Head Tilt Test Research Articles

Clinical features and surgical outcomes of isolated inferior rectus muscle paralysis

Purpose: To describe clinical features of patients with unilateral isolated inferior rectus (IR) muscle paralysis along with type of surgical treatment and results after surgery.Methods: Patients diagnosed with unilateral isolated IR muscle palsy between 2009 and 2012 that required surgical treatment were included in the study. Diagnosis of IR muscle palsy was done by hypertropia with the largest angle in depression and abduction and inferior rectus muscle underaction.Results: Twenty-two patients remained in the study; 17 patients (77.3%) had left eye involvement. IR muscle paresis was traumatic in 12 patients (54.5%), congenital in 9 patients (40.9%), and vascular in 1 patient (4.5%). Limitation of duction in the gaze of IR muscle was −2 to −3 in all cases. 3 patients, paradoxically, had contralateral compensatory head tilt (compensatory head tilt to the opposite side of IR muscle palsy). Intraoperatively, we did not detect any gross abnormalities in the IR muscles. The surgical plan at the first operation was IR muscle resection alone in 13 patients (59.1%). At the last follow-up visit, 15 patients (68%) had no deviations in primary position and downgaze. Three cases needed reoperation.Conclusion: The presence of both ipsilateral and contralateral compensatory head postures in our patients showed that three-step or head-tilt test is not helpful in the diagnosis of IR muscle palsy. In comparison with other studies, more patients in our study were treated with IR muscle resection alone. Also, our reoperation rate was lower than other studies. Absence of gross abnormality in the IR muscles at the operation and partial nature of the paresis may explain these good results. Thus, a considerable number of IR muscle palsy cases with the above characteristics may be treated successfully by one muscle surgery (IR muscle resection).

The Sensitivity of the Bielschowsky Head-Tilt Test in Diagnosing Acquired Bilateral Superior Oblique Paresis

To determine the sensitivity of the Bielschowsky head-tilt test and other commonly used criteria in identifying patients with true bilateral superior oblique paresis. A retrospective chart review was performed to identify patients seen between 1978 and 2009 who were diagnosed with acquired bilateral superior oblique paresis. All patients had a confirmed history of head trauma or brain surgery with altered consciousness followed by symptomatic diplopia. Bilateral superior oblique paresis was defined and diagnosed by the above history, including the presence of greater extorsion in downgaze than upgaze on Lancaster red-green testing, a V-pattern strabismus, and bilateral fundus extorsion. We analyzed findings of the Bielschowsky head-tilt test, the Parks 3-step test, and reversal of the hypertropia from straight-ahead gaze to the other 8 diagnostic positions of gaze to determine these tests' sensitivity in identifying true bilateral superior oblique paresis. Twenty-five patients were identified with the diagnosis of true bilateral superior oblique paresis. The Bielschowsky head-tilt test had a 40% sensitivity, the Parks 3-step test had a sensitivity of 24%, and reversal of the hypertropia had a sensitivity of 60% in making the diagnosis of true bilateral superior oblique paresis. What previously has been described as masked bilateral superior oblique paresis simply may be a reflection of inherent poor sensitivity of the Bielschowsky head-tilt test, the Parks 3-step test, and reversal of the hypertropia in diagnosing bilateral superior oblique paresis. Hence, none of these tests should be relied on exclusively to make this diagnosis.

The influence of body position on Bielschowsky's test.

To investigate the veracity of Jampolsky's statement that Bielschowsky's head tilt test is inverted if performed with the patient in the upside-down position and to interpret its neuromuscular mechanism. We present a series of 10 patients selected from a referred sample who were diagnosed with superior oblique paresis. Hypertropia was measured in the primary position, with the head erect and tilted toward both shoulders with the patient in the erect, supine, and upside-down positions. The last position was achieved by hanging the patient upside-down. As expected, our results showed the veracity of Jampolsky's statement. The forced head tilt difference was inverted or significantly decreased when the test was performed in the upside-down position. Moreover, in all patients, Bielschowsky's phenomenon was neutralized in the supine body position, in which hypertropia with the head erect tended to vanish. In 3 patients, it disappeared completely. This study showed that, in patients with superior oblique paresis, differences in the extent of hypertropia in Bielschowsky's test tended to vanish when the test was performed with the patient in the supine position and invert when it was performed with the patient in the upside-down position.

Computer-assisted diagnosis of monocular elevation deficiency

Our aim is to demonstrate the benefits of using a computer model to support the clinical diagnosis of complex eye motility disorders. For diagnosis and differential diagnosis we compared the clinical data of a patient with suspected monocular elevation deficiency (MED) and the corresponding computer simulation with the simulations of rectus superior palsy, vertical Duane miswiring syndrome and two simulations of asymmetric gaze palsy. We used our biomechanical eye model SEE-KID for the computer simulations, which is partly based on ideas and concepts of the software system Orbit™ by Joel Miller. A young patient with the clinical characteristics of congenital MED, unilateral limitation of up-gaze above midline, with accompanying ptosis on the affected right side, mild head posture, chin-up position, partial binocular functions and Bell's phenomenon was examined. Pupillary situation, cover test, version and duction movements, saccadic test, Parks-Bielschowsky phenomenon and head tilt test, stereopsis test, Bagolini striated lens test and forced duction test were assessed. Up to the age of 5 years we used the prism cover test in the nine main gaze positions; later we switched to the Hess-Lancaster test for analyzing deviations. We also used our computer model for evaluating the diagnosis and for differential diagnosis of our patient. The simulation results from the SEE-KID model support the diagnosis of supranuclear MED, which can be achieved in the model by varying central innervations, contrary to the modification of muscle forces in the simulation of a rectus superior palsy. It is necessary to distinguish between supranuclear, nuclear, interstitial or peripheral lesions with regard to monocular elevation deficit. Simulations of patients with similar pathologies in a way that the simulations correspond to the patient-measured values support (beside the clinical signs) the diagnosis of supranuclear or infranuclear lesions.

Sudden syncopal attack after postobstructed diuresis under combined spinal epidural anesthesia

Micturition is clinically well-known as a factor that may cause hypotension, bradycardia, and if severe, syncope. However, the mechanism of syncope during micturition is not completely understood. Vasodilatation, bradycardia, and reflex car diovascular depression are all called by various terms including vasovagal syncope, Bazold-Jarisch reflex, and neurocardiogenic syncope [1]. The neurally-mediated syncope includes true and situational syncope that can take place in various situations such as blood loss, cough, sneeze, micturition and lifting up a heavy load. A case of a 71 year-old man under combined spinal epidural anesthesia for total knee replacement, in which the operation were performed without knowing that a Foley catheter installed had been obstructed, and severe bradycardia, hypotension, and loss of consciousness occurred immediately after moving the pa tient to the recovery room following micturition were described. The patient had a history of syncope. Preoperative cardiac test was normal. At the operation room, heart rate and blood pressure were 70 /min and 170/90 mmHg. Beginning with the sufficient administration of fluid, the regional anesthesia was performed and the sensory block was verified up to the T4 der matome. A forced air warmer was used to maintain the body temperature. At the end of operation, 8 ml of 0.15% levobupivacaine was injected through the epidural catheter, and then a mixture of anesthetics was continuously injected. Intraoperative systolic blood pressure were ranged from 110 to 190 mmHg, diastolic pressure 65 to 105 mmHg, heart rate 52 to 70 /min, and estimated blood loss was approximately 500 ml. Although the total amount of fluid was approximately 1,000 ml, no urine out put was observed. Just before leaving the operation room, it was found that the tip of the Foley catheter was obstructed. When the catheter was opened, about 700 ml of urine was discharged. At that time, the vital signs were normal and consciousness clear. Finding that the sensory block level had come down to the T12 dermatome, the patient was moved to the recovery room. Immediately after arriving at the recovery room, the heart rate was drastically reduced from 70 /min to 30 /min or below, the blood pressure was 50/30 mmHg, and consciousness was lost. Promptly, 0.5 mg of atropine sulfate and 10 mg of ephedrine were administered, and the patient-controlled epidural anal gesia (PCEA) was stopped. Following the treatment, the heart rate recovered to 60 /min and the blood pressure to 110/80 mmHg, and subsequently, the consciousness of the patient was recovered. While the patient remained in the recovery room, no abnormal findings were observed. Micturition syncope was con firmed that head-tilt test done after the operation was positive. The main causes of consciousness loss when awakening from anesthesia include metabolic anomalies such as hypoglycemia, hyponatremia, hypoxia and severe cardiovascular collapse. However, based on the fact that the patient had no findings of cardiac abnormalities, the patient in this case might have experienced reflex micturition syncope. Micturition syncope is one type of situational syncope that occurs due to neural mediation, and usually occurs in healthy men after alcohol hyperingestion [2]. Sumiyoshi et al. [2] mentioned sleeping under warm blankets and administration of a vasodilator can be factors that cause a reduction in the peripheral arterial blood resistance in the lower extremities and reported that the Valsalva maneuver is a factor

Vertical synergistic divergence: To be or not to be, that is the quintessential question

Dear Editor, We do not concur and reiterate that clinical picture cascades down consummately to a hallmark bilateral Brown Syndrome (BBS) presentation.[1–3] Documentation of forced duction test results, ductions, measurements of deviation in prism diopters in nine cardinal gazes with either eye fixing, fundus photographs for torsion, in tandem with findings on neuroimaging/surgical exploration and surgical outcomes would be seminal in sifting the maze, but reports skirt all of that.[1,3] Full bilateral elevation in abduction with gross bilateral limitation of elevation in adduction with down-shoot of adducted eye consistently in side, up and down gazes, with globes nailed in down position and negative head tilt test results, unequivocally cohere to a diagnosis of BBS. An alternative diagnosis can only be entertained in the presence of negative exaggerated forced duction tests, which were not done.[1,3] The report is cryptic as to whether one or both eyes are having 3rd nerve palsy, the extent of involvement, recovery and aberrant innervation, if any present.[1,3] Either eye is dipping in adduction, and the left eye will also dip if the right eye is allowed to fixate and elevate in slight abduction.[3] No light is shed on the plausible location/pathway/mechanism/causation of the expounded synergistic vertical divergence involving only the right eye, in view of the facts that up gaze fibers freely cross in the posterior commissure, whereas down gaze fibers are uncrossed, and the superior rectus (SR) receives crossed innervation through the opposite subnucleus. It follows that proposed synergistic divergence/convergence cannot be conflated via up gaze fibers at the supranuclear level. Neither can it be conflated at the nuclear/infranuclear level. Superior oblique (SO) overactions (not known whether it is primary or secondary) as propounded[1,3] do not produce globes nailed-in down gaze in adduction. In 3rd nerve palsy, as the depressor action of SO is compromised, they instead cause intorsion. Thus, bilateral overdepression in adduction sans intorsion cannot be ascribed to bilaterally overacting SOs due to (right) 3rd nerve palsy as surmised.[1,3] There is nothing proximate to “no significant ocular torsion,” as torsional position of the globe is a state and, therefore, it may only be normal or abnormal.[3] Further, the downshoot is only in adduction, not in abduction, and therefore cannot be explained by aberrant innervation of SR as SRs act in abduction.[1,3] The SR has to be paretic to undergo aberrant innervation; the report does not state so[3] and resultant cocontraction of vertical recti on up gaze will engender convergence retraction instead. Overaction of SOs, downshoot and widening of palpebral fissure in adduction is known in Brown Syndromes, and is the likely cause of asymmetrical underdepression of both eyes in abduction, the hallmark finding militating against BBS as per the report.[1] No perfidy will be committed anyway if congenital 3rd nerve palsy and BBS coexist. In the absence of irrefutable documentary evidence on forced duction tests against BBS and nine gaze deviations fixing with either eye, no meaningful conclusions can be drawn about muscle overactions/underactions and any abstruse synergistic vertical divergence/convergence. Thus, the proposed esoteric expositions about misinnervation and synergistic divergence are bereft of any neuroanatomical substrate at supranuclear/nuclear/infranuclear levels, and are overtly speculative, emanating from a skewed interpretation of a hallmark congenital BBS presentation.[1,3]

Diplopia Due to Skew Deviation Following Neurotologic Procedures

To describe and characterize diplopia resulting from skew deviation after cerebellopontine angle (CPA) surgery and labyrinthectomy. Retrospective case series of 4 patients who developed vertical diplopia from skew deviation after resection of tumors in the CPA or labyrinthectomy Complete neuro-opthalmologic examination including opticokinetic testing, confrontational visual field assessment, color plate, pupillary reflex, slit lamp examination, and head tilt test. Four patients with residual hearing preoperatively developed skew deviation immediately after surgical intervention, including translabyrinthine (n = 1) and retrosigmoid (n = 2) approaches to the CPA and labyrinthectomy (n = 1). Neuro-ophthalmologic examination demonstrated intact extraocular movements, and 2- to 14-mm prism diopter hypertropia on both primary gaze and head tilt testing. In all cases, skew deviation resolved spontaneously with normalization of the neuro-ophthalmologic examination within 10 weeks. Patients undergoing CPA surgery or labyrinthectomy can develop postoperative diplopia due to skew deviation as a consequence of acute vestibular deafferentation. Patients with significant hearing preoperatively, a probable marker for residual vestibular function, may be especially at risk for developing skew deviation postoperatively.

Positive Bielschowsky head tilt test in cases of comitant exotropia

Purpose: We aimed to study the incidence and factors influencing positive Bielschowsky head tilt test (BHTT) in cases of comitant exotropia.

Anterior Transposition of the Inferior Oblique Muscle in the Treatment of Unilateral Superior Oblique Palsy

To determine whether unilateral inferior oblique anterior transposition alone could be an effective procedure for treating superior oblique palsy with inferior oblique overaction. The records of 38 patients who underwent unilateral inferior oblique anterior transposition for unilateral superior oblique palsy with inferior oblique overaction were evaluated. A comprehensive ocular examination including best-corrected visual acuity measurements, ductions, versions, and deviations at near and distance, head tilt test, abnormal head position, dilated fundus examination, and Titmus test was performed prior to and after surgery. The mean patient age was 29 years, the mean follow-up was 32 months, the mean preoperative hypertropia in primary position was 14.29 ± 7.7 prism diopters (PD), and the mean inferior oblique overaction was 3.63 ± 0.67. Anterior transposition of the inferior oblique muscle was effective across a wide range of preoperative primary position hypertropia (4 to 35 PD) with a mean reduction in postoperative hypertropia of 12 PD. Inferior oblique overaction was reduced in all patients. No patient demonstrated postoperative primary position hypotropia. Surgery improved stereoacuity nearly two units using the Titmus stereoacuity scale. Anterior transposition of the inferior oblique muscle is effective in correcting inferior oblique overaction and primary position hypertropia in the treatment of unilateral superior oblique palsy.

Horizontal Misalignment in Patients with Unilateral Superior Oblique Palsy

To determine the frequency and distribution of horizontal misalignment in patients with unilateral superior oblique palsy (SOP) and to determine the indications for combining horizontal with vertical strabismus surgery. Patients included in the study had a vertical heterophoria or tropia that fit Parks three-step test for SOP and had no previous strabismus surgery or other ocular motility disturbance. Ocular motility and alignment were recorded. Outcomes between patients who had vertical surgery alone and those who had combined vertical and horizontal surgery were compared using the Student's t test. Of 205 patients, 121 (59.0%) had a horizontal misalignment in addition to vertical strabismus. Ninety-six patients (46.8%) required strabismus surgery. Of these, 29 had 8 prism diopters (PD) or more horizontal deviation. Twenty-two had vertical combined with horizontal surgery (V+H group). Although their initial deviation was greater, these patients had better surgical outcomes than patients who had vertical surgery alone (V group). The V+H group had a final mean horizontal deviation of 2.18 PD compared with 6.85 PD in the V group (P < .01). Postoperative vertical alignment in the V+H group was also superior with a final mean vertical deviation of 3.7 versus 6.8 PD for the V group (P = .12). These results indicate that horizontal misalignment is common in patients with SOP. Patients with 8 PD or more horizontal deviation benefited from surgical correction of the horizontal deviation in addition to the vertical surgery.

A Case of Congenital Absence of the Superior Oblique Muscle Treated With Anterior and Nasal Transposition of the Inferior Oblique Muscle

Purpose: To report a patient with absence of the superior oblique (SO) muscle of the left eye, who showed improvement after anterior and nasal transposition of the inferior oblique muscle for left hyperdeviation and right head tilt. Case summary: A two-year-old boy presented with hypertropia of the left eye and right head tilt. Alternate prism-cover test in the primary position demonstrated 18 prism diopters (PD) of left hypertropia, which increased to 35 PD in the left head tilt position. A version test demonstrated overaction of the left inferior oblique muscle and underaction of the left superior oblique muscle. As an orbit CT scan showed absence of the SO muscle, the patient was diagnosed with congenital absence of SO and left anterior and nasal transposition of the inferior oblique muscle was performed. Three weeks after surgery, the patient presented with orthotropia at distant and near. The version test revealed normal oblique muscles. There was no vertical deviation shown on the Bielschowsky head tilt test. The abnormal head posturing was no longer observed. Conclusions: The authorsreport a patient manifesting abnormal head posture and hypertropia, diagnosed with absence of SO muscle, which was successfully corrected using anterior and nasal transposition of the inferior oblique muscle.

Right trochlear and left oculomotor palsies

In this patient, a left paramedian midbrain infarction, as shown by the restricted diffusion and T2 hyperintensity on MRI, resulted in an ipsilateral (left) oculomotor palsy and contralateral (right) trochlear palsy. The presence of right hypertropia and worse diplopia on left lateral gaze and on tilting the head to the right is consistent with right superior oblique weakness due to right trochlear palsy. The Hess chart, performed 2 weeks after presentation, demonstrates under action of the right superior oblique, and the similarity in right and left eye ‘‘box size” suggests a degree of compensation. The mild ipsilateral ataxia may have been due to involvement of fibres of the superior cerebellar peduncule, caudal to their decussation. Although midbrain infarction can lead to vertical ocular misalignment or skew deviation, this would be expected to result in contralateral eye hypodeviation – in this patient a right eye hypodeviation, rather than the observed right hypertropia. Furthermore, the head tilt test is usually negative in skew deviation, unless there is a spread of comitance. Intorsion of the uppermost and extorsion of the lowermost eye is expected, whereas in trochlear palsy, the uppermost eye is typically extorted. In the presence of an oculomotor palsy, a concomitant ipsilateral trochlear lesion can be identified if intorsion is impaired or absent; however, a concomitant contralateral trochlear lesion is difficult to discern as both lesions result in vertical misalignment, with the ipsilateral eye showing hypodeviation and the contralateral eye, hyperdeviation. The combination of left oculomotor and right trochlear palsies is puzzling until midbrain anatomy is recalled. Oculomotor fibres project ipsilaterally, but trochlear fibres decussate within the medullary vellum to innervate the contralateral superior oblique (Fig. 1). Similar presentations have been reported after dorsal paramedian infarction including ipsilateral internuclear ophthalmoplegia with contralateral trochlear palsy, ipsilateral Horner’s

Intracranial dermoid cyst presenting as an isolated fourth nerve palsy

Sirs: A 68-year-old man presented with 4 months of painless vertical diplopia on left gaze. Examination revealed a right fourth nerve palsy, which was confirmed by the Bielschowsky head tilt test and demonstrated on the Hess chart. There was a normal vertical fusion range, no corrective head posture or further neurological abnormality detected. Systemic examination found borderline hypertension (145/ 91 mmHg) and a normal fasting glucose. He denied any history of trauma. His only medical history was treatment for dyslipidemia. MRI scan revealed a 1–2 cm strongly hyperintense welldefined rounded mass on T1and T2-weighted images (Figs. 1, 2). The lipid-containing mass was applied to the dorsum of the tectum and left of the midline. Its appearance was hypointense on the fat-suppressed pulse sequence images (Fig. 3). These findings are characteristic of dermoid cysts. On consultation with the neurosurgical team, the decision was made to observe this intracranial dermoid cyst. At 16 months follow-up there has been no clinical progression. He remains under neuro-ophthalmic review. A space-occupying lesion is an uncommon cause of any isolated pupil sparing third, fourth or sixth cranial nerve palsy. A presumed microvascular palsy is a common aetiology and the majority of these resolve within 6 months. It has been recommended that sudden onset and isolated cranial nerve palsy can be observed, using neuroimaging if there is an insidious onset, progression (i.e. is no longer isolated) or non-resolution [1, 2]. In the case presented the onset of vertical diplopia was over the period of 4 months, and hence due to the insidious onset was scanned urgently. The radiological differential diagnosis of the hyperintense mass on T1-weighted images (Fig. 2) would include haematomas, aneurysms and lipid rich masses. High signal intensity on T1-weighted images and a hypointense T2 appearance, in this location, would be demonstrated by a dermoid cyst, a thrombosed berry aneurysm, an intracranial tetratoma or a quadrigeminal cistern lipoma. Fat suppression and inversion recovery sequences are therefore helpful to narrow the differential diagnosis and prove the mass is lipid containing (Fig. 3) [3]. Further image characteristics, such as chemical shift artefact, can differentiate between a dermoid cyst and a lipoma. Dermoids are typically well-circumscribed lesions that can contain lipid metabolites, hair and hair follicles, calcifications, sebaceous and sweat glands and decomposed epithelial cells containing cholesterol and keratin [4]. The composition determines their appearance: a typical high signal intensity on T1-weighted images, due to the high fat content; and a heterogeneous signal on T2-weighted sequences, due to the mixed content of the lesion [3]. Dermoid cysts are rare, congenital, non-neoplastic lesions that account for 0.7–1.8% of all intracranial tumours, with the posterior cranial fossa being the commonest location [4]. Supratentorial lesions have been reported presenting as an isolated third nerve palsy and other symptoms, with infratentorial dermoids causing sixth nerve palsy and cerebellar signs [5]. To our knowledge, an intracranial dermoid presenting as an isolated trochlear nerve palsy has not been described. R. Tailor S. P. Mollan (&) M. A. Burdon Birmingham and Midland Eye Centre, City Hospital, Dudley Road, Birmingham B18 7QH, UK e-mail: soozmollan@doctors.org.uk

The Clinical Characteristics of Superior Oblique Palsy Associated With Intermittent Exotropia

Purpose: The goal of this study was to determine the clinical characteristics of patients with intermittent exotropia (IXT) associated with hypertropia. Methods: This study recruited 268 hospital patients with IXT associated with hypertropia. After taking history, measuring the angle of deviation, conducting an ocular motor examination, performing a Bielschowsky head tilt test and taking a fundus photograph, the clinical characteristics of 23 patients diagnosed with superior oblique palsy (SOP) were investigated. Results: Twenty-three patients (8.6%) of the 268 subjects with IXT associated with hypertropia were diagnosed with SOP. The average angle of exodeviation was 17.13.8PD and the angle of hypertropia at primary position was 12.95.9PD. Excyclotorsion of an eyeball was observed in 19 patients (82.6%), the Bielschowsky head tilt test was positive in all patients, and head tilt or face turn was found in 12 (52.2%) patients. All subjects had inferior oblique overaction, and 20 (86.9%) had superior oblique underaction. Operations to weaken the inferior oblique muscle of the paralytic eye and for horizontal muscles were conducted at the same time. The angle of exodeviation and the angle of hypertropia were, on average, 1.83.6PD and 2.42.2PD, respectively, 6 months after the operation. Conclusions: When patients with intermittent exotropia have hypertropia, the possibility of SOP should be considered. SOP can be detected by determining a history of head tilt and conducting a Bielschowsky head tilt test. Surgical treatment for SOP is advised.

Clinico-Radiologic Findings of Entrapped Inferior Oblique Muscle in a Fracture of the Orbital Floor

A 51-year old man presented with vertical and torsional diplopia after reduction of a blowout fracture at another hospital one year ago. He had no anormalies of head position and 14 prism diopters (PD) right hypertropia (RHT) in the primary position. In upgaze no vertical deviation was found, and hyperdeviation on downgaze was 35PD. Bielschowsky head tilt test showed a negative response. Distinct superior oblique (SO) and inferior rectus (IR) underaction of the right eye was noted but IO overaction was mild on the ocular version test. Double Maddox rod test (DMRT) revealed 10-degree extorsion, but fundus extorsion was minimal in the right eye.Thin-section coronal CT scan showed that there was no fracture line on the anterior orbital floor, but a fracture remained on the posterior orbital floor. Also, the anterior part of the right inferior oblique muscle was vertically reoriented and the medial portion of the inferior oblique muscle was not traced on the coronal CT scan. The patient underwent 14 mm right IO recession and 3 mm right IR resection. One month after the surgery, his vertical and torsional diplopia were eliminated in the primary position.

The Effect of Acute Superior Oblique Palsy on Torsional Optokinetic Nystagmus in Monkeys

To investigate the effects of acquired superior oblique palsy (SOP) and corrective strabismus surgery on torsional optokinetic nystagmus (tOKN) in monkeys. The trochlear nerve was severed intracranially in two rhesus monkeys (M1 and M2). For each monkey, more than 4 months after the SOP, the ipsilateral inferior oblique muscle was denervated and extirpated. For M2, 4 months later, the contralateral inferior rectus muscle was recessed by 2 mm. tOKN was elicited during monocular viewing of a rotating stimulus that was rear projected onto a screen 43.5 cm in front of the animal. Angular rotation of the stimulus about the center was 40 deg/s clockwise or counterclockwise. The main findings after trochlear nerve sectioning were (1) the amplitude and peak velocity of torsional quick and slow phases of the paretic eye was less than that in the normal eye for both intorsion and extorsion, and (2) the vertical motion of the paretic eye increased during both torsional slow and quick phases. After corrective inferior oblique surgery, both of these effects were even greater. Acquired SOP and corrective inferior oblique-weakening surgery create characteristic patterns of change in tOKN that reflect alterations in the dynamic properties of the extraocular muscles involved in eye torsion. tOKN also provides information complementary to that provided by the traditional Bielschowsky head-tilt test and potentially can help distinguish among different causes of vertical ocular misalignment.

Dissociated vertical deviation in patients with intermittent exotropia

To determine whether the age of strabismus onset and the degree of stereopsis are related to the development of dissociated vertical deviation (DVD) in patients with intermittent exotropia and to describe the characteristics of DVD in patients with intermittent exotropia and DVD. Retrospective record review of patients with (1) intermittent exotropia with DVD; (2) infantile esotropia with DVD; and (3) intermittent exotropia without DVD. Age of strabismus onset, stereopsis, strabismus measurements, and the response of DVD to the Bielschowsky head-tilt test were compared among the three groups. Fifty-two children with intermittent exotropia and DVD were identified. In patients with intermittent exotropia with DVD and intermittent exotropia without DVD group, the mean age of strabismus onset was 12.7 months and 28.9 months, respectively (p = 0.03), and mean stereopsis was 147 arcsec and 65 arcsec (p = 0.02). In patients with intermittent exotropia with DVD and infantile esotropia with DVD, the mean amount of DVD was 9.7(Delta) and 17.2(Delta), respectively (p < 0.01). Bielschowsky head-tilt test showed an increase of DVD on ipsilateral head tilt in 91% and 63.3%, respectively. Intermittent exotropia with DVD is characterized by earlier onset of strabismus and worse stereopsis, suggesting that these factors may be related to the development of DVD in patients with intermittent exotropia. Unlike DVD in infantile esotropia, DVD in intermittent exotropia was smaller in amount and demonstrated a more uniform response to the Bielschowsky head-tilt test.

Displacement of the rectus muscle pulleys simulating superior oblique palsy

To investigate the structural basis of three cases of apparent superior oblique (SO) palsy caused by extraocular muscle (EOM) pulley heterotopy. Three subjects were diagnosed as having decompensated idiopathic left SO palsy on the basis of misalignment in diagnostic gaze positions, response to the head tilt test, and results of the Hess screen test. Magnetic resonance imaging of the orbits in coronal planes was used to determine SO muscle size and contractility and to define the rectus EOM pulley locations. Orbit 1.8 computer simulation was performed for each subject by using measured rectus pulley locations. Simulated binocular alignment was compared with the measurements. The maximal SO cross sections of both eyes of each subject were similar, and exhibited similar contractile thickening from supraduction to infraduction. The superior rectus muscle pulleys in three eyes exhibited significant temporal displacement, while the lateral rectus muscle pulleys in five eyes and the medial rectus muscle pulleys in two eyes were displaced significantly inferiorly compared with published norms. Simulations based on observed pulley position abnormalities alone predicted measured Hess screen data better than did simulations incorporating SO weakness, either alone or combined with other structural abnormalities. Heterotopy of the rectus EOM pulleys may be associated with cyclovertical strabismus that simulates SO palsy.

Computer-Based Simulation of the Bielschowsky Head-Tilt Test Using the SEE++ Software System

Introduction: Latest measurements of the vestibulo-ocular reflex (VOR) allowed the integration of the simulation of the Bielschowsky head-tilt test (BHTT) into the SEE++ software system. SEE++ realizes a biomechanical model of the human eye in order to simulate eye motility disorders and strabismus surgeries. With the addition of the BHTT it can now also be used for differential-diagnostic simulations of complex disorders (e.g., superior oblique palsies). Methods: In order to simulate the BHTT in SEE++, the user can freely choose the desired head-tilt angle from −45° to +45°. The chosen angle is shown in the 3D view with a human body model and is also used in the calculation of the Hess-Lancaster test. Results: The integration of the BHTT offers an additional improvement of the possibilities for simulating eye motility disorders. Moreover, SEE++ allows the creation of a video of the “virtual patient” while tilting the head from one side to the other, which shows dynamic changes in the simulated Hess-diagrams. Discussion: Comparisons of simulation results with patient-measured data showed a good correlation between the simulated and the measured data. Further comparisons with patient data are planned.

A Case of Congenital Inferior Oblique Palsy

Purpose: Paresis of the inferior oblique is the least likely to result in paralysis. We report a patient without a history of trauma successfully treated using contralateral IO recession and SR recession. Case summary: A 25-year-old male patient presented to us with an extended history of abnormal head posture, manifested by a marked habitual left head tilt with a face turn to the right. A cover test in the primary position demonstrated 15 prism diopter right hypertropia, which increased to 25 prism diopter right hypertropia in right gaze and 20 prism diopter right hypertropia in right head tilt. The patient was diagnosed with IO palsy, and a right IO recession was performed. Results: Following the IO recession, head tilt was completely resolved and face turn to the right was slightly resolved. Cover test in the primary position demonstrated 12 prism diopter right hypertropia, which increased to 20 prism diopter right hypertropia in right gaze. A head tilt test demonstrated a symmetrical 12 prism diopter right hypertropia. We performed a right SR recession to decrease face turn and hypertropia in the primary position. Conclusions: We report a patient manifesting abnormal head posture diagnosed with IO palsy, which was successfully treated using contralateral IO recession and SR recession.