movement, unintentionally performs a similar body movement or alters the way that a body movement is performed. automatic imitation rarely involves overt execution of matching responses. instead the effects typically consist of reaction time, rather than accuracy, differences between compatible and incompatible trials. research reveals that the existence of automatic imitation, which is a covert form of imitation, is distinct from spatial compatibility. it also indicates that, although automatic imitation is subject to input modulation by attentional processes, and output modulation by inhibitory processes, it is mediated by learned, long-term sensorimotor associations that cannot be altered directly by intentional processes. many researchers believe that automatic imitation is mediated by the mirror neuron system. additionally, there are data that demonstrate that our postural control is impaired when people listen to sentences about other actions. for example, if the task is to maintain posture, people do it worse when they listen to sentences like this: "i get up, put on my slippers, go to the bathroom." this phenomenon may be due to the fact that during action perception there is similar motor cortex activation as if a human being performed the same action (mirror neurons system). motor mimicry in contrast with automatic imitation, motor mimicry is observed in (1) naturalistic social situations and (2) via measures of action frequency within a session rather than measures of speed and/or accuracy within trials. the integration of research on motor mimicry and automatic imitation could reveal plausible indications that these phenomena depend on the same psychological and neural processes. preliminary evidence however comes from studies showing that social priming has similar effects on motor mimicry. nevertheless, the similarities between automatic imitation, mirror effects, and motor mimicry have led some researchers to propose that automatic imitation is mediated by the mirror neuron system and that it is a tightly controlled laboratory equivalent of the motor mimicry observed in naturalistic social contexts. if true, then automatic imitation can be used as a tool to investigate how the mirror neuron system contributes to cognitive functioning and how motor mimicry promotes prosocial attitudes and behavior. meta-analysis of imitation studies in humans suggest that there is enough evidence of mirror system activation during imitation that mirror neuron involvement is likely, even though no published studies have recorded the activities of singular neurons. however, it is likely insufficient for motor imitation. studies show that regions of the frontal and parietal lobes that extend beyond the classical mirror system are equally activated during imitation. this suggests that other areas, along with the mirror system are crucial to imitation behaviors. autism it has also been proposed that problems with the mirror neuron system may underlie cognitive disorders, particularly autism. however the connection between mirror neuron dysfunction and autism is tentative and it remains to be demonstrated how mirror neurons are related to many of the important characteristics of autism. some researchers claim there is a link between mirror neuron deficiency and autism. eeg recordings from motor areas are suppressed when someone watches another person move, a signal that may relate to mirror neuron system. this suppression was less in children with autism. although these findings have been replicated by several groups, other studies have not found evidence of a dysfunctional mirror neuron system in autism. in 2008, oberman et al. published a research paper that presented conflicting eeg evidence. oberman and ramachandran found typical mu-suppression for familiar stimuli, but not for unfamiliar stimuli, leading them to conclude that the mirror neuron system of children with asd (autism spectrum disorder) was functional, but less sensitive than that of typical children. based on the conflicting evidence presented by mu-wave suppression experiments, patricia churchland has cautioned that mu-wave suppression results cannot be used as a valid index for measuring the performance of mirror neuron systems. recent research indicates that mirror neurons do not play a role in autism: ...no clear cut evidence emerges for a fundamental mirror system deficit in autism. behavioural studies have shown that people with autism have a good understanding of action goals. furthermore, two independent neuroimaging studies have reported that the parietal component of the mirror system is functioning typically in individuals with autism. some anatomical differences have been found in the mirror neuron related brain areas in adults with autism spectrum disorders, compared to non-autistic adults. all these cortical areas were thinner and the degree of thinning was correlated with autism symptom severity, a correlation nearly restricted to these brain regions. based on these results, some researchers claim that autism is caused by impairments in the mirror neuron system, leading to disabilities in social skills, imitation, empathy and theory of mind. many researchers have pointed out that the "broken mirrors" theory of autism is overly simplistic, and mirror neurons alone cannot explain the differences found in individuals with autism. first of all, as noted above, none of these studies were direct measures of mirror neuron activity - in other words fmri activity or eeg rhythm suppression do not unequivocally index mirror neurons. dinstein and colleagues found normal mirror neuron activity in people with autism using fmri. in individuals with autism, deficits in intention understanding, action understanding and biological motion perception (the key functions of mirror neurons) are not always found, or are task dependent. today, very few people believe an all-or-nothing problem with the mirror system can underlie autism. instead, "additional research needs to be done, and more caution should be used when reaching out to the media." research from 2010 concluded that autistic individuals do not exhibit mirror neuron dysfunction, although the small sample size limits the extent to which these results can be generalized. more recent research has still found no neurological evidence to support this “broken-mirror theory” of autism. theory of mind in philosophy of mind, mirror neurons have become the primary rallying call of simulation theorists concerning our "theory of mind." "theory of mind" refers to our ability to infer another person's mental state (i.e., beliefs and desires) from experiences or their behaviour. there are several competing models which attempt to account for our theory of mind; the most notable in relation to mirror neurons is simulation theory. according to simulation theory, theory of mind is available because we subconsciously empathize with the person we're observing and, accounting for relevant differences, imagine what we would desire and believe in that scenario. mirror neurons have been interpreted as the mechanism by which we simulate others in order to better understand them, and therefore their discovery has been taken by some as a validation of simulation theory (which appeared a decade before the discovery of mirror neurons). more recently, theory of mind and simulation have been seen as complementary systems, with different developmental time courses. at the neuronal-level, in a 2015 study by keren haroush and ziv williams using jointly interacting primates performing an iterated prisoner's dilemma game, the authors identified neurons in the anterior cingulate cortex that selectively predicted an opponent's yet unknown decisions or covert state of mind. these "other-predictive neurons" differentiated between self and other decisions and were uniquely sensitive to social context, but they did not encode the opponent's observed actions or receipt of reward. these cingulate cells may therefore importantly complement the function of mirror neurons by providing additional information about other social agents that is not immediately observable or known. sex differences a series of recent studies conducted by yawei cheng, using a variety of neurophysiological measures, including meg, spinal reflex excitability, electroencephalography, have documented the presence of a gender difference in the human mirror neuron system, with female participants exhibiting stronger motor resonance than male participants. in another study, sex-based differences among mirror neuron mechanisms was reinforced in that the data showed enhanced empathetic ability in females relative to males. during an emotional social interaction, females showed a greater ability in emotional perspective taking than did males when interacting with another person face-to-face. however, in the study, data showed that when it came to recognizing the emotions of others, all participants' abilities were very similar and there was no key difference between the male and female subjects. sleep paralysis baland jalal and v. s. ramachandran have hypothesized that the mirror neuron system is important in giving rise to the intruder hallucination and out-of-body experiences during sleep paralysis. according to this theory, sleep paralysis leads to disinhibition of the mirror neuron system, paving the way for hallucinations of human-like shadowy beings. the deafferentation of sensory information during sleep paralysis is proposed as the mechanism for such mirror neuron disinhibition. the authors suggest that their hypothesis on the role of the mirror neuron system could be tested: "these ideas could be explored using neuroimaging, to examine the selective activation of brain regions associated with mirror neuron activity, when the individual is hallucinating an intruder or having an out-of-body experience during sleep paralysis ." mirror neuron function, psychosis, and empathy in schizophrenia recent research, which measured mu-wave suppression, suggests that mirror neuron activity is positively correlated with psychotic symptoms (i.e., greater mu suppression/mirror neuron activity was highest among subjects with the greater severity of psychotic symptoms). researchers concluded that "higher mirror neuron activity may be the underpinning of schizophrenia sensory gating deficits and may contribute to sensory misattributions particularly in response to socially relevant stimuli, and be a putative mechanism for delusions and hallucinations."