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C Lajeunesse

Publications and source records attributed to C Lajeunesse.

At least 19 recordsLinked to original sources
PubMed1992

[Use of low doses of bromocriptine in chronic schizophrenia resistant to neuroleptics. A preliminary study].

In this work, we report the efficiency of bromocriptine (1.25 and 2.5 mg/day) in 9 neuroleptic resistant chronic schizophrenics. Following an initial four-week placebo period, the subjects successively received bromocriptine (1.25 mg/day), placebo and bromocriptine (2.5 mg/day). The 2 bromocriptine treatments significantly improved the global psychiatric symptomatology and different scores and factors related to the more specific schizophrenic symptomatology. An escape phenomenon seems to occur during the 4th week of the first bromocriptine treatment (1.25 mg/day) but is not observed with the second treatment (2.5 mg/day). All patients improved.

Adult↗
PubMed1988

Lithium, thyroid function and antithyroid antibodies.

1. Lithium is known to affect thyroid function. It can cause both subclinical and overt hypothyroidism that may involve in some instances an autoimmune mechanism. 2. Sixty (60) psychiatric patients, already under treatment with lithium for at least 6 months, were administered additional thyroid tests and monitored over a one-year period to study the implication of the autoimmune system in the development of hypothyroidism and thyroiditis during lithium therapy. 3. At the beginning of the study, 16 patients presented biological hypothyroidism (laboratory values under normal limits) and only 4 of them showed some slight clinical symptoms. Initially, antithyroid antibodies were detected in 20% of the patients (6 hypothyroids and 6 euthyroids): 12 had antimicrosomal antibodies and only 8 antithyroglobulin antibodies. 4. During the study, only one additional patient (euthyroid) developed antimicrosomal antibodies. All patients with antithyroglobulin antibodies had antimicrosomal antibodies and 6 hypothyroid patients had both types of antibodies.

Adult↗
PubMed1988

[Clinical aspects of tardive dyskinesias induced by neuroleptics].

Initially, the reality of the existence of tardive dyskinesia raised some controversy, but rapidly this syndrome was recognized as a complication arising from usually long-term administration of neuroleptics. These extrapyramidal abnormal movements represent an important problem due to their prevalence, their potential irreversibility, their complex and still disputed physiopathologic mechanism, the absence of specific and generally effective treatment, and more recently the medico-legal problems entailed. At first, it was believed that these dyskinetic movements, of various intensity, were localized only at the oro-facial area (face, tongue, maxillary), or consisted of limited or generalized choreo-athetosic movements, or were a mixture of both types of movements. However, digestive and respiratory tardive dyskinesia also occur. Tardive dyskinesia can develop insidiously during neuroleptic treatment, or appear when this medication is decreased or ceased. It can coexist with parkinsonian signs. Age (over 50) and gender (female) appear to be risk factors. Other types of tardive syndromes associated with neuroleptic administration have been reported, such as tardive akathisia, tardive dystonia and a tardive Tourette-like syndrome. Involuntary movements resembling tardive dyskinesia can be observed in elderly individuals who never received neuroleptic medication. With respect to the rabbit syndrome, a rapid tremor of the perioral area, with a rhythmicity similar to the parkinsonian tremor, it is clearly different from tardive dyskinesia. It is essential to detect as precociously as possible tardive dyskinesia. The diagnosis is sometimes difficult and even if the clinical features seem pathognomonic of tardive dyskinesia, it is nevertheless important to establish a differential diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Antipsychotic Agents↗
PubMed1988

[The treatment of psychopathologic disorders associated with tardive dyskinesias].

Tardive dyskinesia, an extrapyramidal syndrome consisting of involuntary hyperkinetic movements, is a serious side effect induced by the administration, usually on a long-term basis, of neuroleptic therapy mostly for psychotic disorders. Therefore, psychopathologic disturbances, florid or residual may coexist with the appearance and persistence of tardive dyskinesia. Thus, the exact nature of the psychopathology observed with the presence of tardive dyskinesia and its origin is difficult to delineate and to assess. Indeed, the psychopathological findings observed can possibly originate from the initial psychiatric disorder itself from the intrinsic effect of the neuroleptic medication on psychic processes, may be specifically related to tardive dyskinesia, or be the result of all these factors. Cognitive, thymic or psychotic disturbances have been closely associated with tardive dyskinesia, but their systematic studies is still scarce. Based on these findings, some tentative therapeutic considerations will be outlined, keeping in mind that exact nature and origin of these disturbances still remains to be elucidated, that no really specific and generally effective treatment of tardive dyskinesia has been found.

Cognition Disorders↗
PubMed1984

[Structural problems in French research in biological psychiatry: survey in several European countries].

While French research is being restructured, psychiatric research, especially biological psychiatry with its clinical component, must seek recognition by the official structures and face a series of administrative difficulties in order to reach its full growth. The Danish, Swedish, British and Belgian psychiatric research organizations possess some particularities that are reviewed.

Belgium↗
PubMed1984

[Plasma and saliva DST (dexamethasone suppression test) in depression. Clinical applications and kinetic approach].

Both plasmatic and salivary DST were simultaneously performed on a sample of 37 patients with a diagnosis of major depressive disorder (DMS III criteria): 22 primary depressions and 15 secondary depressions. Salivary DST showed a similar specificity but a decreased sensitivity in comparison with plasmatic DST. Essentially, the simultaneous use of both tests resulted in a better specificity for primary depression.

Adult↗
PubMedDate not supplied

[Cognitive inhibition and psychopathology: toward a less simplistic conceptualization].

"Cognitive inhibition" is a concept that has found a firm place in the interpretation of performance by normal subjects on tasks involving adherence to a plan and suppression of incorrect responses to distractors. The presence of "negative priming" is the classical indicator of cognitive inhibition. Negative priming occurs when, in a sequence of stimuli each of which is composed of a target and a distractor, the distractor of the first stimulus becomes the target of the second stimulus: reaction time to the second stimulus is slowed because of the inhibition applied to the distractor of the first stimulus. The concept has been extended to the interpretation of pathological behavior and symptoms. Pathological subjects have been found to show deficient negative priming. Thus, negative ideation in depression as well as intrusive paranoid associations in schizophrenia have been related to a deficit in the capacity to inhibit inappropriate representations. In this paper, we briefly review some of the experimental evidence from normal subjects that has contributed to the acceptance of cognitive inhibition as a key process in the control of normal cognition, as well as more recent evidence that has led to a revision of the concept. Negative priming in normal subjects has been found to be dependent upon characteristics of the experimental situation as perceived by the subject. In particular, priming is observed when the subject anticipates difficulty in determining the response and proceeds with caution. Thus, inhibition is not an automatic "brake" applied to irrelevant material, but rather the product of strategic considerations within the experimental situation. This revision of the cognitive inhibition hypothesis leads to a re-interpretation of the apparently deficient cognitive inhibition seen in depressed or schizophrenic subjects. According to this more recent interpretation, deficient cognitive inhibition in pathological subjects can be seen as a less adaptive strategic adjustment to the task. The pathology seems to touch higher-level executive functions rather than a deficient inhibitory "brake". In depressed subjects, abnormal performance in selective attention tasks could be related to the underlying pathology in two ways: some depressed subjects show a marked lack of energy and a psychomotor slowing: these subjects do not exhibit normal negative priming, probably because of a reduction of cognitive resources. Other depressed subjects show abnormal performance as reflected by negative priming greater than normal: this result could be related to an exaggerated tendency to verify a correct response. Schizophrenic subjects show a lack of negative priming that seems most plausibly to be related to an ineffectual integration of the experimental instructions concerning both speed and accuracy in the response. This re-interpretation of the cognitive deficiency in pathological patients provides a better fit with recent experimental results from normal subjects, and with cognitive deficits measured in pathological subjects.

Association Learning↗
PubMedDate not supplied

[Tardive dyskinesia. After more than 2 decades].

The clinical aspects of tardive dyskinesia are describe, outlining the difficulties and the limits encountered by the clinician. The tools for its evaluation are reviewed, as well the epidemiology data and the current neuropathological hypothesis.

Animals↗
PubMedDate not supplied

[Lithium, pregnancy and breast feeding].

Due to its teratogenic potential and its passage in the maternal milk, the administration of lithium during pregnancy and post-partum, if breast-feeding is contemplated, raises specific issues. The kinetics of lithium during pregnancy is reviewed, as well as its influence on the foetus during this period and during breast-feeding. Its teratogenicity affects particularly the cardiovascular system, the Ebstein's anomaly being the most typical and frequent malformation. As a general rule, the administration of lithium should be avoided during pregnancy, at least during the first trimester. However, pregnancy and breast-feeding do not represent an absolute contraindication for the continuation of lithium therapy if it is deemed necessary, in spite of the risks that can be incurred and of which the patient should be informed.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

[Neuropsychology of a psycho-organic syndrome caused by idiopathic hypoparathyroidism. Apropos of a case].

A case of organic psychosis secondary to an idiopathic hypoparathyroidism with intracranial calcifications affecting the basal ganglia and the cortico-medullary junction is described. The results of the skull X-ray, cerebral TACO and nuclear magnetic resonance imaging analyses are presented, as well as a battery of neuropsychological tests. In spite of the extensive calcifications found, deficits on the neuropsychological tests were minimal or non-existent; possible explanations of this discrepancy are discussed.

Adult↗