Modern physiology of orienting response

Also called "novelty detection." Novelty detection is crucial for learning and for cognitive flexibility. Novel events are better remembered (von Restorff H 1933). Molecular links of novelty are established to the short arm of chromosome 11 and the D4 receptor gene.

Structural network encompasses the dorsolateral prefrontal cortex, temporoparietal junction, hippocampus and cingululate gyrus.

Physiological detection is accomplished with an "oddball"task eg. P300 stimulus, MEEG and ERP. Maximal amplitude occurs over the parietal area of scalp. Frontal activation increases with task difficulty. Human lesions typically show inferior parietal, superior temporal, thalamic and cingulate activation.

Involuntary and voluntary attention to novelty have different physiologies. The (involuntary) P300 (P3a) has a frontoscalp distribution, peaks in 50 msec (earlier) and habituates over 5-10 presentations. P3a recordings show activation of multiple areas. The hippocampal recorded (voluntary) ERP, like the scalp P3b, does not habituate over repeated presentation of stimulus. Conversely, the hippocampal novelty ERP like the P3a scalp recording, rapidly habituates. The P3a is thought to be a CNS marker of the orienting response.

Prefrontal lesions differentially reduce P3a but not P3b. Patients with orbitofrontal damage have an orthogonal response with a heightened p3a amplitude, perhaps correlating with increased startle and and labile behavior. Moreover with prefrontal damage, p3a response is muted over the entire hemisphere. This supports a modulating role for prefrontal cortex over the rest of the hemisphere.

The hippocampus is involved in novelty mismatch (Sokolov and Vinogradova). The artery of Uchimara irrigates the hippocampus, especially the posterior part. Patients have normal parietal p3b but abnormal frontal p3a associated with novelty. ERP recordings suggest the prefrontal cortex processes the initial novelty detection and then alerts the hippocampus which fires afterwards. The fibers alerting the hippocampus may traverse the retrosplenial cortex. fMRI as of (old data) depended upon field strength and technique to show the changes seen by other techniques.

Norepinephrine may also be important in novelty detection. See post on pharmacotherapy with NE for orienting response.
Selected references
Benjamin J , Li L, Patterson BD et al. Population and familial association between the D$ dopamine receptor gene and measures of novelty seeking. Nature Genetics 12: 81-84.

Chao LL, Knight RT. Human prefrontal lesions increase distractibility to irrelevant sensory inputs. Neuroreport 6:1605-1610. 1995.

Ibid. 1998. Contribution of human DL prefrontal cortex ti delay performance. J COgn Neuroscience 10:167-177.

Courchesne E. Hillyard SAm Galambos R 1975. Stimulus novelty task relevance and the visual evoked potential in man. EEG Clin Neurophys 39: 131-143.

Picton TW 1995. The P300 wave of the human event related potential. J Clin Neurophysiol 9: 456-479.

Woods DL , Knight RT. 1986. Electrophysiological evidence of increased distractibility after dorsolateral prefrontal lesions. Neurology 36; 212-216.