During the last few weeks, an 85-year-old Alzheimer’s patient has been opening and closing a case that contains her deceased husband's jewelry and a box of her rings. She does this for hours. One night, she repeated this behavior for five hours. I unplugged the light by the nightstand where she keeps the jewelry, but she now uses another light. I've tried keeping her up during the day, but it doesn't work. Do you have any suggestions? [ 06/27/11 ]
A repetitive behavior such as this may reflect a variety of causes, and it's tough to figure out which are most relevant without a more detailed analysis. I wonder if this repetitive behavior reflects feelings about her husband's absence. Also, have you've tried to sit down with her and reminisce about her late husband by looking at pictures and sharing fond recollections? Perhaps that would be a way of giving her some relief from the need to interact in this way with his possessions. Other possible explanations for her behavior might include anxiety (her deceased husband's jewelry may provide a comforting effect), a manic reaction (accounting for the sleep disturbance), or just lack of other activities that might occupy her (such as a jigsaw puzzle to work on) if she experiences disrupted sleep and wants to get up during the night.
My mother, who is 89 years old, is suffering from Alzheimer disease. Her doctor prescribed risperidone or haloperidol for her irritability. I did not have these prescriptions filled because of the following FDA warning: Risperidone and haloperidol are not for use in psychotic conditions that are related to dementia. They have caused fatal heart attack and stroke in older adults with dementia-related conditions. Based on this data, what drug can my mother take for her irritability instead of these medications? [ 06/24/11 ]
The antipsychotic medications all carry a warning on their prescribing information for increased risk of various medical complications, including an increased risk for death, yet they continue to be used because there are few alternative drugs from which to choose. The antipsychotics can often be helpful to a limited degree, but patients taking them must be monitored carefully for adverse effects and prescribers should be using the lowest effective dosage for the shortest amount of time needed. Though I can't comment on your mother's specific needs, there are certainly other medications used to treat irritability in Alzheimer's disease patients. Citalopram has been suggested as an alternative, base on some evidence, and other options that are less well evidence-supported include trazodone, divalproex, and gabapentin. Please consult your mother's prescribing clinician for more details on the risks and benefits applicable in her specific case.
My stepfather is 84 years old and has Alzheimer’s disease. He is currently using the Exelon patch. He does not think that it helps, and his doctor just shrugs his shoulder and tells him to do whatever he wants. He has a host of other medical problems, including several aortic aneurisms. Should we stop using the patch? [ 06/23/11 ]
The Exelon patch (rivastigmine transdermal) is helpful in a modest way for symptoms of cognitive impairment and for overall level of functioning, but it's quite difficult to be sure any of the cognitive enhancing medications are “working” when patients continue to get worse. Unfortunately, gradual worsening is a characteristic of Alzheimer's disease and the medicines indicated for treatment do not indefinitely prevent the disease from worsening. Though I can't advise about this decision for your stepfather, consultation with his prescribing clinician may clarify the pros and cons of such a decision.
Does any of the research on Alzheimer’s disease also apply to primary progressive aphasia (PPA)? Would the new oral slow-release medication that has been shown to have a positive effect on mice engineered to show features of Alzheimer’s and Huntington's diseases also help with PPA? I never see specific research on PPA, so I'm always hoping that Alzheimer’s research might also apply to this neurological condition. [ 06/22/11 ]
Primary progressive aphasia is a neurodegenerative disorder characterized by increasing difficulty with finding words. Ultimately there can be a profound disturbance of language function, often accompanied by other cognitive difficulties. There is no cure and there continues to be controversy about PPA's appropriate classification. It is most commonly considered a form of frontotemporal dementia; however, autopsy studies identify a significant number of individuals diagnosed during their lives with PPA who actually had Alzheimer's disease. Typically, PPA is treated with supportive medications to manage anxiety, depression, or insomnia, if these occur, and the central language deficit is addressed with speech therapy. The treatments for Alzheimer's disease might be worth trying in some cases, on the assumption that a subset of people diagnosed with PPA might actually have Alzheimer's disease that has presented in an atypical way. Most cases of PPA, however, are believed to represent a different disease process and therefore might not be responsive to current or experimental Alzheimer's treatments.
Can you please comment on what peer-reviewed studies indicate concerning homocysteine, Alzheimer’s disease, and general brain health? [ 06/01/11 ]
For several decades, there has been interest in whether homocysteine plays a role in various medical disorders, and evidence has been identified to connect elevated homocysteine levels with conditions including coronary artery disease, stroke, silent white matter infarcts, Alzheimer's disease, and possibly Parkinson's disease. A genetic disorder associated with elevated homocysteine levels includes, among other damaging symptoms, a heightened risk for mental retardation. Peer-reviewed, influential findings from the Framingham Study linked elevated homocysteine levels with an increased risk for development of Alzheimer's disease, and subsequent research suggested that homocysteine makes hippocampal neurons more vulnerable to the toxic effects of beta amyloid, which is produced in this neurological disease. Efforts to reduce the symptoms of Alzheimer's disease through dietary supplementation with B12 and folic acid, however, have produced inconsistent results and have not supported initial hopes that dementia symptoms could be reduced by lowering elevated homocysteine levels. Although the information above provides evidence of a connection between homocysteine and a number of medical conditions, there is no conclusive evidence in humans linking diet to incidence of Alzheimer's disease.
I have read that there is a new 23 milligram Aricept tablet. Does that mean two tablets of 10 milligrams can be taken twice each day? My mother has been on 10 milligrams for about four years, and I am wondering if we should double the dosage as she is showing signs of deterioration. [ 05/20/11 ]
Aricept (brand name for donepezil), is one of several “cholinesterase inhibitors” approved for the treatment of Alzheimer's disease, and is thought to work by increasing the availability of the important neurotransmitter acetylcholine. Previously available in 5 and 10 milligram tablets, the FDA has also recently approved (in July 2010) a 23 milligram pill that allows a higher once-daily dosage. A randomized, controlled study of donepezil, using 23 milligrams per day, showed a small improvement in cognitive functioning, versus the 10 milligram per day dose, in moderate to severe Alzheimer's disease subjects, but there was no statistically significant difference in the global functioning assessment test. It is likely that some patients who take the higher dose of donepezil will show a clinical benefit, but the benefit may be limited, and is accompanied by an increased risk for side effects.
It is inevitable that clinicians, caregivers, and patients will consider using two 10 milligram tablets daily instead of the single 23 milligram tablet. On the plus side, this might provide a similarly increased dose at a lower cost, if generic donepezil is used. Other considerations, however, are the following:
- The 10 milligram tablets are not FDA indicated for use above 10 milligrams per day.
- The 23 milligram tablet is formulated for single dosage and may produce a slower release of medication, which would lead to a more tolerable blood level peak than would occur with administration of two 10 milligram tablets
- Giving the donepezil on a twice daily basis might increase side effects such as daytime gastrointestinal problems or nighttime disruption of sleep.
- A twice-daily schedule is more prone to forgetful omission of a dose than is a once-daily schedule.
If your mother's disease has progressed, an increase in donepezil is only one of several possible treatment choices. Your prescribing clinician can work with you and your mother to determine the most appropriate choice regarding donepezil dosage, and whether an increase by either means is the right intervention at this time.
One year ago, at the age of 52, I was struck by a truck when crossing a street, and I suffered severe and multiple traumatic brain injuries. My only residual effects include anosmia (olfactory nerve damage) and benign paroxysmal positional vertigo. A neurological rehabilitation doctor stated that I am at higher risk now for developing Alzheimer’s disease. My maternal grandfather died with during the early stages of Alzheimer’s disease from a heart problem, but there is no other familial history. Now, I become deeply distressed when I have difficulty recalling a specific word or confuse an appointment time because such things rarely happening to me prior to the accident. Given my situation, what are my odds of developing Alzheimer’s now or in the future? Are my symptoms early signs of the Alzheimer’s disease process, residual effects of the traumatic brain injuries, or simply the result of normal aging? [ 05/19/11 ]
Traumatic brain injuries, particularly severe and/or repetitive ones, have been linked with an increase in the risk of developing Alzheimer's disease. Anosmia is known to accompany early Alzheimer's disease, but your anosmia is almost certainly post-traumatic rather than associated with dementia, if there was a sudden onset of this symptom after your injury. Your family history is positive, but not alarming, if your grandfather was elderly at the time of his death because Alzheimer's disease is so very common among the elderly. It is not unusual for someone who is 54 years old to occasionally experience minor difficulties such as you describe, and thank goodness (since they are so very common!) these may be signs of normal aging rather than approaching dementia. Anxiety, such as you experience when you consider the worst case scenarios that might be causing momentary lapses, will only make them worse and more distressing.
It will eventually be possible, I believe, to refine our estimate of risk for individuals, like yourself, through the use of such tests as MRI, CSF biomarkers, and genotyping—but presently, perhaps the most important advice is to make appropriate lifestyle decisions that can help you stay as healthy as possible. For example, it would be prudent to properly manage medical illnesses, and make time in your life for exercise, stress reduction, diet, cognitive stimulation, and meaningful social connections. If forgetfulness or other cognitive changes are of more than limited concern, please consider seeking evaluation with a neurologist or psychiatrist experienced in the evaluation of cognitive symptoms. Neuropsychological testing at a memory clinic, in addition, may contribute to an overall assessment of your current condition and prognosis.
What methods are biologists using to try and solve the problem of Alzheimer's disease? Specifically, can you talk about some of the new treatment modalities, such as the drug called bapineuzumab? [ 05/18/11 ]
We are fortunate that this is an era of important advances in the understanding the causes of Alzheimer's disease (AD). Furthermore, progress is likely to be accelerated as a result of recommendations from a recent task force that redefines clinical Alzheimer's disease as the final stage of a disorder that begins with a long pres-symptomatic phase (demonstrable through the use of cerebrospinal fluid and PET scan measurements, among other biomarkers), followed by a symptomatic pre-dementia phase (mild cognitive impairment), during which individuals may be more amenable to therapeutic interventions. Studies of individuals in these earlier disease phases are likely to increase our understanding of the risk factors for development of AD, the mechanisms by which it develops, and the therapeutic approaches most helpful in delaying or preventing AD's damaging effects.
Currently, much interest in the treatment of AD focuses on reducing the amount of beta amyloid that is produced and accumulated in the brain. Researchers have been enthusiastic about “immunotherapeutic” approaches that attempt to lower beta amyloid levels through immunologic mechanisms. Initial testing of a vaccine (which is an “active immunotherapy” because it induces the formation of amyloid-reducing antibodies in the vaccine recipient) was aborted due to unacceptable adverse effects, ushering in an era of testing “passive immunotherapies.” These medications are called “passive” because they provide pre-made antibodies rather than inducing production of antibodies in the patient. These antibodies attach to the damaging beta amyloid molecules and help the body remove them. Bapineuzumab is one of several “passive immunotherapy” interventions currently in testing and has been in the news, in part, because a large phase III clinical trial is nearing completion, the results of which are eagerly awaited.