Motor Excitation and Inhibition In Internuclear Palsy

Loeffler, John D.; Hoyt, William F.; Slatt, Bernard J.

doi:10.1001/archneur.1966.00470180104012

Cited by 27 publications

(9 citation statements)

References 13 publications

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“…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.…”

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confidence: 90%

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Experimental internuclear ophthalmoplegia.

Burde¹,

Lehman²,

Roper-Hall³

et al. 1977

British Journal of Ophthalmology

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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...

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confidence: 90%

“…Neither in their own nor in the clinical studies of INO which they reviewed did Loeffler et al (1966) mention EMG abnormalities of lateral rectus activity.…”

Section: Discussionmentioning

confidence: 99%

Experimental internuclear ophthalmoplegia.

Burde¹,

Lehman²,

Roper-Hall³

et al. 1977

British Journal of Ophthalmology

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“…Bilateral interruption of this connection and of both MLF, however, was followed by bilateral INO and bilateral loss of lateral rectus inhibition but only mild impairment of medial rectus inhibition [71]. Moreover, loss of excitatory MLF fibre activity is not associated with a reduced tonic resting activity of the medial rectus muscle [81-83]. These findings do not support the concept that inhibition of excitatory abducens nucleus internuclear neurons is important for medial rectus inhibition.…”

Section: Discussionmentioning

confidence: 99%

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

Thömke

Hopf

2001

BMC Neurol

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“…They postulated the existence of inhibitory MLF fibers crossing at the oculomotor nucleus level. However, (a) this would neither cause hypermetric nor slowed abduction saccades on the ipsilateral eye (10,12,14); (b) impaired medial rectus inhibition has always been observed on the eye ipsilateral, not contralateral to the MLF lesion (6, [24][25][26]; and (c) crossing of MLF-fibers, as postulated, has not been demonstrated so far (29-3 1).…”

Section: Inmentioning

confidence: 99%

Abduction nystagmus in internuclear ophthalmoplegia

Thömke

Hopf

1992

Acta Neurologica Scandinavica

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Direct current electro-oculography revealed abduction nystagmus with hypermetric abduction saccades in 35 of 64 patients with unilateral and 55 of 66 patients with bilateral internuclear ophthalmoplegia. Slowing of abduction saccades occurred in 27 unilateral cases, mainly ipsilateral to the paretic eye, and in 36 bilateral cases. Abduction nystagmus with hypermetric abduction saccades of normal velocity is explained by an increased phasic innervation adjusted to adduction paresis. Slowed abduction saccades are attributed to impaired inhibition of the medial rectus muscle. Superposition of impaired medial rectus inhibition and increased phasic innervation best explains abduction nystagmus with slowed hypermetric (6 unilateral and 23 bilateral cases) or normometric abduction saccades (9 unilateral and 5 bilateral cases).

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Motor Excitation and Inhibition In Internuclear Palsy

Cited by 27 publications

References 13 publications

Experimental internuclear ophthalmoplegia.

Experimental internuclear ophthalmoplegia.

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

Abduction nystagmus in internuclear ophthalmoplegia

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