Concordant Pre- and Postsynaptic Deficits of Dopaminergic Neurotransmission in Neurologic Wilson Disease
Henryk Barthela,
Wieland Hermannb,
Regine Klugea,
Swen Hessea,
David R. Collingridgec,
Armin Wagnerb and
Osama Sabria
a Department of Nuclear Medicine, University of Leipzig, Germany
b Department of Neurology, University of Leipzig, Germany
c Cyclotron Unit, MRC Clinical Sciences Centre, Hammersmith Hospital, London, England
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FIG 1. Typical examples of [123I]ß-CIT (top row) and [123I]IBZM (bottom row) SPECT images in a subject from the control group (left), a non-neurologic WD patient (middle), and a neurologic WD patient (right). Transverse sections at the level of maximal diameter of the striatum are shown. No differences were noted between the control subject and the non-neurologic WD patient. In contrast, specific binding is reduced for both radiotracers in the striata of the neurologic WD patient.
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FIG 2. Box plots show the striatal [123I]ß-CIT and [123I]IBZM binding ratios in non-neurologic and neurologic WD patients, given in percentages, as related to those in the control group. No differences were noted in the non-neurologic WD patients, but a highly significant deficit was observed in neurologic WD patients. *** indicates P < .001.
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FIG 3. Scatter plot shows the positive correlation between the [123I]ß-CIT and [123I]IBZM binding ratios in the striatum of non-neurologic WD patients (solid dots) and neurologic WD patients (open dots). The correlation was proved to be linear and highly significant.
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