Brain Plasticity is Key to Surviving a Stroke

Although we think that the adult brain remains formed and static, we are finding that the brain changes and heals itself. Even early psychologists like William James (1890) argued that our brain is flexible and changing when he wrote The Principles of Psychology.  He called this “plasticity”. But it took another 70 years to provide evidence for this concept. One of the first pioneers was Joseph Altman who first discovered brain cell regeneration—or neurogenesis—in 1962. More recently, by 1999 the psychologist Elizabeth Gould of Princeton University reported that memories can be recorded in neurons that are generated daily.

We are now in the age of bran plasticity. Neurologists and psychologist accept the idea that the brain and its function are not fixed throughout adulthood. Brain plasticity refers to the brain's ability to change throughout life. We continue to learn because the brain keeps reorganizing itself and forming new connections between brain cells. And we have come to understand the method the brain uses to change. Donald Hebb in 1949 wrote The Organization of Behavior and provided us with the Hebbian Theory which specifies that neurons that fire together wire together. If I reward a behavior, my brain will associate that behavior with the reward and encourage that brain connection. In the 1950, after his father suffered a massive stroke, the New York neurologist Paul Bach-y-Rita become interested in how the brain can receive information from different organs. He invented an electrically stimulated chair. Behind the chair, a large camera scanned the area, sending electrical signals of the image to four hundred vibrating stimulators on the chair against the patient's skin. The blind patient could “see” the diffuse image from the senses on his back. He developed this technique into a tongue sensor that goes on top of the tongue while wearing a camera that translates the image to these tongue sensors. The tongue replaces the eye and receives the feedback that the brain “sees”. More recently these techniques have been popularized by Michael Merzenich and Norman Doidge. They developed the idea of both positive and negative plasticity.

We all appreciate positive plasticity. We develop memories and learn new things. Our neurons and white matter that comprise our brain organize in such a way that we form an internal representation of learning and experiences. Representing multiple impressions of the same event under different criterion (smell, look, feel, association, importance, relevance etc.) With positive plasticity we learn new skills and improve our thinking by developing better and more efficient communication between sensory and motor pathways. But with negative plasticity we have followed exactly the same growth but for the wrong outcome. We learn how to behave in ways that are not helpful, and this is not intentional. Negative plasticity causes an increased sense of pain, drug use and compulsive behavior among other negative behaviors. Pain, for example, is generated in the brain, and the only way to stop pain is to retrain the brain. Opioids lead to morphine and eventually leads to a situation where no medication is able to stop the brain from feeling the pain. We have retrained the brain to develop more neural pathways to feel the pain every time we try and numb the pain by medication. The death of Prince and Michael Jackson is a testament to how strong the brain is in feeling pain.

Stroke offers us a window into how fast and dramatic brain plasticity can be. A stroke occurs when a part of the brain dies. It can be caused by a blood clot or obstruction of an artery (Ischemia). Or alternatively where a ruptured artery and the neurons are flooded (Hemorrhage). There are other repercussions from these two events, with an accumulation of fluid/pressure on the brain (Edema) and the disruption of the sodium-potassium pump.

In the Copenhagen stroke study, a study headed by Henrik Jørgensen from Bispebjerg Hospital, Copenhagen, Denmark reported that one in five stroke patients died during hospital stay, one in seven were discharged to nursing home, and over half of stroke patients were discharged to their own home. Half of those that went home improved. What happens to these lucky quarter of the stroke victims who improve is a testament about brain plasticity. With all strokes there is a shadow that surrounds the dead tissue in the brain--penumbra. Penumbra are cells waiting to die. Whether these cells die or recover is dependent upon how fast the brain uses these cells for learning. And the clock is ticking. Every minute of delay to treatment is said to cost a patient 1.9 million brain cells.  By early referral to physiotherapy, occupational therapy, and speech language pathologist services the brain heals itself.

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We have an ageist view of health. Instead of referring older adults to therapy we instead shuffle them over to wards. Brain plasticity is still available for older adults. But in our ageist view we judge older adults as ready to die and we fulfill this judgement by not helping their brain become re-engaged.

© USA Copyrighted 2016 Mario D. Garrett

Can I grow a new brain to stop dementia developing?

So the good news is that all of us, especially older adults, have dementia. Yes, that is the good news. Because although we all have some of the biological mess in our brain—amyloid-beta plaques, and tau-protein tangles--we deal with this on a daily basis. We overcome these plaques and tangles through brain plasticity. We push ourselves to learn new things and that develops new brain pathways.  As with cancer, which we all have, our body deals with it effectively. It is only when our body stops dealing with these biological messes that these become a major health hazard. Most of the time however, we deal with these complications because our body is always changing. That is our natural state.

There are 37.2 trillion cells in the human body. All vibrating with activity and they are always changing. Our body is in reality only about 11 years old. It keeps replacing parts on a daily basis. Jonas Frisen from Karolinska Institute in Stockholm have been studying how quickly our organs are replaced. He reports the following turnover of organs:  Intestines (2-3 days); Taste buds (10 days); Skin and lungs (2-4 weeks); Liver is replaced (5 months); Nails (6-10 months); Red Blood cells  (4 months);  Hair (3-6 years); Bones (10 years); and Heart--most of it (20 years). So how come I do not look 11 years old?

In the process of replication some mistakes are made, and some damage cannot be corrected. There are also some cells that cannot be replaced. Cells like the inner lens cells of the eye, or some of the valves and muscle cells of the heart and also cartilage. If we have the brain mess in our brain can we heal ourselves? And the answer is yes.

We are not sure what causes dementia. The antiquated idea that it is caused by plaques (amyloid beta) has not been proven. To date most of the treatments tested in human clinical trials are drugs that remove plaques have not resulted in any positive outcomes. Although the drugs were successful in removing the plaques from the brains of patients with dementia their dementia grew. The focus on brain mess now has been directed at the tangles (tau-protein), although again we are finding that there are different types of these errant proteins (18 so far) that have different ways of infecting the brain. And we are not sure that they are the sole cause of the disease. It is telling that between one in five people--and as high as two out of three people--who have the “disease” in their brain do not show dementia. We still do not know what causes Alzheimer’s disease.

We are also still struggling to diagnose Alzheimer’s disease correctly. We confuse Alzheimer’s disease with Creutzfeldt-Jakob disease, Lewy Body dementia and Vascular dementia. There is also confusion with anxiety, low education, cultural variability and—the main cause of misdiagnoses—depression. Our diagnostic tools are too crude to differentiate these other problems with our thinking. Primarily because we are measuring how strong the problems are rather than the type of problems.

More telling is that the “brain mess” is less likely to cause Alzheimer’s disease as we age. What this means is that there are other problems with the brain as we age. Half of older people with dementia do not have enough brain mess to explain their dementia. Strangely enough, half without dementia have enough brain mess to be diagnosed with Alzheimer’s disease but they do not have it. The sad part about research in Alzheimer’s disease is that around one in ten residents in nursing homes and assisted living facilities have a type of disease that can be reversed. It is caused by water pressure accumulating inside the brain. They are likely misdiagnosed with Alzheimer’s disease when it can be cured. We are too quick to label someone with dementia, especially in older age. It is not that these diseases do not exist, but that there are so many problems with the brain and not all are Alzheimer’s disease. We are too quick to label someone and then this labelling has negative repercussions.

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The husband and wife team of professors Alex and Catherine Haslam with the University of Queensland in Australia looked at how stereotypes play a significant role in diagnosis of dementia. What is referred to as stereotype-threat-related, by reading a short sentence or two about how older adults suffer from dementia when they have memory problems, physicians are more likely to then diagnose someone with dementia. In one study, seven out of ten physicians were more likely to diagnose an older adult who has memory issue as having dementia rather than when there is no stereotyping (only one in seven). Unfortunately, in response, when older adults are faced with negative stereotypes about their age and their thinking, their memory gets worse. We perform worse when we are stressed and we tend to conform to how people expect us to behave. This is not to say that Alzheimer’s disease is made up. But the negative stereotype stops us from performing our best in combating the everyday brain mess that accumulates.   Negative stereotypes stop us doing our best. Stop us from trying harder and pushing the brain to develop new pathways. Negative stereotypes stop us trying. Helping the brain mess to take over. Never stop learning, we are never too old.

© USA Copyrighted 2016 Mario D. Garrett

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Fluid and Crystalized in Intelligence in Older Age

When refer to “fluid” and “crystallized” intelligence of older adults we are still using 1950s constructs. Constructs that are antiquated, eugenic constructs.  Rarely do we see such references for younger people. There is not one article reporting that younger people’s crystalized intelligence is immature. But somehow these construct explain older adults diminished capacity for intelligence. By looking deeper into the use of these indicators of intelligence shows a glaring ageist perspective. 

The Cattell-Horn Theory of Fluid and Crystallized Intelligence has been a resilient theory in psychology for more than 50 years, especially when referring to older adults. First proposed by the British psychologist Raymond Bernard Cattell in 1941 and later much refined with his student John L. Horn in 1964, Cattell believed that intelligence was a genetic attribute. He held eugenicist views that race played a major part in determining our intelligence. In line with the time, he also saw aging as a period of loss and decline.

Although Cattell is also credited with developing an influential theory of personality--16 personality factor model of personality--and creating new methods for statistical analysis--multivariate analyses, and with Charles Spearman developed Factor Analysis--his lasting legacy has been the proposal that intelligence is a reflection of some 100 discrete abilities which can be categorized broadly into two different sets of abilities: Fluid and Crystalized intelligence.  These abilities have quite different trajectories over the course of development from childhood through adulthood. While Crystallized intelligence continues to incremental improve, Fluid intelligence peaks at around 20 years of age and then declines slowly by age 65.

Table: Fluid and Crystalized Intelligence across the Lifespan

(from Baltes P B, Lindenberger U, Staudinger U M, 1998)

Fluid intelligence is one of the discrete factors of general intelligence, proposed to be an innate and inherent learning capacity of all individuals. Fluid intelligence is independent of one’s education, learning and experience and reflects an individual’s natural mental ability. This is your “smarts.”  Such capacity also includes your capacity for learning, problem solving and pattern recognition. Fluid intelligence is thinking on your feet…this is what Piaget refers to as “Intelligence is what you use when you don't know what to do.”

Crystallized intelligence on the other hand is the more stable memory-based intelligence. It is the accumulation of expertise through learning and skill development. It can be manipulated, mimicked. These are things that you ‘know.’ As such they are seen as a repository of clever things.

Initially there was much talk of specific areas of the brain responsible for each individual aspect of intelligence. However, the distinction between the two types of intelligence is not in brain structures. In 2014, Aron K. Barbey and his colleagues with the University of Illinois studied 158 human brain lesions of male patients who had an average age of 58, to investigate the neural foundations of key competencies for fluid intelligence and working memory. Although they found that both type of cognitive activities are active in the fronto-parietal network—a region of the brain on the top of the head above the ears—there were distinct patterns of activation for fluid intelligence and what they call working memory (crystalized intelligence).

However, none of these studies tested older adults or women. More importantly they have no predictive quality. Knowing which part of the brain is active most, does not inform you what the person is thinking. There might be distinct areas of the brain becoming more active depending on the type of task being performed rather than the type of thinking being used.  It is likely that there are no distinct types of intelligence. It is also likely that only distinct tests we use to measure intelligence can be distinguished under two general types and that there are no distinct intelligence. There are also no different areas of the brain used for different types of intelligence. It could be that different tasks might use a part of the brain more than others. The variability among people is also under-reported. What might be activated in your brain might be different from how my brain reacts to the same task.   This criticism is not to discount the value of doing fMRI studies, but to calm the generalization from these studies. The impression given is that there are distinct types of intelligence that use distinct areas of the brain. The corollary of this is that with aging brains we will see diminished capacity in some type of intelligence related to that part of the diminished brain. But this is not the case.  To understand why this is not the case we have to go back to the beginning and explore how Cattell defined the two sets of intelligence in the first place.

The 1950s was a great time for psychology. While psychiatry was moving towards biology, pharmacology and brain surgery—using such barbaric but seemingly efficacious techniques such as prefrontal lobotomy, insulin shock therapy, and ECT; and while psychoanalyses shed its Freudian skin and was moving towards behavioral and cognitive therapy (later to morph into humanistic therapy); Psychology was being engulfed by the behaviorists and the emergence of statistics as the method of choice. The belief was that the human mind is a black box that we can never know. But through scientific rigor and with enough experimentation and statistical strength we can predict--but not understand--the black box. This was Cattell’s world. With sheer statistical strength we can force through a predictive model of the brain.

Using over 100 discrete tests for intelligence, Cattell put them all in a statistical hopper, shook them up, and saw which ones relate to each other. Using this method of defining clusters--called Factor Analysis--he defined two main groupings which he later called Fluid and Crystalized Intelligence. The clusters relate to the tests used, not to some innate distinction of intelligence. The expectation is that the breadth of the test used somehow represents the full capacity of our intelligence. By today’s standards, this assumption will be considered fanciful.

Once in the statistical hopper, how you determine what unique entities are related, and what unique entities are not related is by looking at their statistical loadings--how much they correlate with each other. If one test score is consistently high while another one is consistently low, then the analysis separates them as distinct. While if two test scores mirror each other, while one goes up the other goes up and then when one goes down the other goes down, then the two tests are related. Although this seems logical, in reality there are no real cut off point in their loading factors. How high and how low is determined not by the statistical analysis but by the researcher. Human judgement make that determination at what loading each variable is considered “in” or “out” of the Factor.

Recent work by the now deceased German gerontologist Paul Baltes and his colleagues demonstrated that older adults benefit markedly from guided practice in cognitive skills and problem-solving strategies. By focusing on the fluid ability, a small sample of 72 healthy older adults were capable of improving their fluid intelligence. They expressed improvement both by themselves and by following tutor-guided training. The ability to improve one’s fluid intelligence is not innate but a function of utility. Use it or lose it.

Practically, if older adults are shown to have an increasing capacity for crystalized intelligence then their need to use fluid intelligence diminishes. It is not that the ability diminishes, it is that their expertise in crystalized intelligence make reliance on fluid intelligence less essential. There are fewer opportunities to “wing it” when you know the outcome. The ageist view that somehow an aging brain losses its capacity for one of the most unknown features of intelligence—fluid intelligence, that capacity to create connections--reflects a shadow of the old eugenicists view that also denigrated older adults as diminished beings. Using these two concepts of Fluid and Crystalized Intelligence do not hold predictive power, and are useless in a clinical setting. It is time to remove the shackles of old eugenics legacy and stop using this ageist construct. Perhaps we can invest in research that starts to admire the model of reality that older people have created in their brain.

References

Cattell, R.B. (1941). Some theoretical issues in adult intelligence testng. Psychological Bulletin, 38, 592.

Barbey, A. K., Colom, R., Paul, E. J., & Grafman, J. (2014). Architecture of fluid intelligence and working memory revealed by lesion mapping. Brain Structure and Function, 219(2), 485-494.

Baltes P B, Lindenberger U, Staudinger U M (1998) Life-span theory in developmental psychology. In: Lerner R M (ed.) Handbook of Child Psychology: Vol. 1. Theoretical Models of Human DeŠelopment, 5th edn. Wiley, New York, pp. 1029–143

Baltes, P. B., Sowarka, D., & Kliegl, R. (1989). Cognitive training research on fluid intelligence

in old age: what can older adults achieve by themselves?. Psychology and aging, 4(2), 217.

Horn, J.L. (1965). Fluid and crystallized intelligence: A factor analytic study of the structure among primary mental abilities. Ph.D. Thesis. University of Illinois.

© USA Copyrighted 2016 Mario D. Garrett