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Temporal slow wave (TSW) on electroencephalography (EEG) is a common finding in the elderly. Several studies have found a correlation between TSW and cerebrovascular diseases.1,2 Klass and Brenner, in their review describing EEG in the elderly, suggested that TSW were associated with aging and concluded that such TSW were within the normal range.3 We investigated the clinical significance of TSW by using the following electrophysiological criteria: irregular delta waves ranging from 2 to 2.5 Hz frequency; 1–2 s duration; propagation toward the earlobe; and superimposition on background EEG waves. We previously reported that such TSW were associated with the existence of small brain infarctions observed on magnetic resonance images (MRI)4 and that TSW were also associated with microangiopathy of the retina in diabetic patients.5 Recently, we reported that TSW were more frequently seen in elderly patients with depression than in age-matched controls.6

It is already known that a significantly high percentage of elderly patients with depression have underlying cerebrovascular lesions. Alexopoulos et al. proposed that such patients be classified as belonging to a subgroup of patients with vascular depression (VDep).7 Likewise, we suggest that TSW can serve as a useful indicator of this type of depression.6 In the present report we discuss the clinical course of a female patient with VDep whose EEG findings demonstrated morphologic changes of TSW.

A 57-year-old woman visited the Department of Psychiatry at Mie University School of Medicine complaining of sudden psychomotor retardation, depressive mood and loss of interest without any psychological factors. At the age of 53 years she had been diagnosed as having major depression (Diagnostic and Statistical Manual of Mental Disorders, 4th edn; DSM-IV8) owing to her complaining of depressive mood, decrease in appetite, insomnia, and general fatigue. She had been successfully treated with several antidepressants and had been stable especially in the last 1 year. However, in spite of having hypertension for several years, she had not been taking medication regularly.

At this consultation she had no neurological abnormalities or cognitive impairments because routine laboratory tests were normal. Her blood pressure was 162/104 mmHg. The MRI and EEG examinations were performed immediately. Magnetic resonance imaging showed multiple small T2 high-intensity lesions in the basal ganglia and deep white matter. Some of them were accompanied by abnormalities also in the T1-weighted image. She was diagnosed as having VDep by the MRI findings and also by reviewing the clinical course using Alexopoulos's criteria.7 The EEG demonstrated TSW, lasting 1–2 s, with an average amplitude of 70 µV on both sides. Treatment for hypertension with calcium channel blocker was started in addition to antidepressants. When MRI and EEG were repeated 10 months later, her depressive symptoms had partly improved. The MRI showed no increase in the number of T2 high-intensity lesions. Treatment with antihypertensives was successful in controling blood pressure and is effective at preventing future strokes. The EEG performed on the same day as the MRI showed that the TSW became inconspicuous. The basic rhythm on both EEG was alpha activity with a predominant frequency of 9.5 Hz, which was not an extraordinary finding for her age.

Sporadic TSW considered to be associated with mild cerebrovascular dysfunction, including temporal irregular slow wave as findings in the present report, show a variety of morphological characteristics.9 These TSW are known to correlate with aging and subclinical cerebrovascular diseases.4,5 The main finding in the present report was that the morphology of TSW differed between two EEG performed at two different clinical stages in the same elderly woman with VDep. Her TSW of medium voltage became inconspicuous 10 months later, upon repeated follow-up EEG. According to this finding, we consider that the appearance and morphological characteristics of TSW might suggest the degree of functional changes in focal areas associated with multiple cerebral infarctions.

In most cases of VDep, brain MRI demonstrate multiple neurologically silent lesions, or old infarction, as was the case in the present patient. We occasionally should assess the functional as well as structural changes in the brain at the time of examination in clinical setting. EEG was more convenient and less invasive than single photon emission computed topography in assessment of functional changes in patients with VDep. In subjects with small cerebral infarctions, the slower frequency of alpha waves is absent on routine EEG, as was the case in the present patient; slight slowing was also observed upon only computerized analysis of the EEG pattern. In visual EEG analysis, the existence of TSW or similar morphological changes on EEG might provide a biological marker for improved assessment of present organic factors in patients with VDep, which could augment or support MRI findings.

Because this report involves only a single case, we still do not have a clear explanation for the mechanisms of morphologic change in the TSW. One possible explanation for the present results is that the degree of dysfunction varies with time after onset; such an explanation is suggested by the observed serial changes in focal blood flow in patients with small infarctions. Further study is needed to account for the present findings.

REFERENCES

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