Optics: eye examining – vision testing and correcting – Eye examining or testing instrument – Eye exercising or training type
Reexamination Certificate
1999-09-27
2002-09-03
Manuel, George (Department: 3737)
Optics: eye examining, vision testing and correcting
Eye examining or testing instrument
Eye exercising or training type
Reexamination Certificate
active
06443572
ABSTRACT:
FIELD OF THE INVENTION
The present invention relates to a method and device for the treatment of conditions such as Dyslexia.
BACKGROUND OF THE INVENTION
Dyslexia is a term used to denote a condition of reduced ability to read and write, in the presence of adequate intelligence, conventional instruction and sociocultural opportunity and without any opthalmoscopically detectable retinal abnormality. A proportion of those with this condition also display an inability to listen in the absence of any impairment in their hearing.
The several manifestations of this condition have been encapsulated in the term ‘Dyslexia’, derived from the Greek ‘dys’—meaning difficult, and ‘lexis’—meaning words. A common expression describes ‘Dyslexia’ as ‘word blindness.’
The condition was first noticed in the 1860's in some patients who had suffered a brain injury. It was later uncovered that the condition was more typically present without brain injury and in far greater numbers than expected.
Some estimates suggest that Dyslexia is present in about fifteen percent of the World population to some degree.
For the untrained person, Dyslexia is difficult to detect. Teachers unskilled in the identification of Dyslexia may misdiagnose children to be lazy, forgetful, inattentive and unintelligent. For this reason, the British Dyslexia Association refers to Dyslexia as the ‘hidden handicap’ because the condition is not obvious to all but the trained.
Chronic academic under achievement, sporting ineptitude and an apparent bumbling nature conspire to form an ingrained loss of self-esteem for the youthful Dyslexic. Later for some, this may develop into anti-social behaviour. Others become suicidal. For all, it is often a lifetime of unjust treatment and a failure to reach potential as an individual.
Although it is difficult to quantify, it is clear that a condition as elusive, pervasive and pernicious as Dyslexia must impose heavy social and economic costs. The British Dyslexia Association says that “Dyslexia cannot be prevented or cured, but by teaching appropriate skills and strategies necessary for learning and life, the problems it causes in and out of school can be eased.”Despite an appellation suggestive of visual disorder, Dyslexia became most often attributed to auditory causes. Hence remediations of the past commonly employed methods and inventions that were based upon phonetic techniques. Some clinics to the current date still are based on the assumption of auditory causes.
In recent years, more searching diagnostic techniques have uncovered differences in the sectors of the brain utilised by Dyslexics for purposes of reading. Dyslexics do not appear to fully use their magnocellular pathways, which had evolved to better process fast moving, low contrast objects.
The frontal lobes of the brain in Dyslexics also revealed a greater activity during reading and writing than in non-Dyslexics.
Autopsies have confirmed that the magnocellular pathways are debilitated in Dyslexics, by revealing smaller, fewer pathway cells, and greater disorganisation in the layers of the visual cortex.
The reaction of those in the profession of treating Dyslexia appears mixed in regard to the scientific findings of a strong visual element to the condition of Dyslexia:
Some, whose treatment was based on an assumption of auditory causes, continued to promote the phonological path as that most preferred. Some, whose treatment was to teach alternative methods of reading that did not depend upon an accurate visual perception of what was written, continued their compensatory approach. Others sought to better utilise the debilitated visual pathways of Dyslexics, by filtering light difficult for these pathways to transmit.
All such treatments for Dyslexia are either essentially palliative in nature or have the objectives of developing compensatory behaviour.
SUMMARY OF THE INVENTION
In accordance with a first aspect of the present invention, there is provided a method for treating Dyslexia in a patient, the method comprising the step employing techniques to achieve a stable fixation of both eyes.
The method may comprise the step of employing techniques to strengthen the magnocellular visual pathways of the patient.
In one embodiment, the method comprises utilising a series of visual image exercises provided so as to achieve the stable fixation and to strengthen the magnocellular visual pathways.
The visual images can comprise one or more series of high frequency striations interposed with a visual work exercise exercising the patient mental faculties.
The visual work exercise can include, for example, one of a puzzle, a drawing or a story.
The visual work exercises are preferably of increasing mental complexity.
In a further modification, the step can further comprise occluding one of the patients eyes during the visual image exercise and/or colour filtering the light transmitted to the patients eyes during the visual image exercise. Preferably a red filter is utilised.
The present invention is different to all known prior treatments for Dyslexia, in that it seeks to address the causes of Dyslexia. The present invention has been developed as a result of extensive observations of those displaying the symptoms of Dyslexia in that they are unable to hold a steady fixation on the fovea. Usually there is a fixation drift in at least one eye. The magnitude of this fixation drift was found to be usually less than that observed for Strabismus or Amblyopia, and again unlike Strabismus and Amblyopia, the fixation was almost always in motion, away from and back again to the fovea, seeming to drift in sympathy with the patient's level of concentration or fatigue.
With the knowledge that a larger fixation error causes the Diplopia of Strabismus or the suppression of one eye in Amblyopia, the inventor has deduced that it is the smaller, constantly moving fixation drift of Dyslexics that causes lack of concentration whether listening to a techer or reading.
This phenomenon may be related to the condition commonly described as ‘word blindness’, which concurs with the numerous descriptions given by Dyslexics themselves when they talk of their affliction in their own words ‘of letters and words disappearing off the page’.
Further, the physical act of reading requires the eyes to scan a stream of symbols varying in fine detail, with speed, accuracy and consistency, and this requires a speed of vision perception for which fully functional magnocellular pathways are essential but are debilitated in Dyslexics.
The resulting method of treatment helps restore functionality to the magnocellular visual pathway systems by forcing them to be utilised in escalating degrees of difficulty.
It is noted here that in the context of this specification it is not intended to limit the present invention to a treatment of Dyslexia only, but rather to the treatment of the particular visual element of Dyslexia, which has been found by the applicants to be the key element of Dyslexia. As such, it will be appreciated by a person skilled in the art that e.g. the treatment of Attention Deficit Disorder (ADD) does also fall within the scope of the present invention where the key element of the condition has been found to be substantially the same visual element as described for Dyslexia hereinbefore.
In that regard, it is further noted that medical terms such as Dyslexia are often interpreted differently by different persons in the medical field, which is a further reason why limitation of the scope of the present invention as per a particular interpretation of the term Dyslexia is not appropriate. Also, the medically same condition may be referred to in praxis by different names in for example different countries.
REFERENCES:
patent: 3955564 (1976-05-01), Lrvinson et al.
patent: 5007838 (1991-04-01), Cochran
Article entitled The magnocellular deficit hypothesis in dyslexia: a review of reported evidence, by J.C. Greatrex and N. Drasdot,Ophthal. Physiol. Opt.,vol. 15, No. 5, pp. 50-1506, 1995.
Fulwider Patton Lee & Utecht LLP
Manuel George
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