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Mental disorders
Sub-Topics
Depression and Manic Depression
Anxiety Disorders
Alzheimer’s-type Dementia

Linked
Help Lien : Traitement m_dicamenteux du trouble anxieux g_n_ralis_ Lien : Les anticonvulsivants Lien : Davis scaring out causes and cures for phobias
Lien : Battle against tranquillisers Lien : Sedative-hypnotics

People who are living with post-traumatic stress disorder (PTSD) tend to have abnormally high levels of epinephrine, norepinephrine, and endorphins, three substances that are secreted in larger amounts when an individual is subjected to stress.

Patients with PTSD also show higher levels of corticotropin-releasing hormone (CRH), which acts something like a switch that initiates any response to stress. This hormone ultimately causes the adrenal glands to produce more cortisol, an anti-inflammatory molecule that also helps the body to mobilize its energy resources in order to cope with stress.

One might therefore expect that patients with PTSD would have higher levels of cortisol, just like patients with generalized anxiety disorder or depression. But in fact, the opposite seems to be true: people who have PTSD or who grew up with parents who had it actually show lower cortisol levels. One explanation for this surprising pattern, which is specific to PTSD, might be that certain parts of the brain become hyper-sensitized to cortisol and therefore try to keep its concentrations as low as possible.

Lien : Post-Traumatic Stress Disorder Expérience : Low Cortisol Levels May Predict PTSD Risk Lien : Stress
Lien : PTSD and the Brain: What's New in Basic Research Lien : Recommendations for Pharmacological Treatment of Acute Stress Reactions
TRANQUILIZERS


barbiturate molecule


benzodiazepine molecule

 

 

A milestone in the history of the medications commonly known as tranquilizers occurred in the early 1960s, when the first benzodiazepines arrived on the market. This new class of medications soon supplanted barbiturates, a powerful class of sedatives that were commonly used at the time and that act on the brain's GABA receptors.



The reason for this rapid success was that benzodiazepines were soon found to have a lower risk-to-benefit ratio than barbiturates. Benzodiazepines are at least as effective as barbiturates, have the same or fewer side effects, and have a far lower acute toxity (an overdose of barbiturates can even result in death).



One caveat, however: as far as dependency is concerned, benzodiazepines are no better than barbiturates. People who use benzodiazepines for a long time must undergo a difficult withdrawal process.

Benzodiazepines such as Valium now represent the largest class of tranquilizers. Each member of this class has several pharmacological properties in varying proportions:


For many benzodiazepines, the dominant effect is, of course, anxiolytic or sedative.

Other benzodiazepines are primarily anti-convulsants and are used to treat epilepsy.

Still other benzodiazepines are used as muscle relaxants.

Most benzodiazepines are fairly similar in their undesirable side effects, but differ fairly widely in how quickly and how long they act (their half-lives, for example, can range from a few hours to a few days).

These differences are due to these drugs' differing affinities for different types of GABA receptors and explain why different benzodiazepines are prescribed for different conditions. For example, for an acute anxiety attack, a physician may prescribe an anxiolytic that acts almost immediately but that often has a marked sedative effect. In contrast, for generalized anxiety disorder , the physician will choose a medication that minimizes sleepiness and risks of dependency.

It should be noted that benzodiazepines do not alleviate obsessive-compulsive disorder and are rarely prescribed for panic disorders.

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