In order to investigate functional topography of human hand somatosensory cortex we recorded somatosensory evoked fields (SEFs) on MEG during the first 40 ms after stimulation of median nerve, ulnar nerve, and the 5 digits. We applied dipole modeling to determine the three-dimensional cortical representations of different peripheral receptive fields. Median nerve and ulnar nerve SEFs exhibited the previously described N20 and P30 components with a magnetic field pattern emerging from the head superior and re-entering the head inferior for the N20 component; the magnetic field pattern of the P30 component was of reversed orientation. Reversals of field direction were oriented along the anterior-posterior axis. SEFs during digit stimulation showed analogous N22 and P32 components and similar magnetic field patterns. Reversals of field direction showed a shift from lateral inferior to medial superior for thumb to little finger. Dipole modeling yielded good fits at these peak latencies accounting for an average of 83% of the data variance. The cortical digit representations were arranged in an orderly somatotopic way from lateral inferior to medial superior in the sequence thumb, index finger, middle finger, ring finger, and little finger. Median nerve cortical representation was lateral inferior to that of ulnar nerve. Isofield maps and dipole locations for these components are consistent with neuronal activity in the posterior bank of central fissure corresponding to area 3b. We conclude that SEFs recorded on MEG in conjunction with source localization techniques are useful to investigate functional topography of human hand somatosensory cortex non-invasively.

Aim of this study was the characterization of the circadian melatonin profile in de novo Parkinson patients (N = 9, age 60.0 +/- 3.2 years, mean +/- SEM) and the comparison of these profiles with those of controls and Parkinson patients treated with l-dopa/decarboxylase inhibitor (l-dopa/DCI). We collected 14 venous blood samples during a period of 24 hours and measured the serum melatonin levels by a radioimmuno assay. De novo Parkinson patients displayed the nocturnal melatonin peak (acrophase) at the same time as controls and significantly later than l-dopa/DCI treated patients (1:54 +/- 15.6 min [average clock time +/- SEM in minutes] vs. 1:45 +/- 15.6 min vs. 0:13 +/- 40.8 min). The amount of secreted melatonin did not differ among the three groups. Stage and duration of Parkinson's disease did not correlate with the amount of secreted melatonin. Patients of the tremor subgroup, however, secreted more melatonin than patients presenting only with rigidity and akinesia. The phase advance in Parkinson patients treated with l-dopa/DCI is possibly due to a central nervous dopaminergic effect elicited by l-dopa administration and not inherent to Parkinson's disease per se.

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Although several studies on the efficacy and the toxicity of exogenous melatonin in Parkinson patients have been carried out, there are no data available on melatonin secretion in these patients. We therefore performed a controlled trial in 9 Parkinson patients (aged 62.1 +/- 8.7 years, x +/- SD) and in 14 control persons (58.0 +/- 10.4 years). Parkinson patients were treated with l-dopa (300-1000 mg per day) in combination with a peripheral decarboxylase inhibitor (benserazide, carbidopa). 14 venous blood samples were taken from each person during a period of 24 hours in order to investigate the circadian secretion pattern of melatonin. Serum melatonin levels were estimated by radioimmuno assay. We found that the circadian secretion patterns of l-dopa-treated Parkinson patients and age-matched controls were very similar except for a phase advance of the nocturnal melatonin elevation in the parkinsonian group.

Physical activity during lifetime was investigated among 32 Parkinson patients (age 65.6 +/- 8.1 yrs, mean +/- SD) retrospectively by means of a structured interview. Data were compared with 31 healthy controls (age 61.7 +/- 5.8 yrs). An objective score was obtained by presenting a list of all kinds of sports, subjective estimation of physical activity was done by visual analogous scales. Until the occurrence of the first symptoms (mean = 58.5 yrs) the patients did not differ from controls. During the course of disease a striking reduction in physical activity but no complete abandonment of sports was found. Swimming, hiking and gymnastics were the favoured sports in both groups. Learning of new sports seemed to be impossible for the patients.

Serum lipids were determined in 97 patients (56 men, 41 women; ages 42 +/- 15 years) undergoing long-term anticonvulsive treatment (longer than 6 months). The total group showed increased total cholesterol, decreased high-density lipoprotein HDL cholesterol, an increased ratio of total to HDL cholesterol, and decreased apolipoprotein A1 and B values compared to population means. Considering males and females separately, all differences were significant (P < 0.01) in men, whereas in women only the differences in HDL cholesterol, ratio of total to HDL cholesterol, and apolipoproteins A1 and B reached the level of statistical significance. Considering the different anticonvulsant groups, cholesterol was significantly increased only in phenytoin-treated males; HDL cholesterol was significantly lowered and the ratio of total to HDL cholesterol significantly increased in all groups. Apolipoprotein A1 levels were significantly decreased in phenytoin-treated females and valproate-treated patients of both sexes. Apolipoprotein B levels were significantly decreased in all groups except carbamazepine-treated males. Especially in men treated with anticonvulsants these lipid levels may be considered a risk factor for atherosclerosis.

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