Intentional Inhibition Research Articles

Inhibition in schizophrenia: association with auditory hallucinations

The study investigated whether auditory hallucinations (AH) in schizophrenia are linked to a deficit in inhibition. Two tasks assessing the intentional suppression of cognitive events—the Hayling Sentence Completion Test (HSCT) [Neuropsychologia 34 (1996) 263] and the Inhibition of Currently Irrelevant Memories Task (ICIM) [Nature Neuroscience 2 (1999) 677]—were administered to 42 patients with schizophrenia and 24 normal controls. Presence and severity of symptoms in the patient group were examined using the Positive and Negative Syndrome Scale (PANSS). Patients performed significantly worse on the measures of inhibition compared to controls. More importantly, among patients, significant positive correlations were obtained between an index of AH severity (defined as an increase in frequency of AH on PANSS) and the number of type A errors on the HSCT and errors in the last three runs of the ICIM. An increase in AH severity was, therefore, associated with increasingly impaired control of intentional inhibition. Furthermore, no significant correlations were found between these indices of inhibition and either negative, general or positive symptoms (excluding AH scores).

Visual marking for search: behavioral and event-related potential analyses

Visual marking is an attentional mechanism of prioritizing the selection of new static or moving objects via top-down intentional inhibition of old objects [ Psychol. Rev. 104 (1997) 90–122]. The present study investigated the operation of visual marking using event-related brain potentials (ERPs). Participants searched a display for one of two target letters among randomly selected letter distractors. Two item set sizes were used in a two-stage display. Half of the items appeared for 1000 ms in the first stage followed by the remainder in the second stage. Three blocked conditions were used. In the Preview condition, targets appeared as one of a set of new items in Display 2. Items in Display 1 could thus be excluded from search by visual marking. In the Control condition, old items changed when new items appeared, and the target was equally likely to be at an old or a new position. In this condition marking is unlikely to be engaged since old locations could contain the target. In the Search condition, targets appeared either in Display 1 (80%) or Display 2 (20%), and Display 1 items did not change. The results showed condition-contingent attentional modulations in the N1/N2 range. In addition, a broadly distributed centrally-preponderant sustained negativity was obtained in the 350–750 ms time range after the onset of Display 1 for the Preview–Control comparison. This latter negativity is interpreted to reflect the processes involved in setting up and maintaining of visual marking. It demonstrated an effect of visual marking well prior to Display 2 onset, thereby ruling out an account of the preview benefit solely due to attentional capture by Display 2 item onset.

Therapeutic and Diagnostic Benefits of Intentional Crosstalk Mediated Ventricular Output Inhibition

Ventricular output inhibition due to crosstalk is generally considered unsafe and something that should be avoided. Special circuits have been incorporated in some dual chamber pacing systems to absolutely prevent this from happening. However, in patients with intact atrioventricular conduction, crosstalk mediated ventricular output inhibition can be beneficial to the evaluation and management of the patient. Utilizing this technique, one can achieve single chamber atrial paced rates which greatly exceed the rates allowed by lower rate limit programming to facilitate an assessment of the integrity of AV nodal conduction and to both convert and suppress some pathological tachyarrhythmias. The methods of achieving crosstalk and its utilization in four patients is discussed in this report.

Interactions between anticonvulsants and other commonly prescribed drugs.

Many drug interactions can be demonstrated, but only a few are so clinically significant that they necessitate adjusting drug dosages. The same drug combination may produce changes of variable extent or direction in different individuals. The reasons for this variability include genetic control of the rate and inducibility of drug metabolism, and environmental factors such as contact with chemicals. Among antimicrobial agents, chloramphenicol may cause accumulation of phenytoin (PHT) and phenobarbital (PB), and isoniazid may cause PHT, carbamazepine (CBZ), and primidone (PRM) to accumulate. Erythromycin may cause accumulation of CBZ. Among anti-ulcer agents, antacids may reduce PHT concentration while cimetidine may cause accumulation of PHT, CBZ, and diazepam (DZP). Salicylates displace strongly binding drugs such as PHT, DZP, or valproate (VPA) from the binding sites in plasma proteins, which may lead to some decline of the total plasma level with an increase in the unbound drug percentage. Conversely, anticonvulsants may influence the dosage requirements of oral anticoagulants by inducing their metabolism. Failures of oral contraceptives have been attributed to anticonvulsants in some patients. Probably the most predictable interaction that necessitates dosage adjustment is accumulation of PB caused by VPA. Intentional inhibition of PRM metabolism by nicotinamide serves as an example of attempts to utilize an interaction for improved therapeutic effect.