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To examine the utility of the dexamethasone suppression test (DST) in the differential diagnosis of depression in elderly demented patients, we reviewed the literature and focused on four components of this question: (1) cortisol nonsuppression rates in dementia; (2) cortisol nonsuppression and dementia severity; (3) cortisol nonsuppression in demented versus depressed patients; and (4) cortisol nonsuppression following antidepressant treatment. A combined analysis of 27 articles showed cortisol nonsuppression in 60% of patients with concurrent dementia and depression, in 47% of patients with depression only, in 41% of patients with dementia only, in 46% of patients with multi-infarct dementia, in 36% of patients with primary degenerative dementia, and in 10% of controls. The abnormal DST rate in demented patients was not significantly different from the abnormal DST rate in depressed patients. Eight of 12 studies (67%) did not find a significant relationship between DST results and dementia severity in dementia patients without depression. Twelve of 13 studies (92%) did not find a relationship between age and DST outcome. The data we reviewed do not support the use of the DST in discriminating between depression and dementia or between dementia subtypes. (
The mechanism by which the A4 (β-amyloid) domain of the Alzheimer amyloid precursor protein (APP) is deposited in plaques is unknown, and limited information is available concerning the extent to which other APP sites are associated with plaques. To address these issues, we prepared antiserum to a peptide adjacent to the N-terminus of the APP (referred to as N1) and examined its distribution in brain relative to A4 by double-immunostaining techniques. Anti-N1 localized to both neurons and glia in control and Alzheimer patients. In the Alzheimer brain, anti-N1 detected plaques. Quantitation revealed that 85% of thioflavin-positive plaques, and 91% of A4-positive plaques were also N1 positive. Double-staining methods directly demonstrated colocalization of distant APP sites. The data suggest that proposed mechanisms for amyloid deposition during plaque formation must take into account the extracytoplasmic domain, in addition to the A4 region, rather than be confined exclusively to the A4 site. (
The records were reviewed for 129 medically ill geriatric inpatients treated with either dextroamphetamine or methylphenidate for secondary depression during a five year period at the Massachusetts General Hospital. Eighty-one percent of patients demonstrated at least some improvement following psychostimulant treatment. Sixty-six percent of these experienced marked to moderate amelioration of their depressive symptoms. Improvement was rapid and usually occurred within the first or second day of treatment. No significant difference in efficacy was noted between the two psychostimulants or across diagnostic categories for depression. Only 8% of patients experienced adverse reactions significant enough to warrant termination of the psychostimulant trial. No instances of anorexia due to psychostimulant treatment were observed. (
Two patients, aged 104 and 91 years, who presented with medical problems and depression were successfully treated with 1.25 to 5 mg of methylphenidate without evidence of tolerance or toxicity. Benefits were sustained for more than 8 months on smaller amounts of this central nervous system stimulant than has been previously reported. (
Several experiments were conducted to validate the use of a two-channel microprocessor-based electroencephalographic (EEG) device for detecting changes in EEG background rhythm in the clinic or at the bedside. The reliability of background measures in healthy individuals was evaluated by obtaining EEG data on 20 control subjects on two occasions separated by at least 1 day. The sensitivity to an experimental toxic encephalopathy was evaluated using measures of EEG and the Buschke Memory Selective Reminding Test after the administration of scopolamine hydrobromide, 0.86 mg subcutaneously, to three healthy volunteers. Postdrug measures of the EEG showed significant group differences from controls at 1 and 2 hours for relative alpha and relative theta power. The drug-induced change for each individual exceeded the predicted range calculated from data on control subjects. These findings suggest the feasibility and the potential utility of this method. This approach was extended to the elderly with measures on 102 subjects (average age, 85 years) living in an institutional setting. EEG measures in the population were of acceptable reliability and were significantly correlated with Mini-Mental State Examination (MMSE) scores (r = -.375 for theta and .357 for beta). Preliminary findings suggest that this method may detect metabolic encephalopathies in the elderly. The study demonstrates the potential value of this approach and suggests the need for further research. (

Previous demonstrations that problem solving deficits may occur early in the course of Parkinson's disease (PD) have been taken to support the view that disturbances in the functioning of the frontal lobes are responsible for the initial cognitive deficits in this disease. However, no specific pattern of responding associated with poor problem solving by PD patients has been observed consistently. In an effort to clarify the nature of the problem solving deficits in PD we administered the Wisconsin Card Sorting Test (WCST) and the California Card Sorting Test (CCST), a new test which provides separate measures of concept generation, concept identification, and concept execution as well as several different measures of perseveration. On both tests PD patients of lower than normal mental status performed poorly and their patterns of performance resembled those previously described for patients with focal frontal lobe lesions, but PD patients of normal mental status performed normally. Because poor problem solving in association with increased perseverative responding was only observed for patients with global cognitive deficits these findings do not necessarily support the idea that frontal dysfunction is the principal cause of impaired cognition in PD. Although the overall pattern of results was similar for the WCST and the CCST, the CCST was more sensitive for detecting deficits than was the WCST. (
A prolonged (interictal) delirium was induced by electroconvulsive therapy (ECT) in 6/36 (17%) elderly depressed patients. Brain magnetic resonance imaging or brain computerized axial tomography revealed structural changes in the basal ganglia and white matter in all six patients who developed delirium. These findings are consistent with our previous work and with several lines of data that have implicated the basal ganglia and subcortical white matter in the development of delirium from other causes. These results suggest that lesions in these areas may predispose one to developing an interictal delirium during a course of ECT. (


