Quantitative Changes in Mesial Temporal Volume, Regional Cerebral Blood Flow, and Cognition in Alzheimer's Disease

MR-based in vivo hippocampal volumetrics: 2. Findings in neuropsychiatric disorders

“…143 Researchers have found that hippocampal volume loss is able to discriminate patients and controls accurately, and that age-and gender-adjusted, normalized MRI-based hippocampal volumetric measurements provide a sensitive marker of the mesial temporal lobe neuroanatomic degeneration in AD. 121,[144][145][146] However, use of hippocampal volume exclusively is not advocated by all authors, [147][148][149] and other structures such as the amygdala and the entorhinal cortex may also need to be measured, [150][151][152][153] or hippocampal N-acetyl aspartate measurements may need to be performed to improve diagnosis. 154 Karas et al 155 performed voxel-based morphometric analysis in AD and found volume loss of other structures to be equally predictive of AD.…”

MR-based in vivo hippocampal volumetrics: 1. Review of methodologies currently employed

“…Another method which has been used quite often (21% of the protocols) is to use division by whole brain volume for normalization. 1,55,69 Surprisingly, a substantial number of protocols (34%) do not use a correction factor at all. Although, in some cases, absolute volumes are needed (in epilepsy research, or when comparing automatic and manual volumetrics, for example) and thus controlling for head size is not warranted.…”

Patterns of cortical activity and memory performance in Alzheimer’s disease

“…Although memory problems are often subtle in the earliest stages of AD, their steady progression may leave the patient in an almost entirely amnestic condition. Recent neuroimaging studies have demonstrated structural (Jobst et al 1992;Pantel et al 1997), spectroscopic (Lazeyras et al 1998), and functional (Mann et al 1992;Pearlson et al 1992;Siegel et al 1995; for reviews, see Santens and Petit 1997;Small and Leiter 1998) cerebral changes in AD. These changes strike primarily the temporal and parietal association cortices but generally extend to the frontal cortex with progression of the disease (Buchsbaum et al 1991;Haxby et al 1988;Mann et al 1992;Mielke et al 1994;Smith et al 1992;Stein et al 1998), especially with secondary depression (Hirono et al 1998a).…”

“…Pearlson et al (1992) and Pantel et al (1997) linked amnestic deficits to reduced left temporo-parietal regional cerebral blood flow (rCBF), or left superior temporal gyrus and left temporal lobe atrophy, respectively. Using positron emission tomography (PET) with 18 F-2-deoxyglucose (FDG) as a tracer, Haxby et al (1988) found parietal hypometabolism to correlate with prominent impairment in verbal comprehension, calculation, and visuospatial tasks, whereas frontal hypometabolism was correlated with more impaired verbal fluency and attention.…”