Excessive compensatory recruitment as a compulsory neurophysiological mechanism in Very Early Alzheimer's Disease as compared to Mild Vascular Dementia and to age-matched normal controls.
This paper supports the theoretical position of the existence of neurophysiological mechanisms of excessive compensatory recruitment of neuronal pools in Very Early Alzheimer's Disease (VEAD) as compared to patients with Mild Vascular Dementia (MVD) and age-matched normal controls. In addition, considering that the very early recognition of Alzheimer's disease is of paramount importance for diagnosis, treatment and clinical follow-up, in the present investigation, we have used Topographic Mapping of ERPs to our Memory Workload Paradigm to delineate excessive compensatory recruitment as a sensitive neurophysiological marker for the accurate detection of VEAD as compared to MVD and to age-matched normal controls. The present findings with the Topographic Mapping of ERPs indicate that VEAD patients displayed significantly larger amplitudes with memory loads as compared to MVD patients (p=0.0001) and to age-matched normal controls (p=0.0001). VEAD patients displayed abnormally high P450 amplitudes (p=0.0001) and shorter P450 latencies (p=0.0001) over parietal and occipital sites as opposed to age-matched normal controls. In addition, contrary to normal controls, VEAD patients exhibited longer latencies over pre-frontal and frontal regions (p=0.0001). On the other hand, P450 latencies for VEAD and MVD patients were not significantly different over anterior and posterior regions (p>0.05). These findings suggest that the delayed P450 latencies found over pre-frontal and frontal regions in both patient populations, reflect the partial disconnection of their neuronal pathways from limbic structures. Specifically, in VEAD patients, this aspect, along with the abnormally high amplitudes found over parietal and occipital regions, support the conclusion that VEAD patients allocate much more cerebral physiological resources and effort to accomplish the memory workload tasks as opposed to age-matched normal controls and to MVD patients. As such, in VEAD, the excessive recruitment of compensatory neuronal pools becomes a compulsory neurophysiological mechanism to meet the demanding tasks of our Memory Workload Paradigm.
Beuzeron-Mangina
Helen
H
Cognitive Psychophysiology Laboratory, Montreal Research and Treatment Center, 3587 University, Montreal, Quebec, Canada. mcgill@ca.inter.net
Mangina
Constantine A
CA
D000368:Aged; D000544:Alzheimer Disease / Q000503:physiopathology* / Q000523:psychology; D001931:Brain Mapping; D015140:Dementia, Vascular / Q000503:physiopathology* / Q000523:psychology; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008568:Memory / Q000502:physiology; D009483:Neuropsychological Tests; D011569:Psychiatric Status Rating Scales; D011999:Recruitment, Neurophysiological / Q000502:physiology*; D014057:Tomography, X-Ray Computed