In other words, disconnection per se may not be enough, as it must occur with a sufficient level of dopamine. However, it could be either an important secondary factor by lowering the threshold for expressing psychosis, or even a requirement for expressing psychotic features on dopamine release. This is in line with the observation that only a minority of normal subjects given amphetamine do become psychotic.88 In such rare cases a cofactor such as a subnormal disconnectivity may exist. A final explanation could be that WM diseases weaken cortical control over dopamine release in the striatum (or directly on the ventral tegmental neurons). This is expected to be the case if the WM lesion is localized between the frontal lobe and the striatum. However, as will be discussed later, frontal WM lesions are more prone to provoking depression than psychosis.
