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115 Cards in this Set
- Front
- Back
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characteristic responses to changes in physical stress
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Decreased (↓ed) stress tolerance
Maintenance of stress tolerance Increased (↑ed) stress tolerance Injury Death |
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What happens when physical stress < maintenance range
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↓ed tissue tolerance to subsequent stresses
Atrophy Tissue degeneration > Tissue production |
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What happens when physical stress > maintenance range
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↑ed tissue tolerance to subsequent stresses
Hypertrophy Tissue production > Tissue degeneration Increases in: X-sectional area Density Volume |
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levels of exposure to physical stress
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Magnitude
Time Duration, repetitions, rate Direction of stress Tension Compression Shear Torsional |
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What kind of stress causes tissue injury
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High magnitude, brief duration
Low magnitude, long duration Moderate magnitude, applied repeatedly |
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Inflammation Follows Tissue injury
May result in |
May result in:
Further tissue injury Less stress tolerance |
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Implications for PT
Evaluation & Intervention |
Physiologic Factors
Medications Age Pathology / Disease Obesity Psychosocial Factors |
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Stages of the healing process
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Inflammatory Response Phase
(Acute Inflammation) Pain at rest or w/ min movement Fibroblastic Repair Phase (Subacute—Tissue Repair Phase) Pain during movement / activity / tissue resistance Maturation and Remodeling Phase Pain after activity / significant tissue resistance I Q |
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Acute inflammation stage
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~ Days 1-4 after injury***
Consists of: Vascular Response I Q Hemostatic Response Cellular Response (phagocytosis) All 3 help prepare tissue for healing and re-growth |
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Vascular response in acute inflammation stage
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Vasoconstriction followed by Vasodilation
Constricting of blood vessels in injured tissues Minimizes blood loss Occurs almost immediately Duration ~ 5-10 minutes Stimulated by chemicals released from endothelial cells and adrenal system Serotonin Nor-epinephrine Dilating or “opening” of the blood vessels Begins within minutes Caused by the release of “chemical mediators” From injured cells From Mast Cells accumulation and adhesion of leukocytes to the epithelial cells of blood vessel walls at the site of injury in the early stages of inflammation. What is net result inc. capillary permeability leading to inc. proteins in interstitial |
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Chemical mediators of vasodilation
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Histamine
Stimulates vasodilation Increases capillary membrane permeability Released by Mast Cells Prostaglandins Stimulate vasodilation React with other substances to cause pain Released from damaged cells BRADYKININS |
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Mast cells release
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Histamine
Stimulates vasodilation Increases capillary membrane permeability Substances that attract leukocytes (WBC’s) Leukotrienes Neutrophil chemotaxic factor Heparin Prevents clotting from occurring too early |
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Purpose of vasodilation
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Increase in blood flow
Increase capillary permeability Both allow delivery of: White blood cells Nutrients for healing |
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Hemostatic response of acute inflammatory phase
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Localizes Inflammatory Process
Controls blood loss / Isolates Area Small blood vessels retract and seal Platelets adhere to collagen fibers in vessel walls exposed by injury Allows additional platelets and leukocytes to adhere and form a “plug” Results in a clot Thromboplastin released from damaged cell Stimulates the conversion of a series of plasma proteins |
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Inflammation events leading to edema
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Vasodilation
Causes an increase in blood and plasma flow to injured tissues Increased capillary permeability Allows more leakage of plasma proteins into interstitial tissues Membranes broken during injury Allows membrane proteins to accumulate in interstitial tissues |
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Collagen types
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Type I
Tendon, ligament, scar, jt. capsules Fibroblast Thick, dense fibrils Resist Tension Type II Hyaline Cartilage Chondroblast Loose fibril network Resist intermittent pressure |
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Crimp
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Waves formed in collagen fibers
Made by attachments of GAG’s Organic molecules in ground substance Crimp waveforms straighten when stretched |
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Myofibroblasts
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“Specialized cells derived from same undifferentiated tissue as fibroblasts”
Have contractile properties Cause scar shrinkage Attach to surrounding tissues and pull margins inward Appear around day 5*** |
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Flowers and Pheasant study
6 weeks cast immobilization uninjured fingers |
Flowers and Pheasant
6 weeks cast immobilization uninjured fingers full ROM restored within minutes PROM |
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Time Frames Associated with CT Changes (Animal Studies):
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In absence of stress and movement:
1st gross disorganization (Atrophy) 2-6 weeks 2nd development of contractures 4-6 weeks → Shortening/contracture >7 weeks → Severe contracture Langenskiold pg 49 Currier and Nelson |
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Connective Tissue Changes Associated with Immobilization
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Atrophy of fibers
Loss of mobility b/w adjacent fibers (Not necessarily a contracture) Attachments b/w fibers Loss of H2O Fibers shortened 2ndary to remodeling (Contractures) |
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Facilitation of healing through joint mobilization
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May accomplish this thru:
↑ed circulation Normalizes joint nutrition ↑ed joint H2O content Therapeutic stresses to connective tissue Prevents further weakening of tissue |
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Why do joint mobs?
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Test for joint restrictions
Reduce joint restrictions Pain relief Reduce muscle guarding Promote normal movement thru proprioceptive training Promote tissue healing Prevent / Minimize complications |
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Maitland's grades of joint mobilization
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Grade I
Small amplitude motion at beginning of available range Grade II Large amplitude motion within available range but not reaching limit of the range Grade III Large amplitude motion performed up to the limit of range Grade IV Small amplitude movement performed at limit of range Grade V Manipulation Small amplitude, high velocity thrust performed at limit of range |
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Characteristics of large diameter afferents
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Thick myelin sheaths
Wide in diameter Fast conduction velocity Because of above aspects Carry non-noxious (non-painful) stimuli 2 types A-alpha A-beta |
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Characteristics of small diameter afferents
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Less myelinated
Smaller in diameter Slower conduction velocity Carry info about: Mechanical, thermal, chemical ∆’s Includes noxious (painful) stimuli 2 types A-delta fibers C fibers |
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Pain transmission pathways
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Transmission of pain and temperature stimuli through CNS follow similar pathways
Pathways are named Spinothalamic tract*** Spinoreticular tract Spinoencephalic tract |
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Gate theory of pain control
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A-beta fibers (non-noxious input) stimulate substantia gelatinosa in SC
Substantia gelatinosa inhibits transmission of impulses from A-delta & C fibers (noxious input) onto 2nd order neurons Inhibition of A-delta & C fiber transmission “closes the gate” |
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Central Biasing Model
(Descending Control Mechanism) |
Brief intense pain stimulus to higher centers of brain
Impulse carried thru higher centers (PAG -> Raphe Nucleus) These relay impulses that descend thru the spinal chord Serotonin is released at spinal level to inhibit the SON Synapse on enkephalin interneuron Blocks substance P |
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Beta endorphin release
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Descending Mechanism of Control
Prolonged intense stimulus to higher centers of brain Passes thru higher centers (Reticular formation, Hypothalamus) Beta endorphin released at Hypothalamus Stimulates other higher centers (PAG, Raphe Nucleus) These relay impulses that descend thru the spinal chord Synapse on enkephalin interneuron Blocks substance P Clinical Sources Analgesia via prolonged intense stimulus TENS Low pulse rate, long pulse width These parameters perceived as uncomfortable or painful Electroacupuncture |
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Which neurons cross to the other side of the spinal cord
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Fine/light touch and proprioception 1st synapse brainstem (ipsilateral ascending)
Pain and temp ( A delta and C )-cross midline within spinal cord |
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More info on beta endorphins
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Descending connections from cerebral cortex may block pain at first synapse. Three brain stem reticular nuclei-PAG, locus ceruleus, and raphe nucleus-relay cortical activity to the dorsal horn to block or decrease pain transmission.
Activation of interneurons that inhibit the activity of tract cells through the action of endogenous opiate neurotransmitter enkephalin. Nuclei within the hypothalamic region of forebrain control the hormones released by the pituitary gland: beta-endorphin. Thus region of cerebral cortex can increase the level of beta-endorphin in blood system. Beta-endorph acts on opiate receptors throughout the nervous system, inhibiting activity in pain systems |
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Direct heating or cooling of tissues
penetration of infrared modalities |
Reality:
Most direct energy emitted from infrared modalities will not penetrate deeper than 1cm. Mainly affects cutaneous tissues and vessels However . . . Possible to indirectly change temperature of deeper tissues thru circulation of warmed or cooled blood But how much? |
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Heating of Deeper Tissues
via Superficial Heat |
Most temp ↑’s at 0.5 cm
Muscle temp at 1-2 cm to lesser degree 3cm depth ↑ of <1 deg C Practical limits to depth of penetration? Using a superficial heating or cooling agent for a deep injury affects the superficial sensory nerves and blood vessels but does not produce the Needed metabolic changes in the traumatized tissues |
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Heating and cooling of circulating blood
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Heat dissipates quickly in circulated blood
Cold dissipates less quickly Why? Heat → Vasodilation Cold → Vasoconstriction Therefore, greater mixing of warm & cool blood in application of heat !!! |
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Counter Irritants
NOT an infra-red modality |
Examples:
Methyl salicylate, camphor, capsaicin Topically applied balms Stimulates skin thermoreceptors ↓ in pain 2ndary to: Massage? Descending mechanisms of pain control? Gate? NO EVIDENCE OF VASODILATION OR TEMP ∆’S WITH COUNTERIRRITANTS !!! |
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A randomized, placebo-controlled double-blinded comparative clinical study of five over-the-counter non-pharmacological topical analgesics for myofascial
pain: single session findings. |
showed significant increases in pain threshold tolerance after a short-term application on a trigger points located in the trapezius muscle
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Does cold increase edema?
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No
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Decision to use continuous passive motion
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The decision to include in early treatment must be made considering
The immediate and long-term benefits relative to costs and hazards Point is… it is not based on pathology Prevent (-) effects associated with immobilization “Motion that is never lost need never be regained” |
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How does continuous passive motion help return of function
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Through:
Earlier return of motion Joint Nutrition Reduction of edema / effusion Reduction of pain Acceleration of healing Earlier return of strength |
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What is the control group in studies assessing long term outcomes of CPM?
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What is the control group in studies assessing long term outcomes?
For the non-compliant patient, CPM use is a must !!! How do we know who will be non-compliant? |
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Cavitation and microstreaming
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micro-streaming
one-directional motion of fluid caused by a sound wave cavitation formation of microscopic bubbles during the application of therapeutic US effects of (non-thermal?) ultrasound |
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Ultrasound frequency
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# cycles / second
Range 1 to 3 MHz Determines depth of penetration 3 MHz Absorbed in superficial tissues (up to 2 cm) 1 MHz Can penetrate superficial layers & be absorbed in deeper tissues (up to 5 cm) |
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Size of US treatment head
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Effective Radiating Area (ERA)
Area of sound head actually producing sound wave General Rule: Treatment area should be no greater than 2-3 times the size of ERA |
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Myofibrils and protein filaments
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Myofibrils and Protein Filaments
Myofibrils: Long thin strands within muscle fibers containing thinner protein filaments (actin and myosin-2 proteins) Make up 90 % of cell volume Protein filaments produce “sliding effect” seen during muscle contraction |
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How does cartilage resist pressure
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Thru 2 forces:
Fluid forces Structural forces Most of ability to resist pressure from fluid forces |
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How does intermittent compression work?
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The mechanical pressure waves force fluids within the venous system back toward the heart
Lymphatic uptake and return is assisted by spreading the edema over a larger area (usually proximally), allowing more lymphatic ducts to absorb the solid matter within the edema |
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How does the foot achieve venous return?
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The foot appears to rely on mechanisms other than contractions or ROM
Decrease arch of the foot Stretch veins causing to empty Venous pump is activated by pressure applied to the plantar aspect of the foot |
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Intermittent pressure for edema
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lower leg edema
35 to 55 mm Hg Inc venous flow velocity 175% 90 to 100 mm Hg Inc venous flow velocity 336% Net results is increase in fresh blood flow to the area, elevation more effective than intermittent compression and elastic wraps |
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Effects (of intermittent compression) on the Injury Response Process (cont’d)
Range of Motion |
Reducing the joint volume assists in decreasing arthrogenic muscle inhibition and restoring normal active ROM by reducing the hydraulic resistance to motion
Swelling of the distal joints decreases ROM; the decreased ROM further promotes distal swelling by limiting the muscle pump and reducing venous and lymphatic outflow |
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Effects (of intermittent compression) on the Injury Response Process (cont’d)
Pain |
Reduces the mechanical pressure caused by the edema and restores normal arterial and vascular function
Reduces ischemic pain by increasing the rate of delivery of oxygen and nutrients to the tissues |
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AMI
(WHAT DOES THAT STAND FOR?) |
Injury response accelerates atrophy
Edema and inflammation stimulate GTO (facilitates relaxation when rapid increase in tension-too much) Muscle atrophies blood supply decreases And innervation of the muscle is hindered Continuing process of atrophy leads to reflex inhibition where effusion and painful impulses create an inhibitory loop, essentially causes patient to forget how to contract |
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The efficacy of intermittent compression for increasing venous flow is widely accepted, but the effects of intermittent compression on ___ is not substantiated
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The efficacy of intermittent compression for increasing venous flow is widely accepted, but the effects of intermittent compression on lymphedema is not substantiated
Conclusive evidence does not exist that intermittent compression is more effective than a compression wrap and elevation for reducing protein-rich pitting edema, but evidence does support That compression units, elevation, and cold do reduce edema more than cryotherapy alone PREVENT SWELLING AND ASSIST IN VENOUS RETURN-practical application |
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Intermittent pressure treatment procedure
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If cold 50-55˚
Select max pressure 30 to 60 mm Hg UE 60 to 100 mm Hg LE (should not exceed diastolic pressure) Select on:off 3:1 (45:15 sec) Treatment time 23-30 min (several hours for lymphadema) Patient report unusual sensations Encourage gentle ROM exercises For best results elevate |
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How long should intermittent pressure treatment last?
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Treatment time 23-30 min (several hours for lymphadema)
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Angle of Pull for traction
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Angle of Pull for traction
May raise or lower table to create this Cervical Typically 25-30° flexion May vary based on amount of flexion-extension desired or patient comfort Lumbar Lesser angles will promote spinal flexion and separation at various levels ~ 10° focus at L5 – S1 Up to 30 ° flexion thru ~ L3 Greater angles may actually induce extension Response may vary with patient build & placement of harness Default to patient comfort (most typically straight pull) |
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Tension/force for cervical traction
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In supine, vertebral separation at force = 7% of body weight
May start lower to judge for tolerance Pre-assess with manual cervical traction For separation of cervical spine to occur, need 20% of body weight with patient reclined |
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Final procedures for traction
starting with safety switch |
Give patient the safety switch and explain its use
Place bell within reach Describe what to do and not to do during treatment “Do” relax “Do” report worsening or new symptoms “Don’t” sleep, cough, or produce large movements Unlock separation tables Set parameters and begin treatment |
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Procedure after traction treatment
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Turn off power
Lock Table Place tension cable on slack Loosen halters DO NOT have patient sit up Relax in same position at least 2-3 minutes THEN transfer safely into sitting via log roll technique |
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Safe limits of strain?
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Area of controversy
Toe region considered to be safe limits of stretch without tissue damage Stretch here mostly due to what? Loss of Crimp Breaking dynamic bonds (weaker easier to break and re-form) Linear region stretching of straightened fibers Further stretch here due to what? Further breaking of bonds Begin denaturing of fibers |
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Creep
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Gradual lengthening of tissue due to a constant load
CT will lengthen over time even though no additional stress placed on it “Good stretch” for rehab (at correct load) Philosophy for splinting, some traction, & other forms of sustained stretch Bonds within tissues shift |
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Scar Tissue Formation (Days 2-4)**
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Initial fibroblast activity; cont. macrophage activity
Earliest deposition is type III collagen Weaker fibers May act as scaffolding for deposition of type I fibers As approach day 4-5 ↑ in type I fibers Scar tissue “very fragile” |
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Scar Tissue Formation (Days 5-21)
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Significant fibroplasia
w/corresponding ↑ in collagen fibers ↑ in Fibroblasts; ↓ in macrophages Myofibroblasts & Scar shrinkage Clinical implications DCT: Slide 46 purpose of myofibroblasts |
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Activity of myofibroblasts
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Usually active up until 3 weeks
Result of extended myofibroblast activity? Decreased diffusion and circulation and contribute to persistent myofibroblasts and expansion of extracellular matrix Myofibroblasts: (Have contractile properties Cause scar shrinkage Attach to surrounding tissues and pull margins inward Appear around day 5***) |
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Scar Tissue Formation
(Days 21-60) |
∆ from mostly cellular → fibrous tissue
~ 4 weeks tissue becomes more organized Greater strength Remodeling !!! Fibroblasts lay down collagen tissue along lines of tension !!! Response to stress |
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Scar Tissue Formation
(Day 60 - 360) |
Further maturation and remodeling
Compact & Large collagen fibers Significantly less fibroplasia Comes to resemble original structure |
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Order of massage strokes
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Effleurage-start with this stroke, and conclude with this
Petrissage Friction Massage Tapotement Vibration |
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Bone Histology: Bone Cells
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Osteoblasts
Bone-forming cells Give bone its strength Osteoclasts Bone-resorbing cells Active during maintenance of bone tissue Osteocytes Mature bone cells Maintenance of bony matrix |
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“Mature bone is a rigid connective tissue”
Like other types of connective tissue bone contains: |
Like other types of connective tissue bone contains:
Cells (Osteocytes, -blasts, -clasts) Fibers (Mostly Type I collagen) Ground Substance (other organic molecules and H2O) The amorphous intercellular material in which the cells and fibers of connective tissue are embedded, composed of proteoglycans, plasma constituents, metabolites, water, and ions present between cells Unlike other CT’s contains crystallized inorganic minerals Mostly Calcium & Phosphate |
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Repair of bone tissue
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Similar progression that occurs in soft tissue healing, but end result is newly formed bone tissue
Stages Hematoma formation Procallus formation Callus formation Ossification & Remodeling |
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Procallus formation
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Formation of a fibrocartilage bond between fx fragments
Fibroblasts & osteoblasts form granulation tissue Capillary budding This new, temporary tissue known as procallus Types I, II, & III collagen laid down as fibrocartilage Begins to stabilize area Movement of fragments very detrimental TYPICALLY 2-3 DAYS TO 2 WEEKS AFTER FX Stages Hematoma formation Procallus formation Callus formation Ossification & Remodeling |
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Hematoma formation
(after bone fracture) |
Hemorrhage of damaged vessels & formation of clot
Clot at ends of fracture fragments and around entire site Other events associated with inflammatory response also occur No stability during this stage Begins immediately Stages Hematoma formation Procallus formation Callus formation Ossification & Remodeling |
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Callus formation
after bone fracture |
Inorganic minerals deposited along with collagen
Typically between 2-6 weeks Calcium & phosphates deposited in bulk Beginning of change from cartilage to bone New tissue begins to mature Beginning of bony union & stability Disruption still possible → Complications in healing Most important in determining the final outcome Stages Hematoma formation Procallus formation Callus formation Ossification & Remodeling |
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Final Ossification and Remodeling
- after bone fracture |
More consistent ossification of cartilage tissue
Extra callus tissue reabsorbed and replaced by mature bone Remodeling thru osteoclasts and osteoblast activity Further change based on stresses Stages Hematoma formation Procallus formation Callus formation Ossification & Remodeling |
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Ionto dosage
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Measured in milli-amp minutes
Intensity x Treatment duration 4mA x 10 minutes = 40 mA·minutes If intensity and or duration are higher then RX can be shorter May be limited by patient tolerance 40 mA·minutes with non-buffered electrodes 80 mA·minutes w/ buffered electrodes |
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Medications/ionic solutions for ionto
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Dexamethasone
Negatively charged, thus apply on cathode Anti-inflammatory Lidocaine Positively charged, thus apply on anode Local anesthetic Trigger points Acetic acid Negatively charged, thus apply on cathode Break down calcium deposits?? |
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Penetration of meds into tissues with ionto
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Approximately ½ inch !!!
Max 2 cm (20 mm) True amount delivered variable & unknown Concurrent use of other modalities not recommended Cryotherapy Vasoconstriction may limit absorption into tissues Heat & US Vasodilation may carry meds away |
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Ionto vs. phono
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Depends on phonophoresis beliefs
Depth ?? Penetration ?? Phono = Benefits of US Ionto = No physiological benefits of e-stim 40 vs. 80 mA·min For superficial, inflamed structure probably more evidence in support of: Ionto |
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E-stim - Biphasic vs Monophasic
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Biphasic vs Monophasic
Monophasic currents have ability to cause chemical changes Use dispersive, currents not equal under electrodes |
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E-stim: current and frequency
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Current Density (amount current flow per cubic volume): Is highest where electrode meet the skin
If electrodes are too close-highest current is relatively superficial With closer electrodes the intensity would be put lower Electrodes farther apart-highest current is deeper Properly prepared and positioned make a difference A large electrode disperses current; smaller concentrates current Higher frequency can be used to produce an increase in muscle tension due to summative effects; low frequency used more for muscle pumping and edema |
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E-Stim: Duration
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Duration: will be able to stimulate more nerve fibers with the same intensity by increasing the length of time that adequate stimulus is available.
Greater number of nerve fibers would react to the same stimulus Low volt stimulators are available for this High volt stimulators usually have pre-set pulse |
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Which is the negative electrode?
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Negative electrode CATHODE
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Placement of neg/pos electrode
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Muscle contraction: cathode is distal, anode is proximal
Tissue-stimulating effect is @ negative electrode Ease of excitation: neg polarity is usually more comfortable because positive polarity requires more intensity to create an action potential Generally negative electrode is distal and positive is proximal-as it replicates natural current flow in the body |
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E-stim FYI: Muscle force is varied by changing
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Muscle force is varied by changing the intensity to recruit more or less motor units
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In what fashion do muscle and nerve respond to e-stim?
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Muscle and nerve respond in an all or none fashion; there is no gradation of response recruitment and contraction are the same
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Changes in frequency and duration of current in e-stim
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Muscle contraction will change according to changes in current. As the frequency of the electric stimulation increases, the muscle will develop more tension as a result of the summation of the contraction of the muscle fiber through progressive mechanical shortening. Increases in intensity spread the current over a larger area and increase the number of motor units activated by the current. Increases in the duration of the current will also cause more motor units to be activated.
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E Stim High Volt Pulsed Current
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Decrease edema using sensory level approach
Negative polarity - BLACK – over edema 120 pps, 30 min, Chattanooga I am going to use electric stimulation to help your body absorb some of the swelling that you continue to have I am going to place an electrode over the area of your swelling, this will help move charged proteins into the lymphatic system. You will feel a tingling sensation primarily under this electrode Let me know if it feels too aggressive, it should not hurt, nor cause a muscle contraction |
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E stim: Decrease edema using sensory level approach
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Decrease edema using sensory level approach
EMPI: HIGH VOLT PPR custom Negative Polarity, 120 pps, on time 10 seconds, off 0 seconds, 30 minutes, lock-NO Small electrode over edema, larger dispersive on large muscle belly-hamstring or back SAME BULLETS AS ABOVE |
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E stim for anterior lateral knee pain
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Anterior lateral knee pain
If use one channel generally negative electrode – BLACK – is distal, which replicates natural e flow Gate/conventional between 80-150 pps; pulse duration 50-125 micr sec HVPC chat pre-set Intensity high as tolerated below muscle twitch Low Frequency between 1-10 pps; pulse duration 200-500 micr sec HVPC chat pre-set Intensity high as tolerated, contraction OK Brief Intense/Noxious greater than 100 pps; pulse duration 300 micro to 10 milli HVPC pre-set Intensity high as tol, contraction OK I am going to set up electric stimulation on the outside of your knee, which should help decrease some of your pain. The stimulation will block the nerves that transfer the pain signals to the brain. I am going to set up electric stimulation which will stimulate receptors in your brain which will block your sensation of the pain This should feel pretty good. I am going to a |
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E-stim for muscle reeducation
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Muscle Re-education
One channel Chatanooga, negative – BLACK – on VMO, red adjacent and proximal. Dispersive could Be on hamstring, low back, etc. 35-50 pps, Chatanooga Pulse Duration is pre-set. Rx 10-20 min. Duty Cycle 10/50 I am going to set up electric stimulation on one of your quadriceps muscles. Since it has been difficult for you to contract that muscle this will help you be able to eventually recruit that muscle on your own. This is called muscle re-education. Let me know when you feel the stimulation. OK now I am going to continue to turn up the electric stimulation. I would like to continue to turn it up until we see this muscle contract. Now I am going to have you attempt to tighten the muscle when you feel the stimulation. I set this for 10 minutes. You will feel the stimulation for 10 seconds and then it will be off for 50 seconds. Just relax the muscle when the stimulation is off. |
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Pre-modulated e-stim
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Pre-modulated is a medium frequency waveform
Current comes out of one channel The current intensity is modulated It increases and decreases at regular intervals Amplitude modulated frequency Shoulder Pain for example Sweep off…then beat is fixed, set at conventional, low frequency, etc Pulse duration is pre-set A symmetrical, bi-phasic current with a long pulse duration which is commonly used for the purpose of controlling acute or sub-acute pain |
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Interferential E-stim
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Sweep off
Beat fixed: 80-150 conventional;1-10 low freq; >100 brief noxious Sweep on Beat low Beat high I am going to set up electric stimulation on your shoulder, which should help decrease some of your pain. The stimulation will block the nerves that transfer the pain signals to the brain. Both channels turn on at the same time Pulse Duration pre-set |
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Elicitation of muscle contraction
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Stimulation of Motor Neurons
Direct depolarization of muscle membrane Denervated muscle Requires very long pulse duration DC current |
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The High Voltage Pulsed Current (HVPC) has a very brief pulse duration characterized by
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The High Voltage Pulsed Current (HVPC) has a very brief pulse duration characterized by two distinct peaks delivered at high voltage. The waveform is monophasic (current flows in
one direction only). The high voltage causes a decreased skin resistance making the current comfortable and easy to tolerate. |
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The Symmetrical Biphasic waveform has a short pulse duration and is capable of
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The Symmetrical Biphasic waveform has a short pulse duration and is capable of strong stimulation of nerve fibers in the skin
and in muscle. This waveform is often used in portable muscle stimulation units, and some TENS devices. Because of its short pulse duration, the patient typically tolerates the current well, even at relatively high intensities. |
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Premodulated Current is a medium frequency waveform. Current
comes out of |
Premodulated Current is a medium frequency waveform. Current
comes out of one channel (two electrodes). The current intensity is modulated: it increases and decreases at a regular frequency (the Amplitude Modulation Frequency). |
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Interferential Current is a medium frequency waveform. Current is distributed through
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Interferential Current is a medium frequency waveform. Current is distributed through two channels (four electrodes). The currents cross each other in the body at the area requiring treatment. The two currents interfere with each other at this crossing point, resulting in a modulation of the intensity (the current intensity increases and decreases at a regular frequency).
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Also with electric induced contraction, you don’t have fine motor coordination
The contractions and recruitments are synchronous Heat does lower skin threshold, will require less stim to depolarize With electric induced muscle contraction type II fibers recruited first Electrodes closer probably require less intensity Know what amplitude represents What’s the difference between ? Alternate current: bi-phasic continuous flow Biphasic symmetrical: bi-phasic, periods non-current flow |
Heat does lower skin threshold, will require less stim to depolarize
With electric induced muscle contraction type II fibers recruited first Electrodes closer probably require less intensity Know what amplitude represents What’s the difference between ? Alternate current: bi-phasic continuous flow Biphasic symmetrical: bi-phasic, periods non-current flow |
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Implications for PT
Evaluation & Intervention Movement & Alignment Factors Extrinsic Factors |
Movement & Alignment Factors
Muscle performance Motor Control Posture & Alignment Physical Activity Extrinsic Factors Orthotics Ergonomics Modalities Gravity |
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Contraindications to Joint Mobilization & Traction
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Inflammatory arthritis
Malignancy Bone Disease Neurological Involvement** Fracture Congenital Bone Deformities Vertebral Artery Compromise* Hypermobility** Connective Tissue Disorders** |
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Contraindications & Cautions for Cryotherapy
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Circulatory insufficiency
Deep Vein Thrombosis Cold Hypersensitivities/Cold urticaria Anesthetic skin Advanced diabetes Wounds – chronic, uncovered open Peripheral vascular disease Raynaud’s phenomenon Lupus Hemoglobinemia 11. Superficial peripheral n |
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Contraindications to Superficial Heat
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Acute injury / inflammation
Impaired circulation (PVD) Thrombophlebitis Neuropathy Open wounds / hemorrhage Malignancy**/neoplasms Poor thermal regulation Closed infection Anestheic areas |
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Cold vs. Heat
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Penetrate deeper vasodilate
Last longer cool in/warm out Vasoconstrict effectiveness Reduce inflam proliferation Restrict by pain restrict by stiff (use if they're restricted by stiffness) |
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Some factors when deciding to use heat or cold
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Is area warm to touch?
Area sensitive to light/moderate touch? Does swelling continue to increase? Swelling increase during activity? Does pain limit ROM? Is acute inflam active? Does patient display improvement with cold modalities? If no, heat can be safely used. More likely to use cold with each yes. |
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Spinothalamic transmits
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Spinothalamic transmits heat and pain
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First-order afferents enter where?
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dorsal horn of the spinal cord at the corresponding spinal level
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contraindications for CPM
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Unstable Fracture (Fx)
Uncontrolled infection Spasticity Deep Vein Thrombosis* Production of unwanted joint forces Precautions In combination with anti-coagulant therapy (blood thinners) Skin sensitivity or sensation issues |
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Evidence for CPM in short and long term
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Short term outcomes
↓ed length of hospital stay ↓ed use of pain meds ↑ed satisfaction at D/C ↑ed ROM (Lenssen, et al., April 2008) Long term outcomes CPM use vs. No CPM use No ultimate difference in pain or ROM !!! With long term NWB-ing, does aid articular cartilage health |
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Contraindications for US
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Thrombophlebitis
Over eyes Over reproductive organs Pregnancy Pacemaker: 6 inches away Malignancy Adolescent/ Child Epiphyseal Plate Infection Plastic Implants |
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Precautions for US
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Acute inflammation
Neuropathy Impaired circulation Over CNS tissue Fracture site Prosthetic components Total joint cement Breast implants |
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Petrissage
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lifting and kneading
stretches and separates muscle fiber and fascia from the skin and scar tissue |
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Friction massage
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deep pressure
Muscle mobilization, tissue separation, including the breakup of scar tissue |
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tapotement
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tapping or pounding
promotes relaxation and desensitization of the skin's nerve endings |
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Contraindications to Mechanical Traction
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Acute soft tissue injury
Highly unstable spinal segments Diseases affecting spinal cord or vertebrae tissue Cancer Meningitis Rheumatoid arthritis Pregnancy -Lumbar (yes) -Cervical ?? Vertebral fractures Severe cardiac or pulmonary involvement Advanced osteoporosis Vertebral artery compromise** Claustrophobia Pain with manual traction techniques |
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Contraindications and precautions for intermittent compression
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Compartment syndromes
Gangrene Peripheral vascular disease Ischemic vascular disease Arteriosclerosis Deep vein thrombosi Thrombophlebitis Congestive heart failure Pulmonary edema Unhealed fractures Unresolved joint dislocations (other musculoskeletal instability) Do not use in the presence of flammable gases…oxygen Patient’s arterial blood supply, including heart rate, blood pressure, and vessel continuity must be sufficient to deliver oxygenated blood to the extremity during the treatment |
