Paretic Eye Research Articles

Treatment of Inferior Oblique Paresis With Superior Oblique Silicone Tendon Expander

Patients with inferior oblique eye muscle paresis may show hypotropia and apparent superior oblique muscle overaction on the side of the presumed weak inferior oblique (IO) muscle. We report 8 such patients successfully treated using unilateral silicone superior oblique (SO) tendon expanders. Eight consecutive cases over the course of 6 years from the authors' private practice are described. None had a history of head trauma or a significant neurologic event. All patients showed IO paresis by 3-step test, with incyclotorsion and SO overacton of the hypotropic (paretic) eye. Forced ductions of the hypotropic eye were normal in all cases, and the vertical strabismus was treated with placement of a 7- mm silicone SO tendon expander in the hypotropic (paretic) eye. Mean preoperative primary position hypotropia was 6.5 prism diopters (PD); mean postoperative was 0.5 PD. Seven of 8 patients had resolution of primary position hypotropia, whereas the eighth was reduced. Mean preoperative SO overaction was 3+; all patients had postoperative resolution of SO overaction. Of 4 patients with preoperative ocular torticollis, mean preoperative head tilt was 9.3 degrees; mean postoperative tilt was 2.9 degrees. Two patients' head tilts had resolved, the other 2 showed improvement. All patients showed preoperative incylclotorsion of the hypotropic (paretic) eye; inclyclotorsion resolved in all patients after the placement of a SO tendon expander. The silicone SO tendon expander effectively restores ocular alignment in IO paresis with apparent SO overaction. Associated ocular torticollis can also be improved.

Recovery of Peripheral Versus Central Nerves Identified by Saccadic Velocity After Abducens Neuropathy

The abducens is the motor nerve with the most substantial course, both within and outside the brain and it innervates only one muscle. Sixth nerve palsy affords an opportunity to compare recovery after central versus peripheral nerve damage by assessing the dynamics of abduction. Horizontal saccade peak velocities and durations in 14 patients with unilateral peripheral sixth nerve palsies (5 acute, 9 chronic) are compared with those in 5 patients with central sixth nerve palsies (2 acute, 3 chronic) and with those in 10 normal subjects. Acutely, abducting saccades in the paretic eye were slow in both central and peripheral palsies, as anticipated from weakness of the lateral rectus muscle. In chronic central palsies, abducting saccadic velocities remained reduced, but in chronic peripheral palsies, they increased to normal within the limited range of excursion. The chronically damaged peripheral nerve behaves like a high-pass filter in transmitting phasic velocity commands, whereas tonic position commands remain defective, accounting for limited abduction but normal velocities within the range of duction. In chronic central (fascicular) palsies, saccade velocities remain reduced. Impaired conduction from damage to central myelin or axons is more persistent in central palsies, consistent with limited regeneration within the brain. Recording of saccade velocities may aid the distinction of fascicular from peripheral palsies. Saccade speed is repaired in peripheral palsies, probably by remyelination, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye in order to drive both eyes rapidly and simultaneously to a target in the paretic field of motion.

Clinical features and surgical treatment of congenital ocular muscle palsy characterized with double elevator dysfunction

To investigate the clinical features of congenital ocular elevator muscle palsy and to evaluate the efficacy of surgical treatment. Pre- and post-operative eye position, superior rectus muscle and inferior oblique muscle function, clinical features were examined and analyzed in 11 patients with congenital double elevator palsy of ocular muscles. When fixated with the nonparetic eye, ten of 11 patients showed hypotropia and pseudoblepharoptosis in the primary position; One of 11 patients fixated with the paretic eye and showed hypotropia in the primary position. All cases were a monocular elevation deficiency in abduction and adduction, and showed pseudoblepharoptosis. In ten patients fixated with the nonparetic eye, two of 10 were undergone inferior rectus recession on paretic eyes; six of 10 were undergone inferior rectus recession and superior oblique tenectomy on paretic eyes; two of 10 were applied inferior rectus recession and superior oblique tenectomy on paretic eyes, superior rectus recession was performed on healthy eyes in six months postoperation. The patient fixated with the paretic -eye were undergone superior rectus recession and inferior oblique tenectomy on healthy eyes. Seven patients with exotropia had lateral rectus muscle surgery performed at the time of their vertical operation. Strabismus were complete corrected in 81.8% (9/11) of patients in our study and 18.2% (2/11) of patients were partial corrected. The functions of superior rectus muscle and inferior oblique muscle were not corrected. Nine patients showed complete correction of the psuedoptosis, one patient showed partial correction of the psuedoptosis, one patient did not showed any improvement of the pseudoptosis. We conclude that superior rectus muscle and inferior oblique muscle insufficiency are the primary factors in the etiology of congenital double ocular elevator palsy. Vertical rectus recession and superior oblique tenectomy on paretic eyes is an effective way of surgical treatment the disease.

Vergence-mediated changes in Listing's plane do not occur in an eye with superior oblique palsy.

As a normal subject looks from far to near, Listing's plane rotates temporally in each eye. Since Listing's plane relates to the control of torsional eye position, mostly by the oblique eye muscles, the current study was conducted to test the hypothesis that a patient with isolated superior oblique palsy would have a problem controlling Listing's plane. Using the three-dimensional scleral search coil technique, binocular Listing's plane was measured in four patients with congenital and in four patients with acquired unilateral superior oblique palsy during far- (94 cm) and near- (15 cm) viewing. The results were compared to previously published Listing's plane data collected under exactly the same conditions from 10 normal subjects. In patients with unilateral superior oblique palsy, either congenital or acquired, Listing's plane in the normal eye rotated temporally on near-viewing, as in normal subjects, while in the paretic eye it failed to do so. In patients with acquired superior oblique palsy, Listing's plane was already rotated temporally during far-viewing and failed to rotate any farther on near-viewing, whereas in patients with congenital superior oblique palsy Listing's plane in the paretic eye was oriented normally during far-viewing and failed to rotate any farther on near-viewing. These results suggest that the superior oblique muscle, at least in part, is responsible for the temporal rotation of Listing's plane that occurs in normal subjects on convergence.

Ocular rotation axes during dynamic Bielschowsky head-tilt testing in unilateral trochlear nerve palsy.

To explain the positive Bielschowsky head-tilt (BHT) sign in unilateral trochlear nerve palsy (uTNP) by the kinematics of three-dimensional eye rotations. Twelve patients with uTNP monocularly fixed on targets on a Hess screen were oscillated (+/- 35 degrees, 0.3 Hz) about the roll axis on a motorized turntable (dynamic BHT). Three-dimensional eye movements were recorded with dual search coils. Normal data were collected from 11 healthy subjects. The rotation axis of the viewing paretic or unaffected eye was nearly parallel to the line of sight. The rotation axis of the covered fellow eye, however, was tilted inward relative to the other axis. This convergence of axes increased with gaze toward the unaffected side. Over entire cycles of head roll, the rotation axis of either eye remained relatively stable in both the viewing and covered conditions. In patients with uTNP, circular gaze trajectories of the covered paretic or unaffected eye during dynamic BHT are a direct consequence of the nasal deviation of the rotation axis from the line of sight. This, in turn, is a geometrical result of decreased force by the superior oblique muscle (SO) of the covered paretic eye or, according to Hering's law, increased force parallel to the paretic SO in the covered unaffected eye. The horizontal incomitance of rotation axes along horizontal eye positions can be explained by the same mechanism.

Principles of Surgical Management of Cranial Nerve Palsies

Background and PurposeCranial nerve palsies following cranial and/or ocular trauma are common. Surgical correction of these patients may be challenging and different concepts in surgical planning are required, as compared to patients with non-paretic or comitant strabismus.MethodsEssay presentation and review of the literature.ResultsDegree of paralysis and severity of ductional deficit is the most important factor when devising a surgical plan for these cases. Efforts should be made to normalize ductions when possible by improving movement of the paretic eye. When this is not feasible, creating ductional deficits in the fellow eye in order to make versions more symmetric should be employed. Chemodenervation and prisms are helpful adjunctive modalities in the management of these patients.ConclusionsAlthough multiple procedures may be required, most patients with ocular motor cranial nerve palsies are significantly improved after strabismus surgery, with acceptable alignment in primary gaze and an enlarged field of single binocular vision.

Adaptations and deficits in the vestibulo-ocular reflex after peripheral ocular motor palsies.

Palsy of a nerve might be expected to lower vestibulo-ocular reflex (VOR) responses in its fields of motion, but effects of peripheral neuromuscular disease were unknown. We recorded the VOR during sinusoidal head rotations in yaw, pitch, and roll at 0.5-2 Hz and static torsional gain in 43 patients with unilateral nerve palsies. Sixth nerve palsy (n = 21) reduced both abduction and adduction VOR gains in darkness. In light, horizontal visually enhanced VOR (VVOR) gains were normal in moderate and mild palsy. In severe palsy, horizontal VVOR gains remained low in the paretic eye when it was fixating, whereas gains in the nonparetic eye became higher than normal. Third nerve palsy (n = 10) decreased VOR and VVOR gains during abduction, adduction, elevation, depression, extorsion, and intorsion. Fourth nerve palsy (n = 13) reduced VOR gains of the paretic eye during intorsion, extorsion, elevation, depression, abduction, and adduction, but in light vertical and horizontal VVOR gains were normal. In the nonparetic eye, all gains were normal. Reduced VOR gains in the direction of paretic muscles and also in the direction of their antagonists, together with normal gains in the nonparetic eye, indicate a selective adjustment to the antagonists of paretic muscles. Increase of VVOR gains to normal in the paretic eye, when used for fixation, without conjugate increase in gains in the occluded nonparetic eye, provides further evidence of selective adaptation for the paretic eye. Motions of the eyes after nerve palsies indicate monocular VOR adaptation in three dimensions.

Primary position and listing's law in acquired and congenital trochlear nerve palsy.

In ocular kinematics, the primary position (PP) of the eye is defined by the position from which movements do not induce ocular rotations around the line of sight (Helmholtz). PP is mathematically linked to the orientation of Listing's plane. This study was conducted to determine whether PP is affected differently in patients with clinically diagnosed congenital (conTNP) and acquired (acqTNP) trochlear nerve palsy. Patients with unilateral conTNP (n = 25) and acqTNP (n = 9) performed a modified Hess screen test. Three-dimensional eye positions were recorded with dual search coils. PP in eyes with acqTNP was significantly more temporal (mean: 21.2 degrees ) than in eyes with conTNP (6.8 degrees ) or healthy eyes (7.2 degrees ). In the pooled data of all patients, the horizontal location of PP significantly correlated with vertical noncomitance with the paretic eye in adduction (R = 0.59). Using a computer model, PP in acqTNP could be reproduced by a neural lesion of the superior oblique (SO) muscle. An additional simulated overaction of the inferior oblique (IO) muscle moved PP back to normal, as in conTNP. Lengthening the SO and shortening the IO muscles could also simulate PP in conTNP. The temporal displacement of PP in acqTNP is a direct consequence of the reduced force of the SO muscle. The reversal of this temporal displacement of PP, which occurs in some patients with conTNP, can be explained by a secondary overaction of the IO muscle. Alternatively, length changes in the SO and IO muscles, or other anatomic anomalies within the orbit, without a neural lesion, may also explain the difference in location of PP between conTNP and acqTNP.

Motor mechanisms of vertical fusion in individuals with superior oblique paresis

Purpose: We wanted to determine the mechanisms of motor vertical fusion in patients with superior oblique paresis and to correlate these mechanisms with surgical outcomes. Methods: Ten patients with superior oblique paresis underwent 3-axis, bilateral, scleral search coil eye movement recordings. Eye movements associated with fusion were analyzed. Results: Six patients had decompensated congenital superior oblique paresis and 4 had acquired superior oblique paresis. All patients with acquired superior oblique paresis relied predominantly on the vertical rectus muscles for motor fusion. Patients with congenital superior oblique paresis were less uniform in their mechanisms for motor fusion: 2 patients used predominantly the oblique muscles, 2 patients used predominantly the vertical recti, and 2 patients used predominantly the superior oblique in the hyperdeviated eye and the superior rectus in the hypodeviated eye. The last 2 patients developed the largest changes in torsional eye alignment relative to changes in vertical eye alignment and were the only patients to develop symptomatic surgical overcorrections. Conclusion: There are 3 different mechanisms for vertical fusion in individuals with superior oblique paresis, with the predominant mechanism being the vertical recti. A subset of patients with superior oblique paresis uses predominantly the superior oblique muscle in the hyperdeviated paretic eye and the superior rectus muscle in the fellow eye for fusion. This results in intorsion of both eyes, causing a large change in torsional alignment. The consequent cyclodisparity, in addition to the existing vertical deviation, may make fusion difficult. The differing patterns of vertical fusional vergence may have implications for surgical treatment. (J AAPOS 2002;6:145-53)

The vestibulo-ocular reflex in fourth nerve palsy: deficits and adaptation

The effects of fourth nerve palsy on the vestibulo-ocular reflex (VOR) had not been systematically investigated. We used the magnetic scleral search coil technique to study the VOR in patients with unilateral fourth nerve palsy during sinusoidal head rotations in yaw, pitch and roll at different frequencies. In darkness, VOR gains are reduced during incyclotorsion, depression and abduction of the paretic eye, as anticipated from paresis of the superior oblique muscle. VOR gains during excyclotorsion, elevation and adduction of the paretic eye are also reduced, whereas gains in the non-paretic eye remain normal, indicating a selective adjustment of innervation to the paretic eye. In light, torsional visually enhanced VOR (VVOR) gains in the paretic eye remain reduced; however, visual input increases vertical and horizontal VVOR gains to normal in the paretic eye, without a conjugate increase in VVOR gains in the non-paretic eye, providing further evidence of selective adaptation in the paretic eye. Motions of the eyes after fourth nerve palsy exemplify monocular adaptation of the VOR, in response to peripheral neuromuscular deficits.

Adaptations and deficits in the vestibulo-ocular reflex after third nerve palsy.

To analyze the vestibulo-ocular reflex (VOR) in patients with unilateral peripheral third nerve palsy. Ten patients and 15 healthy subjects were studied using magnetic search coils. Subjects made sinusoidal +/-10 degrees head-on-body rotations in yaw, pitch, and roll in darkness and during monocular viewing in light. Horizontal VOR and visually enhanced VOR (VVOR) gains of the paretic eye were decreased during both abduction and adduction. Vertical VOR and VVOR gains of the paretic eye were decreased during both elevation and depression. Dynamic and static torsional VOR and VVOR gains of the paretic eye were reduced during both excyclotorsion and incyclotorsion. Horizontal, vertical, and torsional VOR and VVOR gains were normal in the nonparetic eye. Adducting VOR gains were reduced as anticipated from medial rectus palsy. Abducting gains were also reduced; the reduction is attributed to an adaptive decrease in innervation to the lateral rectus to achieve symmetry of the horizontal VOR in the paretic eye. Torsional VOR gains were reduced during excyclotorsion from palsy of the inferior oblique muscle. Gains were also reduced during incyclotorsion, which can be explained by an adaptive decrease in innervation to the superior oblique to restore symmetry of the torsional VOR in the paretic eye. Monocular adaptation in the VOR of the paretic eye reduces asymmetrical movement of retinal images during head motion, prevents nystagmus, and reduces retinal image disparity.

Smooth pursuit eye movements in patients with ocular motor nerve palsies: A preliminary report

The trajectories, velocity, and co-ordination of smooth pursuit eye movements were investigated in 30 patients with ocular motor nerve palsies (including palsies of cranial nerves III, IV and VI). The recordings of horizontal and vertical eye movements were obtained by video-oculography under monocular viewing conditions. During the recordings, horizontal, vertical, and oblique target movements of 10°/s constant velocity were presented to the subjects in succession. In contrast to normal subjects, smooth pursuit eye movements in patients with ocular nerve palsies showed considerable differences in dependence on the fixating eye. The smooth pursuit gain of the paretic eye was reduced for eye movements in the pulling plane of the paretic muscle. When viewing with the paretic eye, the tracking of the target was achieved by a series of refixation saccades, which also occurred in the occluded normal eye. Consequently, the sound eye position overshot the target. The transition from a smooth to a saccadic pursuit pattern was accompanied by a spatial deviation of the eye movement trajectories from the path of the fixation target.

Peripheral oculomotor palsy affects orienting of visuospatial attention.

Patients affected by VI cranial nerve palsy were required to orient their attention in monocular vision and to detect a stimulus appearing either in attended or in unattended locations. Results showed that while during non-paretic eye vision stimulus detection in the attended location was faster than that in the unattended one, during paretic eye vision no difference in detection speed was present. However, in this latter condition, detection speed in both attended and un attended locations were as fast as that measured during non-paretic eye vision in attended location. Demonstration that peripheral oculomotor impairment influences monocular covert orienting of visuospatial attention strongly support the idea that visuospatial attention and oculomotor mechanisms share similar cortical networks.

Myectomy of Lateral Rectus Muscle for Third Nerve Palsy

Purpose To introduce myectomy of the lateral rectus muscle for correcting exotropia in patients with third nerve palsy. Methods The lateral rectus muscle of the paretic eye was myectomized without suturing it to the globe. This was combined with a medial rectus muscle resection and a contralateral lateral rectus muscle recession. Magnetic resonance imaging was performed to observe the re-attachment of the lateral rectus muscle to the globe. Results The patient was able to fuse in the primary position without any noticeable limitation in abduction. Magnetic resonance imaging showed that the lateral rectus muscle was attached to the globe through fibrous tissue. Conclusion Myectomy of the lateral rectus muscle is an effective and simple procedure to accomplish a super-maximal weakening effect of abduction in patients with complete third nerve palsy.

Adaptive Phänomene bei internukleärer Ophthalmoplegie

Introduction: Abduction nystagmus and hypermetric abduction saccades are the main abnormalities on the non-paretic eye in internuclear ophthalmoplegia (INO). Their origin is still debated and includes an adaptively increased phasic innervation adjusted to the paretic medial rectus muscle (adaptation hypothesis). This hypothesis predicts a relation between the degree of the adduction paresis and the degree of the abduction overshoot and the occurrence of an abduction nystagmus in opposite eye. The present study investigates these predictions. Material and Methods: Direct-current electro-oculography and analysis of horizontal saccades in 50 consecutive patients with unilateral and 25 with bilateral INO. Results: All patients had overshooting abduction saccades on the eye opposite to the adduction paresis. In patients with unilateral and bilateral INO, linear regression showed negative correlations between adduction saccade velocity on the paretic eye and the degree of abduction overshoot and the duration of the phasic innervation on the other eye (correlation coefficients between r = -0.515 and -0.675). The frequency of abduction nystagmus increased with increasing degree of the adduction paresis. Patients with abduction nystagmus had a significantly higher degree of abduction overshoot and significantly longer duration of the phasic innervation of abduction saccades. Conclusions: These findings add further evidence to the existence of an adaptively increased phasic innervation adjusted to the paretic medial rectus muscle in patients with unilateral and bilateral INO. Such adaptation explains overshooting abduction saccades and abduction nystagmus present in most patients with INO on the non-paretic abducting eye.

Proprioceptive and retinal afference modify postsaccadic ocular drift.

Drift of the eyes after saccades produces motion of images on the retina (retinal slip) that degrades visual acuity. In this study, we examined the contributions of proprioceptive and retinal afference to the suppression of postsaccadic drift induced by a unilateral ocular muscle paresis. Eye movements were recorded in three rhesus monkeys with a unilateral weakness of one vertical extraocular muscle before and after proprioceptive deafferentation of the paretic eye. Postsaccadic drift was examined in four visual states: monocular viewing with the normal eye (4-wk period); binocular viewing (2-wk period); binocular viewing with a disparity-reducing prism (2-wk period); and monocular viewing with the paretic eye (2-wk period). The muscle paresis produced vertical postsaccadic drift in the paretic eye, and this drift was suppressed in the binocular viewing condition even when the animals could not fuse. When the animals viewed binocularly with a disparity-reducing prism, the drift in the paretic eye was suppressed in two monkeys (with superior oblique pareses) but generally was enhanced in one animal (with a tenotomy of the inferior rectus). When drift movements were enhanced, they reduced the retinal disparity that was present at the end of the saccade. In the paretic-eye-viewing condition, postsaccadic drift was suppressed in the paretic eye and was induced in the normal eye. After deafferentation in the normal-eye-viewing state, there was a change in the vertical postsaccadic drift of the paretic eye. This change in drift was idiosyncratic and variably affected the amplitude and velocity of the postsaccadic drift movements of the paretic eye. Deafferentation of the paretic eye did not affect the postsaccadic drift of the normal eye nor did it impair visually mediated adaptation of postsaccadic drift. The results demonstrate several new findings concerning the roles of visual and proprioceptive afference in the control of postsaccadic drift: disconjugate adaptation of postsaccadic drift does not require binocular fusion; slow, postsaccadic drift movements that reduce retinal disparity but concurrently increase retinal slip can be induced in the binocular viewing state; postsaccadic drift is modified by proprioception from the extraocular muscles, but these modifications do not serve to minimize retinal slip or to correct errors in saccade amplitude; and visually mediated adaptation of postsaccadic drift does not require proprioceptive afference from the paretic eye.

Internuclear ophthalmoplegia and contralateral exotropia Nonparalytic pontine exotropia and WEBINO syndrome

To examine whether nonparalytic pontine exotropia, i.e., contralateral exotropia with internuclear ophthalmoplegia (INO), is caused by conjugate deviation by an ipsilateral paramedian pontine reticular formation (PPRF) lesion, we retrospectively reviewed seven patients with this disorder and two with wall-eyed bilateral INO (WEBINO) syndrome. In agreement with a hypothesis that this conjugate deviation is involved, one patient showed a transition from the paralytic to the nonparalytic form as the gaze palsy was resolved. Slowing of saccades toward the lesion was detected in another three patients. Unexpectedly, a milder outward deviation of the eye on the INO side was discovered during eye closure in three patients, implying the participation of a secondary deviation by fixating with the exotropic paretic eye. The presence of abduction nystagmus during fixation with the paretic eye supports this concept. In the two patients with WEBINO syndrome, deprivation of visual fixation with Frenzel goggles and eye closure similarly diminished exotropia, while one eye fixation elicited the marked outward deviation of the other eye with abduction nystagmus. In addition to conjugate deviation, therefore, our results show that secondary deviation induced by over-excitation of contralateral PPRF under fixation with the paretic eye is also involved in the development or aggravation of pontine exotropia.

Vertical muscle transposition augmented with lateral fixation

Introduction: Full vertical rectus muscle transpositions have been shown to be an effective treatment for lateral rectus palsies and type I Duane syndrome. This operation is usually accompanied by mechanical or botulinum toxin treatment of one or both medial rectus muscles. This series evaluates the effect of augmenting the transposed muscles with lateral fixation sutures. Methods: Transposition of the vertical rectus muscles to the lateral rectus muscle was performed in 23 eyes of 21 patients; transposition to the medial rectus muscle was performed in one eye of one of these 21 patients. A lateral fixation suture of 5-0 Dacron polyester filament was placed in the sclera 16 mm posterior to the limbus and adjacent to the lateral rectus muscle, incorporating one fourth of the transposed vertical rectus muscle. Of the 21 patients, five had type I Duane syndrome with a face turn and esotropia in the primary position, seven had a unilateral lateral rectus palsy, two had bilateral lateral rectus palsy, four had an ipsilateral lateral rectus palsy combined with a contralateral lateral rectus paresis (a recess resect procedure was performed on the paretic eye along with the augmented transposition on the paralyzed eye), two had gaze palsies, and one had a unilateral lateral rectus palsy with recurrent esotropia after a transposition procedure performed 16 years previously. Lateral fixation sutures alone were used in the last case listed. Postoperative diplopia-free fields were measured when possible (10 cases). Results: In most cases ( 19 23 eyes), alignment was achieved in the primary position with the use of the augmented transposition procedure alone. On average, 20 degrees of binocular fusion into the abducted field was obtained. No postoperative limitation of adduction in the transposed eye was noted. Among the patients with Duane syndrome, 80% had elimination of the face turn; one patient had 5 degrees of residual face turn.The one patient with previous transposition surgery alone had an 80% (16 PD) reduction of the recurrent esotropia after placement of lateral fixation sutures. After augmented transpositions, induced vertical deviations in the primary position were uncommon ( 4 20 patients) and not greater than 2 PD. Significant lid fissure changes were not seen. Conclusions: The addition of lateral fixation sutures to full vertical rectus muscle transpositions improves the tonic abducting force of the procedure for patients with lateral rectus palsy and type I Duane syndrome without compromising adduction.

The contribution of Alfred K. Graefe to surgical treatment of paretic squint in the second half of the 19th century

Alfred Graefe is one of the three important ophthalmologists of the Graefe family in the nineteenth century, who were engaged scientifically with squint. He dealt with disorders of ocular motility in twenty publications. In: "The indication of operative treatment of paretic eye deviations" Graefe suggested three operative principles: Resection of the paretic muscle, tenotomy of the ipsilateral antagonist and tenotomy of the contralateral synergist. Depending on the amount of the motility disturbance Graefe recommended one or several of these methods. Concerning the vertical muscles Graefe emphasized the importance of parallelism of the retinal meridians. Hence, in the case of superior oblique palsy he favoured a tenotomy of the contralateral inferior rectus.

Some observations on abduction nystagmus in internuclear ophthalmoplegia

The findings in 220 consecutive patients with internuclear ophthalmoplegia (INO) investigated by direct-current electro-oculography (EOG) are reported. Abduction nystagmus is significantly more frequent in patients with severe INO and increases with increasing lateral movements in the direction of the paretic medial rectus muscle. In a series of 12 unselected patients, additional recordings were made immediately after patching the paretic eye, and in six of them also immediately after patching the non-pa-retic eye. Patching the paretic eye was followed by a decreased pulse-step mismatch and a decreased pulse duration causing decreased amplitudes of abduction and adduction saccades in most patients. Patching the non-paretic eye was followed by an increased pulse-step mismatch and an increased pulse duration causing increased amplitudes of abduction and adduction saccades in most patients. The author's findings support the adaptation hypothesis of abduction nystagmus in most patients with INO, and are in accordance with Hering's law of equal innervation. The increased innervation is adjusted to the adduction paresis and generated immediately after onset of the paresis. Abduction nystagmus in INO depends on the medial rectus paresis and presumably is initiated by a visual error signal.