Abstract:
Muller and colleagues provide behavioral, physiological and neuroanatomical correlates of our ability to rapidly allocate attention to different regions of visual space
Muller and colleagues provide behavioral, physiological and neuroanatomical correlates of our ability to rapidly allocate attention to different regions of visual space
Sharon L. Thompson-Schill
Diane Swick
Martha J. Farah
Mark D'Esposito
Irene P. Kan
Robert T. Knight
Date: 1998
PubMed: 9861060
What are the neural bases of semantic mem- ory? Traditional beliefs that the temporal lobes subserve the retrieval of semantic knowledge, arising from lesion studies, have been recently called into question by functional neuro- imaging studies finding correlations between semantic re- trieval and activity in left prefrontal cortex. Has neuroimag- ing taught us something new about the neural bases of cognition that older methods could not reveal or has it merely identified brain activity that is correlated with but not caus- ally related to the process of semantic retrieval? We examined the ability of patients with focal frontal lesions to perform a task commonly used in neuroimaging experiments, the gen- eration of semantically appropriate action words for concrete nouns, and found evidence of the necessity of the left inferior frontal gyrus for certain components of the verb generation task. Notably, these components did not include semantic retrieval per se.
Auditory sensory memory is a critical first stage in auditory perception that permits listeners to integrate incoming acoustic information with stored representations of preceding auditory events. Here, we investigated the neural circuits of sensory memory using behavioral and electrophysiological measures of auditory processing in patients with unilateral brain damage to dorsolateral prefrontal cortex, posterior association cortex, or the hippocampus. We used a neurophysiological marker of an automatic component of sensory memory, the mismatch negativity (MMN), which can be recorded without overt attention. In comparison with control subjects, temporal-parietal patients had impaired auditory discrimination and reduced MMN amplitudes with both effects evident only following stimuli presented in the ear contralateral to the lesioned hemisphere. This suggests that auditory sensory memories are predominantly stored in auditory cortex contralateral to the ear of presentation. Dorsolateral prefrontal damage impaired performance and reduced MMNs elicited by deviant stimuli presented in either ear, implying that dorsolateral prefrontal cortices have a bilateral facilitatory effect on sensory memory storage. Hippocampal lesions did not affect either performance or electrophysiological measures. The results provide evidence of a temporal-prefrontal neocortical network critical for the transient storage of auditory stimuli.
According to the competition account of lexical selection in word production, conceptually driven word retrieval involves the activation of a set of candidate words in left temporal cortex and competitive selection of the intended word from this set, regulated by frontal cortical mechanisms. However, the relative contribution of these brain regions to competitive lexical selection is uncertain. In the present study, five patients with left prefrontal cortex lesions (overlapping in ventral and dorsal lateral cortex), eight patients with left lateral temporal cortex lesions (overlapping in middle temporal gyrus), and 13 matched controls performed a picture-word interference task. Distractor words were semantically related or unrelated to the picture, or the name of the picture (congruent condition). Semantic interference (related vs. unrelated), tapping into competitive lexical selection, was examined. An overall semantic interference effect was observed for the control and left-temporal groups separately. The left-frontal patients did not show a reliable semantic interference effect as a group. The left-temporal patients had increased semantic interference in the error rates relative to controls. Error distribution analyses indicated that these patients had more hesitant responses for the related than for the unrelated condition. We propose that left middle temporal lesions affect the lexical activation component, making lexical selection more susceptible to errors.
Robert T. Knight
Diane Swick
Date: 1998
Lesion studies of prefrontal cortex and attention. In The Attentive Brain, R. Parasura- man, ed. Cambridge, Mass.: Bradford Books, MIT Press, pp. 143-162.
Precise timing of sensory information from multiple sensory streams is essential for many aspects of human perception and action. Animal and human research implicates the basal ganglia and cerebellar systems in timekeeping operations, but investigations into the role of the cerebral cortex have been limited. Individuals with focal left (LHD) or right hemisphere (RHD) lesions and control subjects performed two time perception tasks (duration perception, wherein the standard tone pair interval was 300 or 600 msec) and a frequency perception task, which controlled for deficits in time-independent processes shared by both tasks. When frequency perception deficits were controlled, only patients with RHD showed time perception deficits. Time perception competency was correlated with an independent test of switching nonspatial attention in the RHD but not the LHD patients, despite attention deficits in both groups. Lesion overlays of patients with RHD and impaired timing showed that 100% of the patients with anterior damage had lesions in premotor and prefrontal cortex (Brodmann areas 6, 8, 9, and 46), and 100% with posterior damage had lesions in the inferior parietal cortex. All LHD patients with normal timing had damage in these same regions, whereas few, if any, RHD patients with normal timing had similar lesion distributions. These results implicate a right hemisphere prefrontal-inferior parietal network in timing. Time-dependent attention and working memory functions may contribute to temporal perception deficits observed after damage to this network.
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).
Andrew P. Yonelinas
Neal E. A. Kroll
Ian G. Dobbins
Michele Lazzara
Robert T. Knight
Date: 1998
PubMed: 9673991
Previous studies using the process dissociation and the remember-know procedures led to conflicting conclusions regarding the effects of anterograde amnesia on recollection and familiarity. We argue that these apparent contradictions arose because different models were used to interpret the results and because differences in false-alarm rates between groups biased the estimates provided by those models. A reanalysis of those studies with a dual-process signal-detection model that incorporates response bias revealed that amnesia led to a pronounced reduction in recollection and smaller but consistent reduction in familiarity. To test the assumptions of the model and to further assess recognition deficits in amnesics, we examined receiver operating characteristics (ROCs) in amnesics and controls. The ROCs of the controls were curved and asymmetrical, whereas those of the amnesics were curved and symmetrical. The results supported the predictions of the model and indicated that amnesia was associated with deficits in both recollection and familiarity.
Novelty detection is a fundamental capacity of all mammalian nervous systems /64/. The ability to orient to unexpected events is critical for both survival and normal memory function /82/. The mechanisms whereby the brain detects and responds to novelty have become of increasing interest to neuroscientists. A review is provided of human electrophysiological and blood flow data focused on delineating the neural systems engaged by novelty. Electrophysiological recording of event-related potentials (ERPs) has shown that novel stimuli activate a distributed network involving prefrontal and posterior association cortex as well as the hippocampus /4,23,24,32,33,36,86,88/. Activation of this network facilitates subsequent memory for novel events /27/. Neural modeling provides additional support for a prominent role of novelty in normal memory function /43/. Blood flow studies employing PET and fMRI have also begun to define the neural regions activated by novelty. The blood flow data provide converging evidence on the role of the hippocampus and cortical association regions in the processing of novelty /30,66,75,76/. The results of the behavioral, ERP and blood flow research confirm that a distributed neocortical-limbic circuit is activated by stimulus novelty. These distributed circuits maintain a template of the recent past /74/. Deviations from the template activate a neocortical-limbic network facilitating behavioral response to and memory storage of novel events.
"Theory of mind," the ability to make inferences about others" mental states, seems to be a modular cognitive capacity that underlies humans" ability to engage in complex social interaction. It develops in several distinct stages, which can be measured with social reasoning tests of increasing difficulty. Individuals with Asperger"s syndrome, a mild form of autism, perform well on simpler theory of mind tests but show deficits on more developmentally advanced theory of mind tests. We tested patients with bilateral damage to orbito-frontal cortex (n = 5) and unilateral damage in left dorsolateral prefrontal cortex (n = 5) on a series of theory of mind tasks varying in difficulty. Bilateral orbito-frontal lesion patients performed similarly to individuals with Asperger"s syndrome, performing well on simpler tests and showing deficits on tasks requiring more subtle social reasoning, such as the ability to recognize a faux pas. In contrast, no specific theory of mind deficits were evident in the unilateral dorsolateral frontal lesion patients. The dorsolateral lesion patients had difficulty only on versions of the tasks that placed demands on working memory.