Malignant Glaucoma (Aqueous Misdirection Syndrome)

Key Points at a Glance

Malignant glaucoma (aqueous misdirection syndrome) is a rare secondary angle-closure glaucoma caused by forward rotation of the ciliary body and abnormal posterior flow of aqueous humor, leading to anterior displacement of the vitreous, angle closure, and elevated intraocular pressure.
It most commonly occurs in eyes with primary angle-closure glaucoma (PACG) after filtration surgery, but can develop after any intraocular surgery, including cataract surgery.
The most important distinguishing feature from pupillary block is that the anterior chamber is uniformly shallow.
Miotic agents (e.g., pilocarpine) are contraindicated because they worsen ciliary block.
Pharmacotherapy is based on the triple combination of atropine eye drops, aqueous suppressants, and hyperosmotic agents, but the response rate is only about 50%.
If medical and laser treatments are ineffective, anterior vitrectomy or vitrectomy is required.
Myopic shift may be the only early sign, so attention should be paid to postoperative refractive changes.

1. What is Malignant Glaucoma (Aqueous Misdirection Syndrome)?

Malignant glaucoma is a condition of elevated intraocular pressure with a markedly shallow anterior chamber, typically occurring after filtration surgery in eyes with angle-closure glaucoma. It is thought to result from angle closure caused by anterior displacement of the vitreous due to forward rotation of the ciliary body and abnormal inflow of aqueous humor into the vitreous cavity. It is also called aqueous misdirection syndrome, ciliary block glaucoma, or direct lens block glaucoma, and multiple terms are used interchangeably. The ICD-10 code is H40.8.

First reported by Von Graefe in 1869 as a refractory shallow anterior chamber after filtration surgery, this is a historic disease concept ³⁾. Subsequently, the pathophysiological concept that aqueous humor is misdirected posteriorly (into the vitreous cavity) rather than following the normal forward pathway was established, and the term “aqueous misdirection” became widely used. It is most commonly encountered in eyes with angle-closure glaucoma after filtration surgery, but it is clinically important that it can occur after any intraocular surgery, including cataract surgery.

Position in secondary angle closure

The Glaucoma Clinical Practice Guidelines (5th edition) classify the mechanisms of intraocular pressure elevation in secondary angle-closure glaucoma into the following four categories ⁶⁾.

Due to pupillary block: lens-induced, lens dislocation, iris bombé due to posterior synechiae, etc.
Anterior movement of the iris-lens diaphragm other than pupillary block: lens-induced, lens dislocation, etc.
Anterior movement of tissues posterior to the lens: nanophthalmos, after panretinal photocoagulation, malignant glaucoma, intraocular tamponade, massive intraocular hemorrhage, etc.
Peripheral anterior synechiae unrelated to anterior chamber depth: neovascular, ICE syndrome, uveitis, etc.

Malignant glaucoma is classified under the third category, “anterior movement of tissues posterior to the lens.” It corresponds to the “posterior pushing mechanism” in the EGS 5th edition ⁵⁾.

Epidemiology

The incidence after filtration surgery is reported to be 0.6–4% ⁵⁾. It is more common in women and usually occurs unilaterally. It is most frequent after filtration surgery in eyes with primary angle-closure glaucoma, but it can occur after any intraocular surgery, including cataract surgery ⁵⁾. Risk factors include short axial length (<21 mm), high hyperopia (≥+6 D), and a history of primary angle-closure glaucoma ⁵⁾. Rare spontaneous cases without prior surgery have also been reported. Trabeculectomy for angle-closure glaucoma is known to have a relatively high risk of causing malignant glaucoma postoperatively, along with shallow anterior chamber and choroidal detachment ⁶⁾.

Q How is aqueous misdirection different from pupillary block glaucoma?

In pupillary block, obstruction of aqueous flow at the pupillary margin causes the peripheral iris to bulge forward (iris bombé). In contrast, in aqueous misdirection, aqueous humor accumulates in the vitreous cavity from behind the lens, resulting in a uniformly shallow anterior chamber. Miotics are effective for pupillary block, but they are contraindicated in aqueous misdirection.

2. Main symptoms and clinical findings

Chang R, Du Y, Peng Z, Lu Y, Zhu X. Acute uveal effusion during phacoemulsification with preoperative central serous chorioretinopathy: a case report. BMC Ophthalmol. 2017;17:137. Figure 1. PMCID: PMC5543589. License: CC BY.

UBM images (a–d): Shallow anterior chamber (*) and anteriorly rotated ciliary processes and iris root (arrows) shown in both eyes. This corresponds to the confirmation of anterior rotation of the ciliary body by UBM discussed in the section “2. Main symptoms and clinical findings.”

Subjective Symptoms

In acute onset, the following symptoms occur.

Eye pain: Severe pain due to rapid intraocular pressure elevation
Vision loss / blurred vision: Due to corneal edema and anterior chamber loss
Halos around lights: Rainbow-colored rings around lights due to corneal edema
Headache, nausea, vomiting: Systemic symptoms due to vagal reflex
Myopic shift: Refractive change due to forward displacement of the lens or IOL. May be the only early sign ³⁾

Symptoms are fluctuant and may become apparent weeks to years after cataract surgery ³⁾. In early stages, intraocular pressure may remain within normal range, leading to delayed diagnosis ⁵⁾. When intraocular pressure rises rapidly, the clinical picture resembles acute glaucoma attack, with rapid progression of vision loss.

Clinical Findings (Findings Confirmed by Physician Examination)

Diagnosis is made by a combination of the following findings. In addition to elevated intraocular pressure, the pattern of anterior chamber depth change is most important for differential diagnosis.

Uniformly shallow anterior chamber to anterior chamber loss: Unlike the peripheral bulging in pupillary block, the shallow depth is uniform including the center ⁵⁾. Anterior chamber depth is markedly reduced, and the cornea may contact the iris in some cases
Forward displacement of the iris-lens diaphragm: The lens or IOL is displaced forward
Elevated intraocular pressure: May reach 40–70 mmHg ¹⁾. However, it may be normal in early stages
Patent peripheral iridotomy (PI): If a patent PI is present but shallow anterior chamber persists, pupillary block is ruled out
Absence of choroidal hemorrhage or detachment: Confirmed by B-scan ultrasound
Decreased or absent pupillary light reflex: Accompanied by moderate mydriasis
Corneal edema: Due to elevated intraocular pressure
Conjunctival injection: Ciliary injection is observed

Anterior segment optical coherence tomography (AS-OCT) has been reported to show plateau iris-like findings (flat central iris but occluded angle) associated with anterior displacement of the CTR (capsular tension ring)-IOL complex ²⁾. Ultrasound biomicroscopy (UBM) can directly confirm anterior displacement of the lens capsule-IOL complex and anterior rotation or positional abnormalities of the ciliary body ⁴⁾. UBM has a high resolution of 20–60 μm and can provide detailed imaging of anterior segment structures such as the iris and ciliary body, so it should be actively performed in cases suspected of malignant glaucoma.

UBM and anterior segment OCT are useful for elucidating the pathophysiology. In particular, while confirming the presence or absence of surgical history, it is important to evaluate whether there is any positional abnormality of the ciliary body.

3. Causes and Risk Factors

The most common trigger is intraocular surgery ⁵⁾.

Filtration surgery: Most common after trabeculectomy in eyes with primary angle-closure glaucoma. Intraoperative anterior chamber collapse increases the risk.
Cataract surgery: Can also occur after routine phacoemulsification ³⁾. Cases have been reported that became apparent about 3 years after surgery.
CTR (capsular tension ring) placement: The CTR-IOL complex may compress the ciliary body space, causing resistance to aqueous humor flow ²⁾.
Others: Can occur after any intraocular surgery. It has also been reported as a rare complication after laser peripheral iridotomy (LPI) ⁵⁾.

Ocular Anatomical Factors

Smaller eyes have a higher risk ⁵⁾.

Short axial length: Less than 21 mm
High hyperopia: +6 D or more
Shallow anterior chamber and narrow angle: Eyes with inherently narrow angles have less room for forward displacement
Nanophthalmos: Axial length is extremely short (usually less than 20 mm) and the sclera is abnormally thickened. This scleral thickening impairs vortex vein drainage, increasing the risk of uveal effusion ¹⁾. Surgery itself is difficult, and there is also a high risk of intraoperative expulsive choroidal hemorrhage

Drug-induced

Topiramate: Increases permeability of ciliary-choroidal vessels, causing ciliary body swelling and forward rotation. Eyes with nanophthalmos are at particularly high risk ¹⁾
SSRIs (selective serotonin reuptake inhibitors): Anticholinergic effects cause mydriasis, which can induce angle closure in eyes with narrow angles ¹⁾

If it occurs in one eye, the risk of developing it in the fellow eye also increases ³⁾. Since the risk is elevated regardless of a history of glaucoma, regular follow-up of the fellow eye is important.

The main risk factors are summarized below.

Risk factor	Specific example
Ocular morphology	Short axial length (<21 mm), high hyperopia (>+6 D), shallow anterior chamber
Surgery	Filtering surgery, cataract surgery, CTR placement
Medication	Topiramate, SSRIs

Q Can it be caused by medications such as topiramate?

Topiramate increases vascular permeability of the ciliary body and choroid, causing ciliary body swelling and forward rotation ¹⁾. In high-risk eyes such as those with microphthalmia, it can trigger aqueous misdirection. SSRIs may also induce angle closure in eyes with narrow angles through a mydriatic effect.

4. Diagnosis and Examination Methods

Malignant glaucoma is a diagnosis of exclusion, established only after systematically ruling out pupillary block, choroidal hemorrhage/detachment, suprachoroidal hemorrhage, and other mechanisms of angle closure ⁴⁾. It is not a disease that can be confirmed by specific laboratory values or imaging findings alone; a comprehensive assessment combining clinical course and multiple examination findings is required.

Suspect this condition when extremely shallow anterior chamber and high intraocular pressure occur early after surgery for angle-closure glaucoma. Hemorrhagic choroidal detachment shows similar slit-lamp findings and can also cause high intraocular pressure, but can be differentiated by fundus examination. In idiopathic cases, diagnosis is more difficult due to the absence of surgery history, and confirmation of abnormal ciliary body position by UBM is key to diagnosis.

Main Examinations

Gonioscopy: Essential for evaluating the degree of angle opening and peripheral anterior synechiae (PAS) ⁶⁾. Confirm the presence of a patent PI to rule out pupillary block.
B-scan ultrasound: Essential for excluding choroidal hemorrhage (high-intensity echo) and choroidal detachment (serous, low-intensity echo).
Ultrasound biomicroscopy (UBM): With a resolution of 20–60 μm, it is suitable for observing fine structures of the anterior segment such as the iris and ciliary body. It can directly visualize forward rotation of the ciliary body, contact between ciliary processes and the lens capsule (or IOL-bag complex), and choroidal effusion ⁴⁾. Malignant glaucoma is listed as a primary indication for UBM. It is superior to other imaging modalities in its ability to directly depict the anterior segment including posterior structures. It also allows angle observation in the dark, and is useful for differentiating from plateau iris syndrome and uveitis.
Anterior segment optical coherence tomography (AS-OCT): Non-invasive and non-contact, it allows quantitative evaluation of anterior chamber depth and angle morphology. Unlike UBM, it does not require a supine position and can be performed quickly in an outpatient setting. Although its ability to depict deeper structures is inferior to UBM, it can detect indirect findings such as angle compression by a CTR-IOL complex ²⁾. Combining UBM and AS-OCT is useful for elucidating the pathophysiology.

Differential Diagnosis

The differentiating points between pupillary block and aqueous misdirection are summarized below.

Pupillary Block

Iris morphology: Peripheral iris bulging forward (iris bombé)

Anterior chamber depth: Particularly shallow in the periphery

PI: Occluded or not performed

Miotics: Effective

Aqueous misdirection

Iris morphology: Iris is displaced forward overall

Anterior chamber depth: Uniformly shallow to absent⁵⁾

PI: Patent

Miotics: Contraindicated (worsens condition)

Other differential diagnoses include the following. All can cause shallow anterior chamber and high intraocular pressure, but the treatment strategy differs because the pathogenesis is different.

Hemorrhagic choroidal detachment: High-intensity echo on B-scan. Can be differentiated by fundus findings (convex choroidal elevation). Particular caution is needed in acute postoperative cases.
Serous choroidal detachment: Low-intensity echo on B-scan. Often associated with inflammatory diseases such as Vogt-Koyanagi-Harada disease or posterior scleritis. Systemic steroid therapy is the first choice, and laser treatment should be used with caution as it may exacerbate inflammation.
Intumescent cataract: Angle closure caused by forward displacement of the iris-lens diaphragm due to lens swelling. If the anterior capsule is perforated during laser iridotomy (LI), it may lead to inflammatory intraocular pressure elevation due to phacolysis, so lens reconstruction is preferable.
Lens subluxation: Angle closure due to lens displacement caused by weakening of the zonules. May be associated with pseudoexfoliation syndrome or Marfan syndrome.
Posterior synechiae: Check for history of iritis or diabetes. Adhesion between the iris and anterior lens capsule at the pupillary margin forms iris bombé.
Intraocular tumor / choroidal hemorrhage: Secondary shallow anterior chamber may occur due to choroidal elevation or space-occupying lesions.

5. Standard Treatment

A stepwise approach of medication → laser therapy → surgery is fundamental. First, medication is used to attempt to relieve ciliary block; if ineffective, laser therapy is performed; if still ineffective, surgery is performed. The ultimate goal of treatment is to create a state where no block occurs between the posterior and anterior chambers (unicameral eye) and to prevent recurrence.

Medication (First Step)

Combination therapy with a parasympatholytic agent (mydriatic / cycloplegic), an aqueous humor suppressant (eye drops and oral), and a hyperosmotic agent (intravenous) is recommended ⁵⁾.

Drug	Dosage	Mechanism of Action
Atropine ophthalmic solution 1%	1–3 times daily	Cycloplegia / mydriasis
Timolol ophthalmic solution 0.5%	Twice daily	Aqueous humor suppression (beta-blockade)
Diamox tablets 250 mg	2 tablets, divided into 2 doses after meals	Aqueous humor suppression (oral CAI)
Mannitol infusion	Intravenous administration	Reduction of vitreous volume

Atropine increases tension of the zonules, moving the lens posteriorly, and triggers aqueous humor that has moved into the vitreous cavity to return forward. Cyclopentolate can also be used as an alternative to atropine ⁵⁾.

Eye drops that suppress aqueous humor production (beta-blockers, carbonic anhydrase inhibitors) are used in combination with intravenous hyperosmotic agents ⁶⁾. Hyperosmotic agents reduce vitreous volume, but their therapeutic effect is temporary, so they are positioned as preoperative treatment ⁶⁾.

The response rate to pharmacotherapy is about 50% (within 5 days), but the recurrence rate with medication alone is high ⁵⁾. Even if the anterior chamber deepens and intraocular pressure normalizes with pharmacotherapy, recurrence often occurs when atropine eye drops are discontinued, so long-term maintenance therapy with atropine eye drops may be necessary. Pharmacotherapy is only an initial measure; definitive treatment often requires laser or surgical intervention.

Laser treatment (second stage)

Nd:YAG laser posterior capsulotomy + anterior vitreous membrane incision

In pseudophakic eyes, Nd:YAG laser posterior capsulotomy is performed, and then the focus is shifted behind the posterior capsule, delivering 10 to 20 shots at 3-4 mJ to disrupt the anterior vitreous membrane. By creating a passage for aqueous humor between the vitreous cavity and the anterior chamber, the block is relieved. If successful, improvement in anterior chamber depth and reduction of intraocular pressure are obtained immediately to the next day.

In pseudophakic or aphakic eyes, YAG laser or surgical anterior vitreous membrane incision and capsulotomy are selected ⁶⁾ (evidence level 2C).

Diode laser cyclophotocoagulation (CPC)

Diode laser cyclophotocoagulation may be considered at any stage of treatment ⁵⁾. It causes coagulation necrosis and atrophy of the ciliary processes, potentially leading to disruption of the ciliary-vitreous interface and posterior rotation of the ciliary body ³⁾. However, the irradiation conditions required to disrupt the ciliary-vitreous interface have not been established.

Surgical treatment (third stage)

If pharmacotherapy and laser treatment are insufficient, or in recurrent cases, surgery is performed. It is important to resolve the condition by vitrectomy with anterior vitreous membrane incision ⁶⁾ (evidence level 2C).

Phakic eyes

Pars plana vitrectomy (PPV) is performed ⁵⁾. In some cases, lens extraction is also performed ⁶⁾ (2C). By combining lens extraction, a unicameral eye is created, completely relieving the block between the posterior and anterior chambers to prevent recurrence.

Pseudophakic eye

Zonulo-hyaloido-vitrectomy (irido-zonulo-anterior hyaloidectomy) is effective ⁵⁾. An approach is made from the peripheral iridectomy site to the anterior chamber, and the zonules around the lens capsule and the anterior hyaloid membrane are excised. This procedure creates a permanent communication between the vitreous cavity and the anterior chamber.

In vitrectomy with anterior hyaloidotomy, some cases require iridectomy to treat the most peripheral anterior hyaloid membrane ⁶⁾ (2C). If the anterior hyaloid membrane and zonules are not sufficiently treated, a block remains between the vitreous cavity and the anterior chamber, which may lead to recurrence. In phakic eyes, the lens is also removed simultaneously to relieve contact between the ciliary processes and the lens equator, creating a unicameral eye.

When CTR-IOL complex is the cause

There is a report that a combination of CTR removal, anterior vitrectomy, and IOL scleral fixation was effective ²⁾.

Q Why can miotics not be used?

Aqueous misdirection is angle closure due to a posterior pushing mechanism of the lens. Miotics contract the ciliary muscle, promoting forward protrusion of the ciliary body and worsening ciliary block, thus they are contraindicated ⁶⁾. In contrast, mydriatic-cycloplegic agents such as atropine relax the ciliary muscle, increase tension of the zonules, and move the lens posteriorly, which is effective in relieving the block.

Q If it occurs in one eye, is there a risk of developing it in the other eye?

Unilateral onset significantly increases the risk in the contralateral eye ³⁾. The risk is elevated regardless of a history of glaucoma, so regular evaluation of intraocular pressure and anterior chamber depth in the contralateral eye is important.

6. Pathophysiology and detailed mechanism of onset

The exact mechanism of malignant glaucoma has not been fully elucidated, but the following two hypotheses have been proposed ⁵⁾.

Choroidal expansion theory

Main mechanism: Increased choroidal volume creates resistance to fluid movement from posterior to anterior ⁵⁾

Result: Aqueous humor accumulates in the vitreous cavity, pushing the iris-lens diaphragm forward

Ciliary block theory

Main mechanism: Abnormal anatomical contact between the ciliary processes and the equator of the lens (or IOL) or the anterior hyaloid membrane

Result: A “malignant cycle” is established, acting as a one-way valve that blocks the forward outflow of aqueous humor

Pathogenesis cascade

The progression of the condition can be understood through the following cascade. In a normal eye, aqueous humor produced by the ciliary body flows from the posterior chamber through the pupil into the anterior chamber and exits via the trabecular meshwork at the angle. In malignant glaucoma, this pathway is disrupted.

Some trigger (surgery, medication, etc.) causes the ciliary body to rotate forward
The ciliary processes come into close contact with the equator of the lens (or IOL)
Part of the aqueous humor produced by the ciliary body flows backward (into the vitreous cavity) instead of the normal forward pathway
If the anterior hyaloid membrane is intact, forward movement of fluid from the vitreous cavity to the anterior chamber is impeded
The fluid volume and pressure in the vitreous cavity increase, causing the anterior vitreous to shift forward
The iris-lens diaphragm is pushed forward, leading to angle closure and elevated intraocular pressure
Elevated intraocular pressure further pushes the ciliary body forward, creating a vicious cycle

Mechanism of action of atropine and pharmacological rationale for contraindication of miotics

Atropine eye drops relax the ciliary muscle, increasing tension on the zonules and moving the lens posteriorly. This may allow aqueous humor that has moved into the vitreous cavity to return forward.

In contrast, miotic agents such as pilocarpine contract the ciliary muscle. This contraction relaxes the zonules, pushing the lens forward and further promoting anterior rotation of the ciliary body, thereby worsening ciliary block ⁶⁾. Therefore, miotics are contraindicated in malignant glaucoma.

Mechanism in Pseudophakic Eyes

In pseudophakic eyes, the horizontal diameter of the IOL-capsule complex is larger than that of the natural lens, making it more likely to contact the ciliary processes ⁴⁾. Some of the aqueous humor produced by the ciliary processes is secreted posteriorly (into the vitreous cavity). If the anterior hyaloid membrane is intact, forward fluid outflow is impeded, creating a pressure gradient and shallowing the anterior chamber.

It has been reported that even in eyes with a history of vitrectomy, the condition can develop if the anterior hyaloid membrane remains ⁴⁾. In a recurrent case with a myopic shift of 3 D or more, a combination of goniosynechialysis, iridectomy, and zonulo-hyaloidectomy restored refraction and intraocular pressure ⁴⁾. Therefore, during vitrectomy, thorough removal of the anterior hyaloid membrane, including the most peripheral areas, is essential to prevent recurrence.

Drug-Induced Mechanism

Topiramate increases the permeability of ciliochoroidal vessels, causing swelling of the ciliary body and choroid and anterior rotation of the ciliary body ¹⁾. In microphthalmia, impaired vortex vein drainage due to scleral thickening further increases the risk of uveal effusion ¹⁾.

Mechanism Involving the CTR-IOL Complex

Placement of a CTR expands and thickens the capsular bag, and the CTR-IOL complex contacts the ciliary body and posterior iris circumferentially ²⁾. This compresses the ciliary sulcus, increasing resistance to the posterior-to-anterior flow of aqueous humor. Because the large diameter of the CTR-IOL complex partially limits anterior displacement, it may present with plateau iris-like angle closure while maintaining anterior chamber depth ²⁾. This atypical finding differs from the classic appearance of malignant glaucoma with uniformly shallow anterior chamber, so detailed evaluation of angle morphology using AS-OCT is key to diagnosis.

7. Latest Research and Future Perspectives (Investigational Reports)

Early Diagnostic Significance of Myopic Shift

Chean et al. (2021) reported a case of aqueous misdirection that developed with myopic surprise as the only initial sign after cataract surgery ³⁾. Intraocular pressure remained within normal range for about three years postoperatively, leading to delayed diagnosis. Even if anterior chamber depth appears normal on biometry, measurement errors can occur in short axial length eyes, so aqueous misdirection should be included in the differential diagnosis when myopic shift is observed.

Stephenson et al. (2023) reported a case of aqueous misdirection with a myopic shift of 3 D or more in an eye with a history of vitrectomy, cataract surgery, and artificial iris implantation ⁴⁾. They showed that even after vitrectomy, if the anterior hyaloid membrane remains, it can still occur, and refraction and intraocular pressure recovered after goniosynechialysis + iridectomy + zonulo-hyaloidectomy.

Non-invasive diagnosis using AS-OCT

Goto et al. (2024) first characterized secondary angle closure due to anterior displacement of the CTR-IOL complex using AS-OCT ²⁾. They reported an atypical plateau iris-like appearance with preserved anterior chamber depth, demonstrating the usefulness of AS-OCT in detecting secondary angle closure after cataract surgery with CTR implantation.

Validation of stepwise treatment strategy

A stepwise approach of medication → Nd:YAG laser → cyclodiode → surgery has been proposed ³⁾. Cyclodiode causes coagulation necrosis and atrophy of the ciliary processes, potentially disrupting the ciliary-vitreous interface and causing posterior rotation of the ciliary body. However, the irradiation conditions required to disrupt the ciliary-vitreous interface have not been established, and when medication and laser alone are insufficient, surgery to create a unicameral eye remains the final treatment option ³⁾.

8. References

Hussain A, Snyder K, Paroya S, et al. Topiramate-Induced Aqueous Misdirection in a Nanophthalmic Eye. Cureus. 2023;15(3):e36529.
Goto K, Tomita R, Hiraiwa J, et al. Secondary Angle Closure Caused by Anterior Displacement of Capsular Tension Ring and Intraocular Lens Due to Aqueous Misdirection. Cureus. 2024;16(3):e55716.
Chean CS, Gabadage D, Mukherji S. Aqueous misdirection syndrome masking as myopic surprise following phacoemulsification surgery. BMJ Case Rep. 2021;14:e242777.
Stephenson A, Chu FB, Snyder ME. A peculiar case of aqueous misdirection from a pseudophakic secluded pupil in a patient with chronic angle closure glaucoma. Am J Ophthalmol Case Reports. 2023;29:101795.
European Glaucoma Society. European Glaucoma Society Terminology and Guidelines for Glaucoma, 5th Edition. Br J Ophthalmol. 2025;109(Suppl 1):s1-s268.
日本緑内障学会. 緑内障診療ガイドライン（第5版）. 日眼会誌. 2022;126(2):85-177.

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