Biomedical subjects

A Kaladjian

Publications and source records attributed to A Kaladjian.

5 recordsLinked to original sources

PubMed2000

On the possibility of linear modelling the human arm neuromuscular apparatus.

It has been widely claimed that linear models of the neuromuscular apparatus give very inaccurate approximations of human arm reaching movements. The present paper examines this claim by quantifying the contributions of the various non-linear effects of muscle force generation on the accuracy of linear approximation. We performed computer simulations of a model of a two-joint arm with six monarticular and biarticular muscles. The global actions of individual muscles resulted in a linear dependence of the joint torques on the joint angles and angular velocities, despite the great nonlinearity of the muscle properties. The effect of time delay in force generation is much more important for model accuracy than all the non-linear effects, while ignoring this time delay in linear approximation results in large errors. Thus, the viscosity coefficients are rather underestimated and some of them can even be paradoxically estimated to be negative. Similarly, our computation showed that ignoring the time delay resulted in large errors in the estimation of the hand equilibrium trajectory. This could explain why experimentally estimated hand equilibrium trajectories may be complex, even during a simple reaching movement. The hand equilibrium trajectory estimated by a linear model becomes simple when the time delay is taken into account, and it is close to that actually used in the non-linear model. The results therefore provide a theoretical basis for estimating the hand equilibrium trajectory during arm reaching movements and hence for estimating the time course of the motor control signals associated with this trajectory, as set out in the equilibrium point hypothesis.

Arm↗

PubMed1999

Clozapine monitoring: plasma or serum levels?

In this study, differences between plasma and serum levels of clozapine and norclozapine were quantified and correlations of these differences with myeloperoxidase (MPO) activities were examined. Fifty-seven patients (34 men and 23 women, mean age 36.6+/-11.4 years) taking clozapine in a daily doses varying from 75 to 800 mg entered the study. All patients were analyzed for clozapine level, 29 were analyzed for norclozapine level and 28 for MPO activity. Significant differences (p<0.001) between plasma and serum levels were found for clozapine (mean decrease 9.99+/-15.8%) and norclozapine (mean decrease 16.0+/-21.2%) and for MPO activities (mean increase 114.1+/-123.9%). No correlation was found between differences of MPO activities and differences of drug levels in plasma and serum. Differences in clozapine and norclozapine levels could reflect chemical instability of these drugs. These compounds should be quantified only in plasma because serum levels underestimate blood levels in patients.

Adult↗

PubMed1993

Clozapine in the treatment of psychotic refractory depression.

A 40-year-old woman suffering from major depression with psychotic features was unresponsive to conventional therapy. After the administration of a wide range of drug treatments and ECT, she received clozapine. Depressive symptoms improved and psychotic features disappeared. It is suggested that clozapine could be efficient in psychotic refractory depression.

Adult↗

PubMedDate not supplied

[Current issues on schizoaffective disorder].

Schizoaffective disorder is relatively common in clinical settings, with studies suggesting that the disorder accounts for 10-30% of admissions to inpatients mental health facilities for functional psychosis. Lifetime prevalence is estimated to be between 0.5 and 0.8%. Since its initial description by Kasanin in 1933, the concept has undergone many changes, moving on from that of acute psychosis toward a position located between affective and schizophrenic disorder. In current classification systems this position seems to be closer to the latter one. However DSM IV and ICD-10 differ according to the nature of symptoms, especially the psychotic ones, and the temporal relationship of the psychotic symptoms to the mood symptoms. Psychotic features may include paranoid, cognitive and negative symptoms but mood-congruent and mood-incongruent psychotic features can also be found during mood episodes. The disorder has an episodic course and a prognosis usually intermediate between that of schizophrenia and affective disorder. It has been commonly subtyped into a bipolar and a depressive type, but more recently a division into a concurrent and a sequential type has been proposed too, based on longitudinal findings. Family studies using current diagnostic criteria show that the pattern of illness in relatives suggests that schizoaffective probands may have as high a familial liability to schizophrenia and affective illness as do those probands with only one of the disorders. In addition to biological and neuroendocrine investigation, schizoaffective disorder has been addressed in some neuroimaging, neuropathological, cognitive and neurodevelopmental studies which tend however to confirm its location between the two disorders, but closer to the schizophrenic pole. Several hypotheses have been proposed to account for the nature of schizoaffective disorder. Current data tend to favor the ranging of the disorder within a unitary spectrum of functional psychosis the diathesis of which could be activated by an episode of mood disorder. In contrast to the extensive research devoted to the development of pharmacologic agents for the treatment of schizophrenia and mood disorders, the optimal pharmacological treatment of schizoaffective disorder has been relatively unstudied which may, for instance, explain the lack of treatment guidelines. Nonetheless, despite the paucity of data in this area, some authors recommend the use of atypical anti-psychotics alone or in combination treatment as first line medi-cations both for the short and long term treatment. Research on schizoaffective disorder has been marred by the variability of its definition. Even if doubts have been expressed about the reliability of current diagnostic criteria, they seem to define a syndrome that differs meaningfully from both schizophrenia and affective disorder. Further studies are however still necessary, especially with regard to the subtyping of the disorder and its pharmacological treatment.

Diagnostic and Statistical Manual of Mental Disord↗

PubMedDate not supplied

[Brain structural abnormalities of bipolar disorder].

The number of structural neuroimaging studies of bipolar disorder have increased during recent years, expanding the literature on the nature of cerebral abnormalities underlying this disorder. The purpose of this paper is to provide a selective review on the main issues concerning this literature. Consistent findings are higher rate of periventricular and deep subcortical white matter hyperintensites seen on MRI. Although there is strong evidence for links between hyper-intense lesions and age or cardio-vascular risk factors, some authors have observed the presence of these abnormalities early in the course of the illness. There are also frequent reports on ventricular enlargement, which has been described as mild and predominant in the right lateral ventricle. Total cerebral volume appears to be preserved. Whereas changes in total grey matter volume are uncertain, evidence suggests that reduced white matter volume reflects genetic factors predisposing to the disorder. Recent studies have reported volume changes in several cortical areas including the subgenual cingular, frontal and temporal cortices. Additionally, a number of reports described morphometric abnormalities in various subcortical structures, such as amygdala, basal ganglia and thalamus. Part of the variability in the morphometric abnormalities might be attributable to differences in clinical status and demographic characteristics of patient groups. Despite some inconsistencies across the studies, it emerges that abnormalities are asymmetrically distributed throughout the two cerebral hemispheres. When increase in volume is reported, it is preferentially localised in the left cerebral hemi-sphere and more specifically in prefrontal and temporal cortices and in amygdala. By contrast, when structural abnormalities concern the right cerebral hemisphere, they are identified as deficits. These latter results are in direct line with those of studies of mania following brain injuries, which report that these secondary mania result mainly from right cerebral lesions. It is also important to notice that most of the abnormalities concern both the cortical and subcortical level, ie frontal, striatal, thalamic and limbic regions. These abnormalities highlight the role in the pathophysiology of bipolar disorder of the loops involved in emotional information processing. The particular role of fronto-limbic loops in the phenomenology of bipolar disorder have been emphasised by recent data from functional neuroimaging studies.

Amygdala↗