Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CATAPLEXY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1995

Cortical electrical stimulation in humans. The negative motor areas.

Summarizing, we have presented evidence in humans for two "negative motor areas" which we had speculated play a significant role in the planning of voluntary motor movements. A review of the more recent experimental literature shows that histological, physiological, and electrical stimulation studies in animals reveal the existence of two frontal regions that from the experimental data also seem to play an essential role in the preparation (as opposed to execution) of voluntary movements. Current available evidence suggests that these two areas (areas F5 and F6 of Rizzolatti et al.) correspond to the negative motor areas we have described in human studies. Also of interest is that Broca's area in the dominant hemisphere overlaps the corresponding negative motor area. This observation suggests that Broca's area has evolved from area F5 of monkeys specializing in the planning of fine movements necessary for speech production. We feel that current evidence suggests the existence of three mechanisms by which cortical stimulation (by electrical stimulation or by epileptic activation) can generate negative motor phenomena: 1. The "silent period," which is consistently contralateral, has a somatotopic distribution, and tends to affect predominantly muscles involved in fine movements. It is of relatively short duration and seems to be generated by the activation of cortical areas in the primary sensorimotor region. The H-reflex is not inhibited during the silent period, suggesting that the silent period is generated by a decrease in the excitatory input through direct corticospinal neurons on the spinal alpha motoneurons. It is possible that in normal individuals this system is used for fine tuning of fine distal movements. The negative myoclonus seen in some patients with focal cortical epilepsy is probably generated by this mechanism. The primary and supplementary "negative motor areas" described in this chapter. This effect also has a somatotopic distribution but can affect muscle bilaterally even if there is a clear predominance contralaterally. The negative motor effect does not influence postural tone and can be prolonged. The negative motor effect is probably produced by activation of agranular cortex immediately in front of the primary and supplementary face motor area. These cortical areas are probably used for organization and integration of fine motor movement. Activation of these areas would produce an apraxia of fine movements. Focal atonic seizures are probably generated by this mechanism. 3. The fast-conducting corticoreticulospinal pathways, which by activation of the brainstem inhibitory centers (NRPo, n.r. magnocellularis dorsal beta, and NRGc), tend to produce bilateral atonia of axial, postural muscles. This system probably does not depend on the presence of the direct corticospinal pathways. By analogy with cataplexy, which is probably produced by activation of similar brainstem inhibitory systems, we would expect the H-reflex to be markedly diminished or even to disappear during the atomic phase (64). This pathway would be used normally for postural adjustments and locomotion. The bilateral massive atonic seizures, seen most frequently in patients with severe and diffuse cortical lesions, are probably produced by this mechanism. However, the bilateral atonic seizures occasionally seen in patients with focal cortical lesions may also be produced by a similar mechanism.

Brain↗
PubMed1995

[Use of antidepressants in sleep disorders: practical considerations].

There is a general tendency to restrict the notion of sleep disorders to insomnia and consequently to limit treatment to the prescription of hypnotics. However, it is very often of benefit to prescribe psychotropic agents, in particular antidepressants, not only in insomnia but also in certain cases of hypersomnia, parasomnia and dysomnia associated with organic diseases. In some conditions, however, antidepressants may either induce or aggravate sleep disorders. This is the case with a number of psychostimulants that occasionally induce insomnia. It is also true of the tricyclic antidepressants, which may worsen or even induce a restlessleg syndrome that is often associated with periodic movement syndrome. On the other hand, the antidepressants may play a therapeutic role in certain sleep disorders : - depression-related insomnia is of course the << primary >> indication for antidepressants. Furthermore, certain antidepressants exhibit a sedative action resulting in a hypnogenic-type effect which appears well before the antidepressant effect; - the other types of insomnia may also often be treated with antidepressants : not acute reactional insomnia, against which hypnotics are remarkably effective, but chronic insomnia. In addition, all antidepressants may eventually correct depressive hypersomnia, but in these cases, it is evidently preferable to prescribe non-sedative drugs. Although some tricyclic antidepressants have been proposed for use in hypersomnia due to sleep apnea, their therapeutic interest is minor compared with mechanical and surgical treatment. In contrast, antidepressants play an important role in the treatment of narcolepsy, particularly for the correction of attacks of cataplexy. Antidepressants have also been used for some time in the treatment of parasomnia related to slow deep sleep (night terrors and sleepwalking), but the antidepressants may also be used in enuresis and in parasomnia related to REM sleep : nightmares, sleep paralysis, behavioral problems associated with REM sleep. Antidepressant (mainly serotoninergic drugs) are often used in the treatment of fibrolitis syndrome. Finally, antidepressants (particularly the serotoninergic antidepressants) play an important role in the drug treatment of fibromyalgia.

Antidepressive Agents↗
PubMedDate not supplied

[Dr. John Baptiste Edouard Gélineau].

With this brief review we honor the memory of the great French doctor Jean Baptiste Edouard Gélineau. Dr. Gélineau was born on December 23, 1828 at Blaye, Gironde, close to the Bordeaux region. His name is connected with the first clinical description of the disease for which he, both by the right of the primacy as well as ad valorem of his first two names, coined the name "narcolepsy". He was the first to notice the intrinsically evanescent symptoms of narcolepsy, such as excessive daytime somnolence, imperative sleep habits and cataplexy or "astasia" as he called it, and incorporate them into a single clinical syndrome. In 1881 Gélineau discussed Kaffe's case of "maladie du sommeil" as a proof of the existence of the new disease described a year before. As a good clinical observer Gélineau noticed the close relation of emotional engagement and astasia. His attitude was that narcolepsy was a nosologic entity, a disease sui generis, but admitted that it could appear purely as a symptom only. This was in discordance with the views in England where (in 1928) Dr. Samuel Alexander Kinnier Wilson repudiated such convictions; in 1930 Lhermitte still shared the same opinion. Gélineau differentiated narcolepsy from epilepsy with the elegance of clinical reasoning. Overall, Gélineau described three elements of the narcoleptic pentade. Sleep paralyses were first described by Mitchell in 1876, and were first attributed to narcolepsy by Wilson in 1928; in 1930 Lhermitte first described hypnapompic, and Daniels, in 1934, hypnagogic sleep paralysis. Hypnagogic hallucinations were described by Maury in 1848 and subsequently by de Saint Denis in 1867. In twenties they were thoroughly studiesed during the epidemic encephalitis and after the Big War in 1922 by Levy. The life story of Dr. Gélineau covers multivarious activities. As a young student of the Rochefort Navy Medical School he took part in the fight against colera which deluged the city of La Rochelle. In 1849 he became the "Intern" of the Navy Hospital and next year a "Surgeon of the Third Class". As a Navy surgeon he visited French colonies in the Indian ocean: first the Reunion island and then Mayotte island of the Commores Archipelago. Of this period he wrote "Voyage a i'lle de la Réunion", memoirs published much later, in 1905, in which he described colonial life and abolition of slavery. The story of Elise, a beauteous Creole woman, a concubine of a young naval Commander, who delivered a child that soon died, inexorably points to the autobiographic character of his work. He defended a doctoral thesis "Aperçu Medical de I'lle de Mayotte" at Montpellier University School of Medicine in 1858, using the data collected during his year-and-a-half stay on a Mayotte island; at that time he was a "Navy Surgeon of the Second Class". For his dedication in fighting against epidemics that broke out during the French-German war in 1870 he was nominated for the Legion of Honor, but received it only later. In 1871 Gélineau introduced "Doctor Gélineau's tablets" for the treatment of epilepsy (contained bromide and arsenic). He was a member of the Société de Médicine, Société d' Hypnologie, La-Société Française d' Hygiène, and a few others. After retirement at the age of 72, Gélineau switched to wine production, continuing the family tradition; for the quality of his Bordeaux wines he was awarded gold medals at the Anvers and Paris Exhibitions. Dr. Gélineau died on March 2, 1906, at Argeles Gazost in Pyrnees honored by the titles of Chevalier de la Légion d' Honneur, Officier d'Academie and Commander of Nichan of the Ottoman Empire.

Epilepsy↗
PubMed1976

Narcolepsy in seven dogs.

Narcolepsy in 7 dogs was tentatively diagnosed on the onset of cataplexy, before or during young adulthood. Confirmatory polygraphic sleep recordings were done in 3 of the dogs. In 2 dogs, treatment with neostigmine did not cause the signs to disappear, thus ruling out myasthenia gravis; trials with imipramine reduced catapletic attacks. Data from case histories, polygraphic recordings, drug trials, and clinical tests were used to compare and contrast the disease in man and in the dog.

Animals↗
PubMed1998

[Idiopathic hypersomnia--review of literatures and clinical experiences on 16 Japanese cases].

The concept of idiopathic hypersomnia (IHS) was reviewed. The minimal criteria for IHS in the International Classification of Sleep Disorders (ICSD) are not clear enough to designate a clinical entity. We propose our criteria for IHS, which consist of 6 items. 1. Recurrent daytime sleep episodes with duration of longer than one hour that occur almost everyday for at least 6 months. 2. Absence of refreshed feeling after the daytime sleep episodes. 3. Length of nocturnal sleep is either normal or prolonged. 4. Total sleep time per day exceeds 10 hours. 5. Absence of cataplexy. 6. Does not meet criteria for other sleep disorders that account for the excessive daytime sleep episodes. Our clinical experiences with 16 Japanese IHS patients were described. Decrease in HLA Cw3 was found.

Adult↗
PubMed1999

Neuronal degeneration in canine narcolepsy.

Narcolepsy is a lifelong illness characterized by persistent sleepiness, hypnagogic hallucinations, and episodes of motor paralysis called cataplexy. We have tested the hypothesis that a transient neurodegenerative process is linked to symptom onset. Using the amino-cupric silver stain on brain sections from canine narcoleptics, we found elevated levels of axonal degeneration in the amygdala, basal forebrain (including the nucleus of the diagonal band, substantia innominata, and preoptic region), entopeduncular nucleus, and medial septal region. Reactive neuronal somata, an indicator of neuronal pathology, were found in the ventral amygdala. Axonal degeneration was maximal at 2-4 months of age. The number of reactive cells was maximal at 1 month of age. These degenerative changes precede or coincide with symptom onset. The forebrain degeneration that we have observed can explain the major symptoms of narcolepsy.

Animals↗