The neural basis of communication disorder in children



The neural basis of communication disorder in children

Identifying brain damage underlying speech deficits in children following traumatic brain injury: A new model for diagnosis and prognosis

Chief Investigator: Dr Angela Morgan

Other Chief Investigators: Professor Alan Connelly, Dr Frederique Liegeois,

Associate Investigators: Professor Vicki Anderson, Professor Sheena Riley, Associate Professor Michael Ditchfield, Dr Jacques- Donald Tournier

Lead Organisation: Murdoch Childrens Research Institute

TAC Neurotrauma Funding $276,079

Project Dates: 1 April 2008 – 31 March 2011

Background:

Good communication skills are critical for success in our everyday lives. After brain injury, many children experience difficulties in their speech or language skills. One particularly debilitating speech disorder after brain injury in children is known as dysarthria. Dysarthria manifests as slow and slurred sounding speech. The neural bases of this disorder remain elusive however, making it difficult to predict who will develop persistent speech disorder following TBI.

Aims:

To identify the neural correlates of chronic dysarthria following TBI in childhood.

Methods:

Researchers from the Murdoch Children’s Research Institute and the Brain Research Institute used cutting-edge Magnetic Resonance Imaging techniques to understand which parts of the brain are most commonly damaged in children with dysarthria. Participants with chronic dysarthria following TBI (TBI+ group) sustained in childhood participated. They were compared to two control groups matched for age and gender: a TBI without dysarthria group (TBI-), and a typically developing control group (TD). A single DWI data set was acquired (3T MRI scanner) for each participant, alongside a high-resolution T1-weighted scan for volumetric and voxel-based morphometry (VBM) analyses. Fractional anisotropy (FA) measures were extracted from three regions of interest within the corticobulbar/spinal tract, namely the corona radiata, the posterior limb of the internal capsule (PLIC), and the upper pons. fMRI data was also collected, with participants performing a speaking task whereby they repeated randomly selected single-words out-loud.

Results:

With respect to global brain measures, white matter was reduced in the TBI+ relative to the TD group only. VBM revealed that the TBI+ group had bilateral reductions in several regions including the corona radiata, the PLIC, the cingulum bundle, and the corpus callosum, relative to the TD group. Relative to the TBI- group, reductions were observed in the right PLIC. DWI analyses showed FA reductions in the TBI+ group bilaterally at the level of the corona radiata relative to the two other groups. In addition, FA was reduced compared to the TD group at the PLIC level (trend) and pons level bilaterally. The fMRI results were in agreement with the white matter findings. Specifically, children with dysarthria following TBI demonstrated reduced bilateral activation in the sensorimotor cortices and putamen in comparison to the children without dysarthria and healthy controls.

Conclusions:

Our data suggest that chronic dysarthria following TBI is associated with severe bilateral damage along the corticobulbar tract. Findings could facilitate earlier identification and management of cases at risk for dysarthria, with a view to enhancing speech outcomes in this population.

Publications:

MORGAN A, MAGEANDRAN SD, MEI C. Incidence and clinical presentation of dysarthria and dysphagia in the acute setting following paediatric traumatic brain injury. Special edition on paediatric TBI. Child: Care, Health and Development. 2010;36(1):44-53.

MORGAN A, LIEGEOIS F. Re-thinking diagnostic classification of the dysarthrias: a developmental perspective. Folia Phoniatr Logop 2010;62:120-126.

Presentations:

MAGEANDRAN SD, MORGAN AT, MEI C. Incidence and clinical presentation of dysarthria and dysphagia in the acute setting following paediatric traumatic brain injury. Speech Pathology Australia national conference; 2009 May 17-21, Adelaide, Australia.

MORGAN AT, MAGEANDRAN SD, MEI C. Incidence and clinical presentation of dysarthria and dysphagia in the acute setting following paediatric traumatic brain injury. Australian Society for the Study of Brain Impairment; 2009 May 7-9, Sydney, Australia.

MAGEANDRAN S, MORGAN A, MEI C. Dysarthria and dysphagia in the acute setting following paediatric traumatic brain injury. Singleheath Duke NUS Scientific Congress; 2010 October 15-16, Singapore.

MORGAN A, LIEGOIS F. Re-thinking diagnostic classification of the dysarthrias: a developmental perspective. International Association of Logopaedics and Phoniatrics; 2010 August 22-26, Athens, Greece.

MAGEANDRAN S-D, MORGAN AT, MEI C. Dysarthria and dysphagia in the acute setting following paediatric traumatic brain injury. Singhealth Duke NUS Scientific Congress; 2010 October 15-16, Singapore.

LIEGOIS F, TOURNIER J, CONNELLY A, PIGDON L, MORGAN A. MRI correlates of chronic dysarthria after childhood traumatic brain injury. European Academy of Childhood Disability; 2011 June 8-11, Rome, Italy.

MORGAN A, PIGDON L, CONNELLY A, LIEGOIS F. Chronic dysarthria following paediatric traumatic brain injury: neural correlates. International Neuropsychology Society; 2011 July 609, New Zealand.

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download