The neural basis of communication disorder in children

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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 voxelbased 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.
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