We recently found that patients with drug-induced parkinsonism (DIP) may have normal (group I) or abnormal (group II) putamen [(123)I]FP-CIT DAT (dopamine transporter) binding. In this study we reassessed clinical features and DAT binding in 19 of the original 32 patients (10 of group I and 9 of group II) after a 19-39-month follow-up period and tested the effects of chronic levodopa treatment in both cohorts of patients. In group I patients, [(123)I]FP-CIT SPET (single photon emission tomography) was still normal in all patients at follow-up; DAT binding and UPDRS (Unified Parkinson's Disease Rating Scale) motor score values did not differ from baseline. In group II patients, [(123)I]FP-CIT SPET was still abnormal at follow-up; putamen DAT binding was significantly reduced and UPDRS III score higher compared to baseline. Levodopa treatment improved motor symptoms in three out of ten patients of group I and in eight out of nine patients of group II. No adverse psychiatric effects were observed in any of the patients. This study shows that DAT binding imaging may help to identify subjects with DIP secondary to a loss of dopamine nerve terminals in the context of a progressive degenerative parkinsonism. Patients with DIP may benefit from levodopa therapy, particularly when dopamine nerve terminal defects are present, and this should be considered in the therapeutic management of these patients.

We assessed the status of dopamine nerve terminals in patients treated with dopamine receptor blocking agents (DRBAs) who had developed drug-induced parkinsonism (DIP). We performed [(123)I]FP-CIT SPET in 32 consecutive patients who were on DRBAs for at least 6 months and developed extrapyramidal signs. The UPDRS-III was used to assess clinical severity. Twenty-six age- and sex-matched healthy subjects served as control group. Putamen [(123)I]FP-CIT SPET binding was reduced in 14 and normal in the remaining 18 patients. There was no difference between the two groups for age, duration of DRBAs treatment, UPDRS III, tremor, rigidity, and bradykinesia subscores for upper and lower limbs. Conversely, symmetry of parkinsonian signs and presence bucco-linguo-masticatory dyskinesias were more frequent in individuals with normal tracer binding. Imaging of the dopamine transporter may help to identify subjects with DIP secondary to a loss of dopamine nerve terminals.

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SUMMARY Li,-Na a countertransport was measured in red blood cells of 58 normotensive subjects (27 females and 31 males), 60 patients with essential hypertension (26 females and 34 males), and in 28 with secondary hypertension (19 females and 9 males). The mean values (± SEM) expressed as mmol Li (1 red cells x hr)" 1 were 0.18 ± 0.02 (females) and 0.20 ± 0.01 (males) in the control group, 0.34 ± 0.04 (females) and 0.39 ± 0.03 (males) in essential hypertension, 0.16 ± 0.03 (females) and 0.19 ± 0.02 (males) in secondary hypertension. The mean value of Li,-Na o countertransport obtained in essential hypertension was statistically different from those obtained in both normals (p < 0.001) and patients with secondary hypertension (p < 0.001). A negative correlation was found between age and Li | -Na o countertransport in normotensive males (r = -0.648; p < 0.001) but neither in normal females nor in patients with essential hypertension. A positive correlation (r = + 0.425; p < 0.05) was found between plasma renin activity after intravenous furosemide and Ll-Na countertransport in essential hypertension. These findings support the hypothesis of a characteristic cation transport across the red blood cell membrane of patient with essential hypertension which might be correlated with the plasma renin activity. (Hypertension 5:529-534, 1983) KEY WORDS •• erythrocyte countertransport • age • plasma renin activity • hypertension A N altered cation transport in red blood cells of essential hypertensive subjects has often been observed and has been sometimes referred to as a useful test differentiating essential from secondary hypertension.1 " 4 The abnormality concerning different mechanisms of sodium transport, has been also detected in normotensive people born to parents with essential hypertension:5 ' 6 it could have a predictive value for a later hypertensive disease. One of the cation transport mechanisms that has been found abnormal in the erythrocytes of patients with essential hypertension is the Li r Na o countertransport, 2 6 albeit a consistent overlap of the values of the countertransport between the normotensive and hypertensive groups has been further reported by several authors. -7 8The aim of the present study was to correlate the Li r Na 0 countertransport in the red blood cells of normotensive and hypertensive people with other clinical and biochemical parameters usually investigated in these subjects and particularly with the plasma renin activityF Methods Selected for study were 58 (27 females and 31 males) normotensives, 60 patients (26 females and 34 males) with essential hypertension, and 28 patients (19 females and 9 males) with secondary hypertension. The mean age of the three groups of patients was 38 ± 15, 46 ± 11, and 41 ± 16 years respectively. Among secondary hypertensives, 13 had hypertension secondary to kidney disease, eight had hyperaldosteronism (6 hyperplasia and 2 adenoma), four had polycystic kidney disease, and three had renovascular hypertension. All patients were untreated for at le...

Abstract:Beta-intetferons like other type I intetferons are produced in response to viral infections by various mammalian cells. These include macrophages, dendritic cells and fibroblasts. Type I intetferons have non-specific antiviral and anti-proliferative effects, as well as a broad spectrum of immunomodulatory activities. On this basis, type I intetferons are used successfully in the treatment of viral infections such as hepatitis C, papilloma and HIV-l virus. They are also used (mostly in combination with other drugs) to treat some forms of cancer, including leukemia. Whilst these effects could be anticipated from the biological function of type I intetferons, it came as a surprise to most when a group of neurologists presented convincing clinical and laboratory evidence of a relevant and important effect of intetferon beta-l b in multiple sclerosis (MS). These effects were first noted with regard to its earlier relapsing-remitting form, which is marked by reversible exacerbation, and subsequently also in secondary progressive MS with its increasing physical and especially motor disability. We describe the development, clinical effects and side effects as well as the mode of action of this new therapeutic approach to MS.