Scientific Basic of Pain

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Scientific Basic of Pain RM Clemmons, DVM, PhD, CVA. CVFT University of Florida

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Scientific Basic of Pain. RM Clemmons, DVM, PhD, CVA. CVFT University of Florida. PAIN. Unpleasant sensory and emotional experience associated with actual or potential tissue damage Functions: Stop Signal Warning of a threat Basis of learning Forces a person to rest. Terminology. - PowerPoint PPT Presentation

Transcript of Scientific Basic of Pain

Page 1: Scientific Basic of Pain

Scientific Basic of Pain

RM Clemmons, DVM, PhD, CVA. CVFTUniversity of Florida

Page 2: Scientific Basic of Pain

PAIN

• Unpleasant sensory and emotional experience associated with actual or potential tissue damage

• Functions: Stop Signal• Warning of a threat• Basis of learning• Forces a person to rest

Shortcut to BotoxHeadache.lnk Shortcut to TeenBackPain.lnk

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Terminology• Noxious – harmful, injurious

• Noxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals)

• Nociceptor – nerve receptors that transmits pain impulses

• Pain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissue

• Pain Tolerance – amount of pain a person is willing or able to tolerate

• Hyperesthesia – abnormal acuteness of sensitivity to touch, pain, or other sensory stimuli

• Paresthesia – abnormal sensation, such as burning, pricking, tingling

• Analgesic – a neurologic or pharmacologic state in which painful stimuli are no longer painful

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Overview of Neural Integration

Figure 15.1

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Neural pathways• Afferent pathways

• Sensory information coming from the sensory receptors through peripheral nerves to the spinal cord and on to the brain

• Efferent pathways• Motor commands coming from the brain and

spinal cord, through peripheral nerves to effecter organs

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Types of Nerves

• Afferent (Ascending) – transmit impulses from the periphery to the brain• First Order neuron• Second Order neuron• Third Order neuron

• Efferent (Descending) – transmit impulses from the brain to the periphery

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• Specialized cell or cell process that monitors specific conditions

• Arriving information is a sensation

• Awareness of a sensation is a perception

Sensory receptor

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• General senses• Pain• Temperature• Physical distortion• Chemical detection

• Receptors for general senses scattered throughout the body

• Special senses• Located in specific sense organs• Structurally complex

Senses

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• Each receptor cell monitors a specific receptive field

• Transduction• A large enough stimulus changes the

receptor potential, reaching generator potential

Sensory receptors

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Figure 15.2

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• Provide information on pain as related to extremes of temperature

• Provide information on pain as related to extremes of mechanical damage

• Provide information on pain as related to extremes of dissolved chemicals

• Myelinated type A fibers carry fast pain• Slower type C fibers carry slow pain

Three types of nociceptor

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• Found in the dermis• Mechaniceptors

• Sensitive to distortion of their membrane• Tactile receptors (six types)• Baroreceptors • Proprioceptors (three groups)

Thermoceptors and mechaniceptors

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Skin Tactile Receptors

Figure 15.3a-f

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Sensory Receptors• Mechanoreceptors – touch, light or deep

pressure• Meissner’s corpuscles (light touch), Pacinian

corpuscles (deep pressure), Merkel’s corpuscles (deep pressure)

• Thermoreceptors - heat, cold• Krause’s end bulbs ( temp & touch), Ruffini corpuscles

(in the skin) – touch, tension, heat; (in joint capsules & ligaments – change of position)

• Proprioceptors – change in length or tension• Muscle Spindles, Golgi Tendon Organs

• Nociceptors – painful stimuli • mechanosensitive• chemosensitive

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Nerve Endings• “A nerve ending is the termination of a nerve fiber

in a peripheral structure.”

• Nerve endings may be sensory (receptor) or motor (effector).

• Nerve endings may: • Respond to phasic activity - produce an impulse when

the stimulus is or , but not during sustained stimulus; adapt to a constant stimulus (Meissner’s corpuscles & Pacinian corpuscles)

• Respond to tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs)

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Nerve Endings• Merkel’s corpuscles/disks -

• Sensitive to touch & vibration• Slow adapting• Superficial location • Most sensitive

• Meissner’s corpuscles – • Sensitive to light touch &

vibrations• Rapid adapting• Superficial location

• Pacinian corpuscles -• Sensitive to deep pressure &

vibrations• Rapid adapting• Deep subcutaneous tissue

location

• Krause’s end bulbs – • Thermoreceptor

• Ruffini corpuscles/endings• Thermoreceptor• Sensitive to touch & tension• Slow adapting

• Free nerve endings -• Afferent • Detects pain, touch,

temperature, mechanical stimuli

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Nociceptors• Sensitive to repeated or prolonged stimulation

• Mechanosensitive – excited by stress & tissue damage

• Chemosensitive – excited by the release of chemical mediators• Bradykinin, Histamine, Prostaglandins, Arachadonic

Acid

• Hyperalgesia• Primary Hyperalgesia – due to injury

• Secondary Hyperalgesia – due to spreading of chemical mediators

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First Order Neurons• Stimulated by sensory receptors

• End in the dorsal horn of the spinal cord

• Types• A-alpha – non-pain impulses• A-beta – non-pain impulses

• Large, myelinated• Low threshold mechanoreceptor; respond to light touch & low-

intensity mechanical info• A-delta – pain impulses due to mechanical pressure

• Large diameter, thinly myelinated• Short duration, sharp, fast, bright, localized sensation (prickling,

stinging, burning)• C – pain impulses due to chemicals or mechanical

• Small diameter, unmyelinated• Delayed onset, diffuse nagging sensation (aching, throbbing)

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Second Order Neurons• Receive impulses from the FON in the dorsal

horn• Lamina II, Substantia Gelatinosa (SG) - determines the

input sent to T cells from peripheral nerve• T Cells (transmission cells): transmission cell that

connects sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain

• Travel along the spinothalmic tract • Pass through Reticular Formation

• Types• Wide range specific

• Receive impulses from A-beta, A-delta, & C• Nociceptive specific

• Receive impulses from A-delta & C

• Ends in thalamus

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Third Order Neurons

• Begins in thalamus

• Ends in specific brain centers (cerebral cortex)• Perceive location, quality, intensity• Allows to feel pain, integrate past

experiences & emotions and determine reaction to stimulus

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Descending Neurons• Descending Pain Modulation (Descending Pain

Control Mechanism)

• Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina)• Periaquaductal Gray Area (PGA) – release enkephalins• Nucleus Raphe Magnus (NRM) – release serotonin• The release of these neurotransmitters inhibit

ascending neurons

• Stimulation of the PGA in the midbrain & NRM in the pons & medulla causes analgesia.

• Endogenous opioid peptides - endorphins & enkephalins

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Neurotransmitters• Chemical substances that allow nerve impulses to move from one

neuron to another

• Found in synapses• Substance P

• thought to be responsible for the transmission of pain-producing impulses• Acetylcholine

• responsible for transmitting motor nerve impulses• Enkephalins

• reduces pain perception by bonding to pain receptor sites• Norepinephrine

• causes vasoconstriction • 2 types of chemical neurotransmitters that mediate pain

• Endorphins• morphine-like neurohormone; thought to pain threshold by binding to receptor sites

• Serotonin • substance that causes local vasodilation & permeability of capillaries

• Both are generated by noxious stimuli, which activate the inhibition of pain transmission

• Can be either excitatory or inhibitory

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• Three major pathways carry sensory information

• Posterior (Dorsal) column pathway

• Anterolateral pathway

• Spinocerebellar pathway

Somatic Sensory Pathways

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Figure 15.6

Ascending Tracts in the Spinal Cord

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• Carries fine touch, pressure and proprioceptive sensations

• Axons ascend within the fasciculus gracilis and fasciculus cuneatus

• Relay information to the thalamus via the medial lemniscus

Posterior column pathway

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Figure 15.8a, b

Dorsal Columns & Spinothalamic Tracts

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• Carries poorly localized sensations of touch, pressure, pain, and temperature

• Axons decussate in the spinal cord and ascend within the anterior and lateral spinothalamic tracts

• Headed toward the ventral nuclei of the thalamus

Spinothalamic pathway

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Role of Thalamus• Second order neurons transmit pain and temperature

signals to thalamus contralateral to stimulated receptor

• VPM processes pain and temperature signals from trigeminal (CNV) analog of spinothalamic system for head and neck

• VPL processes pain and temperature signals from peripheral regions of the body such as viscera, trunk and limbs

• Medial (intralaminar) thalamic nuclei process pain and temperature signals from reticular formation (spinoreticular fibers) such as raphe nuclei and locus coruleus

• Central (thalamic) pain signals cannot be localized (e.g., metastatic cancer) and central (thalamic) pain syndrome is relieved by producing electrical lesions in a thalamotomy procedure

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Role of Cerebral Cortex• Pain and temperature signals transmitted from VPL and

VPM (specific thalamic nuclei) to somatosensory cortices SI and SII for localization

• Pain and temperature signals transmitted from medial intralaminar (nonspecific) nuclei to all regions of cerebral cortex for “alerting” response, which induce wakefulness and inhibit sleep

• Pain and temperature signals also transmitted from intralaminar nonspecific nuclei to limbic system, hypothalamus and associated structures for emotional, endocrine, stress and autonomic responses which produce fear, suffering, cardiovascular, respiratory, gastrointestinal, urogenital and stress-related hormonal responses

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Where Does Pain Come From?• Cutaneous Pain

• sharp, bright, burning; can have a fast or slow onset

• Deep Somatic Pain • stems from tendons, muscles, joints, periosteum, & b.

vessels

• Visceral Pain • originates from internal organs; diffused @ 1st & later

may be localized (i.e. appendicitis)

• Psychogenic Pain • individual feels pain but cause is emotional rather than

physical

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Types of Pain: Classification by Duration

Acute pain•An unpleasant experience with emotional, cognitive, and sensory features, resulting from tissue trauma • Usually associated with

significant, observable tissue pathology

• Resolves with healing of causative injury

• Protective biological function to protect against further injury; protective reflexes include withdrawal, muscle spasm, and autonomic reactions

Acute vs chronic1

Chronic pain• Pain lasting beyond

expected recovery period and identifiable pathology insufficient to explain the pain state

• Disrupts sleep and normal activities of living

• Does not serve a protective, adaptive function

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Types of Pain: Classification by Etiology

Nociceptive pain• Results from normal function of

the nervous system• Caused when a noxious

stimulus (eg, trauma, inflammation, infection) activates A-delta and C nociceptors

— Visceral pain: originates in internal organs

— Somatic pain: originates in skin, muscle, skeletal structures

Nociceptive vs neuropathic1 Neuropathic pain

• Abnormal nociceptive signaling caused by an impairment of the nervous system

• Serves no functional or adaptive purpose

• Causes and examples— Metabolic: diabetic neuropathy— Infectious: herpes zoster— Trauma: nerve entrapment

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The Neurophysiology of Pain

• Nociception: process by which information about tissue

damage reaches the central nervous system • Transduction • Transmission• Perception• Modulation

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Pain Transduction• Nociceptor = pain receptor: specialized receptor for detecting

tissue injury/damage• Two classes of nociceptive afferent fibers

A-delta axon C axon

Type A-delta C

Caliber Small diameter, thinly myelinated

Small diameter, unmyelinated

Stimuli Thermal & high-threshold mechanical

Polymodal: high-intensity mechanical, chemical,

heat, cold

Conduction velocity (meters/sec)

5-30 0.5-2

Effect of activation Short, sharp, prickling pain More prolonged sensation

of dull pain

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Pain Transduction• Nociceptors do not spontaneously depolarize:

they send impulses (action potentials) only when stimulated

• No specialized pain “receptors”• The receptor region of the nociceptor is the free

terminal of the axon

• Ion channels in nerve terminal open in response to noxious stimuli, initiating an action potential, the “pain signal”

• Peripheral sensitization: local tissue injury with release of inflammatory mediators can enhance nociceptor response

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Small Diameter Afferent Fibers• Cutaneous mechanoreceptors

• Respond to nondiscriminative tactile stimuli

• Pinch, rub, stretch, squeeze• A-delta and C fiber, high-threshold

• Cutaneous thermoreceptors• Respond to transient change in

temperature• Innocuous ward and cool stimuli

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Small Diameter Afferent Fibers• Cutaneous nociceptors – cutaneous pain

• A-delta mechanoreceptors• Mechanical tissue damage

• C-polymodal nociceptors• Mechanical tissue damage, noxious thermal stimuli, endogenous

algesic chemicals

• C-fiber mechanonociceptors

• A-delta heat thermonociceptors

• A-delta, C-fiber cold thermonociceptors

• C-fiber chemonociceptors – algesic chemicals

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Pain Transmission• Nociceptors (primary sensory afferents) have cell body

in dorsal root ganglia; synapse to second-order neurons in dorsal horn of spinal cord

• Pain impulses can trigger a withdrawal reflex via connections to motor neurons in the spinal cord

• Impulses ascend to brain via various ascending tracts

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CNS Neurotransmitters of A-delta and C-fibers

• Substance P (Neuropeptide)

• Calcitonin Gene Related Peptide (CGRP)

• Excitatory amino acids – e.g., glutamate• Release in ischemia/hypoxia - neurotoxicity

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Pain Perception• Perception of and reaction to pain are influenced by social

and environmental cues, as well as by cultural norms and personal experience

• Both cortical and limbic systems are involved in conscious awareness (perception) of pain

• Recognition of location, intensity, and quality of pain is mediated by processing of signals from the spinothalamic tract > thalamus > somatosensory cortex

• Pain information processing in the brainstem, midbrain, and limbic system appear to mediate affective, motivational, and behavioral responses to painful stimuli

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Pain Modulation• Gate control theory advanced by Melzack and Wall

in 1965 focused on descending pathways from the brain to the spinal cord that inhibit pain signaling

• • Current view: signals originating in the brain can both

inhibit and facilitate pain signal transmission

• Neurotransmitters involved in these pathways include• Endogenous opiates (enkephalins, dynorphins, beta-

endorphins)• Serotonin• Norepinephrine

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Pain Control Theories• Gate Control Theory

• Central Biasing Theory

• Endogenous Opiates Theory

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Gate Control Theory• Melzack & Wall, 1965

• Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate’ – only allows one type of impulses to connect with the SON

• Transmission Cell (T-cell) – distal end of the SON

• If A-beta neurons are stimulated – SG is activated which closes the gate to A-delta & C neurons

• If A-delta & C neurons are stimulated – SG is blocked which closes the gate to A-beta neurons

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Gate Control Theory• Gate - located in the dorsal horn of the spinal cord

• Smaller, slower n. carry pain impulses

• Larger, faster n. fibers carry other sensations

• Impulses from faster fibers arriving @ gate 1st inhibit pain impulses (acupuncture/pressure, cold, heat, chem. skin irritation).

Brain

Pain

Heat, Cold, Mechanical

Gate (T cells/ SG)

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Central Biasing Theory• Descending neurons are activated by:

stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectations

• Cause release of enkephalins (PAG) and serotonin (NRM)

• Enkephalin interneuron in area of the SG blocks A-delta & C neurons

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Endogenous Opiates Theory• Least understood of all the theories

• Stimulation of A-delta & C fibers causes release of B-endorphins from the PAG & NRM

Or• ACTH/B-lipotropin is released from the anterior

pituitary in response to pain – broken down into B-endorphins and corticosteroids

• Mechanism of action – similar to enkephalins to block ascending nerve impulses

• Examples: TENS (low freq. & long pulse duration)

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Goals in Managing Pain

• Reduce pain!

• Control acute pain!

• Protect the patient from further injury while encouraging progressive exercise

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Other ways to control pain• Encourage central biasing – motivation,

relaxation, positive thinking

• Minimize tissue damage

• Maintain communication

• If possible, allow exercise

• Medications

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Opportunities for Pain Control

Local AP effects

Local & Segmental AP effects

Segmental AP effects

Systemic AP effects

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Romance• 10 month old Golden

Retriever

• 2 weeks history of lip twitches & abnormal behavior

• Mild CP deficit in R rear leg

S

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Romance• Localization of Lesion

• D• A• M• N• N• I• I• I• T• T• VO

Cerebral (Forebrain)

Genetic

EncephalitisGME

Brain Tumor

Liver Disease

Epilepsy

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Romance

P

• Problem List • Differential Dx• ?

• Diagnostic Approach• ?

• Treatment• ?

1. Facial Twiches

2. Ataxia

3. Behavioral Change

1. Inf/Inflam2. Neoplasia3. Inborn Error4. Liver5. Epilepsy

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Romance- -Diagnostic Approach• MDB

• CBC• Chemistry Profile• UA• Chest & Abdominal

Radiographs• Abdominal Ultrasound• Bile Acids• Cholinesterase• Ammonia level

• Neurologic Tests• EEG• CSF Analysis

• Cisternal• Titers• MRI

• Client EducationP

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Romance- -CBC

O

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Romance- -Chemistry

O

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Romance- -UA

O

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Romance- -MRI

L L

O

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Romance- -CSF Analysis• SPECIMEN: CSF – AO

• Color/Transparency: colorless/clear• Protein mg/dL 16• RBC/μL 46• WBC/μL 14

• A 32 cell differential count yielded the following:• 13 Neutrophils• 5 Lymphocytes• 14 Mononuclear phagocytes

• Two cytospin preparations are stained and microscopically examined. The slides are of adequate staining and preservation of cellular detail with scant hemodilution present against a colorless background that contains occasional squamous epithelial contaminants. Approximately equal numbers of mature, nondegenerate neutrophils and variably reactive mononuclear phagocytes are the predominant cell types. Small, well-differentiated lymphocytes are infrequently identified.

• No infectious agents or neoplastic cells are identified.

• Interpretation: Mild, mixed pleocytosis.

O

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Romance- -Titers (Serum)

• 3DX - Negative for Dirofilaria immitis antigen, Borrelia burgdorferi and Ehrlichia canis antibody.

• RMS - Negative for Rickettsia rickettsii IgG AB by IFA: Titer <64

• BLM - Negative for Blastomyces by AGID.

• DIS - CDV IgG AB: 50IgM AB: Negative

• CRC - Negative for Cryptococcus antigen by latex agglutination test

• TO1 – Toxoplasma IgG AB: NegativeIgM AB: Negative

• NEO - Negative for Neospora caninurn IgG AB by IFA: Titer <50

O

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Romance- -Final Diagnosis

Seizures Secondary toGME

A

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Romance- -Client Education• The prognosis is guarded to poor

• May continue to progress over 3-6 months

• Treat • phenobarbital• anti-inflammatory and anti-cancer drugs

• Consider CAVM & TCVM approaches to augment or instead of Western therapyP

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Romance- -TCVM exam• Tongue

• Red/purple

• Pulse• Superficial• Slippery• Fast

• Sensitivity• BL 15• Nao Shu

• TCVM Diagnosis

• Damp Heat with Internal Wind

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Romance- -TCVM Therapy• AP

• Cranial points• GV 20• GV 21• An Shen• Meng Men (staple)• GB 20

• Cancer points• LI 4• PC 6• GV 14• SP 9• ST 40• LIV 3

• Herbal

• Mind Damp Heat Formula• Jing Tang

• Di Tan Tang• Jing Tang

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Mansion of Mind Damp-Heat

Lonicera Jin Yin Hua Clear heat, Expel wind 20 gmForsynthia Lian Qiao Clear heat, Detoxify 20 gmIsatidis Ban Lan Gen Clear heat, Cool blood 20 gmAstragalus Huang Qi Move Qi (stimulate immune system) 20 gmAkebia Mu Tong Drain Damp-Heat 10 gmPlatycodon Jie Geng Transporter 15 gmLicorice Gan Cao Harmonizer 10 gm

Encephalitis, SRME, GME

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Cody• History of brainstem

tumor• leading to secondary

hydrocephalus• ~2.5cm mass• Probable

meningioma

• TCVM Dx• Blood Stagnation

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Cody (13 months)

• Western Rx• Phenobarbital• Prednisone

• TCVM• Stasis in Mansion of

Mind formula• Di Tan Tang• Max formula

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History• After electro-acupuncture (EA) analgesia was found

effectively to perform a surgery in China in the early 1970's, EA has been widely used in TCM practice.

Electro-acupuncture techniques

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Advantage: • More effective• Less treatments• Less acupoints• Save labor to manipulate the needles (Classically, the

needles should be manipulated every 2 to 3 minutes).• Objective control of frequency and amplitude

• Amplitude (intensity of stimulation): a tolerance level• Frequency:

• Low level: pain ----> beta endorphin mediated• High level: internal medicine> serotonin mediated

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Acupuncture Points: 6 to 10 pointsFrequency: 20 Hz Or 80 to 120 HzElectrical intensity: gradually goes to the

points the patient can tolerate.

Methods:

• Pain management• Bi syndromes (arthritis)• Soft tissue injuries• Disc problems• Colic/abdominal pain

• Peripheral nerve paralysis• Facial• Radial• Others

• Gastrointestinal conditions: vomiting, diarrhea, constipation, indigestion

•• Muscle atrophy

Indications:

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Contraindications:

• 1) Weak/deficient patients• 2) Heart problems• 3) Seizure/epilepsy• 4) Tumor

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1. Dial the AMPLITUDE and FREQUENCY to zero;2. Plug the wire leads into sockets 1 to 7 and fasten the clips to the handles of

needles;3. Set the desirable frequencies and wave forms

Frequency:

• Low frequency (F1 = 20-30 Hz)• Indication: pain conditions---Endorphin & Enkephalin release

• Moderate frequency (F1=80 to 120 Hz)• Indications: internal medical conditions (diarrhea etc)- -Dynorphin release

• High frequency (F1=200 Hz)• Indication: pain conditions- -Serotonin release

How to Use EA

Dynorphins

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Wave Form: depends on how F1 and F2 is set up

• Continuing Wave: F1=20-200; F2=0• Indications: pain conditions

• Intermittent wave: F1=0; F2=40• Indications: muscular atrophy

• Dense and Disperse (DD) wave: F1=80; F2 =120• Indications: nerve paralysis and internal medical conditions

How to Use EA

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4. Turn on the power 3

5. Gradually increase AMPLITUDE buttons until the patient can tolerate.a) Can increase amplitude a little bit every 5 minutes.

6. The duration of a treatment session: 10 to 30 minutes.

7. Turn off power to terminate the acupuncture treatment.

How to Use EA

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EA: how to pair the points

• 1) Bilateral connection• a. Pair BL-54 on left side to right BL54 for hip dysplasia;• b. Hua-tuo-jia-ji on the left to right side for disk diseases• c. BL-21 on the left to right BL-21 for vomiting• d. KID-1 on the left to right KID-1 for rear weakness• e. Left Ding-chuan + right Ding-chuan for cough

• 2) Same Channel connection.• a. GV-14 + Bai-hui for disk disease• b. LI-10 + LI-15 on the same side for shoulder pain• c. Tip of tail + GV-20 for vestibular dx, disk disease

• 3) Local connection• a. TH-14 + LI-15 on the same side for shoulder pain• b. GB-34 + ST-35 on the same side for stifle pain

• 4) Same energetic connection• ST-36 + GB-34 on the same side for vomiting, rear weakness• ST-36 + BL-20 on the same side for SP Qi deficiency

The general rules: The same lead to pair 2 points

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• 5) From the top to bottoms for paralysis • a. BL-54 + KID-1 for rear limb paralysis• b. PC-8 + GV-14 for front limb paralysis• c. GB-21 + HT-3 for front limb paralysis

• 6) Cover large areas• a. BL-20 on the left + right BL28 for T-L-S IVDD

• 7) Normal area to sick area• a. BL-21 to KID-1 for no deep pain caudal to BL-22• b. ST-5 left to right for right facial paralysis

EA: how to pair the points

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• But, we must pay attention to the following:• 1) The wire (lead) should NOT be connected around

the abdominal areas for pregnant moms.

• 2) The wire (lead) should NOT be connected through the chest if the patient has a pacemaker.

• 3) The wire (lead) should NOT be connected through the tumor mass.

• 4) Caution for seizure dogs when using EA

EA: how to pair the points

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GOD cures, Doctors send the bill!

-Mark Twain