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Biomedical subjects

A Barocka

Publications and source records attributed to A Barocka.

At least 19 recordsLinked to original sources
PubMed2004

[Messy house syndrome].

The messy house syndrome (Diogenes syndrome) is present when, owing to a disordering of the personality structure, a person is unable to keep order, for example, in the household or his finances. Such persons are also referred to as "messies". Useless objects are hoarded in such quantities that the apartment can no longer be lived in. In many cases, the disorder is due to an underlying mental problem such as dementia, schizophrenia, ADHS or obsessive-compulsive disorders. The Prader-Willi syndrome is also associated with an unusual compulsion to hoard things or food. In the first instance, treatment is aimed at the underlying condition (neuroleptic agents, SSRI). New studies appear to suggest that the particular concomitant cognitive and emotional disturbances associated with hoarding respond to cognitive behavioral therapy.

Aged↗
PubMed2002

[Patient education, medication and physical therapy. Balm for "cardiac neurosis"].

In the management of psychogenic chest pain, the family doctor has a key role to play. His main task is to exclude physical or organic causes and identify the underlying psychogenesis--admittedly without wishing to establish a definitive (ICD-10) diagnosis. For this purpose, empathic reassurance of the patient is of major importance. Wherever possible, hospitalization of the patient for a diagnostic clarification should be avoided. Therapeutic options comprise suitable physiotherapy, psychohygienic measures, and appropriate pharmacotherapy. Major goals of such an approach are the establishment of a trusting relationship, and improving the patient's sleep patterns, physical fitness and emotional status. In the event of long-term persistence of the condition or a severe course, referral to a specialist is indicated.

Anti-Anxiety Agents↗
PubMed2000

Specific sensory detection, discrimination, and hedonic estimation of nicotine enantiomers in smokers and nonsmokers: are there limitations in replacing the sensory components of nicotine?

The aim of this study was to investigate in smokers and nonsmokers (1) the olfactory and trigeminal detection of R(+)- and S(-)-nicotine and (2) the discrimination ability and hedonic estimation of nicotine enantiomers in olfactory and trigeminal concentrations. Thirty healthy male subjects (15 smokers, 15 nonsmokers) participated in the experiments. A randomized sequence of R(+)- and S(-)-nicotine stimuli (seven R(+)- and seven S(-)-nicotine stimuli) were introduced into the right nostril of the subjects using a Kobal-olfactometer. The subjects were instructed to group the stimuli into two categories (A and B). To test the role of the olfactory and the trigeminal system in this discrimination task, the authors studied the olfactory detection threshold for the "odorous" sensation and the trigeminal detection thresholds for the "burning" and "stinging" sensations. Nicotine enantiomers were presented at the individual "olfactory" and "trigeminal" concentration levels. The subjects estimated the hedonic properties using a bipolar visual analog scale (from "very unpleasant" to "very pleasant"). A statistical evaluation (t-test) revealed that the subjects were able to identify R(+)- and S(-)-nicotine at olfactory and trigeminal concentrations (p < or = 0.01, p < or = 0.001, respectively). At concentrations near the detection thresholds, i.e., clearly below subjective pain thresholds, smokers rated both nicotine stereoisomers to be significantly more pleasant than did nonsmokers (t-test, R(+)-nicotine: p < or = 0.05; S(-)-nicotine: p < or = 0.01). Increasing the concentrations to above trigeminal thresholds resulted in a difference in hedonic estimates. Smokers perceived the S(-)-isomer as being less unpleasant than nonsmokers at trigeminal concentrations (t-test, p < or = 0.001). This difference in perception might be explained by the smokers' experience with S(-)-nicotine, which is the natural nicotine enantiomer in tobacco.

Adult↗
PubMed1999

Dose-dependent stereoselective activation of the trigeminal sensory system by nicotine in man.

RATIONALE: Nicotine applied to the nasal cavity can evoke 'odorous' sensations in the concentration range near the detection threshold by the activation of the olfactory sensory system and at higher concentrations 'burning' and 'stinging' sensations by the dose-dependent recruitment of C- and Adelta-fibers of the trigeminal sensory system. Neuronal nicotinic acetylcholine receptor (nAchR) subunits are expressed in trigeminal primary afferents and could constitute the receptors involved in nicotine perception. OBJECTIVE: In the present study, we dose-dependently investigated the stereoselective effects of R(+)- and S(-)-nicotine on the trigeminal and olfactory sensory system in man. METHODS: Trigeminal detection thresholds for the 'burning' and 'stinging' sensations and the olfactory detection threshold for the 'odorous' sensation were determined. In order to quantify trigeminal activation, we recorded summated electrical responses from the respiratory nasal mucosa during stimulation with R(+)-and S(-)-nicotine vapor (40, 80, 120, 160 ng/ml; stimulus duration: 250 ms). In addition, subjects rated the intensity of 'odorous', 'burning' and 'stinging' sensations. For chemical stimulation with nicotine enantiomers, a vapor-dilution olfactometer (constant flow rate: 140 ml/s, humidity: 80%, temperature: 37 degrees C, stimulus duration 250 ms) was employed. RESULTS: We found significant stereoselective differences for the trigeminal but not for the olfactory system, i.e. higher summated responses, higher trigeminal intensity estimates, and lower trigeminal detection thresholds for S(-)- compared to R(+)-nicotine. CONCLUSION: Our results clearly demonstrate the different stereoselective activation of the trigeminal sensory system by R(+)-and S(-)-nicotine, indicating the presence of specific stereoselective receptors on trigeminal nociceptive Adelta- and C-fibers.

Adult↗
PubMed1999

Spontaneous slow and fast MEG activity in male schizophrenics treated with clozapine.

RATIONALE: The atypical neuroleptic clozapine induces specific electroencephalogram changes, which have not been investigated using the technique of magnetoencephalography (MEG). OBJECTIVE: The present study investigated whether spontaneous magnetoencephalographic (MEG) activity in patients treated with clozapine differs from that in patients treated with haloperidol and untreated control subjects. METHODS: A 2 x 37 channel biomagnetic system was used to record spontaneous magnetic activity for the frequency ranges (2-6 Hz), (7.5-12 Hz), (12.5-30 Hz) in schizophrenic patients and controls in two trials within 3 weeks. After data acquisition, the processed data were digitally filtered and the spatial distribution of dipoles was determined by a 3-D convolution with a Gaussian envelope. The dipole localisation was calculated by the dipole density plot and the principal component analysis. The target parameters were absolute dipole values and the dipole localisations. The relationship between absolute dipole values, dipole localisations and psychopathological findings (documented by the use of the PANSS, BPRS-scale) during a 3 week period with constant doses of clozapine and haloperidol was investigated using correlation analysis. RESULTS: Our results lend strong support to the assumption of a significant elevation of absolute dipole values [dipole density maximum (Dmax), dipole number (Dtotal), absolute and relative dipole density] in the fast frequency range (12.5-30 Hz) over the left hemisphere, especially in the temporoparietal region by clozapine. In this area, we found a dipole concentration effect only in patients treated with the atypical neuroleptic, whereas the dipole distribution in patients treated with haloperidol and healthy controls was concentrated in the central region. With regard to the absolute dipole values in the frequency ranges 2-6 Hz (delta, theta) and 7.5-12 Hz (alpha), we found no statistically significant differences between the groups investigated. In the slow frequency range (2-6 Hz) no difference was found between the clozapine and haloperidol group for the dipole localisation, which predominated in the temporoparietal region, in contrast to the central dipole distribution in control subjects. CONCLUSIONS: The results of an increase in beta activity under clozapine demonstrate a smaller reduction in activity in terms of unspecific sensory and motor paradigms in comparison with typical neuroleptics. The temporoparietal concentration of dipoles, in particular over the left half of the brain, might illustrate either their special role in the disease process, or the effects of the medication. The latter possibility was supported by the differing dipole distribution in the clozapine group with a left temporoparietal centre in both frequency ranges, and a deviating central dipole localisation in the fast activity range in the haloperidol group.

Adult↗
PubMed1999

[The concept of negative and positive symptoms in a historical perspective].

Over the last years, the modern psychopathological classification of schizophrenic symptoms into the groups of negative and positive symptoms has gained more relevance to the diagnosis, therapy and prognosis of this disorder. We delineate the historical concept of negative and positive elements, which was developed by the British neurologist John Hughlings Jackson (1835-1911) to explain the pathophysiology of psychic disorders. These definitions are elucidated in view of the scientific context at the end of the 19th century, when evolutionism, positivism, psycho-physical parallelism, and the knowledge of neurosciences played an important part. In addition, the reception of Jackson's ideas by psychiatry is shown. Freud was essentially influenced by Jackson in developing his psychoanalytical theory of neurosis. Bleuler joined Freud and defined "primäre" and "sekundäre" symptoms of schizophrenia. In the phenomenological concept of schizophrenia of Huber, "Basissymptome" are distinguished from "End- und Uberbausymptome", which in part correspond to the negative and positive symptoms of today, respectively. The paper provides a historical survey of the Jacksonian influences on concepts of schizophrenia.

History, 19th Century↗
PubMed1998

Effects of tryptophan depletion in drug-free depressed patients who responded to total sleep deprivation.

BACKGROUND: There is some evidence that sleep deprivation (SD) might exert its antidepressant properties by involving serotonergic mechanisms. We investigated the effects of short-term tryptophan depletion (TD) on depressed patients who responded to a single night of total SD. METHODS: Drug-free depressed inpatients (n = 30) were randomly assigned to either TD or sham depletion. Tryptophan depletion was induced by a 24-hour low-tryptophan diet (day 1) followed the next morning by ingestion of a tryptophan-free amino acid mixture (day 2). During sham depletion, the diet and the amino acid beverage were supplemented with tryptophan. Sleep deprivation was performed from day 1 until day 2. Only SD responders received the amino acid beverage the morning after SD. Behavioral ratings and total and free plasma tryptophan levels were obtained before and after the test sessions. RESULTS: Twenty-two of 30 patients showed a favorable outcome after SD. As predicted, TD significantly lowered total and free plasma tryptophan levels, whereas both levels increased during sham depletion. No acute effects on mood were observed during the day after SD in either treatment group. Unexpectedly, TD, but not control testing, prevented the depressive relapse after the recovery night in most of the patients. CONCLUSIONS: Tryptophan depletion did not reverse the antidepressant effects of SD, but it prevented the relapse beyond a night of recovery sleep. These findings suggest that SD does not act via a single monoamine-related mechanism, but they allow the assumption that TD may induce neurochemical alterations that transiently improve depression.

Adult↗
PubMed1998

Neuropsychological results of craniopharyngioma surgery in adults: a prospective study.

BACKGROUND: The optimal management of craniopharyngiomas is a topic of ongoing debate. Supporters of limited surgery for craniopharyngiomas claim that more radical approaches are afflicted with adverse neuropsychological sequelae. Since prospective studies on this issue have not yet been performed, we assessed neuropsychological functioning in adults before and after craniopharyngioma surgery. METHODS: Thirteen adults with an age range of 17-76 years (mean, 45 years) were included in the study. Surgery included a transcranial procedure in 10 patients. The bifrontal interhemispheric approach predominated (n = 7). Neuropsychological evaluation was performed before and 3 months after surgery. The test battery was adjusted to evaluate function related to structures in the operative trajectory and at the tumor site. RESULTS: A complete tumor removal was accomplished in eight patients and subtotal removal in three patients. IQ scores for verbal intelligence were in the normal range and not affected by surgery (mean IQ score preoperative: 106.8; postoperative 107.4). In 12 of 13 patients, immediate recall, delayed recall and recognition memory were not impaired after surgery. Postoperative results for abstract thinking were in the normal or above-normal range. Cognitive speed was impaired in three patients preoperatively and in two patients postoperatively. Overall results were significantly better after surgery. Word fluency was not affected by surgery. Quality of life for the category "sleep" was impaired preoperatively, and this improved after surgery. Otherwise, quality of life was normal both before and after surgery. CONCLUSIONS: Neuropsychological performance and quality of life are generally not impaired after surgical removal of craniopharyngiomas. The findings support the attitude that the initial therapy of craniopharyngiomas should be an attempt at total removal.

Adolescent↗
PubMed1998

Effects of tryptophan depletion in fully remitted patients with seasonal affective disorder during summer.

BACKGROUND: Deficiencies in brain serotonin function are believed to play an important role in the pathophysiology of seasonal affective disorder/winter type (SAD). However, no direct evidence has been reported so far that lowered brain serotonin activity causes the symptoms of SAD. METHODS: We studied 11 SAD patients who had suffered recurrent winter depressive episodes of SAD and were fully recovered and off treatment during the summer. In a randomized, balanced, double-blind crossover design patients received two amino acid beverages, one containing tryptophan and the other containing no tryptophan but otherwise identical. Behavioural ratings and plasma total and free tryptophan concentrations were assessed at baseline before administration of the amino acid beverages and at several time points afterwards. RESULTS: The tryptophan-free amino acid beverage induced significant decreases of plasma total and free tryptophan levels and both levels increased during sham depletion (condition x time interaction: P < 0.001). Tryptophan depletion, but not sham depletion caused a transient return of depressive symptoms (condition x time interaction: P < 0.001). CONCLUSIONS: The present study demonstrates that SAD patients in remission during the summer are vulnerable to a return of depression when depleted of tryptophan. This finding supports the importance of serotonergic mechanisms in the pathophysiology of SAD.

Adult↗
PubMed1998

Weight of adrenal glands may be increased in persons who commit suicide.

In a previous study, increased weight of the adrenal glands was found in a small group of persons who committed violent suicides. This finding was confirmed in our study, which comprised a group of 42 suicide cases and 37 control cases. Further analysis with special consideration toward a "relative adrenal weight" (weight/body surface) revealed that a relative combined adrenal weight >6 g/m2 may be a morphologic sign of a depressive disorder prior to death if no other disease with a known effect on the adrenals is present. These results are consistent with clinical computed tomographic findings of enlarged adrenals in depressed patients. In all suicide cases the police records were reviewed and a postmortem psychiatric diagnosis conducted to investigate whether a correlation between adrenal weight and the "severity" of depression or type of psychiatric disorder exists. In thirteen cases, psychiatric treatment prior to death was known, and a postmortem severity score of depressive disease was formed. No influence of this score or the postmortem diagnosis on the adrenal weight, however, could be detected. Also, the increase in weight of adrenal glands could not be explained by a suspected or proven preceding drug therapy or use. The effect on the pituitary-adrenal-axis by depressive disorders and changes in serotonin metabolism have been investigated repeatedly; mainly reported are increased levels of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) in the depressive interval, which may lead to a growth of the adrenal glands.

Adrenal Glands↗
PubMed1997

Duration of lithium treatment and brain lithium concentration in patients with unipolar and schizoaffective disorder--a study with magnetic resonance spectroscopy.

Twenty psychiatric patients on lithium medication were examined with 7-Li-magnetic resonance spectroscopy of the brain. Patients on long-term lithium treatment (> 6 months) were compared with a short-term group who had been taking lithium for between 4 and 8 weeks. Patients met DSM-III-R criteria for either recurrent unipolar depressive disorder (DSM-III-R 296.3x) or schizoaffective disorder, depressive type (DSM-III-R 295.70). The brain:serum lithium ratio was 0.76 +/- 0.26; there was no significant difference between short-term and long-term treatment. In the group of long-term treatment patients there was a positive correlation between lithium dose per day and brain lithium concentration (R = .72, p < .01), and between lithium plasma concentration and brain lithium concentration (R = .65, p < .05). In the short-term group, however, there was no significant correlation for these parameters. No differences between unipolar and schizoaffective disorder were found.

Adult↗
PubMed1997

Influence of season on manifestation of schizophrenic subtypes.

In the modern classification systems ICD-10 and DSM-III-R, the term seasonality has been given a separate significance in the diagnostic categorization of affective disorders. Its definition is oriented not merely to the increased seasonal prevalence in the autumn and winter months, but also to symptoms that do not occur in nonseasonal attacks. To date, research work on seasonality in schizophrenia has concentrated on birth seasonality, while no results based on large populations of patients have yet become available on the manifestation seasonality of schizophrenic subtypes. Within the framework of a retrospective study carried out in the period between 1983 and 1995, involving 2, 119 patients suffering from recurrent attacks of schizophrenia, seasonal manifestations were recorded in accordance with the criteria defined in DSM-III-R. It was found that the two subtypes of paranoid hallucinatory and schizoaffective psychoses met the criterion of seasonality significantly more frequently than did the subtypes disorganized and catatonic disorders. In addition, seasonal courses within the groups just mentioned clearly differed from the nonseasonal forms in terms of their symptomatology.

Adult↗
PubMed1997

Rapid tryptophan depletion in drug-free depressed patients with seasonal affective disorder.

OBJECTIVE: Brain serotonin systems might be involved in the pathophysiology of seasonal affective disorder. The authors tested whether tryptophan depletion alters the mood of depressed patients with seasonal affective disorder. METHOD: Eleven drug-free depressed patients with seasonal affective disorder underwent tryptophan depletion in a placebo-controlled, double-blind crossover study. Tryptophan depletion was induced by a 24-hour low-tryptophan diet and by ingestion of a tryptophan-free amino acid beverage. During control testing the diet and the beverage were supplemented with tryptophan. Behavioral ratings and plasma total and free tryptophan levels were obtained before the diet started and several times after administration of the beverages. RESULTS: The diet and the tryptophan-free amino acid drink reduced plasma total and free tryptophan levels by 79.0% and 87.5%, respectively. Both levels increased during control testing. No significant behavioral changes were induced by tryptophan depletion or control testing. CONCLUSIONS: The failure of tryptophan depletion to exacerbate the depressive syndrome suggests that dysfunctional serotonergic activity does not play a primary, direct role in the pathogenesis of winter depression.

Acute Disease↗
PubMed1995

Residual symptoms after partial remission: an important outcome in depression.

This paper draws attention to an important adverse outcome in depression, the occurrence of residual symptoms after partial remission. Among patients with definite major depression followed every 3 months to remission and thereafter, residual symptoms reaching 8 or more on the Hamilton Depression Scale 17-item total were present in 32% (19) of the 60 who remitted below major depression by 15 months. The pattern was of mild but typical depressive symptoms. Residual symptoms were more common in subjects with more severe initial illness, but were not related to any other predictors, including longer prior illness, dysthymia, or lower dose of drug treatment during the illness episode. There were weak associations with personality that might have been consequences of symptom presence. Residual symptoms were very strong predictors of subsequent early relapse, which occurred in 76% (13/17) of those with residual symptoms and 25% (10/40) of those without.

Adolescent↗
PubMed1994

Single photon emission computerized tomography assessment of cerebral dopamine D2 receptor blockade in depression before and after sleep deprivation--preliminary results.

The antidepressant properties of total sleep deprivation (TSD) have been well established. There is some evidence that TSD may improve depression by altering central dopamine (DA) function. We therefore studied five depressed TSD responders and five TSD nonresponders after sleep and after TSD and five controls after sleep with IBZM single photon emission computerized tomography (SPECT). Responders showed a significant decrease (Wilcoxon--test p < 0.05) of relative basal ganglia D2 receptor occupancy after TSD compared to nonresponders (change score responders versus nonresponders p < 0.05, U-test). The data are interpreted as a sign of an enhanced DA release in responders. The results confirm previous hypotheses of dopaminergic involvement in the therapeutic action of TSD and indirectly support a dopamine hypotheses of depression.

Adult↗