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Disinhibitory Effect of Benzodiazepines

When benzodiazepines are prescribed for anxiety and the behavioral disorders of dementia, there is a well-documented risk of dizziness, sedation, falls, fractures subsequent to falls, and cognitive impairment associated with these agents in the elderly. In addition, the concept of disinhibition should be considered as a possible complication of therapy in this population. The release of previously suppressed behavior has been called the disinhibitory effect.

“Benzodiazepines dilute the controlling capacity of the ego, allowing one to lose the intensity of normal control mechanisms,” says Lucy Rea Sarkis, M.D., Executive Director, South Beach Psychiatric Center, Staten Island, NY. “The premorbid personality determines how disinhibition is expressed clinically.” Dr. Sarkis elaborates, “It depends on the normal tendencies of the individual.” For instance, in an elderly individual with a premorbid personality possessing sexual preoccupation, a benzodiazepine may precipitate sexually inappropriate behavior. If an aging adult had a premorbid personality possessing obsessive-compulsive features, an increase in anxiety and ritualistic behavior may follow the introduction of a benzodiazepine. If paranoid thinking and/or tendencies existed premorbidly, a benzodiazepine may induce an increase in verbally abusive behavior and an increase in paranoid thinking and behavior.

Furthermore, “in dementia, the area of compromise is very often the determinant of benzodiazepine response variability,” explains Dr. Sarkis. For instance, she adds, if the cerebellum is compromised, a benzodiazepine may increase the risk of falling; with a compromised hippocampus, the center of emotional response, a benzodiazepine may elicit emotional lability; alternatively, a benzodiazepine used with a compromised frontal lobe may produce significant cognitive impairment.

For treating uncomplicated, generalized anxiety in the elderly, shorter-acting benzodiazepines are recommended with scheduled dosing at lower doses than those for younger patients (Table 3). They are relatively rapid in action and effective in reducing feelings of panic, fear, and tension. They should not, however, be prescribed casually for simple situations resulting in tension and anxiety, or for those who suffer from chronic anxiety. The course of therapy is often short (e.g., up to 4 to 6 weeks) since most bouts of anxiety are short-lived, although recurrent in nature. Discontinuation after extended use is difficult due to psychologic and physical dependence; gradual tapering every few days over 3 to 4 weeks is recommended, as withdrawal may lead to rebound anxiety. In a dying patient who appears uncomfortably anxious, an assessment for treatable causes (e.g., hypoxemia, pain, fear) should be undertaken, and if necessary, a short-acting benzodiazepine is recommended.

An alternative to the benzodiazepines is buspirone, initially dosed at 5 mg BID and usually up to 10 mg BID or TID. Using the slow titration guideline of increasing by 5 mg/day every 2 to 3 days as needed up to 20 to 30 mg/day (maximum daily dose of 60 mg/day) helps to avoid or minimize side effects (e.g., dizziness, drowsiness) while providing adequate dosing for effectiveness. Response to treatment is generally seen within 1 to 2 weeks of continuous therapy, with a maximum effect after 3 to 4 weeks. Although this delay in onset of action may be perceived as a disadvantage to buspirone therapy, it should be noted that there is little potential for abuse with this agent.

Hydroxyzine — due to its potent anticholinergic properties — and meprobamate — due to its highly addictive and sedating properties — are not recommended for use in the elderly. Due to adverse effects associated with the antipsychotic drugs (noted above), they should not be used for anxiety disorders unless frank psychotic symptoms (e.g., paranoia, delusions, hallucinations) are present.

In the elderly with anxiety disorders, for whom the tricyclic antidepressants (TCAs) are indicated, imipramine and nortriptyline are well tolerated (75 mg at bedtime; range 50-150 mg/day). Due to strong anticholinergic and sedating properties, amitriptyline is rarely the TCA of choice in the elderly. The TCAs are contraindicated in patients with narrow-angle glaucoma, a frequent comorbidity in older adults. The selective serotonin reuptake inhibitors (SSRIs), also indicated in anxiety disorders, may be useful in patients at risk for sedation, hypotension, and anticholinergic effects of TCAs.The benzodiazepines are often used adjunctively for anxiety disorders, on an intermittent basis, with the TCAs or SSRIs.

Conclusion

Benzodiazepines have demonstrated their utility in relieving anxiety, including the anxiety that accompanies dementia. However, along with other documented potential adverse effects in this patient population, disinhibition may occur. In disinhibition, inappropriate social behavior such as sexual advances or verbal abuse/pananoid behavior may manifest as a side effect. The best outcome from benzodiazepine use in the elderly is obtained from short-term use (4 to 6 weeks) of smaller doses of shorter-acting benzodiazepines.

Behavioral disturbances in the elderly are probably the most important facet of dementia prompting institutionalization. The referral for pharmacologic intervention is often the result of the need for management of mood and behavior. Symptoms tend to be superficially described as “agitated,” “combative,” “depressed,” “acting out,” “inappropriately accusing,” etc., by spouses, family members, and caregivers.

Dementia may be the most common cause of anxiety in the elderly, with an increased risk of anxiety seen in patients initially transferred to a long-term care facility from the hospital or from home. Trauma or a stressful event may induce an acute, short-lived, situational anxiety. Anxiety disorders (also known as anxiety and phobic neuroses) are classified as phobic disorders, posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), obsessive-compulsive disorder (OCD), and panic disorder (Table 1).

Attempts at alleviating anxiety in the elderly, and especially in those with dementia, should be attempted through nonpharmacologic intervention whenever possible. This may include providing a more structured environment with consistent routines, simplifying everyday tasks, avoiding over- or understimulation in the environment, providing soothing background music, and providing support to caregivers. Testing for adequate hearing and vision is also essential. Supportive psychotherapy, behavioral therapy, biofeedback, relaxation therapy, and paced exercise therapy may be used as nonpharmacologic and adjunctive therapy where appropriate.

Reversible etiologies of anxiety related to adverse drug effects and concomitant medical disorders should not be overlooked. When possible, eliminating medications known to contribute to or induce anxiety and treating medical conditions that may cause anxiety or similar symptoms (Table 2) may help avoid unnecessary intervention with an anxiolytic. For example, eliminating anxiety and agitation secondary to depression with the use of an antidepressant may be sufficient.

Benzodiazepines are often prescribed for elderly dementia patients with behavioral disorders because of a prescriber preference over the antipsychotics that carry a liability of extrapyramidal symptoms (EPS) and tardive dyskinesia (TD). Extrapyramidal reactions are more common in the elderly, with up to 50% of patients developing these reactions after age 60; incidence may be more common in dementia patients. The prevalence rate of tardive dyskinesia in the elderly may be as high as 40%; elderly women are especially at risk. Up to 20% of older adults take benzodiazepines, and their use is more common among women than men. Benzodiazepines are useful in treating general anxiety disorders, panic disorders, and depression, as an adjunct to antidepressants. They are also indicated in insomnia, on a short-term basis. In addition, they are useful for preprocedure/preoperative sedation (e.g., dental procedures, MRI screenings) and in cases of status epilepticus.

If you’ve ever had a stomachache before an exam or important meeting, or developed a headache during an argument, you have some idea of what somatization is. Although it’s common to experience these types of medically unexplained symptoms, such as pain and digestive upset under stress, somatization is often a part of serious disorders such as depression, anxiety, and schizophrenia.

“Somatization is a normal, daily experience. It’s highly situational, [with] marked individual differences and marked cultural differences, and associated clearly with psychosocial stress,” stated Normal Jensen, M.D., a professor at the University of Wisconsin in Madison. Jensen addressed an audience of physicians at the annual meeting of the American College of Physicians/American Society of Internal Medicine in Philadelphia last week.

Although “full blown” somatization disorder is fairly rare — less than two percent of Americans are diagnosed with it — Jensen explained that features of the disorder are common. “In primary care, anywhere up to three quarters of our patients have medically unexplained symptoms,” he reported. “The impact on health care services is HUGE.”

Physicians who see patients with complaints that can’t be explained are often distressed and frustrated, noted Jensen. And that frustration is shared by patients, who often consult a long series of physicians and specialists who fail to identify what’s wrong. Some doctors, Jensen said, may turn their frustration on the patient, telling them “it’s all in their head.”

But somatization, he emphasized, is real. Our understanding of pain and other somatic complaints has evolved in recent decades to reveal that sensations are affected by thoughts, emotions, and prior experience. In addition, new discoveries about the role of opioid receptors in the nervous system have provided increasing evidence for a physical basis for somatic complaints.

“Patients appreciate knowing that there are possible molecular and neurophysiological reasons for why their sensations vary from [those of] others, and within themselves from day to day,” Jensen explained.

Patients with these kinds of symptoms shouldn’t be told that there’s no physical reason for their complaints, said Jensen. “I tell them that in fact there is a good physiological reason for their symptoms. I tell them that ‘you’ve either acquired, or were born with, an abnormal nervous system.’ I tell them that ‘your nervous system is allowing you to feel sensations that normal people, or you when you are normal, don’t feel.’

“The nervous system quite naturally filters out unnecessary, confusing, distracting information,” Jensen continued. “Think how it would be if I was constantly aware of my clothes, and my watch, and my jewelry. If I had to process all that information all the time, what else would I be able to do? I wouldn’t even be able to read a book!”

One of the difficulties in treating patients with somatic symptoms is that many patients have an additional illness. “It’s not just somatization. It’s somatization with an anxiety disorder, or with a bad mood disorder, or a thought disorder, or a personality disorder,” said Jensen. He noted that he refers patients to psychiatrists when he wants “to be sure that there isn’t a comorbid condition… or when I want help with treating one of these disorders.”

Another concern, according to Jensen, is that one patient may consult a number of doctors, and specialists may diagnose serious medical conditions based on a patient’s complaints. “These people can get in trouble, because if you look closely enough at any of us, you’re going to find something wrong that could be treated,” he explained.

“What that means is that [generalists] and [their] sub-specialty colleagues have to learn to work together with our patients,” stated Jensen.

Right now, there are no medications that modify sensory perception by targeting opioid receptors, and none specifically for somatization symptoms, noted Jensen. In his own practice, he reported, he looks for symptoms of depression and/or anxiety, and tries antidepressant or anti-anxiety medications if the patient has such symptoms, even if they don’t meet the diagnostic criteria for one of these disorders.

Cognitive behavior therapy has proven helpful for patients with somatic symptoms, too. This therapy, which can be delivered by a trained general practitioner or by a mental health professional, focuses on the relationship between variability of a patient’s symptoms and changes in mood and life events.

As for the future, Jensen reports that there has been some recent evidence that gabapentin (neurontin), an anti-epileptic medication used to prevent seizures, may affect the body’s opioid receptors and thus alter sensory perceptions.

It’s important to remember that somatic symptoms can also mask emotional distress, said Jensen. Patients who have been taught or conditioned not to express emotions, particularly negative ones, may not even realize they’re depressed, anxious, fearful, or grief-stricken. “I do believe that there is a sort of transformation of psychological distress into physical symptoms,” he stated.