Neurolimbic Research Laboratory
Since 1993, I have employed neuroanatomy, histology, Positron Emission Tomography (PET), functional Magnetic Resonance Imaging (fMRI), Diffusion Tensor Imaging (DTI), electroencephalography (EEG), magnetoencephalography (MEG) as well as behavioral methods, including eye-tracking, to study the normal and the diseased brain.
My MD thesis was focused on anatomical studies of the human visual cortex, examining the callosal connections between different visual regions of the human brain. My PhD thesis was devoted to emotion perception in autism.
As a postdoctoral fellow at the Karolinska Institute, Stockholm, Sweden, I used PET to study crossmodal matching between touch and vision, and was able to show for the first time communication between modality specific areas through the claustrum.
In my research at the MGH-Martinos Center, I have been using different methods of brain imaging (fMRI, EEG, MEG) to better characterize the different functional components of our visual system. Using fMRI, I discovered and characterized the area of the brain that is responsible for color vision. Using this extensive base of knowledge of the functional organization of the brain, I extended the scope of my research beyond the visual system, in the broader context of neurological diseases such as brain damage following focal lesions, migraine, and developmental disorders such as autism.
The neurolimbic system is interestingly at the core of these two conditions, namely migraine and autism. In migraine, it is involved in the perception of pain and in the sensitization of the cortex over time, which can lead to the progression from episodic to chronic migraine, and may be connected with some of the co-morbidities associated with migraine, including mood and anxiety disorders; in autism, we know since the pioneering work from Bauman and Kemper (1985) that there are anatomical abnormalities in the amygdala, and dysfuntions of the limbic system are participating to the social and emotional difficulties encountered by individuals with autism.
Migraine is a very common yet poorly understood phenomenon. In about a third of patients, the headache is preceded by a visual phenomenon called the aura. For the first time, our group was able to show that the aura of migraine was a phenomenon similar cortical spreading depression, invalidating the old vascular theory of migraine and opening new perspectives in the treatment of this common and debilitating disorder. This work has been cited more than 1000 times and referenced in a review article in Nature Neuroscience as being “the most thorough investigation of changes in neuronal activity during migraine aura”. Presently, our group is working on extending our understanding of the pathophysiology of migraine, and examining the long-term consequences of this disease on the brain, including in the perception of pain.
is a neurodevelopmental disease that affects one in 64 children. The etiology of this syndrome is still not well understood, and the links between behavioral deficits in autism and their biological substrate are just starting to emerge. Based on my extensive knowledge of the organization of the
visual system, our group was able to demonstrate that "low level" visual
processing is normal in individuals with autism, ruling out a bottom-up deficit.
Moreover, we were the first to provide data disproving a popular theory
stating that individuals with autism are lacking the brain area devoted to face
identification (the “fusiform face area”, or FFA), opening new hypotheses on the etiology of some of the behavioral
aspects of autism potential new therapeutic strategies. Our anatomical and functional studies have demonstrated the presence of abnormalities in the so-called “mirror neuron” areas (which enable us to mimic and mentally simulate the emotions, behavior and movement of others) of young adults with high-functioning autism .These findings suggest a possible deficit that could be addressed with behavioral training. In fact, recent results indicate that imitation training, an activity that will activate the mirroring mechanisms, does significantly improve autistic behavior. On the other hand, we have shown that mirror mechanisms are intact for the perception of pain in ASD, showing that social functions are specifically affected. Our current work is dedicated to understand the neural bases of the deficits of social instinct in ASD, and to develop neural biomarkers that will help to objectify the effect of therapeutic approaches, both behavioral and pharmacological. We are also interested in the neural bases of gaze behavior in ASD.
A couple of years ago, we published a paper showing that contrary to what had been thought, individuals with autism do not lack affective empathy and that their seemingly uncaring behavior stems from personal distress and lack of ability to reappraise when observing pain in others, rather than from an absence of concern.
More recently, we have shown that the reason behind the fact that individuals with autism do not look in the eyes of others is actually due to the fact that they are over-sensitive to eye contact, and that forcing them to look in the eyes provokes hyperactivation of the subcortical face-processing system, including the amygdala.
Emotion perception has been studied using functional imaging for several years, but to date has been concentrated primarily on processes associated with viewing facial expressions. However, from an evolutionary perspective, investigations of expressive body movements may be just as important for understanding the neurobiology of emotional behavior. We published the first functional study on the perception of body expression of emotion in normal subjects, and we are using this new and fascinating model of emotion perception to examine neurodevelopmental disorders and intend to explore this aspect of emotional cognition in autism.
Face perception Neurological syndromes following focal lesions provide
a way to better understand the functional organization of the brain. We have
been using this approach to investigate the network of areas involved in face
recognition. Examining the responses of lesioned brains to stimuli characterized
in normal controls can cast light on the potential plasticity and help identify
appropriate strategies to adopt for rehabilitation.
Face perceptionis already present at birth, supported to the subcortical system, and develops over time, together with the social brain, making typical people 'face experts'. Because we are so good at detecting faces, we can be subject to pareidolia, this phenomenon where we perceive faces in random patterns, including in objects. Toddlers with autism seem to have abnormal orientation towards face-like objects, pointing to a possible abnormal tuning of the subcortical system.
Neurological syndromes following focal lesions provide a way to better understand the functional organization of the brain. We have been using this approach to investigate the network of areas involved in face recognition. Examining the responses of lesioned brains to stimuli characterized in normal controls can cast light on the potential plasticity and help identify appropriate strategies to adopt for rehabilitation.