Orbitofrontal cortex governs working memory for temporal order

abstract:

How do we think about time? Converging lesion and neuroimaging evidence indicates that orbitofrontal cortex (OFC) supports the encoding and retrieval of temporal context in long-term memory, which may contribute to confabulation in individuals with OFC damage. Here, we reveal that OFC damage diminishes working memory for temporal order, that is, the ability to disentangle the relative recency of events as they unfold. OFC lesions reduced working memory for temporal order but not spatial position, and individual deficits were commensurate with lesion size. Comparable effects were absent in patients with lesions restricted to lateral prefrontal cortex (PFC). Based on these findings, we propose that OFC supports understanding of the order of events. Well-documented behavioral changes in individuals with OFC damage may relate to impaired temporal-order understanding.

authors:

• Elizabeth L Johnson

• William K Chang

• Callum D Dewar

• Donna Sorensen

• Jack J Lin

• Anne-Kristin Solbakk

• Tor Endestad

• Pal G Larsson

• Jugoslav Ivanovic

• Torstein R Meling

• Donatella Scabini

• Robert T Knight

Date: 2022

DOI: https:// doi.org/10.1016/j.cub.2022.03.074.

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Orbitofrontal cortex governs working memory for temporal order

Abstract:

How do we think about time? Converging lesion and neuroimaging evidence indicates that orbitofrontal cortex (OFC) supports the encoding and retrieval of temporal context in long-term memory1, which may contribute to confabulation in individuals with OFC damage2. Here, we reveal that OFC damage diminishes working memory for temporal order, that is, the ability to disentangle the relative recency of events as they unfold. OFC lesions reduced working memory for temporal order but not spatial position, and individual deficits were commensurate with lesion size. Comparable effects were absent in patients with lesions restricted to lateral prefrontal cortex (PFC). Based on these findings, we propose that OFC supports understanding of the order of events. Well-documented behavioral changes in individuals with OFC damage2 may relate to impaired temporal-order understanding.

Authors:

• Elizabeth L. Johnson

• William K. Chang

• Callum D. Dewar

• Donna Sorensen

• Jack J. Lin

• Anne-Kristin Solbakk

• Tor Endestad

• Pal G. Larsson

• Jugoslav Ivanovic

• Torstein R. Meling

• Donatella Scabini

• Robert T. Knight

Date: 2022

DOI: https://doi.org/10.1016/j.cub.2022.03.074

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Patients with basal ganglia damage show preserved learning in an economic game

Abstract:

Both basal ganglia (BG) and orbitofrontal cortex (OFC) have been widely implicated in social and non-social decision-making. However, unlike OFC damage, BG pathology is not typically associated with disturbances in social functioning. Here we studied the behavior of patients with focal lesions to either BG or OFC in a multi-strategy competitive game known to engage these regions. We find that whereas OFC patients are significantly impaired, BG patients show intact learning in the economic game. By contrast, when information about the strategic context is absent, both cohorts are significantly impaired. Computational modeling further shows a preserved ability in BG patients to learn by anticipating and responding to the behavior of others using the strategic context. These results suggest that apparently divergent findings on BG contribution to social decision-making may instead reflect a model where higher-order learning processes are dissociable from trial-and-error learning, and can be preserved despite BG damage.

Authors:

• Lusha Zhu

• Yaomin Jiang

• Donatella Scabini

• Robert T. Knight

• Ming Hsu

Date: 2019

DOI: https://doi.org/10.1038/s41467-019-08766-1

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Anatomic Bases of Event-Related Potentials and Their Relationship to Novelty Detection in Humans

ABSTRACT

Voluntary of involuntary detection of an infrequent stimulus generates a large scalp P300 response. This P300 ERP (P for positive; 300 for the approximate peak latency poststimulation) has been widely used to study phasic attention and memory mechanisms. The P300 phenomenon, first reported in 1965 (Desmedt et al., 1965; Sutton et al., 1965) has been the subject of extensive research in normal, neurologic, and psychiatric populations. P300-like potentials have been described in rats(Ehlers et al., 1991; Yamaguchi et al., 1993), cats(Katayama et al., 1985; O'Connor and Starr, 1985; Wilder et al., 1981), and monkeys(Arthur and Starr, 1984; Neville and Foote, 1984; Paller et al., 1988; Pineda et al., 1989) supporting a broad ethologic significance of this electrophysiological marker of cognition(Fig. 1) (Swick et al., 1994).Theorists have focused on attention and memory formulations to account for the cognitive basis of the P300, although no clear consensus has emerged(Donchin and Coles, 1988; Verleger, 1988). Some of this disagreement results from the fact that the P300 does not represent a unitary brain potential arising from a discrete brain region or cognitive process as initially proposed. Instead, scalp positivities generated in the 300- to 700-ms poststimulus delivery measure activation of multiple neocortical and limbic regions dependent on the degree of voluntary and involuntary attention allocated to a stimulus. Support for this contention is provided by scalp topographic studies in normal subjects(Courchesne et al., 1975; Squires and Hillyard, 1975; Ruchkin et al., 1990a, 1992; Yamaguchi and Knight, 1991a; Bruyant et al., 1993), intracranial recording in epileptic patients (McCarthy et al., 1989; Puce et al., 1991; Paller et al., 1992; Baudena et al., 1995; Halgren et al., 1995a,b) and lesion studies in neurologic patients(Knight, 1984, 1997a; Knight et al., 1989; Yamaguchi and Knight, 1991b, 1992; Scabini, 1992).

AUTHORS

• Robert T. Knight

• Donatella Scabini

Date: 1998

DOI: 10.1097/00004691-199801000-00003

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Anatomical substrates of auditory selective attention: behavioral and electrophysiological effects of posterior association cortex lesions

ABSTRACT

Even-related brain potentials (ERPs) and reaction times (RTs) were recorded in an auditory selective attention task in control subjects and two groups of patients with lesions centered in (1) the temporal/parietal junction (T/P, n = 9); and (2) the inferior parietal lobe (IPL, n = 7). High pitched tones were presented to one ear and low pitched tones to the other in random sequences that included infrequent longer-duration tones and occasional novel sounds. Subjects attended to a specified ear and pressed a button to the longer-duration tones in that ear. IPL and T/P lesions slowed reaction times (RTs) and increased error rates, but improved one aspect of performance — patients showed less distraction than controls when targets followed novel sounds. T/P lesions reduced the amplitude of early sensory ERPs, initially over the damaged hemisphere (N1a, 70–110 ms) and then bilaterally (N1b, 110–130 ms, and N1c 130–160 ms). The reduction was accentuated for tones presented contralateral to the lesion, suggesting that N1 generators receive excitatory input primarily from the contralateral ear. IPL lesions reduced N1 amplitudes to both low frequency tones and novel sounds. Nd components associated with attentional selection were diminished over both hemispheres in the T/P group and over the lesioned hemisphere in the IPL group independent of ear of stimulation. Target and novel N2s tended to be diminished by IPL lesions but were unaffected by T/P lesions. The mismatch negativity was unaffected by either T/P or IPL lesions. The results support different roles of T/P and IPL cortex in auditory selective attention.

AUTHORS

• David L. Woods

• Robert T. Knight

• Donatella Scabini

Date: 1993

DOI: 10.1016/0926-6410(93)90007-R

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Gamma-Aminobutyric Acid-Induced Potentiation of Cortical Hemiplegia

Authors:

• Simon Brailowsky

• Robert T. Knight

• Katherine Blood

• Donatella Scabini

Date: 1986

PubMed: 3942881

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Abstract:

A novel model of hemiplegia in young and aged rats is described. Osmotic minipumps were used to deliver a chronic (7 days), localized application of gamma-aminobutyric acid (GABA) (100 micrograms/microliter/h), to the somatomotor cortex of unrestrained rats. This resulted in an easily quantifiable, contralateral and reversible motor syndrome in both young and aged animals. In the young group, the motor deficit cleared over 5-day period, while in the aged animals it persisted for at least a 2-week period. Control animals treated with saline-filled minipumps did not develop a long-lasting motor deficit. The GABA-induced facilitation of hemiplegia due to small motor cortex lesions and the age effects on behavioral recovery of function are discussed. Cortical inhibitory mechanisms may play a role in debilitating syndromes such as stroke or post-epileptic paralysis.