Vertical Fusional Amplitudes Research Articles

Vertical Comitance of Hypertropia in Congenital and Acquired Superior Oblique Palsy.

Ivanir and Trobe have claimed that hypertropia (HT) that is greater in upgaze than downgaze, or equal to it, is characteristic of decompensated congenital superior oblique (SO) palsy and never present in ischemic, traumatic, or tumorous SO palsy. The reliability of this claim was tested in patients with SO palsy confirmed by MRI demonstration of subnormal ipsilesional SO size. Quasi-coronal, surface coil MRI was performed in target-controlled central gaze to identify patients with a unilateral reduction in SO cross section indicative of palsy. Nine patients gave an unequivocal history or had markedly increased vertical fusional amplitudes indicative of congenital onset (mean age 38 ± 16 years, SD). Seven patients had unequivocal acquired onset (age 47 ± 14 years and symptom duration 5.4 ± 4.8 years), including 2 with demonstrated trochlear Schwannoma and 5 with onset after severe head trauma. Fifteen patients had gradually progressive onset unequivocally not congenital yet not associated with any identifiable precipitating event (age 52 ± 20 years and symptom duration 13 ± 14 years). Maximum SO cross section averaged 8.6 ± 3.9 mm2 in congenital palsy, not significantly different from 11.3 ± 3.5 mm2 in acquired palsy (P = 0.08) either unequivocally or progressively acquired, but significantly less than about 19 mm2 contralesionally in SO palsy (P < 10-4). Although mean central gaze HT was greater at 20.6 ± 8.0Δ in 9 cases of congenital than that in 22 acquired cases at 11.4 ± 6.8Δ (P = 0.002), HT was 8.4 ± 16.3Δ less in upgaze than downgaze in congenital SO palsy and 3.7 ± 11.2Δ less in acquired SO palsy. In congenital palsy, 33% of patients had HT greater in upgaze than downgaze while in 67% HT was greater in downgaze (by up to 42Δ). In acquired SO palsy, HT was greater in upgaze than downgaze or equal to it in 8 cases (36%, P = 0.87, X2). In acquired SO palsy, HT was greater in upgaze than downgaze in 37% and greater in downgaze than upgaze in 59% of cases. The HT was equal in upgaze and centralgaze in no congenital and 3 acquired cases of SO palsy. Trends were similar in unequivocal acquired and progressive acquired (noncongenital) SO palsy (P > 0.4). Hypertropia is not characteristically greater in upgaze than downgaze in congenital SO palsy proven by SO atrophy on MRI. In fact, average HT is greater in downgaze than upgaze in both acquired and congenital palsy, sometimes strikingly so in the latter. The finding of HT greater in upgaze than downgaze, or equal to it, does not reliably indicate that SO palsy is congenital, nor does maximum SO cross section.

Understanding and evaluating diplopia

Diplopia or double vision is a frequent reason for ophthalmology consultation. Monocular diplopia is usually ocular or retinal in origin, whereas binocular diplopia is often due to neurological causes. Detailed history beginning with any childhood visual disorders or head tilt and covering comorbid conditions and drug intake is essential. The alignment of images and direction of maximum separation point to the muscle(s) are involved. Temporal profile including onset, progression, and fluctuations along with comorbid conditions helps to narrow down the etiology. Refraction, ocular examination, and fundoscopy can identify ocular and retinal conditions; meticulous examination of ocular ductions and versions is mandatory to localize the cause of diplopia and to initiate investigations for the underlying disease process. Isolated ocular motor palsies are mostly due to microvascular ischemia; in the absence of red flags, investigation may be deferred for 6–8 weeks. Large vertical fusional amplitudes may be a clue to a decompensated congenital trochlear palsy. A partial third nerve palsy with early pupillary involvement, progressive signs, involvement of multiple cranial nerves, and elderly patients with rapid Erythrocyte Sedimentation Rate (ESR) are some situations warranting early imaging and other investigation. Myasthenia gravis and thyroid disease may present with diplopia and ophthalmic manifestations alone without systemic symptomatology. Immunoglobulin G4-related orbital myositis and anti-GQ1b antibody-mediated ocular neuropathies are relatively recently recognized immune-mediated conditions that may present with diplopia to an ophthalmologist. Ophthalmoplegic migraine has been renamed recurrent ophthalmoplegic neuropathy and is a diagnosis of exclusion at initial presentation.

The symptomatic IV nerve palsy

The majority of IV nerve palsies are benign, either idiopathic, congenital, or the result of known trauma. This report describes the stories and atypical features of five patients with isolated IV nerve palsies on examination, who proved to have underlying structural lesions. The first case had a trochlear schwannoma that caused a IV nerve palsy that recurred years later. The second had an orbital apex metastasis that caused a IV nerve palsy with a history of mild fluctuating ptosis. The third had a cavernous sinus fistula that presented with an unusual month-long prodrome of headaches and eye pain prior to diplopia. The fourth was a young patient who suffered a hemorrhage along the tentorium cerebelli from excessive anticoagulation. The fifth had an arachnoid cyst posterior to the cavernous sinus that presented with long-standing head tilt, suggesting a congenital palsy, but normal vertical fusional amplitudes. Detailed imaging of the sella with coronal and axial sections and gadolinium administration was critical to diagnosing most of the lesions causing these symptomatic IV nerve palsies. In most, atypical aspects of their history were key indicators of the need for imaging in this usually benign type of nerve palsy.

Quantifying the vertical fusion range at four distances of fixation in a normal population

Aim: To compare the vertical fusional amplitudes in isometropic participants with normal binocular single vision at four distances of fixation: 33 cm, 1 m, 4 m, 6 m. Methods: Vertical fusion ranges (break point and recovery point) were measured with a Gulden vertical prism bar with the participant fixing a 6/12 Snellen equivalent letter, twice at each distance. Order effects were controlled with randomisation of both fixation distance and prism direction. Results: Twenty-seven participants were examined (aged 20.4 ± 1.05 years). Base up and base down measurements were similar, therefore measurements were combined to give a total vertical range. Median values for the break points were: 33 cm, 6(Δ) ; 1 m, 6(Δ); 4 m, 5.5(Δ); 6 m, 5.5(Δ); and for the recovery points were: 33 cm, 4(Δ); 1 m, 4(Δ); 4 m, 3.5(Δ); 6 m, 3.5(Δ). The difference was significant between either of the near measures (i.e. 33 cm and 1 m) and either of the far measures (i.e. 4 m and 6 m). Conclusions: The vertical fusion range appears to be slightly greater at near than distance. However, the difference is not clinically significant. Measurements for distance, in a normal population, appear to be the same whether a fixation distance of 4 m or 6 m is used.

Vertical fusional amplitudes in patients wearing vertical anisometropic correction

Objective To examine the relationship between vertical anisometropic spectacle correction and vertical fusional amplitudes in patients. Design Comparative observational case series. Participants Twenty-one patients exposed to greater than 0.5 diopters of vertical anisometropic spectacle correction were compared with 46 patients not exposed to anisometropic correction. Methods Vertical fusional amplitudes were recorded in all patients using a prism bar. Main outcome measures Vertical fusional amplitudes and vertical anisometropia. Results In patients exposed to greater than 0.5 diopters of vertical anisometropic spectacle correction, vertical fusional amplitudes measured 5.2 ± 1.4 prism diopters. Patients not exposed to anisometropic correction had vertical fusional amplitudes of 2.7 ± 1.2 prism diopters ( P < 0.0001). Conclusion Patients with vertical anisometropic correction have increased vertical fusional amplitudes. This finding is relevant when evaluating patients with ocular motility disorders, especially with regard to distinguishing acquired versus longstanding deviations.

Pituitary macroadenoma manifesting as an isolated fourth nerve palsy

PURPOSE: To describe an unusual ophthalmic manifestion of a pituitary adenoma.METHODS: Case report.RESULTS: A 32-year-old man had left supraorbital and frontal headaches and new-onset vertical diplopia. Examination showed a left fourth nerve palsy and increased vertical fusional amplitudes. Magnetic resonance imaging disclosed a sellar mass consistent with a pituitary macroadenoma.CONCLUSION: A pituitary adenoma may rarely manifest with an isolated fourth nerve palsy.

Facial asymmetry in superior oblique muscle palsy.

Facial asymmetry is an underrecognized association or sequela of torticollis in congenital or very early onset superior oblique muscle palsy, which when present in an adult, helps to confirm chronicity and prevent unnecessary neurologic evaluation. Nineteen cases of superior oblique muscle palsy were studied prospectively. Of 12 unilateral palsies presenting in adulthood, 9 were considered congenital by history and 7 (77%) of these had facial asymmetry. Large vertical fusional vergence amplitudes and torticollis, on review of childhood photographs, confirmed the early onset of the palsy in each facial asymmetry patient. In addition, two children presenting at age 18 months and 3 years of age with constant head tilting had facial asymmetry. If torticollis is corrected before maturation of the facial structure, resolution of the asymmetry may occur.

Superior Oblique Palsy as a Complication of Anterior Ethmoidal Artery Ligation?

To the Editor. —We read with interest the article by Couch et al1in the August 1990 issue of theArchives. It is especially important in reporting complications of surgery that one document compelling evidence that the problem was not preexisting and appropriate examinations were performed to relate the complication to the surgery performed. In the cases reported by Couch et al, the authors did not discuss the possibility that breakdown of a preexisting vertical phoria may have caused these patients' diplopia.2Studies of superior oblique palsy have documented that one of the most common, if not the most common,3causes of superior oblique palsy is congenital. One may distinguish acute from chronic palsies by review of old photographs for head tilt, measurement of vertical fusional amplitudes, and spread of comitance. In case 1, no mention is made of preexisting head tilt or vertical fusional amplitudes. The

Horizontal and vertical vergence training and its effect on vergences, fixation disparity curves, and prism adaptation: II. Vertical data.

The purpose of this study was to assess the effects of horizontal and vertical vergence training on vertical fusional amplitudes, the vertical fixation disparity (VFD) curve, and prism adaptation. Thirty-four subjects were divided into three groups. One-third served as controls and the other two-thirds underwent 5 h of supervised horizontal and vertical vergence training, respectively. We hypothesized that subjects in the vertical group would manifest increased vertical vergence amplitude and coefficients of adaptation in concert with flatter VFD slopes. Before and after the 4-week training period, vertical vergences, fixation disparity (FD) curves, and coefficients of vertical prism adaptation were measured by a single individual who was intentionally uninformed of each subject's group. Analysis of the data suggests that changes in the vertical fusional amplitudes increased slightly. Although changes in the VFD slope and coefficient of prism adaptation were not statistically significant, the changes were much greater in the vertical group and in the hypothesized direction. We suggest that the results offer preliminary support for our hypothesis.

Interaction between horizontal and vertical fusional responses.

Human fusional responses to combinations of horizontal and vertical disparity presentations were studied in order to determine how the horizontal and vertical fusional components are utilized during the response. Vertical fusional amplitudes decreased in the presence of large horizontal disparities. The reaction time to a vertical-step disparity increased when a horizontalstep disparity was simultaneously presented. Neither horizontal fusional amplitudes nor horizontal vergence responses to step or ramp disparity presentations were affected by the presence of vertical disparities. Thus, the results indicate a unilateral interaction between horizontal and vertical fusional components, one in which the fusibility of a compound disparity is affected by the order in which the disparity components are introduced.

Effect of stimulus size on fusion and vergence.

Objective measurements were carried out to determine the effect of stimulus size on fusional and vergence amplitudes. It was shown that increasing the stimulus size to include peripheral retinal regions results in significant increases in horizontal and vertical fusional amplitudes. This increase is realized by proportionate increases in both motor (vergence) and nonmotor components.

Absence of Spontaneous Head Tilt in Superior Oblique Muscle Palsy

We used the head-tilt test--based on an imbalance between the function of a paretic superior oblique muscle and its homonymous superior rectus muscle, rather than on an anomaly of cycloversion-to test three patients with superior oblique muscle palsies. Spontaneous ocular torticollis was absent if a patient had poor vision in one eye or if his vertical fusional amplitudes were of such magnitude that he was able to overcome his vertical deviation in all positions of gaze. These latter instances, though rare, may be more common than reports indicate.

Observations on vertical divergences and hyperphorias.

THE VERTICAL prism vergences (variously called vertical fusional amplitudes and maximal vertical divergences) of most subjects are of the order of ±2.5 to ±3 Δ.1With repeated or prolonged testing it may sometimes be possible to increase these limits a little.2Ophthalmologists usually regard this range of vertical prism vergences as implying fixed limits in the ability of neuromuscular apparatus and the fusion powers of the two eyes to make vertical divergences. Hyperphorias are considered of real significance so far as their magnitudes encroach upon these limits of divergence. Yet, clinically speaking, if small hyperphorias were thought to be the cause of symptoms, they were corrected by prisms, even though the vertical prism vergences were equal and normal. In this paper it will be shown that the eyes of most persons are capable of compensating for, or adapting to, much larger degrees of vertical divergence. With this adaptation