The Neurobiology of Learning Disabilities

The specific learning disabilities (LD) category, dating back to its origin in the early 1960s, was built on the assumption that central nervous system dysfunction was the underlying cause of why these individuals struggled to achieve at levels commensurate with their peers. More than three decades of testing and classifying, teaching and implementing programs of related services and support has left us with a definition of LD that includes:
 

• at least average intellectual capacity
• a significant (and unexplained) discrepancy between achievement and expected potential
• the exclusion of mental retardation, emotional disturbance, sensory impairment, cultural differences or lack of opportunity to learn
• central nervous system dysfunction as the basis of the presenting problem(s)

While our systems for identifying learning disabilities and for providing instruction and support to these individuals in school and in the workplace have undergone considerable change (for the better) during these years, our understanding of the neurobiology of learning disabilities has lagged behind. This is due, in great part, to the complex nature of the brain, the unique ways that each person processes information, and the ever-changing interrelationship between the brain and a person's experiences in the world.

What We Know and What We Presume 

We know that:

• learning disabilities are a heterogeneous group of disorders that have a negative impact on learning. And LD in reading is the area about which we currently know the most. Dating back to the 1800s, it was shown that variations in brain development (discovered by autopsy) were connected in some way to difficulties in learning to read. Today, using sophisticated brain imaging tools in healthy subjects, we can now say with assurance that a number of regions and structures in the brain are associated with particular skills that support the development of reading. (Drs. Sally & Bennett Shaywitz of Yale University refer to a "neural" signature for phonological processing' characterizing weaknesses evident in dyslexia.)
• learning disabilities are persistent throughout the lifespan and that there is a strong genetic component in the development of these disorders, with rates of reading disabilities in families estimated to be as high as 35-45%. (The Institute for Behavioral Genetics at the University of Colorado is a fine resource for more information about this topic.)
• some learning disabilities are congenital in nature, meaning that they can be traced to biological influences during prenatal gestation; fetal alcohol effects, fetal cocaine exposure, and perhaps even maternal cigarette smoking are examples of these types of contributing factors to LD.
• learning disabilities are both familial and heritable, meaning that they can be caused by both environmental influences and family genetics. This is an important finding because it provides opportunities for early identification of children who are 'at-risk' and even help with the formal identification of LD in adults.

We presume that:

• learning disabilities are the product of neurological "damage" which can occur either during fetal development and/or during the childhood years.
• neurological "glitches" can be structural or functional, and the variations in development and behavior that result are unique to each individual (although patterns of behavior are often seen and can even be predicted and followed over time).
• learning disabilities in adulthood can (often) be traced to neurological conditions in childhood that may or may not have been discovered or understood.

A Word of Caution

In our eagerness to provide help and opportunities for success to individuals with LD, it is often human nature to grab onto preventive measures and treatment approaches that have practical appeal, that "make sense" or that at worst, seem as thought they could do "no harm." Parents and educators often find themselves bombarded with information about purposed cures and treatments including special diets and therapies that "train the brain." In most cases, the treatments being suggested have little or no connection to the etiology (or source) of the problem and few have any real science behind them to demonstrate (or prove) their effectiveness. Keep in mind that:
 

• if it sounds too good to be true, it probably is!
• we should be suspicious of treatments that offer to "cure" LD or that are recommended for a laundry list of different types of problems.
• we shouldn't pay attention to advertisements for products or approaches that promise results using words like "immediate," "complete," "guaranteed" and "remarkable."
• an endorsement by a "doctor" is not sufficient to evaluate the credibility or efficacy of a product or approach.
• learning to overcome the barriers imposed by LD is a life-long and ever-changing process, and one that should not be the cause of isolation or embarrassment; seek information and support at LD.org for reliable sources.