Unilateral Horizontal Gaze Palsy

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Identifier 167-10
Title Unilateral Horizontal Gaze Palsy
Creator Shirley H. Wray, MD, PhD, FRCP
Contributors Ray Balhorn, Video Compressionist
Affiliation (SHW) Professor of Neurology, Harvard Medical School; Director, Unit for Neurovisual Disorders, Massachusetts General Hospital, Boston, Massachusetts
Subject Unilateral Horizontal Gaze Palsy; Conjugate Deviation of the Eyes; Normal Convergence; Oculocephalic Reflex Normal; Pontine Infarct; Unilateral Horizontal Gaze Palsy Infarct
History The patient is a 62 year old woman with known hypertension. She was referred by her PCP because she could not move her eyes fully and look left. Neuro-ophthalmological examination: Visual acuity, fields, pupils and fundi normal Ocular Motility: • Slight head turn to the left • Conjugate deviation of her eyes to the right • Complete horizontal gaze palsy to the left (saccadic and pursuit) with inability to move her eyes past the midline • Horizontal gaze to the right normal • Normal convergence • Full vertical gaze • Normal oculocephalic reflexes (Doll's head maneuver) Neurological examination: Normal No facial palsy The patient's ocular motility signs localized to a left pontine lesion. She was admitted for a stroke workup. Differential Diagnosis: Pontine hemorrhage Pontine infarct Pontine tumor Brain CT: No hemorrhage or mass lesion Diagnosis: Pontine infarct (small vessel disease secondary to hypertension) The patient was discharged on blood pressure medication. On follow-up two months later her eye movements were normal. This case should be reviewed alongside ID905-1, a patient with a unilateral horizontal gaze palsy and an ipsilateral hemorrhage into a pontine metastasis from adenocarcinoma of the breast.
Anatomy Horizontal gaze palsy. There are four theoretical possibilities to account for the ipsilateral horizontal gaze palsy. It may be due to a single unilateral lesion affecting: 1. The ipsilateral paramedial pontine reticular formation (PPRF) only 2. The ipsilateral abducens nucleus alone 3. Both the ipsilateral paramedial pontine reticular formation (PPRF) and the abducens nucleus, or, when two lesions are involved 4. The motoneuron root fibers of the ipsilateral abducens nucleus to the lateral rectus and the contralateral medial longitudinal fasciculus (MLF). Paramedial pontine reticular formation. The medial portions of the nucleus reticularis magnocellularis (or nucleus centralis pontis oralis and caudalis) have been designated the "paramedian pontine reticular formation" (PPRF), rostral to the abducens nucleus. The region extends from the abducens nucleus in a rostral direction toward the brachium conjunctivum and trochlear nucleus. It has been defined functionally because there are no distinct histologic boundaries. But anatomically, Graybiel, Büttner-Ennever, and others all showed inputs from discrete areas. Clinical findings with PPRF lesion: • Loss of horizontal saccades towards the side of the lesion • Contralateral gaze deviation, in acute phase • Gaze-evoked nystagmus on looking contralateral to the lesion • Impaired smooth pursuit and vestibular eye movements may be preserved or impaired • Bilateral lesions cause total horizontal gaze palsy and slowing of vertical saccades Abducens nucleus. The abducens nucleus contains typical motoneurons that give rise to root fibers that innervate the lateral rectus as well as internuclear neurons whose axons cross the midline and ascend via the contralateral MLF to the medial rectus subnucleus in the contralateral oculomotor (third nerve) nucleus. This projection is the main excitatory input to medial rectus motoneurons in lateral gaze. An old clinicopathologic case published by Bennett and Savill (1) described a unilateral gaze palsy with an associated "patch of softening" in the abducens nucleus without apparent involvement of neighboring structures. Clinical findings with lesion of the abducens nuclei • Loss of all conjugate movements towards the side of the lesion - "ipsilateral, horizontal gaze palsy" • Contralateral gaze deviation, in acute phase • Vergence and vertical movements are spared • In the intact hemifield of gaze, horizontal movements may be preserved, but ipsilaterally directed saccades are slow • Horizontal gaze-evoked nystagmus on looking contralaterally • Ipsilateral lower motor neuron facial palsy often associated due to involvement of the genu of the seventh cranial nerve. The gustatory fibers are spared, because these fibers are carried in the intermediate branch of the facial nerve to the nucleus solitarius of the medulla. Damage to motor neurons, in the abducens nucleus innervating the left lateral rectus muscle or damage to the fascicular portion of the sixth nerve accounts for the ipsilateral sixth nerve palsy and esotropia. Clinical distinction PPRF: Abducens nucleus. At the bedside distinction can be made between the manifestations of gaze palsies in lesions of the PPRF in the upper pons from those of the PPRF in the lower pons at the level of the abducens nucleus. With PPRF lesions rostral to the abducens, there is ipsilateral paralysis of saccades and pursuit, but the eyes can be driven to the side of the gaze palsy with vestibular stimulation by the oculocephalic reflex and/or cold calorics. At the level of the abducens nucleus, lesions of the PPRF are associated with ipsilateral gaze palsy and loss of reflex vestibular (and tonic neck) movements. This presumes that there is a critical synapse within the caudal PPRF for the vestibulo-ocular pathways or that, at the very least, the functional integrity of the PPRF at that level is necessary for vestibulo-ocular eye movements. Abducens nucleus and contralateral medial longitudinal fasciculus (MLF) An identical ipsilateral gaze palsy can be produced by damage to axons of abducens neurons as they course through the brainstem, namely, the ipsilateral sixth nerve fascicle and those axons which ascend the contralateral MLF. Separation of these two anatomic sites suggests two lesions. A lateral gaze palsy that always remains conjugate is consistent with one lesion of the abducens nucleus, whereas one that is not conjugate at any time would better fit two lesions.
Pathology Small vessel disease-infarction
Disease/Diagnosis Pontine infarct
Clinical This patient with a unilateral pontine infarct had: • Horizontal gaze palsy to the left • Slight head turn to the left • Conjugate deviation of her eyes to the right • Complete horizontal gaze palsy to the left (saccadic and pursuit) with inability to move her eyes past the midline • Conjugate gaze to the right normal • Normal convergence • Full vertical gaze • Normal oculocephalic reflexes (Doll's head maneuver) The horizontal gaze palsy was attributed to an ipsilateral infarct involving the paramedial pontine reticular formation rostral to the abducens nucleus.
Presenting Symptom Inability to look left
Ocular Movements Unilateral Horizontal Gaze Palsy; Conjugate Deviation of the Eyes; Normal Convergence; Oculocephalic Reflex Normal
Neuroimaging Neuroimaging studies are not available in this patient
Etiology Pontine infarct
Date 1978
References 1. Bronstein AM, Rudge P, Gresty MA, Du Boulay G, Morris J. Abnormalities of horizontal gaze. Clinical, oculographic and magnetic resonance imaging findings. II. Gaze palsy and internuclear ophthalmoplegia. J Neurol Neurosurg Psychiatry. 1990 March; 53(3): 200-207. http://www.ncbi.nlm.nih.gov/pubmed/2324752 2. Horn AKE, Buttner-Ennever JA, Buttner U. Saccadic premotor neurons in the brainstem: functional neuroanatomy and clinical implications. Neuro-ophthalmology. 1996 16, 229-240. 3. Leigh RJ, Zee DS. Diagnosis of Central Disorders of Ocular Motility. Chp 12;598-719. In: The Neurology of Eye Movements 4th Edition. Oxford University Press, New York, 2006. 4. Meienberg, O, Buttner-Ennever, JA, Kraus-Ruppert, R. Unilateral paralysis of conjugate gaze due to lesion of the abducens nucleus. Neuro-ophthalmology. 1981 2, 47-52. 5. Miller NR, Biousse V, Hwang T, Patel S, Newman NJ, Zee DS. Isolated acquired unilateral horizontal gaze paresis from a putative lesion of the abducens nucleus. J Neuroophthalmol. 2002 Sep;22(3):204-207. http://www.ncbi.nlm.nih.gov/pubmed/12352583 6. Müri RM, Chermann JF, Cohen L, Rivaud S, Pierrot-Deseilligny C. Ocular motor consequences of damage to the abducens nucleus area in humans. J Neuroophthalmol. 1996 Sep;16(3):191-195. http://www.ncbi.nlm.nih.gov/pubmed/8865013 7. Oommen KJ, Smith MS, Labadie EL. Pontine hemorrhage causing Fisher one-and-a-half syndrome with facial paralysis. J Clin Neuroophthalmol. 1982 Jun;2(2):129-132. http://www.ncbi.nlm.nih.gov/pubmed/6226696 8. Pierrot-Deseilligny C, Chain F, Gray F, Escourolle R, Castaigne P. [Supranuclear lateral gaze palsy of pontine origin. Report of 2 clinicopathologic cases with electrooculographic and electromyographic data]. Rev Neurol (Paris). 1979;135(11):741-762. http://www.ncbi.nlm.nih.gov/pubmed/555017
Language eng
Format video/mp4
Type Image/MovingImage
Source 16 mm film
Relation is Part of 905-1
Collection Neuro-Ophthalmology Virtual Education Library - Shirley H. Wray Neuro-Ophthalmology Collection: https://novel.utah.edu/Wray/
Publisher North American Neuro-Ophthalmology Society
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management Copyright 2002. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
ARK ark:/87278/s6j41q38
Setname ehsl_novel_shw
ID 188642
Reference URL https://collections.lib.utah.edu/ark:/87278/s6j41q38
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