J Neurol Neurosurg Psychiatry 52:108-111 doi:10.1136/jnnp.52.1.108
  • Research Article

Does signal-attenuation on high-field T2-weighted MRI of the brain reflect regional cerebral iron deposition? Observations on the relationship between regional cerebral water proton T2 values and iron levels.

  1. D J Brooks,
  2. P Luthert,
  3. D Gadian,
  4. C D Marsden
  1. Institute of Neurology, National Hospital for Nervous Diseases, Queen Square, London, UK.


      T2-weighted MRI shows attenuated signals from the basal ganglia, such signal attenuation being more evident at high magnetic field strengths of 1.5 tesla (T). The basal ganglia contain high levels of iron, and it has been suggested that these iron deposits lead to shortening of bulk water T2 protons via a mechanism involving diffusion of water through local magnetic field gradients generated by the iron. This mechanism generates a relaxation contribution that is proportional to the square of the applied static field B0, and if it is significant the relaxation rate 1/T2 should be strongly dependent on Bo. T2-weighted MRI would then provide a potential means of imaging regional cerebral iron levels at field strengths that are high enough for this mechanism to be important. The bulk water proton spin-spin relaxation times (T2) of samples from caudate nucleus, frontal cortex, and white matter, taken from fresh cerebral necropsy material of four subjects dying of non-neurological conditions, and one subject with Parkinson's disease have been measured. T2 values were compared with regional cerebral iron content. At high field strengths (2.35 T and 8.5 T) no significant variation in regional cerebral water proton T2 values was found; caudate, cortex and white matter had similar water proton spin-spin relaxation times in spite of the variation in their iron content. Increasing the field strength from 2.35 T to 8.5 T resulted in a generalised 50% decrease in mean regional cerebral T2 values, as opposed to the 13-fold decrease expected if T2 relaxation was dominated by a mechanism that is dependent on B02. It was thus not possible to provide evidence that iron deposition per se is responsible for the attenuated signal obtained from the basal ganglia in T2-weighted MRI.