Abstract
Among 78 carefully diagnosed dementia of Alzheimer type (DAT) patients, periodic synchronous discharges (PSD) on electroencephalograms (EEGs) were obserbed in 12 advanced cases. Although several case studies have been made since 1970, it is not widely recognized that PSD can be observed in advanced DAT patients. In this study the clinical picture, the nature of PSD, background activity of EEGs and 2 autopsied cases have been clinicopathologically investigated.
The mean duration of the disease in the 12 cases was 6.7 years. The mean age of onset of the disease was 67 years of age. Among the 12 cases, 9 patients presented akinetic mutism or symptoms closely resembling akinetic mutism, who were completely bed-ridden with their extremities fixed in flexion. The other 3 patients were severely demented. They presented various degrees of Parkinsonian syndromes or paratonic rigidity accompanied by some infection and general fatigue. In one of these 3 patients, PSD were observed during the transient apallic state and the PSD themselves were also transient.
The basic rhythm in EEGs were 4-6 c/s: middle amplitude theta waves dominant with delta waves on frontal leads. Triphasic delta, theta and sharp waves of PSD were dominant on centro-parieto-occipital leads. Background activity was not suppressed differing from that of Creutzfeld Jacob disease (CJD). According to the interval histograms of PSD, the majority presented an interval of 1-2 s (1.5 s mean) with some lability which was relatively slower than that of CJD. Fronto-parieto-occipital delay was not observed. By 1 c/s photic stimulation, PSD was not driven. From the stand point of the ordinary course of EEG change, which can be seen as the clinical stage of DAT advances, the EEGs of these 12 cases were situated on the so called subcortical slow wave stage or on the transitional stage between the cortical slow wave stage and the subcortical slow wave stage.
Form the above results, it was assumed that the etiology of PSD does not depend on the rapidity of clinical progress itself but on spread of lesion to the subcortical area in addition to the primary cortical lesion.
The clinicopathological evaluation of the 2 autopsied cases, sponginess and gliosis of cortical gray matter, and severe gliosis of subcortical white and gray matter were marked changes as the most case studies point out. In one of the cases, diffuse cortical Lewy bodies were observed. According to this case and the case which presented transient PSD, it seems that some functional change contribute to the etiology of PSD. With more careful and detailed examination of EEGs of advanced DAT, cases that present PSD are likely to be found.
