The human entorhinal region consists of a number of areas; however, there is no generally accepted nomenclature for these cytoarchitectonic fields, and the designation of its constituent layers or strata is a matter of controversy. Here, we consider a hitherto neglected adjacent field, the preamygdaloid claustrocortex. Its medial subfield has a small common border with the rostromedial entorhinal region (width maximal 2 mm). Both fields are cytoarchitectonically rather similar. The rostromedial oral entorhinal field lacks ascending terminal islands. Its unusually small pre-alpha cells are arranged in a thin band or small clusters consisting of pyramidal, triangular, or polymorphic cells. The conspicuous chromophilic pre-beta cell clusters are composed of a variety of cell types, including groups of ‘immature’ spindle-shaped or bipolar nerve cells. Furthermore, a rare sulcus within the entorhinal region (central sulcus of the entorhinal region: observed in 4% of the 450 brains examined) is associated with an unusual lamination of the entorhinal layers in its wall and floor. Both the specific shape and arrangement of neurones in the claustrocortical-rostral entorhinal border region and the unusual lamination within the rare central entorhinal sulcus are regarded as reflecting neurodevelopmental disturbances characteristic of schizophrenic brains. In contrast, our observations in a large sample of serially sectioned brains from controls, schizophrenics, and patients suffering from neuropsychiatric diseases other than schizophrenia do not support this assumption.
Influence of dopamine-agonists on the pharmacokinetics and pharmacodynamics of levodopaBackground: Despite the broad clinical use of levodopa and dopamine-agonists and their well established clinical efficacy in parkinsonian patients, little is known about the exact pharmacodynamics of both substances and their pharmaeodynamic interactions. However, exact knowledge of pharmacodynarrdcs is essentially for the optimization of therapeutic regimens and maximal clinical efficacy especially in fluctuating patients.Methods: An oral single dose challenge using 100 mg levodopa 25 mg benserazide was performed under standardized conditions in 10 parkinsonian patients with clear-cut wearing-off fluctuations. A continuous s.c. infusion of apomorphine in a clinical subthreshold dosage was coadmimstered to the levodopa challenge under double blind conditions vs. NaC1 in each patient. Levodopa serum-concentrations (LSC) and the actual motor disability (AMD) as the efficacy parameter were measured in 15 rain intervalls over 4 h. AMD was semiquantitatively measured by Columbia-University-Rating-Scale (CURS) sum-scoring, LSC was measured by HPLC. Calculation of main pharmacodynamic parameters (LPC-effect analysis) was performed individually using a semiparametric approach. Data were fitted by an Emax model.Results: Levodopa pharmacokinetics were not significantly influenced by the coadministration of apomorphine with exception of a slight increase of AUC. Pharmacodynamics were significantly altered by apomorphine. Starting from a similar level of basic disability Emax (19.9 _+ 7.7 vs. 19.7 -+ 7.7 pts.) was similar under both regimen but clear differences were seen in Teq (26-+ 8 vs. 19 + 10 min), MRTe (1.9 + 0.5 vs. 3.0 + 0.9 h) and EC50 (430 _+ 163 vs. 315 + 123 ng/ml). The slope factor N showed some decrease under apomorphine but remained still on a high level (17 vs. 7). Our data have shown that the "all or nothing" character of the motor response to levodopa ist preserved under coadministration of a dopamine-agonist and that the mnplitude of motor improvement remains unchanged whereas the duration of the on phase is clearly increased.
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