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Neural Bases of Childhood Speech Disorders: Lateralization and Plasticity for Speech Functions During Development

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Neural Bases of Childhood Speech Disorders: Lateralization and Plasticity for Speech Functions During Development Neuroscience and Biobehavioral Reviews 36 (2012) 439–458 Contents lists available at ScienceDirect Neuroscience and Biobehavioral Reviews jou rnal homepage: www.elsevier.com/locate/neubiorev Review Neural bases of childhood speech disorders: Lateralization and plasticity for speech functions during development a,∗ b,c,d Frédérique J. Liégeois , Angela T. Morgan a Developmental Cognitive Neuroscience Unit, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK b Murdoch Childrens Research Institute, Melbourne, Australia c Royal Childrens Hospital, Melbourne, Australia d Department of Paediatrics, University of Melbourne, Melbourne, Australia a r t i c l e i n f o a b s t r a c t Article history: Current models of speech production in adults emphasize the crucial role played by the left perisylvian Received 3 June 2011 cortex, primary and pre-motor cortices, the basal ganglia, and the cerebellum for normal speech pro- Received in revised form 7 July 2011 duction. Whether similar brain–behaviour relationships and leftward cortical dominance are found in Accepted 23 July 2011 childhood remains unclear. Here we reviewed recent evidence linking motor speech disorders (apraxia of speech and dysarthria) and brain abnormalities in children and adolescents with developmental, pro- Keywords: gressive, or childhood-acquired conditions. We found no evidence that unilateral damage can result in Speech apraxia of speech, or that left hemisphere lesions are more likely to result in dysarthria than lesion to Neuroimaging Development the right. The few studies reporting on childhood apraxia of speech converged towards morphological, Dysarthria structural, metabolic or epileptic anomalies affecting the basal ganglia, perisylvian and rolandic cortices Apraxia of speech bilaterally. Persistent dysarthria, similarly, was commonly reported in individuals with syndromes and conditions affecting these same structures bilaterally. In conclusion, for the first time we provide evidence that longterm and severe childhood speech disorders result predominantly from bilateral disruption of the neural networks involved in speech production. © 2011 Elsevier Ltd. All rights reserved. Contents 1. Introduction . 440 1.1. Adult models of speech production . 440 1.2. Motor speech disorders. 440 1.2.1. Neural correlates of dysarthria . 441 1.2.2. Neural correlates of apraxia of speech . 441 2. Methods . 441 2.1. Search strategy . 441 2.2. Step 1: search criteria and abstract extraction . 441 2.3. Step 2: abstract selection . 441 2.4. Step 3: article selection . 441 3. Results . 442 4. Discussion . 442 4.1. Neural bases of childhood apraxia of speech. 442 4.1.1. Genetic disorders (idiopathic form) . 442 4.1.2. Epilepsy disorders . 444 4.1.3. Metabolic disorders . 444 4.1.4. Syndromes of unknown origin . 444 4.1.5. Infarcts . 444 Abbreviations: CAS, childhood apraxia of speech; MRI, magnetic resonance imaging; CT, computed tomography. ∗ Corresponding author. Tel.: +44 020 7905 2728; fax: +44 020 7905 2616. E-mail address: [email protected] (F.J. Liégeois). 0149-7634/$ – see front matter © 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.neubiorev.2011.07.011 440 F.J. Liégeois, A.T. Morgan / Neuroscience and Biobehavioral Reviews 36 (2012) 439–458 4.1.6. Childhood apraxia of speech: concluding comments . 444 4.2. Neural bases of childhood dysarthria . 451 4.2.1. Metabolic disorders . 451 4.2.2. Syndromic conditions. 451 4.2.3. Traumatic brain injury . 451 4.2.4. Posterior fossa tumour removal . 453 4.2.5. Epilepsy disorders . 453 4.2.6. Infarcts . 453 4.2.7. Neurodegenerative and progressive diseases . 455 4.2.8. Miscellaneous conditions . ..
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