Neurobehavioral research on the role of impulsivity in gambling disorder (GD) has produced heterogeneous findings. Impulsivity is multifaceted with different experimental tasks measuring different subprocesses, such as response inhibition and distractor interference. Little is known about the neurochemistry of inhibition and interference in GD.

We investigated inhibition with the stop signal task (SST) and interference with the Eriksen Flanker task, and related performance to metabolite levels in individuals with and without GD. We employed magnetic resonance spectroscopy (MRS) to record glutamate–glutamine (Glx/Cr) and inhibitory, γ-aminobutyric acid (GABA+/Cr) levels in the dorsal ACC (dACC), right dorsolateral prefrontal cortex (dlPFC), and an occipital control voxel.

We found slower processing of complex stimuli in the Flanker task in GD (P < .001, η2 p = 0.78), and no group differences in SST performance. Levels of dACC Glx/Cr and frequency of incongruent errors were correlated positively in GD only (r = 0.92, P = .001). Larger positive correlations were found for those with GD between dACC GABA+/Cr and SST Go error response times (z = 2.83, P = .004), as well as between dACC Glx/Cr and frequency of Go errors (z = 2.23, P = .03), indicating general Glx-related error processing deficits. Both groups expressed equivalent positive correlations between posterror slowing and Glx/Cr in the right dlPFC (GD: r = 0.74, P = .02; non-GD: r = .71, P = .01).

Inhibition and interference impairments are reflected in dACC baseline metabolite levels and error processing deficits in GD.

Thought insertion is commonly regarded as diagnostic of schizophrenia. Little is known of its aetiology or pathophysiology.

To examine the definition and application of thought insertion in psychiatric and allied literatures.

A semi-structured literature review and conceptual analysis.

When ‘narrowly’ defined, thought insertion is reliably identified but not specific to schizophrenia. There is a range of related phenomena (‘alienated’, ‘influenced’, ‘made’ and ‘passivity’ thinking), less consistently defined but also not specific to schizophrenia. Whether thought insertion is solely an abnormal belief (or may also be an experience) is open to question. Nevertheless, the symptom has been used to explain schizophrenia, predict dangerousness and advance theories of ‘normal’ agency. Most applications have been subject to critique.

Despite its widespread occurrence and diagnostic application, thought insertion is an ill-understood and under researched symptom of psychosis. Its pathophysiology remains obscure.