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The cephalic trim technique is a popular maneuver that often leads to tip deformities, most notably postsurgical alar retraction (PSAR). We advocate using the external rhinoplasty approach to correct PSAR by (1) releasing and repositioning the retracted alar margin, (2) strengthening and immobilizing the central tip complex using a septal extension graft, (3) suspending and longitudinally tightening the mobilized lateral crural remnant by adjusting crural length to match the sidewall span, and (4) providing direct skeletal support to the repositioned alar margin using articulated alar rim grafts. Using this structural treatment paradigm, we have corrected severe PSAR in the preponderance of secondary rhinoplasty cases.

Objectives Sialolithiasis is the primary etiology for parotid and submandibular swelling, potentially resulting in discomfort, bacterial infections, and hospitalization. The etiology of sialolith formation is unknown. Currently, the proposed etiologies range from inflammation, coalescence of organic molecules, sialomicrolith formation, pH changes, and biofilm formation. In this study, we performed a descriptive analysis of images obtained through electron microscopy of sialoliths. Based on our findings and descriptive analysis, we hypothesize that sialolith formation is likely multifactorial and begins with biofilm formation. Biofilm formation then triggers a host immune response, and it is the interaction of biofilm with host immune cells and calcium nanoparticles that forms the nidus and creates a favorable environment for calcium precipitation. Methods Sialoliths were extracted from patients and imaged under light and scanning electron microscopy. Specimens for light microscopy were prepared using a diamond saw. Specimens for electron microscopy were freeze-fractured, thus providing an undisturbed view of the core of the sialolith. Results We were able to identify clear evidence of biofilm caves at the core of each sialolith. These biofilm caves were complex with the presence of bacteria and dehydrated extrapolysaccharide matrix, host cells (immune cells, platelets and erythrocytes), and calcium nanoparticles. Conclusion The etiology of sialolith formation is likely multifactorial. We propose that biofilm formation within a single salivary gland or duct leads to local ductal injury, which results in the influx of host immune cells that interact with the biofilm and calcium nanoparticles, creating a scaffold upon which further calcium deposition can occur. Level of evidence NA Laryngoscope, 130:69-74, 2020.

The cephalic trim technique is a popular maneuver that often leads to tip deformities, most notably postsurgical alar retraction (PSAR). We advocate using the external rhinoplasty approach to correct PSAR by (1) releasing and repositioning the retracted alar margin, (2) strengthening and immobilizing the central tip complex using a septal extension graft, (3) suspending and longitudinally tightening the mobilized lateral crural remnant by adjusting crural length to match the sidewall span, and (4) providing direct skeletal support to the repositioned alar margin using articulated alar rim grafts. Using this structural treatment paradigm, we have corrected severe PSAR in the preponderance of secondary rhinoplasty cases.

In the current value-based health-care environment, 30-day unplanned hospital readmissions have been identified as a quality measure and an opportunity to help reduce health-care costs. The LACE Index Scoring Tool for Risk Assessment of Death and Readmission utilizes length of stay, acuity of admission, comorbidities, and emergency department visits to stratify patients into high and low risk of readmission. A retrospective chart review of 161 patients who underwent a tracheotomy or laryngectomy for head and neck indications at a tertiary care academic center demonstrated that the readmitted patient cohort was not statistically or clinically different from the nonreadmitted cohort when comparing LACE scores ( P = .789), length of hospital stay ( P = .237), discharge disposition ( P = .569), or insurance status ( P = .85). Addressing the problem of unplanned 30-day readmissions will likely require enhanced patient education, improved coordination of care, and further research.

Objective Pseudomonas aeruginosa, a known biofilm-forming organism, is an opportunistic pathogen that plays an important role in chronic otitis media, tracheitis, cholesteatoma, chronic wounds, and implant infections. Eradication of biofilm infections has been a challenge because the biofilm phenotype provides bacteria with a protective environment from the immune system and antibiotics; thus, there has been great interest in adjunctive molecules that may inhibit biofilm formation or cause biofilm dispersal. There are reports that D-amino acids may inhibit biofilms. In this study, we test the ability of various D-amino acids to inhibit P. aeruginosa biofilm formation in vitro. Study design We evaluated the effect of D-alanine (10 mM), D-leucine (10 mM), D-methionine (10 mM), D-tryptophan (10 mM), and D-tyrosine (10 uM and 1 mM) on biofilm formation in two commonly studied laboratory strains of P. aeruginosa: PAO1 and PA14. Methods Biofilms were grown in 24-well and 96-well tissue culture plates, documented photographically and stained with 0.1% crystal violet and solubilized in 33% glacial acetic acid for quantification. Results In strains PAO1 and PA14, the addition of D-amino acids did not result in an inhibitory effect on biofilm growth in 24-well plates. Repeating the study in 96-well plates confirmed our findings that D-amino acids do not inhibit biofilm formation of P. aeruginosa. Conclusion We conclude that D-amino acids only slow the production of biofilms rather than completely prevent biofilm formation; therefore, D-amino acids represent a poor option for potential clinically therapeutic interventions. Level of evidence N/A.

Objectives/hypothesis Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder with an incidence between 10.7 and 17.3 per 100,000 persons per year. The mechanism for BPPV has been postulated to involve displaced otoconia resulting in canalithiasis. Although particulate matter has been observed in the endolymph of affected patients undergoing posterior canal occlusion surgery, an otoconial origin for the disease is still questioned. Study design In this study, particulate matter was extracted from the posterior semicircular canal of two patients and examined with scanning electron microscopy. Methods The samples were obtained from two patients intraoperatively during posterior semicircular canal occlusion. The particles were fixed, stored in ethanol, and chemically dehydrated. The samples were sputter coated and viewed under a scanning electron microscope. Digital images were obtained. Results Intact and degenerating otoconia with and without linking filaments were found attached to amorphous particulate matter. Many otoconia appeared to be partially embedded in a gel matrix, presumably that which encases and anchors the otoconia within the otolith membrane, whereas others stood alone with no attached filaments and matrix. The otoconia measured roughly 2 to 8 μm in length and displayed a uniform outer shape with a cylindrical bulbous body and a 3 + 3 rhombohedral plane at each end. Conclusions These findings suggest that the source of the particulate matter in the semicircular canals of patients with BPPV is broken off fragments of the utricular otolithic membrane with attached and detached otoconia. Level of evidence NA Laryngoscope, 127:709-714, 2017.

Hypothesis Bacterial biofilm formation within cholesteatomas is responsible for increased persistence and tissue destruction and Pseudomonas aeruginosa deficient in biofilm formation (PAO1 ΔfleQ) are less virulent than the parent bacteria. Background Infected aural cholesteatomas have been demonstrated to be more destructive than uninfected cholesteatomas and infections are more persistent. The chronicity and persistence of infections within cholesteatomas may be because of the presence of biofilm formation. Methods Twenty-seven mutant strains of PAO1 were screened for surface adherence. These strains were also screened for static biofilm formation. The biofilms were quantified by staining with crystal violet. Aural cholesteatomas were then induced in Mongolian gerbils by ligation of the ear canal. At the time of ligation, the ear canals were inoculated with wild-type PAO1 and a biofilm deficient PAO1 ΔfleQ strain of P. aeruginosa. A 7 weeks course of ciprofloxacin (20 mg/kg/day) was started on postoperative day 7. Eight weeks after induction of cholesteatomas, the cholesteatoma size, levels of bone destruction, and levels of bone remodeling were evaluated using microCT imaging. Results PAO1 ΔfleQ was identified as a poorly adherent and deficient biofilm forming mutant strain of P. aeruginosa. Infected cholesteatomas had more growth, bone destruction and bone remodeling than uninfected cholesteatomas. However, there was no difference observed between cholesteatomas infected with PAO1 (biofilm competent strain) and PAO1 ΔfleQ (biofilm deficient strain). Conclusion We demonstrate that the biofilm phenotype is not an important virulence factor in cholesteatomas infected with P. aeruginosa.

Stickler syndrome is a collagenopathy that is typically inherited as autosomal dominant disease caused by monoallelic mutations in COL2A1, COL11A2, and COL11A1. Rarely, biallelic mutations in COL9A1, COL9A2, and COL9A3 cause an autosomal recessive Stickler syndrome. One previous report described two siblings with Stickler syndrome and a homozygous mutation in LOXL3, suggesting that biallelic mutations in LOXL3 can also cause autosomal recessive Stickler syndrome. LOXL3 is a member of the lysyl oxidase family of genes which encode enzymes oxidizing the side chain of peptidyl lysine permitting the covalent crosslinking of collagen and elastin chains. Therefore, LOXL3 deficiency is expected to result in collagen defect. Furthermore, Loxl3 deficient mouse model demonstrated features overlapping with Stickler syndrome. In this report, we describe a child and his father who had clinical features consistent with Stickler syndrome and found to have a homozygous novel mutation c.1036C>T (p.Arg346Trp) in LOXL3. This report not only supports that biallelic LOXL3 mutations cause autosomal recessive Stickler syndrome, but also further delineates the phenotype associated with LOXL3 mutations. In addition, the family described here shows an interesting example for pseudodominance, which can be observed in recessive diseases when one parent is affected and the other is heterozygous carrier.

Objective Pseudomonas aeruginosa, a known biofilm‐forming organism, is an opportunistic pathogen that plays an important role in chronic otitis media, tracheitis, cholesteatoma, chronic wounds, and implant infections. Eradication of biofilm infections has been a challenge because the biofilm phenotype provides bacteria with a protective environment from the immune system and antibiotics; thus, there has been great interest in adjunctive molecules that may inhibit biofilm formation or cause biofilm dispersal. There are reports that D‐amino acids may inhibit biofilms. In this study, we test the ability of various D‐amino acids to inhibit P. aeruginosa biofilm formation in vitro. Study Design We evaluated the effect of D‐alanine (10 mM), D‐leucine (10 mM), D‐methionine (10 mM), D‐tryptophan (10 mM), and D‐tyrosine (10 uM and 1 mM) on biofilm formation in two commonly studied laboratory strains of P. aeruginosa: PAO1 and PA14. Methods Biofilms were grown in 24‐well and 96‐well tissue culture plates, documented photographically and stained with 0.1% crystal violet and solubilized in 33% glacial acetic acid for quantification. Results In strains PAO1 and PA14, the addition of D‐amino acids did not result in an inhibitory effect on biofilm growth in 24‐well plates. Repeating the study in 96‐well plates confirmed our findings that D‐amino acids do not inhibit biofilm formation of P. aeruginosa. Conclusion We conclude that D‐amino acids only slow the production of biofilms rather than completely prevent biofilm formation; therefore, D‐amino acids represent a poor option for potential clinically therapeutic interventions. Level of Evidence N/A.

Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder with an incidence between 10.7 and 17.3 per 100,000 persons per year. The mechanism for BPPV has been postulated to involve displaced otoconia resulting in canalithiasis. Although particulate matter has been observed in the endolymph of affected patients undergoing posterior canal occlusion surgery, an otoconial origin for the disease is still questioned.In this study, particulate matter was extracted from the posterior semicircular canal of two patients and examined with scanning electron microscopy.The samples were obtained from two patients intraoperatively during posterior semicircular canal occlusion. The particles were fixed, stored in ethanol, and chemically dehydrated. The samples were sputter coated and viewed under a scanning electron microscope. Digital images were obtained.Intact and degenerating otoconia with and without linking filaments were found attached to amorphous particulate matter. Many otoconia appeared to be partially embedded in a gel matrix, presumably that which encases and anchors the otoconia within the otolith membrane, whereas others stood alone with no attached filaments and matrix. The otoconia measured roughly 2 to 8 μm in length and displayed a uniform outer shape with a cylindrical bulbous body and a 3 + 3 rhombohedral plane at each end.These findings suggest that the source of the particulate matter in the semicircular canals of patients with BPPV is broken off fragments of the utricular otolithic membrane with attached and detached otoconia.NA Laryngoscope, 127:709-714, 2017.

Out-of-pocket (OOP) payments are the principal means of financing health care throughout much of Asia. We estimate the magnitude and distribution of OOP payments for health care in fourteen countries and territories accounting for 81% of the Asian population. We focus on payments that are catastrophic, in the sense of severely disrupting household living standards, and approximate such payments by those absorbing a large fraction of household resources. Bangladesh, China, India, Nepal and Vietnam rely most heavily on OOP financing and have the highest incidence of catastrophic payments. Sri Lanka, Thailand and Malaysia stand out as low to middle income countries that have constrained both the OOP share of health financing and the catastrophic impact of direct payments. In most low/middle-income countries, the better-off are more likely to spend a large fraction of total household resources on health care. This may reflect the inability of the poorest of the poor to divert resources from other basic needs and possibly the protection of the poor from user charges offered in some countries. But in China, Kyrgyz and Vietnam, where there are no exemptions of the poor from charges, they are as, or even more, likely to incur catastrophic payments.

Signs of chronic or acute inflammation have been demonstrated in most cardiovascular diseases of multifactorial pathogenesis, including atherosclerosis and chronic heart failure. The triggers and mechanisms leading to inflammation may vary between clinical conditions but they share many common mediators, including specific patterns of eicosanoid and cytokine production. Certain cocoa-based products can be rich in a subclass of flavonoids known as flavanols, some of which have been found in model systems to possess potential anti-inflammatory activity relevant to cardiovascular health. Indeed, experimental evidence demonstrates that some cocoa-derived flavanols can reduce the production and effect of pro-inflammatory mediators either directly or by acting on signaling pathways. However, it should be noted that the evidence for any beneficial effects of cocoa flavanols in providing a meaningful anti-inflammatory action has been gathered predominantly from in vitro experiments. Therefore, additional research in well-designed human clinical experiments, using cocoa properly characterized in terms of flavanol content, would be a welcome addition to the evidence base to determine unambiguously if this benefit does indeed exist. If so, then flavanol-rich cocoa could be a potential candidate for the treatment, or possibly prevention, of the broad array of chronic diseases that are linked to dysfunctional inflammatory responses.

Epidemiological data suggest that environmental factors may trigger autoimmunity in genetically susceptible individuals. In primary biliary cirrhosis (PBC), it has been postulated that halogenated xenobiotics can modify self-molecules, facilitating the breakdown of tolerance to mitochondrial antigens. The transport and metabolism of xenobiotics is highly dependent on key genetic polymorphisms that alter enzymatic phenotype. We analyzed genomic DNA from 169 patients with PBC and 225 geographically and sex-matched healthy subjects for polymorphisms of genes coding for cytochromes P450 (CYPs) 2D6 (CYP2D6*4, CYP2D6*3, CYP2D6*5, and CYP2D6*6) and 2E1 (c1/c2), multidrug resistance 1 (MDR1 C3435T) P-glycoprotein, and pregnane X receptor (PXR C-25385T, C8055T, and A7635G). We compared the genotype frequencies in patients and controls and also correlated polymorphisms with PBC severity. The distributions of the studied genotypes did not significantly differ between patients and controls. However, when clinical characteristics of patients with PBC were compared according to genotype, the CYP2E1 c2 allele was associated with signs of more severe disease. In conclusion, genetic polymorphisms of CYP 2D6 and 2E1, PXR, and MDR1 do not appear to play a role in the onset of PBC. (HEPATOLOGY 2005;41:55–63.)

The E2 component of mitochondrial pyruvate dehydrogenase complex (PDC-E2) is the immunodominant autoantigen of primary biliary cirrhosis. Whereas lipoylation of PDC-E2 is essential for enzymatic activity and predominates under normal conditions, other biochemical systems exist that also target the lysine residue, including acylation of fatty acids or xenobiotics and ubiquitinylation. More importantly, the immunogenicity can be affected by derivatization of the lysine residue, as the recognition of lipoylated PDC-E2 by patient autoantibodies is enhanced compared with octanoylated PDC-E2. Furthermore, our laboratory has shown that various xenobiotic modifications of a peptide representing the immunodominant region of PDC-E2 are immunoreactive against patient sera. The only purported regulatory system that prevents the accumulation of potentially autoreactive PDC-E2 is glutathionylation, in which the lysine-lipoic acid moiety is further modified with glutathione during apoptosis. Interestingly, this system is found in several cell lines, including HeLa, Jurkat, and Caco-2 cells, but not in cholangiocytes and salivary gland epithelial cells, both of which are targets for destruction in primary biliary cirrhosis. Hence, the failure of this or other regulatory system(s) may overwhelm the immune system with immunogenic PDC-E2 that can initiate the breakdown of tolerance in a genetically susceptible individual. In this review the authors survey the data available on the biochemical life of PDC-E2, with particular emphasis on the lysine residue and its known interactions with machinery involved in various posttranslational modifications.

Evidence suggests that certain flavan-3-ols and procyanidins (FP) can have a positive influence on cardiovascular health. It has been previously reported that FP isolated from cocoa can potentially modulate the level and production of several signaling molecules associated with immune function and inflammation, including several cytokines and eicosanoids. In the present study, we examined whether FP fractions monomers through decamers modulate secretion of the cytokine transforming growth factor (TGF)-β1 from resting human peripheral blood mononuclear cells (PBMC). A total of 13 healthy subjects were studied and grouped according to their baseline production of TGF-β1. When cells from individuals with low baseline levels of TGF-β1 (n = 7) were stimulated by individual FP fractions (25 μg/ml), TGF-β1 release was enhanced in the range of 15%–66% over baseline (P < 0.05; monomer, dimer, and tetramer). The low-molecular-weight FP fractions (≤pentamer) were more effective at augmenting TGF-β1 secretion than their larger counterparts (≥hexamer), with the monomer and dimer inducing the greatest increases (66% and 68%, respectively). In contrast to the above, TGF-β1 secretion from high TGF-β1 baseline subjects (n = 6) was inhibited by individual FP fractions (P < 0.05; trimer through decamer). The inhibition was most pronounced with trimeric through decameric fractions (28%–42%), and monomers and dimers moderately inhibited TGF-β1 release (17% and 23%, respectively). Given the vascular actions associated with TGF-β1, we suggest that in healthy individuals, homeostatic modulation of its production by FP offers an additional mechanism by which FP-rich foods can potentially benefit cardiovascular health.

The use of herbal and other botanical products, including those used extensively in traditional Chinese medicine, has increased dramatically in the last decade. Yet, little scientific research exists concerning their efficacy and safety. We examined the effects of Immune+, a combination of five botanicals frequently used in traditional Chinese medicine, on the production of two cytokines. For this purpose, unstimulated or phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells from healthy volunteers were incubated with different concentrations of Immune+. The secretion of interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma) was measured after 72 hours of incubation. At the highest concentration tested (100 micro g/ml), Immune+ significantly increased the secretion of IL-1beta. Importantly, PHA alone had no effect on IL-1beta production, and the combination of PHA with Immune+ resulted in the same increase in IL-1beta production as seen with the botanical extract alone. Immune+ did not have any detectable effect on either unstimulated or PHA-stimulated IFN-gamma synthesis. These in vitro data support the concept that Immune+ may enhance human immune responses.

We examined whether cocoa, in its isolated procyanidin fractions (monomer through decamer), would modulate cytokine production at the levels of transcription and protein secretion in both resting and phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC). In resting cells, interleukin (IL)-1beta and IL-4 gene expression from cocoa-treated cells varied markedly among the subjects tested. However, at the protein level, the larger fractions (pentamer through decamer) stimulated a dramatic increase in IL-1beta concentration (up to ninefold) with increasing degree of polymerization. Similarly, these larger fractions augmented IL-4 concentration by as much as 2 pg/ml, whereas the control displayed levels nearly undetectable. In the presence of PHA, gene expression also seemed to be most affected by the larger procyanidin fractions. The pentameric through decameric fractions increased IL-1 beta expression by 7-19% compared with PHA control, whereas the hexameric through decameric fractions significantly inhibited PHA-induced IL-4 transcription in the range of 71-86%. This observation at the transcription level for IL-1 beta was reflected at the protein level in PHA-stimulated PBMC. Significant reductions in mitogen-induced IL-4 production were also seen at the protein level with the hexamer, heptamer and octamer. Individual oligomeric cocoa fractions were unstimulatory for IL-2 in resting PBMC. However, when induced with PHA, the pentamer, hexamer and heptamer fractions caused a 61-73% inhibition in IL-2 gene expression. This study offers additional data for the consideration of the health benefits of dietary polyphenols from a wide variety of foods, including those benefits associated specifically with cocoa and chocolate consumption.

Given the widespread ingestion of cocoa in many cultures, we investigated whether cocoa, in its isolated procyanidin fractions (monomer through decamer), would modulate synthesis of the antiinflammatory cytokine, interleukin-4 (IL-4). Both resting and phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) were investigated at the protein secretion level. The smaller-sized cocoa fractions (tetramer or less) were unable to induce an IL-4 response (i.e., values fell below the detection limit of 0.25 pg/ml). The larger oligomeric procyanidins (pentamer or greater) stimulated secretion of IL-4 in resting PBMC by as much as 1.42 pg/ml, as shown by the nonamer. However, only the hexameric, heptameric, and decameric fractions proved to be statistically significant. Cells coincubated with PHA showed an immense increase in secretory IL-4 (21.1 ± 1.1 pg/ml). Only the monomeric fraction was able to enhance PHA-induced secretion by 48%. The other procyanidin oligomers suppressed IL-4 production;...

Recent data has demonstrated that cacao liquor polyphenols (procyanidins) have antioxidant activity, inhibit mRNA expression of interleukin-2 and are potent inhibitors of acute inflammation. Given the widespread ingestion of cocoa in many cultures, we investigated whether cocoa, in its isolated procyanidin fractions (monomer through decamer), would modulate synthesis of the pro-inflammatory cytokine, interleukin-1 beta. Both resting and phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) were investigated at the levels of transcription and protein secretion. Individual cocoa fractions were shown to augment constitutive IL-1 beta gene expression, although values varied between subjects. Interestingly, the smaller fractions of cocoa (monomer-tetramer) consistently reduced IL-1 beta expression of PHA-stimulated cells by 1-15%, while the larger oligomers (pentamer-decamer) increased expression by 4-52%. These data, observed at the transcription level, were reflected in protein levels in PHA-induced PBMC. The presence or absence of PHA did not alter the effects of the cocoa procyanidins with the exception of the pentamer. This study offers additional data for the consideration of the health-benefits of dietary polyphenols from a wide variety of foods, including those benefits associated specifically with cocoa and chocolate consumption.

The purpose of this study was to evaluate the immunomodulatory activity of Spirulina, a bluegreen alga used as a food supplement. The effects of Spirulina on the secretion of three cytokines from unstimulated and stimulated human peripheral blood mononuclear cells (PBMC) were examined. In resting PBMC, Spirulina stimulated secretion of interleukin (IL)-1beta, IL-4, and interferon (IFN)-gamma to nearly 2.0, 3.3, and 13.6 times basal levels, respectively. Spirulina induced levels of IFN-gamma (229 +/- 104 pg/ml) that were comparable to those seen after phytohemagglutinin (PHA) stimulation (476 +/- 121 pg/ml). However, it was much less mitogenic than PHA (13.1 +/- 6.9 pg/ml) with respect to the induction of IL-4 secretion (0.34 +/- 0.1 pg/ml). In PHA-stimulated cells, Spirulina enhanced secretion of IL-1beta, IL-4, and IFN-beta by 2.9, 4.0., and 1.6 times, respectively. Although Spirulina stimulates several cytokines, it is clearly more effective in the generation of a Thl-type response. This in vitro study offers additional data for consideration of the potential therapeutic benefits of Spirulina.

Purpose Adjustable suture technique (AST) has been shown to be an effective treatment method in adult strabismus. The application of AST is not well studied in children due to potential poor cooperation during adjustment and the concern that the adjustment process can not be completed. The present series evaluates the efficacy and safety of this technique in a preselected group of children between 7 and 15 years of age. Methods A retrospective review of 89 consecutive children undergoing AST was completed to assess: (1) the ability to perform and complete adjustment in children; (2) the frequency of need to perform adjustment; and (3) accuracy of surgical alignment. Only patients with horizontal rectus muscle surgery were included. Results All children successfully completed the AST on the first post-operative day. Of the 89 patients, 24 (27%) required further adjustment by the AST. The mean follow-up period was 13.1 months. Fifty-three patients (60%) had previous strabismus surgery (range 1 to 5 operations). Sixty-six (74%) patients achieved successful alignment. Complications included slipped muscles in 1 case and difficulty in recession of the lateral rectus muscle in 1 patient. Conclusions Twenty-seven per cent of the patients required post-operative adjustment. The AST achieved an overall 74% successful alignment. Application of the AST should be considered in children with horizontal deviations over age 7 years, especially in the reoperations of esotropia.

Introduction: Absence of an extraocular muscle was considered rare when demonstrable only by surgical exploration or necropsy. This study presents advances in orbital imaging to correlate clinical findings with absence of the superior oblique (SO) muscle. Methods: We performed high-resolution coronal orbital imaging by magnetic resonance imaging (222 orbits) or computerized radiographic tomography (32 orbits) in 127 patients with strabismus. We reviewed the histories and ocular motility examinations in patients who had absence of 1 or both SO muscles. Findings were compared with patients who were clinically diagnosed with SO palsy but had demonstrable SO muscles on orbital imaging. Results: SO muscles were absent in 6 patients. All had histories suggesting congenital strabismus. In patients old enough for quantitative testing who had unilateral SO muscle absence, visual acuity was a least 20/25 in all and stereopsis was better than 80 arc/s in one. Three patients were orthotropic in primary position. Five patients with unilateral SO muscle absence had clinical findings variably consistent with SO palsy, whereas a sixth patient with Duane syndrome had clinically unsuspected bilateral SO muscle absence. Versions and patterns of hypertropia in patients with SO muscle absence overlapped findings of 20 patients with SO palsy but demonstrable SO muscles. Conclusions: Imaging can frequently demonstrate absence of the SO muscle in patients with SO palsy. Such patients may have good vision and stereopsis and clinical findings indistinguishable from SO palsy without absence of the SO muscle. Orbital imaging should be considered in the evaluation of congenital SO palsy to facilitate planning of effective surgical correction. (J AAPOS 1999;3:143-50)