There are those who say that, if the previous century was the century of genetics, the current century is that of the brain. Certainly, as the years of these first decades have gone by, we have come to understand a little more how the brain functions and how it interacts with the environment to help us adapt to it. Studies of people who have had a brain injury have contributed a great deal but as is often the case, the more we know, the more questions arise: How is it possible that recovery manifests differently in people with similar damage? Why, sometimes, similar injuries do not involve the same type of clinical signs? Cognitive reserve is one of the paradigms that attempts to address these answers.
Cognitive reserve (CR) is not a recent paradigm but is a term that in recent years has become increasingly prominent in our conversations about neuropsychology and brain injury. An example of this can be seen in the increase in the number of publications on this subject in their title (Source: PubMed), which has gone from 183 in the first decade of the 21st century to 967 in the current decade that has not yet ended (the evolution can be seen in the following graph).
Publications on Cognitive Reserve
Is brain reserve the same as cognitive reserve?
The actual problem with the concept of cognitive reserve lies in understanding its meaning and what it may or may not contribute to our daily work. To this end, it is interesting to differentiate between brain reserve (BR) and cognitive reserve, terms that are often used interchangeably, even when they each represent a different hypothesis. First, the term ‘brain reserve’ stems from post-mortem examinations that Katzman and colleagues (1) performed in a cohort of healthy elders with Alzheimer’s, finding that there was a lack of direct relationship between amyloid load and cognitive signs showed by patients. Katzman et al speculated that individuals, even though they had sustained damage consistent with an Alzheimer’s diagnosis, did not show any sign of it in their lifetime because their brains were larger. And this was directly linked to genetic factors, general intelligence (linked to hereditary factors) and formal education influencing neural development, thereby leading to an increase in synaptic density (2). However, BR is a passive model (there is a threshold at which impairment will occur for everyone) and is limited at the intervention level. In a way, this model also reflects older (more structural) conceptions of brain function.
The idea of brain reserve was considered relevant and led to the use of gross measures of brain size, such as the contour of the skull. However, this idea fell short, especially as knowledge of how the brain functions progressed, thanks in part to functional neuroimaging techniques. In fact, based on brain functioning, Stern (3) proposed an active model of reserve on the basis that there really are brains that are more efficient or have greater ability for compensation regardless of size. That is, there are individuals who can better maintain cognitive function in the face of brain damage than others and, therefore, the threshold of brain damage varies greatly from one person to another. The most interesting thing about this hypothesis is that it suggests the ability to modify that reserve (use it or lose it) dependent on lifestyle factors, cognitively stimulating activities, physical activity or the social component as ways to do so.
While these are two different models (although the terminology is sometimes used loosely), the truth is that it could be argued that both interact. Each of us has a genetic endowment, but in turn what is done with it is what will help to have or not more cognitive reserve.
How does this reserve work?
The word reserve refers to “accumulate” something so, in theory, the term cognitive reserve could be understood as “an accumulation of cognition”; in fact, the basic idea behind this reserve is precisely to have additional “cognition” to maintain normal cognitive function when brain damage occurs (or accumulates progressively). The main basis for this accumulation derives from the term neuroplasticity, that is, the brain’s ability to react to the environment and be modified by exposure to it.
The idea of positive and negative neuroplasticity (4), dependent on lifestyle habits, certainly gives us the ability to decide on a personal level how we want our brains to feel with the passage of time. Based on this, the ‘use it or lose it’ (5) hypothesis fits well with the idea of neuroplasticity regarding deterioration due to a lack of use or, if talking about the brain, how efficiency ceases without any stimulation. For this reason, one of the sources of cognitive reserve can be to carry out activities that are novel (which are, therefore, far from automatic) and have a cognitive component. Thus, promoting brain efficiency could delay the clinical manifestations of the progression of a neurodegenerative disease or more efficiently compensate for brain damage (6).
Are there tests in Spain to measure cognitive reserve?
How to measure this reserve is often the main issue we come across. Research in recent decades has allowed us to understand a little better how this reserve can be built as well as what we must pay attention to when trying to quantify it (7,8). In Spain, we currently have several scales available that may be useful. For example, the Cognitive Reserve Questionnaire (CRQ) (9) consists of 8 items that collect information on cognitive reserve proxies such as formal education, parent’s education, occupation, and musical training among others.
In addition, we also have the Cognitive Reserve Scale (CRS) (10), which measures participation in activities both during a person’s young adulthood, adulthood, and late adulthood; the CRS scores various aspects related to training, hobbies or social life.
Finally, the cognitively stimulating activities scale (11)—recently validated in an elderly population—includes 10 activities that can be considered to build cognitive reserve or that, at least, seem to be related to better cognitive function in older adults.
In this respect, it is quite possible that in the future we will see more research shedding some light on the functioning of cognitive reserve and perhaps more importantly, how to learn to use it in the clinical context to assess the progress of people with brain injury and how to introduce it in treatment.
- Katzman R, Aronson M, Fuld P, Kawas C, Brown T, Morgenstern H, et al. Development of dementing illnesses in an 80-year-old volunteer cohort. Ann Neurol. April 1989;25(4):317-24.
- Satz P. Brain reserve capacity on symptom onset after brain injury: A formulation and review of evidence for threshold theory. Neuropsychology. 1993;7(3):273-95.
- Stern Y. What is cognitive reserve? Theory and research application of the reserve concept. J Int Neuropsychol Soc JINS. March 2002;8(3):448-60.
- Vance DE, Wright MA. Positive and negative neuroplasticity: implications for age-related cognitive declines. J Gerontol Nurs. junio de 2009;35(6):11-7; quiz 18-9.
- Hultsch DF, Hertzog C, Small BJ, Dixon RA. Use it or lose it: engaged lifestyle as a buffer of cognitive decline in aging? Psychol Aging. June 1999;14(2):245-63.
- Scarmeas N, Stern Y. Cognitive reserve and lifestyle. J Clin Exp Neuropsychol. August 2003;25(5):625-33.
- Schinka JA, McBride A, Vanderploeg RD, Tennyson K, Borenstein AR, Mortimer JA. Florida Cognitive Activities Scale: initial development and validation. J Int Neuropsychol Soc. January 2005;11(1):108-16.
- Salthouse TA, Berish DE, Miles JD. The role of cognitive stimulation on the relations between age and cognitive functioning. Psychol Aging. December 2002;17(4):548-57.
- Rami L, Valls-Pedret C, Bartrés-Faz D, Caprile C, Solé-Padullés C, Castellví M, et al. Cuestionario de reserva cognitiva. Valores obtenidos en población anciana sana y con enfermedad de Alzheimer. Rev Neurol. 2011;52(4):195-201.
- León I, García-García J, Roldán-Tapia L. Estimating Cognitive Reserve in Healthy Adults Using the Cognitive Reserve Scale. PLOS ONE. 22 July 2014;9(7):e102632.
- Morales Ortiz M, Fernández A. Assessment of Cognitively Stimulating Activity in a Spanish Population. Assessment.1 May 2018;1073191118774620.
Neuropsicólogo Clínico en Centro Integral de Valoración y Educación Terapéutico (CIVET) en Sevilla. Especializado en daño cerebral adquirido, demencias y específicamente en la rehabilitación de las afasias. Además es docente en varios máster de neuropsicología clínica infantil y de adultos.
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