Monocular Elevation Paresis Caused by a Central Nervous System Lesion

Jampel, Robert S.; Fells, P

doi:10.1001/archopht.1968.00980050047008

Cited by 91 publications

(18 citation statements)

References 5 publications

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“…Only three of these retained a Bell's phenomenon. This loss of both voluntary and reflex eye movements with apparent supranuclear lesions has been noted in patients with presumed supranuclear monocular elevation paresis 25 and loss of vertical gaze due to ischemic cerebrovascular disease. 2627 Jacobs' patient with downgaze paresis had absent dolls eyes (table 1A).…”

Section: Figure 7 Photographs Of the Eye Movements In Case 3 A Largmentioning

confidence: 71%

Vertical gaze ophthalmoplegia from infarction in the area of the posterior thalamo-subthalamic paramedian artery.

Wall¹,

Slamovits²,

Weisberg³

et al. 1986

Stroke

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SUMMARY Three cases of a stroke syndrome of acute supranuclear vertical gaze ophthalmoplegia are presented. Voluntary vertical gaze and the vertical vestibulo-ocular reflex were absent or diminished initially in all three patients. The patients also had loss of convergence and alteration hi their mental status. Computed tomography scans showed lesions in the regkm of the rostral midbrain and lower diencephalon in the area surrounding the third ventricle. The blood supply, ischemic stroke syndrome and function of this region with reference to the supranuclear control of vertical gaze are discussed. Stroke Vol 17, No 3, 1986 THE NEURAL SUBSTRATES for vertical gaze are located at the junction of the mesencephalon and diencephalon ( fig. 1). The area currently thought to be of most importance in the function of vertical gaze saccades is the rostral interstitial nucleus of the medial longitudinal fasciculus (rostral iMLF).1 The rostral dorsolateral portion of this nucleus has been shown to be important in the production of downgaze. -2 The caudal ventromedial aspect of this nucleus has been implicated in the premotor control of upward gaze 2 as has the region of the posterior commissure and the pretectal area.3 ' 4 This region of the rostral midbrain is supplied by the posterior thalamo-subthalamic branch of the basilar communicating artery, a branch off the basilar tip. 5 In this report lesions are demonstrated in the region supplied by the posterior thalamo-subthalamic paramedian artery and the vertical gaze ophthalmoplegia and associated findings are discussed. Case Reports Case 1This 56-year-old right handed man was in his usual state of good health until the evening prior to admission when he noted the sudden onset of double vision when looking straight ahead. He was aware of both vertical and horizontal components to the double vision which persisted in all fields of gaze. He then went to sleep, but when he failed to respond to his alarm clock his friend attempted unsuccessfully to awaken him and called an ambulance. While in the ambulance he awoke, confused and combative. At the time of admission to the hospital, he was drowsy but arousable when stimulated. He was disoriented with poor recall of the recent preceding events. There was slight flattening of the right nasolabial fold and mild weakness of the right upper extremity. His tendon reflexes were slightly brisker on the right than his left. He had flexor plantar responses bilaterally. There was slight dysmetria with movement of the left arm and left leg. Sensory examination was within normal limits.Neuro-ophthalmologic examination showed normal visual acuity, visual fields and fundi. His pupils were 5 mm, slightly irregular and did not react to light or to a near target. Ocular motility examination ( fig. 2) showed an alternating exotropia in the primary position of about 30 diopters. Lancaster red-green testing showed an eight diopter right hyperphoria which increased to 16 diopters on gaze up and to the right and a ten diopter left hyperphoria on gaz...

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Section: Figure 7 Photographs Of the Eye Movements In Case 3 A Largmentioning

confidence: 71%

Vertical gaze ophthalmoplegia from infarction in the area of the posterior thalamo-subthalamic paramedian artery.

Wall¹,

Slamovits²,

Weisberg³

et al. 1986

Stroke

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“…There is speculation that both these phenomenon occur due to an abnormality at the supranuclear or nuclear level [2,3,[11][12][13]. Using electromyographic studies in MGJWS, Hepler et al showed that during mastication, anomalous firing of inhibitory interneurons in the midbrain mediated trigemino-oculomotor response [11].…”

Section: Discussionmentioning

confidence: 99%

“…These inhibitory interneurons were reported to be reticular in origin and located in the area of the oculomotor complex [11]. Similarly, Jampel and Fells believed that a lesion in the midbrain tectum or pretectum near the oculomotor nucleus is likely to account for MED [12].…”

Section: Discussionmentioning

confidence: 99%

Bilateral Marcus Gunn jaw winking synkinesis with monocular elevation deficiency: a case report and literature review

Shah¹,

Kumar

Kothari

2012

Int Ophthalmol

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Marcus Gunn jaw winking synkinesis (MGJWS) occurs due to an aberrant innervation of the levator palpebrae superioris muscle by a branch of the motor division of the trigeminal nerve that supplies the muscles of mastication. MGJWS is mostly unilateral occurring in isolation and is less frequently associated with ocular or systemic abnormalities. Although MGJWS is mostly unilateral, few bilateral cases have been reported. Here we describe a rare case of bilateral MGJWS in an 18 year-old male patient with asymmetric bilateral ptosis and monocular elevation deficiency in the right eye.

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“…In acquired MED however, bothersome vertical diplopia is present. [19][20] Abnormal Head Posture (AHP): If binocular fusion is present, a chin elevation is usually seen. 12 Taking fixation with the affected eye is very rare, but has been reported.…”

Section: 13mentioning

confidence: 99%