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Mind-blindness is a state where the ToM has not been developed or lost in an individual.
An alternative approach to the social impairment observed in mind-blindness focuses on emotion of subjects.
Some studies have shown that the orbitofrontal cortex is not directly associated with the theory of the mind or mind-blindness.
Disruption of this neural network leads to mind-blindness in schizophrenic individuals.
Mind-blindness can be described as a cognitive disorder where an individual is unable to attribute mental states to the self and other.
People with schizophrenia also show deficits associated with mind-blindness.
They could even understand that because of that mind-blindness, human society had different imperatives from those of their own.
Another clue towards a possible explanation of mind-blindness in autism was done by Castelli and colleagues.
A study by Bowler concluded that mind-blindness and social impairment is not as straightforward as previously thought.
Conversely the absence or impairment of the ToM that leads to mind-blindness does not lead to social impairments.
These are considered important regions for the activation of the ToM regions and are associated with the mind-blindness.
However it is still debated whether the inactivation of the medial frontal lobe is involved in mind-blindness.
The delay facilitates mind-blindness.
Brain lesion studies show that there are differences seen in the laterality of brain that account for mind-blindness.
Mind-blindness is associated with autism and Asperger's syndrome (AS) patients who tend to show deficits in social insight.
Mind-blindness is usually associated with patients with pervasive developmental disorders such as autism and Asperger's Syndrome.
Many have also pointed out that Mind-blindness wrongly categorizes autism as a problem to be fixed, rather than a condition to be accommodated.
Prof Baron-Cohen defines autism as a kind of mind-blindness in which the brain cannot deal with unexpected changes – and human behaviour can be very unpredictable.
In patients suffering from semantic dementia, the temporal regions of these patients undergo atrophy and lead to certain deficits which can cause mind-blindness.
The cells of the ACC develops at the age of 4 months suggesting that the manifestations of mind-blindness may occur around this time.
It is suspected that the damage to the orbitofrontal cortex brings upon subtle impairments, but not a total loss of the ToM that would to mind-blindness.
However there is an ongoing debate as to whether individuals with schizophrenia have an impaired ToM leading to mind-blindness or display an exaggerated ToM.
There is some evidence that suggests that certain patients develop a rudimentary ToM and do not suffer from complete lack of ToM causing mind-blindness.
Furthermore Frith has predicted that the extent of mind-blindness depends on whether the objective/behavioural or subjective symptoms of ToM abilities prevail.
The cognitive impairment linked to mind-blindness is best explained by a modular theory; the domain specific capabilities that account for mindreading and mentalization are lost in schizophrenia.