Base rates of "impaired" neuropsychological test performance among healthy older adults.

Base rates of deficient neuropsychological test performance were evaluated among 132 neurologically healthy older normal adults using a variety of measures commonly employed in the "flexible-battery"approach to neuropsychological assessment. Subjects were divided into three age groups (50 to 59, 60 to 69, and 70 to 79 years). Despite the healthy status of our sample, most tests yielded at least some proportion of subjects earning scores in the borderline and impaired ranges (1.3 and 2.0 standard deviations below the age-group mean, respectively). Across the battery of measures, 73% of subjects earned a borderline score on at least one measure, and 20% of subjects earned at least two scores in the impaired range on separate tests. The proportion of subjects consistently earning borderline or impaired scores across multiple measures within specific cognitive domains was generally lower. Results illustrate the problems in interpreting isolated low scores, and the need to consider false-positive base rates in drawing inferences from poor test performance.

Neuropsychological deficits among older depressed patients with predominantly psychological or vegetative symptoms.

Depressed outpatients having primarily psychological or vegetative symptoms, as defined by the factor analytically developed Hamilton Depression Scale superfactors described by Rhoades and Overall (1983), were compared with similarly aged normal controls on a comprehensive neuropsychological battery. The vegetative group evidenced poorer performance than controls on several measures associated with right hemisphere functioning and on a task associated with executive functioning. In contrast, the psychological group did not significantly differ from controls on any measure, and had significantly better performance than the vegetative group on several tasks. These findings suggest that neuropsychological deficits associated with depression may be limited to those patients with primarily vegetative symptoms.

Cognition and white matter hyperintensities in older depressed patients.

OBJECTIVE: The authors compared amounts of white matter hyperintensity in late- and early-onset depressed patients and never-depressed older subjects, compared neuropsychological function in these groups, and investigated the association between white matter hyperintensities and cognitive function in depression. METHOD: Sixty currently depressed patients whose first depression occurred after age 50 years, 35 depressed patients over age 50 whose first depression occurred before age 35, and 165 nonpsychiatrically ill subjects over age 50 underwent magnetic resonance imaging (MRI) and neuropsychological evaluation. Areas of white matter hyperintensity were measured from MRI images. RESULTS: The late-onset patients had more white matter hyperintensity than either of the other groups. Compared to the nondepressed subjects, the patients had significantly lower scores in the cognitive domains of nonverbal intelligence, nonverbal memory, constructional ability, executive ability, and information processing speed. The cognitive abnormalities were mostly confined to the late-onset patients, and the presence of a large amount of white matter hyperintensity was associated with significantly poorer executive skills. However, most of the scores were not in the significantly impaired range. CONCLUSIONS: Large amounts of white matter hyperintensity are more frequent in patients with late-onsetdepression than in elderly subjects with early-onset or no depression. Both late- and early-onset elderly depressed patients show mild decrements in some "right hemisphere" cognitive skills; the late-onset subjects also show deterioration in information processing speed and executive functions. Patients with large amounts of white matter hyperintensity have significantly poorer executive function.

Chronic myeloid leukaemia and a myasthenic syndrome.

This is the first report of a case of chronic myeloid leukaemia (CML) complicated by myasthenic syndrome. The patient suffered two prolonged periods of idiosyncratic busulphan-induced marrow aplasia, the first occurring 5 months after busulphan was stopped. Between these two episodes, and at a time when no therapy was required for the leukaemia, myasthenic syndrome developed. After the patient recovered from the second episode, the myasthenic syndrome disappeared, and, despite subsequent recrudescence of CML, there were no further myasthenic symptoms, and treatment with neostigmine was discontinued.