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Transcript
Steele Taylor
presents:
A Neuro-Endocrine Approach to
The Obstetric and Pediatric Applications
of Tactile-Kinesthetic Stimulation Therapy
questions: [email protected]
slide show (fair use images removed): www.uvm.edu/~jstaylor/TKST.ppt
notes and citations: www.uvm.edu/~jstaylor/TKST.doc
The Touch Research Institute
http://www.miami.edu/touch-research/
•
•
•
http://www6.miami.edu/touch-research/research.htm
Research designs explore the following benefits that might be derived from massage:
– Alleviation of depression and anxiety
– Improved quality of sleep
– Pain reduction on neurological and soft-tissue levels
– Prevention of premature delivery
– Weight gain and cognitive/behavioral advances in premature infants
– Improved immune function and reduction of symptoms in auto-immune disorders
– Alleviation of eating disorders and dissonant body-perceptions
– Reduced anxiety and sense of empowerment in the practitioner or parent
– Improved social dynamic between practitioner and recipient (mother-infant, etc.)
Studies that compare massage to general relaxation methods demonstrate that tactilekinesthetic pathways are somehow involved to produce an effect that is beyond that of
relaxation
Inadequate elucidation of the physiological underpinnings, yet valuable information such as changes in hormone
and neurotransmitter levels in response to massage so that outsiders may produce their own hypotheses and
interpretations as to the underlying mechanisms
Some Complicating Endocrine Considerations
• Receptor Type+Expression+Signal Cascades Determine the Response
–
–
Selective Estrogen Receptor Modulation
Cardiovascular Epinephrine Receptors
–
–
Estrogen feedback to hypothalamus becomes positive to initiate ovulation
Clearance of steroid hormones
–
–
Non-genomic: Open/ close ion channels, activate/deactivate enzymes, perform exocytosis
Genomic: protein synthesis, cellular proliferation, cellular differentiation
–
–
Glucocorticoid (GC) permissive effects @ epinephrine binding sites
Action of estriol to influence oxytocin receptor expression during parturition
–
–
Fetal-Placental unit: substrates, precursors, active hormones
Levels are difficult to measure because activity is primarily local
–
–
Stress responses and coping behaviors
Placebo and somatoform phenomena
–
–
–
Thyroid, Adrenal Cortex, and Gonads profoundly impact brain development and function
Might be considered as peripheral-diffuse-modulatory-systems
Adipose, GI, and other tissues also hormonally regulate behavior
• Duration of the Signal Can Alter Feedback and Response
• Genomic Versus Non-Genomic Effects
• Inter-Hormonal Interactions
• Temporary Endocrine Glands
• Behavioral/Environmental Activators
• Endocrine Regulation of Brain/Behavior
Obstetric/Pediatric Complications
Treatable with Massage and
Explainable via Neuro-Endocrine Principles
1)
2)
3)
Back Pain / general discomfort during pregnancy
Depression/anxiety/stress during and/or after pregnancy
Premature or low birth weight delivery
Alex Grey www.alexgrey.com
Pain During Pregnancy:
•
•
Back pain affects over half of all pregnant women and may
significantly impact outlook, mood, daily activities, and sleep
Back Pain: Two Types
1) Lower Back
• Center of gravity moves anteriorly
• Loss of abdominal tone→ lumbar lordosis and spasm
• Increased pressure on intervertebral discs
2) Pelvic
• Relaxin - induced softening of pelvic ligaments and pubic
symphysis to produce pelvic widening
•
•
•
Crucial for successful delivery, not very convenient otherwise
Walking, lifting, rotating can become painful
Referred pain from inferior vena cava
•
Proper positioning to alleviate pressure
Mechanisms of Referred Pain
• Visceral and cutaneous nociceptor
•
•
•
•
axons converge on the same
interneurons in the spinal cord
Signal becomes mixed and visceral
pain is perceived as cutaneous
Important warning sign/diagnostic tool
Angina pectoralis is the classic
example
During pregnancy, pressure on the
inferior vena cava produces referrals to
the pelvic region and lower back
–
–
–
Immediate relief: positioning (left-sidelying)
Long term relief: yoga, chi gung, etc.
Ultimate relief: delivery!
http://www.mona.uwi.edu/fpas/courses/physiology/
neurophysiology/ReferredPainMech.gif
Pain Regulation in the Spinal Cord:
The Gate Theory
• Cutaneous nociceptors (pain) and
•
mechanoreceptors (touch, pressure)
interact with ‘gating’ interneurons in
the dorsal horns
Mechanical stimulation at the site of
pain may override/inhibit the
projection of a pain signal up the
spinothalamic tract
–
–
Instinctively rubbing/compressing
bruised tissue
Broad gliding, friction, and vibrating
massage strokes
www.burtonreport.com/images/GateTheory432GIF.gif
http://www.nursece.com/onlinecourses/imagesPain/Fig2.gif
Pain Regulation in the Brain:
The Mother’s Kiss and Placebo Mechanisms
http://www.annkullberg.com/Shows/2003/Hild.jpg
•
•
•
http://www.sciencemag.org/cgi/content/full/288/5472/1769
Cross-talk occurs between higher emotional regions, ascending pain-signals, ascending pressure signals,
pain-localization regions, pain-anticipatory and avoidance regions, analgesia anticipatory regions (placebo
regulators), and pain regulating pathways
Emotional status powerfully influences the degree of pain that is perceived
Sympathetically maintained pain = centrally produced hyperalgesia
–
•
•
Nociceptors become sensitive to and activated by norepinephrine due to prolonged exposure
Periaqueductal gray matter (PAG) of the midbrain, appears to be a critical mechanism in pain regulation,
and may be innervated by endorphin producing neurons of the hypothalamus, as well as other regions
– Electrical stimulation of the PAG produces remarkable analgesic effects
– Top-Down Effect: PAG activates serotonergic cells in the rostral ventral medial nuclei (RVM) of the
brainstem, which projects axons down the spinal cord that can effectively stifle pain signals
Distracting tasks are highly effective analgesic tools
– Lamaze breathing, visualization, massage, other
Pain Regulation at the Soft Tissue Level
www.amazingbirths.com/images/massage.jpg
www.yogaretreats.ie/images/Nataraj2.jpg
• Muscle tightness/spasm may compress nerves or obstruct vascular supply
• Hypoxia / ischemia triggers pain pathways via vascular signals and irritating waste
products from anaerobic muscle metabolism
–
Inflammation may also occur as a result, causing local hyperalgesia
• Massage therapy shuts off spasm/holding patterns on a neurological level
• Golgi tendon organs reflexes inhibit muscle contraction
• Disruption of holding patterns generated beneath the awareness of the brain
•
– Massage therapy improves local circulation thus alleviating local ischemia
• Performed gradually and over a series of treatments to avoid reperfusion injury
Massage, stretching, and strengthening all help to stabilize and maintain normal joint
position and function, especially in the lower back and pelvic regions
Potential Factors Promoting and Alleviating
Stress During Pregnancy
Psychoendocrinological research cites the following factors as activators and deactivators of stress responses,
as determined by GC levels, skin conductance response, sympathoadrenal activity, etc.
STRESSOR
1) Uncertainty, lack of control,
inadequacy (perceived):
•
•
labor (acute)
motherhood (perpetual)
1)
COUNTER-STRESSOR
Gain mastery of situation
•
Education, planning, birthing classes,
strategizing, networking, nesting, etc.
2) Frustration: inability to perform
tasks previously capable of
performing
2) Find new rewarding tasks, future
3) Environmental withdrawal and/or
exposure to novel settings
3) Embrace and network in new env.
•
•
Movement, consumption, career,
travel, etc.
Workplace withdrawal, new
dwelling, new community, etc.
4) Social withdrawal, low social
support, novel social settings
•
Spouse/father, family, friends,
colleagues
5) Pain and discomfort
oriented versus prisoner of the past
•
•
•
Walking, yoga, swimming, etc.
Consume flavorful, colorful, and
intriguing foods and beverages:
Nesting behavior: prepare dwelling
for amazing new occupant
4) Embrace and pursue supportive/
rewarding relationships
•
Fetus, family, spouse, friends with
children
5) Go Shopping…
(many of these stimuli/stressors are non-removable and beyond our scope as health
care practitioners…treatment must occur on the level of adaptation and coping)
Fetal Consequences of Traditionally Prescribed
Anti-Depressant and Anxiolytic Agents
•
•
•
•
Benefits/risks must be weighed before use during pregnancy
Tricyclic antidepressants, SSRI’s, MAOI’s, benzodiazepenes, etc.
Most are not likely teratogens, yet most are grade C or lower and cross placenta
Neonatal-withdrawal is a common result of fetal exposure
–
–
Inconsolable crying, irritability, feeding difficulties, tachycardia, blood sugar abnormalities
May last weeks to months
–
–
Growth Malformations (imipramine, amitriptyline and relatives)
Neonatal Withdrawal
–
Growth Malformations (tranylcypromine, isocarboxazid)
–
More research necessary, caution recommended
–
–
Neonatal Withdrawal Symptoms
Cleft-Palate and other malformations (diazepam, chlordiazepoxide)
–
–
–
–
May be necessary if severe epilepsy or severe anxiety prior to labor
Minor congenital defects
Fetal hemorrhage
Neonatal withdrawal
• Tricyclic antidepressants: Grade B-D
• MAOI’s: Grade C
• SSRI’s: Grade B (fluoxetine, sertraline, etc.), C (fluvoxamine)
• Benzodiazepenes: Grade D
• Barbiturates: just don’t
General Adaptation Syndrome Model
Alarm →
Maintenance →
Exhaustion
Sympathoadrenal
Activation
Glucocorticoid
Activation
Prolonged
Exposure
• (Occurs via brainstem and
amygdala input to hypothalamus)
• Glycogenolysis and
gluconeogenesis (without muscle
proteolysis)
• Increased heart rate
• Shunting of blood to brain,
lungs, and skeletal muscle
• Bronchial dilation
• Inhibition of enteric division of
ANS
• Pupil dilation
• Sustained catecholamine action
• Continued gluconeogenesis with
additional muscle proteolysis
• Continued lipolysis
• Reduced inflammation
•(stabilize lysosomal membranes)
•(inhibit leukocyte migration to
affected tissue)
• Behavioral/emotional
adaptations
(Or inability to either accept
(habituate/cope) or take control
over a non-removable stimuli)
• Muscle wasting
• Hyperglycemia and
diabetogenesis
•Immuno-atrophy
•Vascular derangement
• GI ulcerations
•Depression / anxiety
• Excess/inappropriate
sympathoadrenal activation
•Polyuria
• Hippocampal atrophy
• Gonadal suppression
Factors Promoting Excess GC Output
• GC’s are a reliable indicator of the degree of stress that is experienced by
•
•
•
•
•
the organism in environmental settings
Prolonged exposure and/or failure to cope will produce over-stimulation of
the hypothalamic-pituitary-adrenal axis
GC’s are lipid soluble and readily diffused across blood-brain-barrier
Widespread receptors in brain account for GC’s ability to influence behavior
Slow clearance from cerebrospinal fluid causes prolonged exposure in brain
Delicate feedback loop increases susceptibility to hypercortisolemia:
– Feedback regulation of hypothalamic CRH secretions is heavily dependent on
inhibition from the hippocampus, which heavily expresses GC receptors
– Ironically, although hippocampal cells rely on GC’s for their development,
repeated exposure can cause hippocampal atrophy and apoptosis
• Reduced feedback causes out of control GC production and vicious cycle
• Hypercortisolemia produces a cascade of physiological impairments and
neurological/behavioral alterations as demonstrated on previous slide
• Infants born to depressed mothers tend to mimic the maternal biochemical
and physiological constitution, including elevated glucocorticoid levels,
reduced serotonin and dopamine levels, and behavioral dysfunction
Can Stress-Related Maternal Hypercortisolaemia
Contribute to the Premature Onset of Parturition?
• IF… Stress and depression during pregnancy produce an increased
risk for premature delivery, and associated complications
• AND… Massage therapy is a highly effective drug-free treatment
for the alleviation of stress and depression
• THEN… Regular massage during pregnancy can dramatically
reduce the occurrence of premature delivery and associated
complications
– To support this we must establish:
1)The role of stress hormones in the onset of parturition
2)The pathways through which massage may alleviate stress
hormone activity
Endocrinology of Parturition
•
Considerable evidence suggests that the fetal lungs and brain are responsible for
the initiation of labor, and that children continue to control their parents
throughout life…
Late in gestation, the fetal adrenal cortex grows considerably, and under the
influence of the CRH-ACTH axis, produces large amounts of GC’s and DHEAS
•
–
–
–
Fetal GC’s stimulate maturation of organs, particularly the lungs
Fetal GC’s stimulate the placenta to increase the conversion of progesterone to estrogens,
particularly to estriol or E3 , ( the fetal adrenal supplies 90% of the precursor: DHEAS)
Estriol acts on the uterus to:
1)
Increase the output of prostaglandins, which prime the contractile proteins
2)
Promote the formation of gap junctions within the uterus, which help to effectively coordinate
expulsion of the fetus
Promote the expression of oxytocin receptors, which help maintain contractions
Promote collagenase enzymes that ripen the cervix by degrading fibrous connective tissue
–
•
3)
4)
Oxytocin, normally antagonized by progesterone, can now operate on uterus
•
Positive feedback loop is generated as uterine proprioceptors prompt the release of more oxytocin
Fetal protection from maternal glucocorticoids:
–
–
–
Placenta deactivates 85% before they reach fetus
ALL fetal tissue expresses enzymes that deactivate maternal cortisol
•
(11-hydroxysteroid dehydrogenase)
Fetus maintains high levels of progesterone, which have a stronger binding affinity for
GCR’s
Preterm Labor Epidemiology
• Stress, depression, infection, preeclampsia, fetal/placental
hypoxia, diabetes, previous PTL, anemia, hyperthyroidism,
smoking, and acute emergency conditions (hemorrhage, etc.) all
contribute to PTL
• In acute cases, it is contraindicated to prevent PTL
• Preventative strategies should be observed by all women, since only
50 % of PTL’s exhibit identifiable risk factors
• USA has a higher PTL rate than most industrialized countries
– Over 10% of pregnancies, with occurrence still rising
– Responsible for 75% of neonatal morbidity and mortality
– Neonatal Intensive Care = $5 billion annually
• Emotional hardship, economic drain, long-term complications
Preterm Labor Onset
1) Infection (vaginal, uterine, intraamniotic)
•
•
•
•
•
•
May cause up to 30% of preterm deliveries
Cytokines released from leukocytes fighting infection may prompt prostaglandin
(PG) release
Bacterial phospholipases may also increase free PG levels
Concurrent reduction in levels of PG dehydrogenase (PGDH), an enzyme that
deactivates PG’s and that is normally maintained at high levels during gestation
Glucocorticoids may also reduce the expression of PGDH
Infection may ultimately be linked to general immunosuppression
resulting from hypercortisolaemia associated with stress and depression
2) Preeclampsia and Fetal-Placental Hypoxia
•
•
•
•
Fetal CRH increases which stimulates increase in placental CRH
Placental CRH operates as a vasodilator
If the attempt to restore blood flow fails, CRH stays high
Fetal adrenal response to CRH-ACTH triggers placenta to initiate labor
3) Disruption of Feedback Systems From Chronic GC Exposure
4) Other Adverse Fetal Environments
Mechanisms Involved In Physiological
Responses to Massage
• Tactile - kinesthetic pathways, including oral, apparently interact
with the brain and particularly the hypothalamus to:
–
–
–
–
–
–
–
Diminish stress responses and reduce mobilization of energy reserves
Increase levels of serotonin, dopamine, and norepinephrine
Improve sleep patterns
Shift relative EEG activity from right frontal cortex to left frontal cortex
Activate pain-reduction pathways and reduce pain at its origins
Release growth-hormone releasing hormone (infants)
Strengthen vagal activity
• Improved gastric motility
• Increased digestive and absorptive hormones such as gastrin and insulin
• Reduce heart rate
• Anatomical interactions between touch receptors and the hypothalamus via
the thalamus and somatosensory cortex are necessary to enable such
dramatic physiological alterations
Tactile-Kinesthetic Stimulation Benefits via
Nonnutritive Suckling, Kangaroo Care and Massage
• Nonnutritive Suckling: the first coping mechanism (98% of NICU’s)
– Powerful instinct upon birth also occurring in womb as early as 5 months gestation
– Analgesic effect reduces fussiness during painful procedures
– Improved sleep patterns (REM), growth rates, and shorter hospital stays
• Kangaroo Care: tactile, kinesthetic, vestibular, and thermal stimulation (97% of
NICU’s)
– Improved breastfeeding habits, reduced infections, and shorter hospital stays
• Massage Therapy: Dynamic tactile – kinesthetic stimulation (39% of NICU’s)
– Deeper pressure is important: light touch may be perceived as aversive
– Enhanced growth, social responsiveness, motor behavior, habituation, parental
interaction, and shorter hospital stays
– (in rats, maternal tongue licking is essential for normal growth and behavior)
A Neonatal Massage Sequence Utilized
In A TRI Experimental Design
• Experimenters treated 40 infants delivered on average 9 weeks preterm and having
•
•
•
•
•
•
•
experienced 3 weeks of intensive care, weighing 2 lbs on average, and free of congenital
heart malformations, CNS disturbances, and other anomalies
Performed through portholes of incubator
Procedure: 45 minutes for 10 days at 3 x 15 minute treatments
– 5 minutes tactile stimulation
– 5 minutes kinesthetic stimulation
– 5 minutes tactile stimulation
Tactile stimulation: Prone
– From top of head to neck and back x 12
– From neck across shoulders and back x 12
– From upper back to waist and back x 12
– From hips to feet and back on both legs x 12
– From shoulders to the hands and back on both arms x 12
Kinesthetic treatment: Supine
– Flexion / extension (bicycling) to individual arms and legs and then both
Results consistent with benefits listed on previous slide
Infants released from hospital on average 6 days earlier than control group!
Field T, Schanberg SM, ScafidiF et al 1986 Tactile / kinesthetic stimulation effects on preterm infants. Originally
published in Pediatrics 77: 654-658, Reproduced in Field T 2000 Touch Therapy. Edinburgh: Churchill Livingston.
Resources:
• Bear MF, Connors BW & Paradiso MA 2007 Neuroscience: Exploring
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the Brain. 3rd edition. Philadelphia: Lippincott Wilkins and Williams.
Briggs GG, Freeman RK & Yaffe SJ 1998 Drugs in Pregnancy and
Lactation. 5th edition. Baltimore: Williams and Wilkins.
Brush FR & Levine S 1989 Psychoendocrinology. San Diego:
Academic Press Inc.
Field T 2000 Touch Therapy. Edinburgh: Churchill Livingston.
Field T 2003 Stimulation of Preterm Infants. Pediatrics in Review.
2003;24:4-11. Hadley ME 2000 Endocrinology. 5th edition. New
Jersey: Prentice Hall
Gilbert ES 2007 Manual of High Risk Pregnancy and Delivery. 4th
edition. St. Louis: Mosby Elsevier.
Karch AM 2006 Focus on Nursing Pharmacology. 3rd edition.
Philadelphia: Lippincott Wilkins and Williams.
McMahon SB & Koltzenburg M 2006 Wall and Melzack’s Textbook of
Pain. 5th edition. Elsevier Churchill Livingston.
Tulchinsky D & Little AB 1994 Maternal – Fetal Endocrinology. 2nd
edition. Philadelphia: W.B. Saunders Company
Van Praag HM, de Kloet R & van Os J 2004 Stress, the Brain and
Depression. Cambridge: Cambridge University Press.