The daily risk for pneumonia decreases with increasing duration of stay in the intensive care unit. Witnessed aspiration and exposure to paralytic agents are potentially modifiable independent risk factors. Exposure to antibiotics was associated with low rates of early ventilator-associated pneumonia, but this effect attenuates over time.

It is widely accepted that autism is associated with disordered emotion processing and, in particular, with deficits of emotional reciprocity such as impaired emotion recognition and reduced empathy. However, a close examination of the literature reveals wide heterogeneity within the autistic population with respect to emotional competence. Here we argue that, where observed, emotional impairments are due to alexithymia—a condition that frequently co-occurs with autism—rather than a feature of autism per se. Alexithymia is a condition characterized by a reduced ability to identify and describe one's own emotion, but which results in reduced empathy and an impaired ability to recognize the emotions of others. We briefly review studies of emotion processing in alexithymia, and in autism, before describing a recent series of studies directly testing this ‘alexithymia hypothesis'. If found to be correct, the alexithymia hypothesis has wide-reaching implications for the study of autism, and how we might best support subgroups of autistic individuals with, and without, accompanying alexithymia. Finally, we note the presence of elevated rates of alexithymia, and inconsistent reports of emotional impairments, in eating disorders, schizophrenia, substance abuse, Parkinson's Disease, multiple sclerosis and anxiety disorders. We speculate that examining the contribution of alexithymia to the emotional symptoms of these disorders may bear fruit in the same way that it is starting to do in autism.

Long abstractThis article argues that mirror neurons originate in sensorimotor associative learning and therefore a new approach is needed to investigate their functions. Mirror neurons were discovered about 20 years ago in the monkey brain, and there is now evidence that they are also present in the human brain. The intriguing feature of many mirror neurons is that they fire not only when the animal is performing an action, such as grasping an object using a power grip, but also when the animal passively observes a similar action performed by another agent. It is widely believed that mirror neurons are a genetic adaptation for action understanding; that they were designed by evolution to fulfill a specific socio-cognitive function. In contrast, we argue that mirror neurons are forged by domain-general processes of associative learning in the course of individual development, and, although they may have psychological functions, they do not necessarily have a specific evolutionary purpose or adaptive function. The evidence supporting this view shows that 1) mirror neurons do not consistently encode action 'goals'; 2) the contingency-and context-sensitive nature of associative learning explains the full range of mirror neuron properties; 3) human infants receive enough sensorimotor experience to support associative learning of mirror neurons ('wealth of the stimulus'); and 4) mirror neurons can be changed in radical ways by sensorimotor training. The associative account implies that reliable information about the function of mirror neurons can be obtained only by research based on developmental history, system-level theory, and careful experimentation. 3 Short abstractMirror neurons have been described as "the neurons that shaped civilization" (Ramachandran, 2009). It is widely assumed that mirror neurons were designed by evolution to enable action understanding. In contrast, we argue that mirror neurons are forged by domain-general processes of associative learning, and do not necessarily have a specific evolutionary purpose or adaptive function. The associative account allows that mirror neurons may have psychological effects or functions. However, it implies that, to get reliable information about the function of mirror neurons, we need a new approach based on developmental history, system-level theory, and careful experimentation. 4Mirror neurons (MNs) were discovered serendipitously in 1992 and given their brilliant name four years later (di Pellegrino, Fadiga, Fogassi, Gallese, & Rizzolatti, 1992;. The striking feature of many MNs is that they fire not only when a monkey is performing an action, such as grasping an object using a power grip, but also when the monkey passively observes a similar action performed by another. Neurons with this capacity to match observed and executed actions, to code both 'my action' and 'your action', were originally found in area F5 of the ventral premotor cortex (PMC) Gallese et al., 1996) and the inferior parietal lobule (IPL) (Bonini et al., 2010;Fogassi et al., 2005) of th...

Considerable research has sought to determine whether face perception is impaired in autism.Clear answers have, however, proved elusive. The present study sought to determine whether comorbid alexithymia (characterized by difficulties interpreting emotional states) may be responsible for face perception deficits previously attributed to autism. Two experiments were conducted to determine the relative contributions of alexithymia and autism to identity and expression recognition using psychophysical procedures. Experiment 1 showed that alexithymia correlates strongly with precision of expression attributions, while autism severity was unrelated to expression recognition ability. Experiment 2 confirmed that alexithymia is not associated with impaired ability to detect expression variation, instead suggesting difficulties interpreting intact sensory descriptions. Neither alexithymia nor autism was associated with biased or imprecise identity attributions. These findings accord with the hypothesis that the 'emotional symptoms' of autism are in fact due to comorbid alexithymia, and that existing diagnostic criteria may need to be revised.3

Alexithymia is a sub-clinical construct, traditionally characterized by difficulties identifying and describing one's own emotions. Despite the clear need for interoception (interpreting physical signals from the body) when identifying one's own emotions, little research has focused on the selectivity of this impairment. While it was originally assumed that the interoceptive deficit in alexithymia is specific to emotion, recent evidence suggests that alexithymia may also be associated with difficulties perceiving some non-affective interoceptive signals, such as one's heart rate. It is therefore possible that the impairment experienced by those with alexithymia is common to all aspects of interoception, such as interpreting signals of hunger, arousal, proprioception, tiredness and temperature. In order to determine whether alexithymia is associated with selectively impaired affective interoception, or general interoceptive impairment, we investigated the association between alexithymia and self-reported non-affective interoceptive ability, and the extent to which individuals perceive similarity between affective and non-affective states (both measured using questionnaires developed for the purpose of the current study), in both typical individuals (n = 105 (89 female), mean age = 27.5 years) and individuals reporting a diagnosis of a psychiatric condition (n = 103 (83 female), mean age = 31.3 years). Findings indicated that alexithymia was associated with poor non-affective interoception and increased perceived similarity between affective and non-affective states, in both the typical and clinical populations. We therefore suggest that rather than being specifically associated with affective impairment, alexithymia is better characterized by a general failure of interoception.