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At least 505 records · Page 28Linked to original sources
PubMed2000

Enhancement of noradrenergic neural transmission: an effective therapy of myasthenia gravis: a report on 52 consecutive patients.

Neurochemical, neuroautonomic and neuropharmacological assessments carried out on all our myasthenia gravis (MG) patients showed that they presented a neural sympathetic deficit plus excessive adrenal-sympathetic activity. These abnormalities were registered during the basal (supine-resting) state, as well as after several stress tests (orthostasis, exercise, oral glucose and buspirone). In addition, MG patients showed increased levels of free-serotonin (f5HT) in the plasma, supposedly associated with the increased platelet aggregability which we found in all MG patients. As the above trio of neurochemical disorders (low noradrenergic-activity + high adrenergic-activity + increased f-5HT plasma levels) is known to favor Th-1 immunosuppression + Th-2 predominance, we outlined a neuropharmacological strategy for reverting the above neurochemical disorder. This treatment provoked sudden (acute), and late sustained improvements. Acute effects have been attributed to the increase of alpha-1 activity at the spinal motoneuron level. Late improvements always paralleled a significant normalization of immunological disorders. Complete normalization was registered only in non-thymectomized MG patients.

Adolescent↗
PubMed2002

Secondary narcolepsy in children with brain tumors.

We report two cases of children with disabling daytime sleepiness associated with suprasellar tumors and hypothalamic obesity. Multiple sleep latency testing demonstrated features consistent with severe narcolepsy, with sleep latencies of 0.25 and 0.75 minutes, and REM latencies of 2.1 and 1.5 minutes, respectively. An additional patient with hypothalamic damage secondary to a brain tumor, who was thought to be in a vegetative state, had features of narcolepsy on polysomnography. All children responded well to treatment with stimulants. We speculate that secondary narcolepsy associated with hypothalamic tumors is due to damage or loss of hypothalamic hypocretin-containing neurons. In view of the good response to treatment, we recommend that all children with excessive daytime sleepiness and hypothalamic damage be evaluated for narcolepsy.

Adolescent↗
PubMed2002

Drugs under investigation for attention-deficit hyperactivity disorder.

There has been substantial development of pharmacological treatments for attention-deficit hyperactivity disorder (ADHD) recently. The greatest change is the approval of new delivery systems for methylphenidate (MPH) and amphetamine (AMP) that permit once a day dosing. There are also a number of new compounds under development for the disorder, including several non-stimulant agents. These compounds target the noradrenergic, histaminergic and dopaminergic systems. The recent developments in the pharmacological treatment of ADHD should increase therapeutic options and the percentage of individuals with the disorder who can be effectively treated.

Animals↗
PubMed2004

Running on dope.

Explore the source record for details and available documents.

Benzhydryl Compounds↗
PubMed2004

Daytime sleepiness and insomnia as correlates of depression.

Insomnia and daytime sleepiness are often associated with depression. The possible relationships between sleep difficulties and depression are numerous. Insomnia and other sleep disturbances can be precursors to the onset of major depressive disorder, so they may act as risk factors for or predictors of depression. The symptomatology of depression also prominently includes insomnia, and sleep disturbances may be residual symptoms after response to antidepressant treatment. Insomnia and the resultant daytime sleepiness may be short-term or long-term side effects of antidepressant treatment as well. Whether insomnia is a precursor, symptom, residual symptom, or side effect of depression or its treatment, clinicians must give serious attention to and attempt to resolve sleep disturbances because of the risk of depression onset, worsening of depressive symptoms, and relapse of depression after response to antidepressant treatment. Remission of depression cannot be fully achieved until the associated insomnia and daytime sleepiness are resolved. This article describes the relationships between insomnia and depression and discusses the effects of various antidepressants on sleep. Finally, several different treatment options, including antidepressant monotherapy and augmentation of antidepressants with other medications, are explored.

Antidepressive Agents↗
PubMed2005

Molecular genetic advances in sleep research and their relevance to sleep medicine.

Neurobiology has been profoundly impacted by the availability of molecular genetic techniques within the past decade, and the sleep research field is no exception to this trend. Genetic influences on normal and pathologic sleep have long been recognized, but only recently have the contributions of discrete genetic loci to the regulation of sleep timing and sleep-related physiologic phenomena begun to be demonstrated, particularly through the use of genetically engineered strains of rodents. The ability to monitor the expression of a large number of genes has also accelerated in recent years, leading to a better understanding of the molecular and neurochemical correlates of sleep and of sleep loss. This article reviews the contributions of molecular genetic studies to our understanding of the processes that underlie sleep and its pathologies, discusses their relevance to the treatment of sleep disorders, and offers some speculation on how the sleep field might further be advanced through molecular genetic analysis.

Animals↗