Authored by Ayse Gul Kocak ALTINTAS*
Abstract
Trochlear nerve palsy is the most common palsy among the other cranial nerve palsies. It causes superior oblique muscle palsy which presents with diplopia and the compensatory head position. Several diverse surgical alternatives are available for both congenital and acquired, superior oblique palsy. Each patient should be extensively evaluated to perform a correct operation with a high success rate. In this review etiologic factors, incidence, clinical findings and different treatment methods of superior oblique muscle palsy is presented.
Introduction
Trochlear nerve palsy (4th cranial nerve) is one of the most frequent palsies among the other cranial nerve palsy. In clinical practice, it presents with Superior oblique muscle palsy (SOP), which is the common cause of vertical and torsional strabismus. In this review etiology, incidence, diagnostic methods, and treatment alternatives with success rates of the SOP are evaluated [1-3].
Incidence
Trochlear nerve (4th cranial nerve) palsy, which innervates the superior oblique (SO) muscle, is considered to be the most common cause of cyclovertical strabismus [1-4] SOP may be congenital or acquired. Helveston et al. [2] observerd that more than 75% of the SOP cases were congenital in their series. Tollefson et al. [3] found that the annual incidence of SOP was 3.4 per 100,000 children younger than 19 years of age. But Martinez‐Thompson et al. [3] reported the annual incidence of adult‐onset SOP to be 6.3 cases per100,000 people in their epidemiological study. The presents of SOP in children is equal by gender but significantly higher in men than women in the adult age group [1-6].
Etiology of Trochlear Never Palsy
The most acquired trochlear nerve palsy develops secondary to trauma because the trochlear nerve is one of the most prolonged and unprotected cranial nerves. The trochlear nerve can be compromised anywhere along its long course from the dorsal midbrain to the SO muscle, mainly traversing intracranial structures, including the rigid tentorium cerebelli and cavernous sinus [1,5]. Vascular malformation, infarction such as cavernous sinus thrombosis, orbital or intracranial inflammation, infection or tumors, iatrogenic factors such as complicating orbital, sinus, or neurologic surgery cause acquired trochlear nerve or SOP [5- 7]. The tendon of muscle may also suffer injuries such as blunt or sharp orbital traumas [1-6,7].
The leading causes of congenital trochlear nerve palsies include hypoplasia of the trochlear nerve itself or its nucleus, anatomical defects, or absence of either trochlea or the superior oblique tendon. Increased laxity, extremely elongation of SO tendon and its insertion anomalies on the sclera may mimic the trochlear nerve palsies [1,6,7].
Clinical Presentation: Diplopia and Abnormal Head Position
Clinical presentation of trochlear nerve palsy is hypertropia, due to decreased depression force and excyclotorsion, caused by paralysis of the anterior fibers of the SO muscle in the eye of the affected side. This vertical and torsional binocular misalignment causes diplopia as the main clinical symptom of SOP. To cope with vertical and torsional diplopia and regain binocular single vision, the patient adopts a compensatory abnormal head position (AHP); by this way, the eyes were placed in a particular field of gaze. The head is generally tilted towards the opposite shoulder from the hypertrophic eye, to minimize torsional diplopia due to insufficient incyclotorsion of SO, and the chin lowered to decrease the vertical deviation. In congenital SOP, the patient usually presents with an AHP; children an unable to realized diplopia because the young developing brain suppresses central perception from the effected, not aligned eye. Adults with acquired SOP complained about vertical and torsional diplopia mainly in reading position, and to compensate this double vision, an AHP was spontaneously developed [5,7-9].
Longstanding, AHP in children can cause persistent and significant contracture of the sternocleidomastoid muscle, ocular torticollis, and secondary facial asymmetry. Clinical features of congenital SOP included ipsilateral hypertropia, head tilt to opposed shoulder, and facial asymmetry [7,8]. The estimated prevalence of childhood torticollis is 1.3% with different etiology. SOP is the most common cause among the 22.6% of non-orthopedic causes of torticollis [9-10]. Kushner reported that incomitant cyclovertical strabismus such as SOP, was the most frequent ocular etiology (62.7%) of torticollis [11]. Head tilt due to trochlear nerve palsy can be objectively measured by using a goniometer, arc perimeter, or surgical protractor with graded markings [12].
Diagnosis of Trochlear Nerve Palsy
Trochlear nerve palsy is present with incomitant strabismus in which the vertical deviation varies in magnitude with different gaze positions relative to the head. The Parks-Bielschowsky threestep test is the gold standard for the diagnosis of cyclovertical strabismus, especially for acute, unilateral SOP.
Parks‐Bielschowsky three‐step test consists of 1) ipsilateral hypertropia in central gaze 2) increased magnitude of hypertropia in contralateral than ipsilateral gaze due to unopposed activity of the palsied SO muscle’s antagonist, the inferior oblique, that increases hypertropia in adduction. 3) greater hypertropia in the head is tilted towards the affected eye than the contralesional side. When the head is tilted towards the shoulder to the affected eye, deficit incyclotorsion from the palsied superior oblique compensated by hyperactivity of ipsilateral superior rectus as the other muscle has incycloduction effect. The hyperactivity of the ipsilateral superior rectus causes the increased magnitude of hypertropia also [13-15].
In the bilateral SOP, hypertropia alternates with both gaze position and head tilt, such as the right eye are hypertrophic in the contralateral side gaze, the left gaze while the left eye is hypertrophic in right gaze. In contrast, the right eye is hypertrophic on the same side the; right head tilt and left eye are hypertrophic on the left head tilt. The degree of excyclotorsion is higher in bilateral SOP than in unilateral cases [15-17].
High-resolution MRI studies of superior oblique structure and contractility demonstrate that Parks‐Bielschowsky three‐step test is only about 70% sensitive and 50% specific [17]. Magnetic resonance imaging (MRI) is an important diagnostic tool for both confirm the clinical diagnosis of trochlear nerve palsy and evaluating the its etiology. After extraocular nerve palsy, neurogenic atrophy occurs rapidly in corresponding denervated muscles. It has been reported by several investigations that superior oblique cross-sectional area significantly decreased after SOP developed. [18-19]. Manchandia and Demer observed that the superior oblique muscle cross-sectional area was decreased to 52% in the SOP side, comparing to the normal contralesional side [17].
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