Marshal F. Folstein

<h3>To the Editor.—</h3> In response (Archives1982;39:1443-1445) to a letter by Ganguli and Saul (Archives1982;39:1442-1443), Robins and Helzer noted that the Mini-Mental State Examination,¹incorporated into the Diagnostic Interview Schedule (DIS) to assess cognitive impairment, had been reported by Folstein et al to differentiate between pseudodementia and true organic brain syndromes. We would like to make that statement more specific. The Mini-Mental State Examination was designed as a clinical method for grading cognitive impairment. It produces a score that can be used to follow the course of patients or as a case detection technique after cutoff scores are established. In a clinical psychiatric setting, a low Mini-Mental score can be associated with many disorders including mental retardation, delirium, manicdepressive disorder, and schizophrenia, as illustrated by Folstein et al in their pre-<i>DSM-III</i>article in 1975.^1,2However, on a medical unit like the one from which Ganguli and

With a psychiatrist's standardized clinical diagnosis as the criterion, the 'Mini-Mental State' Examination (MMSE) was 87% sensitive and 82% specific in detecting dementia and delirium among hospital patients on a general medical ward. The false positive ratio was 39% and the false negative ratio was 5%. All false positives had less than 9 years of education; many were 60 years of age or older. Performance on specific MMSE items was related to education or age. These findings confirm the MMSE's value as a screen instrument for dementia and delirium when later, more intensive diagnostic enquiry is possible; they reinforce earlier suggestions that the MMSE alone cannot yield a diagnosis for these conditions.

D2 dopamine and S2 serotonin receptors were imaged and measured in healthy human subjects by positron emission tomography after intravenous injection of 11C-labeled 3-N-methylspiperone. Levels of receptor in the caudate nucleus, putamen, and frontal cerebral cortex declined over the age span studied (19 to 73 years). The decline in D2 receptor in males was different from that in females.