Morris Friedell MorrisFF@aol.com



(Draft—feedback gratefully accepted.)


According to a contemporary theory, a primary feature of Alzheimer’s disease is neuronal hypoactivity, resulting in progressively decreased processing capacity and lowered stress threshold. This suggests the hypothesis that the qualitative symptoms of moderate AD, disorientation, gross forgetfulness, and loss of abstraction and judgment, are susceptible to rehabilitative intervention.  The intensive rehabilitation available to TBI survivors but apparently untried on AD patients may be effective for them as well.  Insofar as a person with AD can relearn activities using a greater number of easier steps, he can regain function.  And there is evidence that substantial capacities for procedural and implicit learning are retained. 


Alzheimer’s disease always progresses to profound disability and death--so why bother? Why bother training myself so I can balance my checkbook for another year, or empathically listen to a friend, when I’m going to lose it anyway? But isn’t this the same “why bother?” question that’s all around us? Why bother trying to do something about ecology or hunger or oppression when the problems are so big and we are so small, and smarter people than we haven’t succeeded? Thirty years ago, when I was a professor, I did a study of the “why bother to vote?” issue. If we think of ourselves each as isolated units, the probability is infinitesimal that our vote in a national election will “count.” But insofar as “no man is an island” the math is more optimistic.

I think there is no “rational” answer to cynical questions. But one can speak of ”God” or “faith” or “the heart.” In my heritage of Judaism there is the concept of the sacred task, which no one is required to complete, but neither is he permitted to refrain from. Elie Wiesel put it simply, “You suffer, therefore I am.”

When I was diagnosed with Alzheimer’s disease (AD) in September, 1998,1 I had a feeling that all I could do was wait for the axes to fall, one after the other. I’d lose my ability to drive, to budget, to speak coherently, to dress myself, to use the toilet. I thought: I must plan to die when I can still do so with dignity. I still believe that’s a meaningful challenge, but the greater challenge is how to live as fully as I can until that time. And that’s where rehabilitation comes in.

One glimmer of hope was Claudia Osborn's Over My Head (1998) http://www.claudiaosborn.com. She was a traumatic brain injury (TBI) victim, and I could identify with her forgetfulness, spaciness and sense that normal life was going by too fast—actually her symptoms were worse than mine would probably  be for years. However, she participated in an excellent rehabilitation program, and was able to put her life together and write a marvelous book about it. By contrast, I and others  with AD were left to dangle in the wind. At first I sadly felt there probably must be a good reason that there is no book on rehabilitation for persons with AD, just as there is no book on psychotherapy, for persons with AD.2 Seemingly, nothing could be done for us except to make us comfortable while we rot, and give us Aricept (it does help me) to slow it down for several months.

However, as a sociologist I was well aware that the “good reasons” why blacks were suited to be slaves and women shouldn’t vote were hollow. Why couldn’t a person with Alzheimer’s substantially benefit from rehabilitation such as given to TBI patients (although only 5% of them fully receive it)? Alert to holes in the helpless and hopeless picture of the AD victim, I  began to make encouraging observations. We are supposed to be unable to learn, but we are notorious for developing the social skills to mask our deficits. Also, ability to play familiar card games requiring memory and judgment is often surprisingly retained. It seems that the deficits in moderate AD may not be due to broken “hard-wiring” for memory, learning and logic, but due to disorganization of behavior resulting from diminished processing capacity, particularly in the parietal lobes. We can no longer “think on our feet” in unfamiliar situations, and tend to react inappropriately. But when stress is low, higher-order mental capacities may remain, or at least be latent.

A recent article contends, “cell death in AD is generally not a major occurring phenomenon, but is restricted to a few brain areas,” “AD is basically a hypometabolic disease,” and “one may assume that restoration of the activity of neurons, either by pharmacological or non-pharmacological stimuli, would lead to diminished cognitive impairment” (Swaab et al., 1999). The effect of cholinesterase inhibitors such as Aricept provides additional evidence for the diminished processing-capacity theory. Increased neuronal activation sets back the symptoms of the disease across-the-board, suggesting that the qualitative impairments result from a quantitative decrement, and thus that the person with AD might regain function if he or she could relearn activities using a greater number of easier steps.

I wondered if the particular vulnerability of the hippocampus and verbal learning in AD might keep persons with moderate AD from benefiting from the rehabilitation available to patients with closed-head injury resulting in diffuse brain trauma including damage to the frontal lobes. But the surprising ability of AD patients to remember emotional material supports the hypothesis that quantitative factors and remediable disorganization are important in AD amnesia. And there is evidence that procedural memory is a separate system which remains relatively unimpaired in AD and can be significantly substituted for hippocampal memory. Thus it seems that, at least before AD becomes severe, all the rehabilitation successes with TBI can be profitably examined.

Myself, I have a probably congenital nonverbal learning disability, and my short-term memory has always been unreliable. I did not find myself losing my keys when I developed AD because ever since my childhood of losing keys, pens and mittens I have coped by using procedural memory for such things. I remember rules for where to put my keys and where to look for them. When AD further impaired my short-term memory and caused me to become more forgetful of appointments, it was easy to extend my ingrained habit of going by rules and shift the burden to procedural memory with the prostheses of an alarm watch and notebook.

But my priority regarding rehabilitation is keeping my personality rather than remembering things I can take notes for. Here I’m encouraged by the TBI data, even on patients with extensive frontal lobe injuries. It seems that as long as a basic repertoire of emotions and a certain level of self-awareness are retained, personality can often be reconstructed (cf. Damasio, 1999). And AD patients often retain these until the disease is far advanced.

I propose that the typical clinical picture of persons with mild to moderate AD is, more than generally recognized, a picture of remediable “excess disability.” Here is Jitka Zgola’s explication of that concept: “Because a person’s initial disability makes it difficult for her to interact effectively with a conventional environment, her behavior becomes anomalous and efforts to do things are often unsuccessful. Repeated failure and frustration eventually cause her to stop doing things and interacting with people. This leads to social isolation and sensory deprivation, which in turn results in more anomalous behavior, more deterioration of function, and even greater social and sensory deprivation So it goes in an  ever-downward spiral, until the person’s functional decline far exceeds the effects of the original disability” (Zgola, 1999, p. 209). Further, imagine this bleak picture superimposed on the contraction of life all too common among the aging in  our society, where the future (vulnerability, decline and death) is feared and avoided, so the past cannot serve as a source of nourishment and encouragement, and even the present is impoverished in desperate measures to avoid depression (cf. Schachter-Shalomi and Miller, 1995). Still other sources of excess disability will be discussed below.

I plan to intensively and systematically explore state-of-the-art rehabilitation while my impairment deepens. I will communicate the results of this experiment as long as I remain capable of doing so. I hope that will be for many years. A major resource for me is George P. Prigatano’s Principles of Neuropsychological Rehabilitation (1999). The following indicates the essence of his approach: ”I have argued that brain injury, regardless of chronological age, catapults individuals into the second half of life. That is, life is no longer the same after brain injury—individuals function with less intelligence, less capacity for memory,less physical strength, and fewer opportunities for the future. Jung recognized that during middle age, people without brain injuries struggle with similar kinds of problems, albeit at a less severe level.... At times I am asked whether patients with severe cognitive difficulties can actually benefit from psychotherapy. The answer is yes. Much depends, however, on the psychotherapist’s capacity to understand patients’ neuropsychological problems and to identify symbols that the patients can relate to. This process is the true spirit of the phenomenological approach and its reliance on the humanities” (pp. 344-345).

Prigatano’s approach is essentially similar to the psychotherapy for responding to the losses associated with aging, which is part of the psychotherapy for loss in general. Though rudiments of similar psychotherapy have been applied to AD patients (see particularly Mills, 1998), an active future-orientation has been, to my knowledge, always lacking. But acceptance and concern for the resolution of painful memories have been effectively provided.

My personal experiment in rehabilitation is innovative in its attempt to apply the same principles of humanistic future-orientation or meaningful living that have been used in concentration camps (Frankl, 1984), cancer (Krauss and Goldfischer,1988; Spiegel, 1993; Spiegel and Classen, 2000), ALS (Schwartz, 1996), aging (Cole and Winkler, 1994; Schachter-Shalomi and Miller, 1995), and TBI (Prigatano, 1999; Osborn, 1998). How could one live for the future in Auschwitz? “The way in which a man accepts his fate and all the suffering it entails, the way in which he takes up his cross, gives him ample opportunity—even under the most difficult circumstances—to add a deeper meaning to his life.” (Frankl, p. 76). Compare Prigatano on the lovability of children with subnormal intelligence: “The child’s value is reflected in so many other capacities than his or her IQ. It is reflected in the child’s honesty, the child’s caring and loving attitude, the child’s capacity for humor, and the child’s capacity to work hard in the face of adversity. These are the virtues that often enable the human spirit to overcome subnormal intelligence or any other hardship. In some form, this spirit must be recaptured when a young adult, a middle-aged adult, or senior citizen suffers a brain injury associated with cognitive losses.” (p. 335).

Frankl and Prigatano are speaking of what Frankl calls “attitudinal values”—he contrasts these with the values of achieving and experiencing. In Auschwitz, TBI, or Alzheimer’s one’s capacity to be productive or to have enjoyable experiences may be severely limited, but the capacity to realize attitudinal values remains, except under the most extreme conditions, and it is the noblest. Rather than struggle for one’s personal place in the sun, one reorients oneself to participation in the spirit of aspiration toward to a better future for humanity or to intimacy with God. (My interpretation of such religious language is deep and powerful metaphor or, as Prigatano would probably say, “symbol.”)

Within this framework of meaning and hope it is possible to grieve one’s losses (Prigatano and Ben-Yishay, 1999). The process of grieving is the work of creating meaning out of memories. My impression is that as long as the capacity for sorrowful perspective is retained so is that for griefwork. Mills’ (1998) study of persons with AD is encouraging in this regard.

Grieving, i.e., lovingly letting go, permits one to rebuild after catastrophic loss. Prigatano proposes work, love and play as “symbols” guiding the creation of a meaningful life after TBI. His discussion of play in the context of TBI is particularly interesting, since there, as in AD, it is hard to sustain gaiety or zestfulness. “Play does not mean recreation. It means the freedom to do what one wants to do in fantasy. By exploring via play and fantasy what individuals want, feel, and desire, a deeper sense of self begins to emerge.... The capacity to develop [the] sense of freedom to be who one is and to do so within the context of play is crucial for the development of individuality. Play is especially difficult for most people—and this statement is true of people both with and without brain injury. Yet, once the capacity for work and love is established, the capacity for play becomes extremely important because play pays closer attention to the inner world” (pp. 211-213). Opportunities for fun are impaired in TBI or AD, but Prigatano points out this is not the essence of play, and slower, more inward exploration can also serve.

Additional encouragement for rehabilitation is implicit in Guy Claxton, Hare Brain, Tortoise Mind (1999). He amasses evidence that slow unconscious or dimly conscious processes of learning through familiarization can have unsuspected power—power which is neglected or even actively inhibited in our culture. Implicit learning may well be relatively preserved in AD and could perhaps be cultivated. Evidence that artistic creativity may blossom in dementia is encouraging here.

Discussion of AD Research  

I will proceed to detail some additional support for my contentions in the Introduction.

The quantitative decrement of processing-capacity hypothesis for impairment is an extension of the extensively studied cognitive reserve theory explaining why ”individuals manifest different thresholds for symptom occurrence with brain dysfunction” (Cummings et al., 1998). The following observations collectively support the quantitative-decrement hypothesis: 1) “Brain changes precede the appearance of the disease by several years and are present when patients show no evidence of a dementia syndrome” (Cummings et al., 1998).  2) Smaller brain size has been associated with an earlier onset of AD (Cummings et al., 1998). 3) “People with Alzheimer’s disease with higher levels of education have been found to have a greater degree of physical deterioration in the brain at the same level of symptomatology as people with less education.” (Tappen, 1997, p. 27)--education has been estimated to retard the development of symptoms as much as 4 or 5 years (Cummings et al., 1998). 4) Fatigue or infection exacerbates symptoms. 5) Progressively lowered stress threshold has been found to be a useful paradigm for symptom development (Hall and Buckwalter, 1987). 6) Memory for an event can be improved by techniques which augment quantity of processing, e.g., by involving the emotions. This can be effective to such an extent that Sandman (1993) reported: “patients had nearly perfect recall for events during days of significant events.”  Arkin (1997) found that moderately to severely demented individuals could benefit from using tape-recorded narratives and quizzes. “Follow-up testing..., one and two weeks after training, indicated substantial retention of information learned, with no intervening rehearsal.”  Further, she reports: “Biographical memory tapes have been used in ongoing therapy sessions by the author and her students with six subjects. Substantial learning gains were made and maintained for three years with one subject, Bee, the experimenter’s mother, and, for one semester, with four out of five subjects with whom it was tried. The subject who was unsuccessful had a Mini-Mental score of only eight.” 7) “Spatial disorientation as an excess disability is suggested by the findings of Browers et al....  In comparing the performance of 4 individuals with Alzheimer’s disease to healthy older volunteers on a road map test, no significant differences were found.” (Dawson, 1993). I.e., disorientation in real-life situations may be due to overload.

In support of the preservation of procedural memory, Eslinger and Damasio (1986) found “no correlation between procedural learning ability and global intellectual level.” And the research of Hirono et al. (1997) “indicates that the neural system subserving procedural memory is not related to the neural systems for the declarative type of memory.” The authors affirm implications for rehabilitation.

The Conative Loss Paradigm   

A principal source of disability in middle to moderate AD is “conative loss,” the inability to set goals and move thoughtfully through the steps to achieve them (Hall and Buckwalter, 1987).  This fact leads to an intriguing mystery: Conation is an executive function, supposedly carried out by the frontal lobes, but both brain scans and the preservation of social skills indicate that frontal lobe function is often retained.  I suggest that conative loss stems from parietal lobe pathology resulting in the loss of ability to make simultaneous quasi-spatial syntheses (Luria, 1973) through procedures that were formerly effective.  We solve problems by using habitual semi-conscious procedures for laying them out in a virtual or metaphorical 3-dimensional space, and the disorientation patients experience in literal space is indicative of their disorientation in virtual space. Presumably AD neuropathology impairs processing capacity, which then becomes inadequate for the implementation of previously reinforced procedures.  This theory of conative loss explains the painful experience of AD patients that trying hard or attempting self-reflection further impairs performance (because of the processing overload).  If trying is unsuccessful, not-trying mitigates the pain of failure and is reinforced —the patient tends to develop learned helplessness on top of his other problems.

I believe the dysfunction is a matter of procedures rather than in the capacity for spatial representation per se because patients can gradually come to orient themselves to unfamiliar surroundings, and also can slowly create paintings which are “3-dimensional” in their expressiveness (e.g., in “Memories in the Making” art projects)3.  If this is true, a powerful avenue for rehabilitation opens up—patients should be able to relearn to problem-solve through slower simpler procedures.  The success of Montessori-based activities with persons with dementia (Camp, 1999) is encouraging to the present line of thought.

In this perspective relearning to problem-solve becomes central to AD rehabilitation, and the severity of the initial disability should not create undue pessimism.  An analogy to learning to problem–solve with simplified procedures is the challenge of the stroke patient who has to learn to live with one usable hand.  She can eventually become amazingly adroit (Mayer, 1996).  Attention to basic emotional issues must be given priority, however, in order that learning may take place in a climate of hope but not demand: “God, grant me the serenity to accept the things I cannot change.…”  Then, inspired by Montessori methodology, problem-solving can be reviewed step-by-step from the simplest tasks of the young child, in accordance with developmental principles and the individual’s biography, branching out to the various areas of life, and finally, if possible, reaching the level of the mature adult.  The person should develop a renewed sense of competence, which can extinguish the mind-set of learned helplessness.  After regaining competence in activities of daily living representative of, say, the eleven-year-old child, emotional issues, reminiscent of the concerns of adolescence, could be reviewed—the goal would be to rehabilitate not only practical competencies but the emotional shallowness that typically afflicts patients.

Excess Disability

I turn now to some additional material on excess disability. If children with learning-disabilities are exposed to anything like the psychosocial environment of AD patients, e.g., given messages that they will inevitably become more and more helpless, stupid and useless, it is well known that there will generally be a profound induction of excess disability. The enormous significance of excess disability in TBI is indicated by Prigatano and Ben-Yishay (1999, p. 281): ”It is our impression, as it has been that of others, that 10 to 15 years after injury fewer than 10 percent of patients with severe TBI are employed. This figure contrasts with the 30 percent who are working 2 to 5 years after injury.”   And “brain injury is not a degenerative disorder.” (McKinlay and Watkiss, 1999, p. 79). (Prigatano (1999) questions this, however.) Analogous growth of disability in AD might falsely be attributed solely to the progression of the disease.  Additional indication of the importance of excess disability is found in a study by Greenspan and MacKenzie (1994), where poverty was a better predictor of long-term outcome than severity of injury in their group of children and adolescents with TBI.  And Ezrachi et al. (1991), in a study of vocational success, found that duration of coma (an index of severity of TBI) accounted for only 8% of the variance, in contrast to psychosocial factors (60%) and cognitive factors (32%).   

There are many interacting sources of excess disability in AD. To review those I’ve mentioned, there is the vicious spiral leading to social isolation with its concomitant sensory deprivation and deprivation of activities. Another is the stereotypes and stigma of aging and the fear of death. All these reinforce each other, especially in a culture where it is not easy to talk about painful realities. Depression is a major source of excess disability, the only one so far given adequate recognition. AD may well directly contribute to depression, certainly depression contributes to cognitive impairment and social isolation. Of course, social isolation contributes to depression. AD disrupts circadian rhythms and creates sleep disturbances, which contribute to depression and to social isolation. Overmedication may occur, to which the impaired and elderly are particularly vulnerable.

Frontal lobe symptoms, apathetic, stereotyped or disinhibited behavior, may result from remediable reactions to stress, just as does analogous behavior in learning-impaired and emotionally-disturbed children. These, of course, contribute to social  isolation and depression, which in turn contribute to stress.

Beyond the above, I have located three other sources of excess disability. One is ease of dissociation, perhaps due to the disorganization of symbolic space induced by parietal lobe pathology. Normally we function in life by involuntarily remembering unpleasant realities which make us uncomfortable but remind us to take action. But, perhaps with the aid of drugs or alcohol, some of us learn to dysfunctionally but pleasantly forget, in a way that gets us into trouble. (The phenomenon of alcoholic blackouts may support the hypothesis of analogous AD amnesia being excess disability.) For me, with AD, “out of sight, out of mind” is an option now like it has not been since when I was a small child. This capacity to dissociate could easily make my life unmanageable, just as it does the addict’s, particularly if I were surrounded by people who believed that the only thing they could do for me when I was upset was distract me.

Also, intermittent reinforcement is a source of excess disability. There is a powerful human tendency to perseverate where there is intermittent success, in accordance with the theory that “practice makes perfect.” But, unfortunately in a way, the AD patient loses an activity not suddenly and totally but with a great deal of intermittency, consistent with the progressively-lowered-stress-threshold paradigm. The principle of intermittent reinforcement, augmented by well-intentioned but superficial social support, makes AD patients waste their scarce mental resources practicing ineffectually. By contrast, aging athletes take intermittency not as a sign to practice harder but to review and modify the fundamentals of their game.

Finally, excess disability is caused by interference from well-learned schemata that are no longer functional due to their processing-capacity requirements (but which may still be intermittently reinforced). My impression is that developmentally disabled persons are less vulnerable to disorganization in speech than comparable persons with AD because they do not waste their scarce mental resources trying to talk in ways too complex for them. In conversation, I use simple, generic words like “nice” or “thing” more than I actually need to at this stage, so I will be better able to keep my train of thought later. By contrast, in writing if I lose my train of thought while groping for a good word, I can easily read the text and get it back.

Putting all these sources of excess disability together, I wonder if perhaps the ”windows of clarity” observed in patients with moderate AD might be representative of how they could function if rehabilitated. However, it is important to emphasize that excess disability does not imply voluntary control. Depression is a good example here. It is generally remediable, but one cannot just “snap out of it.” Skilled psychotherapeutic or pharmacological intervention may be required. Remediation of other sources of excess disability has analogous requirements.

The Question of the Frontal Lobes

Next, I maintain that frontal-lobe impairment may well be no bar to the retention of personality through moderate AD. True, organizing the presentation of this material feels beyond me at the moment, and I’m tempted to raid the refrigerator. But I remind myself that I felt that way long before AD. Highly-functioning frontal lobes are required for rapidly negotiating the complexities of the sophisticated business deal or dinner-party, but is that what life is about? Mightn’t our reverence for the frontal lobes stem from our culture of power and productivity, which slights the child, the elder, and the loser in the global marketplace?

The reason, of course, that I can continue to write like this despite my cognitive impairment, though my performance at a dinner party (never very good) has sunk through the floor, is the lack of demand for real-time performance. (It does take longer to write now, and it tends to wipe me out for a while.) Thus it’s not surprising that Claudia Osborn can write thoughtful and animated prose about the frontal-lobe injury that turned her into a social “zero.”

The shallow responses and “catastrophic reactions” of TBI and AD patients may represent excess disability rather than extent of frontal-lobe damage. Kurt Goldstein wrote, in a seminal article, “They [the patients] are often afraid that they may not be able to react correctly, and that they will be in a catastrophic condition. Therefore, when they believe they have the right answer, they answer as quickly as possible.... Their quick response is an effect of their strong necessity to release tension...” (quoted in Prigatano, 1999, p. 34). Shallow responses significantly stem from avoidance of painful emotion rather than directly from brain-impairment. Nobody is deep and thoughtful when fleeing from pain. Just as in therapy for addiction, rehabilitation requires compassionately confronting and working through painful emotions.

Prigatano and Ben-Yishay (1999) report an inspiring instance of rehabilitation of a wounded Israeli soldier: “Upon regaining consciousness, Matthew exhibited an array of bifrontal symptoms. He lacked initiation and spontaneity and had a robotlike, compliant attitude. He also had significant memory deficits and impairment of higher-level cognitive functions.” For the next two years “he led a sterile and robotlike existence. He uttered few words and responded in monosyllables.” Despite this picture, Matthew’s therapists were convinced that his fiancee’s abandonment of him was significant. They mined for all the shreds of memory they could find, and then they staged a powerful, creative and sustained psychodrama, reminiscent of a Biblical narrative in its fullness and depth of feeling, to bring Matthew back to emotional life. After doing so they challenged him: “So now, this intelligent, resourceful, brave, and resilient man is finished for good? Or will he bounce back?” The upshot was that Matthew’s rehabilitation took off, and he was eventually able to marry and hold down a job.

Apparently, nothing at all like this has ever been tried on an AD patient. But Mills’ report of her analogous therapeutic explorations for persons with AD, though feeble and tentative by comparison, is encouraging. Frontal lobe impairment may foster apathy, but passionate motivation may overcome it. Tappen, to introduce Interventions for Alzheimer’s Disease, (1997) quotes Nietzsche, “He who has a why to live can bear with almost any how.”

Holistic Neuropsychological Rehabilitation

The spirit of the psychosocial side of rehabilitation has been indicated above.  Vital are acceptance of reality and drawing on one’s spiritual resources for self-redefinition.  Then a new life is created through grief-work, life-review, retelling one’s story and participating in community.  This life emphasizes participation in “living symbols” (Prigatano) or realizing “attitudinal values” (Frankl) which transcend the conventional values of experiencing and achieving. Put simply: “Search your heart, paint a picture, live the picture.” 

The cognitive side of rehabilitation emphasizes task hierarchies based on an analysis of deficits.  Sensitive fading of prompts helps the patient learn with a minimum of errors.  Careful attention is paid to the development of transfer to real-life situations. 

My impression is that in mild to moderate AD memory-loss can be effectively compensated for by note-taking or memo-recording procedures and frontal-lobe impairment is generally not severe.   The principal rehabilitation challenge becomes conative loss with its concomitant learned-helplessness.  As indicated above, Montessori-inspired methods are promising.

Implications for the Caregiver

Can my perhaps utopian picture of rehabilitation potentialities offer anything to the caregiver of the typical passive demoralized Alzheimer’s patient? I believe so—its focus on emotion ought to be broadly applicable. Naomi’s Feil’s The Validation Breakthrough (1993) shows one can engage in supportive emotional communication even with advanced nonverbal patients, and she reports that orientation and speech is thereby often improved. This is consistent with the “paradox of acceptance,” whereby compassionate nonjudgmental acceptance (not approval) of an unfortunate trait combined with unconditional positive regard for its possessor frequently permits a person to let go of that trait. Beyond Feil, Mills (1998) and Kitwood (1997) indicate potentialities for warm, rich and supportive emotional environments for persons with dementia. Eden Alternative facilities (www.edenalt.com/home/index.htm) are of this sort.

After emotional support is established, the key question is inspiring the patient to find a purpose in life. (What might your purpose be, reader, if you had Alzheimer’s? Where would you look forward to being a year from now?) Persons with dementia often want very much to be helpful or do useful things. They can find their creativity, as in a “Memories in the Making” project. They can tap spiritual resources (e.g., religious beliefs such as that God has a plan for each person).  Then Montessori-inspired activities may rehabilitate instrumental activities of daily living.


“Why bother?” I asked at the beginning of this article? I have argued at length that the neuronal hypoactivity theory of Alzheimer’s combined with an analysis of conative loss excess disability and offers scope for surprisingly optimistic results. But most important for rehabilitation is faith in the infinite preciousness of a human life, because that enables one to face and transcend the pain in griefwork. In religious language, we are children of God. By attending to my own rehabilitation and helping others I’d like to leave this message for my children.


I’m grateful to Yehudah Ben-Yishay, Tiffany Chow and Amy Tan for their help and encouragement.


1. I was diagnosed at UCLA in September, 1998, at age 58, principally by PET scan.  Mild global atrophy and mild global hypometabolism was found, with superimposed mild hypometabolism over the right temporal lobe and bilateral parietal lobes.  

2. Later I found Tappen (1997) and Mills (1998) which, while not devoted to these subjects, make valuable contributions.   And now an excellent  book on psychotherapy, Cheston and Bender, Understanding Dementia, has finally become available.

3. See the Orange County CA Alzheimer’s Assn.’s expressive calendar: (phone) 714-283-1111.  


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Sport Psychology

I’ve been reading about the psychology of getting peak athletic performance from a normal brain, and wonder if the equivalent for getting peak performance in daily living has ever been seriously tried on an impaired brain. To introduce my line of thought, here is Prigatano (op. cit., 1999) on a stroke patient:

“When asked to perform the subtraction ‘42 - 28 = what?’ he began the task by stating, ‘Normally, I would subtract 30 from 42 and the answer is 14. Then I would subtract 2 from this in order to get the correct answer since 28 was two points less than 30.’ He said the answer must be ‘12’ but seemed uncomfortable with his response. After pausing and thinking, he said it appeared this answer was wrong. He sensed that something was wrong and was unsure of his answer. At that point, he said that his mind went blank, and he did not know how to try to reapproach the problem. He was obviously upset.... Confusion ... takes the person out of a problem-solving loop.... This feature is a hallmark of a dysfunctional brain.”

This is from Cogan and Vidmar, Gymnastics (2000) discussing mental blocks: “One day the gymnast feels a little disoriented and doesn’t throw the double full on floor quite right, or maybe her timing is off. She starts twisting too early off the ground and doesn’t know where she is in the air. From there, things deteriorate until she can’t do the skill at all.”

There’s a lot of similarity in these two vignettes. I suspect that the same principles of sport psychology that can help the athlete overcome her mental block can help the stroke (or TBI or AD) patient recover his capacity to do arithmetic or to remember.

Myself, I’ve become aware that my capacity to use my memory to navigate daily life is continuing to improve, although there are certain signs that my disease is slowly progressing. I have profited from the TBI literature, but I think I’m developing a certain facility and flow beyond what I’ve read about in that literature. Yet I’ve not put a great deal of effort into either memorizing or studying memorizing techniques. However, I think I’ve been using, almost unconsciously, sport psychology.

The rationale for applying sport psychology to AD is that Alzheimer’s symptoms are well-interpreted as resulting from progressively-lowered stress-tolerance, and sport psychology teaches one how to function effectively under conditions of enormous overload. (It’s obvious that basketball means coping with overload, but the golf swing does as well. It involves the coordination of multiple muscle groups and, though there is no input from the external environment to deal with, the necessity for homeostasis (constantly rapidly making minute corrections) makes the problem of golf fundamentally not that different from the problem of basketball—thus one can speak of a general sport psychology, central to which is the theory and practice of effective performance under overload.)

A key concept in sport psychology is that muscles are not tensed more than necessary, so that fatigue is minimal, or less than necessary, so that priming is available, and the simplest moves compatible with maximal performance are employed. Each muscle or muscle group has optimal tone at any given time in, say, the golf swing. The poor athlete will just be concerned to make the “right moves,” whereas for the pro the harmonization of the different muscles during the course of the swing or stroke might be compared to a symphony. The subjective experience of this is “flow,” sustained optimal engagement. Flow is highly pleasurable, hence reinforcing.

When I developed AD I lost most of my capacity for flow and thought I’d never regain it. At best I’d be able to learn to operate myself like a marionette. I had, as it were, to make a map whenever I took a step. If it was this way now, what would it be like when the disease worsened?

Now, with a regained feel for flow, I can be almost as casual about where I leave my glasses as before AD. This despite being quite oblivious if you were to ask me to describe the furniture in an unfamiliar room. I don’t even try to remember where I put my glasses, instead I have a rule for searching for them—I’m not even fully conscious of what it is--(e.g., “right next to the computer, on the bedtable, on one of the largest surfaces in the room as long as there’s nothing else near it”). I put my glasses where I feel I can easily find them; I have a vital meta-rule—don’t use the rule if it doesn’t feel easy to use! If I don’t feel comfortable with letting go of something I clutch it as if it would drop thousands of feet into cloudy oblivion, until I make a note and place the note where I will find it when I need it (in accordance with my rules for notes). It’s like in martial arts, turning weakness into strength—I lean on the sense of easiness and milk it.

Here is how I memorize three words representing diverse objects given, say, 15 seconds, to be able to recall them after 15 minutes and with a series of other tasks in between: Initially there is the creation of an amusing visual image. E.g., when the words were “chef,” “blue,” “horse,” I imagined a chef in a white hat bending over an enormous cauldron in which a blue horse was being simmered. Implanting the image into my long-term memory (for me 15 minutes is long-term) is like watching a Polaroid develop. (I’ve enjoyed sharing this experience with my grandchildren.) My attention pendulates, and on the downswing I relax into the image. Intermittently I give pulses of attention to the specific words paired with the images. I expect interruption and the need to subordinate the memorizing to other tasks (“embrace the tiger”). The feeling of amusement (i.e., the feeling of a touch of a smile) serves as an efficient and effective anchor for the visual memory. Also, I have cultivated a sense of when the Polaroid has sufficiently developed, so my memorizing doesn’t peter out with an unpleasant affect the expectation of which impairs the process. This is analogous to “follow through” in golf. Thus there is a sense of flow and closure in my memorizing process analogous to that in a golf swing, albeit much slower. And like the golfer I am pleasurably engaged in the process, rather than trying as hard as I can to hit the green.


Feng Shui

Studies of the rehabilitative success achieved when stroke patients are forced to use a disabled limbs suggest that it may be helpful for persons with early AD to make meaningful decisions in contexts where the frontal lobes are relatively inactive.  Arranging one’s environment in accordance with some of the principles of feng shui (Kingston, 1999), in particular eliminating clutter, would be therapeutic and revitalizing.


Liberation Neuropsychology

Tedd Judd (1999) having worked in rehabilitation among the poor in Central America, proposes a “liberation neuropsychology” that would be sensitive to indigenous culture, political oppression, and spirituality.


Additional References:

Cogan, K. D.  and Vidmar, P. Gymnastics, Morgantown, WV: Fitness Information Technology, 2000. 

Judd, T. Neuropsychology and Community Integration, New York: Kluwer, 1999.

Kingston, K. Clear Your Clutter with Feng Shui, New York: Broadway, 1999.



Again, I welcome your comments:   MorrisFF@aol.com