Skip to main content
placeholder image

Evoked cardiac response components in cognitive processing: Differential effects of amyotrophic lateral sclerosis

Journal Article


Abstract


  • We investigated the mechanism of two evoked cardiac response components associated with different aspects of information processing. Innocuous stimuli presented in an irrelevant condition elicit a simple cardiac deceleration termed ECR1. The same stimuli presented in a relevant condition (such as results from requesting subjects to silently count the stimuli) elicit a complex biphasic response with a large secondary acceleration in heart rate. This difference is attributed to the additional effect of cognitive task performance, resulting in an addition response component, ECR2. This may be realised by subtraction of the two responses. We investigated the mechanisms involved by comparing cardiac response profiles from a neurologically-impaired group with those from a control group, amyotrophic lateral sclerosis (ALS) has been associated with a loss of synaptic connections in the frontal lobe. Twelve ALS clinically non-demented patients were age-matched with twelve neurological patients without pathological changes in the brain. Cardiac response profiles for ECR1 and ECR2 were examined as a function of group. ECR1 did not differ between the groups, but ECR2 was significantly impaired in the ALS patients. The results are discussed in terms of different brain regions associated with these two cardiac response components. ECR1 may be associated with automatic preattentive stimulus registration involving, in the case of auditory stimuli, the auditory analyser and associated pathways, while ECR2 appears to be a correlate of controlled executive processing, involving the frontal cortex.

Publication Date


  • 1999

Citation


  • Kaiser, J., Wronka, E., Barry, R. J., & Szczudlik, A. (1999). Evoked cardiac response components in cognitive processing: Differential effects of amyotrophic lateral sclerosis. Acta Neurobiologiae Experimentalis, 59(4), 329-334.

Scopus Eid


  • 2-s2.0-0032754159

Start Page


  • 329

End Page


  • 334

Volume


  • 59

Issue


  • 4

Abstract


  • We investigated the mechanism of two evoked cardiac response components associated with different aspects of information processing. Innocuous stimuli presented in an irrelevant condition elicit a simple cardiac deceleration termed ECR1. The same stimuli presented in a relevant condition (such as results from requesting subjects to silently count the stimuli) elicit a complex biphasic response with a large secondary acceleration in heart rate. This difference is attributed to the additional effect of cognitive task performance, resulting in an addition response component, ECR2. This may be realised by subtraction of the two responses. We investigated the mechanisms involved by comparing cardiac response profiles from a neurologically-impaired group with those from a control group, amyotrophic lateral sclerosis (ALS) has been associated with a loss of synaptic connections in the frontal lobe. Twelve ALS clinically non-demented patients were age-matched with twelve neurological patients without pathological changes in the brain. Cardiac response profiles for ECR1 and ECR2 were examined as a function of group. ECR1 did not differ between the groups, but ECR2 was significantly impaired in the ALS patients. The results are discussed in terms of different brain regions associated with these two cardiac response components. ECR1 may be associated with automatic preattentive stimulus registration involving, in the case of auditory stimuli, the auditory analyser and associated pathways, while ECR2 appears to be a correlate of controlled executive processing, involving the frontal cortex.

Publication Date


  • 1999

Citation


  • Kaiser, J., Wronka, E., Barry, R. J., & Szczudlik, A. (1999). Evoked cardiac response components in cognitive processing: Differential effects of amyotrophic lateral sclerosis. Acta Neurobiologiae Experimentalis, 59(4), 329-334.

Scopus Eid


  • 2-s2.0-0032754159

Start Page


  • 329

End Page


  • 334

Volume


  • 59

Issue


  • 4