Some TBI Patients Show Dopamine Pathway Deficits
Still untested: whether dopamine enhancing drugs help with symptoms
From MedPage Today | By John Gever
BOSTON — A subset of patients experiencing cognitive problems following traumatic brain injury (TBI) show evidence of diminished dopaminergic activity, suggesting that dopamine-enhancing therapies such as those used in Parkinson’s disease might be useful, a researcher said here.
Iodinated SPECT scans in 42 patients with history of TBI at least 6 months previously showed that mean levels of the dopamine transporter (DAT) molecule were significantly lower than in a group of 20 unaffected control individuals, reported Peter Jenkins, BMBCh, of Imperial College London, at the American Academy of Neurology's annual meeting.
Among the patients, 14 showed substantially abnormal DAT levels, Jenkins said. The caudate region was most strongly affected, and DAT levels within this region were correlated with cognitive function as measured with trail-making and Stroop tests.
Moreover, compared with control, substantia nigra volume was lower on average, and this was related to striatal binding ratio in the putamen and nucleus accumbens. Together, the results point to a Parkinson-like degeneration in dopaminergic pathways that might be amenable to drug therapies that boost dopamine activity, Jenkins said, although he emphasized that the current study did not test that hypothesis.
Some previous studies had also suggested that dopaminergic function is disrupted after TBI, he explained in introducing his presentation. Although Parkinson-like motor symptoms are seldom seen, persistent cognitive problems are very common.
The specifics of how TBI may damage dopaminergic pathways have not been well studied. For the current study, Jenkins and colleagues recruited patients who had experienced TBIs. Mean time since injury was 73 months and ranged up to more than 30 years.
In addition to the iodinated SPECT scans, patients also underwent diffusion tensor imaging and volumetric analyses of specific brain regions. Not all patients in the study with cognitive deficits showed the dopaminergic abnormalities.
Still, Jenkins suggested that in TBI patients showing persistent cognitive deficits, brain scans could — at least in theory — identify those for whom dopamine-boosting therapies may be beneficial. The first step, of course, will be to perform clinical trials to confirm that such treatments are, in fact, helpful.
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