Event-related potential measurement of deficits in information processing following moderate to severe closed head injury

Abstract

Event-related potentials may offer more precision than behavioural measures for understanding the extent and timing of information processing difficulties that follow closed head injury (CHI). Behavioural tests consistently indicate a general reduction in cognitive function but lack adequate diagnostic or prognostic function. This study compares a group of seven CHI patients, in which time since injury varied between 1 and 5 years following injury, with 10 matched controls on a three-tone discrimination task. Abnormality in the processing of tones as early as 200 ms following their onset, as measured by the P2 and N2 components of the event-related potential, indicated a general difficulty with tone discrimination. This abnormality was obtained despite differing damage profiles over patients and is likely to be due to the diffuse aspects of damage normal in CHI. These results also indicate that functional deficits in CHI patients can extend up to 5 years or more. A correlation between P2/N2 amplitudes and time since injury, however, suggests that both these components normalize with the passage of time and offers the prospect of a sensitive, non-behavioural measure of recovery in cognitive processing.

Closed head injury-related information processing deficits: An event-related potential analysis

“…Others (Heinze et al, 1992), however, including those in which it was quantified in the difference wave- Table 4 Closed head-injury effects on visual ERPs Sangal and Sangal (1996) Sangal and Sangal (1996) Polo et al (2002) Entries reflect comparisons between head-injury survivors and healthy controls. Kaipio et al (1999) Clark et al (1992) Packard and Ham (1996) Curry (1980 Keren et al (1998 Potter and Barrett (1999) Packard and Ham (1996) forms (Duncan et al, , 2005, have found significant reductions in visual N200 amplitude. Of the long latency components, P300 has been the most studied in investigations of head-injury survivors (Campbell and de Lugt, 1995).…”

“…N200 is thought to reflect detection and discrimination of features of a deviant stimulus. In one group of studies (Clark et al, 1992;Duncan et al, 2003Duncan et al, , 2005Solbakk et al, 1999), N200 was reduced and/or its scalp distribution altered, suggesting that such processing is impaired in head-injury survivors. However, in a second group of studies, auditory N200 was reported to be unchanged (e.g., Bernstein, 2002;Potter et al, 2002;Segalowitz et al, 2001) or larger (Curry, 1980;Ford and Khalil, 1996;Rugg et al, 1988) in survivors.…”

“…Only three of the 13 papers assessing P200 reported amplitude reductions in this component (Clark et al, 1992;Keren et al, 1998;Reinvang et al, 2000).…”

Decreased prefrontal cortex activity in mild traumatic brain injury during performance of an auditory oddball task

“…A reduction in P3b amplitude in TBI patients suggests a corresponding reduction in attentional resources allocated to updating working memory traces as compared with healthy controls (Duncan et al 2005). Only a small proportion of existing TBI ERP studies reported abnormalities in N2 or an earlier-peaking P3a ERP thought to more directly reflect attentional-orienting (Curry 1980;Clark et al 1992;Ford and Khalil 1996;Solbakk et al 1999;Potter et al 2001;Duncan et al 2003Duncan et al , 2005, which strongly suggests inquiry should focus on any abnormalities of P3b-related (i.e., target-detection) brain activity.…”

Coma Outcome Prediction Using Event-Related Potentials: P₃ and Mismatch Negativity

“…Firstly P 3 does not always follow MMN, which is independent of conscious attention to the stimulus; secondly P 3 is perhaps more significantly affected by the age of the subject, and thirdly the MMN arises principally from a supratemporal origin close to the auditory cortex, whilst the P 3 is generated by multiple cortical and subcortical centres, including paralimbic, frontoparietocingular and ventral temporofrontal cortices [Halgren et al, 1998]. In two studies of patients investigated 6 months or more after head injury, it was shown that N 2 (of which the MMN is a part) was more sensitive than P 3 to the effects of traumatic brain injury, because of their different roles in information processing [Rugg et al, 1988], and that the N 2 may normalize with time [Clark et al, 1992].…”