Diffusion kurtosis imaging in the basal ganglia, as compared with conventional diffusion-tensor imaging, can improve the diagnosis of PD.

Objective-Theta burst stimulation, a form of repetitive transcranial magnetic stimulation, can induce lasting changes in corticospinal excitability that are thought to involve long-term potentiation/depression (LTD/LTD)-like effects on cortical synapses. The pattern of delivery of TBS is crucial in determining the direction of change in synaptic efficiency. Previously we explained this by postulating (1) that a single burst of stimulation induces a mixture of excitatory and inhibitory effects and (2) those effects may cascade to produce long-lasting effects. Here we formalise those ideas into a simple mathematical model. Methods-The model is based on a simplified description of the glutamatergic synapse in which postsynaptic Ca 2+ entry initiates processes leading to different amount of potentiation and depression of synaptic transmission. The final effect on the synapse results from summation of the two effects.Results-The model using these assumptions can fit reported data. Metaplastic effects of voluntary contraction on the response to TBS can be incorporated by changing time constants in the model. Conclusions-The pattern-dependent after-effects and interactions with voluntary contraction can be successfully modelled by using reasonable assumptions about known cellular mechanisms of plasticity. Significance-The model could provide insight into development of new plasticity induction protocols using TMS.

PINK1 was recently found to be associated with PARK6 as the causative gene. We performed mutation analysis in eight inbred families whose haplotypes link to the PARK6 region. We identified six pathogenic mutations (R246X, H271Q, E417G, L347P, and Q239X/R492X) in six unrelated families. All sites of mutations were novel, suggesting that PINK1 may be the second most common causative gene next to parkin in parkinsonism with the recessive mode of inheritance.

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