Steinberg calls attention to the work of Dr. J. Douglas Bremner who does research on Post-traumatic Stress Disorder (PTSD). In an on-line article Bremner writes: “Recent studies have shown that victims of childhood abuse and combat veterans actually experience physical changes to the hippocampus, a part of the brain involved in learning and memory, as well as in the handling of stress. The hippocampus also works closely with the medial prefrontal cortex, an area of the brain that regulates our emotional response to fear and stress. PTSD sufferers often have impairments in one or both of these brain regions. Studies of children have found that these impairments can lead to problems with learning and academic achievement.” Bremner goes on to say: “Memory problems play a large part in PTSD.” He explains that PTSD patients report deficits in declarative memory, such as being able to remember facts or lists, fragmentation of memory, and dissociative amnesia, which involves gaps in memory lasting from minutes to days.
To see video from a PBS special on epigenetics, link to NOVA Science Now.
An expert on the brain…Richard M. Restak explains that “Fibers from all four lobes, along with association fibers uniting these separate connections into one unified experience, converge into the hippocampal region.” Restak writes: “Thanks to extensive two-way connections, with other brain areas the hippocampus and its immediate connecting structures integrate and coordinate both our outer- and inner-world experiences into a unity.” The hippocampi and other structures—such as the amygdalae—that process and integrate stimuli provide input to the autonomic nervous system (ANS; see ANS—the autonomic nervous system). So one can experience all the autonomic consequences of fear at the mere memory of a traumatic event.
If attachment is hard wired in animals including humans, then one must ask what happens if circumstances disrupt attachment? The result, I think, can often be described as frustration. And although there are a wide range of etiologies for the onset of depression and obsessive-compulsive symptoms, I contend that frustration or chronic stress related to attachment issues can sometimes cause depression and initiate or otherwise kindle existing or latent OCD symptoms. Frustration can, I think, activate and potentiate atavistic fixed-action patterns encoded in the animal brain, turning such patterns into dangerous stereotypies.
What we often fail to realize is that the same animal brain circuitry that generates stereotyped behavior in animals under stressful conditions can also generate stereotyped behavior in humans under stressful conditions. Human stressors exacerbate ADHD, OCD, PTSD, Tourette syndrome, and compulsive grooming symptoms. In Why Zebras Don’t Get Ulcers: The Acclaimed Guide to Stress, Stress-Related Diseases, and Coping (2004), Robert M. Sapolsky writes: “When it comes to what makes for psychological stress, a lack of predictability and control are at the top of the list of things you want to avoid.”
In Affective Neuroscience, Panksepp explains that “with excessive DA [dopamine] activity, animals begin to exhibit repetitive behavior patterns known as stereotypies; with low NE [norepinephrine] activity, they tend to perseverate on a task despite changes in stimulus contingencies (presumably because of attentional deficits).” Panksepp cites research to conclude: “Existing evidence suggests that NE promotes sensory arousal, while DA promotes motor arousal. As we would expect from such functional considerations, NE terminals are concentrated in sensory projection areas of the cortex, while DA terminals are more prominent in motor areas.”
In regard to human illnesses such as OCD and ADHD, then, I think it may therefore be appropriate to say that excessive dopamine often drives compulsions whereas inadequate norepinephrine and/or inadequate dopamine often drives perseveration.
Researchers have suggested that high levels of dopamine transporters are associated with ADHD. During some of my research on dopamine, I found a 2006 report titled “High Dopamine Transporter Levels Not Correlated with ADHD.” The U.S. Department of Energy’s Brookhaven National Laboratory, in collaboration with Mount Sinai School of Medicine in New York, produced the report. Researchers used positron emission tomography (PET) technology to study dopamine transporters in the brain. PET scan images such as the ones below (link to source) show that patients in the study with ADHD had lower levels of dopamine transporters in the nucleus accumbens when compared to control subjects.
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