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Biomedical subjects

R Rimon

Publications and source records attributed to R Rimon.

At least 19 recordsLinked to original sources
PubMed2000

Akathisia masked by hypokinesia.

Here, we will discuss the concept of subjective akathisia and present a patient case. Our patient was suffering from neuroleptic-induced hypokinesia and akathisia at the same time. The typical motor manifestations of akathisia were masked by hypokinesia, which made the diagnosis difficult. However, the subjective symptoms of akathisia were evident and distressing. Although not observable to bare eye, the pathognomonic pattern of motor activity detected in akathisia was demonstrated by actometric recording. Changing the conventional neuroleptic to an atypical one brought relief to the subjective symptoms of akathisia and hypokinesia, while the motor activity was clearly diminished in actometric recording. Actometric recording may be useful in diagnosing akathisia masked by hypokinesia, but the typical subjective symptoms of akathisia should not be ignored, even when actometry is not available to demonstrate the missing motor component of akathisia. Not only akathisia defined by DSM-IV but also subjective akathisia should be adequately treated to relieve the subjective distress, and to diminish the unfavorable effects on psychotic symptoms, behavior, and drug compliance.

Adult↗
PubMed1999

Measuring neuroleptic-induced akathisia by three-channel actometry.

Three-channel actometry was used to study neuroleptic-induced akathisia (NIA), a common and often serious disorder in association of traditional neuroleptic therapy. The aim was to explore the diagnostic possibilities of actometry in NIA and to examine in detail the motor phenomenology of the disorder in detail. The actometers were attached to the ankles and waists of ten patients, suffering from NIA, and to ten matched healthy controls. Five of the patients were changed to olanzapine treatment, and these patients were re-examined during the no-NIA condition. NIA was associated with manyfold movement activity during controlled rest (sitting) but not with increased daily overall motor activity. Movement frequencies in NIA seemed to be pathognomonic. Actometry is promising for investigation and clinical assessment of NIA. Olanzapine proved to be an adequate treatment choice for NIA patients.

Adult↗
PubMed1997

Long-term efficacy and safety of milnacipran compared to clomipramine in patients with major depression.

Milnacipran is a new antidepressive drug, a combined noradrenaline/serotonin (NA/5-HT) reuptake inhibitor, which has been suggested to be as effective as and better tolerated than tricyclic antidepressants. Since long-term studies are lacking, we compared the efficacy, safety and tolerability of milnacipran and clomipramine in a double-blind, randomized, parallel-group study setting during 26 weeks of treatment in patients with major depression. A total of 107 patients were treated with either milnacipran (n=52) or clomipramine (n=55). Due to active treatment of duration less than 12 days in four patients and protocol deviation in one patient, in total 47 milnacipran-treated patients were eligible for efficacy analysis. Nine patients in the clomipramine group continued on active treatment for less than 12 days. Thus 46 clomipramine-treated patients were finally included in the efficacy analysis. After 1 week of dose escalation, there was a fixed dosage regimen of either milnacipran (200 mg daily) or clomipramine (150 mg daily) during weeks 2 to 10, followed by flexible dosing of milnacipran (100, 150 or 200 mg daily) or clomipramine (75, 100 or 150 mg daily) during weeks 11 to 26. A total of 53 patients (49%) completed the 26-week study period; 21% (11/52) of the patients in the milnacipran group and 38% (21/55) of the patients in the clomipramine group discontinued their medication prematurely due to adverse events, whereas 19% (10/52) of those on milnacipran and 7% (4/55) of those on clomipramine treatment withdrew due to either lack of efficacy or clinical deterioration. The mean change (+/-SD) in the Hamilton Depression Rating Scale (HAMD) score between the baseline and the last rating ranged from 23.7+/-3.1 to 12.0+/-9.5 in the milnacipran-treated patients and from 23.1+/-3.5 to 8.0+/-8.5 in the clomipramine-treated patients, revealing a significant difference in favour of clomipramine. In total 58% of the milnacipran-treated patients vs. 72% of the clomipramine-treated patients showed a > or = 50% reduction in their baseline HAMD scores and 45% vs. 63% had an HAMD score of < or = 7 at the last rating, respectively. Moreover, the time to the onset of the antidepressant action (defined as > or = 50% reduction of the baseline HAMD score) showed a significant difference in favour of clomipramine. In addition, clomipramine was significantly more efficacious in patients with a baseline HAMD score of > or = 24 as evidenced by the analysis of the HAMD score at week 6 and at the last rating. The Montgomery Asberg Depression Rating Scale (MADRS) and the Clinical Global Impression (CGI) scale did not show significant differences between the treatment groups. The safety analysis did not reveal any differences of clinical significance in cardiovascular variables between the study drugs. Dry mouth was significantly less frequently reported by the milnacipran-treated patients during the early and later phases (weeks 6 to 26) of the study, while insomnia was more common in the milnacipran group during weeks 1 to 6. In conclusion, milnacipran appeared to be less effective than clomipramine in the long-term treatment of depression. The side-effects of the drugs differed to a certain extent, and milnacipran tended to be somewhat better tolerated than clomipramine.

Adolescent↗
PubMed1996

The effect of clozapine on the course of illness in chronic schizophrenia: focus on treatment outcome in out-patients.

Forty-eight consecutive schizophrenic patients treated with clozapine (mean daily dose 436 mg) for at least 1 year (mean 7.6, range 2.2-14.8 years) were studied retrospectively. The most favourable changes in the course of illness were observed in 39 out-patients, whose duration of hospitalization per year continuously and significantly declined after the introduction of clozapine. The out-patients who continued with clozapine treatment for more than 10 years (n = 8) did not need hospitalization at all during the last year of the observation period. The improvement in social functioning in the out-patient group correlated positively with the duration of clozapine medication (r = 0.384, p = 0.016) and with the duration of hospitalization (r = 0.372, p = 0.020) after introduction of clozapine. Out-patients with disorganized schizophrenia (later called hebephrenic according to the Finish version of DSM-III) showed more noticeable clinical (U = 226, p = 0.032) and social (U = 233, p = 0.024) improvements than non-hebephrenic patients. There appears to be a subgroup of hebephrenic patients who benefit from clozapine more than patients with other types of schizophrenia.

Adolescent↗
PubMed1993

The use of clozapine in treatment-refractory schizophrenia.

The effects of clozapine on positive and negative symptoms were studied in 103 patients with treatment-refractory schizophrenia. The evaluation of symptom profile was made before and after clozapine treatment. Overt psychopathology did not vary significantly before clozapine treatment. Significant decreases in positive and negative symptoms were noted by the third month on clozapine. No further significant progress could be observed after 6 months of treatment. No fatal cases were observed, although two patients developed agranulocytosis during clozapine treatment.

Adult↗
PubMed1992

Inadequate treatment response to des-enkephalin-gamma-endorphin compared with thioridazine and placebo in schizophrenia.

The possibility of an involvement of peptidergic systems in schizophrenia has been under investigation for a number of years. Studies of the efficacy of des-tyr-gamma-endorphin were equivocal; more recent studies with des-enkephalin-gamma-endorphin have reported some activity but the peptide has only been investigated as an adjunct to neuroleptic medication, apart from one very small active reference comparator study. In the multicentre study reported here, 96 patients suffering from schizophrenia (DSM-III with a current exacerbation if chronic) were allocated randomly to double-blind treatment with either des-enkephalin-gamma-endorphin (DE-gamma-E) (Org 5878) 10 mg given as a once daily intramuscular injection for 4 weeks, thioridazine 400 mg orally in 2 divided doses or placebo using a double-dummy technique to preserve blindness. There was a significant advantage for thioridazine compared with placebo registered on all measures at weeks 3 and 4. There was no difference between DE-gamma-E and placebo. There was a significant difference between thioridazine and DE-gamma-E at weeks 3 and 4 registered on the MSS and at week 3 registered on the BPRS. The lack of efficacy of DE-gamma-E suggests that the theories that the endorphins have an important role in schizophrenia have to be revised. The need for well designed placebo controlled studies for assessing efficacy in schizophrenia is emphasized.

Adult↗
PubMed1987

Plasma endogenous opioids and dexamethasone suppression test in depression.

Plasma levels of beta-endorphin plus beta-lipotropin were determined in 35 hospital patients with depression and in 23 controls before and after administration of 1 mg of dexamethasone (dxm). Dxm suppressed opioid secretion in both groups. The opioid levels of the patients were significantly higher than those of the controls both before and after dxm. All the controls were cortisol suppressors. Among the patients the post-dxm opioid levels of cortisol nonsuppressors (n = 14) were higher than those of cortisol suppressors (n = 21). A significant correlation between the opioid and cortisol levels was found in the patients. There was a significant association between the use of neuroleptics and high opioid levels, but the difference between the patients and the controls was not explained by the effect of any single class of drugs. The results support the concept of hypersecretion of corticotropin-releasing factor in depression.

Adult↗
PubMed1987

Effects of propiomazine on the EEG sleep of normal subjects.

The effects of 25 mg propiomazine were examined in ten healthy volunteers in a sleep laboratory setting. A significant decrease in sleep latency and a corresponding decrement in subjectively assessed sleep latency was found during drug treatment. The distribution of the different sleep stages was affected to a relatively small extent. Some evidence for a suppression of REM-sleep in the early part of the treatment period was found. Based on subjective assessment, the subjects rated their sleep quality as significantly improved during treatment. Ratings of "drowsiness in the morning" were not different during baseline and drug treatment, but there was a significant decrease at withdrawal.

Adult↗
PubMed1986

Mood alterations and sleep.

We have reviewed literatures about neurobiological aspect of mood disorders in the light of abnormalities of REM sleep. A shortened REM latency is a consistent finding in depressed patients and may be considered a biological marker for depression. Most depressed patients with shortened REM latency also show non-suppression on dexamethasone-suppression test (DST). The commonly used antidepressant drugs cause a significant reduction in REM sleep. Patients with abnormal DST show a better response to sleep deprivation than those with normal DST. Recent studies indicated that borderline patients, primary dysthymic patients and obsessive-compulsive patients (OCD) have shortened REM latency. Farthermore, patients with OCD have a fairly good response to antidepressant clomipramine. Diagnostic and therapeutic strategies can conceivably be related on the examination of sleep patterns of psychiatric patients.

Affective Disorders, Psychotic↗
PubMed1985

Evidence for the presence of 'ouabain like' compound in human cerebrospinal fluid.

Material extracted and partially purified from human cerebrospinal fluid (CSF) is capable of: a, inhibiting [3H]ouabain binding to rat brain synaptosomes; b, inhibiting the activity of purified pig kidney Na+,K+-ATPase; and c, inhibiting ouabain sensitive induced 86Rb influx to tissue cultured fibroblasts. These results demonstrate the existence of an 'ouabain like' compound (OLC) in human CSF, and are consistent with the hypothesis of the function of this compound as a neuromodulator.

Binding Sites↗
PubMed1983

Low cerebrospinal fluid 5-hydroxyindoleacetic acid concentration differentiates impulsive from nonimpulsive violent behavior.

Relationships of impulsive and nonimpulsive violent behavior to cerebrospinal fluid (CSF) monoamines and their metabolic concentrations were studied in thirty-six violent offenders. A relatively low 5-hydroxyindoleacetic acid (5HIAA) concentration was found in the CSF of impulsive violent offenders. This was not true for the offenders who had premeditated their acts. Other CSF monoamine or metabolite concentrations were not significantly different between the two groups. Of the groups studied, impulsive violent offenders who had attempted suicide had the lowest 5HIAA levels. A low CSF 5HIAA concentration may be a marker of impulsivity rather than violence.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Neuroleptic malignant syndrome due to depot fluphenazine.

The parenteral long-acting phenothiazines are drugs frequently used in the treatment of hospitalized and ambulatory psychiatric patients. The usual side effects of these drugs are familiar to psychiatrists. However, the "Neuroleptic malignant syndrome" reported in this paper can give rise to considerable diagnostic difficulty. The clinical characteristics and differential diagnosis of this syndrome are described with a care report. The need for prompt initiation of adequate therapy is stressed.

Adult↗