Extramotor involvement in ALS: PET studies with the GABA(A) ligand [11C]flumazenil

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  • C. M. Lloyd, King's College London, Hammersmith Hospital
  • ,
  • M. P. Richardson, Hammersmith Hospital, Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London
  • ,
  • D. J. Brooks
  • A. Al-Chalabi, King's College London
  • ,
  • P. N. Leigh, King's College London

We used the benzodiazepine GABA(A) marker [11C] flumazenil to study cerebral dysfunction in amyotrophic lateral sclerosis (ALS) with PET. Seventeen non-demented patients with clinically definite or probable ALS were scanned and statistical parametric maps were derived to localize changes in regional flumazenil volumes of distribution (FMZVD), which correlate closely with receptor density (B(max)), and the results were compared with those of 17 controls. The ALS group showed statistically significant decreases in relative FMZVD in the prefrontal cortex (areas 9 and 10 bilaterally), parietal cortex (area 7 bilaterally), visual association cortex (area 18 bilaterally) and left motor/premotor cortex (including area 4) (P < 0.001). Relative reductions in FMZVD were also seen in the left ventrolateral and dorsolateral prefrontal cortex (areas 45, 46 and 47), Broca's area and the right temporal (area 21) and right visual association cortex (area 19). These observations suggest that cerebral dysfunction in ALS involves motor/premotor and extramotor areas, particularly the prefrontal regions.

Original languageEnglish
Pages (from-to)2289-2296
Number of pages8
Publication statusPublished - 1 Jan 2000
Externally publishedYes

    Research areas

  • Amyotrophic lateral sclerosis, Extramotor cortex, PET, [C]flumazenil

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