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Biomedical subjects

Antonio R Damasio

Publications and source records attributed to Antonio R Damasio.

5 recordsLinked to original sources
PubMed2003

Differential distribution of calbindin D28k and parvalbumin among functionally distinctive sets of structures in the macaque brainstem.

In a study of brainstem in the cynomolgus monkey, we found that the distribution of calbindin D28K (CB) and parvalbumin (PV) is nonoverlapping among functionally distinct sets of brainstem structures. Nuclei involved in representation and regulation of the organism's internal state contain CB, whereas those involved in the representation of the external environment and the representation or execution of externally directed actions contain only PV. Moreover, our findings indicate that different nuclei known as components of the ascending reticular activating system (ARAS) contain either CB or PV or both, suggesting that this system in primates operates with both CB and PV. In line with previously reported findings, we also found that unmyelinated pathways contain only CB, whereas myelinated pathways contain PV. Distribution of CB and PV in the macaque brainstem follows a pattern comparable to, but in some instances significantly different than, the pattern previously reported in the rat. We argue that the nonoverlapping distribution of CB and PV among different structures of the brainstem might reflect underlying differences in the physiological, anatomic, and perhaps phylogenetic properties of these structures. Considering our recent findings of selective vulnerability of brainstem structures to Alzheimer's disease, the present data suggest that the majority of macaque brainstem nuclei that contain CB are vulnerable to neurofibrillary tangles in humans. By contrast, only few nuclei that contain PV exhibit pathologic changes. Some of these nuclei are affected with a high number of neuritic plaques without ever developing neurofibrillary tangles.

Animals↗
PubMed2003

Neuroanatomical correlates of brainstem coma.

The brainstem tegmentum, including the reticular formation, contains distinct nuclei, each of which has a set of chemical, physiological and anatomical features. Damage to the brainstem tegmentum is known to cause coma, the most radical disturbance of consciousness. However, it has remained unclear which nuclei within the tegmentum are crucial for the maintenance of consciousness in humans. Accordingly, we initiated a retrospective study of MRIs obtained from 47 patients with brainstem stroke. The lesion boundaries were charted on patient MRIs and transferred onto a corresponding series of 4.7 T MRIs obtained from a control brainstem specimen that later was cut on a freezing microtome and analysed histologically. In addition, medical charts and available post-mortem materials were used to obtain relevant clinical and anatomical data to verify the MRI readings in each case. We found that in the 38 patients who did not have coma, brainstem damage either was located outside the tegmentum (n = 29) or produced a very small and unilateral compromise of the tegmentum (n = 9). In contrast, in patients who had coma (n = 9), the lesions in the tegmentum were mostly bilateral (n = 7) and were located either in the pons alone (n = 4) or in the upper pons and the midbrain (n = 5). The maximum overlap territory of the lesions coincided with the location of the rostral raphe complex, locus coeruleus, laterodorsal tegmental nucleus, nucleus pontis oralis, parabrachial nucleus and the white matter in between these nuclei. We also found that four coma subjects developed hyperthermia and died in the absence of any infections. In these cases, the maximum lesion overlap was centred in the core of pontine tegmentum. Our findings suggest that lesions confined to the upper pons can cause coma in humans even in the absence of damage to the midbrain. The findings also point to the brainstem nuclei whose lesions are likely to be associated with loss of consciousness and fatal hyperthermia in humans.

Adult↗
PubMed2003

Dissociable neural systems for recognizing emotions.

This study tested the hypothesis that the recognition of emotions would draw upon anatomically separable brain regions, depending on whether the stimuli were static or explicitly conveyed information regarding actions. We investigated the hypothesis in a rare subject with extensive bilateral brain lesions, patient B., by administering tasks that assessed recognition and naming of emotions from visual and verbal stimuli, some of which depicted actions and some of which did not. B. could not recognize any primary emotion other than happiness, when emotions were shown as static images or given as single verbal labels. By contrast, with the notable exception of disgust, he correctly recognized primary emotions from dynamic displays of facial expressions as well as from stories that described actions. Our findings are consistent with the idea that information about actions is processed in occipitoparietal and dorsal frontal cortices, all of which are intact in B.'s brain. Such information subsequently would be linked to knowledge about emotions that depends on structures mapping somatic states, many of which are also intact in B.'s brain. However, one of these somatosensory structures, the insula, is bilaterally damaged, perhaps accounting for B.'s uniformly impaired recognition of disgust (from both static and action stimuli). Other structures that are damaged in B.'s brain, including bilateral inferior and anterior temporal lobe and medial frontal cortices, appear to be critical for linking perception of static stimuli to recognition of emotions. Thus the retrieval of knowledge regarding emotions draws upon widely distributed and partly distinct sets of neural structures, depending on the attributes of the stimulus.

Affect↗
PubMed2003

Role of the amygdala in decision-making.

The somatic marker hypothesis proposes that both the amygdala and the orbitofrontal cortex are parts of a neural circuit critical for judgment and decision-making. Although both structures couple exteroceptive sensory information with interoceptive information concerning somatic/emotional states, they do so at different levels, thus making different contributions to the process. We define "primary inducers" as stimuli that unconditionally, or through learning (e.g., conditioning and semantic knowledge), can (perceptually or subliminally) produce states that are pleasurable or aversive. Encountering a fear object (e.g., a snake), a stimulus predictive of a snake, or semantic information such as winning or losing a large sum of money are all examples of primary inducers. "Secondary inducers" are entities generated by the recall of a personal or hypothetical emotional event or perceiving a primary inducer that generates "thoughts" and "memories" about the inducer, all of which, when they are brought to memory, elicit a somatic state. The episodic memory of encountering a snake, losing a large sum of money, imagining the gain of a large sum of money, or hearing or looking at primary inducers that bring to memory "thoughts" pertaining to an emotional event are all examples of secondary inducers. We present evidence in support of the hypothesis that the amygdala is a critical substrate in the neural system necessary for triggering somatic states from primary inducers. The ventromedial cortex is a critical substrate in the neural system necessary for the triggering of somatic states from secondary inducers. The amygdala system is a priori a necessary step for the normal development of the orbitofrontal system for triggering somatic states from secondary inducers. However, once this orbitofrontal system is developed, the induction of somatic states by secondary inducers via the orbitofrontal system is less dependent on the amygdala system. Perhaps the amygdala is equivalent to the hippocampus with regard to emotions, that is, necessary for acquiring new emotional attributes (anterograde emotions), but not for retrieving old emotional attributes (retrograde emotions). Given the numerous lesion and functional neuroimaging studies illustrating the involvement of the amygdala in complex cognitive and behavioral functions, including "social cognition," we suggest that this involvement is a manifestation of a more fundamental function mediated by the amygdala, which is to couple stimuli/entities with their emotional attributes, that is, the processing of somatic states from primary inducers.

Amygdala↗