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Slide 1 Jack M. Stagge P.T., O.C.S
F.A.A.O.M.P.T.International Manual Therapy
Seminars www.internationalmanualtherapy.com
presents:
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Slide 2
Neuropathic or Peripheral Nerve Pain in the Causation and
Maintenance of many Orthopedic Diagnosis's
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Slide 3 I.F.O.M.P.T. 2000Perth Australia
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Slide 4 For the sake of this Breakout Session Neuropathic Pain=CRPS I=
Peripheral Nerve Pain=Peripheral Nerve Sensitzation
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 5 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 6
Review of PathophysiologicalConsiderations in:
CRPS I,Peripheral Nerve Pain, Peripheral
Nerve Sensitzation
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Slide 7 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 8 Adherance
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Slide 9 Physiological, Inflammatory and Neuropathic Pain
“A region of potential abnormal impulse initiation may not become symptomatic untl 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 10 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 12 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 13
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Slide 14 “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 15
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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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 17
Central Sensitization
Repeated injury to the ipsilateral or contralateral nerve root or its corresponding
peripheral nerves.
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Slide 22 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 23 Neuropathic 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 24
Pain Drawings
Analog Pain Scale
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Slide 25 NeuPSIG Guidelines
IASP 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 26 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 27 Strength and Reflex Testing in a Provoked Position.Patient’s limb or spine can be placed in a specific provoked position and strength or reflexes retested
against neutral positioning.
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Slide 28 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 29
Posture
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Neural tissue sensitivity, provocation tests and protective reflex muscle activity.
Protective antalgic posture. The recognition of protective muscle
hypertonicity.
Coppieters M. 2003, Hall T 1996, Sherrington CS 1900
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Slide 31
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“Transformation of flexion withdrawal reflex from
high threshold phasic to low threshold tonic.”
May cause symptoms of their ownor maintain neural irritability.
Woolf C J 1987, Patterson, M. 1986
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Active DysfunctionAdd and Subtract Nerve Provocation
Positions
Patterson 1986, Woolf 1987,
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Biomechanics of NeuromeningealTissues Involved in Active and Passive
Testing
Upper Limb and Lower Limb “Provocation” Testing
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Slide 42 Muscular Recruitment Patterns with and
without Provocation.Use of surface electrode EMG
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Modified Slump Test
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Testing of “Slump” and Modified SLR in Normals
Boyd et al, Breig, Butler, Coppieters et al,
Davis, Gajdosik et al, Johnson et al,
Philip K. et al, Zusman et al
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Slide 47 Passive Dysfunction
(Add and Subtract Nerve Provocation Positions)
Elvey 1984, Keneally 1993, Hall 1996, Coveney 1997, Friberg2000, Cooppieters 2000, 2003,
Van de Heide 2001, Jull 2003, 2010, Shacklock 2003,
Brown 2011
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Slide 48 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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Slide 49
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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Slide 52
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Slide 53 Muscular tightness in and out of provocation.
Mid‐scalene with median bias
Mid‐scalene with ulnarbias
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Slide 54
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 55 “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 56 Nerve Trunk Palpation
• Sciatic Nerve‐L4,L5, S1,S2,S3 Through the buttocks at neck of femur.
• Common Peroneal Nerve L4,L5,S1,S2 Neck of fibular
• Tibial Nerve S1,S2 At the level of the calcaneum, post. To the post. Tibial artery
• Femoral Nerve L2,L3,L4. At the inguinal region lateral to the femoral artery .
• Saphenous Nerve L2,L3,L4. Medial tibial condylar plateau.
• Lateral Cutaneous Nerve of thigh L2,L3. Medial to the ASIS
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Slide 57 Reliability, validity and diagnostic
accuracy of palpation of the sciatic, tibialand common peroneal nerves in the
examination of low back related leg pain
Walsh, Hall. Manual Therapy 14 (2009) 623‐629
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Slide 58 Algometer: Mechanical AlodyniaPressure Pain Thresholds (PPT) and Max Pain
Pressure Thresholds (MPPT)
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Slide 59
Tender PointsWill be Found in Muscles Innervated by
Involved Nerve
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Slide 60 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 61
Putting it All Together
• Meshing Subjective, Objective, and Patient History to come to a
Differential Diagnosis
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Slide 62 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 63 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: Plantar Fascitis…. L45, L5S1)
.
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Slide 64 3. Must have specific correlation between provocation tests of neural tissue and spinal
segmental signs.(ex. Positive Obturator Nerve Tests and L5S1 Segment Dysfunction= NO CORRELATION)
4. There must be specific correlation between neural palpation tests and provocation test of
neural tissue.(Example:Positive Femoral Nerve Palpation with
Positive Femoral Provocation Tests= CORRELATION)
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Slide 65 5. Trigger Points or “Tender Points” should correlate with Spinal Level of Involvement unless only postural.. ie..Quad Lumborum, Hip Ext. Rotators, Hamstrings etc. (Example: L5,S1 dysfunction and Trigger Point or Tender point in the Gastrocs)
6. Should be able to “turn on” and “turn off” findings by use of specific provoking and relieving positions.
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Slide 66
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 67 “Orthopedic”, or “Sports Medicine” Patient Diagnosis That May Have Neuropathic Causation
or in Whom Symptoms are Maintained by Neuropathic Input. (Lower Quadrant)
• Failed Back Syndrome
• Piriformis Syndromes
• Sciatic Scoliosis
• Chronic TrochantericBursitis
• Fibromyalgia‐TRP’s.
• Chronic Hamstring Tears
• Chronic Plantar Fascitis
• Chronic PeronealTendonitis/Tears
• Chronic Achilles Tendonitis
• Chronic Adductor Strains
• Compartment/Tunnel Syndromes
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Slide 68 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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