Different contributions of the human amygdala and ventromedial prefrontal cortex to decision-making.

The somatic marker hypothesis proposes that decision-making is a process that depends on emotion. Studies have shown that damage of the ventromedial prefrontal (VMF) cortex precludes the ability to use somatic (emotional) signals that are necessary for guiding decisions in the advantageous direction. However, given the role of the amygdala in emotional processing, we asked whether amygdala damage also would interfere with decision-making. Furthermore, we asked whether there might be a difference between the roles that the amygdala and VMF cortex play in decision-making. To address these two questions, we studied a group of patients with bilateral amygdala, but not VMF, damage and a group of patients with bilateral VMF, but not amygdala, damage. We used the "gambling task" to measure decision-making performance and electrodermal activity (skin conductance responses, SCR) as an index of somatic state activation. All patients, those with amygdala damage as well as those with VMF damage, were (1) impaired on the gambling task and (2) unable to develop anticipatory SCRs while they pondered risky choices. However, VMF patients were able to generate SCRs when they received a reward or a punishment (play money), whereas amygdala patients failed to do so. In a Pavlovian conditioning experiment the VMF patients acquired a conditioned SCR to visual stimuli paired with an aversive loud sound, whereas amygdala patients failed to do so. The results suggest that amygdala damage is associated with impairment in decision-making and that the roles played by the amygdala and VMF in decision-making are different.

Parahippocampal projections to posterior auditory association cortex (area Tpt) in Old-World monkeys.

Retrograde and anterograde tracing methods were used to study the connections between the parahippocampal gyrus and the posterior auditory association cortex (area Tpt) in the Old-World monkey. Nine monkeys received injections of tritiated amino acids in different areas of the parahippocampal gyrus, and three monkeys received injections of the retrograde tracer fast blue in area Tpt of the auditory association cortex. It was observed that the medial part of the posterior portion of the parahippocampal gyrus (area TH) gives rise to projections that terminate in layers I-III of area Tpt. Using complementary retrograde tracing experiments, the cells of origin for this projection were identified in layers V and VI of area TH. The findings reveal a direct structural coupling between auditory association cortices and a temporal region thought to play a role in learning and memory. These connections may form part of a neural system in the monkey that is related to acoustic learning and memory. Homologous systems in humans may be involved in auditory learning and language acquisition.

Nonhaemorrhagic thalamic infarction. Clinical, neuropsychological and electrophysiological findings in four anatomical groups defined by computerized tomography.

Twenty-five patients with nonhaemorrhagic infarcts of the thalamus were studied clinically and by neuropsychological testing, computerized tomography and somatosensory evoked response (SER) recordings. Our aim was to determine whether the findings in these different tests would form distinct symptom clusters associated with different anatomical territories of the thalamus. Infarction conforming to the tuberothalamic arterial territory caused a facial paresis for emotional movements, severe neuropsychological deficits and a delay of the SER after P14. Infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER. Infarction conforming to the anterior choroidal territory caused a hemiparesis, moderate neuropsychological deficits and varied sensory evoked responses. Patients with infarctions conforming to the entire geniculothalamic territory had sensory loss in multiple modalities, minimal neuropsychological deficits and absence of sensory evoked responses after P14. A lacune in this territory caused pure hemisensory loss involving part of the body for the modalities of pain and light touch but not proprioception or vibration. Neuropsychological deficits were uncommon and N32 and N60 were delayed in the SER.

Nonhemorrhagic infarction of the thalamus: behavioral, anatomic, and physiologic correlates.

We studied five patients with nonhemorrhagic thalamic infarction with neuropsychological tests, CT, and somatosensory evoked responses (SERs). The three patients with left thalamic lesions had abnormalities of language, memory, visuospatial processing, intellect, and personality-changes compatible with dementia. The two patients with right thalamic lesions were not aphasic and did not have verbal memory defects, but were otherwise comparable. Four lesions occurred in the tuberothalamic artery territory and one in the deep interpeduncular artery territory. SERs revealed a delay in the first negative peak after P14 in the tuberothalamic patients, and a delay in the third negative peak (N60) in all patients.

Olfactory dysfunction in man: anatomical and behavioral aspects.

We reviewed studies examining the olfaction of patients with brain damage for the purpose of discerning correlations between disordered structure and function. Patient samples included those with neurological disorders and neurosurgical interventions and recording of spontaneous or elicited neuronal activity. Brain areas involved in olfaction include the olfactory bulbs, the orbitofrontal and medial temporal cortices, the thalamus, and the amygdala. Despite recent advances in olfactory anatomy, understanding of how these structures are related to olfactory detection, discrimination, and recognition continues to be limited. Inadequate localization of brain lesions and lack of comprehensive behavioral assessment have thus far prevented a detailed account of the organization of olfaction in the human brain.

Aphasia with nonhemorrhagic lesions in the basal ganglia and internal capsule.

Atypical aphasia syndromes were associated with circumscribed nonhemorrhagic infarctions of the anterior limb of the internal capsule and of the striatum, in the dominant hemisphere. None of the several cases could be classified in terms of the classic cortical aphasia syndromes, nor did they correspond to the description of aphasia produced by hemorrhage in the thalamus or putamen. Control subjects without aphasia had lesions in the same structures of the nondominant hemisphere, or they had comparably circumscribed damage, which was located lateral or caudal to the previously indicated locus. The findings raise the question of participation of the dominant striatum, and of the connectional systems that course in the anterior limb of the internal capsule, in language processing.

A neurological model for childhood autism.

We analyze the behavioral and motor disturbances in childhood autism. On the basis of analogy to signs and conditions seen in adult neurology, we propose that the syndrome results from dysfunction in a system of bilateral neural structures that includes the ring of mesolimbic cortex located in the mesial frontal and temporal lobes, the neostriatum, and the anterior and medial nuclear groups of the thalamus. The mesolimbic cortex is cytoarchitectonically, angioarchitectonically, and neurochemically distinct and, along with the striatum, forms the entire target area of dopaminergic mesencephalic neurons. This raises the possibility that autism is related to neuromediator imbalance in those structures. Such dysfunction might be the result of macroscopic or microscopic changes in the target area or in structures functionally influencing them, consequent to a variety of causes such as perinatal viral infection, insult to the periventricular watershed area, or genetically determined neurochemical abnormalities.