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Neurology (Expert Forum)
benzodiazepines, brain atrophy, and much more...
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benzodiazepines, brain atrophy, and much more...
by ontherecord, Mar 14, 2004 12:00AM
There has some been research correlating long term benzodiazepine use with premature brain atrophy, but the correlation is not definite. Benzos act on the brain in much the same way alcohol does, and long-term alcohol use leads to brain shrinkage. Is benzo induced brain atrophy possible?
First, how would you handle a patient who would benefit from MILD daily benzo use, long-term but is concerned about premature brain atrophy? Since stress is a high risk factor for MI (since most MI's happen on Monday), which is the lesser of two evils: benzo use, or stress?
Second, define "long-term" use?
Third, is brain atrophy manifest by deficits characteristic of dementia?
Fourth, research has not ruled out the possibility that prolonged cell phone use can cause neurlogical problems (Alzheimer's, Parkinsons)...what do you make of this connection? It seems logical to me that EMF waves can affect the brain both locally and globally. Is it prudent to minimize cell phone use or use an earpiece?
Fifth, there is a correlation between moderate and severe head injuries and idiopathic alz. disease. What do you make of the conclusion that sustaining a mod/severe head injury increases one's risk of developing AD?
Sixth, what is the role of norepinephrine on emotion? If an SNRI does what an SSRI does + more, why isn't it first-line treatment?
Seventh, why is physiologic brain injury often dismissed by clinicians as psychological sequelae?
Eight, what area of the brain controls eye movement?
Ninth, is the Mini-Mental SE sensitive to mild cognitive impairment?
First, how would you handle a patient who would benefit from MILD daily benzo use, long-term but is concerned about premature brain atrophy? Since stress is a high risk factor for MI (since most MI's happen on Monday), which is the lesser of two evils: benzo use, or stress?
Second, define "long-term" use?
Third, is brain atrophy manifest by deficits characteristic of dementia?
Fourth, research has not ruled out the possibility that prolonged cell phone use can cause neurlogical problems (Alzheimer's, Parkinsons)...what do you make of this connection? It seems logical to me that EMF waves can affect the brain both locally and globally. Is it prudent to minimize cell phone use or use an earpiece?
Fifth, there is a correlation between moderate and severe head injuries and idiopathic alz. disease. What do you make of the conclusion that sustaining a mod/severe head injury increases one's risk of developing AD?
Sixth, what is the role of norepinephrine on emotion? If an SNRI does what an SSRI does + more, why isn't it first-line treatment?
Seventh, why is physiologic brain injury often dismissed by clinicians as psychological sequelae?
Eight, what area of the brain controls eye movement?
Ninth, is the Mini-Mental SE sensitive to mild cognitive impairment?
Doctor's Answer
by CCF-Neuro-M.D.-CS, Mar 19, 2004 12:00AM
The data within the literature has not concluded that benzodiazepines cause brain atrophy. The initial studies reported this, but recent studies did not support this. Therefore, at this time I cannot say whether benzodiazepines cause brain atrophy. I also can not define long term use. These medications have been available since the 70's, and I am sure there are patients who have been using them since then.
Brain atrophy can cause dementia, but also can cause mild cognitive impairment, or no deficits at all. Formal neuropsychological testing can help identify if certain areas of the brain are functioning properly.
I am not aware of the literature on EMF waves and neurodegenerative disorders.
Based on the literature, there is evidence that brain injury may predispose an idividual to dementia of the Alzheimer's type, or excelerate the process. However, whether this is truely pathologically confirmed Alzheimer's is controversial. Therefore, I think it would be reasonable to say that head trauma predisposes an idividual to dementia, and possibly Alzheimer's.
The neurepinephrine re-uptake inhibitors have been associated with causing seizures, and this is one of the main reasons why they are not used as primary therapy. This is not an absolute, and there are many patients who use these medications. However, the SSRI's typically have a better side effect profile, and are used more commonly.
Volitional eye movements are controlled by an area in the frontal lobes bilaterally.
The mini-mental examination may not detect changes in individuals with mild cognitive changes, or individuals with more severe disease who were high functioning before disease onset. A formal neuropsychological evaluation may be helpful in this setting.
I hope this information helps you. I would recommend discussing these issues with your physician for further clarification. Good luck.
Brain atrophy can cause dementia, but also can cause mild cognitive impairment, or no deficits at all. Formal neuropsychological testing can help identify if certain areas of the brain are functioning properly.
I am not aware of the literature on EMF waves and neurodegenerative disorders.
Based on the literature, there is evidence that brain injury may predispose an idividual to dementia of the Alzheimer's type, or excelerate the process. However, whether this is truely pathologically confirmed Alzheimer's is controversial. Therefore, I think it would be reasonable to say that head trauma predisposes an idividual to dementia, and possibly Alzheimer's.
The neurepinephrine re-uptake inhibitors have been associated with causing seizures, and this is one of the main reasons why they are not used as primary therapy. This is not an absolute, and there are many patients who use these medications. However, the SSRI's typically have a better side effect profile, and are used more commonly.
Volitional eye movements are controlled by an area in the frontal lobes bilaterally.
The mini-mental examination may not detect changes in individuals with mild cognitive changes, or individuals with more severe disease who were high functioning before disease onset. A formal neuropsychological evaluation may be helpful in this setting.
I hope this information helps you. I would recommend discussing these issues with your physician for further clarification. Good luck.
Related discussions
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Why is this happening to me? (2 replies):I have been on Ativan reguarly for about three months. ...[more]
1. Yes, benzodiazepine induced brain atrophy is indeed possible. Although the issue has not been studied extensively here in the U.S., studies published in UK journals of medicine indicate that participants in at least one study who had used benzodiazepines for an average of 13.2 years had shrinkage greater than their peers in the control group. Of course, another issue that must be analyzed is whether this correlation is dose-dependent. By analogy, someone who drinks 6 drinks or more every day for a period of x years is clearly different from the person who drinks 1-2 drinks a day for x years. Peter Breggin, M.D. also alludes to the correlation between benzodiazepine use and brain atrophy in Chapter 11 of Toxic Psychiatry.
1-A Presented with such a patient, I would recommend at most a mild, therapeutic dose subject to follow-ups. Since half of all heart attacks cannot be explained by risk factors such as cholesterol, family history, hypertension, and obesity, stress is the greater evil over a therapeutic, mild dose.
2. Long-term means daily for an period greater than 5 years. Bear in mind, however, that the FDA has approved benzodiazepines for only short-term use up to 12 weeks. However, the natural flaw is that the people who benefit from benzodiazepines will not only relapse to their pre-treatment anxiety, but also iatrogenic rebound anxiety. Also bear in mind that 15 million benzodiazepine prescriptions are dispensed every year in the U.S., and 10% (1.5 million people) become addicted each year. It is actually a significant societal problem with great costs to the system that is justified by attributing addiction to a person's predisposition (i.e., it wasn't the benzodiazepine, but the person taking it who was predisposed to addiction).
3. Cognitive deficits characteristic of brain atrophy are different than the deficits characteristic of dementia. The former are more localized, the latter more global. However, that said, both share some fundamental similarities such as shrinkage evinced on CT or MRI.
4. Cell phone use is generally safe from what we know, up to 3 years. We cannot say what the long-term effects are at this time. However, there was one study that showed neurological effects in rats after merely 2 hours of exposure. Caveat emptor -- buyer beware is my recommendation. Like cigarettes during the turn of the century, which were smoked with reckless abandon until people in the mid-1900's starting dying from lung cancer, I surmise that cell phones will come with warnings within a decade or two.
5. The study showed a correlation between idiopathic Alzheimer's disease and moderate to severe head injury in a retrospective study (not as good as prospective) of primarily war veterans relying heavily on self-reporting. Although somewhat flawed, the correlation seems logical. Given how little is known about Alzheimer's (hence "idiopathic" -- a fancy way of saying "we don't know why it happens"), and how little is known about head injuries, especially ones that do not induce structural damage, the correlation cannot be definitively proved or disproved. In any event, protecting the head is the only preventive measure.
6. Norepinephrine affects the limbic system, and is responsible for motivation in large part. SNRI's (like Effexor) are not first line treatment because they are generally not as well tolerated as SSRI's and have greater potential for interaction by virtue of their added benefit (of inhibiting the reuptake of norepinephrine). Every benefit comes with a potential side effect.
7. I don't know for sure, but I'm guessing several cranial nerves and the brainstem.
8. Physiologic brain injury is often dismissed a psychological sequelae because the MRI and/or CT does not show structural damage and clinicians have to rely on subjective complaints that often interplay with psychological factors that vary greatly from person to person. In essence, there is no objective demonstrable way to quantify physiologic brain injury. It doesn't mean brain injury didn't occur though, and a person could very well have long-lasting or even permanent deficits. There is an excellent article on the topic by Julie Frank, M.D.
9. The MMSE is not sensitive to mild cognitive impairment. Neuropsychological testing supposedly is. It provides a baseline. Unlike neuropsychological testing, the Mini-Mental Status Exam does not take into account a person's level of education.
Now tell me, what are you taking atvian for? What sort of medication is it? Is it a benzodiazepine?
As for taking benzodiazepines for longer than the prescribed period, my final conclusion is that it is not advisable if you're taking a MODERARATE to HIGH dose. if you're taking a mild dose, either once a day or titrated in several doses, then I don't envision long-term use becoming a real problem. Taking a mild dose of benzodiazepine is literally like having a shot or two of whiskey and has much the same effect. If you either take a moderate to high dose or drink 5 shots of whiskey a night, then you're asking for trouble. The biggest challenge is staying at that mild dose and not increasing it over time. Doctors are more concerned about addiction than they are about brain atrophy. It's very easy to develop a tolerance and increase your dosage over time to the point where it does become dangerous. And unfortunately, many people who take benzidiazepines daily do develop a tolerance in much the same way we develop a tolerance to alcohol. So that's the rub. At mild therapuetic doses, I think it's ok. At higher doses, it's not. Bottom line: until you have your symptoms checked out, I'd say keeping taking it, but don't overdo it. And then have this exact same conversation with your neurologist.
Well, 5 months isn't all that long, and when people talk long-term, they're generally referring to a period of like 5 years or greater. However, truth be told (as I am a benzodiazepine user too, currently -- xanax, .25 mg, 3 times day), it doesn't take 5 years to get addicted; it could take as little as 4 weeks as I am sure you're aware. There is a psychological addiction (of using it as a crutch, to relax) and a physical component (withdrawal symptoms) so it is in fact a complicated issue. Now, there are two antidepressants that have an anxiolytic effect: Buspar and Effexor. Buspar is somewhat controversial and newer, so I wouldn't recommend it. Effexor however, may reduce anxiety *somewhat* but definitely NOT like benzodiazepines do, which are both quick and effective. Again, truth be told, and all political correctness aside, honestly the only two options IF you want or need the relief, are alcohol and benzodiazepines. I know -- it's a tough choice, and a lesser of two evils type of thing. At least with alcohol, you know what you're getting; a lot remains unknown about the long-term effects of benzos. But, you can't have a beer or two 3 times a day, so it gets tricky. Also, as you know, the benzo-induced state of mind is more pleasant and less abrasive. So I don't know what to tell you. Hopefully the neurologist can shed some light on your symptoms or they possibly just go away with time. But there is no easy answer, unfortunately to the benzo question. Sometimes I feel like I am on my way to addiction (and I used to drink pretty heavily too, but no longer do today, so I know where you're coming from with regard to the addiction angle).
Bottom line: if you cut your dosage by half, and stayed there, my best guess is that you're not likely to become addicted (in the true sense of the word) and it's not likely to have adverse neurological consequences. But that's just my best guess, and no doctor -- here or elsewhere -- can tell you with certainty what's a safe dose or what isn't, or how long it's safe to take them without adverse consequences.
In any event, feel free to respond with any thoughts, and please keep me updated on your condition.