Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
“CARDIAC DISTRESS and Efferent Autonomic Drive” Presented by Michael D. Allen, DC, NMD, DIBAK, DABCN Chiropractic Neurologist HealthBuilderS® The Educational Arm of Allen Chiropractic, PC “Our Name is What We Do Best!”® © HealthBuilderS® 2006 Allen Chiropractic A Professional Corporation Sync-Think® Learning Lab “Brain-Based Learning with You in Mind!”® 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 2 CARDIAC DISTRESS & 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 3 CARDIAC DISTRESS & Efferent Autonomic Drive “…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.” © HealthBuilderS® 2006 4 CARDIAC DISTRESS & Efferent Autonomic Drive “…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 5 CARDIAC DISTRESS & Efferent Autonomic Drive “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.” © HealthBuilderS® 2006 6 CARDIAC DISTRESS & Efferent Autonomic Drive “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.” © HealthBuilderS® 2006 7 CARDIAC DISTRESS & Efferent Autonomic Drive “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.” © HealthBuilderS® 2006 8 CARDIAC DISTRESS & Efferent Autonomic Drive “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 9 CARDIAC DISTRESS & Efferent Autonomic Drive “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 10 CARDIAC DISTRESS & Efferent Autonomic Drive “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 11 CARDIAC DISTRESS & Efferent Autonomic Drive “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.” © HealthBuilderS® 2006 12 CARDIAC DISTRESS & Efferent Autonomic Drive “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 13 CARDIAC DISTRESS & Efferent Autonomic Drive 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 14 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 15 CARDIAC DISTRESS & Efferent Autonomic Drive “Decreased Potentiation of Normal Reciprocal Movements Impairs Cognitive Abilities” © HealthBuilderS® 2006 16 CARDIAC DISTRESS & Efferent Autonomic Drive 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 17 CARDIAC DISTRESS & Efferent Autonomic Drive The cortical outflow is the sum of the effect of afferent and the resultant efferent quality. Quality = Timing Afferentation vs. Deafferentation © HealthBuilderS® 2006 18 CARDIAC DISTRESS & Efferent Autonomic Drive “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 © HealthBuilderS® 2006 19 CARDIAC DISTRESS & Efferent Autonomic Drive 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! © HealthBuilderS® 2006 20 CARDIAC DISTRESS & Efferent Autonomic Drive 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 21 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 22 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 23 CARDIAC DISTRESS & Efferent Autonomic Drive Receptor-driven cerebellar and midbrain afferents © HealthBuilderS® 2006 24 CARDIAC DISTRESS & Efferent Autonomic Drive 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.) © HealthBuilderS® 2006 25 CARDIAC DISTRESS & Efferent Autonomic Drive 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 26 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 Unmyelinated; nociception, temperature & crude touch; small Same as Type C fibers 27 CARDIAC DISTRESS & Efferent Autonomic Drive 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 28 CARDIAC DISTRESS & Efferent Autonomic Drive 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 29 CARDIAC DISTRESS & Efferent Autonomic Drive 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 30 © HealthBuilderS 2006 CARDIAC DISTRESS & Efferent Autonomic Drive …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. 31 CARDIAC DISTRESS & Efferent Autonomic Drive “…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 ® © HealthBuilderS 2006 CARDIAC DISTRESS & Efferent Autonomic Drive Within the somatosensory cortex is a representation of the human body called the homunculus or " little man". © HealthBuilderS® 2006 33 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 34 CARDIAC DISTRESS & Efferent Autonomic Drive Genetic expression and coupled manipulation techniques: Deafferentation Coupled treatment Neuraxis Cell Nucleus Genetic Changes Protein Replication in Muscle Enhanced Abilities Enhanced Cortical Expression © HealthBuilderS® 2006 35 CARDIAC DISTRESS & Efferent Autonomic Drive “…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 36 CARDIAC DISTRESS & Efferent Autonomic Drive “…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 37 CARDIAC DISTRESS & Efferent Autonomic Drive “…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 38 CARDIAC DISTRESS & Efferent Autonomic Drive The Cerebral Cortex and Motor Strip © HealthBuilderS® 2006 39 CARDIAC DISTRESS & Efferent Autonomic Drive “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 © HealthBuilderS® 2006 40 CARDIAC DISTRESS & Efferent Autonomic Drive Major Cortical Fields in Planning and Execution of “Purposeful” Movements © HealthBuilderS® 2006 41 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 42 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 43 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 44 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 45 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 46 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 47 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 48 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS 2006 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 50 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 51 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 52 CARDIAC DISTRESS & Efferent Autonomic Drive Parallel, Climbing, Mossy & Purkinje Fibers with Golgi, Stellate, Granule & Basket Cells © HealthBuilderS® 2006 53 CARDIAC DISTRESS & Efferent Autonomic Drive ® 2006 © HealthBuilderS From Surround Inhibition – The Miracle F ig u r e 4 of Upright Posture by Michael D. Allen, DC, NMD 54 CARDIAC DISTRESS & Efferent Autonomic Drive 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 55 CARDIAC DISTRESS & Efferent Autonomic Drive “…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 56 CARDIAC DISTRESS & Efferent Autonomic Drive Contralateral Ipsilateral Cortex Thalamus Cerebellum Posture Autonomics © HealthBuilderS® 2006 Joints 57 CARDIAC DISTRESS & Efferent Autonomic Drive The integration of each of the basal nuclei requires both temporal and spatial summation of the vast array of information to the basal ganglia. © HealthBuilderS® 2006 58 CARDIAC DISTRESS & Efferent Autonomic Drive 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 © HealthBuilderS® 2006 59 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 60 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 61 CARDIAC DISTRESS & Efferent Autonomic Drive 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) © HealthBuilderS® 2006 62 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 63 CARDIAC DISTRESS & Efferent Autonomic Drive “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 64 ® © HealthBuilderS 2006 CARDIAC DISTRESS & Efferent Autonomic Drive © HealthBuilderS® 2006 65 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 66 CARDIAC DISTRESS & Efferent Autonomic Drive © HealthBuilderS® 2006 67 CARDIAC DISTRESS & Efferent Autonomic Drive The Basal Gangliae modulate and regulate specific cortical functions. They are important for: Emotional Behavior Learning of Movement Memory of Movement © HealthBuilderS® 2006 68 CARDIAC DISTRESS & Efferent Autonomic Drive There are three basic aspects of movement: Preparation Planning Execution © HealthBuilderS® 2006 Efferent Copy Feedback Feed Forward 69 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 70 CARDIAC DISTRESS & Efferent Autonomic Drive The basal ganglia integrates a vast number of “neurobehavioral variables”: Muscle contraction patterns Limb movement patterns Target location Memory Motivation © HealthBuilderS® 2006 71 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 72 CARDIAC DISTRESS & Efferent Autonomic Drive Computing a Voluntary Movement Reaching Movement: Three Functional Levels Input/Output of Cortical Motor Areas © HealthBuilderS® 2006 73 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 Th _ Thalamocortical Neuronal Loop Pathways DIRECT PATHWAY 75 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 © HealthBuilderS® 2006 STh _+ _ _ _ Th _ Thalamocortical Neuronal Loop Pathways DIRECT PATHWAY INDIRECT PATHWAY 76 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 77 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 STh _+ _ _ _ Th _ Thalamocortical Neuronal Loop Pathways DIRECT PATHWAY INDIRECT PATHWAY GABA DOPA GLUT 80 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 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 © HealthBuilderS® 2006 85 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 86 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 87 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 88 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 89 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 90 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 91 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 92 CARDIAC DISTRESS & Efferent Autonomic Drive “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 © HealthBuilderS® 2006 93 CARDIAC DISTRESS & Efferent Autonomic Drive 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. © HealthBuilderS® 2006 94 CARDIAC DISTRESS & Efferent Autonomic Drive 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!” © HealthBuilderS® 2006 95