1
Stroke infarct Causes Right Horizontal Gaze Palsy
ABSTRACT
Introduction: Stroke is the second leading cause of death globally. There are 68%
ocular motility abnormalities which can happed caused by stroke lesion, included horizontal gaze palsy. Prompt management perhaps can prevent impairing quality of life.
Purpose: To report clinical manifestation and management of right horizontal gaze palsy case which caused by history of stroke infarct
Case Illustration: A 46 years old female patient presented with chief complain of double vision for 5 days before admitted to hospital. She had history of hypertension, hypercholesterolemia and three times of stroke attack. Ophthalmic examination revealed fifteen degrees of esotropia in right eye with or without cover and uncover test. The result of red glass test was uncrossed diplopia. Patient had restriction of ocular movement on right gaze. There was restriction of -3 on right eye and -2 on left eye when patient looked to the right side. The result of CT-scan examination showed that there was infarction area in paramidline pons. There was increase of low-density lipoprotein (LDL) and normal blood glucose in result of ischemic laboratory result. Patient was diagnosed with right horizontal gaze palsy caused by infarct lesion in pons caused by ischemic condition with hypertension, history of stroke and hypercholesterolemia.
Discussion: The horizontal gaze palsy can happen 11.59% following stroke lesion.
Multidiscipline management might be the appropriate management which can resolve paralysis of gaze
Conclusion: Horizontal gaze palsy will impair quality of life caused by paralysis of gaze and double vision as visual impairment. Promptly management can prevent further damage and resolve the paralysis
Keyword: Horizontal gaze palsy, infarct stroke
I. Introduction
Stroke is the second leading cause of death globally. The ocular movement abnormalities are considered as some of the most common disorders which can happen caused by stroke lesion. It is rare condition, but there are 68% ocular motility abnormalities which happen caused by stroke lesion. The horizontal gaze palsy can happen 11.59% following stroke lesion.1–3
Abducens nuclei, medial longitudinal fasciculus (MLF), oculomotor nuclei and paramedian pontine reticular formation (PPRF) are complex which controls horizontal gaze. Any lesions affecting the pathways and structures that were described can lead to abnormalities ocular movements, included horizontal gaze
palsy. The etiology of this case can be caused by ischemia, infiltration, trauma, inflammation and compression.2,4,5
The aim of management in horizontal gaze palsy is to resolve the paralysis and prevent impairing quality of life. Multidisciplinary team have been required for management of horizontal gaze palsy which caused by ischemic lesion.2,4,6 The purpose of this study is to report clinical manifestation and management of right horizontal gaze palsy case which caused by history of stroke infarct.
II. Case Report
A 46 years old female came to Neuro-ophthalmology unit in Cicendo Hospital with chief complaint of double vision for five days before admitted to hospital. She felt that double vision would be diminished if she had covered her one eye. Her complaint was not accompanied by recurrent red eye, blurred vision, pain, headache, nausea or vomit. There was no history of eyeglasses use, ocular surgery or trauma before the double vision happened. She had no family members who have the same complaint like her. Patient had history of hypertension for thirteen years and high cholesterolemia for one year, but she did not take any medicine regularly.
She also had history three times of stroke attack in 2020, 2021 and 2022. There was no history of diabetes or cardiac disease. She denied using tobacco or alcohol.
Picture 2.1 Result of eye alignment and eye movement examination: There was restriction of ocular movement on right gaze (yellow arrow)
Patient had blood pressure in 140/80, but the others vital sign was within normal limit. Ophthalmology examination revealed visual acuity was 1.0 in both eyes.
There was fifteen degrees of esotropia in right eye with or without cover and uncover test. The result of red glass test was diplopia. Patient had restriction of ocular movement on right gaze. There was restriction of -3 on right eye and -2 on left eye when patient looked to the right side. The result of accommodative convergent and vertical eye movement examination was within normal limit. Intraocular pressure was 17 mmHg in both eyes from Non-Contact Tonometry (NCT) examination. Anterior segment dan posterior segment examination was within normal limit for both eyes. Light reflex examination showed within normal limit and no relative afferent pupillary defect (RAPD) in both eyes.
Picture 2.2 Result of fundus photograph in both eyes: within normal limit
The result of color vision with ishihara, contrast sensitivity and amsler grid examination was within normal limit. Patient had no neurological deficit in cranial nerve and motoric examination. The result of visual field examination with Humphrey 30:2 showed in picture 2.3. There was generalized reduction in both eyes, but the result was unreliable which caused by high false negative errors.
Average of retinal nerve fiber layer thickness in both eyes was still within normal limit for result of optical coherence tomography (OCT) in picture 2.4.
Patient was diagnosed with right horizontal gaze palsy caused by suspect pons lesion with hypertension and history of stroke. Patient was given citicoline 1000 milligrams (mg) once in a day. Patient had to continue antihypertensive therapy from general practitioner. Patient was planned for having head and orbita computed tomography scan (CT-scan) examination.
Picture 2.3 Result of visual field examination with Humphrey 30:2 (A) Left eye (B) Right eye: There was generalized reduction in both eyes, but the result was unreliable.
Patient came to follow up in two weeks. She had no any further complaint, but she still had felt double vision. The result of blood pressure examination was 135/82. Ophthalmology examination revealed visual acuity was 1.0 in both eyes.
There was fifteen degrees of esotropia in right eye with or without cover and uncover test. The result of red glass test was diplopia. Patient had restriction of ocular movement on right gaze. There was restriction of -3 on right eye and -2 on left eye when patient looked to the right side. Anterior segment dan posterior segment examination was within normal limit for both eyes. Light reflex examination showed within normal limit and no relative afferent pupillary defect (RAPD) in both eyes. The result of color vision with ishihara, contrast sensitivity and amsler grid examination was within normal limit. The result of CT-scan
examination showed that there was infarction area in paramidline pons. There was no impairment in optic nerve, bulbus oculi and retrobulbar space. The result of CT- scan examination was showed in picture 2.5.
Picture 2.4 Result of OCT optic disc: Average of retinal nerve fiber layer thickness in both eyes was still within normal limit
Patient was diagnosed with right horizontal gaze palsy caused by infarct lesion in pons caused by ischemic condition with hypertension and history of stroke.
Patient was given citicoline 1000 mg once in a day. Patient was planned to have consultation to neurology department and ischemic laboratory test.
Patient came to follow up in one week. There was no additional complaint which patient felt, but she felt that headache was getting rare. Ophthalmology examination revealed visual acuity was 1.0 in both eyes. There was fifteen degrees of esotropia in right eye with or without cover and uncover test. The result of red glass test was diplopia. Patient had restriction of ocular movement on right gaze. There was restriction of -3 on right eye and -2 on left eye when patient looked to the right side.
Anterior segment dan posterior segment examination was within normal limit for both eyes. Light reflex examination showed within normal limit and no relative
afferent pupillary defect (RAPD) in both eyes. The result of color vision with ishihara, contrast sensitivity and amsler grid examination was within normal limit.
Blood test results showed that there was increase of low-density lipoprotein (LDL) and normal blood glucose.
Patient was diagnosed with right horizontal gaze palsy caused by infarct lesion in pons caused by ischemic condition with hypertension, history of stroke and hypercholesterolemia. Patient was given citicoline 1000 mg once in a day. Patient had consultation to internist. She got amlodipine 10 mg once in a day and atorvastatin calcium 20 mg once in a day from internist. Patient was planned to have consultation to neurology department.
Picture 2.5 Result of Head and Orbita CT-scan examination (A) Axial view (B) Sagital view (C) Coronal view: There was infarction area in paramidline pons (black circle)
Patient came to follow up in three weeks. She had no any further complaint. She already had no felt headache and double vision. Patient had ophthalmology examination revealed visual acuity was 1.0 in both eyes. There was seven degrees of esotropia in right eye with or without cover and uncover test. The result of red glass test was diplopia. Patient still had restriction of ocular movement on right gaze. There was restriction of -1 on right eye and -0.5 on left eye when patient looked to the right side. Anterior segment dan posterior segment examination was within normal limit for both eyes. Light reflex examination showed within normal limit and no relative afferent pupillary defect (RAPD) in both eyes. The result of color vision with ishihara, contrast sensitivity and amsler grid examination was within normal limit.
Picture 2.6 Result of eye alignment and eye movement examination: There was improvement in restriction of ocular movement on right gaze (yellow arrow)
Patient underwent transcranial doppler in neurology unit. The result of this examination showed that there was increase of index pulsation, but no stenosis wave. Patient was diagnosed with right horizontal gaze palsy caused by infarct lesion in pons caused by ischemic condition with hypertension, history of stroke
and hypercholesterolemia. Patient was given citicoline 1000 mg once in a day, acetylsalicylic acid 80 mg once in a day from neurologist, amlodipine 10 mg once in a day and atorvastatin calcium 20 mg once in a day from internist. She was recommended came back for follow up in two weeks.
Patient came to follow up in two weeks. She had no any further complaint. She already had taken acetylsalicylic acid in two weeks. Patient had ophthalmology examination revealed visual acuity was 1.0 in both eyes. There was seven degrees of esotropia in right eye with or without cover and uncover test. The result of red glass test was diplopia. Patient had improvement of ocular movement in the right gaze. There was only restriction of -1 on right eye when patient looked to the right side. Anterior segment dan posterior segment examination was within normal limit for both eyes. Light reflex examination showed within normal limit and no relative afferent pupillary defect (RAPD) in both eyes. The result of color vision with ishihara, contrast sensitivity and amsler grid examination was within normal limit.
Picture 2.7 Result of eye alignment and eye movement examination: There was only restriction of -1 on right eye when patient looked to the right side
Patient was diagnosed with right horizontal gaze palsy caused by infarct lesion in pons caused by ischemic condition with hypertension, history of stroke and hypercholesterolemia. Patient was given citicoline 1000 mg once in a day, acetylsalicylic acid 80 mg once in a day, amlodipine 10 mg once in a day and atorvastatin calcium 20 mg once in a day. She was recommended came back for follow up in one month.
III.Discussion
Stroke is acute risk of cerebral perfusion or an unexpected beginning of a neurological deficit, which resulted from acute focal damage on the nervous system for vascular reasons. It is the second leading cause of death globally. Stroke affects 13.7 million people in the world annually. The incidence of stroke increases with age, but strokes in people aged 20-54 years increased from 12.9 – 18.6% of all cases globally between 1990 – 2016. There is no predilection gender in occurrence of stroke. There were 85% risen strokes have ischemic causes. Risk in increased when individual has medical condition like hypertension, coronary artery disease or hyperlipidemia.1,7,8
There is wide range of visual disorder that occur following stroke. The ocular movement abnormalities are considered as some of the most common disorders.
There are 68% ocular motility abnormalities which happen caused by stroke lesion.
The horizontal gaze palsy is ocular movement disorder that can make paralysis of abduction accompany with adduction paralysis toward side of the lesion. It is rare condition following stroke lesion, but it can still happen in 11.59% cases.2,3,5 Patient in this study was a 46 years old female with chief complaint double vision with history of hypertension, hypercholesterolemia and three times of stroke attack.
There are several parts which controls the horizontal gaze. Abducens nuclei, MLF and oculomotor nuclei are responsible for lateral gaze. There are two pathways of nerve fibers are originated from the abducens nuclei. Abducens nucleus contains motoneurons that innervate ipsilateral lateral rectus muscle and bodies of internuclear neuron that cross midline and ascend in the contralateral MLF to synapse in the contralateral subnucleus of medial rectus muscle. The PPRF
comprises multiple excitatory and inhibitory cell groups, which are arranged functionally in the reticular formation of the pons and medulla. Efferent connections from the PPRF exert their effects on the ipsilateral abducens nucleus, and therefore, their role in the initiation or suspension of conjugate horizontal eye movements. Any lesions affecting the pathways and structures that were described can lead to abnormalities ocular movements.4,5,9
Picture 3.1 Anatomical scheme for the synthesis of horizontal eye movements.5
Gaze palsy is a symmetric limitation of the movements of both eyes in the same direction. Bilateral horizontal gaze palsy can be caused by bilateral abducens nuclei lesion or MLF lesion. Isolated MLF lesion will cause the classic internuclear ophthamoplegia (INO) that characterized with eye abduction is preserved, but the ipsilateral eye will not be able to be adducted on conjugate horizontal gaze. Lesions in PPRF can cause horizontal gaze palsy similar to the involvement of two sets nerve fiber abducens nuclei. It is caused by PPRF acts as a relay center that connects the frontal eye fields in the cerebral cortex to the abducens nuclei. The PPRF is also coordinate vertical saccadic movement, so the PPRF lesion will decrease velocity of vertical eye movements as additional manifestation.4,5,9
The horizontal gaze palsy can occur from damage to abducent nucleus. Lesions affecting the abducens nuclei will cause ipsilateral horizontal gaze palsy, because of damage to motor neurons and internuclear neurons originating from the nuclei.
The horizontal gaze palsy that occurs from damage to abducens nucleus is not always symmetric. It can happen caused by cell bodies of the abducens motoneurons are more vulnerable than those of the internuclear neurons. Ipsilateral upper and lower facial weakness can also present with a nuclear abducens palsy due to involvement of the adjacent facial nerve fascicle.3,4,9 Patient in this study had chief complaint double vision and headache for five days before admitted to hospital. She had history of hypertension, hypercholesterolemia and three times of stroke attack There was fifteen degrees of esotrophia in right eye with or without cover and uncover test. The result of red glass test was diplopia. Patient had restriction of ocular movement on right gaze. There was restriction of -3 on right eye and -1 on left eye when patient looked to the right side.
The etiology of this palsy can be caused by ischemia, infiltration, trauma, inflammation and compression. In the case of strokes, restriction of horizontal gaze on one side is usually due to damage of the contralateral frontal cortex or ipsilateral pontine area. The damage can be caused by obstruction of blood flow in focal area.
This condition can increase oxidative stress which can induce cell death and impair of neurological focal function.1,3,4 Patient in this study had history of three times stroke attack which showed infarction area in paramidline pons from CT-scan result examination. Infarction around abducens nuclei area in paramidline pons can make impair neurological function. The position infarct in CT-scan result concerned to right abducens nuclei area.
Horizontal gaze palsy which caused by ischemic can recover completely within 2 - 4 months. Management of ischemia factors from internist or others department can be done. Neuroimaging is mandatory to exclude others pathology, such as tumor, stroke or aneurysm. It sometimes does not recover within 3 to 6 months.
Strabismus surgery can be done at least six months without improvement of alignment in primary position or persistent diplopia. One eye occlusion can be used to overcome diplopia. Chemodenervation of the antagonist MR muscle with
botulinum toxin can be used to treat patients with both acute and chronic case.2,4,5,10 Patient in this study already had consultation to internist and neurologist to improve hypertension, hypercholesterolemia and history of stroke infarct as ischemic factors which be causes horizontal gaze palsy. Patient already had showed improvement in two months after she admitted to hospital.
Prognosis ad vitam in this patient was dubia caused by patient had systemic disease, history of stroke and infarct lesion in pons which can increase mortality rate 31% within five years. Prognosis ad functionam in this patient was dubia ad bonam caused by there was improvement of ocular movement, no diplopia and no headache in the last follow up. Prognosis ad sanationam in this patient was dubia caused by ischemic condition in this patient as reason of palsy can induce recurrency of palsy.
IV. Conclusion
There are 11.59% horizontal gaze palsy which happen caused by stroke lesion.
Stroke can cause obstruction of blood flow and impair neurological function in focal area especially ipsilateral pontine area or contralateral frontal cortex in horizontal gaze palsy case. Clinical manifestation of horizontal gaze palsy is ocular movement disorder that can make paralysis of abduction accompany with adduction paralysis toward side of the lesion. Horizontal gaze palsy which caused by ischemic factor can resolve completely within 2 - 4 months. Consultation to others department as multidisciplinary team can be used for management in this case.
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