Figure 1.

A pathophysiological schematic of the syndrome of right temporal lobe atrophy. The Figure diagrams key brain regions, networks and cognitive processes implicated in the pathogenesis of the syndrome of right temporal lobe atrophy (RTLA). The main cartoon is oriented following radiological convention with the right temporal lobe projected on the left, as in the inset coronal T1-weighted structural brain MRI section (derived from a patient with a clinical syndrome of RTLA). We argue that the clinical syndrome of RTLA reflects the intersection of four large-scale neural networks in the anterior, inferior and mesial right temporal lobe, each mediating a cognitive process that is core to the expression of the RTLA syndrome: complex sensory analysis (green); homeostasis and assignment of hedonic value (red); semantic appraisal of sensory signals (gold); and inference about and response to others' mental states, mentalising or ‘theory of mind' (blue). Note that each of these networks extends beyond the right temporal lobe, to the left temporal lobe and beyond. The cognitive processes mediated by these networks interact extensively; these interactions are likely to fundamentally underpin the diverse phenotypic repertoire of RTLA. Although the core functional neural circuit lesion of RTLA has not been defined, a plausible candidate (relevant to all the cognitive operations schematised here) is impaired neural template-matching (see text). a-h, amygdala and hippocampus; EC, entorhinal cortex; FG, fusiform gyrus; ins, insula; ITG, inferior temporal gyrus; MTG, middle temporal gyrus; OFC, orbitofrontal cortex; R, right; STG, superior temporal gyrus; ToM, theory of mind; TP, temporal pole; vmPFC, ventromedial prefrontal cortex; vs, ventral striatum.