Individual Differences in Mental Abilities Cognition

Nature of Cognition

Ever since Simon and Binet developed the first intelligence test in 1905, the field of psychology has maintained a strong interest in the nature of intelligence. How do we think? Why are some people better problem solvers than others? What is cognition, the ability to think about our environment? Why are some people consistently more able to use their brains to think, to remember, and to problem-solve than others?

The first IQ tests were devised to determine which children were mentally retarded. These children were pulled away from mainstream education. However, the tests did an effective job of predicting school success for all students, and their use was broadened (Sternberg, 1999). Multiple tests were developed to measure cognition, which might be defined as the ability to think abstractly. Markman (2001) described it in this way:

Cognition depends on the ability to imagine or represent objects and events that are not physically present at a given moment. Cognitive functions include attention, perception, thinking, judging, decision-making, problem solving, memory, and linguistic ability.

One of the most basic cognitive functions is the ability to conceptualize, or group individual items together as instances of a single concept or category, such as 'apple' or 'chair.'"

The ability to reason about things which aren't in our immediate vicinity, or which are abstract concepts, allow us to think beyond the concrete limitations of our environment. Markman lists some of these kinds of abstract thinking as "deductive reasoning, induction, mental simulation, and analogy" (Markman, 2001). Much research has been done on the nature of what cognition is, and on why some people are consistently much stronger or much weaker in their ability to think, remember and reason (often measured as an IQ score). This paper will look at what cognition might be, and what some of the causes are for the condition known as "mental retardation, where the individual has markedly diminished ability to use cognitive skills to both learn and to retrieve information when compared to most people. However, Sternberg (1999) makes the important point that since we are just beginning to explore how the brain is, any tests we have devised so far are by necessity incomplete measures of the wide variety of ways in which people can "think."

Complicating the exploration of cognition is the fact that the brain uses multiple functions to process information. For instance, memory is more than one thing. Immediate short-term memory (sometimes called "active working memory") allows us to examine things while they are present, such as a phone number. We may need to remember it only long enough to dial it, and immediately forget it. Or we may deliberately commit it to memory, or it may end up there simply because it has been repeated enough to be permanently stored for recall. The ability to recall information is crucial to our ability to compare new information to old, to categorize, and to develop new information, and even to have a sense of self.

Another issue in cognition is that of both quantity and speed. Measures of intelligence often include both the amount of information known ("Who was the first President of the United States") and processing speed, or how quickly we can recall or manipulate information (Wenger, 2000).

Recent attempts have been made to measure some of these brain functions. For instance, can attention be measured? Can we quantify how much information a person can hold in active working memory at one time? Wenger (2000) considered in some research whether these skills are static or changeable. Perhaps the size of this memory buffer varies according to the stimulus. Thus, a musician with little math ability might remember a melody better than a series. Wenger (2000) makes the point that the ability to use this very-short-term memory might include the ability to draw on multiple other functions of cognition at the same time. Nothing in how we think seems to be as simple as is presented, on the surface, in IQ Tests. Nevertheless, they are the best-quantified measures we have right now to determine who has significant cognitive problems. Their use to identify those with cognitive limitations has encouraged research of the phenomenon, which has provided important new information about both the brain and genetics.

Causes of low cognitive ability

What causes one person to have such impaired cognitive abilities that he or she has marked difficulties not only in school but also in functioning in every day life activities? While researchers don't have all the answers yet, two major groups of causes have been identified: environmental and genetic causes. Environmentally, prematurity, prenatal exposure to alcohol and lead poisoning will be looked at. Genetically, some of the lesser known causes will be considered: a new, unnamed genetic difference, Fragile X, Rett Syndrome, and Williams Syndrome will be looked at.

Environmental

Prematurity has often been considered a risk factor, and in the past it was assumed that the smaller the baby, the more likely significant neurological damage was. However, McGrath (2000) has completed interesting research that measures the risk factors more precisely.

She devised a scale to evaluate the severity of the infant's difficulties while developing to term weight. In the study, a composite Neonatal Risk Index including both medical and neurological complications was the best predictor of outcomes. She then tracked the children's progress, using a control group of babies born at full term, for eight years (measured by due date).

She found that later cognitive difficulties correlated with the level of neurological difficulties rather than birth weight. In other words, some very small babies did markedly better than some larger but still premature infants, later on. She also described a "sleeper effect," that is, that difficulties apparent by age eight were not always detectible at younger ages. Some of these difficulties included motor skill lags and difficulties learning that weren't apparent at a pre-school age.

Her research is important because in the past, some research has suggested that prematurity is a major cause of learning problems while other research has shown that the children will catch up by school age (reported by McGrath, 2000). The children were matched for socio-economic status of families and other factors that might have acted as uncontrolled variables. Information was gathered in an unbiased way from the babies' medical charts.

In McGrath's study, neurological assessments were performed at 18 and 30 months (adjusted for each child's prematurity). The evaluators achieved a very high rate of agreement (95%) They also noted the presence of cerebral palsy, blindness, deafness, hydrocephalus (treated) and seizures not under control (McGrath, 2000). Evaluations were done again at the ages of 4 and 8.

At ages 4 and 8, developmentally appropriate gross and fine motor skills were included, such as gait, motor weakness, muscle tone, or movement difficulties. At age 8, children were evaluated for attention deficit hyperactivity disorder (ADHD). Information on cognition, any medical diagnoses and socioeconomic information was updated.

One of the findings in McGrath's study was that the full-term group of children had significantly higher IQ's than the premature children, as a group. The full term group was more stable by every measure, although some of those children did show developmental difficulties by age eight. In addition, the more severely neurologically involved children as a group had significantly lower IQ scores, typically in the seventies and eighties, compared to the full term group, whose average IQ was 104. While all groups had children who required special services, the children who showed neurological impairments from premature birth required significantly higher levels of intervention.

However, it is clear from this study that there is no direct cause/effect relationship between premature birth and subsequent impaired cognitive function. Events subsequent to the birth resulting in greater difficulty for the newborn were the controlling variables, and sometimes babies born very early did relatively well later on.

Fetal alcohol effects were first noted in animal research, but clinicians soon realized that maternal consumption of alcohol during pregnancy could cause problems for the developing fetus. These effects include growth and behavior problems as well as cognitive difficulties (AAP, 2000). The difficulties occur on a continuum, and they may not all be present at birth, although some children have facial anomalies that make the problem apparent immediately. These children typically have disabilities that last all their lives. The AAP cited research tracking children with maternal alcohol-related disabilities and described them as "profound, pervasive, and persistent" in nature. They noted significant cognitive problems including "specific mathematical deficiency, difficulty with abstraction (eg, time and space, cause-and-effect), and problems with generalizing from one situation to another,... poor attention and concentration skills, memory deficits, and impaired judgment, comprehension, and abstract reasoning."

The children often had behavior problems that ranged from ADHD-type symptoms (hyperactivity and impulsivity) to oppositional behavior to more serious incidents of lying and even stealing. The behavioral differences are not typical of those typically seen in other kinds of mental retardation, where the behaviors are more typical of the individual's mental age (AAP, 2000).

Lead poisoning is another common cause of low cognitive function in children, and like fetal alcohol syndrome, is avoidable.

While Soong (1999) reported cases where eliminating or reducing the exposure diminished the negative effects of the lead exposure, other research has not found this. The children involved were of kindergarten age, and Soong acknowledges that lead poisoning in younger children, especially two years old and younger, causes more devastating disabilities. It was once thought that lead levels as high as 25 [micro]g/dl] would be safe, but Soong found that exposure as low as 25 could cause measurable and irreversible neurological damage, and some believe that measures as low as 10 [micro]g/dl] might be cause for concern. Lead poisoning is preventable by vigilant monitoring of lead levels in children's blood.

Genetic

Physicians have known for some time that chromosomal abnormalities can cause cognitive difficulties (ex: Down Syndrome). However, intense genetic research such as that done with the Human Genome Project is uncovering more genetic causes for mental retardation.

Bower (1999) reports of a recent finding in Great Britain of a new genetic difference recently discovered. It involves a subtle rearrangement at the ends of some chromosomes. The researchers at Radcliffe College in Oxford, England, found that this genetic difference could explain 40% of the cases of mental retardation for which they previously could find no cause. They believe it to be the second most common cause for low cognitive abilities after Down Syndrome. They found that this genetic pattern was familial and involved unusally short strands of DNA. All the children had parents of normal IQ.

Another genetic cause of retardation is Rett Syndrome. It is the most common cause of retardation in females, but does not typically occur among multiple family members. Its signs can first be spotted by 18 months old because it affects skills that develop at that age - speech and eye-hand skills (Bake,1999).

Fragile X Syndrome occurs in about 1 out of 2,000 to 4.000 births (Eliez, 2000). It includes physical as well as mental characteristics, and is markedly different than the form of retardation recently described in England because it is marked by unusually long DNA strands. The components are arranged incorrectly causing the strand to curve incorrectly. How this chromosomal difference translates into impaired function and physical abnormalities is not known at this time. In addition to cognitive weaknesses, these children often exhibit somewhat autistic behaviors.

Fragile X: Fragile X syndrome is a common form of mental retardation with an estimated incidence of 1 per 2,000 to 4,000 in the general population. The physical manifestations associated with the syndrome include macroorchidism, large ears, a prominent jaw, moderate to severe mental retardation, and autistic-like behavior. (Eliez, 2000) Eliez reports that cognitive difficulties include "... executive, visual-spatial, and visual motor abilities, behavioral symptoms of autism, attention deficit hyperactivity disorder, and social anxiety: Morphological variations of brain structure have been observed in this population and include abnormalities in the cerebellar vermis, caudate, hippocampus, and lateral ventricles." (Eliez, 2000) Only mothers can pass on Fragile X.

Williams Syndrome is considerably more rare than Fragile X or Rett Syndrome, occurring in about 1 in 20,000 births (Osborne, 2001). It includes mild mental retardation (typical IQ's are 55-60), shortened stature, various physical differences (very often including serious cardiac complications, and an exceptionally friendly personality (Osborne, 2001). It is caused by a deficit on chromosome 7. Osborne reports a variety of neurological difficulties including "hyperreactivity, sensory integration dysfunction, delayed expressive and receptive language skills, and multiple developmental motor disabilities affecting balance, strength, coordination, and motor planning" (Osborne, 2001). Many of the children have anxiety disorders such as phobias not common in such friendly children.