Note: I am traveling to Colombia this week attending a neuroscience congress and I won’t be able to answer any comments or emails to this or other posts in an expedited manner.
Back in my college days I had the opportunity to learn about animal behavior when I volunteered to work in several different laboratories with my favorite professors. Although I consider myself an animal lover, I was deeply terrified by some of the caged animals. Baboons, so lovely and peaceful as babies, will rip your fingers if you ever touch their cages. My fear didn’t change much if rather than in cages the animals were free ranging. Near Puerto Rico there is a small island inhabited primarily by monkeys. Researchers from all over the world go there to study their behavior. I just remember that the monkeys would gang up whenever we approached by boat to bring them food. Again, I was markedly afraid that one day my luck would run out and several hundred of them would attack me- which brings me to my subject fear and behavior.
Among the many researchers that went to study the monkeys in that remote island was a man named Arthur Kling. I never met him personally, he was there way before my time. However, he did some of the most important work ever recorded in regards to how lesions in one area of the brain, called the amygdala, affected behavior. He found that lesions of this structure affected sociability (e.g. bonding behaviors) and emotions. In regards to the latter, some lesioned monkeys not only seemingly lacked fear but also showed an inability to read emotions in other animals. Thus a low ranking animal would be oblivious to the threatening gestures of an alpha monkey and end up being frequently beaten. Given the constant abuse, these monkeys would run away from the colony and even suicide! Furthermore, many of the symptoms would depend on the age at which the monkey was lesioned, the gender of the animal, and whether it occurred while in a caged or free ranging environment. Many of these observations served to sustain the opinion that this brain structure was substantially impaired in psychiatric conditions such as schizophrenia or autism.
Indeed, some pioneering microscopic studies by Bauman and Kemper’s suggested reduced neuronal size and increased density in the amygdala and other structures of the so-called limbic system of autistic individuals. However, using an optical fractionator, Stereoinvestigator software, and a detailed description of anatomical guidelines to define subdivisions of the human amygdala, Schumann and Amaral were unable to corroborate the presence of decreased neuronal size or increased cell packing density in autism. A difference between the series of Schuman and Amaral and that of Bauman and Kemper was the exclusion in the former of individuals with seizures.
Almost half a century ago, Penfield and Perot recorded the experiences of epilepsy patients during electrical stimulation of certain parts of their brains. The images thus elicited were so vivid that they considered them to be memory traces of past experiences. According to this theory, the images elicited would be the enagram that was closest to the stimulating electrode. Most commonly, patients during stimulation would relate hearing or watching another person’s actions and speech. It is intriguing that of all the possible responses, some were seldom elicited. These included experiences in which the patient himself or herself was engaged in speaking, thinking, or performing some skilled behavior]. At present, some investigators consider that the phenomenon described by Penfield and Perot did not reflect the recall of past experiences but instead represented vivid experiences that were dependent on the preexisting personality, cognitive state, and expectation of the patients.
Results of behavioral studies in monkeys after complete amygdalectomy have varied depending on the age, sex, and postoperative testing environment. Surgically operated adult and juvenile male monkeys exhibited a fall through the social hierarchy and a diminution in their aggressive behavior. Occasionally, some of the lesioned monkeys were subjected to an increased number of attacks by normal members of the colony. Contrary to these observations, amygdalectomized adult female monkeys occasionally increased their aggressive behavior and rose in social rank. Maternal behavior was never seen in lesioned females; rather, they abused and/or neglected their infants. Operated juveniles presented still a different behavioral conduct consisting of heightened oral and sexual activity, whereas infants with similar lesions displayed a grossly normal interaction with their mothers. It may be worth adding that lesioned infants later (at 2–3 years of age, or roughly at the onset of puberty) exhibited aberrant behavior. The absence of early symptomatology in these brain-injured infants was attributed to the immaturity of the central nervous system and the strong mother–infant bond that can be established despite the lack of reinforcement by the young. After release to their natural environment, amygdalectomized adult animals failed to resocialize and never re-entered their troop. Although tame in a cage situation, when they were free, they did not allow experimenters to recapture them. According to Kling, the social drift in these operated animals seems related to entorhinal cortex damage, whereas abnormalities in sexual behavior (part of the Klüver-Bucy syndrome) were the result of lesions in the lateral nuclei of the amygdala. Partial ablation of the amygdala with sparing of the uncal cortex decreased aggressive behavior while simultaneously allowing for resocialization, albeit at a lower social rank. It is therefore unsurprising that organic processes such as encephalitides, cerebrovascular accidents, tumors, and head injury leading to damage of these structures may present with schizophreniform symptoms. Topographical analysis of these abnormalities indicates that the incidence of psychosis is highest for those lesions of presumed developmental origin lying toward the medial aspects of the temporal lobes (i.e, the entorhinal cortex).