Effects of low dose lithium on hippocampal neuropathology in people at ultra-high risk for psychosis
Wood, Stephen J., Berger, Gregor, Dell'Ollio, Margaret, Hamer, Clare A., Wellard, R. Mark, Pell, Gaby S., Phillips, L. J., Nelson, Barnaby, Manji, Husseini, Jackson, Graeme J., Pantelis, Christos, & McGorry, Patrick D. (2007) Effects of low dose lithium on hippocampal neuropathology in people at ultra-high risk for psychosis. In Biological Psychiatry, Society of Biological Psychiatry, San Diego, USA, 259S-260S.
Background: Indicated intervention prior to the onset of psychosis may help
to delay, attenuate or even prevent the illness. To date, successful intervention
trials using atypical antipsychotics and/or cognitive behavioural therapy
have been reported, but it is not clear that these treatments are targeting the
underlying brain pathology. Given our previous findings of progressive grey
matter loss over the transition to psychosis, agents that can prevent this, such as
lithium, might be useful for preventing or delaying the onset of psychosis.
Methods: In this open-label trial, 11 ultra-high-risk patients who received low-
dose lithium treatment for four months were compared with 10 similar patients
who received only needs-based intervention. Magnetic resonance imaging,
including T2 relaxometry and proton spectroscopy was performed prior to
initiation of treatment and after four months.
Results: Hippocampal T2 declined significantly in the treatment group
(p=0.018). No significant group x time effects were seen for brain metabolites,
although N-acetyl aspartate (NAA), myo-inositol, creatine and choline
all tended to increase with lithium administration and decrease or remain
unchanged in the comparison group.
Conclusions: Decreased T2 relaxation time and increased concentrations
of NAA are indicators of increased neuronal function/viability. Low-dose
lithium may help regulate synaptic pruning and reduce neuronal dysfunction
associated with the onset of psychosis.
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