Voxel-based mapping of brain hypometabolism in permanent amnesia with PET.

In this study, we used voxel-based mapping methods to compare the resting cerebral metabolic rate of glucose (CMRglc) measured with PET in five patients with permanent amnesia (three with chronic Wernicke-Korsakoff and two with postanoxia syndrome) to that of nine healthy age-matched subjects. We assessed (i) a group pattern of relative hypometabolism; and (ii) the consistency of this group pattern, if any, in individual subjects, according to etiology. The results from the group analysis documented that permanent amnesia is associated with hypometabolism in the thalamus, posterior cingulate cortex, and mesial prefrontal cortex (near the anterior cingulate gyrus), bilaterally, as well as in the left supramarginal and middle temporal gyri. The individual analysis showed that this group pattern was found in essentially each patient, regardless of the cause of amnesia. Thus, permanent amnesia is subtended by dysfunction in structures belonging to Papez/limbic circuits as well as in left-hemisphere areas typically concerned with verbal functions, probably through a mechanism of thalamo-cortical disconnection and possibly involved in retrograde amnesia. The use of a voxel-based method allowed us to map a common network of synaptic dysfunction in a neuropsychological syndrome regardless of etiology. Our results indicate that this should be a powerful method in functional neuropsychology.

Functional neuroanatomy of amnesia: positron emission tomography studies.

In this article, we review the principles of, and provide examples for, the new approach of functional neuropsychology in the field of amnesia. In the permanent amnesic syndrome, positron emission tomography (PET) can provide statistical maps of the brain regions with significantly impaired resting metabolism in comparison with control subjects. These regions include not only Papez's circuit but also the left supramarginal gyrus, which may explain in part the retrograde amnesia present in most cases of amnesic syndrome. This approach is also of great interest in transient global amnesia (TGA) because the defect of episodic memory is highly selective and occurs without permanent damage. The few available PET studies in TGA suggest the dysfunction of a distributed network including the hippocampal region and the prefrontal cortex, with a different pattern individually. Further studies will be necessary to better understand the relationships between the precise cognitive deficits in TGA and the pattern of brain hypometabolism. In Alzheimer's disease (AD), the study of the correlations between memory test scores and metabolic values across a sample of subjects provides a map of those brain structures whose synaptic pathology dysfunction underlies the particular neuropsychological alteration. The distribution of the sites of correlations shows striking differences according to each memory system. This approach should open the way for the unravelling of the neurobiological substrates of both cognitive impairment and compensatory mechanisms in neurodegenerative diseases. Over and above their applications in neurological research, such studies in brain-diseased subjects are particularly useful for establishing cognitive and neurobiological models of human memory, because they allow the highlighting of the neural networks that are essential for memory function. From a cognitive neuroscience perspective, the functional neuropsychology of amnesia is, therefore, complementary to the classic activation paradigm in normal subjects, which identifies the cerebral structures that are involved with, but not necessarily indispensable for, the execution of the task.

[Function imaging of the hippocampus in Korsakoff's syndrome]. / Imagerie fonctionnelle des hippocampes dans le syndrome de Korsakoff.

A case of alcoholic Korsakoff syndrome is reported in a 47 year-old-man. Neuropsychological examination revealed an important both anterograd and retrograd amnesia but procedural and short-term memory were not affected nor was intellectual capacity. Cerebral IRM was normal. Pet scan demonstrated a previously unsuspected fact: the diminution of glucose metabolism in the two hippocampus and in the mamillary bodies.