What is a neuropsychological evaluation, what good is it, and how is it best done? Let’s start by making a distinction between testing and evaluation. Tests are rigid, standardized, formal measuring tools to determine things like mastery of information, placement in school programs, and outcomes for clinical trials of drugs. The test administrator needs to be consistent, neutral, not help, and not give feedback that may influence the results. Many neuropsychologists administer “tests.”

On the other hand, an evaluation is more flexible. The interaction is less formal and can be modified to meet the needs and personalities of those needing evaluation. For example, memory evaluations start by observing whether the client is on time. Did he or she remember the paperwork? Can he or she find the office? Find their insurance cards? Know their birthdate? Remember a list of words? Evaluation can be more relaxed, friendly. The intention is to put the client at ease. After all, in forensic work the client may want to look as bad as possible. However, no one wants to look demented. Cheating and exaggeration are unlikely.

Neuropsychological evaluation is like blood work – but no one has ever fainted on me. The question addressed is that one has a set of brain skills that have served them well throughout life. The intent is to determine if those skills are holding or declining. Skills may include memory, thinking, problem solving, attention, judgment, using language, nonverbal problem solving. This is the stuff of independence and competence. When well done, the results describe strengths and weaknesses in a way that informs treatment of any deficiencies and takes advantages of strengths. The results inform caregivers of what they are managing and how to help compensate for weaknesses. The results scale the severity of the problem and serve as tracking devices to determine patterns over time and effects of treatments.

I feel strongly that family members should be part of the process. After all, if someone forgets that they forget they can’t tell you what you need to know. Indeed, not including family in the evaluation of memory is a formula for making mistakes that lead to incorrect treatment plans or incorrect assessment of severity of the problem. Furthermore, family members should sit in on the “testing.” That way they better see what they are dealing with. The assessment is part of the treatment and for memory disorders this is a family issue. Being there also enhances feedback, which should be in detail and understandable. Assessment is a teaching device for family members as well as clients with memory concerns.

Diagnosis is a minor part of the process. It informs physicians of treatment parameters. But neuropsychological assessment can be so much more. It is a human interaction. Clients and family deserve to understand not only the findings but also the implications as well as practical guidance of how to deal with often-difficult issues. Assessments should help understanding of how to have a good life despite memory loss as well as to inform decision-making.


It seems that there is a mass sense of awaiting the magic bullet – the medication or the supplement – which we can take to make neurological disease go away. I hear so often how disappointed my audience is when I honestly say there is no magic potion available nor is there one that I can see on the horizon. We have come to expect medicine to offer a cure for Alzheimer’s or Parkinson’s disease just as it can offer antibiotics for certain infections or analgesics that make a migraine go away.

However, if we actually understand how the brain functions, there are treatments right under our nose. I recently read Norman Doidge’s article in the Wall Street Journal (February 7/8, 2015) “Brain, Heal Thyself” with great interest. He points out how our evolving metaphors of the brain, despite having immense heuristic value, have constrained our thinking about treatment of brain diseases.

The French philosopher Rene Descartes proposed an early model. He proposed the brain functioned as a machine. His model was further refined by the added proposition based on the brain’s electrical nature that the brain consists of circuits that have specific roles. Of course, this evolved into the current metaphors of the brain as a computer. These models limit our thinking as the focus on “hardware” and “software” that make the brain inflexible and mechanical. It is something to manipulate from the outside via a chemical or a surgery.

But the brain is anything but static. The brain is a fluid, dynamic organ that defines and constantly redefines itself from birth. The brain creates and refines its skills, microcircuitry, from experiences. It learns. It elaborates skills and parts it uses and it weakens those not needed or used. Consider the miracle of language. We learn language by experience without effort in our early years when all languages are possible. The brain is not fixed but rather it is flexible and evolving. It elaborates itself by use and wastes away by underuse.

Mr. Doidge discusses some interesting implications of this understanding for treating neurological disease. For example, Alzheimer’s disease can be understood as a progressive loss of the brain’s plasticity. It has diminishing returns of benefits from experience. As Alzheimer’s disease unfolds over decades and only becomes disabling at the end of its course, it is treated by lifestyle interventions like found in a recent epidemiological study. The results indicated that the “risk of dementia” is reduced by healthy eating, maintaining normal weight, limited alcohol, not smoking, walking at least the equivalent of 2 miles a day. These interventions appear to mitigate some of the decline attributed to normal or abnormal aging.

Consider also the frustrations of those with Parkinson/s disease that Doidge describes as the “tightening noose.” Fast walking helps motor function in Parkinson/s disease. But the rub is that this becomes increasingly difficult as the disease progresses so those afflicted back off on walking fast further adds to the disability by “learned nonuse.” Also, there is a disengagement of rhythmicity of motor execution in Parkinson/s disease. This may explain why walking on treadmill or dancing to music helps as these activities aid rhythms and help increase speed.

All of this is encouraging. We can treat neurologic disease as well as balance changes from aging by taking advantage of the brain’s natural placidity. We need to better understand these treatments, quit waiting for the magic bullet, buying unproven computer games, and take advantage of the brain’s natural ability to manage itself.


It’s not just those who have memory disorders that want to remember better. In everyday life, at school, or at work we rely on memory to stay engaged, advance, and track information. Seems so simple. It is not. Ever try to remember which movies you have seen over the last 6 months? What books have you read (who wrote them? Details for discussion?)? What you have to do at 3:00? Here are some strategies that help.

1. Read physical books. Reading is reading, right? Apparently not. Turns out that reading a physical book leads to better memory than reading on an electronic reader. Also, taking written notes leads to better learning than transcribing notes on a computer or tablet. When I don’t care if I remember (like for reading just for fun novels), I read electronically. If I am reading to remember, I read hard copy as active notes seem to work better than highlighting functions on electronic readers.
2. Being married. Two memories are better than one. Additionally there can be division of memory labor. Pamela remembers some things better than I and I remember some things better than her. Together we construct a more complete memory of our past and present.
3. Write things down. The act of writing – especially elaborative writing – locks in memory better than single quick experiences or information that are not pondered. Even better, try to teach someone else what you want to remember. Being able to convey information beyond the self creates better understanding as well as better future recall.
4. Walk through the woods or on the beach. A recent study compared the recall of new learning between a group of participants that walked around in a forest to a group who walked around in an urban environment. The persons who walked in the forest did better on a later memory test.
5. Make associations. The best way to learn new information is to associate it with something you already know. Make a story. Draw a sketch. Associate the information with a song. Mark Twain used to walk a familiar route on his estate as he learned new speeches.
6. Review. Takes notes. Review notes often over increasing intervals. Quiz yourself.
7. Don’t ignore the One Minute Rule. This is the old science of mnemonics. The more time, effort, and thought you put into something, the better you understand and remember it.


There are multiple memory systems in the brain. Each has its own organization and structure as well as unique role in our adaptively managing the world about us. I most often discuss short-term and long-term memory as these are so critical for our understanding of senior moments as well as common memory disorders. Short-term memory is the systems that allow new learning and is like the save command in a computer. Long-term memory is autobiographical information, knowledge, habits, sense of self and is like the hard drive of a computer.

Working memory is the memory system that manages the complex inputs we are constantly bombarded with from within (thoughts, feelings) and without. It consists of awareness, near awareness, and rapid decision-making. It is constantly juggling multiple inputs and deciding what to attend to, what to process further, and what to ignore. It is the desktop on a computer, it is the processor on the computer, and it is your active involvement with deciding what to do with all of the possible information and tasks available to you on a computer.

Working memory is a limited capacity system. It is part like the sport light of attention, constantly screening out distraction and focusing on what is import in the moment and in the near future. It allows us to follow conversation. It allows us to hold a phone number long enough to dial it. It allows us to know what we have to do at 3:00. It’s the system that allows us to do mental arithmetic.

Working memory switches from one task to another rapidly and slows more with each demand placed on it. We cannot do two things as quickly as one. Furthermore, as with most skills it slows and becomes less efficient as we age. We are able to juggle fewer things less efficiently, which adds to senior moments.

Hence it becomes essential as we age to actively optimize working memory by spending our cognitive resources and energy more wisely, another manifestation of the One Minute Rule. Here are some suggestions that will help:
1. Reduce and manage stress. Being distressed and overwhelmed takes resources away from working memory. Practice relaxation as a skill, increase mindfulness.
2. Stay fit. A conditioned body optimizes brain function.
3. Become an “expert.” The more we practice a skill or a talent, the more elaborate the brain circuitry underlying the skill, the greater the associations, and the more automatic the execution and the less we need to use working memory. This applies to learning athletic skills, creating knowledge, doing crossword puzzles, playing Bridge, doing art, as well as playing a musical instrument.
4. Get enough rest. Working memory slows when we are tired. Do cognitively demanding work when you are alert and rested.
5. Realize that many drugs (e.g., alcohol) and medications (benzodiazepines, pain medications) compromise working memory.
6. Limit interference (turn off the ringer on the phone) and unnecessary multitasking as much as possible.


I was invited to participate in a panel discussion at Avow Hospice. The theme was “what are the three things that you want all of your clients to know.” This is an interesting challenge for two reasons. First, each panel member has only ten minutes to make their point, Second, as I have recently turned 70 and am rapidly approaching retirement, what do I need to know for myself as I am not immune to the complex cognitive and physical changes that accompany both normal, true senior moments, and abnormal aging, memory and physical loss.

1. We do not yet know what causes Alzheimer’s disease. A recent issue of the ARRP newsletter states that the problem is a lack of research funding. But the issue is more complex. Where do we put the money? Amyloid treatments are a bust despite the fact that amyloid theories have caused mass tunnel vision within the scientific and medical community. We need a paradigm shift. The good news is that Alzheimer’s disease gives advanced warning so we can make plans to have a good life in the face of future memory loss. Furthermore, not everyone with the pathology of Alzheimer’s disease becomes demented and not everyone with dementia has Alzheimer’s disease.
2. The key to treatment of Alzheimer’s disease is short-term memory. There are slowly progressing changes in the ability to learn new information or skills that unfold over the course of a decade before dementia (read as disability) sets in. There is adequate time to strategically plan both to compensate for memory changes and for a higher quality of life for those who are forgetful as well as those who live with them. Make your life plan before you forget that you forget.
3. Treating short-term memory loss requires planning how to remember – the One Minute Rule. Simply, anything given less than one minute of thought will fade from your memory. Moreover, the more minutes you spend the better you will remember something. Quit trying to remember. Plan on how you will remember. A well-placed Post-it note trumps a good intention. Write things down in an organized way. Live by your calendar that contains both what you love to do and what you have to do. Organize your memory tools. The time and effort pays off.

Plan to have a good life even if you don’t remember it.


The cholinesterase inhibitors like Aricept (i.e., donepezil, rivastigmine, and galantamine) have been available for treatment of dementias such as Alzheimer’s disease since the mid 1990s. These medications slow the progression of Alzheimer’s disease (in those who tolerate them) and discontinuing them after extended use may induce a rapid decline even in those so impaired that they are in skilled nursing facilities. Despite these facts, the cholinesterase inhibitors are often maligned, not used, or discontinued too soon because they do not produce dramatic effects and do not arrest or reverse decline.

Although Alzheimer’s and similar dementias are classified as memory disorders, they actually have an impact on many brains skills or domains. In addition to memory, Alzheimer’s disease may produce impairments in attention, language such as word finding, visuospatial skills like drawing/handiwork, personality, mood, and/or executive functions. All of these skills are affected by changes in acetylcholine, the neurotransmitter that is increased by use of cholinesterase inhibitors. If we were to understand the benefits of these medications as consumers, it would be helpful to know what specific domains of possible benefits to expect.

This was the question addressed by “Treatment effects in multiple cognitive domains in Alzheimer’s disease: a two-year cohort study (Alzheimer’s Research and Therapy, 2014, 6, 48-60, PMID 25484926). As pointed out by the authors, there have been 4 large clinical trials demonstrating the benefits of cholinesterase inhibitors on global cognitive functioning (such as changes in the total score on the MMSE) for at least two years when compared to untreated matched control cases. However, there has been very little study of the specific domains or brain skills that respond to this treatment. It is especially important to understand the effects on executive functions as they are strongly correlated with activities such as cooking, driving, shopping, and managing the checkbook.

The focus of the study was to determine the effects of cholinesterase inhibitors on treated and untreated persons with Alzheimer’s disease for up to two years. Both measures of global functioning (MMSE and Dementia Rating Scale (DRS) total scores) and domain specific (e.g., memory, executive function) scores were obtained. The two groups were well matched in terms of age, education, and beginning MMSE and DRS scores. Treatment produced benefits on total score on both the MMSE and the DRS. For example; the average MMSE score began at 24.2 and declined to 20.2 in the treated group but declined from 22.9 to 16.4 in the untreated group.

More importantly, the major effects of treatment were in the domains of attention, visuoconstructive skills, and executive function. Despite being thought of as memory enhancers, these medications had little benefit on memory. In short, cholinesterase inhibitors do not improve short-term memory. Rather they slow the rate of decline in critical skills such as word finding, engaging in the world, and thinking abstractly. They reduce the burden of care by keeping together routines and self care skills longer than in the absence of treatment. These are important benefits despite the progressive nature of these dementias; treatment with cholinesterase inhibitors buys time.


Alzheimer’s disease and other progressive dementias are not the only cause of cognitive impairment. It is commonly known that as the heart goes, so goes the brain. An estimated 5 million Americans suffer from heart failure and this number is expected to double over the next 40 years (“Heart failure and cognitive dysfunction,” International Journal of Cardiology, 2014, 178, 12-23, PMID 25464210). Cognitive impairment is common in those with heart failure with a prevalence ranging from 25% to 75% with greater degree of heart failure associated with higher levels of cognitive impairment. Those in heart failure with a left ventricular ejection fraction of less than 45% are especially prone to cognitive impairment that is at least mild.

Cognitive impairment may involve any one or all of several brain functions. These include attention, memory, executive function, language, speed of thinking, and/or constructive ability. Heart failure causes hypoperfusion (decreased blood flow) of the brain, which reduces oxygen and delivery of glucose to the brain. This in turn may lead to the destruction of neurons. The risk for cognitive impairment in heart failure is greatest for those with diabetes, systolic blood pressure of greater than 180, or diastolic blood pressure less than 65. There does not appear to be an association with low systolic or high diastolic blood pressure.

There are a multitude of secondary effects of heart failure that may contribute alone or together to increase cognitive impairment. Among these factors is depression, which may be severe or mild. Many medications that regulate blood pressure and heart function have anticholinergic side effects that are notorious for inducing confusion. Diabetes is known to induce cardiomyopathy, heart disease, and hypoglycemia. Inflammatory cytokines are released and are associated with cognitive impairment. Homocysteine, an amino acid, is elevated in heart failure and associated with cognitive impairment and decline. Finally, atrial fibrillation is strongly associated with cognitive and functional decline if left untreated.

Cognitive impairment associated with heart failure has a number of consequences. It compromises the skills necessary to manage a complicated treatment routine including managing medications, tracking follow up appointments, and managing heart healthy diet. It also may compromise the ability to recognize symptoms in oneself. On a practical level these changes may impair IADLs like driving, managing finances, paying bills, or preparing meals. In the extreme, cognitive impairment may lead to hospitalization and increased mortality in heart patients, mortality in heart failure with cognitive impairment is 18% at one year versus 3% in those with normal mentation.

The bottom line is that heart disease adds cognitive burden that affects treatment and outcome. The cognitive changes may be subtle or obvious, temporary or persisting. Assessment of cognitive function is an essential component in managing and treating heart disease.


Alzheimer’s disease does not develop suddenly. It emerges over the course of decades. There is a history of short-term memory loss that often dates back a decade before more obvious symptoms arise. Onset is subtle. How many of us have had senior moments? How do we know if they are benign or the hallmark of progressive cognitive decline? Changes are complex and differ across individuals depending on the region of the brain that is affected.

One way to make sense of these complicated pathways is to have a category that reflects significant changes in memory that fall short of a dementia. The solution has been to create a category – diagnosis if you like – for individuals who have memory changes but are not demented. This is Mild Cognitive Impairment (MCI) (“Mild cognitive impairment and mild dementia: a clinical perspective,” David Knopman and Ronald Peterson, Mayo Clinic Proceedings, 2014, 89, 1452-1459, PMID 25282431).

MCI (the amnestic type) is memory decline that is greater than the inefficiencies of normal aging. It is marked by cognitive impairment that falls short of a dementia. The afflicted person remains independent but there are concerns as well as performance on objective tests that are lower than expected from those with similar age and education. A person with MCI can still pay bills, shop, and prepare meals. MCI marks the risk of future decline that is greater than for those with normal memory.

How is MCI different from mild dementia? Those with mild dementia also have poorer memory than either those who age normally or those with MCI. Mild dementia is marked by substantial decline at work or at home in abilities such as paying bills, shopping, or taking medications. However, personal care like dressing, preparing snacks, and grooming are fine. Persons with mild dementia almost always decline over time whereas some with MCI do not.

How are these conditions diagnosed? Mostly by a careful history obtained from the person of concern and an informant such as a family member or close friend. Despite the advancements in imaging techniques, a good clinical interview and objective cognitive tests are the gold standard for diagnosing MCI and mild dementias. If these assessments suggest decline further medical evaluation is necessary to determine if the problems are a result of a medical disorder such as stroke, thyroid disorder, or diabetes.

What should you look for in everyday life to indicate that someone may be at risk for progressive decline? Mostly the early signs will show as functional changes. Look at abilities like paying bills, balancing the checkbook, getting taxes ready, managing affairs, organizing papers, being able to shop alone, preparing meals, tracking current events/interests, following movies/TV shows, taking medications, finding one’s way around. If any of these skills are of concern, seek assessment.


Treatment of Alzheimer’s disease begins with early detection of memory loss, well before any serious symptoms are present and there is an impact on independence. In other words, we need to have a reliable, valid way to detect minor changes in memory that exceed the inefficiencies of aging. At the present time we rely on medical screening with a test that is very insensitive to mild decline in memory – the Mini-Mental State Exam. The major problem with this approach is that it misses all but the most obvious changes in memory. Alternatively, we can seek neuropsychological evaluation to thoroughly measure and describe cognitive skills. This approach is much more sensitive but involves greater time and expense.

More simply we can ask the simple question, “How’s your memory?” After all, most medical and psychological evaluation begins with self-report and a good history. Some are very aware of their own changes in memory. The problem here is that we are asking someone who may be very forgetful to remember. In many memory loss clients, the problem is that they forget that they forget. They are not aware of their problem and will be unable to have insight into their deficits. The technical term for this is anosagnosia.

There is a good supplemental source of information that is easy to use and quite reliable and valid. One can ask family members for their appraisal. I am surprised how often spouses are not an integral part of memory assessment. After all memory loss is a family problem – affects not only the forgetful but also those who live with them. The point of assessment is to help those who are or may become caregivers to better understand what they are dealing with – I always involve family in all of my evaluations.

For example, one could give both the client and the spouse a questionnaire like the PRMQ (Prospective and Retrospective Memory Questionnaire). This is a simple set of questions about memory issues like being able to remember appointments, being able to remember to take medications, or being able to remember to do chores. Indeed, informant corroborated memory loss is superior to self-reported memory loss in assessing memory function in Alzheimer’s disease (The clinical utility of informant appraisals on prospective and retrospective memory in patients with Alzheimer’s disease, PloS One, 2014 19, E112210, PMID 25383950).

Informant’s ratings are highly correlated with objective measures of memory and overall cognitive ability. Informant’s ratings have good specificity and sensitivity for memory loss. Finally, informant’s ratings provide incremental value to both objective test scores and demographics. We need to paint a broader and more accurate picture of the range and scope of memory loss if we are to develop and implement better treatments. We have to include the family in all steps of the evaluation process.


There has been a long standing debate about whether undergoing anesthesia can trigger dementia (see article by Roni Jacobson in Scientific American, October, 2014). Despite large, well-publicized studies claiming there is no significant association between anesthesia and dementia, there are too many cases to dismiss the phenomenon as coincidence. The cases appear to be statistical outliers in that they are not the norm.
However, that does not make them any less real just infrequent.

What is widely accepted is that a portion of those who undergo general anesthesia experience what is called “postoperative cognitive decline.” This marked by lapses of memory and attention (mild to severe delirium) that lasts from a few hours to a few weeks before it clears. Most who experience anesthesia do not show these effects for more than a very brief time and do not go on to experience a progressive, irreversible dementia (disability and loss of independence).

The question is whether anesthesia causes or is the first link in those who experience progressive decline after anesthesia. One obstacle to answering this question is that we still do not understand how anesthesia really works. The effects are very diffuse and produced by the deactivation of proteins that modulate sleep, attention, memory, and learning. Anesthesia targets sleep and arousal by deactivating neural networks that allow various brain systems to communicate. Like any drug, anesthetics can trigger unforeseen adverse events or side effects that have nothing to do with anesthesia per se. Drugs are never as specific in action as many might think.

Animal studies have shown that anesthetics can increase the levels of toxic amyloid proteins in the brain. Furthermore, they can also inflame brain tissues. But it is a long way from animal models to human brain function. Epidemiological studies with humans so far have not clearly shown a link between anesthesia and triggering of dementia.

That being said, there are many complicating factors in pursuing answers to the question of casual links between anesthetics and dementia. There may be many individual differences in susceptibility to adverse effects of anesthesia. What are the factors that cause some of us to be more affected? Are there preexisting conditions that put some at risk for dementia? We know that postoperative decline is more likely with cardiac surgery. It is also more likely in the aged, the diabetic, and the hypertensive. Are there medical factors that predispose to dementia after anesthesia? How do we separate the effects of anesthesia from the general effects of the trauma of surgery?

We have few practical answers regarding the link between anesthesia and dementia so far. The best concrete advice given the risks and uncertainty is to avoid elective surgeries. Also, carefully consider the risks and benefits of any surgery.

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