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Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
http://www.baillement.com 
 
mystery of yawning

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mise à jour du
31 décembre 2003
lexique
Bibliographie de références en attente

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Postgrad Med 2000 Oct;108(5):175-6, 179-82
Is it a tic or tourette's? Clues for differentiating simple from more complex tic disorders
Evidente VG Parkinson's Disease and Movement Disorders Center, Mayo Clinic Scottsdale, AZ 85359, USA.
Tics are characterized by sterotyped, purposeless, and irregularly repetitive movements and usually can be classified as chronic motor or vocal tic disorders, transient tic disorders, or Tourette's syndrome. The latter is a complex disorder associated with multiple tics and often accompanied by other conditions, such as ADHD and obsessive-compulsive disorder. Treatment can be difficult, and drug therapy should begin with agents least likely to cause problems for the patient. Education of the patient and family and support from the physician and other care providers are essential elements of effective management.
 
Arch Gen Psychiatry 2000 Aug;57(8):741-8
A functional neuroanatomy of tics in Tourette syndrome.
Stern E, Silbersweig DA, Chee KY, Holmes A, Robertson MM, Trimble M, Frith CD, Frackowiak RS, Dolan RJ Functional Neuroimaging Laboratory, Department of Psychiatry, Box 140, Room 1304, Weill Medical College of Cornell University, 525 E 68th St, New York, NY 10021, USA.
Tics are involuntary, brief, stereotyped motor and vocal behaviors often associated with irresistible urges. They are a defining symptom of the classic neuropsychiatric disorder, Tourette syndrome (TS), and constitute an example of disordered human volition. The neural correlates of tics are not well understood and have not been imaged selectively. METHODS: Event-related [(15)O]H(2)O positron emission tomography techniques combined with time-synchronized audio and videotaping were used to determine the duration of, frequency of, and radiotracer input during tics in each of 72 scans from 6 patients with TS. This permitted a voxel-by-voxel correlational analysis within Statistical Parametric Mapping of patterns of neural activity associated with the tics. RESULTS: Brain regions in which activity was significantly correlated with tic occurrence in the group included medial and lateral premotor cortices, anterior cingulate cortex, dorsolateral-rostral prefrontal cortex, inferior parietal cortex, putamen, and caudate, as well as primary motor cortex, the Broca's area, superior temporal gyrus, insula, and claustrum. In an individual patient with prominent coprolalia, such vocal tics were associated with activity in prerolandic and postrolandic language regions, insula, caudate, thalamus, and cerebellum, while activity in sensorimotor cortex was noted with motor tics. CONCLUSIONS: Aberrant activity in the interrelated sensorimotor, language, executive, and paralimbic circuits identified in this study may account for the initiation and execution of diverse motor and vocal behaviors that characterize tics in TS, as well as for the urges that often accompany them.
 
Int J Neurosci 1995 Mar;81(1-2):95-100
Cholinergic mechanisms in Gilles de la Tourette's syndrome.
Sandyk R NeuroCommunication Research Laboratories, Danbury, CT 06811, USA.
Gilles de la Tourette syndrome (GTS), a chronic, familial, neuropsychiatric disorder of unknown etiology, is characterized clinically by the presence of motor and vocal tics that wax and wane in severity over time and by the occurrence of a variety of neurobehavioral disturbances including hyperactivity, self-mutilatory behavior, obsessive compulsive behavior, learning disabilities, and conduct disorder. Pharmacological studies suggest that the tics of GTS result from dysfunction of monoaminergic systems, more specifically from increased dopaminergic activity due to postsynaptic dopamine receptor supersensitivity. However, given that striatal dopaminergic and cholinergic systems exhibit reciprocal antagonism in other movement disorders such as Parkinsonism and chorea, it is conceivable that the cholinergic system is implicated in the disease. In the present communication it is proposed that: (a) the emergence of motor and vocal tics in GTS is associated with increased central cholinergic activity; (b) cholinergic overactivity is involved in the manifestation of other symptoms in GTS including depression, sleep disorders, motion sickness, pain, sensory tics, and the waxing and waning course of the disease; (c) abnormalities of the cholinergic system support previous evidence linking GTS with delayed cerebral maturation in a subset of young patients; and (d) drugs which stimulate cholinergic receptors may exacerbate symptoms of GTS, and as with dopamine agonists, should be avoided in patients with GTS.
 
Int J Neurosci 1996 Feb;84(1-4):187-94
Effects of picotesla flux electromagnetic fields on dopaminergic transmission in Tourette's syndrome.
Sandyk R NeuroCommunication Research Laboratories, Danbury, CT 06811, USA.
Tourette's syndrome (TS), a chronic familial neuropsychiatric disorder ofunknown etiology, is characterized clinically by the presence of motor and vocal tics that wax and wane in severity over the time and by the occurrence of a variety of neurobehavioral disorders. It is believed that the tics of TS result from increased dopamine (DA) activity caused by postsynaptic DA receptor supersensitivity. The synthesis and release of DA is regulated presynaptically by a specific class of DA D2 receptors, termed autoreceptors activation of which causes inhibition of DA synthesis and release. In experimental animals and humans administration of small doses of apomorphine, a DA D2 autoreceptor agonist, produces yawning. Recurrent episodes of yawning followed by increased motor tic activity was observed in two patients with TS during exposure to brief, extracranial applications of picotesla flux electromagnetic fields(EMFs). On the basis of these observations it is suggested that recurrent episodes of yawning in response to application of EMFs was induced by activation of presynaptic DA D2 autoreceptors while further exposure to these EMFs caused excessive stimulation of postsynaptic DA D2 receptors resulting in exacerbation of the tics. Thus, the dual effects of picotesla flux EMFs on the DA D2 autoreceptor and the postsynaptic receptor resemble the biphasic pharmacological and behavioral properties of apomorphine, a DA agonist which activates the autoreceptors in low doses while in higher doses causes stimulation of the postsynaptic receptors producing exacerbation of symptoms of TS. These findings demonstrate that picotesla flux EMFs applied extracerebrally may influence nigrostriatal DA transmission at pre- and postsynaptic DA D2 receptor sites.
 
 
Panminerva Med 2000 Mar;42(1):61-7
Tourette's syndrome in children: neurobiological issues in pathophysiology.
Masi G, Brovedani PDivision of Child Neurology and Psychiatry, University of Pisa, IRCCS Stella Maris, Calambrone, Italy.
In recent decades significant advances in the understanding of neurobiological substrates of Tourette's Syndrome (TS) have led to the formulation of hypotheses regarding the ways in which the most salient features of the syndrome may occur. Pathophysiology of TS involves multiple intertwined neurobiological issues in different areas of the Central Nervous System. This review considers neuroimaging studies (MRI, PET, SPECT) in patients with TS. Neurochemical neurophysiological and electrophysiological studies are also reviewed. The role of the neuroendocrine and neuroimmunologic mechanism on pathogenesis of the disease is discussed. Advances in diagnostic techniques (fMRI, mMRI, PET, SPECT) and in neurophysiological research on neurotransmitter systems will allow us to better understand the pathophysiology of TS and to use more specific treatments.
 
Eur Child Adolesc Psychiatry 2000;9 Suppl 1:I60-75
Gilles de la Tourette syndrome: symptomatic treatment based on evidence.
Robertson MM, Stern JS Department of Psychiatry and Behavioural Sciences, Royal Free and UniversityCollege Medical School, University College, London, UK.
The treatment of the Gilles de la Tourette syndrome has evolved from case reports, clinical experience and more recently blinded trials usually in small numbers of patients. We have reviewed the evidence available to clinicians. The oldest and still most widely prescribed drug, haloperidol, should now not be considered the first-line agent in children as other agents have superior adverse effects profiles. Symptomatic treatment should be targeted to the specific additional psychopathologies seen in the syndrome. For the treatment of tics, sulpiride, tiapride, possibly pimozide and in some cases clonidine may be considered first-line agents. Although a body of data supports pimozide, caution has to be exercised in relation to possible cardiac effects. Antidepressants and stimulants have an important place in the management of depression, obsessionality and attention deficit hyperactivity disorder. The latter also responds to clonidine making it a rational first choice where ADHD coexists with GTS. There are a multitude of other drugs advocated in the literature in addition to reports of neurosurgery and the novel use of immune modulation. Therapeutic trials for GTS are challenging. However, further data from blinded trials are required before many of these treatments can be considered to be mainstream treatment options.
 
Addict Dis 1975;2(1-2):187-99
A study of factors that influence the severity of neonatal narcotic withdrawal.
Ostrea EM Jr, Chavez CJ, Strauss ME
1. History is unreliable in assessing maternal drug habit. Morphine was detected in significant amounts in maternal and fetal urine regardless of whether the mother was on a methadone program or whether she denied any use of heroin during the last trimester of pregnancy. 2. Infants born to drug-addicted mothers were, in general, of birthweight normal and appropriate for gestational age (i.e., greater that 10th percentile). The infants born to mothers on a methadone clinic program had a higher birthweight compared to those whose mothers were not on any methadone program. 3. In order of frequency, the signs and symptoms of withdrawal were: central nervous system manifestations-fist sucking, irritability, tremors, sneezing, high-pitch cry, hypertonia; vasomotor in the form of stuffy nose; and gastrointestinal in the form of sweating, diarrhea, vomiting and yawning. Convulsions were not noted. No death occurred. 4. The severity of neonatal narcotic withdrawal did not correlate with the infant's gestational age, APGAR, sex or race; nor with maternal age, parity, duration of heroin addiction or duration of methadone intake. Also, it did not correlate with the total morphine level measured either in infant's or mother's urine or in cord blood. The serum levels of calcium and glucose were normal and identical in either mild or severe withdrawal. 5. The severity of neonatal withdrawal correlated significantly with the methadone dose per day of the mother (in initial, final or average dose). A maternal methadone dose of more than 20 mg per day was associated with a higher incidence of moderate to severe withdrawal in their babies. As a corollary, it was also noted that infants whose mothers were on a high methadone dose (i.e., greater than 20 mg per day) had a greater postnatal weight loss despite a significantly higher birthweight initially, and stayed in the hospital longer. 6. Finally, the modification of the environment to reduce external stimuli to the infant born to a drug-dependent mother, does not prevent or diminish the severity of neonatal narcotic withdrawal. Thus, there is no need to manage these infants in a special nursery.
 
Rev Neurol (Paris) 1985;141(6-7):429-39
Role of alpha-MSH and related peptides in the central nervous system
Delbende C, Jegou S, Tranchand-Bunel D, Leroux P, Tonon MC, Mocaer E, Pelletier G, Vaudry H
Alpha-melanocyte stimulating hormone (alpha-MSH) is a tridecapeptide secreted by intermediate lobe cells and synthesized in the brain as well. As a hormonal peptide, the physiological function of alpha-MSH consists mainly in the control of pigment movements within dermal melanophores.At the pituitary level, alpha-MSH secretion is under multifactorial control: it is inhibited by dopamine and GABA and stimulated by corticoliberin (CRF), thyroliberin (TRH), beta-adrenergic agonists and (or) serotonin. Identification of alpha-MSH containing neurons in the hypothalamus and other brain regions (septum, thalamus, mid-brain, striatum, hippocampus, cerebral cortex and spinal cord) has been carried out by means of immunological and biochemical techniques combined with bioassays. In the central nervous system (CNS) as in the hypophysis, alpha-MSH is synthesized from a high molecular weight precursor, pro-opiomelanocortin (POMC). Maturation of this protein yield similar end products in the hypothalamus and the intermediate lobe. Several peptides chemically related to alpha-MSH are generated including the desacetyl and monoacetyl (authentic alpha-MSH) forms; the latter has the greatest behavioral activity. The demonstration that alpha-MSH has numerous central nervous system effects has raised the possibility that this neuropeptide acts as a neuromodulator or a neurotransmitter. In the rat, intra-cerebroventricular administration of ACTH/MSH peptides induces the stretching-yawning syndrome (SYS) which is frequently preceded by excessive grooming. This excessive grooming is blocked by neuroleptics indicating that the central dopaminergic neurons are implicated in this behavioral effect of the peptide. alpha-MSH is involved in memory, arousal and attention; in hypophysectomized animals, the learning ability is restored after administration of MSH or related peptides. Injection of alpha-MSH delays also extinction of passive avoidance behavior and affects performances motivated by hunger as well as aggressive behavior. Recent studies concerning the role of alpha-MSH have been undertaken in human beings. The effects of MSH-related peptides favour a role of these peptides in arousal: they maintain a high level of vigilance and improve visual discrimination. These behavioral changes were accompanied by marked changes in CNS electrophysiology. Current studies, which aim at establishing a neurotransmitter function for alpha-MSH, concern the distribution and characterization of alpha-MSH receptors in the central nervous system and the mechanism controlling the release of neuronal alpha-MSH.
 
Rinsho Shinkeigaku 1982 Feb;22(2):112-9
Ide M, Kataoka A, Koriyama T, Osame M, Igata A
New accompaning signs and symptoms of adrenoleukodystrophy. Adrenoleukomyeloneuropathy with hypoparathyroidism, cerebral calcification, and frequent yawning
 
Pharmacol Biochem Behav 1976;5(Suppl 1):159-63
Neurologically active peptides
Barbeau A, Gonce M, Kastin AJ
This paper reviews recent evidence that a number of small peptides found in the brain are active in the central nervous system and behaviorally. Attention is focused on MSH/ACTH 4-10, alpha- and beta-MSH, and the prohormone beta-LPH, as they produce a syndrome of yawning and stretching. Studies with substance P and mainly with MIF-I are also reviewed. It is shown that substance P is an excitatory transmitter or modulator in the dorsal spinal cord with that MIF-I has antiparkinson properties. It is concluded that many polypeptides have direct actions on the central nervous system independent of their neuroendocrine properties
 
Eur J Pharmacol 1999 Jun 30;375(1-3):1-11
Behavioral pharmacology of neuropeptides related to melanocortins and the neurohypophyseal hormones.
de Wied D Rudolf Magnus Institute for Neurosciences, Department of Medical Pharmacology, Utrecht University, The Netherlands.
Neuropeptides are peptides which affect the nervous system. They are derived from large precursor molecules. These are converted to neurohormones, neuropeptides of the "first generation", which can be further converted to neuropeptides of the "second generation". This review is a brief survey of the nervous system effects of neuropeptides derived from pro-opiomelanocortin (POMC) and the neurohypophyseal hormones. Processing of these molecules results in neuropeptides of the first and second generation which have similar, different, more selective or even opposite effects. Among those are effects on learning and memory processes, grooming, stretching and yawning, social, sexual and rewarded behavior, aging and nerve regeneration, thermoregulation, pain, sensitivity to seizures, and cardiovascular control. Results of animal studies as well as those of clinical studies suggest that these neuropeptides may be beneficial in aging, neuropathy, memory disturbances and schizophrenia. Most of these nervous system effects in animal studies were found before receptors in the nervous system for the various neuropeptides were detected. G-protein-coupled receptors for the neuropeptides of the "first generation", i.e., melanocortin receptors, opioid receptors, and neurohypophyseal hormone receptors have been found, in contrast to the receptors for neuropeptides of the "second generation", although there are indications that G-protein coupled receptors for these may be present in the brain.
 
 
Biol Rev Camb Philos Soc 1999 Aug;74(3):347-74
Miklosi A. Department of Ethology, Eotvos University, Budapest, Hungary.
The ethological analysis of imitation.
Theorists and experimental researchers have long debated whether animals are able to imitate. A variety of definitions of imitation have been proposed to describe this complex form of social learning. Experimental research on imitation has often been hampered by either a too loose 'anthropomorphic' approach or by too narrow 'behaviourist' definitions. At present neither associative nor cognitive theories are able to offer an exhaustive explanation of imitation in animals. An ethological approach to imitation offers a different perspective. By integrating questions on function, mechanism, development and evolution one can identify possible directions for future research. At present, however, we are still far from developing a comprehensive theory of imitation. A functional approach to imitation shows that, despite some evidence for imitative learning in food processing in apes, such learning has not been shown to be involved in the social transmission of either tool-use skills or communicative signals. Recently developed procedures offer possible ways of clarifying the role of imitation in tool use and visual communication. The role of imitation in explorative play in apes is also investigated and the available data suggest that copying during play might represent a behavioural homologue of human imitation. It is proposed that the ability to copy the behaviour of a companion is under a strong genetic influence in many social species. Many important factors have not been examined experimentally, e.g. the effect of the demonstrator, the influence of attention and memory and the ability to generalize. The potential importance of reinforcement raises the possibility that copying abilities serving divergent functions might be partly under the control of different mechanisms.
 
Child Dev 1983 Jun;54(3):702-9
Newborn infants imitate adult facial gestures.
Meltzoff AN, Moore MK.
Newborn infants ranging in age from 0.7 to 71 hours old were tested for their ability to imitate 2 adult facial gestures: mouth opening and tongue protrusion. Each subject acted as his or her own control in a repeated-measures design counterbalanced for order of stimulus presentation. The subjects were tested in low illumination using infrared-sensitive video equipment. The videotaped records were scored by an observer who was uninformed about the gesture shown to the infants. Both frequency and duration of neonatal mouth openings and tongue protrusions were tallied. The results showed that newborn infants can imitate both adult displays. 3 possible mechanisms underlying this early imitative behavior are suggested: instrumental or associative learning, innate releasing mechanisms, and active intermodal matching. It is argued that the data favor the third account.
 
Revue du praticien 1991, 41, 1 p7-15
G. Couly Development of the face in the embryo
The facial complex and the brain develop separately from a common embryonic structure called ectoblast. The neural crest cells which migrate early on from the neural groove differentiate into facial parenchyma, so that the embryological origin of the face is a neural one. The cephalic pole bas a primitive encephalofacial and encephalocervical segmentation with strict topographical correspondence : the nasofrontral and premaxillary structures are related to the anterior brain, whereas the maxi! Io-mandi bular and anterior cervical structures are related to the brainstem and its nerves. Thus the face is a qualitative, quantitative and topographical marker of the central nervous system. At the beginning of the third month the embryo becomes a fœtus due to the appearance of the first oral and pharyngeal motor sequences which are dependent upon the neurological development of the brainstent. This sum of embryological knowledge has clinical semiological applications : the face and its functions play the predictive role in the search for associated malformations of the same neural origin (brain, eye, neck, thorax). Such malformations are neurocristopathies.