DEFINITION
A disorder characterized by marked impairments in social interaction and communication accompanied by a pattern of repetitive, stereotyped behaviors and activities. Developmental delays in social interaction and language surface prior to age 3 years.
NCI Thesaurus, 2012
ANATOMY OF THE HUMAN MIRROR SYSTEM
In humans the observation of goal-directed motor-acts activates, besides visual areas, the inferior parietal lobule (IPL) and the premotor cortex, mostly its ventral part, plus the caudal part of the inferior frontal gyrus (IFG) roughly corresponding to the pars opercularis of Broca’s area. These two regions form the core of the human parieto-frontal mirror system.
MIRROR NEURONS HYPOTHESIS
Cognitive symptoms:
Understanding the intentions of others is a major deficiency of '* Autism * characterized by the complete absence of relationship with other people. It has been recently demonstrated that in many cases of autism there is a deficit of the mirror neuron system.
Currently autism is defined as a disorder that generally affects the brain function, for which the person suffering from this disease show a marked decrease of the capacity of social integration and communication. Attempts to description of the disease dates back to 1940. Since then, researchers have developed several theories about the cause, but have not yet been possible to identify them uniquely. The recent discovery in the nineties of the century just ended, a group of motor neurons with sensitive peculiarity also called mirror neurons, has opened new horizons in research and therapy even in field of autism. Autism affects 5-20 people per 10,000 population. It is a multiform disorder: each individual is a universe in itself, has very particular characteristics, both in skills possessed, as in deficit. The 50% of subjects with autism is not able to communicate verbally, and those capable of using the language speak in many occasions in a bizarre manner. The echolalia, which is the involuntary repetition of words heard, and once quite common in individuals with autism, can be immediate or deferred. Autistic spectrum disorder ( ASD) is a heterogeneous syndrome characterized by impairment in social skills, verbal and non verbal communication, coupled with restricted, and repetitive behaviors (DSM-IV-TR 2000). Deficits in the domains of affective links and emotional behavior are other aspects of ASD.
Mirror neurons studies:
Autism affects a variety of nervous structures, from the cerebral cortex to the cerebellum and braistem. However, in the context of a broader neurodevelopmental deficit a set of ASD symptoms (impairment in communication, language, and the capacity to understand others) appears to match functions mediated by the mirror mechanism. The hypothesis that this specific set of deficits might depend on an impairment of the mirror mechanism has therefore been advanced. Additional evidence for an impaired mirror mechanism in autism came from behavioral and Transcranic Magnetic Stimulation (TMS) studies . Avikainen et al showed that , unlike TD individuals, who, when viewing persons face-to-face, tend to imitate them in a mirror way, children with autism do not show this preference. This imitation peculiarity is most likely due to a deficit of mirror mechanism coding other person’s movements on one’s own. It was demonstrated an impaired motor facilitation in children with autism during action observation by using TMS.
Taken together, this data indicate that children with autism process the actions done by others in a manner different from that of TD children. The simplest way to account for these differences is to postulate that children with ASD have an impairment of the mirror mechanism. This hypothesis is also known as the “broken mirror” hypothesis.
Specchi infranti, una teoria sull'autismo, 2006
In the winter of 1991, Giacomo Rizzolatti sent to Nature a report on a surprising set of neurons that he and other authors had found in the ventral premotor cortex of the monkey. The fundamental characteristic of these neurons was that discharged both when the monkey performed a certain motor act ( e.g; grasping an object) and when it observed another individual ( monkey or human) performing that or a similar motor act. These neurons are known as mirror neurons.
Mirror neurons and their clinical relevance
Some F5 neurons discharged not when the monkey looked at the food, but when the experimenter grasped it.
In 1996 were published two articles which first reported the existence of the mirror areas in humans. The rational of the experiment was as follows: if mirror mechanism exists in humans the observation of actions done by another individual should activate, besides visual areas, also areas that have motor properties.
Mirror neurons: from discovery to autism 2009
h3.PATHOPHYSIOLOGY
Autism is a multifactorial disease of hereditary basis.
We will consider the biochemical mechanisms involved in the correlation of mirror neurons with the disease.
Some studies converge on the possibility that mirror neurons used primarily dopamine as a neurotransmitter and is involved in the phenomenon of cognitive associations.
The dopamine binds to metabotropic receptors, G protein-coupled which determine an increase (D1) or a decrease (D2) of cAMP, expressed mainly in the SNC. These receptors are implicated in many neurological processes: motivation, pleasure, cognition, memory, spatial memory, emotions, learning, fine motor control and modulation of neuroendocrine signal. One of the most important function of transduction molecules in the control of behavior. The multiple roles are a reflection of the different structure of dopamine receptors (labeled D1 to D7) and the particular density in brain areas. The drugs are dopamine antagonists used as antipsychotic, while agonists act as psychostimulants.
During the Autism Conference in Las Vegas in July 1994, the dr.Luke Y.Tsai did a report on neurotransmitters and psychopharmacology in autism. In addition to identify different neurotransmitters, neuroscientists have also found problems related to them, then in the presence of too many or too few neurotransmitters.
Too much dopamine in the limbic system of the brain (the center of emotions), and too little in the cortex (the seat of reason), it can cause suspicion and inability to process information at a normal pace of social interactions.
The sequence of gratifications includes the release of serotonin, which in turn stimulates the enkephalin which in turn inhibits the GABA in the substantia nigra, which in turn tunes the amount of DA. It is known that under normal circumstances the DA works to maintain our normal function. In fact, the DA has been called the pleasure molecule or antistress molecule.
As a result, a decrease in D2 receptors causes the individual is subject to compulsive behaviors, impulsive, autism, antisocial behavior.
Managing Vital Neurotransmitters in Autism 2008
TREATMENT
The discovery of the deficit in mirror neurons in people with autism opens new avenues for the diagnosis and treatment of disease.
A therapeutic strategy could be based on the correction of biochemical imbalances that disable the mirror neurons.
The partial loss of “empathogen” neurotransmitters would explain the lack of emotional empathy found in autism, so you should use compounds that stimulate the release of neurotransmitters, or they simulate the effects on mirror neurons. One possible candidate is the MDMA, better known as ecstasy, which has been shown to promote emotional closeness and communication. Researchers should be able to change the mixture developing a safe and effective therapy that is able to alleviate at least some of the symptoms of autism.
Unfortunately, treatment of this type may result in only partial relief, because other symptoms (repetitive movements, rocking back and forth, avoiding eye contact, hypersensitivity and aversion to certain sounds) are not explained by the hypothesis of mirror neurons.
VALLERO MARIA ELENA, SCARAFIA CARLOTTA
