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Biomedical subjects

J Constantinidis

Publications and source records attributed to J Constantinidis.

At least 109 records · Page 6Linked to original sources
PubMed1977

[Syndrome of senile dementia with dilatation of the cerebral ventricles without other lesions (apropos of 18 observations anatomo-clinical)].

Study of 18 anatomo-clinical observations with dilatation of the cerebral ventricles (without vascular, degenerative or other cerebral lesions), and neuropsychiatric syydrome during the senile period of life. In the morphological and pathogenetic point of view, for one half of these cases a traumatic, microhemorrhagic, or inflammatory aetiology could be taken into consideration; for the other half, the hydrocephalus could be considered as idiopathic.

Aged↗
PubMed1975

[Abnormal movements induced by L-dopa. New therapeutic possibilities].

One of the major difficulties in the treatment of Parkinson's disease with L-Dopa alone or associated with a decarboxylase inhibitor lies in the frequent occurrence of involuntary movements. In some cases these movements can be prevented (eliminated) by increasing the plasma DCI concentration or by associating 3-oxy-methyl-dopa. In resistant cases the authors have conducted a trial with EP 19-088, which belongs to a new class of tricyclic derivatives of indenopyridine. The trial population comprised 42 patients. In 12 of these there was complete cessation of symptoms. In 9 patients a marked improvement was noted, while in 10 others the improvement was slight but definite. The treatment was discontinued in 2 cases due to episodes of increased confusion. In the other 9 patients the experimental treatment had no effect. No side effects were observed in 24 of the 42 patients tested. In addition to symptoms such as nausea or transient heartburn, the remaining patients reported either a slight worsening of their parkinsonian symptoms or an increase in diurnal fatigability.

Heartburn↗
PubMed1975

[Formation of norapinephrine in the rat brain after administration of ((+)-erythro-3,4-dihydroxyphenylserine(author's transl)].

Fluorescence microscopy of rat brains after administration of (+)-erythro-DOPS has been studied. (+)-erythro-DOPS induced an increase of brain NE part of which was formed in the capillary walls. The slight diminution of this increase when (+)-erythro-DOPS was administered after inhibition of peripheral decarboxylase, might result from the algebraic sum of two inversely acting processes: suppression of NE synthesis in the capillary walls and enhancement of parenchymatous NE in some brain areas. (+)-erythro-DOPS enters different brain structures non specifically and NE is formed in DA and 5-HT systems, displacing the amines especially at the terminals; the NE formed by (+)-erythro-DOPS in NE systems should be rapidly catabolised. Possible pharmacological effects of (+)-erythro-DOPS administration involve consideration of the lack of topical specificity of NE formation; the displacement of 5-HT and DA; and the fact (+)-erythro-DOPS produces (+)-NE, and not naturally occurring NE.

Animals↗
PubMed1975

Specificity of the clinical diagnosis of dementia.

The specificity of anatomo-clinical observations were investigated on 776 out of 982 consecutive persons hospitalized at the University Psychiatric Clinic of Geneva. Discriminant function analysis shows that most of the anatomical classes (no dementia, senile dementia, Alzheimerized senile dementia and Alzheimer's presenile dementia, vascular dementia, combined dementia nnd undefined form of encephalopathy) are at least partially separable (less than 50% overlap). On the basis of anatomical criteria, Alzheimer's presenile dementia is not separable from Alzheimerized senile dementia, and senile dementia is not separable from combined dementia. Differentiation between the anatomical classes is improved by a preliminary analysis based on clinical diagnosis. Senile plaques account for 43.4% of the total variation between the anatomical classes. The coefficient of agreement between anatomical and clinical diagnosis is 0.27, which is highly significant. The diagnosis of senile dementia has a poor specificity, while the diagnosis of senile Alzheimerized dementia has a better one. The diagnosis of combined dementia has to be reserved for cases with a similar intensity of vascular and degenerative changes. Alzheimer's presenile dementia has a distinct dominant hereditary pattern and must be considered a separate entity. The high specificity of the diagnosis of Alzheimer's presenile dementia makes it possible to conduct epidemiologic and genetic surveys based on clinical data.

Age Factors↗
PubMed1975

Effect of peripheral decarboxylase inhibition on HVA and 5HIAA in cerebrospinal fluid of depressed patients.

The effects of benserazide on the level of homovanillic acid and 5-hydroxyindoleacetic acid in CSF have been investigated in 1 manic and 11 depressed patients. Benserazide induced no change on both metabolites. This negative result supports the view that monoamine metabolites in CSF, in the absence of loading with an exogenous precursor, originate mostly from brain parenchyma, without significant contribution of the metabolism in capillary walls.

Adult↗
PubMed1975

The stereoisomers of 3,4-dihydroxyphenylserine as precursors of norepinephrine.

The action of the four stereoisomers of 3,4-dihydroxyphenylserine (DOPS) on the monoamine content of brain and heart was investigated with biochemical and histochemical methods. The (+)-erythro-DOPS (50-250 mg/kg i.p.), due to its alphaS configuration, was readily decarboxylated in vivo leading to an accumulation of norepinephrine (NE) in brain and heart. The amino probably corresponded to the unnatural (+) form since the amino acid shows betaS configuration. The NE was located in brain regions rich in noradrenergic (hypothalamus, locus ceruleus), dopaminergic (neostriatum, substantia nigra) and 5-hydroxytryptaminergic (raph'e nuclei) neurons. In addition, (+)-erythro-DOPS decreased the level of endogenous 5-hydroxytryptamine and dopamine and increased that of 5-hydroxyindoleacetic and homovanillic acid in the brain indicating a displacement of 5-hydroxytryptamine and dopamine, respectively, from their storage sites. Inhibitors of extracerebral decarboxylase (benserazid and carbidopa) diminished the (+)-erythro-DOPS-induced increase in cerebral NE by inhibiting the decarboxylation of the amino acid in the walls of the brain capillaries. The (-)-threo-DOPS, which also show alphaS configuration, was decarboxylated too, leading to a rise in cardiac NE. The amine was likely to correspond to the natural(-)-isomer since (-)-threo-DOPS has betaR configuration. This increase in NE lasted much longer than that caused by (+)-erythro-DOPS. In the brain, the accumulation of NE was negligible after i.p. administration of (-)-threo-DOPS but marked after injection of the isomer into a cerebral ventricle indicating a poor penetration of (-)-threo-DOPS through the blood-brain barrier. High doses (500 and 1000 mg/kg i.p.) of (-)-erythro- and (+)-threo-DOPS caused only a slight increase in cerebral and cardiac NE since, due to their alphaR configuration, they were probably not decarboxylated to a major extent. In conclusion, (+)-NE formed from (+)-erythro-DOPS probably accumulates in the storage sites of the endogenous monoamines where it might function as a false neurotransmitter.

Animals↗