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Re: Help - trigger - scared

Posted by morganpmiller on June 24, 2009, at 1:55:19

In reply to Re: Help - trigger - scared, posted by morganpmiller on June 24, 2009, at 1:52:10

OOps, I thought that would be something you could click on, sorry.



Benzodiazepines
Brain-Disabling Effects Of Benzodiazepines

By Peter R. Breggin, M.D.
From Brain-Disabling Treatments in Psychiatry
This is the first page of a two page article.

The benzodiazepines (BZs) have for several decades been recognized in the literature and clinical practice for their capacity to cause mental and behavioral abnormalities.

Xanax (alprazolam), and to an even greater extent, Halcion (triazolam), have a significantly different profile from other benzodiazepines due to their greater capacity to bind to receptors and their shorter half-life.

Halcion's very short half-life led to the hope that it would make a particularly good sleeping medication but it has proven especially dangerous.

The brain-disabling or toxic effects of the Bzs in general can be divided into several somewhat overlapping categories:

(1) The primary clinical effect of inducing sedation (tranquility) or hypnosis (sleep), which is indistinguishable from a toxic effect except in degree;
(2) Cognitive dysfunction, ranging from short-term memory impairment and confusion to delirium;
(3) Disinhibition and other behavioral aberrations-- including extreme agitation, psychosis, paranoia, and depression, sometimes with violence toward self or others;
(4) Withdrawal, in which the individual experiences a continuum of symptoms from anxiety and insomnia after routine use to psychosis and seizures after the abrupt termination of long-term, larger doses;
(5) Rebound, an aspect of withdrawal, in which the individual develops anxiety, insomnia, or other serious emotional reactions that are more intense than before drug treatment began. Withdrawal can take place between doses during the routine administration of Bzs, especially the short-acting ones.
(6) Habituation and addiction, along a continuum from feeling dependent on the drug to compulsively organizing one's behavior in a self-destructive manner around obtaining large amounts of the agent.

The Mechanism of Brain-Disability Neurophysiological studies show that the BZs potentiate the neuronal inhibition that is mediated by gamma-aminobutyric acid (GABA).

In doses used clinically, this results in a generalized suppression of both spontaneous and evoked electrical activity of the large neurons throughout all regions of the brain and spinal cord (Ballenger, 1995).

The binding of BZs to the GABA receptors is most intense in the cerebral cortex. Some BZs, such as Xanax and Halcion, bind especially tightly, increasing their tendency to produce more intense sedation and hypnosis, and also more severe cognitive deficits, behavioral abnormalities, rebound, and withdrawal.

Some advocates of the BZs have argued for a specific anti-anxiety effect separate from the general sedative effect, but there's no substantial evidence for this.

Rall (1990) concludes: The question whether the so-called antianxiety effects of the benzodiazepines are the same or different from the sedative and hypnotic effects has not been resolved.

People who use BZs to calm their anxiety will frequently use alcohol and other sedatives interchangeably for the same purpose, either in combination or at different times.

As they switch from drug to drug, they tend to find little or no difference in the anti-anxiety effect. This confirms the brain-disabling principle that BZs have no specificity for anxiety in comparison to other sedative/hypnotic agents. The Mechanism for Producing Behavioral Abnormalities.

There are at least two probable causes for the abnormal behavior produced by BZs. One mechanism is direct intoxication, resulting in impaired executive and cognitive function, including reduced judgment and impulse control.

Fogel and Stone (1992, p. 341) observe Benzodiazepines, given to reduce arousal or possibly to treat a hypomanic state, may aggravate impulsive behavior by impairing the inhibition mechanism of the frontal lobes. Barbiturates may have similar effects.

Especially in regard to the BZs, a second mechanism, rebound, has been demonstrated, and is a probable cause of many more severe reactions.

Rebound or discontinuation symptoms occur when the BZs are withdrawn or when they begin to lose their effectiveness (American Psychiatric Association, 1990). As the BZ disappears from the GABA receptor sites, the receptors may have become down-regulated (less sensitive).

Or there may be a reduction in GABA itself in response to the drugs, once again leaving the GABA system relatively inactive. Without the inhibiting effects of the GABA system, the disinhibited brain over-reacts.

The American Psychiatric Association (1990) task force report, Benzodiazepine Dependence, Toxicity, and Abuse, theorized that discontinuation symptoms arise from the abrupt withdrawal of BZs from their receptor sites. Before GABA can retake these positions, there is an acute reduction of GABA, and a loss of GABA inhibitory tone.

BZ disinhibition differs in some ways from alcohol disinhibition. It can occur without a noticeable sedative intoxication, such as slurred speech, lack of coordination, or impaired consciousness. Furthermore, the BZs are prescribed by a physician, often without providing the patient a warning about possible disinhibition.

Unlike the experienced alcohol user, the trusting BZ user has little reason to anticipate losing control. Expecting to be helped, and not harmed, by the drug, the patient is less able to understand or manage potentially overwhelming feelings of anger or violence, or other untoward emotional responses.

Also unlike alcohol, some of the worst BZ behavioral reactions occur during withdrawal, or in between doses, adding to the patient's confusion concerning what is happening. At the time, the patient may have little idea what is driving the unfamiliar behavior, and in retrospect it may seem like a fragmented, poorly recalled nightmare.

Adverse Reactions to the BZs as a Group Standard textbooks and reviews spanning more than two decades, as well as a variety of clinical studies, confirm widespread recognition of BZ-induced behavioral abnormalities (DiMascio and Shader, 1970; Kochansky, Salzman, Shader, Harmatz, and Ogeltree, 1975; Shader and DiMascio, 1977; Rosenbaum, Woods, Groves, et al., 1984; Arana and S. Hyman, 1991; Maxmen, 1991; Maxmen and Ward, 1994; Ashton, 1995).

Salzman, Kochansky, Shader, Porrino, Harmatz, and Swett (1974), in a placebo controlled study, showed that volunteers taking chlordiazepoxide became more hostile when confronted with a situation of interpersonal frustration.

In 1988, Dietch and Jennings reviewed the literature concerning reports about disinhibition whose Manifestations range from irritability to increased verbal hostility and frank assault.

They found a variety of studies that demonstrate an increase in feelings of hostility or in verbal hostility. They did not come to a definitive conclusion concerning the existence of the phenomenon, but estimated it was probably rare. Salzman (1992) reviewed the literature.

He too pointed out the controversial nature of BZ-induced violence, but went on to assert, Recent observations, however, have confirmed that hostility can be seen with all benzodiazepines, including alprazolam and clonazepam (citations omitted).

Writing in Goodman and Gilman's The Pharmacological Basis of Therapeutics, Rall (1990) summarized: AAdverse psychological effects: Benzodiazepines may cause paradoxical effects.

Nitrazepam frequently and flurazepam occasionally increase the incidence of nightmares, especially during the first week of use. Flurazepam occasionally causes garrulousness, anxiety, irritability, tachycardia, and sweating.

Euphoria, restlessness, hallucinations, and hypomania behavior have been reported to occur during the use of various benzodiazepines.

Antianxiety benzodiazepines have been reported to release bizarre uninhibited behavior in some users with low levels of anxiety; hostility and rage may occur in others. Paranoia, depression, and suicidal ideation occasionally also accompany the use of these agents.

Rall believed that the incidence of such paradoxical reactions is extremely small. Whether or not that is true, they are extremely hazardous. They are more common in regard to the short-acting Bzs.

The APA task force report on BZs (1990, p. 18) presents a table of discontinuation symptoms. The complete list of frequent discontinuation symptoms includes anxiety, insomnia, restlessness, agitation, irritability, muscle tension.

Among many symptoms that are common but less frequent, it lists depression and nightmares, as well as lethargy. Clinical experience indicates that the combination of anxiety, insomnia, restlessness, agitation, irritability, nightmares, and depression can produce a spectrum of behavioral abnormalities, including suicide and violence.

Adding to the dangers, the task force's complete list of uncommon symptoms includes psychosis, seizures, persistent tinnitus, confusion, paranoid delusions, hallucinations.


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URL: http://www.dr-bob.org/babble/20090620/msgs/902877.html