Download “Cardiac Distress and Efferent Autonomic Drive”

“CARDIAC DISTRESS
and
Efferent Autonomic Drive”
Presented by
Michael D. Allen, DC, NMD, DIBAK, DABCN
Chiropractic Neurologist
HealthBuilderS®
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CARDIAC DISTRESS &
Efferent Autonomic Drive
The article entitled, “Mental
Stress and Sudden Cardiac
Death: Asymmetric Midbrain
Activity as a Linking
Mechanism,” reports that
cardiac arrhythmia and
sudden cardiac death can be
related to specific
neurological, psychiatric, or
cardiovascular conditions.
(Brain, 2005;
http://brain.oxfordjournals.org/cgi/reprint/128/1/75?maxtoshow=&HITS=10
&hits=10&RESULTFORMAT=&fulltext=mental+stress&searchid=1&FIRST
INDEX=0&resourcetype=HWCIT ),
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“…We therefore
undertook a study to
identify the brain
mechanisms by which
stress can induce
cardiac arrhythmia
through efferent
autonomic drive.”
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“…Across the patient group,
we observed a robust
positive relationship between
right-lateralized asymmetry
in midbrain activity and
proarrhythmic abnormalities
of cardiac repolarization…
during stress.”
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CARDIAC DISTRESS &
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“…lateralization of central
autonomic drive during stress
results in imbalanced activity
in right and left cardiac
sympathetic nerves.” This
sympathetic drive asymmetry
disrupts the heart’s ability to
repolarize, leading to a
predisposition to arrhythmia.
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“Each subject was scanned using H215O PET while
performing two replications of mental and
physical stress tasks and corresponding control
conditions. In the mental stress task, the
subject was required to perform (to
themselves) rapid continuous serial subtractions
of 7 from a cued starting point over a 3
minute period. In the corresponding low-stress
‘effortless’ control condition, the subject was
required to count to themselves slowly from a
cued starting point over 3 minutes.”
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CARDIAC DISTRESS &
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“Importantly, we directly explored the hypothesis
that predisposition to arrhythmia may arise from
imbalanced right-left shifts in the central
autonomic drive to the heart (Friston, 2003). In
order that observed effects were attributable to
stress-related autonomic activity (independent of
task modality), we ensured that they were present
independently in both exercise and mental arithmetic
conditions [formally tested using conjunction
analyses (Price and Friston. 1997: Friston et al.,
1999)] thereby excluding activity that was specific
only to either cognitive or physical task modality.”
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CARDIAC DISTRESS &
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“Brain activity associated with increased
TWR (“T-wave residua”; i.e., proportion of
the non-dipolar components of the Twave) in response to stress was also
observed unilaterally in right midbrain,
extending into adjoining thalamus and
hypothalamus.”
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CARDIAC DISTRESS &
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“Many neurological, psychiatric and cardiological patient groups are
at risk from arrhythmia and sudden death attributable to a central
neurogenic cause (Lown et al., 1977; Oppenheimer et al., 1990;
Oppenheimer, 1994; Lane and Jennings, 1995; DiPasquale et al.,
1998; Hennessey et al., 2002; Cheung and Hachinski, 2003;
Macmillan et al., 2003; Nei et al., 2004). For example, sudden
arrhythmic death in epilepsy is likely to originate from seizure
activity driving efferent autonomic effects on the heart (Mameli et
al., 1988; Oppenheimer, 1994; Nei et al., 2004). Emotional
challenges and mental and physical stress are associated with
arrhythmogenesis, again via efferent autonomic activity, and
patients with pre-existing cardiac disease are especially vulnerable
(Lampert et al., 2000). Our findings indicate a mechanism by
which brain activity associated with stress and autonomic arousal
may be translated into a proarrhythmic state of the heart.”
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“Electrophysiological studies suggest that increased electrical
inhomogeneity of the myocardium, during the repolarization phase of
the cardiac cycle, is a major factor in the susceptibility to ventricular
arrhythmias (Batchvarov et al., 2003). If parts of the heart recover
and are ready to contract before neighbouring regions, the likelihood
of an abnormal heart rhythm is greatly increased. The left- and rightsided autonomic (sympathetic) nerves are distributed asymmetrically
over the ventricles, and unilateral stimulation of either side may alter
repolarization inhomogeneity (Yanowitz et al., 1966). Thus,
repolarization inhomogeneity may reflect ‘upstream’ influences on the
right-left symmetry of sympathetic cardiac drive, for example
asymmetric brain activation in response to stress. This key question
was the focus of the present study, which, for the first time,
provides evidence for a mechanistic link between stress and cardiac
arrhythmias at the level of the brain.”
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“Mental and physical stress is widely recognized as
playing an important role in ventricular arrhythmias
and sudden cardiac death. One group of subjects
particularly at risk are patients with coronary artery
disease. Much research has focused on describing
local cardiac causes for arrhythmia, such as
ischemia. In fact, mental and physical stress can
cause ischemia, and ischemia may precipitate
ventricular tachycardia and ventricular fibrillation
(Janse and Wit, 1989). Nevertheless, in a substantial
number of cardiological patients, arrhythmia and death
are thought to occur in the absence of ischemia
(Lampert et al., 2000).”
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“A brain mechanism underlying the generation of arrhythmia is suggested by the clinical
association of arrhythmia with neurological conditions such as epilepsy (Oppenheimer,
1994; Nei et al., 2004), focal brain lesions (Cheung and Hachinski, 2003) and subarachnoid
haemorrhage (DiPasquale et al., 1998; Macmillan et al., 2003), and the experimental
induction of arrhythmia by focal brain stimulation (Lown et al., 1977; Mameli et al., 1988).
Existing evidence suggests that proarrhythmic states of inhomogeneous electrical
repolarization observed in our patients during stress may result from asymmetrical
sympathetic drive to the heart. In identifying neural correlates of cardiac inhomogeneity,
we have localized a putative substrate underlying asymmetric autonomic influences on the
heart. Anatomically, there is evidence for subcortical lateralization of efferent
sympathetic pathways, with segregation of left and right responses maintained at the level
of brainstem and spinal cord (Mangina and Beuzeron Mangina, 1996). Our results suggest
that a critical transitional locus exists in the midbrain region. When midbrain activation in
response to stress was bilaterally symmetrical, the repolarization inhomogeneity in the
heart was unchanged. However, when stress-induced midbrain activation was lateralized to
the right, repolarization inhomogeneity (i.e. the arrhythmogenic substrate) was enhanced
(see Fig. 4). It is noteworthy that within our limited sample of cardiology patients,
the magnitude of proarrhythmic changes did not appear to be predicted by the
severity of coronary artery disease, whereas these effects are apparent in some
patients with normal coronary arteries.”
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CARDIAC DISTRESS &
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“At the level of the cerebral cortex, evidence from
clinical studies and PET neuroimaging experiments suggests
a right-sided dominance of cortical regions, particularly
right insular and anterior cingulate cortices, in the
generation of sympathetic responses (Oppenheimer et al.,
1990; Oppenheimer, 1994; Critchley et al., 2000, 2001).
There may be, therefore, a right hemispheric predominance
of cortical influences on sub-cortical autonomic centres
during mental and physical stress and this tendency may be
expressed as a relative predominance of right sympathetic
responses. Our evidence, as illustrated in Figs 2 and 3,
suggests that a threshold may exist at which central
sympathetic drive reaches a critical right-left imbalance at
the level of the midbrain.”
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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Although they say that the
neurological means are poorly understood,
the authors of the article found that these
heart problems may start in vulnerable
patients via centrally driven autonomic
nervous system responses. In other words,
heart attacks can start in the brain. The
authors go on to say that the mechanisms
may be induced through efferent autonomic
drive and not necessarily inherent to heart.
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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Because the key to this issue is the “efferent
autonomic drive”, this class will discuss and
demonstrate the functional neurological
mechanisms of spinal cord performance that
trigger cortical modulation of efferent
autonomic drive.
The goal of the discussion is to promote the
doctor’s understanding of cardiac
performance via improved afferentation and
resultant autonomic influence.
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CARDIAC DISTRESS &
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“Decreased Potentiation of
Normal Reciprocal Movements
Impairs Cognitive Abilities”
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CARDIAC DISTRESS &
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The greatest thing we can do for our
patients is help them better express
what it means to have a uniquely
human nervous system, but we must
be sure of what we are seeing
before we treat it.
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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The cortical outflow is the sum
of the effect of afferent and
the resultant efferent quality.
Quality = Timing
Afferentation vs. Deafferentation
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CARDIAC DISTRESS &
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“Consciousness, like locomotion, might
be more a case of intrinsic activity
than of sensory drive. Consciousness
has to do with timing.”
Llinas, Ribary, Contreras & Pedroarena; The Neuronal Basis for Consciousness; Philos Trans R
Soc Lond B Biol Sci. 1998 Nov 29;353(1377):1841-9
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CARDIAC DISTRESS &
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The Human Brain: What is it?
– Nerve cells connected by ~1.5 million km (900,000
miles) of nerve fiber (RT moon 2x)
– 90% of brain cells are glial cells (structure,
transport, maintenance,…interneurons)
– 10% of brain cells are neurons - “active” cells for
thinking, learning, etc…
– A fruit fly has 100,000 neurons; a monkey has 10
billion neurons; a human has 100 billion neurons
– Each neuron makes up to 20,000 connections
– An adult has half the neurons of 2 year old
– We lose >10,000 neurons per day!
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CARDIAC DISTRESS &
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Receptors are specialized
sensory organs that make
up the anatomic basis for
sensation. They are the
peripheral endings of
afferent nerve fibers,
capable of registering
certain changes in their
vicinity and within the
organism, and of
transmitting these stimuli
as impulses.
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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Receptors
 Pain and temperature endings are
found quite uniformly over the body
surface
 Touch and pressure sense
receptors are found in most body
surfaces
 Position and vibratory sense
receptors are found in the muscle
fibers, fascia, tendons and in joint
capsules
 Receptors of deep sensibility are
for proprioception and related to
muscles and their performance
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CARDIAC DISTRESS &
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Receptors
 Muscle Spindle Fibers and
Golgi Tendon Organs are
related to muscles
 Ruffini corpuscles sense hot
 Pacinian corpuscles sense
pressure
 There are other receptors
that have other functions
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CARDIAC DISTRESS &
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Receptor-driven
cerebellar and
midbrain afferents
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CARDIAC DISTRESS &
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Anterior view of dermatomes (left) and cutaneous areas supplied by individual peripheral nerves (right).
(Modified from Carpenter MB, Sutin J: Human neuroanatomy, Baltimore, 1983, Williams & Wilkins:
Isselbacher KJ et al, editors: Harrison's principles of internal medicine, ed 13, New York, 1994, McGrawHill.)
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CARDIAC DISTRESS &
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Posterior view of dermatomes (left) and cutaneous areas supplied by individual peripheral nerves (right).
(Modified from Carpenter MB, Sutin J: Human neuroanatomy, Baltimore, 1983, Williams & Wilkins: Isselbacher
KJ et al, editors: Harrison's principles of internal medicine, ed 13, New York, 1994, McGraw-Hill.)
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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We know that specifically stimulated receptors
send afferent signals according to their central
integrative state, at specific speeds
Type
Type A
Group Speed
Group Ia 120M/s
Annulospiral Endings of Muscle Spindles (Nuclear Bag)
Same as α-Type A fibers
Group Ib
Golgi Tendon Organs
Same as β-Type A fibers
Group II
Tactile Receptors & Flower Spray Endings (Nuclear Chain)
Same as β & γ-Type A fibers
Group III
Carry temperature, nociception, crude touch & prickling
pain sensations
Same as γ & δ-Type A fibers
Type B
Type C
Characteristics
Preganglionic parasympathetic
Motor only
Lack much of an after hyperpolarization
Group IV 0.5M/s
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Unmyelinated; nociception, temperature & crude touch; small
Same as Type C fibers
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CARDIAC DISTRESS &
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LOCATION
NERVE
SA
SE
VE
NOTE 1
I
Special Sensory
II
Special Sensory
Mes~
III


“
IV


“
V (Sensory)
Branchial afferent (BA)
Pons
V
Branchial efferent (BE)
“
VI
“
VII
“
VIII
Medulla
IX
“
X
“
XI
“
XII
Spinal Cord
C1(-C8)
“
C2-8
“
“


EWN; the highest
representation of
the autonomic NS
NOTE 2
Ciliary Ganglia to the
pupillary constrictor
muscle;
Episcleral Nerve to clilary
muscle and lens

BA, BE
Superior Salvatory Nucleus
to the Sphenopalatine
Ganglion and the lacremal
glands;
Submandibilar Nucleus to
the salvatory glands
Special Sensory
Cochlear and Vestibular
Divisions

BA, BE
Inferior Salvatory Nucleus
to the Otic ganglion and
parotid glands

BA, BE
Dorsal Motor Nucleus and
several others

BA, BE



()


()
T1-L2



L3-S2


()
“
® 2006S2-4
© HealthBuilderS



No DRG
IMLCC
By Synapse Back to L3S2
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CARDIAC DISTRESS &
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Primary receptor afferents terminate in
the dorsal horn where the signal can
actually do any one or a combination of
12 different things…
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CARDIAC DISTRESS &
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Twelve Things Primary Afferents Do:
All primary afferents:
 Are excitatory to the intermediolateral cell column. This allows for
dilation of arterioles to muscles, capillaries to skin, piloerector tissue and
sweat glands
 Inhibit pain (excites inhibitory interneurons to inhibit nociception)
 Excite alpha motor neurons of the homologous muscles, i.e., right upper
extremity flexors
 Inhibit alpha motor neurons of antagonistic muscles, i.e., right upper
extremity extensors
 Excite left upper extremity extensors
 Inhibit left upper extremity flexors
 Excite right lower extremity extensors
 Inhibit right lower extremity flexors
 Excite left lower extremity flexors
 Inhibit left lower extremity extensors
 Ascend up to the medulla
 Ascend ®up to the cerebellum
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© HealthBuilderS 2006
CARDIAC DISTRESS &
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…This signal
participates in
reflexive
coordination
leading to some
sort of efferent
response via the
anterior horn -“the final common
pathway”.
© HealthBuilderS® 2006
We discuss the effect of “Global
Binding” and its influence on the
“central integrative state” of the
anterior horn of the spinal cord
in other classes.
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CARDIAC DISTRESS &
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“…How the sensory homunculus develops is not well
understood, and previous work in this area had
focused on the incoming neural connections
(sensory afferents). It argued that densely
innervated areas, including the lips and tongue, sent
large cohorts of neurons into the brain, and that
their intense activity enabled them to claim a large
territory in cortical layer 4, which handles incoming
sensory information. The cortex itself was thought
to have only a small instructive role, if any.”
(Emphasis added)
Genes or Environment: What Shapes the Sensory Homunculus?; Protein shown to help build
body maps raises questions about individual differences in function; Harvard Medical School,
Boston, MA, 03/30/00
32
®
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CARDIAC DISTRESS &
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Within the somatosensory cortex is a representation of the
human body called the homunculus or " little man".
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Researchers from Harvard Medical
School have found that a single gene
expressed in the brain can change a
long-standing icon (the sensory
homunculus) of basic neuroscience that
was until now thought to be shaped
mostly by neural input from the body's
periphery. (Emphasis added)
Genes or Environment: What Shapes the Sensory Homunculus?; Protein shown to help build
body maps raises questions about individual differences in function; Harvard Medical
School, Boston, MA, 03/30/00
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CARDIAC DISTRESS &
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Genetic expression and coupled
manipulation techniques:
 Deafferentation
 Coupled treatment
 Neuraxis
Cell Nucleus
 Genetic Changes
 Protein Replication in Muscle
 Enhanced Abilities
Enhanced Cortical Expression
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CARDIAC DISTRESS &
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“…The current work does not negate
the importance of neural activity by
incoming neurons to determining
brain maps. It says for the first
time, however, that the cortex
also has a hand in divvying up
brain space, and that this
influence is genetic.”
Genes or Environment: What Shapes the Sensory Homunculus?; Protein shown to help build
body maps raises questions about individual differences in function; Harvard Medical
School, Boston, MA, 03/30/00
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“…The idea is that incoming neurons
negotiate (this crossfire of labels) with
the combination of receptors they
carry. In the end, each neuron finds its
proper spot in a spatial pattern that
reflects the outside world.”
“…The molecular mechanism by which this
occurs is poorly understood.”
Genes or Environment: What Shapes the Sensory Homunculus?; Protein shown to help build
body maps raises questions about individual differences in function; Harvard Medical
School, Boston, MA, 03/30/00
© HealthBuilderS® 2006
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“…Lastly, lest someone feels
misrepresented by the homunculus,
Flanagan adds that it is not about
mere sensitivity, but ability to
resolve tactile information. We do
feel pain when pinched in the ribs
or lower leg, but would not use
these parts to read Braille.”
Genes or Environment: What Shapes the Sensory Homunculus?; Protein shown to help build
body maps raises questions about individual differences in function; Harvard Medical
School, Boston, MA, 03/30/00
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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The Cerebral Cortex and Motor Strip
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CARDIAC DISTRESS &
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“With few exceptions, all
activities of the CNS, receiving,
processing and integrating
information, ultimately find
expression in contraction of a
muscle. Muscle activity may
occur in terms of purposeful
motion… or of postural control.”
-Despopoulous & Silbernagl, Color Atlas of Physiology. pg 264
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CARDIAC DISTRESS &
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Major Cortical Fields in Planning and
Execution of “Purposeful” Movements
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CARDIAC DISTRESS &
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Physiological reflexes, when
working properly, display their
influence according to preprogrammed human performance
patterns. Any display other than
that which is normal must be
considered pathological.
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CARDIAC DISTRESS &
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Because reflexes are dynamic, they require
a constant against which they can be
compared. That constant is unchangeable
throughout all the earth.
Gravity is that constant – it is the only
constant environmental stimulus. It is
always present and is monitored by highly
specialized neurologic sense organs in the
muscles. They detect muscle stretch as
we move about and try to resist gravity.
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CARDIAC DISTRESS &
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 The reflexive response to gravity is not
constant even though gravity is constant.
 The effects of gravity ultimately influence
the higher brain centers - the thalamus and
cerebellum - by being constant.
 Gravity is the stimulus but proprioception
is the modality.
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CARDIAC DISTRESS &
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The Deep Tendon
(Patellar) Reflex
Rate the reflex with the following scale:
5+
Sustained clonus
4+
Very brisk, hyperreflexive, with clonus
3+
Brisker or more reflexive than normally.
2+
Normal
1+
Low normal, diminished
0.5+ A reflex that is only elicited with reinforcement
0
No response
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CARDIAC DISTRESS &
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Tonic Neck Reflexes (TNR)
The tonic neck reflexes are present
around 18 weeks in utero. Some
authorities believe that they become
inhibited or suppressed between 6-8
months after birth, when awake, and
persists up to three and one half
years when asleep.
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CARDIAC DISTRESS &
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Flexor Withdrawal Reflex
• Onset - begins at 28 weeks gestation
• Integration - 2 months for normal child;
may persist in developmentally delayed
and/or CP child
• Testing position - child supine, head
midline, lower extremities extended
• Procedure - apply a noxious stimulus to the
sole of the foot
• Response observed - withdrawal of the
foot from the stimulus employing hip and
knee flexion
• Developmental significance - failure to
attain and integrate this reflex may
indicate sensorimotor delay and/or CNS
depression
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CARDIAC DISTRESS &
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Crossed Extensor Reflex
• Onset - begins at 28 weeks gestation
• Integration - 1-2 month
• Testing position - child in supine, head in midline,
lower extremities extended
• Procedure - Holding one leg in extension at the knee,
apply firm pressure to the sole of this foot
• Response observed - child’s opposite leg will flex,
adduct, and then extend
• Functional significance - this reflex can interfere
with reciprocal kicking and later functional activities
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CARDIAC DISTRESS &
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Twelve Things Primary Afferents Do:
All primary afferents:
 Are excitatory to the intermediolateral cell column. This allows for
dilation of arterioles to muscles, capillaries to skin, piloerector tissue and
sweat glands
 Inhibit pain (excites inhibitory interneurons to inhibit nociception)
 Excite alpha motor neurons of the homologous muscles, i.e., right upper
extremity flexors
 Inhibit alpha motor neurons of antagonistic muscles, i.e., right upper
extremity extensors
 Excite left upper extremity extensors
 Inhibit left upper extremity flexors
 Excite right lower extremity extensors
 Inhibit right lower extremity flexors
 Excite left lower extremity flexors
 Inhibit left lower extremity extensors
 Ascend up to the medulla
 Ascend ®up to the cerebellum
49
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CARDIAC DISTRESS &
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Proprioceptors are found everywhere, primarily in
the joints – muscles, tendons and ligaments, etc.
Their input is processed primarily through the
cerebellum, which constantly updates its
environmental responses from all other sources.
Proprioceptors influence body movements and
direct the postural background for fine muscle
coordination.
Distorted information coming from any one of these
sources will also affect proprioception –
deafferentation.
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CARDIAC DISTRESS &
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Cerebellar function is essential to
human development, and its
moderating activities are referred
to as, “Surround Inhibition”.
The cerebellum coordinates with all
other sensory sources (JMRs, etc)
to influence body movements and
coordinates fine muscle movement.
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CARDIAC DISTRESS &
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Drawing from Ramón y Cajal's first publication on the central nervous system, showing the five classes of
neurons in the cerebellum: A, Purkinje cell; D, stellate cell; F, Golgi cell; H, granule cell; S, basket cell
axons., From the Instituto de Neurobiología "Ramón y Cajal", Madrid, Spain.
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CARDIAC DISTRESS &
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Parallel, Climbing, Mossy & Purkinje Fibers with Golgi, Stellate,
Granule & Basket Cells
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CARDIAC DISTRESS &
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® 2006
© HealthBuilderS
From
Surround Inhibition – The Miracle
F
ig
u
r
e
4 of Upright Posture by Michael D. Allen, DC, NMD
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CARDIAC DISTRESS &
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Muscle and bone signals both go
to the thalamus, but the muscle
signals also go to the
cerebellum – it gets no signal
from bones. When the
thalamus and cerebellum
collect all the incoming
information, it gets sent to
the brain. All this
afferentation sets the stage
for neurologic
synchronization. All the
information that comes in from
the special senses — like touch,
vision, hearing, smell, taste, etc
— cause us to respond to our
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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“…the thalamus, the last relay
station of tactile information
from the body's surface.”
Genes or Environment: What Shapes the Sensory Homunculus?; Protein shown to
help build body maps raises questions about individual differences in
function; Harvard Medical School, Boston, MA, 03/30/00
© HealthBuilderS® 2006
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CARDIAC DISTRESS &
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Contralateral
Ipsilateral
Cortex
Thalamus
Cerebellum
Posture Autonomics
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Joints
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The integration of each of the basal
nuclei requires both temporal and
spatial summation of the vast array
of information to the basal ganglia.
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CARDIAC DISTRESS &
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There are three currently recognized
ways that signals are exchanged
between the cortex, thalamus and
cerebellum, and all the structures in
between. They are:
 Efferent Copy
 Feed Back
 Feed Forward
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CARDIAC DISTRESS &
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A Grand Unification Theory of the Brain
Professor Rodolfo Llinás of the New York University
School of Medicine has argued and demonstrated that
electromagnetic arrhythmias – out-of-phase signals
between the thalamus and other centers of the brain –
may account for disorders ranging from depression and
obsessive-compulsive disorders to Parkinson’s disease
and chronic pain. (Emphasis added)
Summarized from an article by Wray Herbert in US News & World Report (January 3rd
2000) monitored for the Global Ideas Bank by Roger Knights.
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CARDIAC DISTRESS &
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In his theory, the symptoms of these
psychiatric and neurological disorders
are all aberrations in the normal
synthesis of sensory information. If
this is true, it would point the way
forward towards the possibility of new
drugs and possibly even implants such as
neurological pacemakers to correct the
out-of-sync timing of the thalamic
messaging system.
Summarized from an article by Wray Herbert in US News & World Report (January
3rd 2000) monitored for the Global Ideas Bank by Roger Knights.
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CARDIAC DISTRESS &
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Llinás' theory moves neuroscience and
cognitive science away from their
emphasis on anatomy as the source of
perception and thought to a closer
study of the thalamus and his theory
that consciousness has to do with
timing. (Emphasis added)
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CARDIAC DISTRESS &
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Llinás believes that the thalamus, rather than
being a mere relay station receiving stimuli from
sense organs and then sending them on for
processing to regions of the brain's cortex, also
functions as the brain's clock. While studying
the brain's electromagnetic waves, he found
that the thalamus is in constant dialogue with
the brain's higher processing centers - not
only do electromagnetic loops send pulses from
the thalamus to the cortex, but the different
sensory centers of the brain also send messages
to the thalamus.
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CARDIAC DISTRESS &
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“Attempting to understand how the brain, as a whole, might be
organized seems, for the first time, to be a serious topic of
inquiry. One aspect of its neuronal organization that seems
particularly central to global function is the rich
thalamocortical interconnectivity, and most particularly the
reciprocal nature of the thalamocortical neuronal loop
function. Moreover, the interaction between the specific and
non-specific thalamic loops suggests that rather than a gate
into the brain, the thalamus represents a hub from which any
site in the cortex can communicate with any other such site or
sites. The goal of this paper is to explore the basic assumption
that large-scale, temporal coincidence of specific and nonspecific thalamic activity generates the functional states that
characterize human cognition”. (Refer to “flywheel” slide)
The Neuronal Basis for Consciousness; Llinas, Ribary, Contreras & Pedroarena. Philos Trans R Soc
Lond B Biol Sci. 1998 Nov 29;353(1377):1841-9
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CARDIAC DISTRESS &
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The basal ganglia plays a huge
role in autonomic display. This
is where because this is where
the command is given to “go” or
“no go” as far as efferent
autonomic drive is concerned.
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CARDIAC DISTRESS &
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CARDIAC DISTRESS &
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The Basal Gangliae modulate and
regulate specific cortical functions.
They are important for:
Emotional Behavior
Learning of Movement
Memory of Movement
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CARDIAC DISTRESS &
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There are three basic aspects of
movement:
 Preparation
 Planning
 Execution
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 Efferent Copy
 Feedback
 Feed Forward
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CARDIAC DISTRESS &
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Rule #3:
Modulation (inhibition) is the
secret to preprogrammed human
performance and reciprocal
movement
Corollary #1: Reciprocal joint motion knocks
out pain.
Corollary #2: Aerobics are the means to
sustained performance.
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CARDIAC DISTRESS &
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The basal ganglia integrates a vast
number of “neurobehavioral
variables”:
Muscle contraction patterns
Limb movement patterns
Target location
Memory
Motivation
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CARDIAC DISTRESS &
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Fig. 1 Cortico—striato—thalamo—cortical circuits. GABA, -aminobutyric acid;
VTA, ventral tegmental area; Gpe, globus pallidum externa; Gpi, globus pallidum
interna; STN, sub-thalamic nucleus.
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CARDIAC DISTRESS &
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Computing a Voluntary Movement
Reaching Movement:
Three Functional Levels
Input/Output of Cortical Motor Areas
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Cortexm
Cortexs
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
GPe
Neostriatum
STh
GPi
SNc
SNr
SC
BS
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Th
The Nuclei of the Basal Ganglia
and their Thalamocortical Neuronal Loop Pathways
Cortexm
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
Cortexs
+
_
GPe
STh
+
Neostriatum
_
SNc
_
GPi
_
SNr
SC
BS
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Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
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Cortexm
Cortexs
+
_
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
_ GPe
+
Neostriatum
+
SNc
GPi
_
SNr
+
SC
BS
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STh
_+
_
_
_
Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
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CARDIAC DISTRESS &
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The overall effect of the
nigrostriatal system is one of
reinforcing cortically initiated
motor activity through a
facilitation of the direct loop and a
suppression of the indirect loop.
The neurotransmitters are the key
to understanding the pathway’s
function.
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Cortexm
Cortexs
+
_
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
_ GPe
+
Neostriatum
+
SNc
GPi
_
SNr
+
SC
BS
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STh
_+
_
_
_
Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA
78
Cortexm
Cortexs
+
_
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
_ GPe
+
Neostriatum
+
SNc
GPi
_
SNr
+
SC
BS
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STh
_+
_
_
_
Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA DOPA
79
Cortexm
Cortexs
+
_
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
_ GPe
+
Neostriatum
+
SNc
SC
GPi
_
SNr
_
+
_
BS
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STh
_+
_
_
_
Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA DOPA GLUT
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Cortexm
(PMC, M1, S-1, PMA)
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
+
_
_ GPe
+
Putamen
SNc
_
Th _
STh
_+
_
GPi
_
SNr
+
SC
BS
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Cortexs
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA DOPA GLUT
Motor Loop
81
Cortexm
(DLPC, PMA, MTVC)
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
Cortexs
+
_
_ GPe
+
Caudate Nucleus
SC
GPi
_
SNr
_
+
BS
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STh
_+
_
SNc
_
Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA DOPA GLUT
Oculomotor Loop
82
Cortexm
(DLPC, PPC, PMC)
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
Cortexs
+
_
_ GPe
+
Caudate Nucleus
GPi
_
SNr
+
SC
BS
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STh
_+
_
SNc
_
Th _
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA DOPA GLUT
Dorsolateral Prefrontal
Cortex (Assoc-1) Loop
83
Cortexm
(POPC, S/M/I Temp & Cing Gyr)
GPe: Globus Pallidus externus
STh: Subthalamus
GPi: Globus Pallidus internus
SNc: Substantia Nigra compacum
SNn: Substantia Nigra
SC: Superior Colliculus
BS: Brain stem
Th: Thalamus
+
_
_ GPe
+
Caudate Nucleus
SNc
_
Th _
STh
_+
_
GPi
_
SNr
+
SC
BS
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Cortexs
Thalamocortical Neuronal Loop Pathways
DIRECT PATHWAY
INDIRECT PATHWAY
GABA DOPA GLUT
Lateral Orbital Frontal
(Assoc-2) Loop
84
Ant Cing & Med Orb/Fr Areas (MOFA)
Cerebral cortex
The limbic loop
describes the vague
Ventral Striatum understanding – but
excellent example –
of intangible
connections
Ventral Pallidum
between emotions
and cognition.
DMmc
(Hippocampal, entorinal cortex,
and S/M/I Temporal gyrus)
Limbic Loop
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Brain centers can only work in their
pre-designed manner when they are
switched ”on”.
Before two bits of information can be
connected, the nervous system must be
”on” and receptive. The problem is
that these centers are not “on” all the
time
Each center has its own specific and
unique rhythm so it can conserve energy.
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Even a simple arm movement follows this
same rule. Although your brain knows
what movement to make, the motor
system must wait for its controllers
to be ”on” before any movement can
occur.
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Two seemingly separate bits of data can be
connected if the centers that deal with the data
are switched ”on” to receive it. When these
streams of input are coupled they can be related
to memory. If the two bits of information arrive
at the same time and only one center is “on” and
able to deal with the data, the signal can go no
further from this point. It is as if the data
locally died for lack of a linkage (i.e., coupling).
One stream of unconnected information means
virtually nothing.
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Two of the major centers for learning are the
cerebellum and thalamus; their jobs are similar, but
they go about them differently. The cerebellum
seems to have 8 to12 “on”/”off” cycles every second
while the thalamus has around 40 to 50 of them per
second. The basal ganglia has its own uniquely
intricate timing systems.
When all these two systems are in time with each
other, they can communicate clearly. Information
that comes in when they are both ”on” is crunched
and it is either used immediately or filed away for
future reference.
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Any “electromagnetic dysrhythmia”
reduces the number of times these
centers are “on” at the same time,
and two bits of information may
never be linked. That’s a processing
or learning problem.
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The internal and external personal
environments can each have a
profound impact on timing.
Internal stresses can cause problems.
Optimally, the nerve centers should
perform at their highest level.
External influences like chemicals,
allergens, sounds, and stress of many
kinds can make some systems work
faster and others work slower.
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The best way to influence nerve performance is
to treat the whole person.
Timing patterns are sensitive to bone and
joint – including muscles – movements.
When they move in uniquely human ways,
clearer nerve signals get sent to the timing
centers and more neurochemicals naturally
get produced, causing a self-regulation
without the need for drugs, medications
and/or implants.
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“Potentiated normal human movement
patterns enhance cognitive abilities”.
Reciprocal movement patterns set free the ability to learn.
Reciprocity is one of the keys to understanding what each
person’s nervous system needs so that they can perform at
their highest human level.
 Stimulates neurological reciprocity
 Produces coupled motion
 Stimulates the neuraxis
 Modulates genetic expression
 Encourages protein replication
 Enhances cognitive abilities
 Eliminates the perception of pain
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To evaluate the efferent autonomic drive we must
recognize that its integrity arises from the
primary afferents that arise in the peripheral
receptors, the greatest population of which is in
the muscles and joints.
We will use the pre-programmed and physiological
human movement patterns – reflexes – to examine
the afferent and efferent motor system
simultaneously, then dissect the functional
deafferentation and demonstrate its effects.
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HealthBuilderS®
“Our Name Is What We Do Best!”
Spring
2006
Clinical Update
The Educational Arm of Allen Chiropractic, a Professional Corporation
Allen Chiropractic
A Professional Corporation
Sync-Think® Learning Lab
“Brain-Based Learning with You in Mind!”
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