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Biomedical subjects

A Erfurth

Publications and source records attributed to A Erfurth.

48 records · Page 3Linked to original sources
PubMed1992

Effects of methiothepin on changes in brain serotonin release induced by repeated administration of high doses of anorectic serotoninergic drugs.

We previously observed, using in vivo microdialysis, that the potassium-evoked release of frontocortical serotonin (5-HT) is suppressed after rats receive high doses (30 mg/kg, i.p., daily for 3 days) of fluoxetine, a selective blocker of 5-HT reuptake. We now describe similar impairments in 5-HT release after repeated administration of two other 5-HT uptake blockers, zimelidine and sertraline (both at 20 mg/kg, i.p. for 3 days) as well as after dexfenfluramine (7.5 mg/kg, i.p. daily for 3 days), a drug which both releases 5-HT and blocks its reuptake. Doses of these indirect serotonin agonists were about 4-6 times the drug's ED50 in producing anorexia, a serotonin-related behavior. In addition, methiothepin (20 microM), a non-selective receptor antagonist, locally perfused through the dialysis probe 24 h after the last drug injection, enhanced K(+)-evoked release of 5-HT at serotoninergic nerve terminals markedly in control rats and slightly in rats treated with high doses of dexfenfluramine or fluoxetine. On the other hand, pretreatment with methiothepin (10 mg/kg, i.p.) one hour before each of the daily doses of fluoxetine or dexfenfluramine given for 3 days, totally prevented the decrease in basal and K(+)-evoked release of 5-HT. Finally, when methiothepin was injected systemically the day before the first of 3 daily injections of dexfenfluramine, it partially attenuated the long-term depletion of brain 5-HT and 5-HIAA levels induced by repeated administration of high doses of dexfenfluramine. These data suggest that drugs which bring about the prolonged blockade of 5-HT reuptake - such as dexfenfluramine and fluoxetine - can, by causing prolonged increases in intrasynaptic 5-HT levels as measured by in vivo microdialysis, produce receptor-mediated long-term changes in the processes controlling serotonin levels and dynamics.

Animals↗
PubMed1990

[Adenosine and methylxanthines in the central nervous system--on their significance for psychiatry and neurology].

In the last 15 years the central effects of adenosine and its importance for neurology and psychiatry have increasingly become an object of investigation. Physiology and metabolism of adenosine have been examined by different research groups. The effects of adenosine in the central nervous system and the various mechanisms of these effects have been described by electrophysiologic methods. The inhibition of the release of several neurotransmitters through adenosine has already been described 10 years ago. In this review studies on binding sites for adenosine receptor ligands are discussed thoroughly. The properties and the highly specific distribution of the distinct receptor subtypes are described. For the functioning of the adenosinergic system the different interactions with other centrally active substances such as benzodiazepines, barbiturates, neuroleptics, anti-depressants, opiates, alcohol and carbamazepine have turned out to be of interest. The results of neuropsychiatric investigations on methylxanthines, which are antagonists at the adenosine receptor, are widely considered. Finally the discussion on the importance of the adenosinergic system in different neurological and psychiatric diseases is summed up. The particular significance of adenosine in the modulation of dopaminergic functions is emphasised.

Adenosine↗
PubMed1989

Tolerability of long term clozapine treatment.

Tolerability of long term clozapine treatment (7-8 years) was investigated in 27 female patients (age 34-77 years). Diagnosis according to ICD 9 was schizophrenia in 21 patients, severe psychomotor agitation with mental deficiency in 4 patients and an "endogenous" depression in 2 patients. All patients had previously been treated with different neuroleptics but with inadequate response or distressing side effects. The duration of the disorder was 10-36 years, duration of hospitalisation 10-36 years. At the day of investigation the total dose of clozapine ranged from 52-826 g, the average total dose being 385 g. The daily dose of clozapine ranged from 75 to 600 mg, the average daily dose being 225 mg. Only 2 patients were treated exclusively with clozapine, the other 25 patients were also receiving other neuroleptics. Seventy eight per cent of the investigated patients complained about hypersalivation and 63% showed overweight. In 37% of the patients the EEG demonstrated abnormalities. Mild parkinsonism was reported in 15% and akathisia in 11% of the patients, all these patients being on combined treatment. Clozapine did not induce tardive dysakinesia (TD) in any of the patients within a treatment period of 7-8 years. It is concluded that a potential benefit of clozapine includes a low incidence of neurological side effects even after long term administration.

Adult↗
PubMed1989

[AIDS disease and psychopathology--observations by the psychiatric consultation service of an internal medicine clinic].

The majority of HIV-infected inpatients are treated in departments of internal medicine. For the conditions of the west-german health service it was studied, if and how psychiatric symptoms of HIV-positive inpatients of a University Hospital for internal medicine require a psychiatrist. The evaluation of the suicide risk and psychopharmacological treatment of depressive syndromes were the most frequent reasons to ask for a psychiatrist. It became evident, that by means of a psychiatric consultation service, treatment of psychiatric complications in HIV-infection is feasible in a department of internal medicine.

AIDS Dementia Complex↗
PubMed1989

[Indications for therapy using MAO inhibitors].

The MAOIs have been an underutilized and overly feared class of medical compounds potentially useful for a wide spectrum of disorders. At one end of the spectrum they have been found effective for several anxiety disorders, especially when phobic or panic reactions are part of the symptoms. At the other end of the spectrum, they are effective in patients with melancholic depressions, especially outpatients who have lack of energy, a history of bipolar disorder, or a nonresponse to conventional treatment with TCAs. However, their major role for psychiatric patients appears to be in the large heterogeneous group of ambulatory depressives who have symptoms of both anxiety and depression. The danger of side effects or toxicity associated with MAOIs has been exaggerated. Most side effects are relatively mild and are controllable by dose reduction or other supportive measures. The adverse reaction of most concern, hypertensive crisis, is great extent preventable with appropriate dietary restrictions. Selective and reversible MAOI's may have a better safety profile compared to classical MAOI's.

Anxiety Disorders↗
PubMed1987

Do cerebral arteriovenous malformations increase in size?

Six patients are reported with cerebral arteriovenous malformations which have enlarged over follow up periods of from 4 to 20 years. The frequency of spontaneous enlargement is estimated to range from 0.2% to 2.8% per annum. This rate of enlargement should be considered when treatment options are reviewed in individual patients, and should be added to the risk of haemorrhage.

Adolescent↗
PubMed1986

Heterogeneity of binding sites for N-ethylcarboxamido[3H]adenosine in rat brain: effects of N-ethylmaleimide.

Binding sites for N-ethylcarboxamido[3H]adenosine (NECA) in rat brain membranes and cryostat sections were examined in relation to their sensitivities to displacement by unlabeled NECA and R(-)-phenylisopropyladenosine (R-PIA). In membrane fractions from cerebral cortex, cerebellum, hippocampus and striatum, nanomolar concentrations of these adenosine receptor agonists displaced [3H]NECA such that R-PIA was more effective than NECA, consistent with the presence of an A1-adenosine receptor. At concentrations of displacing agent higher than 1 microM, R-PIA was unable to displace [3H]NECA further in cerebral cortex, cerebellum and hippocampus. In striatum, a second R-PIA-sensitive component of [3H]NECA binding was evident which was more sensitive to NECA than to R-PIA, i.e. it showed the characteristics of an A2-adenosine receptor. In striatum, however, R-PIA was also unable to displace [3H]NECA binding completely. Similar results were obtained in quantitative autoradiographic studies. Preincubation of cryostat sections with N-ethylmaleimide (NEM) abolished both the A1- and R-PIA-insensitive binding components such that both NECA and R-PIA were able to displace [3H]NECA binding completely. The remaining sites showed IC50 values of 0.13 and 3.68 microM for NECA and R-PIA, respectively. These A2-like [3H]NECA binding sites had a highly specific distribution in the brain, being concentrated in the striatum, nucleus accumbens and olfactory tubercle. The results indicate the presence in brain tissue of at least 3 classes of [3H]NECA binding sites, an A1-site, an A2-site and a third, unidentified R-PIA-insensitive site.

2-Chloroadenosine↗
PubMed1986

Properties of binding sites for [3H]cyclohexyladenosine in the hippocampus and other regions of rat brain: a quantitative autoradiographic study.

The properties of binding sites for the adenosine receptor ligand, [3H]cyclohexyladenosine ([3H]CHA), were investigated in rat brain using quantitative autoradiography. Scatchard analysis of the binding data showed that there were no significant differences between Kd values for [3H]CHA in any of the regions investigated. The highest concentrations of [3H]CHA binding sites were found in the cerebellum (molecular layer) and the stratum oriens and stratum radiatum of the hippocampus (CAI region). Displacement curves obtained using N-ethylcarboxamidoadenosine (NECA) and the R- and S-diastereoisomers of phenylisopropyl adenosine (PIA) showed the [3H]CHA binding sites to have the pharmacological properties of A1-adenosine receptors, i.e. the order of potency for these derivatives was R-PIA greater than NECA greater than S-PIA, in all regions tested. Further, [3H]CHA binding was in all cases attenuated by the guanosine triphosphate derivative, beta, gamma-imidoguanosine triphosphate. These results indicate that [3H]CHA binding sites throughout the central nervous system have the properties of A1-adenosine receptors and that these are in all regions associated with guanine nucleotide regulatory proteins.

Adenosine↗
PubMedDate not supplied

An open label study of gabapentin in the treatment of acute mania.

Recent anecdotal single case reports have suggested that the new antiepileptic drug gabapentin might be effective in the treatment of manic episodes and in the prophylaxis of bipolar disorder. In the present open trial, 14 patients with acute mania were treated for up to 21 days with gabapentin in a dose range from 1200 to 4800 mg/day. Six patients were treated with gabapentin as add-on medication and 8 patients were treated with a high dose of gabapentin alone. Gabapentin was both efficacious and safe when applied in combination with other drugs such as lithium and valproic acid. All patients in the add-on group and 4/8 patients on gabapentin monotherapy finished the 21 day protocol. Analysis of the scores of the Bech-Rafaelsen Mania Assessment Scale (BRMAS) of these patients showed that the mean BRMAS score declined from 37.7 to 7.8 on day 21 in the add-on group and from 27.8 to 9.0 in 4/8 patients finishing 21 days in the monotherapy group. It is suggested that gabapentin monotherapy might be useful in selected patients to treat modest but not severe manic states. In addition, gabapentin in conjunction with other effective mood stabilisers seems to be safe and efficacious in the treatment of severe mania.

Acetates↗
PubMedDate not supplied

Trimipramine fails to exert antimanic efficacy: a case of the discrepancy between in vitro rationale and clinical efficacy.

Standard mood stabilizers, such as lithium and haloperidol, and anticonvulsants show effectiveness in a maximum of 60%-70% of acutely manic patients. Obviously, there is a clinical need to evaluate other treatment options. Current pathophysiologic concepts suggest that substances with an ameliorating effect on dopaminergic hyperfunction, serotonergic hypofunction, or GABAergic hypofunction might be useful, as may be substances with calcium-antagonistic effects. In vitro, the antidepressant trimipramine exerts dopamine- and calcium-antagonistic properties. Therefore, we conducted an open trial to screen it for antimanic action. We found no clinical benefit in four acutely manic patients receiving up to 400 mg/d of trimipramine. It is concluded that, at least in the case of trimipramine, the pharmacologic profile is not helpful in predicting potential effectiveness in mania.

Adolescent↗