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  1. Peter O Jenkins1,3,
  2. Sara De Simoni1,
  3. Jessica Fleminger1,
  4. Niall Bourke1,
  5. Amy Jolly1,
  6. James Cole1,
  7. Daniel Darian2,
  8. David Sharp1
  1. 1Imperial College, London
  2. 2Imperial College Healthcare NHS Trust
  3. 3ABN Fellow


Background Traumatic brain injury (TBI) causes dopaminergic disruption. The cause, however, is unclear and may relate to damage to the dopaminergic nuclei or their ascending projections.

Objectives To investigate whether: (1) TBI reduces striatal dopamine transporter (DAT) levels; (2) TBI causes structural changes to the substantia nigra, striatum and/or nigrostriatal tract; (3) DAT levels following TBI correlate with substantia nigra or nigrostriatal tract damage.

Methods 24 moderate/severe TBI patients and 13 controls underwent an ioflupane (123I) SPECT scan (DaTscan) to measure striatal DAT levels. MRI was used to calculate substantia nigra and striatal volumes, and nigrostriatal tract diffusion metrics.

Results 66% of TBI patients' clinical DaTscan reports were abnormal. Quantitative assessment showed reduced DAT levels in TBI patients. Patients had substantia nigra and striatal atrophy, as well as increased mean diffusivity in the nigrostriatal tract. Striatal DAT levels correlated negatively with nigrostriatal tract mean diffusivity.

Conclusions The reduced DAT levels in TBI patients implies a disruption to their dopaminergic systems. The abnormalities of MRI structural measures may provide surrogate markers of dopaminergic system integrity. The relationship between DAT levels and nigrostriatal tract mean diffusivity supports a possible causal relationship between damage to this pathway by TBI and dopaminergic dysfunction.

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