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, which are claimed to occur in the absence of any sort of inner experience of rage.[1] These behavioral changes are reversed with small lesions in hypothalamus.[2]

The term sham rage was in use by Walter Bradford Cannon and Sydney William Britton as early as 1925.[3] Cannon and Britton did 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] The concept has been rejected by many affective neuroscientists on the grounds that nonhuman animals displaying rage behaviors do indeed experience rage. This is the view of Jaak Panksepp, for example,[5][6] who was among the first to describe the neural generators of rage.[6][7]

Symptoms

The physiological symptoms of sham rage include rise in blood sugar, pulse, respiratory rates, and blood pressure.[8] These symptoms can occur spontaneously and may also be evoked by sensory stimulations.[9] 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.[10] 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.[11]

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.[12] 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.[13]

Prevalence in humans

In some cases, human sham rage appears to be caused by "uninhibited hypothalamic discharge".[14] This is not surprising, as the role of the hypothalamus in generating the internal experience of rage has been mapped in rats, cats, and humans.[15] Three known causes of hypothalamic discharge are depolarization of the hypothalamus via electrode stimulation,[16][17] 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".[18] Although a person will express emotion during moments of sham rage, it does not indicate that the individual is actually feeling that emotion. However, there is no reason to suspect that the individual is not actually feeling the emotion, and the concept of sham rage, i.e., the expression of rage behaviors during increased activation in the hypothalamus in the absence of the internal experience of rage, is likely a false concept, and an artifact of the politics of the period of science during which the concept was created.[5] 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.[18]

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. Bibcode:1969PNAS...64..108R. 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" (PDF). 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. doi:10.1152/ajplegacy.1925.72.2.283.
  4. Cannon, W.B.; S.W. Britton (1925). "Pseudoaffective medulliadrenal secretion". American Journal of Psychology. 72: 283.
  5. Panksepp, Jaak (2005). "Affective consciousness: Core emotional feelings in animals and humans". Consciousness and Cognition. 14 (1): 30–80. doi:10.1016/j.concog.2004.10.004. PMID 15766890. Many still prefer to envision these systems as psychologically vacuous "output" components. The matter was well presented by Walter Hess (1957, p.23), who received the Nobel prize for his work on brain stimulation induced autonomic and behavioral changes in cats from the hypothalamus, including the first descriptions of brain stimulation induced anger responses. In considering such subcortical brain functions, including the rage facilitated by decortication, he noted that "American investigators label this condition sham rage. In our opinion, the behavior that we find manifested here should be interpreted as true rage, and its appearance is aided by the suppression of inhibitions that go out from the cortex" Because of behavioristic anti-mind biases, this reasonable perspective never became a mainstream hypothesis on the Anglo-American scene, and there is little discussion of the varieties of affective states in animals among behavioral neuroscientists to this day.
  6. Panksepp, Jaak (1982). "Toward a general psychobiological theory of emotions". Behavioral and Brain Sciences. 5 (3): 407–422. doi:10.1017/s0140525x00012759.
  7. Panksepp, J; Zellner, MR (2004). "Towards a neurobiologically based unified theory of aggression". Revue Internationale de Psychologie Sociale. 17: 37–62.
  8. 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". American Journal of Physiology. Legacy Content. 149 (1): 246–253. doi:10.1152/ajplegacy.1947.149.1.246. PMID 20291968.
  9. Dow, Robert S. (1958). The Physiology and Pathology of the Cerebellum. Minneapolis: University of Minnesota. p. 295.
  10. 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.
  11. Bard, P.P. (1934). "On emotional expression after decortication with some remarks on certain theoretical views: Part II". Psychological Review. 5. 41 (5): 424–449. doi:10.1037/h0071731.
  12. Reis, Donald J.; Kjell Fuxe (Sep 15, 1969). "Proceedings of the National Academy of Sciences of the United States of America". 1. 64: 108–112. Cite journal requires |journal= (help)
  13. Reis, Donald J.; Lars-Magnus Gunne (23 July 1965). "Brain Catecholamines: Relation to the Defense Reaction Evoked by Amygdaloid Stimulation in Cat". Science. New Series. 149 (3682): 450–451. Bibcode:1965Sci...149..450R. doi:10.1126/science.149.3682.450. PMID 17809420.
  14. Wortis, Herman (1 March 1942). ""Sham Rage" in Man". Am J Psychiatry. 98 (5): 638–644. doi:10.1176/ajp.98.5.638.
  15. Panksepp, J; Zellner, MR (2004). "Towards a neurobiologically based unified theory of aggression". Revue Internationale de Psychologie Sociale. 17: 37–62. This affective attack or RAGE response is mediated by neurons in the corticomedial amygdala, the rostro-caudal extent of the medial hypothalamus (MH) and the dorsolateral region of the midbrain periaqueductal gray (PAG); this is known because rage behavior can be reliably and consistently elicited through electrical stimulation of these regions. Many areas of the hypothalamus also modulate the behavior because of the capacity of this brain area to regulate the internal environment of the body and monitor various kinds of homeostatic imbalances, such as hunger, thirst, temperature, and sexual arousal. When stimulated, the medial hypothalamus projects information to the PAG. The PAG and surrounding tectal areas are the neural substrates for some of the essential sensory and motor representations of the core self, both visceral and somatic, and is centrally involved in pain perception.
  16. Skultety, Miles (1963). "Stimulation of periaqueductal gray and hypothalamus". Archives of Neurology. 8 (6): 608–620. doi:10.1001/archneur.1963.00460060038004. PMID 14059332.
  17. Zanchetti, Alberto; Zoccolini, Adriana (1954). "Autonomic hypothalamic outbursts elicited by cerebellar stimulation". Journal of Neurophysiology. doi:10.1152/jn.1954.17.5.475.
  18. Campbell, Robert Jean (2009). Campbell's Psychiatric Dictionary. New York: Oxford University Press.

Further reading
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