title: Metabolic abnormalities in developmental dyslexia detected by 1H magnetic resonance spectroscopy.
abstract: BACKGROUND
  Neurological and physiological deficits have been reported in the brain in developmental dyslexia. The temporoparietal cortex has been directly implicated in dyslexic dysfunction, and substantial indirect evidence suggests that the cerebellum is also implicated. We wanted to find out whether the neurological and physiological deficits manifested as biochemical changes in the brain.
  
  
  METHODS
  We obtained localised proton magnetic resonance spectra bilaterally from the temporo-parietal cortex and cerebellum of 14 well-defined dyslexic men and 15 control men of similar age.
  
  
  RESULTS
  We found biochemical differences between dyslexic men and controls in the left temporo-parietal lobe (ratio of choline-containing compounds [Cho] to N-acetylaspartate [NA] p< or =0.01) and right cerebellum (Cho/NA, p< or = 0.01; creatine [Cre] to NA p< or =0.05; (not significant). We found lateral biochemical differences in dyslexic men in both these brain regions (Cho/NA in temporo-parietal lobe, left vs right, p< or =0.01; Cre/NA in cerebellum, left vs right, p< or =0.001). We found no such lateral differences in controls. There was no significant relation between the degree of contralateral chemical difference and handedness in dyslexic or control men.
  
  
  CONCLUSIONS
  We suggest that the observed differences reflect changes in cell density in the temporo-parietal lobe in developmental dyslexia and that the altered cerebral structural symmetry in dyslexia is associated with abnormal development of cells or intracellular connections or both. The cerebellum is biochemically asymmetric in dyslexic men, indicating altered development of this organ. These differences provide direct evidence of the involvement of the cerebellum in dyslexic dysfunction.
authors.affiliation: MRC Biochemical and Clinical Magnetic Resonance Unit, John Radcliffe Hospital, Oxford, UK. crae@biochem.usyd.edu.au
authors.forename: C
authors.initials: C
authors.lastname: Rae
authors.forename: M A
authors.initials: MA
authors.lastname: Lee
authors.forename: R M
authors.initials: RM
authors.lastname: Dixon
authors.forename: A M
authors.initials: AM
authors.lastname: Blamire
authors.forename: C H
authors.initials: CH
authors.lastname: Thompson
authors.forename: P
authors.initials: P
authors.lastname: Styles
authors.forename: J
authors.initials: J
authors.lastname: Talcott
authors.forename: A J
authors.initials: AJ
authors.lastname: Richardson
authors.forename: J F
authors.initials: JF
authors.lastname: Stein
mesh_terms: D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000032:analysis; D001923:Brain Chemistry; D016022:Case-Control Studies; D002452:Cell Count; D002531:Cerebellum / Q000737:chemistry / Q000378:metabolism*; D002794:Choline / Q000032:analysis; D003401:Creatine / Q000032:analysis; D004410:Dyslexia / Q000378:metabolism*; D004734:Energy Metabolism; D006801:Humans; D007805:Language Development Disorders / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D010296:Parietal Lobe / Q000737:chemistry / Q000378:metabolism*; D013702:Temporal Lobe / Q000737:chemistry / Q000378:metabolism*
chemical_list: D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline