Definition of a Learning Dysfunction
©1987, revised January 1996
Barbara Arrowsmith Young, January 1996
Definitions of learning disabilities state that the cause of a specific learning disability is known or suspected to be the result of a problem in the central nervous system (ACLD 1986 definition, Interagency Committee on Learning Disabilities 1987 definition, National Joint Committee on Learning Disabilities 1987 definition). Hammill, on reviewing the eight most widely used definitions of learning disabilities, found that seven referred to central nervous system dysfunction as the source of the learning disability. Mercer et. al. found that 64% of the 50 states used the concept of neurological impairment in their definition of a learning disability. Reiff et. al., on asking 57 learning disabled adults to define the term learning disability, found that “many of these individuals felt or believed that their problems with learning… were caused by some processing dysfunction in the brain” (p. 124).
The nature of this neurological impairment and its functional relationship to specific mental and behavioral processes has been defined less clearly. The purpose of this paper is to describe the relationship between a neurological impairment and a learning disability based on research originating from neuroscience and the research of Arrowsmith School. Before describing this relationship, it is necessary to state a neuroscientific model of how the brain works.
It has been established that the human cerebral cortex is made up of brain areas that are distinctly different from one another based on their cellular makeup or cytoarchitecture (Brodmann, 1909 cited in Luria, 1980 p. 37). According to Brodmann’s analysis, which is most widely used, there are 52 different brain areas (Pansky et. al., 1988, p. 204).
Each of these brain areas has its own particular or characteristic function. For example, area 6 in the left hemisphere, the premotor region, is responsible for the conversion of individual motor impulses into a smoothly and consecutively organized skilled movement. Skilled movement consists of a series of consecutive links between motor impulses requiring smooth changes from one link of the series to another. As Luria (1973) describes it, “Individual motor impulses are synthesized and combined into ‘kinetic melodies’ when a single impulse is sufficient to activate a complete dynamic stereotype of automatically changing elements” (p.176). Writing out the alphabet would be one such kinetic melody. The smooth, automatized performance of an arithmetic procedure requiring the use of a complex sequential chain of elements is another such kinetic melody. The fluent, smooth and automatic switching in speech expression from one element to another which allows for the unfolding of the dynamic structure of the whole speech expression also involves kinetic melodies. This brain area contributes its own characteristic form of mental activity or operation to each of the higher mental processes that it is involved in (e.g., writing, arithmetic, speaking).
Complex mental and behavioral processes (e.g., speaking, reading, writing, playing chess, skiing, etc.) “…may exist only as a result of interaction between highly differentiated brain structures [referred to as brain areas in this paper] and that individually these structures make their own specific contributions to the dynamic whole and play their own roles in the functional system” (Vygotskii, 1960 pp. 375 – 393 cited in Luria, 1980 pp. 34). A functional system, according to Luria (1966, 1970a, 1970b, 1973,1980), is a group of brain areas working together to carry out a specific higher mental process to which each component brain area makes its own particular contribution according to its own individual characteristic of mental functioning or activity. Individual brain areas may be components of different functional systems and take part in different higher mental processes. For example, as described in the preceding paragraph, the premotor region is involved in the processes of writing, arithmetic and speaking. Thus, each brain area concerned in a specific functional system introduces its own particular contribution which is essential to the normal performance of that functional system.
In order to illustrate the concept of a functional system Luria (1980) describes the higher mental process of writing from dictation:
It follows that the act of writing cannot by any means be regarded as the result of the activity of any one “center;” its performance requires a complete system of interconnected but highly differentiated cortical zones. The performance of the act of writing is conditional on the integrity of the primary and, in particular, of the secondary fields of the auditory cortex of the left temporal region, which together with the inferior portion of the postcentral (kinesthetic) and premotor portions of the cortex takes part in the phonematic analysis and integration of speech. Another essential requirement is integrity of the visual-kinesthetic areas of the cortex, without which recoding of the phonematic structure into a system of graphemes, with maintenance of the topological characteristics and spatial coordinates, is impossible. Integrity of the kinesthetic and motor (postcentral and premotor) portions of the cortex is also essential for normal writing activity, i.e., for the recoding of graphic schemes into smooth kinetic “melodies” of motor acts…. It can therefore be stated with justification that normal writing can be carried out only if a highly complex group of cortical zones remains intact (p. 80).
Lassen et. al. confirmed the proposition that higher mental processes involve specific functional systems comprised of particular groups of brain areas working together by measuring the changes in blood flow to specific brain areas when a person was engaged in different tasks. An increase in blood flow directly relates to an increase in cortical activity. These researchers stated, “The analysis of cortical activation during reading illustrates that a complex task is carried out by several circumscribed cortical regions brought into action in a specific pattern. …. In general our results confirm a conclusion reached by the late A. R. Luria of Moscow State University on the basis of his neuropsychological analyses of patients with brain damage: ‘Complex behavioral processes are in fact not localized but are distributed in the brain, and the contribution of each cortical zone to the entire functional system is very specific'” (p. 70).
What happens then if one or more brain areas suffer traumatic damage? The bulk of Luria’s work was in studying the characteristic way in which various functional systems were disturbed by damage to a particular brain area. Luria states, “When a particular factor is incapacitated by a brain lesion, all the complex behavior processes that involve the factor are disturbed and all others remain normal” (p. 72). A problem in any one brain area will affect higher mental processes in a particular way depending on the mental operations or activities carried out by that specific brain area in its contribution to the functional system. Since the same brain area may be a component of several different functional systems “the presence of a primary defect, interfering with the proper function of a given part of the brain, inevitably leads to disturbances of a group of functional systems, i.e., to the appearance of a symptom-complex, or syndrome, composed of externally heterogeneous but, in fact, internally interconnected symptoms” (Luria, 1980, p. 83).
For example, when there is a lesion in Brodmann’s area 6 in the left hemisphere, the premotor zone described earlier in this paper, there is an effect on the functional system involved in the writing process. Luria (1980) says, “Handwriting begins to change; the letters forming whole words begin to be written separately, and subsequently, every stroke forming a grapheme requires a separate effort of will” (p. 220). The individual is no longer capable of executing complex kinetic melodies and the skilled writing movements are replaced by the isolated delineation of individual letters with signs of perseveration (continued writing of the component letters over and over again). Disturbances are found in their writing “…in which the order of the elements is lost and the smooth transition from one component of a word to another and the retention of the required sequence are impossible, and in which the pathological perseveration of a word once written is clearly apparent, so that these patients cannot write properly” (Luria, 1973, p. 185).
There are also effects on the other functional systems of which Brodmann’s area 6 is a part such as speaking and carrying out arithmetic operations. In speech, there is a loss of fluency and automaticity of expression with frequent stumbling, hesitations, words slipping out incorrectly and fragmentation of speech. Finding an individual word may require a special impulse and part of the dynamic structure of the speech process breaks down. In arithmetic, there is a disturbance of the smooth automatized performance of arithmetic operations. There is a loss of the dynamic schemes of arithmetic procedures. For example, adding breaks down to a simple counting act.
Thus, each of these three functional systems (writing, speaking, and arithmetic) is disturbed in the same characteristic way when there is damage to the premotor zone. Luria (1966) states, “The nucleus of this syndrome is a disturbance of the smooth course of forms of mental activity consisting of a series of consecutive actions or what we may call the higher automatisms” (p.290).
Luria’s neuropsychological investigations demonstrate that mental processes which on the surface seem to have nothing in common are actually related through dependence on a particular brain area. At first glance, performing mathematical operations, understanding logical grammatical structures and naming objects do not appear to have anything in common. yet all of these processes are adversely affected by the same lesion to the parieto-tempero-occipital zone in the left hemisphere. In all cases there is a disturbance in the analysis and understanding of symbolic relationships. “The primary difficulty lies in the integration of details into a single pattern, the recognition of relationships, the unification of individual elements into a single simultaneously- beheld system” ( Luria, 1970b, p. 230). In arithmetic there is a disintegration of the categorical structure of number and of the system of mathematical relationships (e.g., the number one thousand and twenty four could be written as 124 or 1000 24; there would be difficulty differentiating between symmetrical numbers 17 – 71; in adding 17 + 25, it could become 1+7+2+5). There is difficulty in comprehending any construction that involves logical grammatical relationships (e.g., brother’s father and father’s brother; Kate is younger than Mary, but older than Jenny. Who is oldest?). Naming of objects becomes difficult because the system of semantic relationships built up around the word which gives that word its specific meaning have been disrupted. In all cases there is a difficulty in the simultaneous integration of separate symbolic elements into a unified whole and the understanding of their structural relationship.
How then does this knowledge of the specific effects of lesions in particular brain areas on the different functional systems they play a role in help us to understand learning disabilities? It is proposed in this paper that the neurological impairment which is the source of a learning dysfunction is a specific brain area that is weaker in functioning, for whatever reason, than the person’s remaining brain areas such that it significantly impairs the mental activities of the functional systems in which it is involved. The specific nature of the learning dysfunction is dependent upon the characteristic mental activities or operations of the particular brain area that is impaired and will be manifested in all the functional systems of which it is a component.
At Arrowsmith School, we are unable to investigate the brain area per se but can investigate the symptom-complex or syndrome arising out of the hypothesized brain area deficit. The term learning dysfunction is used by this author to denote the specific syndrome arising from the hypothesized brain area deficit as opposed to the more general term learning disability. An individual referred to Arrowsmith School is typically found to have a combination of learning dysfynctions. The specific combination of learning dysfunctions is different for each individual with certain dysfunctions being identified with greater frequency. An individual with five or more specific learning dysfunctions is faced with the difficulty of attempting certain tasks in which not one but several of the mental components involved in the functional systems required for schoolwork are weak or deficient. Clinical investigation has found that an individual with one or two learning dysfunctions is usually able to cope with normal curricular demands although he/she does not achieve up to his/her full intellectual potential. It is argued here that what has been traditionally referred to as a learning disability in the literature is five or more specific learning dysfunctions (weaker mental components) each of which is involved in the functional systems of the mental processes of the brain operating in learning activities at school.
Due to the fact that these learning dysfunctions occur in combinations, and that each separate learning dysfunction has its own specific characteristics which operate in each of the functional systems of higher mental processes of which it is a part, the resulting picture of symptoms from these combined learning dysfunctions operating together could be very confusing. One individual could have the same learning dysfunction as another individual resulting in the same symptoms but then have other learning dysfunctions which were different. An observer looking at these different individuals labelled as learning disabled and trying to understand a common factor could have difficulty.
It is not surprising that a proliferation of different definitions of what a learning disability is exist. Rather than going from a theoretical neuroscientific model of how the brain works to the concept of specific learning dysfunctions which explain the observed symptoms, investigators in the field of learning disabilities frequently have gone from the observed symptoms to build the concept of a learning disability. Thus the descriptive definitions vary according to the symptoms observed. It is argued in this paper that a neuroscientific model provides a useful framework within which to understand learning disabilities.
A research finding by Duffy (cited in McKean ) using a technique called brain electrical mapping, lends support to the hypothesis of deficient or weaker mental components as being the source of learning dysfunctions. It was found that “when compared with normal children, the dyslexic group showed stronger alpha waves (thought to show an inactive brain) in the ‘supplementary motor area.’ This is the part of the brain that helps plan complicated motor activity; it had not previously been implicated in dyslexia.” (p. 33). Lassen et al. from their blood flow analysis study “concluded that the upper premotor cortex, including the Quantification Sense area, is involved in the planning of sequential motor tasks” (p. 69). They found that this area was active in reading silently and aloud, speaking, operating a typewriter and counting numbers inside one’s head. According to Luria’s investigations, this area would also be active during writing. Duffy’s finding that the 13 dyslexics who had difficulty with reading and writing showed less activity in this brain area than nondyslexics is consistent with the research findings of the function of this brain area. Thus it is argued that less activity in this brain area would adversely affect all the functional systems it was a part of (reading, speaking, writing, doing mental mathematics, typing) in its own characteristic way given this brain areas specific form of mental activity.
Arrowsmith School has identified 19 specific learning dysfunctions based on its clinical research. Each of these specific learning dysfunctions is as Luria describes “a symptom-complex, or syndrome, composed of externally heterogeneous but, in fact, internally connected symptoms” (1980, p.83). This list of 19 is only a beginning, a brief description of the many potential learning dysfunctions.
For each of the 19 learning dysfunctions, a parallel can be drawn between the symptom-complex resulting from damage to a specific brain area as described in the neuroscience literature and the symptom-complex identified in Arrowsmith School’s clinical population. For example, there is a parallel between the symptom-complex arising from damage to the left hemisphere premotor zone and the symptom-complex of the motor symbol sequencing dysfunction identified in Arrowsmith School’s research. This learning dysfunction has the same qualitative characteristics of impaired functioning, to a lesser degree of severity, in writing, arithmetic and speech expression as those described by Luria in cases of traumatic brain damage. The same parallel can be drawn between the characteristic functional impairment due to a lesion to the parieto-tempero-occipital region described by Luria and the symbol relations dysfunction identified at Arrowsmith School.
Certain learning dysfunctions have not been commonly considered in the broad category of learning disabilities even though they significantly impair the functional systems they are involved in. The term learning disability has traditionally referred to difficulties in academic performance in school with some acknowledgment that there may be effects in social situations as well. The concept of a learning dysfunction, as proposed in this paper, includes a much wider range of discretely different problems. For example, the spatial reasoning dysfunction identified at Arrowsmith School would not significantly interfere with academic performance but would interfere with everyday life functioning in that the person would frequently get lost and forget where they had left things.
Wells argues that the most critical issues facing the area of research in the field of learning disabilities are those of identification and remediation. This paper argues for the use of a neuroscientific model within which to understand and further investigate the nature of specific learning dysfunctions. It is believed that use of this model will contribute to a more differentiated identification of learning disabilities by breaking them down into their component learning dysfunctions. Further research is necessary in order to be able to clearly identify the various possible learning dysfunctions and the symptom-complexes associated with each. Once the characteristic deficit in the functioning of a mental component responsible for a specific learning dysfunction is fully understood then remediation can be tailor-made to treat that deficit.
Arrowsmith School has been developing and implementing methods to increase the capacity of specific mental components.
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