Functional Imaging of Human Extraocular Muscles In Head Tilt Dependent Hypertropia

Demer, Joseph L.; Kung, Jennifer; Clark, Robert A.

doi:10.1167/iovs.10-6596

Cited by 38 publications

(54 citation statements)

References 33 publications

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“…16 For instance, a recent study showed that the three-step test was only about 50% specific, with 10 of 22 patients fulfilling the three-step test lacking superior oblique atrophy on MRI. 22 The present study challenges the sensitivity of the three-step test, which missed 30% of cases with demonstrated superior oblique atrophy.…”

Section: Discussionmentioning

confidence: 70%

“…21 Superior oblique palsy is also accompanied by shifts in the medial rectus, lateral rectus, and inferior rectus pulleys. 22,23 Finally, there is MRI evidence that differential compartmental contraction in the lateral rectus and medial rectus muscles elicits cyclovertical actions that might modulate alignment in superior oblique palsy. 24,25 …”

Section: Discussionmentioning

confidence: 99%

“…Our finding that ipsilesional superior oblique cross section in presumed superior oblique palsy was 52% of the contralesional and control superior oblique muscles is consistent with previous studies of superior oblique palsy. 6,11,21,22,26 …”

Section: Discussionmentioning

confidence: 99%

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Sensitivity of the three-step test in diagnosis of superior oblique palsy

Manchandia

Demer

2014

Journal of American Association for Pediatric Ophthalmology and

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Purpose Although the Parks-Bielschowsky three-step test is the cornerstone of cyclovertical strabismus diagnosis, it has not been validated against an external benchmark. We evaluated the test’s sensitivity in clinical diagnosis of superior oblique palsy in patients with unequivocal magnetic resonance imaging (MRI) evidence of superior oblique atrophy. Methods A total of 73 strabismic patients were selected from a prospective MRI study because they exhibited superior oblique atrophy indicative of superior oblique denervation and thus confirmatory of superior oblique palsy. Of these, 50 patients who had no confounding factors were included for detailed study. Ocular motility data were evaluated to determine sensitivity of single and combined clinical findings in diagnosis of superior oblique palsy. Results Maximum mean ipsilesional superior oblique cross section was reduced to 9.6 ± 0.6 mm2 (mean ± standard error) in superior oblique palsy, representing 52% of the 18.5 ± 0.6 mm2 contralesional superior oblique maximum cross section and 52% of the 18.4 ± 0.4 mm2 control maximum superior oblique cross section (P < 0.001). Of the 50 patients, 35 (70%) with superior oblique atrophy fulfilled the entire three-step test. In 14 (28%) patients two steps were fulfilled; in 1 patient (2%), only one step. Affected superior oblique cross section was similar in orbits that fulfilled the three-step test (9.8 ± 0.9 mm2) and those that did not (9.1 ± 0.7 mm2; P = 0.58). Conclusions The complete three-step test fails to detect 30% of cases of superior oblique atrophy. Often only two of three steps are positive in superior oblique palsy.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

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Sensitivity of the three-step test in diagnosis of superior oblique palsy

Manchandia

Demer

2014

Journal of American Association for Pediatric Ophthalmology and

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“…Yet, most cases of congenital SO palsy, which is an unequivocal CCDD, are not associated with BrS. [23][24][25][26] Moreover, in a recent MRI study of congenital BrS, Kim and Hwang 27 found qualitatively normal trochlear nerves and SO muscles in nine cases. This implies that innervational and mechanical causes of BrS may be dissociated.…”

Section: Discussionmentioning

confidence: 98%

Size of the Oblique Extraocular Muscles and Superior Oblique Muscle Contractility in Brown Syndrome

Suh

Demer

2015

Invest. Ophthalmol. Vis. Sci.

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Citation: Suh SY, Le A, Demer JL. Size of the oblique extraocular muscles and superior oblique muscle contractility in Brown syndrome. Invest Ophthalmol Vis Sci. 2015;56:6114-6120. DOI:10.1167/iovs.15-17276 PURPOSE. This study employed magnetic resonance imaging (MRI) to investigate possible size and contractility changes in the superior oblique (SO) muscle, and possible isometric hypertrophy in the inferior oblique (IO) muscle, resulting from abnormal mechanical loading in Brown syndrome (BrS).METHODS. High resolution orbital MRI was obtained in 4 congenital and 11 acquired cases of BrS, and compared with 44 normal subjects. Maximal cross-section areas and posterior partial volumes (PPVs) of the SO were analyzed in central gaze, supraduction, and infraduction for the SO, and in central gaze only for the IO.RESULTS. In congenital BrS, mean maximum SO cross-sectional areas were 24% and 20% less than normal in affected and unaffected eyes, respectively (P ¼ 0.0002). Mean PPV in congenital BrS was also significantly subnormal bilaterally (29% and 34% less in affected and unaffected eyes, respectively, P ¼ 0.001). However, SO muscle size and volume were normal in acquired cases. The SO muscle did not relax in supraduction in BrS, although there was normal contractile thickening in infraduction. The IO muscle had normal size bilaterally in BrS.CONCLUSIONS. Congenital BrS may be associated with SO hypoplasia that could reflect hypoinnervation. However, unique isometric loading of oblique extraocular muscles due to restrictive hypotropia in adduction in BrS is generally not associated with changes in muscle bulk or in SO contractility. Unlike skeletal muscles, the bulk and contractility of extraocular muscles can therefore be regarded as independent of isometric exercise history. Restriction to elevation in BrS typically arises in the trochlea-tendon complex.Keywords: extraocular muscle, magnetic resonance imaging, strabismus T he hallmark of Brown syndrome (BrS) is restrictive limitation to supraduction in adduction. In 1950, Harold Whaley Brown first coined the term ''superior oblique tendon sheath syndrome,'' supposing a short superior oblique (SO) tendon sheath as the cause. 1 In 1975, Parks 2 reported that a restrictive band posterior and inferior to the globe limited elevation in adduction in BrS. In 1982, Helveston 3 suggested fluid accumulation or concretion in the bursa-like space, or vascular distention in the SO tendon sheath, as causes of acquired BrS, impairing SO tendon travel through the trochlea. Subsequent studies have confirmed that pathology generally lies in abnormal SO tendon-trochlea complex, 4,5 although another mechanism involving inferior slip of the lateral rectus pulley has also been identified. 6 The classical mechanism of BrS provides a unique window into extraocular muscle physiology. Impaired SO tendon travel through the trochlea in BrS prevents the SO muscle from elongating during its innervational relaxation in attempted supraduction in adduction. Consequently, the SO experiences unu...

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“…[1][2][3][4][5][6][7][8][9][10][11][12] Previous studies of SOP by using MR imaging have consistently shown a variable degree of hypoplasia of the paretic superior oblique muscle (SO) and variable trochlear nerve absence. [1][2][3][4][5] In our recent study of patients with congenital SOP, 73% had ipsilateral trochlear nerve absence and a variable degree of SO hypoplasia, while the remaining 27% had a normal-appearing SO and trochlear nerve on both sides, suggesting a different etiology.…”

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confidence: 99%