes had improved visual function after repeat optic nerve sheath decompression. We believe that patients with acute papilledema and visual loss should be offered optic nerve sheath decompression, and if symptoms recur, repeat optic nerve sheath decompression is a safe and effective treatment option.

We performed optic nerve sheath decompression on four patients (five eyes) with visual loss secondary to nonarteritic anterior ischemic optic neuropathy. Four of the five eyes had marked improvement in visual function after the operation. Optic nerve sheath decompression is an effective treatment for patients with nonarteritic ischemic optic neuropathy and progressive visual loss.

We reviewed 241 patients (178 black and 63 white) who were examined and treated at the Detroit Medical Center between 1980 and 1989 for traumatic hyphema. Secondary hemorrhage occurred in 46 patients (19%) and was significantly higher in black patients (P less than .005). Thirty-one patients (67%) developing secondary hemorrhage had an initial hyphema filling less than 25% of the anterior chamber. Patients treated with aminocaproic acid had secondary hemorrhages at a rate of 11% (six patients) compared to 21% (40 patients) in patients who were not treated with aminocaproic acid. The high risk of secondary hemorrhage with potential ocular damage in patients with traumatic hyphema, especially black patients, supports the benefit of hospitalization and the administration of aminocaproic acid.

Thirteen patients (20 eyes) were diagnosed with pseudotumor cerebri and subsequently underwent an optic nerve sheath decompression. In addition to improvement in visual function, an ultrasound examination demonstrated a significant change in the size of the optic nerve immediately posterior to the globe post-operatively. The posterior nerve measurements did not significantly change. These findings are useful in determining the possible mechanisms involved in optic nerve decompression.

We investigated retinal vascular changes in nine patients undergoing optic nerve sheath decompression for vision-threatening papilledema associated with pseudotumor cerebri. Two major (one superior and one inferior) retinal venous and arterial calibers were measured before and 1.1 ± 0.1 months, 3.2 ± 0.2 months, 5.0 ± 0.2 months, 7.6 ± 0.2 months, and 13.0 ±1.9 months after surgery. The retinal venous caliber decreased significantly, and the decrease progressed until 3.2 months after surgery. The venous caliber in the contralateral unoperated eyes also decreased significantly. The decrease in the venous caliber in the contralateral unoperated eye as well as in the operated eye following the surgery supports the hypothesis that slow filtration is the mechanism of successful optic nerve sheath decompression. Retinal venous caliber measurement, in either the operated eye or the unoperated fellow eye, can be used to quantitatively monitor the status of papilledema associated with pseudotumor cerebri.

The occurrence of ptosis after trabeculectomy has been a common postoperative complication. Many factors have been implicated in the development of postoperative ptosis. The purpose of this study was to investigate the incidence of ptosis following trabeculectomy and whether or not it was influenced by combined cataract surgery, type of conjunctival flap, and previous intraocular surgery. We reviewed 386 eyes of 386 patients who underwent either trabeculectomy alone or trabeculectomy combined with cataract surgery, with greater than 6 month follow-up. Ptosis occurred in 10.7% (18 of 150 eyes) after trabeculectomy alone and in 12.7% (30 of 236 eyes) after trabeculectomy with combined cataract surgery (p = 0.96). The incidence of ptosis was 12.3% (10 of 81 eyes) after limbus-based conjunctival flap and 12.5% (38 of 305 eyes) after fornix-based conjunctival flap (p = 0.98). There was no significant difference in the incidence of ptosis between primary surgery eyes (12.5%, 34 of 273 eyes) and secondary surgery eyes (12.4%, 14 of 113 eyes) (p = 0.97). The incidence of ptosis after trabeculectomy was about 12% overall and not significantly influenced by combined cataract surgery, type of conjunctival flap or previous ocular surgery.

We read with interest the report by Jablons et al 1 in the January 1993 issue of theArchivesof 26 patients who underwent optic nerve sheath fenestration for treatment of progressive ischemic optic neuropathy. Although we have had different results in our series of 23 eyes, 2 our sample may be significantly different from the series from the Bascom Palmer Eye Institute, Miami, Fla. Only one (6%) of 17 patients tested had intranerve sheath fluid on 30° A-scan echography in the Bascom Palmer series. 3 In our series, 12 of 12 subjects tested positive for intranerve sheath fluid and 11 (92%) of 12 experienced improvement of 2 or more lines after optic nerve sheath decompression (ONSD). If this is analyzed according to visual acuity, nine of 10 patients with visual acuity of 20/60 or worse experienced improvement of 2 or more lines. These results are significantly better than those

Aiello et al 1 reported two cases of spontaneous improvement of progressive anterior ischemic optic neuropathy (AION). They argued that since the conditions of patients with AION may spontaneously improve, it is reasonable to conduct a randomized clinical trial comparing the natural history of AION with AION treated with optic nerve sheath decompression (ONSD). While a trial may answer these questions, we are concerned that some issues are obfuscated in their cases. We have examined many 45- to 65-year-old patients with acute loss of visual acuity. Some of these patients have intranerve sheath fluid on standardized echography. It has been suggested that these patients have optic neuritis of the elderly. If this is true, we would expect final visual acuities to be similar to those reported in the optic neuritis treatment trial, in which median visual acuity was 20/20 after 6 months of follow-up. None of our patients with fluidassociated

Ocular involvement and visual symptoms from non-Hodgkin's lymphoma may occur from direct tumor involvement of the iris, choroid, retina, vitreous, and optic nerves.1We describe visual loss due to retinopathy resulting from renovascular hypertension in a patient with renal artery stenosis due to non-Hodgkin's lymphoma. Report of a Case. —A 19-year-old white man had intermittent headaches for 2 months and painless, progressive visual loss for 10 days in his right eye. Stage IV highgrade non-Hodgkin's lymphoma was diagnosed 2 years earlier following a right hemicolectomy for a cecal mass. The patient received chemotherapy. Six months later he had an autologous bone marrow transplant after a preparative regimen of high-dose cyclophosphamide and total-body irradiation (12 Gy). He had no spot radiation to the kidneys and was disease free for 18 months subsequent to the transplant. He had no history of ocular problems or hypertension. Best corrected visual acuities were 20/800

Nine patients with blepharoptosis and no levator palpebrae superioris muscle function were treated by fixating irradiated fascia lata to the tarsus and frontalis muscles under direct visualization. No recurrences were noted on follow-up, which ranged from four to 24 months. There were no postoperative infections or granuloma reactions. Cosmetically, the height, contour, and symmetry of the eyelid margin and eyelid crease were predictable and satisfactory. This modified method of frontalis suspension may provide a more predictable and cosmetically pleasing result in the treatment of blepharoptosis when minimal or no levator muscle function is present.

We studied optic nerve sheath decompressions for pseudotumor cerebri performed at the Kresge Eye Institute, Detroit, over the past year. Six patients (ten eyes) were operated on. Visual function improved in all ten eyes. A decision to operate was based on progressive loss of visual acuity or visual field unresponsive to medical therapy, accompanied by echographic evidence of a distended optic nerve sheath (positive 30 degrees test). Follow-up ranged from four to 11 months. Four patients underwent subarachnoid iopamidol (Isovue) contrast injection followed by orbital computed tomography. The subarachnoid space totally filled in all patients. No evidence of fibrosis or obstruction of the optic nerve sheath existed; however, leakage of dye from the optic nerve sheath could not be demonstrated. Postoperative complications included transient diplopia and transient atonic pupil (one patient each). Our results indicate that optic nerve sheath decompression improves and protects visual function in patients with pseudotumor cerebri who demonstrate progressive visual field loss and fluid in the optic nerve sheath.

Twelve consecutive patients with optic neuritis of unknown etiology treated with 250 to 500 mg methylprednisolone every 6 hours are described. All patients improved, some dramatically and rapidly. Patients with swollen discs and visual loss for less than 6 weeks improved uniformly, rapidly, and completely. In some patients, progressive visual deterioration was reversed rapidly. Serum serologies and cerebrospinal fluids findings were of limited use in determining etiology or prognosis with treatment. Side effects included exacerbation of a preexisting psychosis, elevated glucose levels, and oral candidiasis. None required cessation of treatment. Patients with optic neuritis may benefit from intravenous megadose corticosteroids.

We repaired four eyes in four patients with impending perforation using a vascular periosteal-temporalis fascia pedicle flap continuous to the periorbita of the orbital wall. Two eyes with extruding keratoprostheses, one eye with severe ocular surface dysfunction and a perforated, infected keratoplasty, and one eye with scleral ectasia were successfully reconstructed. Excellent visual acuity (20/25) was attained in one eye and functional visual acuity (20/100) was maintained in another. Structural integrity was maintained in all eyes. A vascularized flap was an excellent source of tissue for reconstructing eyes with impending perforation and scleral melting.

We compared the clinical course and histopathologic findings in five patients with malignant gliomas originating from the optic nerve pathways with those in previously reported cases to elucidate further the clinical features of this tumor and facilitate future diagnoses. Patients with malignant optic nerve pathway gliomas had unilateral or bilateral visual dysfunction, which was often accompanied by periorbital discomfort in an otherwise asymptomatic adult. Regardless of origin, the clinical course invariably was bilateral blindness rapidly followed by death. Occasionally, the diagnosis was made preoperatively and was confirmed by surgical exploration and biopsy.

A 49-year-old woman had a 12-year history of a localized left orbital tumor that required five subtotal excisions, orbital radiotherapy, and finally an exenteration. The last procedure was performed after visual function had deteriorated and in order to prevent spread of the tumor into a surrounding compartment. The biopsy specimens from the first four surgeries showed a stroma-free spindle cell tumor with benign cytologic features and no mitotic activity, which exhibited palisading of nuclei, imbrication of delicate cytoplasmic processes (neuropil), true perivascular rosettes with cytoplasmic processes oriented perpendicular to vessel walls, and Wright rosettes. The biopsy after radiotherapy and the exenteration specimen contained more polyhedral (gemistocytoid) tumor cells with abundant eosinophilic cytoplasm and tapering cell processes; nuclear pleomorphism without mitotic activity was also seen. Electron microscopy showed the presence of neurosecretory dense-core granules in the perikaryon region of the tumor cells and in the myriad interweaving cytoplasmic processes (neurites); neither Nissl substance nor synapses were identified. Immunohistochemical staining for neuron-specific enolase was positive, but glial fibrillary acidic protein stained negative. This previously undescribed orbital tumor is interpreted as a primary differentiated neuroblastoma without evidence of ganglion cell differentiation that exhibited locally aggressive behavior. The distinctions between neuroblastic and neuroendocrine tumors are discussed.

To the Editor. —A recent report by McCartney and Char 1 describing return of visual function, albeit limited, after 36 hours of postoperative blindness treated with orbital decompression, prompts us to report a similar experience following intracanalicular optic nerve decompression. Herein we describe the restoration of vision in a patient with no light perception acuity after five days of unsuccessful treatment with intravenous megadose corticosteroids. Report of a Case. —A 28-year-old man received a stab wound through his right nostril, immediately losing vision in his right eye. Evaluation revealed no light perception acuity in the right eye and a paralysis of cranial nerves III, IV, and VI. It was presumed that the knife injured the optic nerve and oculomotor nerves at the apex with penetration of the weapon intracranially. The sole finding on computed tomographic imaging studies was pneumocephalus. The patient was treated with intravenous methylprednisolone, 250 mg every six

• Forty-three patients with traumatic hyphema were studied prospectively in a controlled, double-blind study. Twenty-three patients received prednisone and 20 received a lactose placebo. Secondary hemorrhages occurred in 16% of all patients. There was no significant difference in the incidence of secondary hemorrhage between the two groups ( P =.85). There is no evidence that prednisone (40 mg/day) decreases the incidence of secondary hemorrhage. There was no significant difference in final visual acuities between the two groups. Patients with initially larger hyphemas do not appear to have worse final visual acuities. Hyphemas without secondary hemorrhage had a uniformly good prognosis. Although final visual acuities were worse in eyes with secondary hemorrhage, associated ocular injuries rather than blood-related complications accounted for the decreased visual acuity.

The Foster Kennedy Syndrome is very uncommon. The literature cited is often confusing. This paper presents a lucid definition of the syndrome that has contemporary diagnostic value and tenacious historical roots. We attempt to “sort-out” the true Foster Kennedy syndrome from its congeners and discuss the misnomers involved. An illustrative case is presented.

• Serious corneal complications occurred in an otherwise successful experience with continuous-wear soft contact lenses (SCLs) for aphakic correction. One hundred twenty eyes were fit, and 92% attained visual acuity of 20/40 or better. Severe corneal complications were observed in 13 eyes, including bacterial ulcers (six), apical erosions (three), and severe superficial vascularization (four). Corneal ulcers occurred in nondiabetic as well as diabetic subjects. Continuouswear SCLs are not innocuous; as for any other drug or device, continuous, longterm medical supervision is necessary to minimize potentially severe complications and visual loss.

• A case of progressive bilateral visual loss of abrupt onset and rapid course is described. Extensive neuroroentgenographic evaluation was normal, and the results of exploratory craniotomy were unremarkable, except for a slight ovality of the left optic nerve. A biopsy of the left optic nerve showed a glioblastoma, apparently originating in the anterior optic pathways.

To the Editor. —I read with interest the article in theArchivesentitled "Optic Neuropathy in Systemic Lupus Erythematosus" by Jabs et al 1 and totally concur with their statement that "in virtually any patient, particularly young women, who develop any type of optic neuropathy, whether unilateral or bilateral, the possibility of SLE [systemic lupus erythematosus] must be considered, and an appropriate history, examination, and serologic studies may be required." I believe, but cannot yet document, that this entity is much more common than we believe and may be a presenting manifestation of an autoimmune disease years before the appearance of convincing clinical signs, symptoms, and serologic abnormalities. I have had excellent success restoring vision in patients with both suspected and known autoimmune disease and visual loss due to an optic neuropathy with pulse dosage of megadose intravenous methylprednisolone. 2 Similar success has been reported by others. 3 I suggest

In three patients we used B-scan ultrasonography to guide the placement of an aspirating needle, which allowed rapid and accurate cytologic diagnosis of retrobulbar orbital neoplasms. This technique spares the patient the greater costs, inconvenience, and morbidity of more invasive procedures.

In Reply. —We read with interest the article by Rynne and Romano. 1 Although the authors stated that they had demonstrated the effectiveness of oral steroids in reducing the rebleeding rate in hyphemas, we believe this definitely was not demonstrated adequately by their article. In their article, their so-called control population consisted of patients with hyphemas treated by other physicians in the same institution. There was no random assignment of patients with hyphema to either the control or study group. There was no use of a placebo mentioned in the article. We also noted that an earlier article by Yasuna 2 also had a poor control series consisting of patients that he had treated before the use of prednisone. There was no random assignment of study patients to either the control series or the series treated with prednisone. We would like to address the specific criticisms of Rynne and Romano.

In Reply. —I regret that Stark et al believe we have "misrepresented the intent and content of [their] past articles on extended-wear contact lenses by stating that [they] reported no significant complications." This was not our intent. However, they reported "... good visual results with a minimum of complications,"1 "... no cases of infectious corneal ulcers or scarring or permanent visual loss," 1 and "... no infectious corneal ulcers and no significant corneal neovascularization" (at 22 months' follow-up). 2 These statements, which we believed connoted minimal complications with continuous wear of soft contact lenses, did prompt us to review and analyze our own experience 3 and that of others. 4,5 As reported, we 3 did note a significant incidence of potentially serious corneal complications. Others have reported a similar incidence of serious corneal complications, including infected corneal ulcers. 4,5 The less than 1% incidence of infected corneal ulcers now described by Stark et

To the Editor. —Complete or partial third nerve palsies may result from compression of the oculomotor nerve by an internal carotid-posterior communicating artery aneurysm. The onset is typically acute with rapid progression to total third nerve involvement. We describe a subtle, stable third nerve paresis that was the presenting sign of a familial intracranial aneurysm and urge awareness that operable internal carotid-posterior communicating artery aneurysms may present as subtle, incomplete third nerve palsies without a rapidly progressive course. Report of a Case. —An 18-year-old girl had a sudden onset of severe occipital headache associated with vomiting. Over the next three days her pain became localized to the left temporal area. She had no photophobia or neck stiffness. On the third day she developed a left upper eyelid ptosis and sought medical attention. Six months previously, the patient's 38-year-old mother had suffered an acute, right, total third nerve palsy. Cerebral arteriography

This book contains 20 chapters. Some of the chapter titles are: The Ruptured Globe: Primary Care; Corneal Trauma, Endophthalmitis; Antibiotic Usage; Radiology of Orbital Trauma; Maxillofacial Fractures; Orbital Infections; and Basic Management of Soft Tissue Injury.

This book contains 20 chapters. Some of the chapter titles are: The Ruptured Globe: Primary Care; Corneal Trauma, Endophthalmitis; Antibiotic Usage; Radiology of Orbital Trauma; Maxillofacial Fractures; Orbital Infections; and Basic Management of Soft Tissue Injury.