Acquired pendular nystagmus in multiple sclerosis and oculopalatal tremor

Tilikete, Caroline; Jasse, Laurence; Pélisson, Denis; Vukusic, Sandra; Durand‐Dubief, Françoise; Urquizar, Christian; Vighetto, Alain

doi:10.1212/wnl.0b013e318219fa9c

Cited by 43 publications

(28 citation statements)

References 28 publications

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“…For our patient 3, several control MRI examinations failed to reveal any contralateral lesion, and the delay between the onset of oscillopsia and MRI was 1 month. Like Kim et al [1] and Tilikete et al [28], we do not have a definite explanation for the presence of nystagmus prominent ipsilaterally to unilateral IONH.…”

Section: Discussioncontrasting

confidence: 84%

“…We found 24 publications on OPT for a total of 82 reported cases [1,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30]. We compiled them with our series of 8 patients, totaling 90 cases of OPT.…”

Section: Resultsmentioning

confidence: 99%

“…This implied that 2 OPT patients in their series exhibited prominent nystagmus on the same side as the IONH, like our patient 3. Similarly, Tilikete et al [28] reported 1 patient with dissociated vertical pendular nystagmus that was also more prominent ipsilaterally to the IONH [28]. Both authors did not provide any explanation for this unusual presentation of OPT.…”

Section: Discussionmentioning

confidence: 99%

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Oculopalatal Tremor: Variations on a Theme by Guillain and Mollaret

Jang

Borruat²

2014

Eur Neurol

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Background: Oculopalatal tremor (OPT) is a delayed complication of a brainstem lesion, characterized by involuntary contractions of the soft palate associated with a synchronized ocular pendular nystagmus. MRI reveals inferior olivary nucleus hypersignal/hypertrophy (IONH). Our objective was to refine the clinical profile of patients with OPT and to report a few oddities in both presentation and evolution. Methods: We performed a retrospective study of patients diagnosed with OPT and a literature search. Results: From our database, we retrieved 5 men and 3 women with a diagnosis of OPT. Eighty-two patients with OPT were retrieved from the literature and were compiled with our series. The average age was 54 years and there was a male predominance. Brainstem vascular lesion was the most common etiology (80%). Prominent vertical pendular nystagmus was found in 90%. Dissociated nystagmus was mostly associated to unilateral contralateral IONH on MRI, while bilateral symmetrical nystagmus was due to a bilateral IONH in the majority of cases. Three oddities were found amongst our 8 patients: prominent nystagmus ipsilateral to IONH; disappearance of IONH on MRI despite persisting nystagmus, and asymptomatic OPT. Conclusion: The clinical profile of OPT is rather stereotyped. Rarely do patients deviate from the classical description of OPT.

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Section: Discussioncontrasting

confidence: 84%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Oculopalatal Tremor: Variations on a Theme by Guillain and Mollaret

Jang

Borruat²

2014

Eur Neurol

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“…Interestingly, the most common cause of acquired nystagmus probably is multiple sclerosis, 31 in which the nerves are demyelinated in the brain and spinal cord. Notably, MANBA (the molecular marker rs228614) has been recently identified as a genetic risk locus for multiple sclerosis by genome-wide association study analyses of a large population, 32 suggesting that this polymorphic allele of MANBA might be associated with nystagmus in multiple sclerosis.…”

Section: Discussionmentioning

confidence: 99%

Lysosomal storage disease in the brain: mutations of the β-mannosidase gene identified in autosomal dominant nystagmus

Yü

Cui

Cai

et al. 2015

Genetics in Medicine

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Monocular pendular nystagmus in a patient with sporadic cerebellar ataxia syndrome

2014

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Dear Editor-in-chief, Pendular nystagmus (PN) corresponds to an enduring toand-fro eye oscillation without resetting quick phases [1]. Multiple sclerosis (MS) and oculopalatal tremor (OPT) are known to be the most common causes of acquired PN. OPT is more frequently associated with lesions in the GuillainMollaret triangle, whereas PN in MS is mainly associated with central (i.e., pontine tegmentum or optic nerve) demyelination [1]. We experienced monocular PN in a patient with progressive cerebellar ataxia but showed no palatal tremor. MRI disclosed diffuse cerebellar atrophy, but the hypertrophic degeneration of the inferior olivary nucleus or a focal lesion involving the Gullain-Mollaret triangle was not observed. Disruption of the cerebellum that influences the gaze-holding neural network in the brainstem may give rise to PN. CaseA 58-year-old man presented with gait disturbance for 4 years. His symptom worsened over the years. He could stand without support but veered to the both sides when walking. From 2 years, he felt dizziness and oscillopsia. There was no family history on progressive gait ataxia. On neurological examination, he had mild dysarthria and PN in the left eye. He showed limb dysmetria on both extremities and gait ataxia but no palatal tremor, postural tremor, or any extrapyramidal signs. In three-dimensional VOG (SMI, Teltow, Germany, resolution of 0.1°, sampling rate of 60 Hz), the peak velocity of PN was 5.5°/s. The frequency and amplitude were 5.5 Hz and 0.5°, respectively, and the horizontal and torsional components were mostly regular (Fig. 1a). The vertical component of oscillation was smaller than the torsional or horizontal component. The nystagmus was not attenuated with visual fixation. The amplitude of horizontal PN was increased on leftward or upward gaze. In the leftward or upward gaze, the amplitude of horizontal PN was 1 degree. Measurement of saccade for 30°target displacement disclosed hypermetria (mean accuracy of first saccade, 115.7 %) of the rightward and downward (mean accuracy of first saccade, 109.4 %) saccades, and slight hypometria of the leftward (mean accuracy of first saccade, 86 %) and upward saccades (mean accuracy of first saccade, 78.3 %) in the both eyes. The Brain MRI showed diffuse atrophy in the cerebellum, but there was no abnormality in other areas including the inferior olivary nucleus (Fig. 1b, c). On ophthalmological examination, visual acuity using Snellen test chart was 0.2 in the both eyes. Funduscopic examination was normal. Pupils were normal without a relative afferent pupillary defect. Motility was full and confrontation visual fields were also full. Visual evoked potential test and optical coherence tomography showed no abnormality. Extensive investigations to exclude other causes including genetic analysis for spinocerebellar ataxia 1, 2, 3, 6, 7 and dentatorubral-pallidoluysian atrophy, and thyroid function test were unremarkable. He was finally diagnosed as having S.-M. Woo and H.-A. Kim equally contributed as co-first authors to this work.

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Acquired pendular nystagmus in multiple sclerosis and oculopalatal tremor

Cited by 43 publications

References 28 publications

Oculopalatal Tremor: Variations on a Theme by Guillain and Mollaret

Oculopalatal Tremor: Variations on a Theme by Guillain and Mollaret

Lysosomal storage disease in the brain: mutations of the β-mannosidase gene identified in autosomal dominant nystagmus

Monocular pendular nystagmus in a patient with sporadic cerebellar ataxia syndrome

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