Intermittent horizontal saccade failure ('ocular motor apraxia') in children.

Harris, Christopher M.; Shawkat, Fatima; Russell‐Eggitt, Isabelle; Wilson, John; Taylor, David

doi:10.1136/bjo.80.2.151

Cited by 80 publications

(60 citation statements)

References 44 publications

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“…5,6 The pathophysiology of OMA remains unclear but structural abnormalities in the cerebrum, cerebellar vermis, brainstem, mid-brain (rostral interstitial nucleus of the medial longitudinal fasciculcus), and basal ganglia have all been previously implicated and reported. 2,3,4,7 In particular, agenesis of the corpus callosum and cerebellar hypoplasia have been repeatedly associated with congenital OMA. 9,10 Agenesis of the corpus callosum frequently occurs in association with cerebellar hypoplasia or with other structural abnormalities, which further complicates the issue.…”

Section: Discussionmentioning

confidence: 99%

“…2,3,4,5 It may also be idiopathic or associated with structural brain abnormalities (e.g. cerebellar hypoplasia, agenesis of the corpus callosum), neurodegenerative disorders (e.g.…”

mentioning

confidence: 99%

“…3,4 This report reviews patients with OMA seen at a paediatric neuroophthalmology clinic. In particular, it examines the neurodevelopmental implications of isolated OMA.…”

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confidence: 99%

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Neurodevelopmental implications of ocular motor apraxia

Marr

Green

Willshaw

2005

Develop Med Child Neuro

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Ocular motor apraxia (OMA), a disorder of saccadic initiation, may be congenital or acquired. While the acquired form is frequently associated with significant neuropathology, the congenital form is often regarded as relatively benign. Many children with congenital OMA who were observed clinically have shown neurodevelopmental disturbance over time. A retrospective review was taken of 34 consecutive patients (22 males and 12 females), seen over a 20–year period, to evaluate the frequency and type of associated neurodevelopmental problems. Age at presentation ranged from 8 weeks to 14 years, with a mean age of 10 years. Of 29 children with congenital OMA, 15 had imaging evidence of structural central nervous system abnormalities (with cerebellar hypoplasia the most frequent abnormality detected). Eleven of the 14 patients with no structural abnormality showed abnormal neurodevelopment. This study suggests that congenital OMA is not a benign diagnosis, even in the absence of overt neurological disturbance at the time of presentation.

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Section: Discussionmentioning

confidence: 99%

“…2,3,4,5 It may also be idiopathic or associated with structural brain abnormalities (e.g. cerebellar hypoplasia, agenesis of the corpus callosum), neurodegenerative disorders (e.g.…”

mentioning

confidence: 99%

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Neurodevelopmental implications of ocular motor apraxia

Marr

Green

Willshaw

2005

Develop Med Child Neuro

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“…Bunların klinik olarak, çok ağır olmadıkları sürece, tanınması oldukça zordur ve genellikle kalitatif olarak tarif edilir. [4][5][6][7] Biz de olgumuzda kalitatif olarak tarif edebildiğimiz yavaş sakkadik göz hareketleri saptadık ve bulgularda postoperatif dönemde düzelme gözlemedik. …”

Section: Discussionunclassified

Abnormal Saccadic Eye Movements and Esotropia in a Patient with Type 3 Gaucher Syndrome: Case Report

Acar¹,

Demir²,

Buttanri³

et al. 2015

Turkiye Klinikleri J Ophthalmol

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“…We suggest that a similar mechanism could also explain ISID in patients with cerebellar vermis hypoplasia and in agenesis or hypoplasia of the corpus callosum. 2,7,10,23 We propose that the fundamental problem underlying saccade initiation delay is a congenital or an acquired disruption or disconnection of axons linking analogous brain regions involved in processing saccades (See the accompanying article on page 779 for further details).…”

Section: Figure 3: Axial T2-weighted Brain Mri Of the Patient Throughmentioning

confidence: 99%