Isolated bilateral horizontal gaze palsy as first manifestation of multiple sclerosis

2014 ◽  
Vol 20 (6) ◽  
pp. 754-755 ◽  
Author(s):  
Stefan Kipfer ◽  
David W Crook

Predilection sites for infratentorial multiple sclerosis lesions are well known and frequently involve the fasciculus longitudinalis medialis leading to classical internuclear ophthalmoplegia. We report a very rare oculomotor disorder due to a demyelinating central nervous system (CNS) lesion in the medial part of the lower pontine tegmentum. A 36-year-old man presented with sudden onset of blurred vision. Clinically there was limited eye adduction and abduction to either side, which corresponds to bilateral horizontal gaze palsy. Brain magnetic resonance imaging (MRI) showed a demyelinating CNS lesion affecting the fasciculus longitudinalis medialis, abducens nuclei or abducens fibres in the medial part of the lower pontine tegmentum. Furthermore there were six further demyelinating white matter lesions fulfilling all Barkhof criteria for multiple sclerosis. Demyelinating CNS lesions causing isolated bilateral horizontal gaze palsy are exceptional and usually associated with further focal neurological deficits, which was not the case in the presenting patient. This is a unique video report of isolated bilateral horizontal gaze palsy as the initial manifestation of demyelinating CNS disease, which lead to definite diagnosis of relapsing remitting multiple sclerosis.

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sheng Zhuang ◽  
Weiye Xie ◽  
Chengjie Mao

Abstract Background Bilateral facial colliculus syndrome is a rare clinical presentation in patient with pontine infarction. We herein described a case of bilateral facial paralysis and complete horizontal gaze palsy possibly caused by paradoxical embolization from patent foramen ovale related stroke. Case presentation A 55-year-old male presented with sudden onset of complete peripheral facial palsy and horizontal gaze palsy after Valsava maneuver. MRI revealed symmetric involvement of bilateral pontine tegmentum in accordance with the location of facial colliculus. CSF analysis and follow-up MRI showed no evidence of central demyelinating disease. Subsequent echocardiography revealed patent foramen ovale and closure surgery was performed. Conclusions Facial colliculus syndrome with symmetric dorsal pontine tegmentum involvement may a rare manifestation in posterior circulation stroke.


BMC Neurology ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Amirhossein Akhavan Sigari ◽  
Masoud Etemadifar ◽  
Mehri Salari

Abstract Background Demyelinating central nervous system diseases include several disorders that multiple sclerosis (MS) is identified as the most common among them. Ocular movement disturbances are a typical presentation in MS patients where lesions affect the complex and interconnected pathways involved in eye motion. Centers for gaze control are located in the pons primarily; therefore, lesions involving these centers can be presented with abnormalities in gaze. However, bilateral lesions in pontine gaze centers are exceptionally rare. Case presentation A 16-year-old girl with bilateral horizontal gaze palsy was referred to the neurology clinic. Magnetic resonance imaging of the patient indicated bilateral hyperintensities in the pons at the level of the paramedian pontine reticular formation. The patient was diagnosed with multiple sclerosis with respect to clinical and imaging findings and managed. Conclusion Ocular movement abnormalities are a commonly encountered manifestation in patients with multiple sclerosis, however, bilateral gaze palsy is an exceptionally rare sign and should guide the physician to contemplate for anticipated lesions in the pons, and suspect MS, especially in childbearing-aged women. Although an extensive workup should also be done to rule out possible mimickers.


SLEEP ◽  
1993 ◽  
Vol 16 (2) ◽  
pp. 184-188 ◽  
Author(s):  
Francesc Valldeoriola ◽  
Joan Santamaria ◽  
Francesc Graus ◽  
Eduardo Tolosa

Author(s):  
Andre C. Felicio ◽  
Denis B. Bichuetti ◽  
Luis F. Marin ◽  
William A.C. dos Santos ◽  
Clecio Godeiro-Junior

2017 ◽  
Vol 91 (6) ◽  
pp. 327-330
Author(s):  
Vanesa Rivero-Gutiérrez ◽  
Cristina Nieto-Gómez ◽  
Emiliano Hernández-Galilea

2021 ◽  
Vol 20 (4) ◽  
pp. 182-188
Author(s):  
Sun Young Lee ◽  
Mi-Ra Park

Purpose: We report a case of multiple sclerosis with bilateral optic neuritis that was atypical in terms of both the clinical signs and symptoms.Case summary: A 34-year-old female visited the department of neurology with a complaint of sudden-onset, left lower extremity weakness and numbness that had developed 3 weeks prior, and bilateral blurred vision that had commenced 2 weeks prior. The patient was diagnosed with multiple sclerosis and prescribed high-dose intravenous methylprednisolone for 3 days, but the blurred vision did not improve. The patient was referred to the ophthalmology department. The initial best-corrected visual acuity was 0.04 in both eyes, and the relative afferent pupillary defect test was positive for the left eye. The Ishihara color test scores were 1/17 for both eyes. No optic disc swelling was evident on fundus examination. Brain and spine magnetic resonance imaging (T2-weighted) performed during the initial visit revealed lesions of high signal intensity in the frontal, subcortical white matter; the optic chiasm; the left retrobulbar optic segment; the medulla; and the spinal C2-5 processes. Aquaproin-4 immunogloblin G antibody (AQP4-IgG Ab) was not detected in serum. One month after prescription of the oral steroid, the vision improved to 1.0 in the right and 0.8 in the left eye. The patient was lost to follow-up after prescription of interferon-beta for 4 years, without recurrence.Conclusions: Binocular optic neuritis accompanied by severe visual loss is a rare form of multiple sclerosis. A thorough diagnosis (with a focus on exclusion) is required, as is appropriate treatment.


2019 ◽  
Vol 18 (6) ◽  
pp. E184-E190 ◽  
Author(s):  
Jaims Lim ◽  
Hussain Shallwani ◽  
Kunal Vakharia ◽  
Adnan H Siddiqui

Abstract BACKGROUND AND IMPORTANCE Few studies describe the use of adenosine-induced cardiac systole for treatment of cerebrovascular pathologies. We describe a midbrain arteriovenous malformation (AVM) treated with transvenous embolization using adenosine-induced asystole to achieve transient systemic hypotension with the purpose of furthering discussion on the technique and operative considerations for adenosine use in endovascular AVM treatments. CLINICAL PRESENTATION A 29-yr-old man presented with sudden onset of severe bilateral headache, blurred vision, and numbness on the right side of his face and tongue. Noncontrast head computed tomography revealed fourth ventricle hemorrhage. Diagnostic cerebral angiography revealed a high-flow midbrain AVM with a posterior wall perforator from the basilar artery terminus and a draining vein into the straight sinus. Transarterial AVM embolization was successful. The patient was discharged with no residual neurological deficits but returned 1 wk later with slurred speech and left-sided dysmetria. Repeat angiography revealed partial AVM filling. Attempts at transarterial embolization were unsuccessful. Thus, transvenous AVM embolization with adenosine-induced cardiac asystole and systemic hypotension was performed. A total of 60 mg of adenosine was administered, followed by 2 additional doses of 60 and 40 mg; and complete cardiac asystole with a mean arterial pressure of 40 mmHg was maintained, resulting in successful embolization of the AVM. No residual filling was visualized on postembolization arterial angiography runs. The patient was neurologically stable and discharged on postoperative day 2. CONCLUSION With appropriate and safe dosing, adenosine-induced asystole and systemic hypotension may be a feasible, safe option to reduce flow and assist endovascular transvenous embolization of high-flow AVMs.


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Fiona J. Rowe ◽  
David Wright ◽  
Darren Brand ◽  
Carole Jackson ◽  
Shirley Harrison ◽  
...  

Aim. To evaluate the profile of ocular gaze abnormalities occurring following stroke. Methods. Prospective multicentre cohort trial. Standardised referral and investigation protocol including assessment of visual acuity, ocular alignment and motility, visual field, and visual perception. Results. 915 patients recruited: mean age 69.18 years (SD 14.19). 498 patients (54%) were diagnosed with ocular motility abnormalities. 207 patients had gaze abnormalities including impaired gaze holding (46), complete gaze palsy (23), horizontal gaze palsy (16), vertical gaze palsy (17), Parinaud’s syndrome (8), INO (20), one and half syndrome (3), saccadic palsy (28), and smooth pursuit palsy (46). These were isolated impairments in 50% of cases and in association with other ocular abnormalities in 50% including impaired convergence, nystagmus, and lid or pupil abnormalities. Areas of brain stroke were frequently the cerebellum, brainstem, and diencephalic areas. Strokes causing gaze dysfunction also involved cortical areas including occipital, parietal, and temporal lobes. Symptoms of diplopia and blurred vision were present in 35%. 37 patients were discharged, 29 referred, and 141 offered review appointments. 107 reviewed patients showed full recovery (4%), partial improvement (66%), and static gaze dysfunction (30%). Conclusions. Gaze dysfunction is common following stroke. Approximately one-third of patients complain of visual symptoms, two thirds show some improvement in ocular motility.


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