Clinical Trial: Speech and Short-term Memory Functions in Dyslexia: a Combined MEG and EEG Study

Study Status: Enrolling by invitation
Recruit Status: Enrolling by invitation
Study Type: Observational

Official Title: Speech and Short-term Memory Functions in Dyslexia: a Combined MEG and EEG Study

Brief Summary: Developmental dyslexia is a highly heritable disorder in which reading skills are compromised despite normal intelligence and appropriate reading instruction. Reading problems in dyslexia are thought to primarily originate from weak speech sound representations or poor phonological skills. Dyslexia has also been associated with short-term or working memory dysfunctions. The current study will address the presence of these problems in dyslexic adults by the means of recording auditory and audio-visual mismatch negativity (MMN) and its magnetic counterpart (MMNm) to determine neural speech sound discrimination, representations and integration of seen and heard language. In addition to analyzing neural processing of syllables or (pseudo-)words, a new approach to MEG acquisition and analysis to characterize the neural responses during comprehension of complex real-life speech will be used. Furthermore, reading, phonological and cognitive skills of these participants will be determined with a neuropsychological test battery. The associations between the neural, neuropsychological and genetic measures will be studied. This project will illuminate the nature of neurocognitive dysfunctions in dyslexia and their relationship with genes.

Detailed Summary:

  1. Background

    Developmental dyslexia is the most prevalent learning disorder impairing reading skill even in individuals having normal intelligence and full availability of education (Lyon et al., 2003). It is highly heritable, and several candidate genes contributing to dyslexia have been identified (Scerri & Schulte-Körne, 2010). A wide range of deficits have been associated with dyslexia, but according to the most prevalent theory its major cause is impaired phonological processing (Ramus, 2001). The MMN, the generators of which overlap with brain areas reported to have anatomical abnormalities in dyslexia, has supported this notion. Diminished MMN amplitudes have systematically been reported in dyslexics for certain speech and non-speech sound features (for a review Kujala & Näätänen, 2001). These effects were even found in children and infants having an inherited risk for dyslexia (Leppänen et al., 2002; Lovio et al., 2010). Furthermore, a recent study in our group has shown that dyslexic children have problems in forming memory traces for words (Kimppa et al., in prep.), whereas both the auditory system of normal-reading adults (Shtyrov et al., 2010) and children (Kimppa et al., in prep.) was shown to rapidly form representations for novel words.

    It was recently suggested that phonological deficits in dyslexia can occur due to impairments in different steps of sound processing. According to this theory, dyslexic individuals can be divided into different subgroups. Ramus and colleagues (2013) suggested that dyslexic individuals show an impairment in phonological representations or at later processing stages as an impairment in phonological skills.

    The current pr
    Sponsor: Helsinki University

    Current Primary Outcome: Magnetic mismatch negativity brain responses to speech sound changes [ Time Frame: 2 hours ]

    Original Primary Outcome: Same as current

    Current Secondary Outcome:

    • Magnetoencephalographic amplitude envelope inter-subject correlation during listening to complex real-life speech [ Time Frame: 2 hours ]
    • Event-related brain responses to pseudowords [ Time Frame: first 25% and last 25% of the measurement time (total 2 hours) ]
    • Correlation of event-related brain responses to susceptibility genes for dyslexia [ Time Frame: 1 year ]
    • Source localization of audio-visual integration processes [ Time Frame: 2 hours ]


    Original Secondary Outcome: Same as current

    Information By: Helsinki University

    Dates:
    Date Received: November 11, 2015
    Date Started: July 2015
    Date Completion: December 2020
    Last Updated: March 2, 2017
    Last Verified: March 2017