3. Are Emotional Indicators Necessary or Sufficient for an Emotional Experience?

In reviewing the literature, one of the more common conceptual disagreements concern whether or not a specific type of indicator is necessary or sufficient for an emotional experience to occur [3,4,17,18]. In the early 1900’s the Body Theory of emotions [12] came under attack [13]. Based on observations that animals who underwent sympathectomy were still capable of producing authentic somatic-motor displays of emotion when appropriately stimulated and observations in sympathectomized patients who reported that they were still able to experience emotions, Canon [13,29] and Bard [30,31] concluded that visceral-autonomic changes were neither sufficient nor necessary for an emotional experience. Furthermore, when human subjects are given pharmacological agents that induce visceral-autonomic reactions, they verbally report either experiencing changes in their physical state without an emotional experience or report experiencing a “cold” “as if” rather than a genuine emotion [32,33]. It has also been reported that when the hypothalamus is stimulated in awake patients undergoing neurosurgical procedures, marked changes in autonomic activity are observed without the patient reporting a concomitant emotional experience [34]. Lastly, if subjects are given pharmacological agents to induce different types of visceral-autonomic reactions and are placed in with group of individuals serving as foils to induce various social-emotional situations, the subjects report experiencing emotions appropriate to the social situation but not specific to the pharmacological agent [15,33].

Another error is assuming that if an emotion indicator is disrupted by a focal brain lesion, the patient is not able to experience emotions. For example, clinical research over the last 40 years has shown unequivocally that acute ischemic lesions involving the right frontal operculum, basal ganglia or medial frontal regions are associated with flattening of affect due to loss of the ability to project emotion into vocal communication, facial expressions and gestures [19,20,34,35,36]. The various affective communication deficits following focal right-brain damage are classified under the term “aprosodia” and the syndromic classification is analogous to the different aphasic syndromes observed after focal left-brain damage [35]. However, patients with affective-communication deficits causing flattening of affect associated with motor-types of aprosodia, are able to experience emotions inwardly (by verbal report), comprehend affective communication of others (by verbal report and formal testing) and are often cognitively aware of that their affective-communication deficits are having a deleterious effect on their interpersonal relationships and psycho-social well-being [34,37]. Even more important, some patients with motor-types of aprosodia may also suffer from a concomitant depression based on their verbal reports of feeling depressed and experiencing anhedonia or suicidal ideation [38,39,40]. Nevertheless, their verbal complaints may be discounted by clinicians because the complaints are not communicated with an appropriate affect.

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Another error is assuming that if a patient or research animal displays somatic-emotional behaviors that they are, in fact, experiencing an emotion. In the early 1900’s, research focused on the hypothalamus as a pivotal structure for engendering emotions because it was observed that decorticated or decerebrated animals (cats, dogs) could be stimulated to engage in attack types behaviors as long as their caudal hypothalamus was intact [30]. In addition, electrical or chemical stimulation of certain regions of the hypothalamus were shown to be able to induced somatic motor display behaviors, specifically attack and rage behaviors, and associated autonomic responses in animals with intact forebrains [31,41], also known as the hypothalamic “savage” syndrome [42]. However, it was concluded that these display behaviors and autonomic responses represented “sham” rather than real emotions [11,29,30,31,41,42] because: (1) the display behaviors could be induced in animals that were decerebrated or decorticated, (2) the display behaviors were generalized and not necessarily object directed and could be induced by trivial sensory stimulation, (3) the display behaviors would occur only during electrical stimulation of the hypothalamus in otherwise neurologically intact animals after which the animal would return to its previous activity, as if nothing had occurred, and (4) electrical stimulation of the hypothalamus could not be used as an unconditioned emotional response to induce a learned conditioned emotional response in experimental animals. Lastly, in awake patients undergoing neurosurgical procedures, it has been observed that electrical stimulation of the hypothalamus produces autonomic changes but does not induce somatic motor displays of emotion or verbal reports of an emotional experience [34].

There is also a well-studied clinical condition that supports the idea that somatic-motor displays of emotion are not necessarily indicative that the patient is actually experiencing an emotion. Pathological regulation of affect is a disorder in which the patient will laugh and/or cry in response to trivial environmental stimuli that do not necessarily have any emotional significance [43,44,45]. The emotional displays are very realistic, are not under voluntary control, and have an “all or none” quality. In most instances, based on the patients’ verbal reports, the displays are not associated with an actual emotional experience and do not reflect their actual mood or emotional state. The patients will often complain of their inability to control these unwanted and socially embarrassing behaviors. The most common cause for pathological regulation of affect is pseudobulbar palsy due to bilateral lesions that injure the bulbar neocortical motor regions or their descending connections to the brainstem motor nuclei [46]. To date [18], clinical studies have not resolved if the lesions need only involve the pyramidal (primary) motor cortices or their descending pathways that course through the posterior limb of the internal capsule [47] or whether the lesions also need to also involve the premotor cortices or their descending pathways that course through the genu and anterior limb of the internal capsule [48]. Pathological regulation of affect has also been associated with unilateral or bilateral lesions or epileptic activity involving the basal forebrain, medial temporal lobe, diencephalon, tegmentum and lower brainstem without the presence of pseudobulbar palsy [43,45,49,50,51,52]. Finally, pathological regulation of affect has been reported in several patients after unilateral ischemic lesions involving the right frontal operculum, causing motor aprosodia, who were also suffering from a major depression [39,40]. Although the patients exhibited, at minimum, left upper-motor-neuron facial weakness, they did not have pseudobulbar palsy or structural lesions involving the basal forebrain, medial temporal limbic system, hypothalamus or brainstem. Despite their depression, the patients reported that the unwanted (pathological) emotional displays did not reflect their depressed mood and were not associated with a congruent emotional experience. Interestingly, their pathological regulation of affect rapidly responded to antidepressant treatment well before their depressed mood responded.

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The observations reported above regarding pathological regulation of affect suggest that critical lesions or disease processes involving either the neocortical bulbar motor system, basal forebrain, temporal limbic structures or diencephalon release deep seated, innate, reflexive (“sham”) emotional displays [13] that are organized in the brainstem consistent with conclusions reached by Bard [29,30] and Cannon [13,28]. More recent animal-based research has suggested that some innate species-specific emotional displays and associated autonomic reactions are organized in a rostral-caudal pattern within the peri-aqueductal gray matter of the midbrain tegmentum [53,54].

The other clinical condition that supports the concept that the reflexive antecedents of primary emotions reside in the brainstem is hydranencephaly. Hydranencephaly is a syndrome in which the neonate is born without cerebral hemispheres either due to genetic factors, ischemic or hypoxic injury or infection [23,55,56,57]. In the most severe cases (anencephaly), the entire forebrain, including the diencephalon, is missing, as is the calvarium, and the midbrain may be malformed or missing [23,55]. In less severe cases (hydranencephaly), the hypothalamus and other regions of the diencephalon, and portions of the inferomedial occipital and temporal cortices and inferomedial frontal cortex may be preserved with the rest of the forebrain replaced by cerebrospinal fluid surrounded by meninges with an intact calvarium. Neonates with less severe forms of hydranencephaly may survive the post-natal period and live for a number of years with markedly reduced development [57,58]. Some neonates with hydranencephaly may not be diagnosed with the condition until several months after birth when developmental milestones are not met [59]. What is of interest, however, is that neonates with anencephaly, if they survive birth, and neonates with severe hydranencephaly will display many of the innate (reflexive) behaviors associated with primary emotions [13,56].

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