© HealthBuilderS ® 2006 “CARDIAC DISTRESS and Efferent Autonomic Drive” Presented by Michael D. Allen, DC, NMD, DIBAK, DABCN Chiropractic Neurologist Sync-Think

© HealthBuilderS®

2006

““CARDIAC DISTRESS CARDIAC DISTRESS and and

Efferent Autonomic Efferent Autonomic DriveDrive””

Presented by

Michael D. Allen, DC, NMD, DIBAK, DABCN

Chiropractic NeurologistSync-Think® Learning

Lab “Brain-Based Learning with You in

Mind!”®

HealthBuilderS®

The Educational Arm of Allen Chiropractic, PC

“Our Name is What We Do Best!”®

Allen Chiropractic A Professional Corporation

2© HealthBuilderS®

2006

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&FIRSTINDEX=0&resourcetype=HWCIT ),


2006



“…We therefore undertook a

study to identify the brain

mechanisms by which stress can induce cardiac

arrhythmia through efferent

autonomic drive.”

“…We therefore undertook a

study to identify the brain

mechanisms by which stress can induce cardiac

arrhythmia through efferent

autonomic drive.”© HealthBuilderS®

2006


2006

“…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.”

“…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.”




2006

“…“…lateralization of central lateralization of central autonomic drive during autonomic drive during

stress results in stress results in imbalanced activity in imbalanced activity in right and left cardiac right and left cardiac sympathetic nerves.” sympathetic nerves.” This sympathetic driveThis sympathetic drive asymmetry disrupts the asymmetry disrupts the

heart’s ability to heart’s ability to repolarize, leading to a repolarize, leading to a

predisposition to predisposition to arrhythmia.arrhythmia.

“…“…lateralization of central lateralization of central autonomic drive during autonomic drive during

stress results in stress results in imbalanced activity in imbalanced activity in right and left cardiac right and left cardiac sympathetic nerves.” sympathetic nerves.” This sympathetic driveThis sympathetic drive asymmetry disrupts the asymmetry disrupts the

heart’s ability to heart’s ability to repolarize, leading to a repolarize, leading to a

predisposition to predisposition to arrhythmia.arrhythmia.




2006

“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.”




2006

“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.”




2006

“Brain activity associated with increased TWR (“T-wave residua”; i.e.,

proportion of the non-dipolar components of the T-wave) in response to stress was also

observed unilaterally in right midbrain, extending into adjoining thalamus and

hypothalamus.”




2006

“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.”




2006

“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 right-sided 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.”




2006

“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).”




2006

“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.”




2006

“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.”




2006

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.




2006

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.




2006

“Decreased Potentiation of Normal Reciprocal

Movements Impairs Cognitive Abilities”




2006

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.




2006



The cortical outflow is the sum of the effect of afferent and the resultant efferent

quality.

Quality = Timing

Afferentation vs. Deafferentation


2006



“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


2006

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!




2006

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.




2006

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




2006

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




2006



Receptor-driven cerebellar and

midbrain afferents

© HealthBuilderS®

2006


2006



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, McGraw-Hill.)


2006



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.)


2006

Type Group Speed CharacteristicsType A Group Ia 120M/s Annulospiral Endings of Muscle Spindles (Nuclear Bag)

Same as α-Type A fibers

Group Ib Golgi Tendon OrgansSame 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 & pricklingpain sensationsSame as γ & δ-Type A fibers

Type B Preganglionic parasympatheticMotor onlyLack much of an after hyperpolarization

Type C Group IV 0.5M/s Unmyelinated; nociception, temperature & crude touch; smallSame as Type C fibers

We know that specifically stimulated receptors send afferent signals according to their central

integrative state, at specific speeds




2006

LOCATION NERVE SA SE VE NOTE 1 NOTE 2

I Special Sensory

II Special Sensory

Mes~ III EWN; the highest

representation of the

autonomic NS

Ciliary Ganglia to the pupillary constrictor

muscle;Episcleral Nerve to

clilary muscle and lens

“ IV

“ V (Sensory) Branchial afferent (BA)

Pons V Branchial efferent (BE)

“ VI

“ VII BA, BE Superior Salvatory Nucleus to the Sphenopalatine

Ganglion and the lacremal glands;

Submandibilar Nucleus to the salvatory glands

“ VIII Special Sensory Cochlear and Vestibular Divisions

Medulla IX BA, BE Inferior Salvatory Nucleus to the Otic

ganglion and parotid glands

“ X BA, BE Dorsal Motor Nucleus and several others

“ XI BA, BE

“ XII

Spinal Cord C1(-C8) () No DRG

“ C2-8 ()

“ T1-L2 IMLCC

“ L3-S2 ()

“ S2-4 By Synapse Back to L3-S2




2006

Primary receptor afferents terminate in the dorsal horn where the signal can actually do any one or a combination

of 12 different things…



© HealthBuilderS®

2006


2006

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




2006

…This signal participates in

reflexive coordination

leading to some sort of efferent

response via the anterior horn --

“the final common

pathway”.

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.




2006

“…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




2006

Within the somatosensory cortex is a representation of the human body called the homunculus or " little man".




2006

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)






2006

Genetic expression and coupled manipulation techniques:

Deafferentation Coupled treatment

NeuraxisCell Nucleus

Genetic Changes Protein Replication in Muscle

Enhanced AbilitiesEnhanced Cortical Expression




2006

“…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




2006

“…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.”






2006

“…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




2006

The Cerebral Cortex and Motor Strip




2006

“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




2006

Major Cortical Fields in Planning and Execution of “Purposeful”

Movements




2006



Physiological reflexes, when working properly, display their

influence according to pre-programmed human

performance patterns. Any display other than that which is normal must be considered

pathological.


2006

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.




2006

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.




2006

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



The Deep Tendon

(Patellar) Reflex


2006

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.




2006

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




2006

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




2006

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




2006

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.




2006

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.




2006

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.




2006

Parallel, Climbing, Mossy & Purkinje Fibers with Golgi, Stellate, Granule & Basket Cells




2006Figure 4

A Schematic of the Pathways of Surround Inhibition

From Surround Inhibition – The Miracle of Upright Posture by Michael D. Allen, DC, NMD




2006

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 environment.




2006

“…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




2006

Contralateral Ipsilateral

Cortex

Thalamus

Cerebellum

PostureAutonomics

Joints




2006

The integration of each of the basal nuclei requires both

temporal and spatial summation of the vast array of information to the

basal ganglia.




2006

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




2006

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.




2006

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.




2006

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)




2006

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.




2006

“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 non-specific 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




2006




2006



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.


2006




2006

The Basal Gangliae modulate and regulate specific cortical

functions.

They are important for:Emotional Behavior

Learning of MovementMemory of Movement



AUTONOMICS

AUTONOMICS


2006

There are three basic aspects of movement:

Preparation Planning Execution

Efferent Copy Feedback

Feed Forward



AUTONOMICS

AUTONOMICS


2006

Rule #3:Modulation (inhibition) is the

secret to preprogrammed human performance and

reciprocal movementCorollary #1: Reciprocal joint motion

knocks out pain.

Corollary #2: Aerobics are the means to sustained performance.



AUTONOMICS

AUTONOMICS


2006

The basal ganglia integrates a vast number of “neurobehavioral

variables”:Muscle contraction patternsLimb movement patterns

Target locationMemory

Motivation



AUTONOMICS

AUTONOMICS


2006

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.




2006

Computing a Voluntary Movement

Reaching Movement:

Three Functional Levels

Input/Output of Cortical Motor Areas



© HealthBuilderS®

2006

Cortexm Cortexs

ThGPe

SThNeostriatum

GPi

SNc

SNr

SC

BS

The Nuclei of the Basal Gangliaand their Thalamocortical Neuronal Loop

Pathways

GPe: Globus Pallidus externusSTh: SubthalamusGPi: Globus Pallidus internusSNc: Substantia Nigra compacumSNn: Substantia Nigra SC: Superior ColliculusBS: Brain stemTh: Thalamus


2006

Cortexm Cortexs

ThGPe

SThNeostriatum

GPi

SNc

SNr

SC

BS

_

_

_

__

+

+

DIRECT PATHWAY


Thalamocortical Neuronal Loop Pathways


2006

Cortexm Cortexs

ThGPe

SThNeostriatum

GPi

SNc

SNr

SC

BS

_

+

_

_

__

_ _

_

++

+

INDIRECT PATHWAYDIRECT PATHWAY

+




2006

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.




2006

Cortexm Cortexs

ThGPe

SThNeostriatum

GPi

SNc

SNr

SC

BSGABA

_

+

_

_

__

_ _

_

++

+

+


INDIRECT PATHWAYDIRECT PATHWAY



2006

Cortexm Cortexs

ThGPe

SThNeostriatum

GPi

SNc

SNr

SC

BS

+

_

_

_

__

_ _

_

++

+

+

DOPA


GABAINDIRECT PATHWAYDIRECT PATHWAY



2006

Cortexm Cortexs

ThGPe

SThNeostriatum

GPi

SNc

SNr

SC

BSGLUT

+

_

_

_

__

_ _

_

+

_

+

+

+

_


DOPAGABAINDIRECT PATHWAYDIRECT PATHWAY



2006

Cortexm Cortexs

(PMC, M1, S-1, PMA) Th

GPe

STh Putamen

GPi

SNc

SNr

SC

BS

+

_

_

_

__

_ _

+

+

Motor Loop

+


GLUTDOPAGABAINDIRECT PATHWAYDIRECT PATHWAY



2006

Cortexm Cortexs

(DLPC, PMA, MTVC) Th

GPe

STh Caudate Nucleus

GPi

SNc

SNr

SC

BS

+

_

_

_

__

_ _

+

+

+

_

Oculomotor Loop





2006

Cortexm Cortexs

(DLPC, PPC, PMC)Th

GPe

STh Caudate Nucleus

GPi

SNc

SNr

SC

BS

+

_

_

_

__

_ _

+

+

+

Dorsolateral PrefrontalCortex (Assoc-1) Loop





2006

Cortexm Cortexs

(POPC, S/M/I Temp & Cing Gyr) Th

GPe

SThCaudate Nucleus

GPi

SNc

SNr

SC

BS

+

_

_

_

__

_ _

+

+

+

Lateral Orbital Frontal(Assoc-2) Loop





2006

The limbic loop describes the

vague understanding –

but excellent example – of

intangible connections

between emotions and cognition.

Limbic Loop

Cerebral cortex

Ventral Striatum

Ventral Pallidum

DMmc

An

t C

ing

& M

ed

Orb

/Fr

Are

as

(MO

FA)

(Hippocampal, entorinal cortex, and S/M/I Temporal gyrus)


2006

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.




2006

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.




2006

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.




2006

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.




2006

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.




2006

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.




2006

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.




2006

“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




2006



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.


2006



Allen Chiropractic A Professional Corporation

Sync-Think® Learning Lab “Brain-Based Learning with You in Mind!”

HealthBuilderS®

“Our Name Is What We Do Best!”

Clinical Update

Spring2006

The Educational Arm of Allen Chiropractic, a Professional Corporation

Documents

© HealthBuilderS ® 2006 “CARDIAC DISTRESS and Efferent Autonomic Drive” Presented by Michael D. Allen, DC, NMD, DIBAK, DABCN Chiropractic Neurologist Sync-Think