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
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-thalamic circuitry, in OCD" (Arai 2000). 4. Research on "Sociality, Stress, and the Corpus Striatum of the Green Anolis Lizard" (Greenberg 2003) confirms that the anole lizard's pushup to a high-stand is mediated by modules of the basal ganglia.
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 globus pallidus) 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
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 II], 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).
See also BROADSIDE DISPLAY, HIGH-STAND DISPLAY.
Copyright 1998 - 2018 (David B. Givens/Center for Nonverbal Studies)
Drawing of "Showing My Nonverbal Side" by my son Aaron Huffman (copyright 2012 by Aaron M. Huffman)