Depressive illness with initial onset after age 60 has different clinical and prognostic features compared to depression beginning at a younger age. We evaluated waking electroencephalograms (EEGs) in 61 elderly depressed patients (32 early onset, 29 late onset) without cognitive impairment and not receiving psychotropic medications. The groups were comparable for age, severity of Hamilton depression score, education, and Folstein Mini-Mental State scores. Conventional visual EEG analysis revealed no significant differences in the mean alpha rhythm, incidence of abnormal records, or types of EEG abnormalities. Computerized spectral EEG analysis was also performed in 48 patients (23 early onset, 25 late onset). There were no significant differences in the pooled parasagittal mean frequency, theta--beta difference, combined delta and theta percentage, or relative power of the frequency bands. Thus, waking EEGs do not differentiate between elderly patients with the initial onset of the depression before or after age 60.
"have more severe or treatment resistant disorders (Brodaty et al., 1991; Brodaty et al., 1997; Conwell et al., 1989; Greenwald & Kramer-Ginsberg, 1988; Heyman et al., 1991; Klein et al., 1999; Reynolds et al., 1998), they do tend to have higher rates of medical comorbidity, notably of concurrent vascular disease, more extensive cerebral changes on magnetic resonance imaging (notably deep white matter and basal ganglia lesions) and a differing pattern of neuropsychological impairment (Hickie et al., 1995, 1997; Naismith et al., 2002, p. 3). "
[Show abstract][Hide abstract] ABSTRACT: Because the determinants of anxiety and depression in late adolescence and early adulthood may differ from those in later life, we investigated the temporal stability and magnitude of genetic and environmental correlates of symptoms of anxiety and depression across the life span. Data were collected from a population-based Australian sample of 4364 complete twin pairs and 777 singletons aged 20 to 96 years who were followed-up over three studies between 1980 and 1996. Each study contained the 14-item self-report DSSI/sAD scale which was used to measure recently experienced symptoms of anxiety and depression. Symptom scores were then divided and assigned to age intervals according to each subject's age at time of participation. We fitted genetic simplex models to take into account the longitudinal nature of the data. For male anxiety and depression, the best fitting simplex models comprised a single genetic innovation at age 20 which was transmitted, and explained genetic variation in anxiety and depression at ages 30, 40, 50 and 60. Most of the lifetime genetic variation in female anxiety and depression could also be explained by innovations at age 20 which were transmitted to all other ages; however, there were also smaller age-dependent genetic innovations at 30 for anxiety and at 40 and 70 for depression. Although the genetic determinants of anxiety and depression appear relatively stable across the lifespan for males and females, there is some evidence to support additional mid-life and late age gene action in females for depression. The fact that midlife onset for anxiety occurs one decade before depression is also consistent with a causal relationship (anxiety leading to depression) between these conditions. These findings have significance for large scale depression prevention projects.
Twin Research 03/2004; 7(1):39-53. DOI:10.1375/13690520460741435
"Diseases of the brain commonly are marked by changes in brain electrical activity. Increases in slow-wave (lower than 8 Hz) and decreases in high-frequency (above 12 Hz) activity are seen commonly in stroke (Ingvar, 1981; Nagata et al., 1984, 1989; Bo et al., 1987) and in a variety of psychiatric illnesses including schizophrenia (Shagass, 1977; Abrams and Taylor, 1979; Morstyn et al., 1983; Karson et al., 1987), depression (Brenner et al., 1988; Heyman et al., 1991; Leuchter et al., 1993), and Alzheimer's disease ~Leuchter et al., 1987; Brenner et al,, 1988). These electro- en6ephal~gra~hi6 (EEG) changes, however, are not considered reliable measures of brain dysfunction. "
[Show abstract][Hide abstract] ABSTRACT: Brain electrical activity is related to cerebral perfusion. The nature of this relationship is unclear, however and surface-recorded activity has not been a reliable indicator of brain perfusion. We studied 27 subjects, all of whom were examined with single photon emission tomography (SPECT) and quantitative electroencephalography (QEEG), to assess associations between QEEG cordance and relative brain perfusion. Cordance has two indicator states: concordance, which may indicate high perfusion; and discordance, which may indicate low perfusion. We used multiple linear regression to assess the association between cordance and SPECT values, and found that cordance values were strongly associated with tissue perfusion. Concordance in the α band was associated both with mean tissue perfusion and the volume of normally perfused tissue and it had a stronger association with perfusion than any other QEEG variable. Discordance in the β1 band was associated with mean perfusion, and it had a stronger association than did relative but not absolute power. These data suggest that cordance may be useful for the noninvasive assessment of brain perfusion.
Psychiatry Research 10/1994; 55(3-55):141-152. DOI:10.1016/0925-4927(94)90022-1 · 2.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To determine the prevalence of electroencephalogram (EEG) abnormalities at different levels of cognitive impairment and to assess the possible diagnostic usefulness of the test.
Combined prospective assessment of subjects receiving EEGs and retrospective chart review of symptoms and medications.
Academic geriatric psychiatry service.
350 adults age 50 and above; 312 were patients being evaluated for possible organic mental syndrome and 38 were normal controls.
All subjects had EEGs and Mini-Mental State Examinations (MMSE) performed at the time of the EEG. EEGs were rated for the presence and type of abnormality, and subjects were stratified according to the severity of impairment. Charts were reviewed by a person blinded to EEG results to determine clinical diagnosis and medications received.
Abnormal EEGs were significantly more common among all patients (67%) in the study than among controls (11%), and the prevalence of abnormality increased with increasing impairment. Many demented patients with equivocal impairment (42%), and most with mild-to-moderate impairment (65%) had abnormal EEGs. An abnormal EEG was not indicative of dementia even when clear cognitive impairment was present, since patients with depression frequently also had abnormal EEG results.
These findings suggest that the EEG is a moderately sensitive but non-specific indicator of brain dysfunction in the elderly. The significance of abnormalities among patients with equivocal impairment should be more fully assessed by longitudinal follow-up to determine if greater cognitive impairment develops.
Journal of the American Geriatrics Society 07/1993; 41(6):605-11. DOI:10.1111/j.1532-5415.1993.tb06730.x · 4.57 Impact Factor
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