“the angry mother in law” · syndromes with regard to the cervical spine, thoracic outlet,...
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“TheAngryMother‐in‐law”
Peripheral Neuropathic Syndromes in Orthopedic & Sports Medicine Patients: (Upper Quarter)
InternationalManualTherapySeminarsJackM.StaggeP.T.,O.C.S.,FAAOMPT
2810RiverwalkPlace
EastWenatchee,WA98802
(509)679‐1657Fax:(509)884‐2811
E‐Mail:[email protected]
website=internationalmanualtherapyseminars.com
Course Description
Course 1A.: The Upper Quarter Pain Puzzle:
Peripheral Neuropathic Syndromes in Orthopedic & Sports Medicine Patients: (Upper Quarter)
This one‐day lab course will present concepts of differential diagnosis and treatment of patients with
upper extremity radicular symptoms pioneered by Bob Elvey P. T., GDMT. Emphasis will be placed on
precise physical evaluation of neural, articular, and muscular tissues in order to allow for specific
treatment of each. This precision evaluation allows for differential diagnosis of upper arm and arm pain
syndromes with regard to the cervical spine, thoracic outlet, glenohumeral joint and peripheral nerves.
Treatment of pain syndromes of neural origin will be explained and demonstrated along the lines of
neural tissue bio‐mechanics and physiological concepts. This course will cover well‐recognized disorders
commonly encountered by the physical and occupational therapist. Such topics as "frozen shoulder,"
CRPS, carpal tunnel, thoracic outlet, and other peripheral neuropathies and their treatment will be
discussed. Neurogenic pain syndromes, associated neuropathic and neurogenic pain syndromes,
including a review of new research into the treatment of CRPS I and CRPS II, will also be presented. Real
patient videos, case presentation, and lab practicals will be used to further allow for application of the
material into the participant's daily practice.
WhoisBobElvey?BobisaninternationallyknownclinicianandlecturerfromSouthPerth,WesternAustralia,whopioneeredanddevelopedevaluationandtreatmenttechniquesinthefieldof“NeuralMobilization”.Hedevelopedandresearchedupperquarterneuraldysfunction’sandpublishedhisfirstarticlesonhisinnovative“UpperLimbTensionTests(U.L.T.T.).inthelate70’s.Hisresearchandinnovativeevaluationandtreatmenttechniqueshaveledtotheworldwidedevelopmentoftreatmentsandresearchintoneurogenicpainsyndromes.BobretiredaftermanyyearsinprivatepracticeandwascoordinatorandseniorlecturerofthepostgraduatemanipulativetherapyprogramatCurtinUniversityinPerthAustralia.MrElveyisapastpresidentoftheInternationalFederationofOrthopaedicManipulativeTherapistsandhasreceivedtheprestigiouslifetimeachievementaward.HeisalsopastpresidentoftheManipulativePhysiotherapistsAssociationofAustralia.BobElveyhaswrittenandcontributedtonumerousarticlesandbooksonthesubjectofNeurogenicPainSyndrome.Hehastaughthis“PhysicalEvaluationandTreatmentofNeuralTissuesinDisordersoftheNeuromusculoskeletalSystem”allovertheworldandhasinfluencedcountlessnumbersofManualTherapistsinthepursuitofexcellence.BobpassedawayinAprilof2013.Heleftalegacyofcompassion,excellence,andaneverendingpursuitofknowledge.Thispresentationisatributetohisspiritandhiswork.
AboutOurInstructor:JackM.StaggeP.T.,OC.S.,F.A.A.O.M.P.T
Receivedhisbachelor’sdegreeinPhysicalTherapyfromCSUFresnoin1978.HereceivedaspecialtycertificationinAdultNeurologyfromU.S.C.in1979.HispostgraduatetrainingincludesextensivemanualtherapycourseworkinNorwegian,Australian,McKenzieandCyriaxprotocols.HewaschosenasasubjectmatterexpertbytheAmericanPhysicalTherapyBoardofSpecialtiesin1988andhelpedinwritingthefirstO.C.S.exam.HewasBoardCertifiedasanOrthopedicClinicalSpecialistinMay1990and1999,andbecameaFellowoftheA.A.O.M.P.T.in2002.Mr.Staggetaught“PhysicalEvaluationandTreatmentofNeuralTissuesinDisordersoftheNeuromusculoskeletalSystem”withMr.RobertL.Elvey,P.T.,G.D.M.T.ofCurtainUniversity,Perth,AustraliaforseveralyearsthroughouttheUnitedStates.Mr.StaggehasbeenafeaturedpresenterattheWorldConfederationforPhysicalTherapy,theAPTA’sNationalScientificmeeting,CombinedSectionMeetings,StateConferences,andtheI.F.O.M.P.T.inPerthAustralia.HehasservedasavisitingprofessorandlectureratseveralgraduateprogramsandisamemberoftheInternationalTeachers’ForumofI.F.O.M.P.T.Mr.StaggehasalsoservedasabookreviewerfortheJournalofOrthopedicandSportsP.T.,andasaconsultantonseveralarticlespublishedonorthopedicmanualtherapy.Mr.StaggeiscurrentlydirectorofInternationalManualTherapySeminarsandcontinuestoconsultandteachintheareaofneurogenicpainsyndromes.
LearningObjectives
1.Participantswillgainanunderstandingofthemechanismsbywhichneuraltissuemayinitselfbeapainsource.2.Participantswillgainanunderstandingofhowneuraltissue,whenitisapainsource,maycausewidespreadeffects.3.Participantswillgainknowledgeofneuraltissuedynamics.4.ParticipantswillgainanunderstandingofhowdysfunctionmayoccurwhenNormalneuraltissuedynamicsispreventedbypain.5.Participantswillgainknowledgeofphysicalexaminationtechniquesofneuraltissueforitsdynamicandfunctionalcompliance.6.Participantswillgainknowledgeoftherollneuraltissuemayplayinconditionscommonlyevaluatedandtreatedbyphysicaltherapistsandmanualmedicinepractitioners.Thisknowledgwillallowforspecificityofdiagnosisandpreventtreatmenterrors.7.Participantswillgainknowledgeofphysicaltreatmenttechniquesdirectedtowardsneuraltissues.8.Participantswillbepresentedwithpostulationsastotheremedialeffectofphysicaltreatmenttechniquesofneuraltissues.9.Participantswillgainanunderstandingforcautioninimplyingthatneuraltissueisthecauseofadisorderandinthetreatmentofneuraltissue.10.Participantswillgainknowledgeofdifferentialdiagnostictechniquesinneuromusculoskeletaldisorders.11.Participantswillbeabletodifferentiallyruleinoroutneurogenicsyndromesaseitherthecauseorthecentraldriverofdiagnosticfindings.
Schedule 8:30....Introduction
Patient profiles
8:45....Orthodiagnosis Types
9:00....Term definition
Compression vs. P.N.S.
9:15....Pathophysiology
Research
9:30....Subjective Evaluation
9:45....Objective Evaluation
DUCK
Posture
Active Testing
10:00....Break
10:15....Demo of Active Testing
10:30....Lab on Active Testing
11:00....Passive Testing
11:15....Demo of Passive Testing
11:30....Lab on Passive Testing
12:00....Lunch
1:00.....Neuropalpation
1:15.....Neuropalpation Demo
1:30.....Lab on Neuropalpation
2:00....Tender Points/Specific Signs of Local Dysfunction
2:15....Demo Trigger Point or Tender Point Palpation/Specific Signs of Local Dysfunction
2:30.... Putting it altogether.
2:45....Ortho and Sports Med Patient Presentation
3:00....Break
3:15....Treatment Demo
3:30....Lab on Treatment
4:00....Home Programs
4:15....Treatment Sequencing...
4:30....Further Considerations/Conclusion
4:45....End of Course
Slide 1 Jack M. Stagge P.T., O.C.S
F.A.A.O.M.P.T.
International Manual Therapy Seminars
www.internationalmanualtherapy.com
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Slide 2 I.F.O.M.P.T. 2000Perth Australia
Bob Elvey P.T., G.D.M.T.
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Slide 3
Peripheral Nerve Sensitization:
“The Angry Mother in Law”in
Upper Quarter Orthopedic and Sports Rehabilitation
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Slide 4 Patient Profile
Subjective: Primary complaint of chronic pain and decrease function.
“Heaviness” and “weakness” reported without objective verification.
Objective: Often Negative MRI. Neg. Nerve Conduction Velocities. Active ROM often evaluated as WNL’s unless neural provocation positions are
added or combined.
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Slide 5 E.M.G Findings
“E. M. G. will probably be negative if nerve is inflamed rather than compressed. Must lose 80% of conduction channels before tests are
definitive.”
Haldeman S., SPINE Vol. 9, No. 1, 1984
Sunderland S., Nerve and Nerve Injury, 1977
Yoshizawa, H. SPINE Vol. 20. No. 4, 1995
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Slide 6 Most patient’s have normally seen several practitioners some labeled as “Chronic Pain
Personalities”. Patient’s with neural irritability many times report worsening symptoms with use of
decompressive techniques such as traction or with patterned exercise such as PNF patterning of the
lower extremity
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Patient’s who have had decompressive surgeries and had both compression and irritability prior to surgery
may display decrease of compressive signs with continued pain complaints.
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Slide 7
Athletes may have failed interventions directed to distal or protective tissues
when neural irritability is the primary pain or movement driver. Noted functional loss and inability to correct normal patterning
despite elite training.
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Slide 8 Research throughout the world is
revealing that 17‐37% of chronic pain patients “may have a neuropathic pain
causation”
Haanpaa, Maija. Diagnosis and Classification of Neuropathic Pain. Pain, Clinical Updates. Vol XVIII, Issue 7, Sept.
2010.
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Slide 9 Upper Quarter “Orthopedic” Patient Diagnosis That
May Have Neurogenic Causation or in whom
symptoms are maintained by Neurogenic Input.
• Adhesive Capsulitis‐”Frozen Shoulder”
• Lateral Epicondylitis• “Whiplash Syndrome”• Dequervan’ Tenosynivitis
• Failed Cervical Decompression
• Tunnel Syndromes
• “Pseudo” Sympathetic Reflex Dystrophy
• Levator Scapular Syndrome
• Shoulder Impingement Syndrome
• Fibromyalgia‐TRP’s• Monarticular Arthritis
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Slide 10 Objective of Orthopedic Manual Evaluation
Determine dysfunction and relate to subjective examination=Diagnosis:
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Slide 11 Areas That Must Be Considered In Evaluation
1. Motion segment
2. Neural tissue
3. Muscle and soft tissue
4. Functional Movement Patterns
5. Emotional aspects
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Slide 12
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Slide 13
Definitions and Termsin
Neuropathic Syndromes
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Slide 14 For the sake of this presentation:Neuropathic Pain=CRPS I=
Peripheral Nerve Pain=Peripheral Nerve Sensitzation
AKA::Angry Mother‐in‐Law
Bennett GJ. , Can we distinguish between inflammatory and neuropathic pain? Pain : Res. Management 2006, vol.11.pg 5‐ 11.
Devor, M., Neuropathic pain and injured nerve peripheral mechanisms. British Medical Journal 47, pgs 619‐623, 1991.
Haanpaa, Maija., Diagnosis and Classification of Neuropathic Pain. Pain, Clinical Updates. Vol XVIII, Issue 7, Sept. 2010.
Schafer, Axel, Interrater Reliability of a New Classification System for Patients with Neural Low Back‐Related Leg Pain. JMMT 2009: 17(2) pgs 109‐117
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Slide 15 Peripheral Nerve Sensitization(PNS)= "Sensitization arising from nerve trunk inflammation causing increased axonal
mechanosensitivity with absent significant denervation."
Eliav Eli, Inflammation with no axonal damage of the rat saphenous nerve trunk induces ectopic discharge and
mechanosensitivity in myelinated axons. Neuroscience Letters 2001; 311(1): 49‐52
Hall, T., Elvey R.L., Management of mechanosensitivity of the nervous system in spinal pain syndromes. Grieves Modern Manual
Therapy. Edinburgh, UK: Churchill Livingstone; 2004
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Slide 16 NeuPSIG GuidelinesIASP 2011
“Common Denominators” that are found in Neuropathic Pain
1. Area of symptoms fits the distribution of a nerve
2. Quantatative—hyper or hypoesthesia
3. Qualitative‐‐‐‐ allodynia or dysesthesia
4. Temporal‐‐‐‐‐‐‐aftersensation , summation.
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Slide 17 Neuropathological Definitions by
Treatment Categories(Instructors Definition Only )
• 1. Compressive
• 2. Inflammatory AKA… P.N.S or Peripheral Nerve Pain
• 3. Combinations
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Slide 18 Compressive
Loss of Neural Function
• Example: Bony or soft tissue stenosis, tunnel syndromes, scar tissue “strangulation”, HNP sequestration, foreign bodies, etc.
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Slide 19 Comparison of Compressive
versus Irritative Evaluation Findings
(May of course have both)
Compressive(Loss of conductivity)
– Loss of Reflex
– Hypoesthesia
– Loss of strength
– Irradiation with compressive positioning.
– Hair loss
– Possible positive electro diagnostics
Irritative‐Inflammatory(Pseudoneuroma, Central Sens.)
– Possible Hyper reflexive
– Hyperesthesia/After sensation‐
– Irradiation with Provocation positions
– Distal “tender points”
– Mechanical Hyperalgesia
– Neg. Electrodiagnostics
– Pain inhibition
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Slide 20 Three Major Causations for Symptom or Sign Manifestations With Peripheral Nerve Pathology
1. Adherance of the epi‐endo‐or perineum leading to loss of elongation for normal functional patterns.
2. Pseudoneuroma formation leading to pain avoidance or direct distal inflammatory responses.
3. Prior peripheral nerve injury leading to excessive protection and physiological reaction to second load or trauma.
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Slide 21 Adherance
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Slide 22 Physiological, Inflammatory and Neuropathic Pain
“A region of potential abnormal impulse initiation may not become symptomatic until local adhesions or a change in posture causes undue mechanical forces to be brought to bear.”
Woolf C JAdvances and Technical Standards in Neurosurgery
Vol 15, pp 39‐62, 1987
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Slide 23 Development of a Pseudoneuroma
Caused by :
• Direct mechanical disruption of the epineureum, perineurium, or endoneurium.
• Rupture of epi or endoneural blood vessels.
• Chemical disruption of the epineurial barrier such as exposure to nucleus pulposus in annular tears.
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Slide 24
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Slide 25 Development of a “Pseudoneuroma”
“Obstruction to the venous outflow from a funiculusslows intrafunicula circulation.”
Increase intrafunicular pressure=Vascular collapse=Breakdown of Blood Nerve Barrier=Decrease
axonal Transport=Stasis=Hypoxia=Excitability”
“Painful Lesion” …… Sjostrands J et al, Lundberg et al.
“Pseudoneuroma”… LeBAn M ET AL, Cavanaugh et al.
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Slide 27 “When pain from localised peripheral neural pathology
becomes widespread, tenderness can be found along
the course of the affected nerve.”
• Devor, Lishman, Quitner, etc.
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Slide 28 Neurogenic Rheumatica
The usual diagnosis of arthritis, bursitis, neuritis, muscular rheumatism, fibrositis should not be made until cervical nerve root irritation has
been considered. Joint swelling may be directly caused by inflamed nerve roots.
Geppetti P 1996, Jackson R 1966, Levine, J. ,1984, Olsen, Y. , 1971, White D.M., 1985,etc.
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Slide 29 Research into "algias" suggest that the
reason that many problems once referred to as "itis", do not have normal
inflammatory product findings. Instead neurogenic inflammatory products are
found such as PABA etc. Possible neurogenic causation of Lat.
Epicondalgia...? Coopetiers, Fernandez‐De‐Las‐Penas
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Slide 30
What Causes Severe Reactions to Minor Afferent Input?
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Slide 31 Causations of Central Sensitization
• Long standing nocioceptive input.(Cavenaugh, Chang , Cheng, Haroutounian, etc.)
• Prior history of radiculopathy or CRPS involving ipsilateral or contralateral limb with new pain inputs involving the same nerve root. Could be Antidromic or Orthodromic.
(Kim, Hunt, etc.)
• “Double Crush” (Summation of inputs) (Osterman…Ang….etc.))
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Slide 36 1st Stage=Peripheral Afferent Sensitivity(Pathological Changes That Occur After Injury)
•Increased Mechanosensitivity. (4x Stretch Receptor, hyper to compression due to hypoxia)
•Altered Chemosensitivity. (Epi, Peri,Endoneural Breakdown)
• Altered Trophic Influence on Peripheral Target Tissue. (Neurogenic Rheumatica.)
• Altered Connections (C‐fiber re‐investment, Phenotypic Switch)•Pain Avoidance Movement Patterns ( Nerve Elongation Avoided)
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Slide 37 Orthodromic vs AntidromicAfferent Sensory Patterns
Orthodromic ImpulsesConduction along an axon (normally thought to be sensory) in its normal direction, away from the target structures. Modified at spinal synapse. Summates. Repetitive input causes ramping.
Antidromic ImpulsesConduction along the axon (thought to be sensory) away from the axon terminal(s) and towards the distal target structures. Monitored by the CNS and both modifies and contributes to pain syndromes. May cause release of chemicals at distal site.
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Slide 38 Does Antidromic Acivation of Nocioceptors
Play a Role in Sciatic Radicular Pain(Xavier ET AL PAIN No.40, Pg. 77‐79, 1990)
Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy.
(Haroutounian, Simon. Pain 155 pgs. 1272‐1279. 2014)
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Slide 39
2nd Stage (normally)
is
Central Sensitization
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Slide 40 Central Sensitization
A) Dorsal Horn Sensitization (WDR Neuron) Cavenaugh,Geppetti,Hanai,Svendsen
B) C N S Sensitization ( Thalmus‐Red Nucleus, Descending Fiber Excitation, Changes in Cortex Mapping, etc)
Butler,Sluka, Kramis
C) Autonomic Over Reactivity
Bennett,Geppetti,
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Evaluationof
“Irritative Inflammatory” or P.N.S.Syndromes
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Slide 42
Subjective Evaluation:
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Slide 43 Newly Developed Subjective Exams
LANSS (Leeds Assessment of Neuropathic Signs and Symptoms) Bennett et all, Pain, Vol. 7.
issue 3, pg 199‐203, Feb. 2007
painDetect
Freynhagen, Current Medical Research and Opinion: vol.22, pgs 1911‐1920 2006
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Slide 44
Pain Drawings
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Slide 45 DERMATOMES
“Not Consistent”
Dalton, P: Australian Journal of Physiotherapy Vol. 35, No. 1
DYNATOMES
Curtis, Slipman –SPINE Vol. 23,
No. 20, 1998
VS
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Slide 48 Pain Descriptions(Individualized)
• May describe “burning”, heaviness, “deep bone ache”, “a headache in my foot”, “cold water running down my leg”, “feels numb”, “hurts to touch”, “lightning”, “tingles and hurts at the same time”, etc. etc. etc.
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Slide 49
Need Analogue Pain Scales
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Slide 50
ObjectiveEvaluation:
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Slide 51
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Slide 52 Objective:Use of Standard Neurological Eval
• Reflexes. Maybe hyper‐reflexive.• Pinwheel. Hyper/hypo pin point sensation, may have
increased receptor fields, after sensation. Rate Pain Responses.
• Vibratome: 128 HZ Tuning Fork: Mechanical Hypoesthesia• Von Frey Fibers: Impaired tactile discrimination, Two point
discrimination.• Strength..Test in provoked position. • Clonus, Babinski etc.
Used to help determine the “health” of the nerve and to rule out other neurological considerations.
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Slide 53
Review of the “Duck”
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Slide 54 Signs of Adverse Response to the Physical Examination of Neural tissues
“THE DUCK” • Posture
• Active Dysfunction
• Passive Dysfunction
• Nerve Trunk Hyperalgesia
• Tender Points
• Specific Signs of Local Dysfunction
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Slide 55
Posture
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Slide 56
Neural Tissue Sensitivity and Protective Reflex Muscle Activity.
Protective antalgic posture. The recognition of protective muscle hypertonicity.
Hall T 1996, Sherrington CS 1900
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Slide 59 “Transformation of flexion withdrawal
reflex from high threshold phasic to low threshold tonic.”
Physiological, Inflammatory and Neuropathic Pain. Woolf C J Advances and Technical Standards in Neurosurgery.
Vol. 15, pp. 39‐62, 1987
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Biomechanics of Neuromeningeal Tissues Involved
in Active and Passive Testing
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Validity of Upper Limb NeurodynamicTests for Detecting Peripheral
Neuropathic Pain.
Nee, R.J. , Jull G., et al, JOSPT Vol. 42,
Number 5, May 2012
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Active Dysfunction
Add and Subtract Specific Nerve Provocation Positions
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Passive Dysfunction
Add and Subtract Nerve Provocation Positions
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Slide 75 Ectopic Sensory Discharges & Paraesthesiae in Patients with Disorders of Peripheral Nerves,
Dorsal Roots & Dorsal Columns.
Provocation Tests showed abnormal discharges on sensory pathways using microneurography
Nordin M. ET AL PAIN Vol. 20, Pgs. 231‐245, 1984
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Muscular Recruitment Patterns with and without Provocation.
Use of surface electrode EMG
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Slide 91
Using Nerve Bias Position to Rule in and Rule Out Muscle Tightness
Example: Scalenes, Levator., Shoulder External Rotators
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Slide 92
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Slide 93
Nerve Trunk Hyperalgesia(Mechanical Alodynia)
Elvey 1981
Fernadez de Las Penas 2010
Hall and Marshall 2009
Hall and Quintner 1996
Lishman, Nordin, M 1994
Devor , M 1991
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Slide 94 “When pain from localised peripheral neural pathology
becomes widespread, tenderness can be found along
the course of the affected nerve.”
• Devor, Lishman, Quitner, etc.
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Slide 95 Neural Hyperalgesia can be Objectified by use of Algometry
• Test Pain Threshold• Test Pain Tolerance
• Hall, Toby. Reliability, validity, and diagnostic accuracy of palpation of the sciatic, tibial, and common peroneal nerves of low back related leg pain. Manual Therapy; 14(6) December 2009; Pages 623‐629
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Slide 96 Specific Mechanical Pain
Hypersensitivity Over Peripheral Nerve Trunks in Women with Either Unilateral
Epicondylalgia or Carpal Tunnel Syndrome
Fernandez‐de‐las‐Penas, Cesar. Journal of Orthopaedic and Sports Physical Therapy.
Vol. 40 No. 11. Nov. 2010
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Slide 97
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Slide 98
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Slide 99
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Slide 100
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Slide 101 Nerve Palpation: In Supine
Trunks of the brachial plexus. C5, 6, 7, 8, T1.Posterior Triangle of the neck at the interscalene cleft and the supraclavicular
fossa, over the first rib. In the infraclavicular fossa. Caudal/medial to the coracoids.
The Peripheral Nerve Trunks: Below the coracobrachialis.
The Median Nerve C5,6,7,8,T1. Along the distal third of the anterior/medial upper arm between biceps and brachialis muscles.
The Ulnar Nerve C7,8,T1. At the posterior/medial elbow. Proximal and distal to the Ulnar Groove.
The Radial Nerve 5,6,7 (primarily) At the posterior arm in the lower one‐third of the Radial Groove .
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Slide 102
In Prone:
The Axillary Nerve C5,6 between posterior deltoid and teres minor.
The Suprascapular Nerve C5,6. Supraspinous and Infraspinous Fossa
Radial Nerve as described in other slide
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Slide 103 Tender Points
Will be Found in Muscles Innervated by
Involved Nerve
Hubbard, D. Myofascial Trigger Points Show Spontaneous Needle EMG Activity. Spine Vol. 18,
Number 13, pp. 1803‐1807, 1993.
Quinter, John L. A critical evaluation of the trigger point phenomenon. Rheumatology Dec. 3, 2014.
Pgs. 270‐278. 2014
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Slide 104 Specific Signs of Local Dysfunction
• Loss of passive joint motion at specific levels of dysfunction. Will have a painful, springy or bogey end feel often with a muscular rebound noted in multifidi etc.
• Should display tenderness from problem site distally, rarely proximally.
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Slide 105
Putting it All Together
• Meshing Subjective, Objective, and Patient History to come to a
Differential Diagnosis
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Slide 106 Subjective 1. Pain diagram and reproduction of symptoms during exam should match. Often produce dominant and specific pain symptom related to original complaints.
2. Complaints of sensitivity (hyperesthesia, allodynia, and temperature abnormalities) should be objectified.
3. Patients lack of ability to precisely describe abnormal sensations should not be regarded as signs of malingering. Often use words such as “heavy”, “puffy”, “electrical”, “burns”, “like a toothache in my……..etc.
4. Pay close attention to reports of multiple trauma involving the same nerve roots. Make sure to question prior history.
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Slide 107 Working With the Duck(Objective Findings)
1. Must determine peripheral neuropathy vs spinal neuropathy or radiculopathy, vs. systemic disease?.
(Reflex, Pinwheel, Strength,Tinel’s, Distalization etc.)
2. Anatomical Relationships between pain locality and spinal motion segments must match if central problem exists.
(Example: Lateral Epicondylitis C45, C56)
.
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Slide 108 3. Must have specific correlation between provocation tests of neural tissue and spinal
segmental signs.(ex. Positive Ulnar Nerve Tests and C4C5 Segment Dysfunction= NO CORRELATION)
4. There must be specific correlation between neural palpation tests and provocation test of
neural tissue.(Example:Median Nerve Palpation with Positive Median Provocation Tests= CORRELATION)
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Slide 109 5. Trigger Points or “Tender Points” should correlate with Spinal Level of Involvement unless only postural.. ie..Levator, Upper Traps etc. (Example: C5C6 dysfunction and Trigger Point or Tender point in the Teres Minor)
6. Should be able to “turn on” and “turn off” findings by use of specific provoking and relieving positions.
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Slide 110
Medical Considerations
•Systemic Disease changes…Diabetes…Shingles…ART meds., radiation
•Sleep Deprivation
•Emotional Overlay
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Slide 111
“Ortho”Case Presentation
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Slide 112
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Slide 113
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Slide 114
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Slide 115
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Slide 116
“Sports Medicine”Patient Presentation
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Slide 117 Treatment of Irritative‐Inflammatory Neural Pain Syndromes, PNP’s, PNS
Patient’s who meet the criteria for irritative or inflammatory dysfunctions, are initiated on the following treatment protocols, dependent on the
severity. Chronicity and complexity of their problems.
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Slide 118 Contraindications
• Some conditions with neurological deficit. CNS disorders or compressive radiculopathies.
• Progressive neurological pathology.
• When treatment exacerbates a condition or causes distal symptoms.
• When another form of treatment or management is indicated. Eg. Joint disorder, metabolic neuropathy, etc.
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Slide 119
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Slide 120 Treatment of neural tissues by techniques of mobilization of
surrounding anatomical tissues or of the neural tissues.
Techniques DO NOT involve stretching. 15% elongation NORMAL neural tissue
causes microvascular stoppage(Lundberg G. et al)
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Slide 121 POSTULATION for Treatment Effect
• Mechanical effect
• Neurophysiological modulation (Central Desensitization)
• Physiological effect
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Slide 122 1. Therapist’s Intervention:
Passive Mobilization of the environment surrounding the affected nerve in very specific
positions and levels determined by the evaluation.
May also include the use of modalities such as Heat, Ultrasound, and, or Electrical Stimulation to
decreased muscle guarding or help with neural irritability. Only used to allow therapist to
administrate mobilization more effectively. In many cases modalities are not needed. Direct segmental
mobilization may of course be needed.
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Slide 123
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Slide 124
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Slide 125
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Slide 126
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Slide 127
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Slide 128
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Slide 129
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Slide 130
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Slide 131
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Slide 132 2. Patient Self Treatment:
Once therapist’s intervention has a carry over between treatments, patients are initiated on
home programs of neuro‐mobilization exercises to allow for continued benefit of movement and to restore function around
inflamed nerve.
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Slide 133
Home Programs
Active Neural Mobilization
Standing
Seated
Flossing
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Slide 134
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Slide 135 Home Nerve Gliding Techniques
“Flossing”
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Slide 136
Additional Home Programs
In addition to Neural “Mobilization”
May include:
Desensitizing, Mirror Box, Loading Techniques etc.
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Slide 137 3. Therapist’s Specific Muscle Re‐
education:
Patient’s normally have developed loss of specific muscular strength and endurance. This is due to disuse atrophy, reflexive inhibition, or neural compression. May require modification of
positioning into unprovoked position to “honor” the “Mother in Law”.
Remember fear avoidance issues!!! Good time to initiate “general ex” programs to break patterns of disability and increase overall physiological return.
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Slide 138 Patient’s Self Specific Movement Re‐
education:
Home exercise, guided by the therapist. Patterned movement ie. Functional patterns of movement that were substituted for when the nerve was injured and need to be restored to allow for return to function including work
activities without re‐injury or injury of another area. Once again remember provoked
positioning and pain memory!!
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Slide 139 Specific Functional Task Education
and Rehabilitation:
Certain heavy demand or labor intensive job tasks require specific “work hardening”
procedures to return many of these “Chronic Pain Patient’s” to prior job or modified job
status.
Communication with treating Therapist
and Rehab Counselor is essential.
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Slide 140
Conclusion
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Slide 141 Patient Specificity
1. Each patient is unique! Find and treat “Their Pain”
2. Must be able to turn on and turn off symptoms.
3. Goal is to reverse process of sensitization, self perpetuation and allow for normal healing of pseudoneuroma.
4. Must remember all aspects of the treatment environment are critical.
5. Hope is given and healing begins with proving diagnosis to yourself and especially the patient. This requires a thorough exam and good communication.
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Slide 142 Remember Regional Intervention.
Treatment of the “Inflamed Nerve”, is only the beginning of functional restoration. By
decreasing and often eliminating the input and secondary reactions to the “Angry Mother in
Law”, we can begin the process of rehabilitation that the pain input did not allow and may have led to an incorrect diagnosis and treatment
plan. None of the treatments presented are an “End All”, but rather a beginning and a
component of the final restorative process.
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Slide 143
Thank You Very Much for Your Participation
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Slide 144
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LabManual
SpecificPhysicalTherapyEvaluationSignsandFeaturesmustbere‐assessable:
Patientssymptomsshouldbereproducedatsomepointofthisprocess!!
1. Observation: Body positioning that decreases elongation or provocation of nerve.
2. Active Movement: Specific motions with and without nerve provocation positions.
3. Passive Movement: Specific motions with and without nerve provocation
positions. These are repeated provocation tests with “Central” and Peripheral
Positions .
4. Nerve and nerve trunk hyperalgesia to mechanical pressures.
5. Trigger Point or “Tender Point” palpation. Look for myotomal distribution
matching neural irritability.
6. Evidence of Central or Peripheral Causation. Must find localized source of
irritability, adhesion, or compression or any combination to effectively treat.
NeuralProvocationEvaluation__________________(UpperQuarter)___________________PosturalPostioning:
ForwardHead___CervicalLateralTilt____Shldr.ElevationR__L__
ElbowPosition_________WristPosition______Fingers_____
ActiveMotionTests:
ShoulderActiveAbductionROM
NeutralCervicalPosition_____ScapulaFixation______________
ScapulaFixatedandHeadinIpsilateralFlexion________________
ContralateralFlexion_____________
Plus:ElbowFlexed_________ElbowExtended_______________
NotedSubstitution______________________________________
PassiveMotionTests(N.T.P.T.)
PeripheraltoCentral
MedianNerve:CervicalNeutral____Contralateral____Ipsilateral_____
RadialNerve:CervicalNeutral_____Contralateral____Ipsilateral_____
UlnarNerve:CervicalNeutral_____Contralateral____Ipsilateral_____
CentraltoPeripheral
DegreesofCervicalLateralFlexionR____L____withUpperExtremityin
_____________________position.Increaseswith__________________
NeuralPalpationTrunks:Superior______Middle_______Inferior________
AxillaryPalpation_________________________________
MedianNerve______Location______________________
RadialNerve_______Location_______________________
UlnarNerve________Location_______________________
AxillaryNerve______Location_______________________
TenderPointsLocation_____________________________________________________________________________________________
SpecificSignsofLocalDysfunctionC3C4____C4C5___C5C6___C6C7___C8T1___T1T2___T2T3
NEURALPALPATION
InSupine:
Trunksofthebrachialplexus.C5,6,7,8,T1.
PosteriorTriangleoftheneckattheinterscalenecleftandthesupraclavicularfossa,overthefirstrib.
Intheinfraclavicularfossa.Caudal/medialtothecoracoids.
ThePeripheralNerveTrunks:Belowthecoracobrachialis.
TheMedianNerveC5,6,7,8,T1.Alongthedistalthirdoftheanterior/medialupperarmbetweenbicepsandbrachialismuscles.
TheUlnarNerveC7,8,T1.Attheposterior/medialelbow.ProximalanddistaltotheUlnarGroove.
TheRadialNerve5,6,7(primarily)Attheposteriorarminthelowerone‐thirdoftheRadialGroove.
InProne:
TheAxillaryNerveC5,6betweenposteriordeltoidandteresminor.
TheSuprascapularNerveC5,6.SupraspinousandInfraspinousFossa
RadialNerveasdescribedabove.
HomeProgramsOncethePatienthasdisplayedcarryoverfromtherapistinterventionwithmanualtechniquesandthepatientdisplaysgoodunderstandingofirritativefactors,thepatientmaybestartedonself‐treatment.Thepatientstandsorsitsinfrontofamirror(elbowsupported)andfirstteststheiractiveROMofCervicalLateralFlexionawayfromthesymptomaticsidewithupperextremityinneutral.ThepatientthenaddsthespecificprovokedpositiononlyupuntilapproximatelyonethirdoftheCervicalLateralFlexionislost.SeventoTenrepetitionsarecompletedwithoutproducingsymptoms.Patientcanexpecttofeeltightnessintheantagonisticmusculature,however,symptomsshouldnotdistalize.Patientcanrepeatthese“treatments”oneortwotimesdaily.Donotrefertothemasexercises.Ifsymptomsincreasethenextday,resttwentyfourtofortyeighthoursandretry.Itisimperativethatpatientsrecheckpositioningeachtimeandtreateachsessionasseparatefromthelastone.
Home Nerve Gliding Techniques“Flossing”
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