Frontotemporal Dementia and the Importance of Accurate Diagnosis

Relatively speaking, of the major leading causes of dementia out there, there is one that has one of the most mercurial of histories in terms of its respective nosology: frontotemporal dementia (FTD). Depending on what variant one is referring to, FTD is variously referred to as “frontotemporal lobar dementia,” “Pick’s Disease,” “sementic dementia,” and “progressive nonfluent aphasia.” Originally called “Picks Disease” (first described by Arnold Pick in 1892) it was originally described as a syndrome characterized by “amnestic aphasia,” a focal pattern of atrophy involving the temporal and frontal lobes of the brain, and the presence of Pick “inclusion bodies,” and accompanied by a characteristic pattern of language impairment.

Depending on the sources you consult, FTD is either the second or third leading cause of dementia worldwide (with dementia of the Alzheimer’s type and vascular dementia taking up the other of the top three slots). Either way, it seems to be a disease that’s most frequently misdiagnosed. Probably this is because when Arnold Pick identified the first cases of FTD he thought it was necessary to identify these agyrophobic inclusion bodies (Pick bodies) on postmortem in order to positively diagnose FTD (of course, now it’s know that this is not the case).

Dementia in general has been traditionally seen as a disease characterized by cognitive loss leading to significant functional loss. However, there is significant heterogeneity in presentation across dementias. In the case of Alzheimer’s disease, memory dysfunction tends to be the earliest and most central complaint. In the case of vascular dementia, gait disturbance, falls, and a “vascular depression” phenomenon may be leading-edge symptoms.

FTD presents differently. One thing to get out of the way is that FTD is not actually a single disease entity – there are actually two sub-variants, first, probably representing the form noted by Arnold Pick is so-called semantic dementia, where a progressive breakdown in semantic knowledge is evidenced in speech and testing, accompanied by a fluent aphasia (often those suffering from this disorder will be able to easily speak, but it sounds nonsensical at times). Interestingly, in the case of semantic dementia (unlike Alzheimers or vascular dementia), episodic memory is well-preserved well into the progression of the disease.

The second sub-variant of FTD is the behavioral variant (bvFTD), which, as you might expect, has a relatively dramatic presentation. Its presentation often takes the form of rather dramatic personality changes. Early symptoms might include mood lability (e.g, anger outbursts), restlessness, and apathy. As the disease progresses, patients lose insight into their deficits, withdraw socially, and may start exhibiting distressing behavior like impulsiveness (often sexual in nature). Criminal behavior is sometimes reported. Another symptom seen prominently in bvFTD sufferers is hyperphagia, where sufferers will uncharacteristically gravitate towards eating large amounts of food, often carbohydrate-laden. Frontal release signs are seen on neurological exam, such as the palmomental reflex (which is something normally seen in newborns).

One of the issues that comes up when I talk about assessment is the question of, “why does it matter”? In other words, I’ve heard it argued (often from family members and occasionally from physicians) that differentiating, say, differential diagnosis of Alzheimer’s from an FTD variant is largely an academic exercise. Dementia is dementia and really all family members and primary care physicians tend to be interested in is how to manage the diversity of behavioral symptoms that come with any dementia.

I think it does matter. In my practice as a geropsychologist I’ve seen more than a handful of cases of dementia that I was reasonably certain were in fact FTD. A case I recall in particular was of a lady whom I assessed, who was at that time living in an assisted living facility in San Francisco. She was in her late 60s and had been diagnosed with Alzheimer’s disease and her family had approached the Institute on Aging to give her a comprehensive examination. One of the issues that was particularly worrisome for her was this woman’s apathy, she was reported by her family to be sleeping “a lot,” she seemed disinterested in activities, and her neuropsychological testing profile indicated severe impairment in executive functioning. On interview, she presented with a prominently “flat” affective expression and poor eye contact. Due to her apathy and listlessness, the rapid decline in her clinical picture, and the cognitive profile evidenced, I diagnosed her with FTD.

One of the most significant recommendations I made in my report on this woman was that her prescription for Aricept (which is a popular medication, belonging to the class of acetylcholinesterase inhibitors, or AChEI, approved to treat Alzheimer’s disease) be discontinued in light of her probable FTD, because depending on who you talk to (for example, see the reference below of Boxer, Trojanowski & Lee et al., 2005) AChEI therapy can make the symptoms of FTD worse, and not better.

After seeing this woman and completing her testing report, weeks later I received a call from her physician, actually, if I remember correctly, 2-3 of them in one week. Initially thinking something was wrong, I called back. The physician excitedly reported to me that he had followed my recommendation to discontinue her Aricept prescription, and had switched her from a less activating antidepressant (Lexapro) to a more activating one (Prozac). Within weeks, the patient had apparently changed dramatically. She had become more interested in activities, her “flat” expression had gone away, and she had proceeded to become her “old self!” I was delighted, of course.

One of the lessons of this assessment was that diagnosis of dementia can matter, and sometimes profoundly. It should be noted that there are no cures for [edit] most forms of dementia (although, as a LinkedIn commenter rightly pointed out – there are some forms of dementia that are reversible, such as in the case of depression, as I pointed out previously here). In the case of FTD, there are also no effective treatments, but there are management techniques that can occasionally make a profound difference. So, when I first see families who approach me for assistance with their loved one suffering from dementia, one of the first things I find out is if a proper assessment has been done. If not, it’s one of the first things I do.

Boxer, A. L., Trojanowski, J. Q., Lee, V. Y. M., & Miller, M. J. (2005). Frontotemporal lobar degeneration. Neurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics.

Bozeat, S., Gregory, C. A., Ralph, M. A. L., & Hodges, J. R. (2000). Which neuropsychiatric and behavioural features distinguish frontal and temporal variants of frontotemporal dementia from Alzheimer’s disease?. Journal of Neurology, Neurosurgery & Psychiatry, 69(2), 178-186.

Lane, G., Ratto, W. (2009). The importance of geriatric assessment in clinical

outcome: A case of frontotemporal dementia. Psychologists in Long Term Care Newsletter, 23 (3), 3-5.

Varma, A. R., Snowden, J. S., Lloyd, J. J., Talbot, P. R., Mann, D. M. A., & Neary, D. (1999). Evaluation of the NINCDS-ADRDA criteria in the differentiation of Alzheimer’s disease and frontotemporal dementia. Journal of Neurology, Neurosurgery & Psychiatry, 66(2), 184-188.

Treating and Preventing Alzheimers

What can we do to treat Alzheimers disease? I watched again a great talk by Dr. Frank Longo MD/PhD at Stanford, a rock star if there ever was one in the Alzheimers research and treatment field. It’s a great little talk and I recommend watching it if you’re a practitioner, researcher, or even just an interested caregiver or patient – there’s a lot here.

We all know about the medications available – there are the FDA approved medication treatments basically in two groups: the so-called cholinesterase inhibitors, such as Donepezil (Aricept), Galantamine (Reminyl, Razadyne), and Rivastigmine (Exelon). And then there are the “NMDA receptor antagonists,” of which there is one medication currently approved and on the market, Memantine (e.g., Namenda).

Basically all of these medications can help, but they are only treatments. Generally a patient who is helped but Aricept or Namenda can expect maybe 6 months where the progression of their dementia (as Alzheimers is a disease of progressive cognitive decline) is effectively halted. In rare cases some improvement in cognitive functioning can occur. However, these drugs all treat the symptom of the disease (e.g., the cognitive dysfunction) and they do not treat the underlying issue – the underlying brain damage that causes the cognitive deficits in the first place. Also, these drugs (like all drugs) have side effects.

So, drug therapies are interesting and as a psychologist who has worked almost exclusively in inpatient medical settings for the past several years, I like to keep abreast of what’s happening in the world of the somatic therapies. There are a lot of research treatments out there as well that we can talk about… I may go into that in a later post. Needless to say, a lot of research is currently going on in the Alzheimers disease treatment front as far as medical treatments go.

However, as a psychologist what I’m personally most interested in are health-related behaviors, like diet, exercise, coping behaviors, et cetera. Are there things that people could be doing to prevent Alzheimers disease or even treat it after it’s taken hold?

The answer is, yes. I was greatly impressed when I heard Dr. Longo speak at last year’s Updates on Dementia in Foster City (which I try to attend every year… pamphlet on the 2013 conference is here if you want to attend). He basically gave the same lecture that I linked to above (although at the conference he included a lot more information about current research on drug therapies and diagnostic techniques). In both lectures, he spoke at length about the nexus of research that relates to the subject of health behaviors and how they relate to Alzheimers disease and prevention. He focused on three areas – diet, exercise, and so-called brain games or brain training activities.

First, there’s the so-called “Mediterranean diet.” This relates to the idea that a diet rich in monounsaturated fats (such as olive oil), low in saturated fats, and high in lean proteins like fish (and low in red meat, which I don’t like to hear), and plenty of vegetables and fruit, somehow imparts a protective effect on people when it comes to development of progressive dementia. There does seem to a significant body of research that indicates that adherence to such a diet can reduce the risk of several forms of dementia, including Alzheimers disease – eating fish two to three times a week probably helps reduce risk of Alzheimers disease, and this probably relates to the positive effects of the Omega-3 fatty acids (which you can also get from flaxseed or chia seeds as well). It may or may not help people who currently suffer from Alzheimers.

Then, there’s exercise and maintaining a proper body weight. One of the things that impressed me is that Dr. Longo cited several studies, both with humans and animal (rat) models that people with excessively high Body Mass Index (BMI) tended to develop higher levels of amyloid plaques than those of normal BMI (which maybe has something to do with the fact that beta-amyloid serves a function in the body of metabolizing cholesterol, and is also related to oxidative stress). So, maintaining a normal BMI may be a critical way to prevent (or treat) Alzheimers disease.

Regarding exercise: Frank Longo cited several studies, including the 2012 EXCEL study (which focused on weight training) and the 2011 study of Erickson et al., both of which demonstrated nothing short of “striking” effects. In the EXCEL study, subjects essentially reversed the effects of their Mild Cognitive Impairment syndrome (often a precursor to full-blown dementia) by engaging in weight training twice per week for six months, and in Erickson et al., subjects engaged in some brisk walking several times per week – and on average subjects increased their hippocampal volumes (the hippocampus being a brain structure crucial to learning and memory) by on average, two percent. In neither case were these exercise programs particularly taxing.

So, both cardiovascular exercise and progressive resistance training appear to impart significant benefits. Engaging in a regular exercise program may not only prevent the onset of Alzheimers disease, but may actually be a treatment as powerful as some of our current FDA approved therapies (!!!). Think about this as a treatment – what if you went to a doctor and they told you they could offer you a treatment that could potentially reverse the shrinkage of your hippocampus, reverse your cognitive impairment issues, and the side effects are all positive, e.g., reversing of your diabetes, healthy weight loss, increased muscle tone, decreased depression, better sleep…. Would you take that treatment? I would!!!

Finally, there’s the question of brain exercises. I’m sure you’ve seen the ads for computer software such as from the companies Posit Science and Luminosity. The idea here is based on some reasonable logic – the idea is when it comes to Alzheimers disease, “use it or lose it” is the watchword. Also, people who have a lifetime history of being intellectually engaged seem to run a reduced risk of developing frank cognitive impairment (based on the well-known observation that higher levels of educational attainment seem to impart a protective effect against Alzheimers disease).

So, here’s the idea: if instead of spending one’s retirement watching reruns of “Gilligan’s Island,” one instead plays these games, or does crossword puzzles… does that prevent or treat Alzheimers or MCI? Unfortunately, Dr. Longo, as well as I, have to give you the bad news. Amongst the three areas outlined here (diet, exercise, and ‘brain exercises’), the literature on this seems to be the poorest. While I would certainly tell you that it’s better to remain intellectually engaged and challenged in late life, and it probably helps, at best the positive effects of playing these “brain games” or making a point of doing the New York Times crossword puzzles on a daily basis, is likely vanishingly small. If active engagement in life truly is an Alzheimers disease preventative – it’s not to be found in brain games, it’s to be found in having a purpose in life, a hobby, social activities, stuff like that.

But do we need research to tell us that? Think about what the boosters of these software packages are telling us – that somehow it’s a good thing for an older adult to sit in front of their computer for even more time in their average day (which an average Baby Boomer does probably enough of anyways) and play computer games as a way to forestall the onset of dementia, INSTEAD of getting out of the house and going to the gym, or just going on a walk?

This is me on my soapbox here – I think the reason why these companies are making so much money based on such a flimsy premise is that it appeals to people in the same way drug therapies do. “Here,” they say, “treating or preventing your Alzheimers disease or dementia is as easy and effortless as taking a pill or playing some computer games (and doesn’t require the hard work and effort involved in making healthy dietary choices or getting a regular exercise program)!” The problem is, pills have side effects, these software programs likely don’t do much, and exercise is essentially free – and it works. So, save the potentially hundreds of dollars you might spend on expensive brain training software and maybe hit Costco and lay up a few filets of salmon, and then use the rest to buy that gym membership you were thinking about (or, maybe just save your money and instead go out and walk!!!!).

(BTW, just wanted to say – before you start any exercise program, it’s probably smart to check with your physician first. Never hurts.)

Behavior Management in Dementia Patients

We’ve done a number of posts about behavior problems in nursing homes. Nursing homes are challenging places for patients to live. Residents suffer from chronic, disabling illness, often with no hope of cure. They may have chronic pain, and about 50-70 percent of the residents may suffer from dementia. Patients are depressed, confused, and sick; this is a recipe for behavior problems. Patients scream and yell inconsolably, they may become assaultive (verbally or physically), they may refuse to eat, they may be tearful and depressed, all sorts of negative things can happen.

So how is behavior management done in the nursing home? Why do we do it?

The second question is easier than the first. We do behavior management (specifically non-pharmacological behavior management strategies) because the alternative is, of course, to throw pills at the problem. Nursing home residents are typically older adults – they are susceptible to falls and increased confusion. They are often less able to physically process drugs due, for example, to impaired kidney and liver function as a result of chronic disease. In short, drugs aren’t a very safe and effective way to control behavior problems in nursing home residents, and even when drugs work, sometimes the side effects are worse than the cure (see my previous posts on use of pharmacological means of behavior management here and here).

So, behavior management is a great idea! Does it work? It depends on a number of factors. First, if a patient is cognitively intact, a provider may wish to directly approach the patient and try to engage him or her in some behavioral contracting. Behavioral contracting is basically a sort of therapeutic “you scratch my back and I’ll scratch yours” deal that providers make with patients. For example, let’s say that Mr. Jones can’t seem to follow the rules against smoking at the local community skilled nursing facility. To encourage him to follow the rules, the nursing staff proposes that if he can go one month without breaking the smoking rules, he can check out an additional DVD from the recreation therapy staff office. Mr. Jones agrees to the contract.

Obviously, this approach doesn’t work very well with demented patients, particularly when the dementia becomes more severe. Because so many dementia patients also have problems with executive functioning, they may be unable to adhere to the terms of a behavioral contract. A provider who tries to implement a contract with such a person is potentially setting the dementia patient up for failure.

Just as behavioral contracting typically does not work well with individuals who suffer from dementia, neither does negotiating, pleading, convincing, or arguing. To work with dementia patients appropriately, it may be necessary to give up on the idea that these individuals have a meaningful level of control over their behavior. For many family caregivers and many paid caregivers, this is a huge shift in thinking to make. Even to this day, I hear nurses tell me, “oh, that Mr. so and so, I know you say he’s demented, but I’m convinced he knows what he’s doing” (and he’s doing it to annoy me!).

Once the care providers in a nursing home have made this shift in thinking, what should the next step be? Research tends to support two approaches that consistently help eliminate problem behaviors (such as aggression and agitation) in adults with dementia. The first approach is to increase the amount of pleasurable, enjoyable activities (so-called “pleasant events”) that this patient is engaging in. The second approach is to try to actively change, via trial and error, what might have been causing the behavior problem in the first place.

According to the “ABC model” (Antecedents, Behaviors & Consequences), every problem behavior in dementia patients is preceded by a predictable pattern of events, and a predictable set of responses then follow. If we can fairly precisely define the problem behavior in question, and carefully identify and change these “triggers” (antecedents) for the behavior, we can potentially reduce the incidence of the behavior. Finally, if we can change the environment’s response to the behavior, we can also reduce the harm of the behavior and its further occurrence.

Let’s take an example. Say that Judy is at home with her husband Sam, who has dementia. Sam exhibits sundowning behavior: every evening as he’s sitting in his comfy chair (where he sits after dinner, usually watching TV with his wife) he starts to get more and more confused and agitated and starts to go for the door, repeating the same worried-sounding phrase over and over again, “I need to go home, I need to go home!” Of course, he is home, and Judy exhaustedly goes through the same routine every night of trying to keep him safe from falls (as he keeps bolting to the door from his comfy chair) and convincing him that he is, in fact, home (which doesn’t seem to reassure him at all). Eventually, they both tire, and often late into the evening, Sam passes out in their bed. Judy is able to maybe get a few minutes to clean up the house before she collapses.

The “ABC model” approaches this scenario as follows:

ANTECEDENTS: Evening hours, after dinner, watching TV.

BEHAVIOR: “I want to go home,” ambulates unsafely, exit-seeking.

CONSEQUENCES: “You’re already home!”

So what do we do? From what we see above, Sam has a full belly, and he’s sitting in his comfy chair. It’s evening – the shadows are longer, the lighting is poorer. He’s probably getting tired. Judy could try not having the TV on, or the couple could sit in a more well-lit area of the house after dinner. Sam could try taking a nap earlier in the day to avoid confusion and agitation at night. None of these ideas are guaranteed to work, but by using trial and error, Judy and Sam can implement changes that might eliminate the triggers for the behavior.

What about Judy’s reaction? In the example, every time Sam complains about wanting to “go home,” Judy responds by trying to convince him that he is, in fact, already home, but this doesn’t seem to quiet him. Instead of challenging Sam’s perception, Judy could try to sooth things over: “all right, Sam, we’ll go home first thing tomorrow. You’re staying with me tonight. It’s a vacation!” Judy could try offering him a stuffed animal (or, if she has six thousand dollars lying around, a Paro Robot), or some other pleasant thing.

The key here is for Judy to track Sam’s behavior after she systematically makes these changes to his environment; this will allow her to determine what works and what doesn’t.

In my training as a geropsychologist, I have found that engaging a caregiver in this type of problem-solving exercise (usually in the form of brainstorming techniques), is by itself an extremely powerful method of getting a handle on behavior problems in the home.

Sometimes, though, behavior problems become so intractable that the use of medications to treat agitation and behavior problems is unavoidable. That’s okay! I am not anti-drug therapy. Medications can help, when used judiciously, when the “start low and go slow” rule is followed, and when polypharmacy is avoided at all costs.

Chemical Restraints and Consent

A brief followup to the rather lengthy post from a week or so ago regarding long-term care and medications.

Advertisements for pharmaceuticals is something we’ve all been exposed to for many years now. Not very long ago, pharmaceutical companies were prohibited from advertising directly to consumers. Now, of course, such advertisements are commonplace – everyone remembers the sparkly butterfly (Lunesta) and the bizarre Rozerem ads with the beaver and Abe Lincoln.

Some of the most popular, best-selling drugs are psychotropic medications. Three of the top ten drugs sold in 2011 were psychiatric medications: Seroquel and Abilify are second and third-generation anti-psychotics, respectively; Cymbalta is an antidepressant with some pain-control properties. All three are routinely used in the long-term care setting.

In this amusing link,, the first few ads feature Thorazine (aka chlorpromazine). Thorazine is a member of the so-called phenothiazine class of medications, one of the most popular and venerable of the so-called “first generation” anti-psychotics, and of the first-generation neuroleptic drugs, probably second perhaps only to Haldol in terms of its fame.

The story that we’ve all been told is that these drugs were revolutionary because they eliminated the need for physical restraints in psychotic patients, allowing them to live normal lives. In truth, of course, these medications simply substitute one form of restraint (physical) for another form (chemical).

Many patients freely choose and prefer to be on these kinds of medications because they do not want to experience a recurrence of the problems they had without them (e.g., psychosis). However, patients with severe dementia are likely unable to consent to the administration of such drugs. The problem is that administering medications is a much more sanitized route to restraining your demented patients than use of physical restraints – it appears much more humane; but it doesn’t solve the problem that caused the agitation, violence, and behavior problems in the first place. Solving that problem takes effort.


Psychotropics in Long-Term Care

There have been a variety of public policy initiatives designed to reduce the use of psychotropic medications in skilled nursing facilities, the most well-known is the so-called Omnibus Budget Reconciliation Act of 1987 (e.g., OBRA-87), which sets comprehensive guidelines for training nursing home staff and guidelines for prescribing psychotropic medications in nursing homes.

OBRA-87 required a number of changes to prescribing habits in nursing homes, all in the name of reducing the use of powerful medications as “chemical restraints.” It required prescribers to carefully document medications to be used for specific problems (e.g., as opposed to prescribing a resident Haldol for “dementia” it had to be for a specific behavioral issue). It asked providers to consider the use of shorter-acting medications rather than longer-acting ones, and to avoid other troublesome medications in older adults, such as cholinergic medications. The law also recommended providers regularly institute dose-reduction trials to see whether patients could function on less medications.

It appears OBRA-87 has had an effect on prescribing habits in nursing homes. According to research by Borson and Doane, prescribing habits have changed substantially over the years (Borson and Doane looked at ’89-’92), presumably due to the pressure brought to bear by the federal government’s purse:

  • Prescriptions for antipsychotics (e.g., Haldol, thorazine, etc.) in LTC fell by 34.8%.
  • Prescriptions for long-acting benzodiazepines (anxiolytics) fell by 70.1%.
  • Antihistamines, lithium, and psychostimulant prescriptions also fell significantly (40%, 24.1%, and 17.1%, respectively)

This all looks good. After all, antipsychotic use in the elderly, particularly the so-called “first generation” antipsychotics, poses particular dangers. Many, if not most of the older adults in nursing homes are prescribed antipsychotics for the purpose of controlling behavior issues secondary to dementia – I personally am very concerned about use of these agents with patients, given the issues related to tardive dyskinesia and how prone a demented older adult might be (particularly as their dementia advances in severity) to developing such issues. Avoiding long-acting benzodiazepines and antihistamines in older adults also seems like a good outcome, given the high risk of falls in the long-term care population.  Lithium, while effective, tends to have a very narrow therapeutic window (it tends to be toxic, particularly to the kidneys – which also are often compromised in older adults).

However, certain drug classes began to be prescribed more, apparently  – particularly short-acting anxiolytics like lorazepam and alprazolam (up by 7.9% and 11.5%, respectively) – and clonazepam prescriptions rose precipitously, up by 368%. While it’s an improvement over longer-acting benzodiazepine meds (like diazepam), in my opinion it’s never a good thing to be prescribing ‘benzos’ of any sort to patients who by their nature are prone to falls and mental confusion.

Prescriptions for buspirone, also known as Buspar, rose by a staggering 557.7%. Buspar is an interesting medication – typically when one wants to use medications to treat anxiety or agitation in anyone, older adult or no, a physician can use the benzodiazepine class of medications. While effective, these have the side effects of increasing confusion and fall risk (particularly in older adults, mentioned above) and of course, are also habit forming. In particularly difficult cases, one can use more powerful first or second-generation antipsychotic medications, but using those with older adults creates the risk of additional problems, such as metabolic side effects and even increased risk of death; this is why the FDA has issued one of it’s rare black box warnings for the entire class of drugs when used with older adult populations with dementia.

Buspar generated a lot of excitement when it was first released on the market in 1986 due to the fact it did not seem to lead to addiction or mental confusion in its users. However, anecdotally (just based on my experience) it doesn’t seem particularly effective, although to be fair it’s supposedly as effective as benzodiazepines for treating anxiety.

Finally, the antidepressant drugs doxepin and amitriptyline also dropped by 24.5 and 35.8 percent, respectively, presumably due to the fact that doxepin is contraindicated for use in people with so-called organic brain syndrome (of which most dementias would qualify).  Amitriptyline isn’t recommended for older folks because of its anticholinergic effects (older adults tend to produce less acetylcholine anyways – so they are more prone to unpleasant side effects from drugs with this tendency).

There continue to be periodic initiatives from governmental and regulatory bodies regarding psychotropic use in long-term care facilities, often with a focus on dementia patients. The latest is a push that began in March of 2012 and ended in December of 2012, which aimed to reduce the use of antipsychotic medications in dementia patients by 15% in all nursing homes.

What’s the alternative to using medications in long-term care facilities to treat behavior issues in dementia patients? In one of my next posts I’ll take that on (the subject of behavior management) – there’s actually lot that can be done, but it’s not as straightforward as giving people a pill or a shot – which is probably why it’s not as easy to do.

Dementia Definitions: A Brief(er) Post

Dementia, as readers of this blog are no doubt well aware, is a health problem which particularly (but not exclusively) strikes the older adult population and, because of the “greying of America” that’s been going on, will only increase in prevalence over the coming years. Increasing age, of course, is a major risk factor for developing dementia.

Let’s define dementia first. Probably one of the most influential definitions of dementia is in the American Psychiatric Associations’ Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text-Revision (DSM-IV-TR for short), which basically says that to have a dementia of any sort, you must have

1) the development of multiple cognitive deficits manifested by both:

a) memory impairment (impaired ability to learn new information or to recall previously learned information); and

b) one (or more) of the following cognitive disturbances:

i) aphasia (language disturbance),

ii) apraxia (impaired ability to carry out motor activities despite intact motor function),

iii) agnosia (failure to recognize or identify objects despite intact sensory function), or

iv) disturbance in executive functioning (i.e., planning, organizing, sequencing, abstracting).

2) The above cognitive deficits need to produce “significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.” Which means that if the person has cognitive deficits as specified above (say, identifiable via neuropsychological testing) but seems to function well, miraculously, in their daily life, then they don’t have dementia and may instead have something milder, say, mild cognitive impairment.

Complexifying things further, the DSM-IV-TR is currently poised to be updated to DSM-V (just when we got comfortable with the mental disorders we already had!), and we already know that the diagnostic criteria for what is considered dementia will likely shift anyways. But we’ll go with the DSM-IV-TR definition, because it’s still current and it works and makes sense for me as a practitioner (except perhaps for the requirement that memory dysfunction always be central to having a dementia).

So what about Alzheimer’s Disease? One of the common misconceptions I run into when talking to people about what I do as a geropsychologist (aside from people constantly mistaking me for a psychiatrist) is that “dementia” and “Alzheimer’s” are synonymous. Alzheimer’s Disease, of course, is only one of many, many difference dementia subtypes – dementia is an umbrella category of which Alzheimer’s disease falls under. There are other dementias, such as vascular (stroke) dementia, Lewy Body dementia (which I plan on posting about in the near future), dementia due to alcohol, Frontotemporal dementia, and many, many others.

Dementia is what I do for a living, basically. Look for more posts about the subject down the line.

Sleep (and specifically Slow-Wave Sleep), Older Adults, and Memory

So wending it’s way through the news cycle about a week or two ago (briefly) was some neuroscience research from folks at UC Berkeley relating to older adulthood, memory retention, and so-called “slow wave sleep.”

What these researchers did is took two groups of ostensibly healthy young adults (in their 20s) and older adults (in their 70s), and subjected them to a word-pair matching memory task where English words and nonsense words were associated and subject to a subsequent forced-choice recognition memory test (they did administer a number of other neuropsychological tests, but the critical one was the word-pair matching task). They selected the word-pair task because it was found in previous research to be sensitive to the effects of sleep in subjects performing the task.

Subjects were assessed immediately after the task, and then after a typical nights sleep for them (if you call typical when you’re wired up in a sleep lab), they were tested again – but the testing the next morning was done with subjects’ brains being monitored via fMRI.

Before I get to the results – what is sleep? When I was starting graduate school, sleep was an activity subdivided into five distinct identifiable stages according to the so-called Rechtschaffen and Kales sleep scoring criteria – this had been the method for identifying sleep stages for approximately the last 40 years. In 2007 the American Academy of Sleep Medicine got into the mix and simplified matters somewhat and made the practice of polysomnography somewhat more straightforward, by collapsing seven sleep stages into four. Thus, a typical sleep cycle looks like this:

N1 → N2 → N3 → N2 → REM

In both methods for scoring sleep, there was little real change in the objective criteria for identifying so-called Rapid Eye Movement, or REM sleep. N1 and N2 (formerly 1 and 2) were the same across both staging methods (representing N1 / 1 being essentially just drowsing, and N2 / 2 being so-called “alpha wave” sleep – where conscious awareness of the environment disappears).

Slow-wave sleep went from being measured across multiple sleep stages (3 & 4) using the R&K criteria and now is now measured in a single sleep stage (N3).

Below is something called a hypnogram, where sleep can be visually represented across the various sleep stages – typically looks like this (peaks on this graph represent waking periods, with lower points representing increasingly deep sleep).hypnogram

The above hypnogram is a fairly typical looking representation of a young adult’s sleep pattern across an entire night. As is typical, there is more slow-wave sleep during the first ½ of the night and more REM sleep during the second half.

Now let’s look at a hypnogram depicting the same, typical young adults’ sleep with that of a typical older adult (from Lichstein & Morin, 2000; Treatment of Late-Life Insomnia – a great book).

(Note that the hypnograms here are scored using the older R&K criteria).

sleep stages

Note a difference? The term used by the sleep folks is that older adults, even ostensibly healthy ones, tend to show evidence of a “fractured sleep architecture,” characterized by more intrasleep arousals (those are the very highest points represented on the hypnogram), a generally shallower “sleep depth,” and significantly less time spent in NREM sleep (e.g., non-REM sleep). Lack of sleep depth and reductions in NREM sleep tend translate into lack of so-called slow-wave sleep.

Slow-wave sleep (SWS), is referred to as such due to the distinctive pattern of 75microvolt (0.5-2 Hz) waves observable on electroencephalogram (EEG) leads during a polysomnogram, and consist of stages 3 and 4 of the R&K criteria (now just stage N3). SWS is not dreaming sleep and typically when subjects are awoken from SWS they do not report dream activity (unlike REM sleep). It’s considered the most physically restorative sleep period, notable by the fact that production of human growth hormone (HGH) peaks during this time of night. Also, when SWS suffers in otherwise healthy young adults (as is the case in patients suffering from narcolepsy), the result is subjective reports of being physically exhausted, despite sleeping several hours a night, such as this person.

Back when I was a lowly predoctoral intern in psychology at UMDNJ in New Jersey, I did a rotation at the hospital’s sleep lab where we saw a number of patients and offered treatments. One of the “rules of thumb” I learned when I was first learning sleep medicine is that SWS is for resting the body, and REM sleep is for resting the mind.

Of course, sleep is an inordinately complex biological process and while it seems likely that REM sleep plays a role in consolidation of certain types of memories, it now seems clear that SWS plays a role in consolidation of memory, particularly declarative memory, as well.

So, back to Mander, Rao, and Lu et al. (2013; the Berkeley study referenced at the beginning of this post). What these researchers found is that SWS deficits observed in older adults were reliably related to performance deficits on the word pair matching task, and that this SWS deficit observed in older adults, moreover, was related to degeneration of a part of the brain called the medial prefrontal cortex (mPFC, part of the frontal lobes of the brain), and finally, was also related to overactivation of the hippocampus the next day.

The idea, of course, is SWS is the mechanism by which memories stored in the hippocampus (sort of a neurobiological memory buffer) are consolidated and shunted to the cerebral cortex for long-term storage, via the mPFC. If the mPFC is malfunctioning, the memories stay stranded in the hippocampal ‘buffer’ until they are overwritten. Which, of course, then provides us with a fascinating account of how those “senior moments” take place, or worse, how dementia begins to show itself in older adults.

The question is, how is this information of practical use? Interestingly, there are a number of ways to boost SWS. Exercise, hot baths, carbo-loading are some easy, drug-free methods. One of the active ingredients in cannabis, THC, is known to increase the duration of SWS. Transcranial stimulation (also known as EMG) is another method.

Hot baths, exercise, and eating sweet treats sounds nice, but may not do the job on their own. Use of cannabis to boost SWS, while it might be effective and with few side effects (aside from perhaps an increased preference for the aforementioned sweet treats) isn’t a particularly practical treatment given its current legal status. EMG is interesting but even more impractical given the expensive and unwieldy equipment required.

Another treatment option for boosting SWS is a prescription medication called Zyrem, also known as sodium oxybate. Zyrem is basically a chemical analogue of gamma-hydroxy-butyrate, also known as GHB. GHB, of course, is a neurochemical that humans produce endogenously (in our brains) and is thought to be related to the maintenance of the human sleep cycle, particularly as it relates to SWS.

Even there, however, the practicality issue makes use of GHB and GHB analogues difficult – GHB is also an illegal drug, like cannabis, and Zyrem is a drug that is more tightly controlled than many narcotic pain medications, and is only approved for use in narcolepsy.

This is unfortunate. Barring the invention of a cheap and portable version of an EMG machine for use in older adults beginning to show signs of memory problems (or even showing signs of frank dementia), direct methods for stimulation of SWS production in older adults is difficult given the practical (legal) limitations on use of agents like cannabis or GHB.

Of course, we should back up for a moment. It’s certainly possible that boosting SWS in older adults may be a successful treatment for memory problems – but it may not be. Recall that in the Berkeley study (Mander et al.), the reduction in SWS was observed to be related to degeneration of the mPFC (part of the frontal lobes of the brain). Its possible (although it seems unlikely) that boosting SWS may not reverse memory problems in older adults because, after all, it’s unclear how boosting SWS would actually reverse the brain damage we know now is associated with dementia. However, this is interesting information and hopefully there will be research taking place.

Paying For Long-Term Care

As a nation, saving money just isn’t something we’re very good at. Causes could include stagnant wages, or possibly our love of shopping, but the result is undisputed: 45% of people age 46 to 64 have less than $25,000 saved for retirement. Between the decline of pensions and the housing crash, it is unlikely that number will improve in the future.

Despite this, about 70% of people age 65 or older will need long-term care services at some point in their lifetime, and the median annual rate for a private nursing home room was $81,030 in 2012. My math skills aren’t the greatest, but these figures tell me there’s a huge (and growing) gap between need and ability to pay when it comes to long-term care.

One solution, perhaps more popular ten years ago than today, is long-term care insurance.  However, the recent low-interest rate environment (combined with rapidly escalating long-term care costs) has resulted in premium hikes many older adults cannot afford to pay.

Unfortunately Medicare only covers the first 100 days of skilled nursing care per illness, provided various requirements are met; Medicare does not cover “custodial care,” designed to help with activities of daily living. Increasingly, even middle-income seniors are turning to Medicaid to cover the cost of long-term care.

Eligibility guidelines for Medicaid vary state by state. In California, Medicaid (known as “Medi-Cal“) covers nursing home care with prior authorization from a health care provider if you qualify.

Determining whether you qualify for Medicaid or Medi-Cal is an extremely complex task. As noted by Disability Benefits 101, there are over 90 eligibility categories, each with its own rules and requirements. An elder law attorney is the best person to contact if you or someone you know may need Medicaid assistance. The National Academy of Elder Law Attorneys (NAELA) has a “find an attorney” feature on its website; this is a very good place to start.

A person may be automatically eligible for Medi-Cal if he or she receives aid from one of the following programs:

  • SSI/SSP (Supplemental Security Income/State Supplemental Program)
  • CalWORKs (California Work Opportunity and Responsibility to Kids). Previously called Aid to Families with Dependent Children (AFDC).
  • Refugee Assistance
  • Foster Care or Adoption Assistance Program.

A person with income above the eligibility levels of no-cost Medi-Cal programs may also qualify as “medically needy” if he or she is, for example, 65 or older, blind, or disabled. This program usually requires the person to pay a monthly share of cost, similar to a co-payment.

Detecting and Preventing Elder Financial Abuse

The ever-present threat of elder abuse and neglect is always a concern for professionals who work with older adults. Elder abuse can be physical, psychological, and financial. Like many other healthcare professionals, as a psychologist I am a mandated reporter: if I suspect an adult over the age of 65 is being physically abused or denied food, hygiene, or medicine, I must report my suspicions in a timely manner to my local county Department of Health (via Adult Protective Services or APS). Failure to do so could subject me to civil or criminal penalties. Conversely, the law protects providers who make reports in good faith from lawsuits.

In California, the primary law that protects older adults from abuse is the Elder Abuse and Dependent Adult Civil Protection Act (EDACPA), codified at Welfare & Institutions Code §§15600 et seq. There are many reasons to be particularly concerned about financial abuse when one is working with this population. Older adults simply by virtue of their age are at higher risk of dementia compared to the general population. Additionally, contemporary research has suggested one of the early warning signs of dementia is increasing episodes of poor financial decision making. Older adults tend to also have higher incidences of physical frailty, and therefore often depend on others for physical care. Combine all of these factors, and you have a recipe for financial disaster.

Often older persons or their families will see the need to hire a home health aide. Unfortunately, these services are particularly expensive if the home health aides are well-trained, licensed, and bonded. Costs can be reduced by hiring home health aides from less reputable sources; however, cost-cutting in such a manner can impart some significant risk.

In my career working with outpatient, homebound older adults, I’ve at times seen geriatric clientele paired with young family members, often a young grandniece, nephew, or grandchild. On the surface this may seem like a good idea, particularly when the younger family member is unemployed or out of school. Unfortunately, the same factors that make this younger family member ideal to “keep an eye” on grandpa or grandma (for example, the younger family member has lots of free time) may be the same ones that make them a risk: older adults, even close family members, may be an irresistible source of income to fund a younger family member’s drug or gambling addiction.

After a report has been made to adult protective services (APS), it’s sometimes found that the best plan for the older adult is to be admitted to long term care, such as an assisted living or a community nursing home. Typically, at this point, APS considers its work over. This doesn’t seem an unreasonable position to take; after all, once the older adult is under the care of a licensed facility that provides 24/7 care and supervision, the responsibility for safeguarding the welfare of the older person has shifted to the facility.

Of course, we all know that residing in long term care facility doesn’t automatically provide an older adult with iron-clad protection against abuse. I’m sure we’ve all seen the occasional lurid news story documenting the rare instances where nursing staff engage in overtly abusive acts, ranging from out-and-out violence to criminal neglect. However, this is in my experience an exceedingly rare event. Not only does the training and hiring process for nursing home providers tend to weed out abusers, it’s also not a particularly convenient environment for an abuser to commit their acts undetected by their fellow employees. Also, nursing homes are, without a doubt in my mind, some of the most highly regulated category of healthcare facilities in the country. Consequently, there is an enormous amount of oversight and considerable incentives for nursing homes to prevent and, if necessary, detect and respond to abuse by staff when it happens.

But what happens when a fellow resident victimizes a vulnerable older adult? This is a particularly sticky problem for a number of reasons. First, patient privacy is at issue here – how do you document that resident X seems to be targeting resident Y in their chart? Given the laws governing patient privacy (for example, HIPAA), this is impossible. Second, although nursing staff are technically responsible for the welfare of their residents, it’s impossible for nurses at a sweeping majority of facilities to be able to keep tabs on their residents all of the time. In the evening hours (what nurses call the “off shifts”) the number of nurses on the floor typically shrinks even further.

I’ll cover this particular issue in more detail in my next post. Suffice it to say, at many nursing homes an underground economy operates: even the most watchful nursing staff do not always detect residents covertly trading contraband and desirable items like cigarettes, food, candy (possibly even drugs and alcohol). What does it mean when one-half to three-quarters of the potential participants in this trade are demented or otherwise have diminished capacity? A number of extremely thorny liability and management issues are potentially in play here.