Experimental internuclear ophthalmoplegia.

Abstract

SUMMARY A midline experimental lesion separating the medial longitudinal fasciculi at and below the level of the abducens nuclei without damaging either fasciculus at the level of the nuclei has produced defects of ocular motility resembling those of clinical internuclear ophthalmoplegia. Electromyographic recordings during lateral gaze demonstrate: (1) lack of inhibition of the lateral rectus muscle in the adducting eye, (2) delayed inhibition of the medial rectus muscle in the abducting eye, and (3) occasional evidence of excitation of the medial rectus muscle of the abducting eye probably associated with pupillary constriction. The presumed physiologic mechanisms involved in conjugate gaze movements are discussed in the light of the experimental findings.Internuclear ophthalmoplegia (INO) is the dissociation of ocular movements during horizontal versions, consisting of an underacting medial rectus muscle (in the adducting eye), often accompanied by abducting nystagmus of the fellow eye. The presence of this movement disorder is considered to be pathognomonic of a lesion in the medial longitudinal fasciculus (MLF) in the brainstem. The pathophysiologic mechanism by which the dissociated nystagmus of the abducting eye is produced has remained elusive. Stroud et al. (1973Stroud et al. ( , 1974 proposed that asymmetric convergence is used to drive the weak medial rectus muscle, which secondarily produces the abducting nystagmus on the uninvolved side. More recently, Pola and Robinson (1976) have postulated that a lesion of one MLF would interrupt both ipsilateral excitatory and contralateral inhibitory fibres to the respective medial rectus subnuclei of the third cranial nerve. This postulate would fit well with clinical findings previously reported by Loeffler et al. (1966). In contrast to Stroud et al. these authors believe that the nystagmus of the abducting eye after a contralateral MLF lesion is due to loss of inhibition of the medial rectus activity of that eye. A third hypothesis attributes the nystagmus to interruption of nerve fibre pathways passing to The purpose of this study was to produce an experimental model of inter-nuclear ophthalmoplegia in the primate without damaging the parapontine gaze centres or their subservient ocular motor nuclei. The animals were studied by electromyography in order to gain an understanding of the underlying pathophysiology of INO. MethodsFour male and one female rhesus monkeys of weights ranging from 9 5 to 12-5 lb (4 3 to 5 7 kg) underwent suboccipital craniectomy under barbiturate anaesthesia. In each case the cerebellar vermis overlying the caudal portion of the fourth ventricle was split in the midline to a depth of approximately 1'5 cm. Under magnification the two cerebellar hemispheres were held apart in this region, and a midline cut was made in the floor of the fourth ventricle with a fine knife.A week or more after surgery the animals were studied in a primate chair with and without head restraint. Motion pictures, 8 and 16 mm, were made of the extraocular mo...

Results of extraocular muscle surgery in WEBINO bilateral internuclear ophthalmoplegia patients

“…19,21,22 Electromyographic evidence in monkeys with INO supports the presence of cocontracture of the medial rectus muscles with conjugate gaze. 4,19,21 Others describe an altered inhibitory input to the lateral rectus muscle or an adaptive alteration in the pulse and step signals from the parapontine reticular formation; the defect can be described as a pulse-step mismatch. 2,13,20,22 This latter hypothesis supports the authors' impression that strengthening the medial rectus muscles by resecting the muscles in WEBINO cases alters feedback to the neural integrators and somehow rectifies the pulse-step mismatch that causes the adduction lag and abducting nystagmus.…”

“…19,21 Some authors believe it is influenced by the vergence system. 19,21,22 Electromyographic evidence in monkeys with INO supports the presence of cocontracture of the medial rectus muscles with conjugate gaze. 4,19,21 Others describe an altered inhibitory input to the lateral rectus muscle or an adaptive alteration in the pulse and step signals from the parapontine reticular formation; the defect can be described as a pulse-step mismatch.…”

“…18 Several mechanisms underlying abducting nystagmus have been described. 2,19 These include a secondary response by an overacting lateral rectus muscle caused by limited adduction of its antagonist 2,18,20 or a compensatory response to the adaptive increase in innervation to the adducting eye. 19,21 Some authors believe it is influenced by the vergence system.…”

“…2,19 These include a secondary response by an overacting lateral rectus muscle caused by limited adduction of its antagonist 2,18,20 or a compensatory response to the adaptive increase in innervation to the adducting eye. 19,21 Some authors believe it is influenced by the vergence system. 19,21,22 Electromyographic evidence in monkeys with INO supports the presence of cocontracture of the medial rectus muscles with conjugate gaze.…”

Abduction paresis with rostral pontine and/or mesencephalic lesions: Pseudoabducens palsy and its relation to the so-called posterior internuclear ophthalmoplegia of Lutz

“…Inhibition of antagonistic eye muscles may cause paresis of vertical and horizontal eye movements despite normal excitation of agonistic eye muscles [23,71-73]. Impaired medial rectus inhibition may occur with midbrain lesions as documented in a patient with an unilateral convergence paresis as a clinical sign of an ipsilateral midbrain dysfunction, who also had an ipsilateral abduction paresis with grossly impaired medial rectus inhibition and normal lateral rectus excitation [23].…”