We’ve been doing kinesiology at New Leaf Natural Therapies for 20 years. LEAP is an integrative approach to supporting better brain function – for moods, stress, survival patterns, learning problems, damaging behaviours, anxiety, suicidal thoughts…
LEAP®: The Learning Enhancement Acupressure Program: Correcting
Learning and Memory Problems with Acupressure and Kinesiology.
By Dr. Charles T. Krebs
ABSTRACT:
The Learning Enhancement Acupressure Program, or LEAP®, has been developed since 1985 inconjunction with clinical psychologists, speech pathologists, neurologists and other health professionals, as a very effective program for the correction of most learning difficulties. LEAP® is based on a new model of learning integrating recent concepts in neurophysiology of the brain and uses highly specific acupressure formatting to address stress within specific brain structures. The application of specific non-invasive acupressure and other energetic techniques can then resolve these stresses resulting in a return to normal function.
In the LEAP® model of learning Gestalt and Logic functions are not simply localised in the right or left cerebral hemisphere as in the popular Right Brain/Left Brain model of learning. But rather, each type of conscious brain function or process appears to have a cerebral “lead” function that is either predominantly Gestalt (Visuo-spatial, Global) or Logic (Linear, Sequential) in nature. These cortical “lead” functions provide a “point of entry” into a widely distributed system comprising many subconscious cortical sub-modules in both hemispheres and many subconscious subcortical modules throughout the limbic system and brainstem.
While the Gestalt and Logic “lead” functions are conscious, these functions are dependent upon many levels of subconscious sensory processing at many levels within the nervous system. While this processing through multiplexing and parallel processing at many different levels is highly efficient, it means that brain processing is “time bound”. Since many components of any mental function are performed in many different parts of the brain, and often at different speeds, coherent output in the form of “thinking” requires integration and synchronisation of all of these separate processes.
Loss of integrated brain function, termed loss of Brain Integration in LEAP®, thus results in the loss of a specific mental capacity, the ability to perform a specific type of mental task. When these specific mental capacities are required for academic performance, their loss can result in Specifi Learning Disabilities.
Specific Learning Disabilities (SLDs) arise in this model by either lack of access to specific subconscious processing modules, either cortical or subcortical, or the de-synchronisation of neural flows in the integrative pathways linking processing modules. Thus to resolve SLDs, you need only “open up” access to the “blocked” processing modules or re-synchronise the timing of information flow between them to re-instate integrated brain function.
The LEAP® program provides an integrated acupressure protocol using direct muscle biofeedback (kinesiology) as a tool to identify “stress” within specific brain nuclei and areas that have “blocked” integrated function. The application of the LEAP® acupressure protocol using acupressure and other energetic based techniques to re-synchronise brain function resolves learning and memory problems in a high percent of cases.
HISTORY OF SPECIFIC LEARNING DIFFICULTIES.
Difficulties with learning academic tasks such as reading, spelling and mathematics have been recognised for over a century, with Kussmaul in 1877 ascribed as the first person to specifically describe an inability to read, that persisted in the presence of intact sight and speech, as word blindness.1 The word dyslexia was coined by Berlin in 1887.2 Within a decade a Glasgow eye surgeon James Hinschelwood (1895) and a Seaford General Practitioner Pringle Morgan (1896) observed students who were incapable of learning to read and hypothesised that this was based on a failure of development of the relevant brain areas which were believed to be absent or abnormal.
This model was based on the assumption that developmental dyslexia (congenital dyslexia) was similar in form to acquired dyslexia, which is dyslexia due to brain damage after a person has already learned to read. Deficits in other types of learning, such as mathematics, would also result from some other underlying brain damage or abnormality.3
Work in the early part of the twentieth century, particularly by Samuel T. Orton in the 1920s and 1930s suggested that learning difficulties such as dyslexia were not based on anatomical absence or abnormality, but rather it was delay in the development of various areas that caused these dysfunctions. This belief was largely ignored until the 1960s when it was revived by a growing interest in neuropsychology. However, more recent developments in neuropsychology and neurophysiology support the hypothesis that dysfunctions within the brain, both anatomical and developmental, may be causal in many learning problems.4
It was not until 1963, in an address given by Samuel Kirk, who argued for better descriptions of children’s school problems that the term “learning disabilities” originated. Since that time there’s been a proliferation of labels that attempt to dissociate the learning disabled from the retarded and brain damaged.
Definitions
In the context of this synopsis, Specific Learning Disorders or Disabilities (SLDs) relates to problems with physical co-ordination and acquiring the academic skills of reading, writing, spelling and mathematics including both Dyslexia and Attention Deficit Disorder (ADD) with or without hyperactivity. ADD with hyperactivity is now commonly called Attention Deficit Hyperactivity Disorder (ADHD) or hyperkinetic disorder in Europe. Historically, Dyslexia has been widely defined in terms of deficits in the areas of reading, spelling and language. However, more recent conceptualisations have included a definition that also encompasses a wide range of problems, including clumsiness and difficulty with rote learning.5 Fawcett and Nicolson have also challenged the prevailing hypothesis that Dyslexia is merely a language based problem, suggesting that it might be a more generalised deficit in the acquisition of skills.6
The term Dyslexia is not defined in the DSM IV (1994) although it is still commonly used in literature discussing various learning difficulties. The term Learning Disorders (DSM IV) currently encompasses various types of learning difficulties including dyslexia and Attention Deficit Disorder (ADD). Learning Disorders are defined in the DSM IV as being essentially a persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than is typically observed in individuals at a comparable level of development. The performance of these individuals on standardised tests for reading, mathematics, or written expression is substantially below, more than 2 standard deviations (SDs), same age peers even though their IQ scores are average or above average.7
Incidence
Frequently, children diagnosed as learning disabled are also inattentive and deficient in linguistic skills, most often in reading.8 Rutter and Yule examined a large population of children from a number of different studies and found 3.5% of Isle of Wight 10-year-olds, 4.5% of 14-year-olds and over 6% of London 10-year-olds showed reading difficulties.9 Gaddes looked at the proportion of children with learning disorders in various studies in both North America and Europe and found that the need for special training for learning disorders ranged between 10-15% of the school age population.10 However, estimates of the prevalence of learning disorders for broad age ranges is problematic because a learning disability is an emergent problem that is often not evident until later years in schooling. Using the criteria of defining learning disorders as being two years behind on standardised tests, less than 1% of 6-year-olds are disabled, 2% of 7-year-olds and so on until at age 19, 25% would be classified as learning disabled. So these children fall progressively behind as they mature and the complexity of work increases.11 In an address given by the Australian Federal Schools Minister, Dr David Kemp, in October 1996, Kemp stated that a study of 28,000 students in four surveys in Australia found 30% of year 9 students lacked basic literacy skills. This high incidence of learning disorders in school children indicates a need for effective treatment. Studies in other countries, both English, French and German support these figures, so specific learning difficulties, which cover all types of learning disabilities from dyslexia, reading problems, ADD to ADHD, probably represent greater than 15% of school-aged children, and may be as high as one third of all school-aged children.
Causes
Currently hypotheses concerning learning disorders suggest that they are primarily the result of one or more of five major factors;
1) structural damage,
2) brain dysfunction,
3) abnormal cerebral lateralisation,
4) maturational lag and
5) environment deprivation.
While none of these theories is unequivocally supported by current data, all of these factors may contribute in varying degrees to learning disabilities.12
Brain damage and overt brain dysfunction would appear to account for a relatively small percentage of children with learning disorders. The great majority of other children with learning disorders do not typically show many of the neurological symptoms associated with brain damage in adults. For instance, EEG and CT studies have not shown structural damage and abnormal EEGs correlated with known brain damage are not consistently observed in children with learning disorders.13 Rather than direct brain damage, there is evidence that abnormal physiological or biochemical processes may be responsible for malfunction in some part of the cerebral cortex.
Electrophysiological recording studies have associated specific high frequency EEG and AEP (averaged evoked potentials) abnormalities with various types of learning disorders.14 Recent studies with SSVEP (Steady state visual evoked potential) have shown that children diagnosed with Attention Deficit Disorder demonstrate similar abnormal SSVEP patterns when compared to normal subjects while performing the same cognitive task.15 The brain dysfunction hypothesis suggests that the dysfunction may be a consequence of defective arousal mechanisms resulting in some form of inadequate cerebral activation.16
This is supported by studies of children with learning disorders that show they have difficulty on continuous performance tests requiring attention and low distractibility; had slower reaction times to stimuli, and increased errors due to impulsivity on tests of visual searching.17 Douglas proposed that the deficits on these tasks resulted from inadequate cerebral activation. Learning disorders of some types at least, do improve with drugs like amphetamines that cause cerebral activation via increasing subcortical arousal. In fact this is the basis of treating hyperactive children with Ritalin.18
An alternative model of learning disorders is based on recent neurophysiological findings that suggest it is the timing and synchronisation of neural activity in separate brain areas that creates high order cognitive functions. Any loss or malfunction of the timing mechanism may cause disintegration of neural activity and hence dysfunction in cognitive tasks.19 Clearly, brain dysfunction due to inadequate cerebral activation may indeed lead to disruption of the timing and synchronisation of neural flows, and thus these two hypotheses may just be different aspects of the same process.
This model supports the approach in the Learning Enhancement Advanced Program (LEAP®) that Dr. Krebs developed in the late 1980s early 1990s.20 In the LEAP® Model, Specific Learning Disorders are based on the disruption or loss of timing and synchronisation between the neural activity in the diverse brain regions, both cortical and subcortical, that must be synchronised in order for successful integration to produce normal cognitive activity. Learning disorders would arise in this model from a lack of integration of functions that occur simultaneously in separate brain regions.
If the brain does integrate separate processes into meaningful combinations we call ‘thought’ or cognitive ability, then the main risk is mis-timing or loss of synchronisation between these processes. To quote Damasio “any malfunction of the timing mechanism would be likely to create spurious integration or disintegration”.21 For synchronous firing of neurons in many separate brain areas to create cognitive functions would require maintenance of focused activity at these different sites long enough for meaningful integration of disparate information and decisions to be made.
THE LEAP® MODEL OF LEARNING:
From a review of the major brain structures and the workings of learning and memory in the neurological literature, it is clear that both memory and learning do not involve a single, global hierarchical system in the brain. But rather, learning involves interplay between many inter-linked sub-systems or modules.22 Also, the timing and synchronisation of information flow between these sub-systems and modules appears to be critical to the success of learning and coherent cognitive function.
However, the sub-systems or modules underlying both learning and memory are both conscious and subconscious with most of the early leveling processing being totally subconscious, and only the highest levels of neural processing reaching consciousness. Yet, it is indeed these conscious modules that initiate and direct the processing to be done by the subconscious modules, as both learning and memory require “conscious” effort to occur. This means that the memory and learning processes can be disrupted at both the conscious and subconscious levels, depending upon which neural substrates or integrative pathways are disrupted.
Sensory processing of all types is initially a relatively linear chain of neural impulses originating from a generator potential of the sensory receptor, and following a chain of neurons into the Central Nervous System (CNS) and brain. However, this initially linear stream of nerve impulses, the data of the CNS, rapidly becomes divergent and multiplexed at higher levels of cortical processing.
Conscious perception only arises at the highest levels of these multiplexed data flows as they are reintegrated back into unified conscious perception by the cortical columns directing all conscious brain activity. Thinking and other cognitive abilities rely upon all of the proceeding levels of subconscious sensory processing, which are predominately bilateral initially, but which become progressively asymmetrical and lateralised with increasing levels of conscious awareness. Sensory information is processed initially as neural flows of increasing complexity that generate preverbal images and symbols, but becomes increasingly defined by language in higher level cognitive processes. And language by its very nature is based upon abstract representations of external reality (called words), that follow linear rules (grammar), and word order linked to meaning (syntax). Hence it is predominately sequential and linear in form, which permits analytical evaluation of the thoughts generated following rational rules of Logic. From the perspective of Logic, the world is interpreted as parts that can be constructed into a whole via deductive reasoning.
Sensory and other mental data not suitable for language-based rational processing is processed via visuo-spatial image and symbols that permit global, holistic comprehension of the whole and is inherently non-rational.23 This global, simultaneous, non-rational visuo-spatial processing has been termed Gestalt (German for pattern or form), with the meaning of the whole extracted via inductive reasoning. From the Gestalt perspective, the world is seen as a “whole” with intuitive understanding of the properties of the whole. There is no rational analysis of “Why?”, it just “Is”.
In the LEAP® Model of Learning, it is recognized that most of the lower level linear sensory processing occurs below conscious perception, that is either subcortical, being processed in the brainstem or other brain nuclei like the hypothalamus, thalamus, basal ganglia, etc., or is palaeocortical and limbic. Even the basal levels of cortical processing are largely bilateral and subconscious, and thus occur outside of conscious perception. All higher level cortical processing, which may become conscious, is thus reliant upon maintenance of integrated function and neural flows at these subconscious levels.
However, the more overtly cognitive components of learning rapidly become lateralised with processing dominated by activation of cortical columns, the functional units of the neocortex, in one hemisphere of the brain or the other. In right-handed people, Logic processing typically activates cortical columns in the left hemisphere, that then process the data in a linear analytical way, while activation of cortical columns in the right hemisphere process data in a Gestalt, visuo-spatial way.
Thus, at the highest levels of conscious neural processing underlying cognition and thought, whether that “thought” be verbally based language of Logic, or global intuitively based “knowing” of Gestalt, the neural processing is highly lateralised and is predominately processed in the right or left hemisphere.
The neural substrates for all “conscious” functions therefore are cortical columns of the neocortex (Fig. 1). Conscious activation of a cortical column acts to initiate a cascade of neural flows that rapidly spread to other cortical areas both conscious and subconscious in both hemispheres, and also into many subcortical structures as well. These consciously activated cortical columns initiate either Gestalt or Logic functions depending in which hemisphere they are located.
In LEAP® we term cortical columns activating Logic functions, Logic “lead” functions, and those activating Gestalt functions, Gestalt “lead” functions. These “lead” functions provide points of entry into an inter-linked set of cortical and subcortical modules that then perform our mental functions.
Figure 1. Cortical Columns. Vertical slabs of cortex consisting of all six distinct cell layers, called cortical columns, are the functional units of the cerebral cortex. Some of the cells like the large pyramidal cells have dendrites that extend through almost all layers and axons that exit the gray matter to become part of the white matter tracts carrying information to other parts of the brain and body. There are also innumerable interneurons connecting the cells within each cell layer and between the layers.
Indeed, it was a misunderstanding about the nature of these “lead” functions from which the popular “Right Brain – Left Brain” model of learning and brain function arose. Because damage to specific cortical columns caused loss of specific conscious functions, e.g. the ability to form an image, or figure out certain types of problems or solve certain types of puzzles, it was assumed that the damaged area actually did that specific function. In reality, all that cortical column did was provide a point of entry into these inter-linked sets of cortical and subcortical modules that actually performed the function lost because of the damage to the cortical “lead” function.
An analogy would be damage to the “K” key on your keyboard. Your consciousness is still intact and able to initiate “K” questions, and your computer system is still able to process and answer “K” questions, but the interface to initiate “K” processing in the computer has been damaged. Like wise, if a Gestalt “lead” function is damaged, the process initiated by this “lead” function no longer activates the inter-linked cortical and subcortical functions that are required for this process to occur. Thus, while damage to the area initiating a function, “blocks” the rest of the processing needed to perform the function, the area initiating function never actually ever “did” the function in the first place. To continue this analogy, in most cases it is not overt “damage” to the cortical “lead” function or subcortical brain areas that prevents effective thinking, but rather “blocked” access to these brain areas due to some stressor that is the problem. Thus, much in the same way a “sticky” key blocks fluent typing, “blocked access” to specific brain areas blocks effective thinking and problem-solving.
Synopsis of the LEAP® Model of Learning:
In summary, the LEAP® Model of Learning is based on the following suppositions about the nature and location of neural processing underlying learning and memory:
• Sensory processing initiated by sensory receptors generates initially linear neural flows that rapidly diverge at each successive processing centre (spinal and cranial nerve ganglia, brainstem nuclei, subcortical nuclei, limbic cortices, and finally neocortical columns) into a number of different complex data streams. All processing below the neocortex is subconscious.
• Each processing centre, at each successive level within the spinal cord, brainstem, diencephalon, basal forebrain and cortex elaborates the sensory data, defining some aspect more than another, or adds additional types of information needed to define the sensory data further at the next level of processing. All processing below the neocortex is subconscious.
• At the higher cortical levels, input from many lower levels both cortical and subcortical is integrated to form a conscious perception of the initial sensory experience.
• These higher cortical levels not only integrate processing of the “raw” sensory data, but also include integration of input from memory areas about past experiences with similar sensory stimuli.
• At the highest cortical levels the conscious perceptions formed at lower cortical levels are further processed asymmetrically in either Gestalt or Logic cortical columns, and hence perceived as a visuos-patial pattern or a Gestalt, or abstractly as a verbal word based language or an abstract symbol based mathematical language.
• The very highest levels of conscious processing that underlie our thinking about conscious perceptions, while dependent upon input from all areas of the brain, are generally frontal lobe and particularly involve working memory areas in the Dorsolateral Frontal Cortex.
• A whole set of basal brainstem mechanisms maintain the organism in a state of homeostasis, such that higher level conscious sensory processing can proceed effectively:
These include the Reticular Activating System, the Periventricular Survival System, the Vestibular System and the Sensory-Motor System. Imbalances within or between these systems may disrupt on-going sensory processing and integration at this and higher levels. Processing at this level is totally subconscious.
• The initial “raw” data stream is “sampled” by the Amygdala and other survival centres in the brainstem, and coloured by the survival emotions paired or associated with the sensory stimuli being analyzed, including the physiological responses to these emotions, and is the basis of Conditioned Learning. These primary survival emotions may disrupt on-going sensory processing and integration at this and higher levels. Processing at this level is subconscious.
• When survival emotions of the Fight or Flight response are activated above some “threshold” value, the amygdala and other brainstem structures such as the Periaqueductal Grey Matter of the midbrain inhibit frontal cortical processing, interfering with reasoning and problem-solving. The cause of this loss of higher level conscious cortical processing is a direct consequence of activation of the subconscious primary survival emotions of the Limbic System and Brainstem.
• Secondary processing of the sensory stimuli in the Brainstem, Limbic System and lower cortical levels generates a series of control functions defining the nature of the sensory data stream (e.g. control of pupils in vision) and second-order integration of this sensory data (e.g. movement, shape and location of object in space). Processing at this level is subconscious.
• Further processing in the palaecortical components of the Limbic System (e.g. hippocampus, cingulate, subcallosal and orbitofrontal cortices) generates secondary emotions relative to the sensory data stream and primary emotions already supplied by the amygdala and other brainstem areas via sampling memory of related events. These secondary limbic emotions may disrupt on-going sensory processing and integration at this and higher levels. Processing at this level is largely subconscious.
• Initial cortical processing is predominately bilateral and subconscious, and is dependent upon earlier processing at brainstem and subcortical levels. Emotions, either primary or secondary, may disrupt on-going sensory processing and integration at this and higher levels.
• At some level of cortical processing the sensory data stream emerges into a conscious perception, and is dependent upon earlier processing at brainstem, subcortical, and earlier cortical levels. Emotions, either primary or secondary, may disrupt on-going integration at this and higher levels
• At the highest levels of cortical processing, the processing is largely done in one hemisphere or the other and perceived consciously as a logical, rational thought or a visuospatial Gestalt, and is dependent upon earlier processing at brainstem, subcortical and cortical levels. Emotions, either primary or secondary, may disrupt on-going integration at this level, and any “thinking” dependent upon this level of processing.
• Thinking about the fully processed and integrated sensory experience in the frontal lobes, based upon remembered sensory experiences relevant to the current experience may lead to decisions, which will be represented neurologically by activation of either Logic or Gestalt “lead” functions or both.
• These “lead” functions will then initiate a cascade of neurological flow, which is initially frontal cortical, but rapidly flows into other cortical areas and subcortical structures like the basal ganglia, thalamus, and cerebellum, which in turn feedback to the cortex and each other. Emotions, either primary or secondary, may disrupt on-going processing and integration at any level of this process, and thus overtly affect the final outcome of the cognitive functions taking place.
• Coherent neurological processing at any stage of the above process is dependent upon both uninterrupted flows along integrative pathways and within integrative processing centres. Disruption or de-synchronisation of the timing of these integrative neural flows or disruption or de-synchronisation of processing in any of the integrative centres may result in loss of cognitive function.
• Maintaining integration along all integrative pathways and within all integrative centres produces optimum function, a state called Brain Integration in LEAP.
• Loss of integrated brain function is the principal cause of dysfunction in both mental and physical performance, called Loss of Brain Integration in LEAP.
• The primary mechanism causing Loss of Brain Integration is de-synchronisation and loss of timing of neural flows along integrative pathways and within integrative centres by inhibition or excitation of these pathways and centres by neural flows originating from brainstem and limbic survival related emotions.
• On-going Loss of Brain Integration is often generated by early childhood trauma that creates long-term disruption of Brain Integration as a mechanism of coping.
• Other factors affecting Brain Integration are genetic, structural, organic brain damage, and environmental stressors:
o Structural defects or abnormalities can be of developmental origin, e.g. neuronal migration problems, or result from toxin exposure at specific critical periods of development, e.g. fetal alcohol syndrome. Many cognitive defects have been shown to correlate with abnormalities in brain structure.24
o Organic Brain Damage may result from a head injury, and this damage often results in sclerosis that disrupts neural flows underlying Brain Integration (e.g. hippocampal sclerosis and subsequent epilepsy are often associated with learning disorders).
o Genetic Factors affecting Brain Integration are often genes that code for specific alleles for specific enzymes involved in maintaining normal levels of neurotransmitters or receptors in brain circuits.25 Deficiencies in either neurotransmitters or receptors will compromise Brain Integration, and have behavioural consequences. This is both the basis of much ADHD behaviour and the justification for drug use to ameliorate these behaviours.26
Other genes may code for alleles that affect fatty acid metabolism and utilisation, especially in maintaining neuronal membrane stability and function. This affects predominately physical co-ordination and reading.27
o Diet and nutritional deficiencies may also compromise brain function and result in loss of Brain Integration. Diets rich in fast or junk foods often create marginal nutritional deficiencies that may disrupt brain function, and often contain various preservatives and additives, like the azo-food dye tartrazine, that may cause a total loss of brain integration in sensitive individuals28.
Indeed, the misbehaviour and academic performance of children and young adults have been shown to improve significantly with diet change or nutritional supplementation29, and several recent books have discussed this aspect of behaviour and learning problems30.
o Environmental factors such as electromagnetic fields emitted from man-made electronic equipment and Geopathic stress from distortions in the earth’s electromagnetic fields may affect the brain integration of sensitive individuals and result in learning problems. 31
Loss of Brain Integration and Compensation
When Brain Integration is lost via disruption of the most efficient neural pathways and/or centres, either by organic damage or by functional inhibition of cortical or subcortical functions due to outputs from survival centres in the brain, specific conscious functions dependent upon this integration is also disrupted. The overt loss of conscious function is, however, often far less than the degree of interference with underlying functions might suggest because the brain is a master at compensation and will automatically compensate for these disrupted flows by using other areas of the brain, both conscious and subconscious to produce the most efficient processing possible.
Thus, even children with considerable organic brain damage will often establish compensatory neurological patterns of activity to produce varying levels of function in spite of massive disruption of neural pathways underlying normal function, e.g. children with cerebral palsy may learn to walk and talk. It is indeed this tremendous compensatory capacity of the brain that allows even highly disintegrated brains to produce some degree of function, however, the level of dysfunction controls the degree of compensation. Thus, the greater the degree of dysfunction present, the lesscompensation that is possible.
If the disruption of integrated function is at the more basal levels of integration, the ability to compensate for the resulting dysfunction is much more limited than if the loss of integration is at a higher level of processing because all higher levels of processing are dependent upon the quality of the data integrated at earlier levels of processing. For instance, while damage to an early component of vision, say the retina or optic nerve totally disrupts sight, damage and hence loss of integration in the V3 area of the occipital cortex may leave the image fully intact, but disrupt only colour vision.
When the highest levels of cortical integration are disrupted directly or lower level cortical or subcortical functions underlying these higher cortical functions are disrupted, we may lose the capacity to “think” in certain ways. For instance, we may maintain Gestalt creative abilities (e.g. be good at art and design), but lose the ability to perform even simple mathematics because of the loss of the ability to abstract (e.g. are hopeless at maths). Specific Learning Disorders result from the loss of integration in of higher-level cortical functions or lower-level subconscious cortical or subcortical functions supporting these higher-level functions directly activated by consciousness.
Children and adults suffering Specific Learning Disorders usually know what they need to do, often even how to do it (e.g. I want to spell this word, so I need to sequence the letters and remember this sequence). But they just cannot activate the necessary subcortical and cortical processing to do what they know how and want to do consciously because of loss of integration at some level of neural processing required to do this function. When this loss of Brain Integration affects their ability to read, spell, write or do mathematics, it results in SLDs. However, they will still attempt to perform these functions, but in some compensated way. For instance, a child that cannot spell words correctly (that is, visually in English), still attempts to spell words, but using phonetics to compensate for the “mind’s eye” image he/she cannot create.
Because the level at which the integration is disrupted is unknown to the consciousness and compensation is largely subconscious and automatic, a person with Specific Learning Disorders is only aware that some function is difficult or not possible to perform, but not why this is so. Most often Brain Integration is lost in subconscious functions that were never accessible to our consciousness in the first place.
