Sham rage

Sham rage is behavior such as biting, clawing, hissing, arching the back and "violent alternating limb movements" produced in animal experiments by removing the cerebral cortex.[1] This behavior is reversed with small lesions in hypothalamus.[2]

The term was in use by Walter Bradford Cannon and Sydney William Britton as early as 1925.[3] Cannon and Britton were doing research on emotional expression resulting from action of subcortical areas. Cats had their neocortices removed but still displayed characteristics of extreme anger resulting from mild stimuli.[4]

Symptoms

The physiological symptoms of sham rage include rise in blood sugar, pulse, respiratory rates, and blood pressure.[5] These symptoms can occur spontaneously and may also be evoked by sensory stimulations.[6] In some cases animals have suffered several convulsive attacks followed by withdrawal of sodium barbital. It has been concluded that the cerebral cortex may play a facilitating part in this type of convulsive process.[7] These physiological effects happen alongside the rage-like symptoms of hissing, clawing, biting, etc.

Causes

There are only a few known causes of sham rage in animals. Most of the experiments done on animals have been done on cats, dogs and rats. The actual symptoms of sham rage are normal anger and defense reactions in animals. It becomes sham rage only when this rage reaction is triggered by unthreatening stimuli. A study by Bard (1934) showed that the removal of the neocortex in cats and dogs produced sham rage. The behavior of each animal was observed before the surgery was performed, noting how calm and friendly the animal was with humans and other animals, as well as their reactions to being handled. After the surgery, Bard observed that the animals would have an extreme rage reaction to stimuli that had previously produced little to no response, like touching the tail. He concluded the reason for this might be that the removal of the neocortex causes a loss of inhibition of the areas involved in the rage reaction, causing those areas to become hyperactive.[8]

A study by Reis and Gunne (1965) found that electrically stimulating the amygdala of cats caused sham rage, which resulted in a decrease in the presence of adrenaline and noradrenaline. They believed this was because the excited defense reaction known as sham rage caused such a huge increase in the release of the neurotransmitters that the brain could not resynthesize noradrenaline fast enough to keep up.[9] Reis and Fuxe (1969) then did a study of cats that went into a sham rage after having a brainstem transection. The purpose was to determine the relationship between the decrease in norepinephrine in sham rage and the magnitude of the sham rage behavior. They found that a more extreme sham rage was correlated with lower levels of norepinephrine. They also found that when they gave these cats protriptyline, which facilitates the actions of norepinephrine, their symptoms got worse and when they gave them haloperidol, which inhibits the functions of norepinephrine, their symptoms were less severe. They concluded that this meant the release of norepinephrine is necessary for sham rage behavior.[10]

Prevalence in Humans

In some cases, human sham rage appears to be caused by "uninhibited hypothalamic discharge"[11] even though the hypothalamus is not considered to be the center of emotion in the brain. Two known causes of this hypothalamic discharge are carbon monoxide poisoning and insulin hypoglycemia. While experiencing sham rage, the human body will show both internal and external signs of physical distress. Bouts of sham rage are never intentional in humans, but the body will show "changes in the internal organs and in the composition of the blood similar to those characteristic of human emotional behavior".[12] Although a person will express emotion during moments of sham rage, it does not indicate that the individual is actually feeling that emotion. Stimuli encountered by a human during an outburst can cause physical reactions such as pupil dilation, exophthalmos, increased pulse rate, an increase in systolic pressure, and widening of the palpebral fissures.[13]

References

  1. ↑ Reis DJ, Fuxe K (September 1969). "Brain norepinephrine: evidence that neuronal release is essential for sham rage behavior following brainstem transection in cat". Proc. Natl. Acad. Sci. U.S.A. 64 (1): 108–12. doi:10.1073/pnas.64.1.108. PMC 286133. PMID 5262991.
  2. ↑ Savard G, Bhanji NH, Dubeau F, Andermann F, Sadikot A (December 2003). "Psychiatric aspects of patients with hypothalamic hamartoma and epilepsy". Epileptic Disord 5 (4): 229–34. PMID 14975791.
  3. ↑ Cannon, Walter B; Britton, Sydney William (1 April 1925). "Studies on the conditions of activity in endocrine glands: XV. Pseudaffective medulliadrenal secretion". Am J Physiol 72 (2): 283–94.
  4. ↑ Cannon, W.B.; S.W. Britton (1925). "Pseudoaffective medulliadrenal secretion". American Journal of Psychology 72: 283.
  5. ↑ Kennard, Margaret A.; C.W. Hampel, M. Dorrit Willner (16 October 1946). "Effect of Frontal Lobectomy on Blood Sugars of Normal Cats and Monkeys and Adrenal Denervated Cats". Departments of Anatomy, Psychiatry and Psysiology, New York College of Medicine: 246.
  6. ↑ Dow, Robert S. (1958). The Physiology and Pathology of the Cerebellum. Minneapolis: University of Minnesota. p. 295.
  7. ↑ Kasamatsu, Takuji; John D. Pettigrew (1979). "Preservation of Binocularity after Monocular Deprivation in the Striate Cortex of Kittens Treated with 6-Hydroxydopamine". Discussion of Biology: 216–276.
  8. ↑ Bard, P.P. (1934). "On emotional expression after decortication with some remarks on certain theoretical views: Part II". Psychological Review. 5 41: 424–449. doi:10.1037/h0071731.
  9. ↑ Reis, Donald J.; Kjell Fuxe (Sep 15, 1969). "Proceedings of the National Academy of Sciences of the United States of America". 1 64. pp. 108–112.
  10. ↑ Reis, Donald J.; Lars-Magnus Gunne (23 July 1965). "Science". New Series. 3682 149: 450–451.
  11. ↑ Wortis, Herman (1 March 1942). ""Sham Rage" in Man". Am J Psychiatry 98 (5): 638–644.
  12. ↑ Campbell, Robert Jean (2009). Campbell's psychiatric dictionary. New York: Oxford University Press.
  13. ↑ Campbell, Robert Jean (2009). Campbell's Psychiatric Dictionary. New York: Oxford University Press.

Further reading