See also Dominance Emotion Cue

Copyright © 1998 - 2001 (David B. Givens/Center for Nonverbal Studies)

Illustration for Sherlock Holmes by Sidney Paget (note the cringing posture behind the door; copyright 1892 by Strand Magazine)



Postural cue. A slight or substantial change in body position, e.g., a. shifting one's weight in a chair, or b. angling one's torso to a new direction at a conference table (see ANGULAR DISTANCE).

Usage: A sudden body-shift may telegraph an unspoken feeling, mood, or opinion, and thus offer a probing point.

Salesmanship. One signal of a prospect's skepticism: "A sudden shift in posture" (Delmar 1984:46).

RESEARCH REPORTS: 1. "Slight postural shifts and the direction of visual focus are [in monkeys] two extremely subtle movements that communicate a potentially changing emotional state and an awareness of surrounding activity or tension" (Dolhinow 1972:231). 2. "Gross changes in body position, such as shifting in the chair, may show negative feelings toward the person one is talking to" (Mehrabian 1974:90).

Neuro-notes. Because they are supplied by segmental spinal nerves directly--rather than by the more elaborate nerve plexuses which govern limb movements--trunk-bending and body-shifting represent a simpler, more straightforward venue for the expression of emotion. This is because, unlike our arm's tangled brachial-nerve plexus (an intricate, evolutionary add-on designed to coordinate the arm's dexterity and movement), our segmental spinal nerves have retained their more primitive role in the control of posture. Thus, governed by paleocircuits of the basal ganglia and brain stem, gross body-shifts may reveal anger, disagreement, and disliking more directly.


Copyright 1999, 2000 (David B. Givens/Center for Nonverbal Studies) Detail of photo by Otto Hagel (copyright Fortune)



Brain. 1. An involuntary motor system of the reptilian brain used to initiate body movements, facial expressions, and postures. 2. Large, rounded masses of forebrain, used subconsciously to adjust, coordinate, and smooth out body movements, e.g., for speaking, smiling, walking, and pointing.

Usage: For neuroanatomist Paul D. MacLean, the basal ganglia are important parts of our reptilian heritage. Territorial gestures and postural displays, e.g., of dominance and submission, are shaped by these subcortical structures. Such status signs are analogous, MacLean thinks, to nonverbal displays of modern reptiles used to show physical presence, to challenge competitors, and to attract mates (MacLean 1990).

RESEARCH REPORTS: 1. The [basal ganglia's] putamen is mainly connected to the premotor and motor cortex and overactivity [i.e., oversupply of dopamine] in this pathway is thought to account for the physical tics in Tourette's syndrome" (Carter 1998:67). 2. The [basal ganglia's] caudate nucleus has more connections to the orbital cortex--an area concerned with higher order planning of activity. Overactivity in this pathway [i.e., dopamine excess] is thought to result in obsessive-compulsive disorder [OCD]" (Carter 1998:67). 3. Studies ". . . suggest the existence of certain pathophysiologically important abnormalities in central neurocircuitries, especially in cortico-striatal [i.e., basal ganglia]-thalamic circuitry, in OCD" (Arai 2000).

Anatomy. Our basal ganglia represent a more ancient motor system than what was to develop millions of years later in the brain's neocortex. Less skilled, e.g., than the neocortex's primary motor area, the basal ganglia control basic movements such as the human arm-swing. While walking, we automatically swing our arms because the basal ganglia assume we are still quadrupeds.

Evolution. In early reptiles, the basal ganglia's archistriatum (i.e., the "most ancient" striatum, or amygdala) and paleostriatum (i.e., the [merely] "ancient" striatum, or globuspallidus) evolved to show identity, power, and submission through programmed movements and postural displays (see ANTIGRAVITY SIGN, CROUCH). In early fishes, the precursor circuits of our present basal ganglia were linked to the primeval "smell brain," and led to swimming motions toward positive chemical signals (e.g., food and mates) and away from negative chemical signs (e.g., of enemies; see AROMA CUE).

Neuro-notes I. Apart from our conscious awareness, the basal ganglia set patterns for key body postures and expressive cues. They turn-on and switch-off ancient spinal circuits for locomotion and postural communication, e.g., and hindbrain circuits for facial expressions and emotional displays (see PALEOCIRCUIT). Basal-ganglia damage from Parkinson's disease shows in a rigid, expressionless, masklike face and a stiff, shuffling gait with non-swinging motionless arms.

Neuro-notes II. 1. ". . . the apparent site of that extra brain power [required for the ability to speak a second language, whether mastered as a child or as an adult] is a deep brain region called the putamen [of the basal ganglia] . . ." (Barinaga 1995:1437). 2. ". . . 'there is some sort of extra control of articulation' required for them to speak their second language" (Barinaga 1995:1437).

Neuro-notes III. 1. "Firstly, the BG provide internal motor cues that enable the release of submovements from the SMA [supplementary motor area; see STEEPLE, Neuro-notes IT], for execution by the motor cortex. The cue (phasic neuronal activity) interacts with the SMA (sustained neuronal activity) to string submovements together in the correct timing sequence. The second function is to contribute to cortical motor set (sustained neuronal activity) which maintains whole movement sequences in readiness for running and execution. This contribution may be to the SMA, premotor area or to both" (Iansek et al. 1995). 2. "The BG is only utilized in these two functions when the movements or sequences are skilled and require few attentional resources for their performance" (Iansek et al. 1995; see NONVERBAL LEARNING). 3. "In Parkinson's disease a defective cue leads to slowing of skilled movement sequences and associated instability of submovements (each submovement cumulatively decreases in amplitude and velocity). This is the phenomenon of hypokinesia. A defect in the contribution to motor set leads to an inability to initiate whole skilled movement sequences (akinesia)" (Iansek et al. 1995; italics added).

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