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Results for “CATAPLEXY”

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At least 793 records · Page 44Linked to original sources
PubMed1984

Comparison of the psychosocial effects of epilepsy and narcolepsy/cataplexy: a controlled study.

A questionnaire survey compared the psychosocial effects of epilepsy in 60 patients without major organic pathology (selected cases with temporal lobe epilepsy or primary generalized epilepsy) with those of matched (duration of illness, sex) patients with narcolepsy/cataplexy and with those of age- and sex-matched controls. Comparing epileptic patients with controls, we confirmed the well-documented marked deleterious effects of epilepsy upon work, education, occupational and household accidents, recreation, personality, interpersonal relations, and other parameters. Comparisons of epileptic and narcoleptic patients, however, showed that, in general, persons with narcolepsy are even more psychosocially impaired. The narcoleptic patients showed greater frequencies of disease-attributed reduced performance at work, poorer driving records, higher accident rates from smoking, greater problems in planning recreation, and other significant differences. Rather dissimilar profiles of psychosocial impairment were found to characterize the two conditions, and these were largely understandable as a function of their symptoms. The only areas in which epileptic patients showed greater problems than those with narcolepsy were in educational achievement and in ability to maintain a driving license. Most of the intergroup differences remained significant even for smaller groups matched also for age. The somewhat greater psychosocial impact of narcolepsy appears to be due to the continuous excessive daytime sleepiness that persists between the diagnostic attacks, whereas persons with epilepsy are relatively alert between seizures.

Accidents↗
PubMed1987

Narcolepsy/cataplexy. IV: Diagnostic value of daytime nap recordings.

Sleep and wakefulness patterns in daytime naps of 50 patients with narcolepsy/cataplexy were compared with those of 50 controls. Each subject was monitored polygraphically during 2 one-hour nap periods. A sleep-onset REM period in either of the 2 daytime naps was observed to have a higher diagnostic sensitivity (78%) than an abnormally shortened sleep latency (68%). However, the specificities of a sleep-onset REM period (88%) or abnormally shortened sleep latency (90%) were quite similar. When the occurrence of either a sleep-onset REM period or a shortened sleep latency was evaluated in either of the two naps, the overall sensitivity was increased to 84% while the specificity was decreased only to 80%. The limitations of and indications for the use of testing for sleep and REM latencies in the diagnosis of narcolepsy in clinical practice are discussed.

Adult↗
PubMedDate not supplied

Multisystemic chromatolytic neuronal degeneration in Cairn terriers. A case with generalized cataplectic episodes.

Multisystemic chromatolytic neuronal degeneration, a newly recognized disease of Cairn Terriers, is described in a second affected North American puppy. In this puppy, the early onset of hind limb weakness at 11 weeks and rapid development of signs of diffuse CNS involvement were distinctive. Signs of cerebellar dysfunction were prominent, but bouts of cataplectic collapse in this puppy constituted the most distinguishing clinical feature. Although electroencephalograph (EEG) recordings lacked a true rapid eye movement (REM) pattern during cataplectic episodes, cervical electromyograph (EMG) potentials ceased or diminished, and imipramine injection was associated with arousal. Postmortem studies revealed that chromatolytic degeneration was very widespread, affecting many neuronal populations in the brain and spinal cord as well as neurons in sensory ganglia. Although the pattern of chromatolysis varied among affected perikarya, chromatolysis was consistently related to dispersion and loss of ribosomes. In this puppy, as opposed to six studied previously, thoracolumbar myelomalacia also occurred symmetrically in the dorsal horns and adjoining funicular white matter. The metabolic derangement underlying this chromatolytic neuronal degeneration and myelomalacia remains unknown.

Animals↗
PubMed2004

Developmental changes in CSF hypocretin-1 (orexin-A) levels in normal and genetically narcoleptic Doberman pinschers.

Loss of hypocretin cells or mutation of hypocretin receptors causes narcolepsy. In canine genetic narcolepsy, produced by a mutation of the Hcrtr2 gene, symptoms develop postnatally with symptom onset at 4 weeks of age and maximal symptom severity by 10-32 weeks of age. Canine narcolepsy can readily be quantified. The large size of the dog cerebrospinal fluid (CSF) cerebellomedullary cistern allows the withdrawal of sufficient volumes of CSF for accurate assay of hypocretin levels, as early as postnatal day 4. We have taken advantage of these features to determine the relation of CSF hypocretin levels to symptom onset and compare hypocretin levels in narcoleptic and normal dogs. We find that by 4 days after birth, Hcrtr2 mutants have significantly higher levels of Hcrt than normal age- and breed-matched dogs. These levels were also significantly higher than those in adult narcoleptic and normal dogs. A reduction followed by an increase in Hcrt levels coincides with symptom onset and increase in the narcoleptics. The Hcrtr2 mutation alters the normal developmental course of hypocretin levels.

Aging↗
PubMed1992

The delayed sleep phase syndrome: clinical and investigative findings in 14 subjects.

Fourteen subjects are described in whom a clinical diagnosis of the delayed sleep phase syndrome was made. The condition is multi-factorial, dependent on lifestyle, mood and personality, as well as on familial factors but no single factor in isolation is sufficient to explain the delay in sleep timing. Refusal to attend school may be important in some instances but will not explain cases with delayed age of onset. In half the subjects the delay in sleep phase started in childhood or adolescence. The syndrome causes severe disruption to education, work and family life. Polysomnography, motor activity monitoring of rest-activity cycles, plasma melatonin profiles and urinary melatonin metabolite excretion are normal. Different patterns of sleep phase delay seen in the syndrome include stable, progressive, irregular and non-24 hour sleep-wake cycles. These patterns may result from different social and other Zeitgebers ("time-markers", for example sunrise, sunset) in the normal environment. Treatment by forced sleep-wake phase advance or with melatonin resulted in a partial sleep-phase advance but this was not maintained on stopping treatment.

Adolescent↗
PubMed2001

Increased and decreased muscle tone with orexin (hypocretin) microinjections in the locus coeruleus and pontine inhibitory area.

Orexin-A (OX-A) and orexin-B (OX-B) (hypocretin 1 and hypocretin 2) are synthesized in neurons of the perifornical, dorsomedial, lateral, and posterior hypothalamus. The locus coeruleus (LC) receives the densest extrahypothalamic projections of the orexin (OX) system. Recent evidence suggests that descending projections of the LC have a facilitatory role in the regulation of muscle tone. The pontine inhibitory area (PIA), located ventral to LC, receives a moderate OX projection and participates in the suppression of muscle tone in rapid-eye-movement sleep. We have examined the role of OX-A and -B in muscle-tone control using microinjections (0.1 microM to 1 mM, 0.2 microl) into the LC and PIA in decerebrate rats. OX-A and -B microinjections into the LC produced ipsi- or bilateral hindlimb muscle-tone facilitation. The activity of LC units was correlated with the extent of hindlimb muscle-tone facilitation after OX microinjections (100 microM, 1 microl) into fourth ventricle. Microinjections of OX-A and -B into the PIA produced muscle-tone inhibition. We did not observe any significant difference in the effect of OX-A and -B on muscle tone at either site. Our data suggest that OX release activates LC units and increases noradrenergic tonus in the CNS. Moreover, OX-A and -B may also regulate the activity of pontine cholinoceptive and cholinergic neurons participating in muscle-tone suppression. Loss of OX function may therefore disturb both facilitatory and inhibitory motor processes.

Animals↗
PubMed1984

Narcolepsy: preliminary retrospective study of psychiatric and psychosocial aspects.

A review of the charts of 24 ambulatory male veterans with narcolepsy or narcolepsy/cataplexy showed an impressive number of psychiatric and psychosocial difficulties in these patients, such as poor adjustment to the illness, high unemployability, and disturbed intrafamily relationships. Sixteen of the patients had psychiatric disorders according to DSM-III criteria, including adjustment disorder, major depressive episode, alcohol dependence, and personality disorder, but excluding any type of psychotic disorder. The study suggests that narcoleptic/cataplectic patients have more of these difficulties than narcoleptic patients do.

Adaptation, Psychological↗
PubMedDate not supplied

Pseudocataplexy.

Explore the source record for details and available documents.

Adolescent↗
PubMed2006

Topiramate effect in catatonia: a case series.

The authors describe four cases of catatonia in which topiramate treatment was used. Commonly effective therapies, including benzodiazepines and divalproex, were proven refractory. In all four cases, subjects experienced complete remission of catatonic symptoms and tolerated treatment well. In one case, all psychotropic medications were discontinued because the patient became delirious. The delirium resolved after discovery and treatment of a urinary tract infection. Catatonic agitation relapsed when topiramate was withdrawn but remitted again when topiramate and lorazepam therapy was restored. In two cases, continued topiramate therapy was accompanied by sustained remission. These case reports present a novel approach to the treatment of catatonia.

Adult↗