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Abstract
Autism is a developmental disorder of neurobiological origin that is defined on the basis of behavioral and developmental features. Apart from pathological findings in the cerebellum and its connections to other brain areas with the correlation of these finding to the motor deficits in autistic children -as discussed earlier-, other precise neurobiological mechanisms have not yet been established. As yet, known direct links between pathophysiology and different behaviors in autism are still rare and have not yet had great influence on treatments or diagnoses.
Then only since few years ago, few researchers began to investigate motor deficits in autistic children. Some of them claimed that these deficits should be essential in diagnosis.
In the current assay, we put the hypothesis of: A good percentage of autistic children have different motor deficits. So, detection and proper intervention of these deficits may have its implications on the management of autistic patients. An extensive review of literature was done to fulfill our aims.
Recently, many researchers have replicated the findings that: - The cerebellum integrate and combine different movements; and movement sequences, with Climbing fibers (utilize Aspartate) acting to learn the task; Mossy fibers (utilize Glutamate) learning the context; and Parallel fibers (utilize Glutamate) integrating the context with the actual motor activity, and even correcting errors. Cerebellar motor learning was hypothesized to be located at the Parallel fiber contacts with the Purkinje cells (utilize GABA) (Figure 9).
This concept of motor learning and defining the underlying neural systems in ”normally” developed children provides a way for better understanding of neuropathology of motor deficits in ”autism”.
The argument that neuropathological onset of autism: either ”Prenatal i.e. neurodevelopmental” or ”Postnatal i.e. neurodegenerative” raises from the parents report either their child was abnormal from birth; or that their child was developmentally normal until sometime after birth then the child began to regress or deteriorate.
Whatever the hypothesis [”prenatal” or ”postnatal”] is, Purkinje cell loss in autism is one of the most consistent neurological abnormalities found by histopathological post-mortem examination in autistics. Several studies showed that Purkinje cell loss results from insult [”prenatal” &/or ”postnatal” ], and that the Purkinje cells are selectively vulnerable to many factors as ischemia; hypoxia; oxidative stress; viral infections; heavy metals (such as mercury & lead)…etc.
Up-to-date, no specific proved evidence based researches about the exact neurotransmitters involved in the pathology of autism generally and its motor domain specifically. All the available researches are just on the hypothetical level and either contradictory or not yet replicated. The noradrenaline and dopamine system only play a rather secondary role, if any at all, and that the role of the serotonin system is unclear.
Very recently, researchers found that neurotransmitters involved in cerebellar Purkinje cell circuit (which explain mostly pathophysiology of motor deficits in autism) are GABA; Glutamate; and Aspartate. This will cause us to challenge our thinking about following the wrong monoamines track in our researches and psychopharmacological trials which proved inconsistency and lack of their beneficial therapeutic effect (if any at all) on motor deficits of autism specifically and all other core features of autism as well. New researches should tackle these new neuromodulators. This will create a new avenue for developing effective and safe medications for children with autism.
Beginning from 2000s (after the concept of ”Triad of Impairment”), many replicated researches which described the motor problems in autistic children emerged. Some studies reported a range of 30% - 75% of autistic individuals have motor deficits as hypotonia which was the most common reported motor symptom in autism (51%).
Motor apraxia was reported in 34% of autistics and showed a tendency to be more prevalent among younger children as compared with older children. Some researchers emphasized that dyspraxia may be a core feature of autism or a marker of the neurological abnormalities underlying the disorder.
One of the most clinical observations in the field of autism is the ”Diagnostic gap” which is the length of time that passed between when the parents began to suspect that something is wrong in their infant and when the diagnosis of autism is established. This gap ranges from 6 - 41 months. As previously discussed, this gap has many explanations.
Yet, prompt early identification of autism can abolish this gap. In clinical settings, early identification of motor deficits can be applied for early detection and assessment of autism through the early reflex markers which are easy to spot and can serve as ”early detection markers” and the early assessment tools that are specific for motor abilities in children aged 0 – 3 years. They have applicability to young autistic children as ”screening tool” or ”diagnostic tool”.
Motor incoordination in autism has many implications on management. Some of these implications direct to and are connected to the others like a vicious cycle. These implications are summarized as follows:
• More awareness of motor deficits will shed light upon more unidentified early cases (early screening and diagnosing autistics) will definitely increase the prevalence of autistic children referred from schools and community to early interventional programs.
• With the help of implementation of motor deficits detection (which are well-evidence based), significant cost-aversion or cost-avoidance may be possible with early intensive identification and intervention programs.
• Yet, one of the difficulties to implement motor deficits in early identification programs is our current classification systems. Diagnosing autism following the current diagnostic criteria of either ICD-10 or DSM-IV is defective because they pay no attention to motor incoordination symptoms and signs which proved to be essential for diagnosis and as important as other social and communication deficits especially very early where these later deficits are not visible yet.
• The lack of clear neurochemical pathology of autism till now which renders the use of new pharmacotherapy agent to be empirical in its nature. The effects on the core autistic symptoms seem to be indirect and limited in scope and effect size. Unfortunately, there are no studies targeting pharmacological interventions of motor deficits in autism. This give the chance for future researches in the domain of new categories of psychopharmacology directed towards other neurotransmitters such as: - GABA; Aspartate; and Glutamate which are known now to be involved in the process of cerebellar motor learning; control; and development in both healthy and autistic children.
• There is little valid research on intervention techniques specifically targeting the motor symptoms of young children with autistic spectrum disorders. This area is small and has been elucidated only very recently. Still, the few published studies added a lot of fruitful implications on the management of autism in the literature.
• With early motor intervention programs, a good percentage of those children were no longer in the autistic spectrum. They could attend regular classrooms without special assistance.
• Several studies have reported positive outcomes for children enrolled in motor intervention programs between the ages of 2 - 4 years.
• Although, until now there is no structured motor rehabilitative programs for autistic children with motor difficulties, autism researchers who specialize in early intervention have the ability to recognize clues to the syndrome in high-risk babies as young as 3 or 4 months. By initiating intensive physical therapy with infants and their parents, therapists hope to prevent a diagnosis of actual autism at 2 or 3 years”.
• ”Brain development is most dynamic (plastic) in the first year of life …….. When you work with infants, you can start to see change not in days but in hours”.
• Physical medicine professionals can establish motor intervention approaches which make the child be able to perform certain movement patterns with appropriate timing; sequencing; and control.
• There are many approaches of motor rehabilitation for motor deficits in autistics. They promote basic motor skills as: body awareness; motor planning; bilateral motor integration; balance skills; gait training; and fine motor coordination.
• These movement programs based on ”motor learning theory” by taking advantage of the plasticity of neuronal centers to initiate
re-organization of neural networks to generate locomotion and re-shaping of the brain development.
• In other words, neural plasticity is the sole of early intervention in autism.