Asperger Syndrome is an Autism Spectrum Disorder (or Pervasive Developmental Disorder) characterized by significant difficulties in social interaction along with restricted and repetitive patterns of behaviors and interests. Those with Asperger Syndrome, or AS, may exhibit a lack of empathy for their peers, clumsiness, and atypical use of language, though none of these symptoms are required for a diagnosis.1
The pain of coming to terms with having Asperger's is still very real for me right now. There is a tremendous sense of grief. Grief for all that I suffered through to try to be "normal" and grief for how short of "normal" I always have been. There is also great relief to know that I am not crazy and that not everything can be traced back to an abusive past in the sense that some of what I experience is not choice/emotional but neurons/physical. The greatest challenge I face right now is trying to figure out which is which. This is not easy.
One of the most common side effects of a number of antidepressant medications is loss of sex drive. I could forgive our friends at fine companies such as Eli Lilly, Bristol Meyers Squibb, and Pfizer if dry mouth, irritability, disrupted sleep patterns, loss of appetite, sloth, and social phobia were the sole issues related to the medications I take on a daily basis. However, it is the sex thing I find most challenging.
Anhedonia is the technical term for the inability to experience joy. When people are in the depths of depression, nothing touches them, not the most intensely pleasurable activities, not the most familiar comforts. They are emotionally frozen. In this state, people either have to get professional help or simply wait for weeks or months until the depression lifts by itself; nothing is going to make them feel better.
Schizophrenia is a mental illness which affects one person in every hundred.
Depression is perhaps the most common of all mental health problems, currently felt to affect one in every four adults to some degree. Depression is a problem with mood/feeling in which the mood is described as sad, feeling down in the dumps, being blue, or feeling low. While the depressed mood is present, evidence is also present which reflects the neurochemical or "brain chemistry" aspects of depression with the depressed individual experiencing poor concentration/attention, loss of energy, accelerated thought/worry, sleep/appetite disturbance, and other physical manifestations. When this diagnosis is present, the individual will exhibit at least five of the following symptoms during the depressive periods:
In the last few years, there has been a revolution in the study of emotions. Our emotions — love, fear, anger, desire — give coloration and meaning to everything in life. Our emotions are indispensable whenever we choose to pursue one goal and not another. The derangement of emotions is what leads to the profound pain and much of the disability experienced in mental illness. The emotions were once thought to reside in the heart, but scientists know now that they originate in the brain.
Scientists have learned to use neuroimaging to see the living, thinking, feeling human brain at work. Neuroimaging tools include functional magnetic resonance imaging (fMRI), which uses magnetic fields and radio waves to elicit signals from the brain, and positron emission tomography (PET), which uses low doses of a radioactive tracer to obtain signals from the brain. Both of these technologies have been designed to reveal signals that correlate with human brain activity. These approaches have been used to study the pathways in the brain involved in sensory processes such as vision, and in a variety of cognitive processes.
Slice 24=forward part of amygdala; Slice 25=backpart of amygdala. Image is viewed as though the person is looking out from the page, so the left amygdala is on the right of the picture. More intense colors show greater activation. 2
We are now at the dawn of an era when we can use these technologies to see pathways in the brain that underlie emotions such as fear and desire. In the near future, these approaches will allow us to see precise abnormalities in brain pathways that produce mental illness.
Fear is the emotion that has been most successfully studied. Fear is required for our survival, but when it is not regulated, it becomes responsible for anxiety disorders and some of the symptoms of depression. We have learned that fear depends on very specific circuits in the brain. In fact, the way that the brain processes emotion is no different from the way it processes vision or voluntary movements, which also rely on their own specific circuitry.
The emotion of fear relies on pathways that involve a structure deep in our brains called the amygdala. The details of this circuitry have been worked out in rat models; however, a series of studies that began in 1996 and have become increasingly sophisticated have demonstrated that showing a fearful face to a normal subject while scanning his/her brain permits us to see activation of the amygdala and associated brain pathways. 1,2,3,4 Subsequent experiments have shown that if humans learn a connection between a neutral signal and something noxious, like a loud buzzing sound, we actually can observe the brain in the act of storing information about the signal that predicts danger.5,6,7 We can see that the brain processes information about threat and fear even when the person is not concentrating on it and may not even consciously remember seeing the danger signal.
Although this research is still in its early phase, success to date in delineating specific fear pathways has encouraged the investigations of emotional pathways in mental illness. We are finding out, for example, whether phobias hitchhike on the same pathways used by normal fear. Soon we will have information about other emotions and conditions such as depression. Over time, these tools will be used to study the effects of medications and psychological therapies on mental illness.
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NIH Publication No. 01-4601
1 Morris J, Frith C, Perrett D, et al. A differential neural response in the human amygdala to fearful and happy facial expressions. Nature, 1996; 383(6603): 812-15.
2 Breiter H, Etcoff N, Whalen P, et al. Response and habituation of the human amygdala during visual processing of facial expression. Neuron, 1996; 17(5): 875-87.
3 Whalen P, Rauch S, Etcoff N, et al. Masked presentations of emotional facial expressions modulate amygdala activity without explicit knowledge. Journal of Neuroscience, 1998; 18(1): 411-18.
4 Hariri A, Bookheimer S, Mazziotta J. Modulating emotional responses: effects of a neocortical network on the limbic system. Neuroreport, 2000; 11(1): 43-8.
5 Buechel C, Dolan R. Classical fear conditioning in functional neuroimaging. Current Opinion in Neurobiology, 2000; 10(2): 219-23.
6 LaBar K, Gatenby J, Gore J, et al. Human amygdala activation during conditioned fear acquisition and extinction: a mixed-trial fMRI study. Neuron, 1998; 20(5): 937-45.
7 Morris J, Ohman A, Dolan R. Conscious and unconscious emotional learning in the human amygdala. Nature, 1998; 393(6684): 467-70.
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