Thalamic and hippocampal volume associated with memory functions in multiple sclerosis.

OBJECTIVES: Although multiple sclerosis (MS) has long been considered to primarily affect white matter, it is now recognized that cognitive deficits in MS are also related to neocortical, thalamic and hippocampal damage. However, the association between damage to these structures and memory deficits in MS is unclear. This study examines whether MS patients with cognitive impairment have a reduction of hippocampal and/or thalamic volumes compared to cognitively intact patients, and whether these volume reductions correlate with various aspects of memory function. METHODOLOGY: Volumetric MRI measures of thalamus and hippocampus of forty-one patients with MS were performed. The patients were divided in two groups depending on the presence or absence of cognitive impairment, based on their neuropsychological tests scores. RESULTS: Right hippocampal volume was found to be associated with learning, and the left thalamic volume was found to predict performance in verbal memory. Cognitively impaired patients had a tendency to have a reduced left thalamic volume compared to cognitively intact patients. CONCLUSIONS: This study does not support a direct relationship between hippocampal atrophy and verbal memory. These results add to the growing evidence of the involvement of thalamus in cognitive impairment in MS and its association with verbal memory deficits.

Correlation between brain volume change and T2 relaxation time induced by dehydration and rehydration: implications for monitoring atrophy in clinical studies.

Brain volume change measured from magnetic resonance imaging (MRI) provides a widely used and useful in vivo measure of irreversible tissue loss. These measurements, however, can be influenced by reversible factors such as shifts in brain water content. Given the strong effect of water on T2 relaxation, we investigated whether an estimate of T2 relaxation time would correlate with brain volume changes induced by physiologically manipulating hydration status. We used a clinically feasible estimate of T2 ("pseudo-T2") computed from a dual turbo spin-echo MRI sequence and correlated pseudo-T2 changes to percent brain volume changes in 12 healthy subjects after dehydration overnight (16-hour thirsting) and rehydration (drinking 1.5 L of water). We found that the brain volume significantly increased between the dehydrated and rehydrated states (mean brain volume change = 0.36%, p = 0.0001) but did not change significantly during the dehydration interval (mean brain volume change = 0.04%, p = 0.57). The changes in brain volume and pseudo-T2 significantly correlated with each other, with marginal and conditional correlations (R (2)) of 0.44 and 0.65, respectively. Our results show that pseudo-T2 may be used in conjunction with the measures of brain volume to distinguish reversible water fluctuations and irreversible brain tissue loss (atrophy) and to investigate disease mechanisms related to neuro-inflammation, e.g., in multiple sclerosis, where edema-related water fluctuations may occur with disease activity and anti-inflammatory treatment.