Wednesday, May 30, 2012

Neurological Mechanisms for Visual Distortions/Perceptions

Spanish researcher Jose Caravaca has been working on a "distortion" theory with regards to individual close encounters with the UFO phenomena.  Mr. Caravaca has shown that external agents (stimuli?) may be an important component of the perceived experience.  The external factors that could influence the experience could range from food ingested prior to the experience to what the individual read or saw (books, magazines, advertisement, radio, television).  What appears to still be elusive is a (the) trigger mechanism.

Before a trigger mechanism(s) can be identified, I believe that looking at neurological mechanisms, from a physiological and pathological point of view, could be beneficial.  Studying cognitive models based on neurological deficits brought about by pathological issues such as neuro-disorders and illnesses can be of help as certain disorders precipitate various states of visual distortion or illusionary misidentification - delusional misidentification.

This is not to imply that all individuals that have experienced what is perceived as a UFO close encounter (visual or abduction) have neurological/psychiatric disorders.  To the contrary, most of these individuals are psychologically healthy and fully functional in our society.  It's the mechanism of perception in the healthy individual that is of interests.

In my line of work (inpatient psychiatric care), I deal with a good percentage of patients that have various forms of dementia (Alzheimer's, Frontal Temporal, Lewy-body, vascular, etc.).  Most, if not all, experience a form of agnosia, that is, they demonstrate the loss of ability to recognize objects, persons, sounds, shapes or smells, yet the specific senses remain intact.  In certain cases, agnosia may be present without any appreciable memory loss.

Agnosia is generally associated with brain injury and neurological illness effecting the brain's occipital - temporal border (ventral stream).  Of interest for this discussion is associative agnosia which the individual can describe visual scenes and objects but still fail to recognize them.  A good example would be attempting to describe a fork versus that of a spoon.

A few months back, I had an 83 year old female patient who consistently mistook me for a long ago (50 years past) friend.  When out in the day room, she was agitated and restless, often yelling out obscenities worried that her parents would be upset that she was not home.  Yet, alone with me in her room her entire demeanor changed.  The hospital room now became her apartment in the North end of Boston back in the late 1940s.  Her mannerisms and speech content was that of someone living back in that time period.  I was "transformed", in her image, to that of a long lost suitor.  Despite her perceptions, I had no personal history with her and we were in San Diego, California.  Yet, the setting was how she visually perceived it.

With  progressive cognitive and functional impairment, executive functioning is degraded.  The individual lacks to ability to appropriately be attentive to his/her's environment.  Planning, judgment, abstract thinking and semantic memory are degraded or totally absent. In reviewing the various memory models.  Short term memory is unable to be consolidated into long term memory.  This consolidation pathway is effectively severed. In using my "pathological" model in an attempt to define Jose Caravaca's external distortion agent, could the "severed" memory pathway provide clues?

In healthy individuals, complex visual information binds with present memories and stored emotional attributes that produce stable and real images of the world.  What of the individual that presents with agnosia?  Stable and real images tend to be distorted in an altered perception of reality.  And what of the stored emotional attributes?  Agnosia could be linked to a dysfunction of the limbic area. (J. Neurospsychiatry and Clinical Neurosciences, 2008)

The limbic system is the part of the brain (sub-cortical) that is sometimes referred to as the "emotional" brain.  It's major components are the Amygdala, Hippocampus, Hypothalamus, and Thalamus.  Since the limbic system deals with the formulation of our various emotions, how does this have any relevance to agnosia or visual distortions?  Perhaps the functions of the amygdala can shed some light.

The amygdala tends to link sensory experiences into emotional relevance.  What happens when the amygdala is damaged or destroyed?  Hayman, et al, looked at amygdala dysfunction caused by Kluver-Bucy Syndrome (KBS). (Hayman, et al, 1998)   KBS is a cluster of behavior changes linked to bilateral amygdala ablation (destruction).  It can be caused secondary to herpes encephalitis, head trauma, hypoxia and various central nervous system diseases.  KBS interupts visual input to the limbic system.  In animal studies, bilateral lesions in the amygdala caused visual agnosia.  In human studies, removal of the amygdala caused dysfunctional facial recognition.  Lesions in the temporal cortex and superior temporal polysensory area mimic the deficits after amygdala ablation.  Hayman believed this to implicate the two cerebral regions supplying the amygdala with information that identifies objects in visual context.

Hayman and his fellow researchers provided a case study to support their hypothesis.  The case study involved a 40-plus year old male diagnosed with liver cancer.  Prior to initiating chemotherapy, the patient's low blood serum sodium was rapidly treated over a 48 hour period.  After chemotherapy, the patient became severely cognitively impaired with symptoms consistent with KBS, he was not able to recognize his wife and son, attempted to eat a plastic cup.  He was unable to identify the use of a comb, simply referring to the comb as a "saw."  There was no evidence to support chemotoxicity.  MRI scans showed that the neurological issues were caused by lesions involving the amygdala and temporal lobe connections.  There was further evidence showing involvement of the Hippocampus and parahippocampus area.  Were the lesions a result of the patient's liver cancer spreading to the brain?  Oddly there was no indication that cancer had invaded the brain.  Hayman found that the neurons in the affected components of the amygdala and hippocampus showed demyelinization of the myelin sheath.  This was caused by the overly aggressive treatment of the patient's low sodium levels causing a condition know as myelinolysis - the destruction of the neuron's myelin sheath which protects nerve cell axons.  With no functional axon, then there is no way to release the various neurotransmitters needed to activate a pathway to the next neuron, thus a needed connectivity pathway is effectively severed. 

Does this mean that an over abundance of sodium in our bodies, even for a short duration of time can possibly illicit visual distortions momentarily disrupting amygdala functions?  By using extreme cases of neurological disorders, illnesses, and syndromes, I've shown what areas and components of the brain are identified with visual distortions and perceptions.  Perhaps a component of Jose Caravaca's Distortion Theory is a variation of agnosia.  In my next post, I'll look at the relationship of the neurotransmitter dopamine and the amygdala.

The reader may be wondering (I would) what this all means concerning perceived UFO close encounters and abductions.  I used a neuro-pathological model to identify mechanisms.  The question that I pose is this:  In a healthy individual, can visual distortions manifest due to abrupt and brief physiological stimuli (anxiety and stress) evoking a brief psychological response, and does this involve the brain's limbic system - amygdala?  My next posting will explore that question.


"A Squint of Brain:  A Capgras Syndrome Variant", Journal of Neuropsychiatry and Clinical Neurosciences, December 9, 2008.

Hayman et al:  Kluver-Bucy Syndrome After Bilateral Selective Damages of the Amygdala and its Cortical Connections, Journal of Neuropsychiatry and Clinical Neurosciences, August 1, 1998.

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