Monoamine oxidase-B (MAO-B) activity of platelets of an age- and sex-matched group of controls was compared with several groups of inpatients having non-familial dementia of Alzheimer type (DAT), Parkinson's disease (PD), multi-infarct dementia (MID), mixed types of these 3 diseases and a group of other central nervous system (CNS) organic disorders. All patients were subjected to several psychometric tests, including the Sandoz Clinical Assessment--Geriatric Scale, Hamilton Rating Scale for Depression, Mini-Mental State Examination and the Organic mental Disorder Scale (OMDS). A statistically significant enhancement of MAO-B activity could be observed in DAT patients and in PD patients, whereas the MID group showed a mean activity similar to that of the control group and the group with other organic CNS disorders. In DAT patients the degree of dementia in the OMDS test and the enhancement of MAO activity were positively correlated, but PD did not show such a correlation. It is concluded that the increase of MAO activity in PD and in DAT might be due to a disease-related enhanced affinity to oxygen and to such oxygen-derived radicals as superoxide or hydroxyl radicals. However, a possible drug-induced enhancement of MAO activity in PD cannot be excluded. Furthermore, the MAO-B activity values in platelets of individual patients or controls are not indicative of diagnosis or prognosis of any of these diseases and are of no disease-related specificity.

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A country-wide search for idiopathic torsion dystonia (ITD) in Israel between 1969 and 1975 revealed 42 patients (41 Jewish and 1 Druze Arab). Prevalence of ITD per million population, age-adjusted to the United States population in 1970, was 10.8 in the total Jewish population (22.0 among Jews of European extraction contrasted with 1.5 among Jews with Afro-Asian forebears). Among Europeans, the highest prevalence was among Jews from Eastern Europe. The average age-adjusted annual incidence rates per million population were 0.43 in the total Jewish population, 0.98 in the Europeans, and 0.11 in the Afro-Asians. Among the 40 patients for whom familial data were available, the majority of cases (26) were sporadic. The other 14 belonged to four unrelated European families, all of Russian-Polish origin. The pattern of inheritance in these four families fits an autosomal dominant model with incomplete penetrance.

Twenty-six patients with migraine attacks were treated for 3 to 16 months with flufenamic acid (125 mg four to six times per attack), an inhibitor of prostaglandin synthesis and action. In 25 patients the drug afforded symptomatic relief in 195 of 200 treated attacks. Side effects observed were mild dyspepsia (eight patients) and severe upper gastrointestinal symptoms (two patients). None of the eight patients treated with placebo reported any relief (20 attacks). The "common" antimigraine drugs afforded symptomatic relief in 12 of the patients, partial relief in seven, and no relief in seven. Treatment with flufenamic acid was based on the hypothesis that prostaglandins are involved in migraine attack and that the drug relieves migraine by inhibition of the vasoactivity of prostaglandins.