Genes on chromosomes 6 and 15 may play some role with SLDs as they have linked to poorer reading, poorer spelling and lower phonemic awareness. Diagnosis
Unlike specific learning disabilities and neurodevelopmental disorders that have been more extensively studied, there is no gold standard for diagnosing dysgraphia. This is likely due to writing systems often differing substantially between countries and languages and there being considerable heterogeneity among the therapists who are charged with diagnosing dysgraphia. Consequently, there are several tests that are used to diagnose dysgraphia like Ajuriaguerra scale, BHK for children or teenagers, the Minnesota Handwriting Assessment, ETCH, SCRIPT, DASH and HHE scale.With devices like drawing tablets, it is now possible to measure the position, tilt, and pressure in real time. From these features, it is possible to compute automatic features like speed and shaking and train a classifier to diagnose automatically children with atypical writing. The features extracted have different importances in the classification through development and allow to characterize different subtypes of dysgraphia that could have different origins, outcomes and could require different remediation strategies.It is not uncommon for dysgraphic individuals to be intellectually gifted, possess a rich vocabulary and have strong comprehension of language when speaking or reading, though their disorder is often not detected or treated; which may also be in part to developmental dyslexia receiving far more academic and medical attention than developmental dysgraphia. In addition, gifted children with transcription disabilities seldom receive programming for their intellectual talents due to their difficulties in completing written assignments.
Thus, it may be necessary to diagnose AON after a period of observation, noting the problem is not behaving as expected for demyelinative disease. Pathogenesis
Approximately 1-2% of patients with defined SLE develop an optic neuropathy during the course of their disease. SLE-associated optic neuritis is rarely the presenting sign of the disease. The molecular pathogenesis is hypothesized, based on clinical features and the emerging understanding of mechanisms in SLE. Inflammation resulting from auto-antibodies, immune complexes, T-cells and complement, probably damages the components of the optic nerve, as well as the blood vessels (vasculitis). The resulting vasculitis causes a loss of blood supply to the nerve (ischemia). This combination of inflammation and ischemia may produce reversible changes such as demyelination alone, or more permanent damage axonal (necrosis), or a combination. The poor recovery of vision in AON despite anti-inflammatory treatment suggests that ischemia from the underlying vasculitis is an important component, but the details have not been established. It may be reasonable to consider that AON pathogenesis represents an incomplete expression of the SLE-associated optic neuropathy disease process. Diagnosis
Treatment
AON is a rare disease and the natural history of the disease process is not well defined. Unlike typical optic neuritis, there is no association with multiple sclerosis, but the visual prognosis for AON is worse than typical optic neuritis. Thus AON patients have different treatment, and often receive chronic immunosuppression. No formal recommendation can be made regarding the best therapeutic approach.