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NEUROPATHODYNAMICS
Dr. LAKSHMI PAVANI P. (PT)
SPINE
Mechanical interface
Neural
Innervated tissue
FLEXION AND EXTENSION
Mechanical interface- spinal canal
Flexion of the whole spine causes elongation of the spinal neural structures because they, and their canal are located behind the axis of rotation of the spinal segments.
Neural tissues-
Tension and strain are the two responses for flexion. The amount of tension is not clearly known but strain from lumbar extension to flexion in lumbar dura can reach 30%, scaral nerve roots 16% (Adams & Logue; Yuan et al 1988)
Sliding and convergence:
Sliding of the neural structures is complex in spine and specific sequences of movements their own sliding. Eg: Neck flexion produces cephalad sliding of neural structures in lumbar region (Breig 1978). However SLR produces caudad sliding of the nerve roots in the lumbosacral foraminae ( Goddard & Reid; Breig 1978).
LATERAL FLEXION AND LATERAL GLIDE
Mechanical interface
The key event with lateral flexion in relation to mechanical interface is that the intervertebral foraminae close down ipsilateral side and open on the contralateral side (Fujiwara et al 2001).
Neural effects:
Lateral flexion produces increased tension in the neural structures on the convex side of the spine and reduce tension on the concave side (selvaratnam et al 1988).
Increase in tension occurs in two ways:
The first is that lateral flexion itself produces elongation of the interface and neural tissues on the convex side.
The second is by causing an increase in distance between the spine and the periphery by sideway translation of the vertebrae (Louis 1981)
Uses: 1.
Structural differentiation
2.
Sensitization
Others: 1.
Contralateral neurodynamics
2.
Bilateral neurodynamic techniques
GENERAL NEUROPATHODYNAMICS
Mechanical interface dysfunctions
Neural dysfunctions
Innervated tissue
dysfunctions
MECHANICAL INTERFACE DYSFUNCTIONS Closing dysfunctions
• Reduced closing
Opening dysfunctions
• Reduced opening
Patho-anatomical dysfunctions Pathophysiological dysfunctions
• Excessive closing
• Excessive opening
• Eg: spondylolisthesis • malignancy • inflammation
CLOSING DYSFUNCTIONS
Reduced closing
Symptoms: Key behavioral aspect is symptoms increase with closing movements. Physical findings: 1.
Posture:
In acute and severe dysfunctions a protective deformity is frequently apparent. This deformity is always in the opening direction so as to reduce the pressure in the adjacent neural structure.
Excessive closing
Symptoms:
Provoked by closing mechanism
Hypermobility, instability or habitual closing exist.
Eg: Hyper-lordotic lumbar spine. History:
Habitual posture or posture imperfection is common.
Sometimes a history of trauma and features of instability also
Opening dysfunctions
Reduced opening
Symptoms:
Usually aches and pains in the localized area with or without referred pain.
Opening movements provoke pain and are usually restricted.
History:
Usually H/O trauma exists in which patient has been forced into opening positions.
The body then compensates during healing process by causing inflammation and muscular spasm such that opening movements are reduced to avoid further provocation.
Eg: spine
Physical findings:
The reduced opening dysfunction produces a protective spasm on the ipsilateral side unlike closing type has on contralateral side. This deformity is specially designed to reduce tension in the interfacing and neural tissues.
Palpation:
tenderness, muscle spasm Eg: L4-S1 segments may be accompanied by tenderness and spasm of the ipsilateral erector spinae as they limit contralateral flexion.
Excessive opening
Symptoms:
Aches and pains and can produce referred pain
Pins and needles, numbness can occur in this dysfunction.
Symptoms are intermittent and they are produced when provoking movements occur.
Physical findings:
No deformity is seen
Opening movements are increased and that is eventually leading to this disorder.
Eg: cervical contralateral flexion and rotation.
Palpation:
Tenderness over specific areas is often present. Hypermobility produces mechanical irritation of the relevant structures.
NEURAL DYSFUNCTIONS
Neural sliding dysfunction Neural tension dysfunction
Hypermobility
AIMS AND OBJECTIVES OF NEUROMOBILIZATION
Neuromobilization is aimed at reconstructing normal neuromechanical condition, i.e. adapting the nervous system to constantly changing loads and mechanical tension.
It involves stretching and pulling nerve trunks, spinal roots, spinal nerves, spinal cord and spinal meninges by effecting movement of joints in precisely isolated positions.
Physiotherapeutic treatment, including neuromobilization, ought to be performed in the earliest possible stage of disease, before the occurrence of irreversible morphological changes and should include all affected tissues.
Neuromobilization should involve the entire length of the nerve trunk.
The primary objective in neuromobilization is to improve neuromechanical function through mobilization of peripheral nerves, spinal roots, spinal meninges and the perineural connective tissue.
Neuromobilization techniques restore normal neuromechanical function of both peripheral nerves and the central nervous system.
CLINICAL TESTS Clinical tests performed in connection with neuromobilization consist of:
Testing of exteroceptive sensation (superficial sensation, two-point discrimination) and proprioceptive sensation ,vibrations.
Examination of indicator muscle function (innervated mostly by one segment)
Testing muscle reflexes
Examination of nerve trunk tension (nerve trunk tension tests)
Examination of nerve trunk mobility (nerve trunk mobility tests)
The essential examination conducted before performing neuromobilization involves nerve trunk tension and mobility tests. Positive results of these tests include:
Elicitation of a symptomatic pain reaction characteristic of a particular condition,
Differential symptoms in symmetry tests (performed on the opposite upper limb)
Confirmation of the symptoms by discriminatory testing of other tissues
Confirmation of the symptoms by palpation of the nerve trunk through irritation.
Tension tests consist in stretching a given nerve, spinal cord or meninges by moving joints in areas where these structures are found in such a way as to enable the maximum possible adjustment of the nervous system.
The stretching effect is increased by angular placement of the joint and also by joint traction.
A positive test result reflects a lack of elasticity in the conducting structures.
Eg: Hematoma located in the perineurium.
Mobility tests induce a shift of the nervous system by placing the examined fragment of neural tissue in a rest (relaxed) position, while a shift in relation to perineural tissues occurs as a consequence of stretching the nerve proximally or distally to the injury site.
A positive test result reveals a limitation in the supportive connective tissue in the nerve or the presence of external compression factors.
Positive results enable the tests to be used as mobilization techniques.
The initial position for a mobilization procedure is determined by a positive tension test or a positive mobility test.
Impulsation (stretching and pulling) is conducted through the joint situated proximally or distally to the treated segment of the nervous system.
Impulses stretching the trunks of peripheral nerves should not stretch the neural tissue more than
up to 8% of the entire nerve length, since that might produce early symptoms of nerve ischemia. (Lundborg et al,1970)
Blood supply is completely blocked when neural tissue is stretched by 15% (Lundborg et al 1970)
Thus, a procedure must correspond to the patient's condition and may never cause pain. The number, duration and frequency of impulses is determined on the basis of patient response.
Initially, two series of impulsation procedures of a few seconds' duration are performed at a frequency of 2-4 impulsations per second.
As the patient's condition improves, the duration of the procedure is extended to 20-30 seconds, with increasing amplitude of movement in the joint through which the impulsation, longer duration of a single impulse and more series of impulsations.
In chronic conditions, between 10 and 60 stretches are performed lasting up to 20 seconds.
However, it must be emphasized that this method is based on the principle of painlessness corresponding with concept of “painlessness and opposite motion”- ( Maigne R et al,1996 ), which holds that the patient should not feel any pain either during or after the procedure.
While producing tension of a nerve trunk, the therapist does not know which structure has caused
the dysfunction. In the course of the procedure the stretching force is received by the tissue which has lost elasticity. The remaining structures gradually adapt to the progressing tension and rearrangement ( Maigne R et al,1996 ).
CONTRAINDICATIONS
Acute injuries to the central and peripheral nervous system,
Tumors of the nervous system and spinal cord,
Infection and acute inflammation,
Fever,
Unstable neurological symptoms,
Pain at rest,
CONTRAINDICATIONS
Cauda equina injury symptoms (disturbed bladder or bowel function, disturbed function of the rectal sphincters, major neurological defects of upper and lower limbs),
Spinal instability (osseous or ligamentous),
Congenital anomaly of the spinal column and peripheral nerves (dysplasia, aplasia, hyperplasia, neoplasia etc.)
Lack of patient compliance.
The above contraindications apply to all neuromobilization techniques.
Following a neuromobilization procedure (which must not cause any pain to the patient), pain is reduced while the scope of painless movement and muscle relaxation improve
A painless procedure will normally not give rise to any undesirable effects.
Properly performed neuromobilization procedures contribute to:
Pain reduction
Improved perfusion of the neural tissue
Reduced edema of the neural tissue
Improved axonal transport (orthodrome and antidrome)
Reduced sympathetic tone
Restoration of normal neuromechanical function
Restoration of normal physiological function of the nerve cells.
NEURODYNAMIC TESTS
Observation
Planning the examination (Levels of examination)
LEVELS OF NEURODYNAMIC TESTING Level 0 (zero): Testing is contraindicated. Any contraindication for manual therapy generally exists for neurodynamic testing Level 1: Limited examination
Indications:
When symptoms are easily provoked and takes long time to settle after movement.
In cases of severe pain.
Presence of any neurological deficit.
When symptoms show a progressive worsening after physical examination.
Level 2: Standard examination Indications:
Problem is not easily provoked and symptoms are not severe.
Neurological impairment is absent.
When pain is not severe during examination.
Contraindications:
When there is bony instability, hypersensitivity, irritability/ co-existing pathology
Level 3 examination:
Indications:
When level 2 testing is normal and didn’t reveal sufficient information
Symptoms are stable and not easily provoked
When there is no co-existing pathology that might adversely affect the nervous system
Contraindications:
Same as level 2
Summary Level 0
• contraindicated
Level 1
• limited
Level 2
• standard • Neurodynamically sensitized
Level 3
• Neurodynamic sequencing • Multi-structural
• Symptomatic position/ movement
GENERAL POINTS TO BE NOTED
Explanation to the patient
Bilateral comparison
Test the unaffected side first
Maintain each movement precisely
Be gentle and do not hurry
Evoke VS provoke
Short duration of testing
The application of neuromobilization in musculoskeletal conditions is effective provided that the patient is properly diagnosed and the pathology is functional.
Neuromobilization procedures should be performed in musculoskeletal system diseases on condition that the results of tension and mobility tests are positive.
Different musculoskeletal conditions require conditionspecific neuromobilization techniques. It must be borne in mind that neuromobilization is a component of conservative treatment and should not be used in monotherapy but included in a therapeutic regimen together with other physiotherapeutic procedures and pharmacotherapy.
REFERENCES
Butler D, Mobilisation of the nervous system. New York: Churchill Livingstone; 1991
Haftek J. Stretch injury of peripheral nerve: acute effects of stretching on rabbit nerve. Joumal of Bone and Joint Surgery 1970; 52B; 354-365.
Lundborg G. Ischemic nerve injury: experimental studies on intraneural microvascular pathophysiology and nerve function in a limb subjected to temporary circulatory arrest. Scandinayian Joumal of Plastic and Reconstructive Surgery 1970; 6: 1-113.
Selander D, Mansson L G, Karlsson L, i wsp. Adrenergetic [RACZEJ adrenergic] vasoconstriction in peripheral nerves in the rabbit. Anesthesiology 1985; 62; 6-10.
Gilliatt R W. Physical injury to peripheral nerves: physiologic and electrodiagnostic aspects. Mayo Clinic Proceedings 1981; 56; 361-370.
Triano J J, Luttges MW. Nerve irritation: a possible model of sciatic neuritis. Spine 1982; 7; 129-136.
Rydevik B, Brown M D, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9: 7-15.
Dahiin L B, Rydeyik B, McLean W G, i wsp. Changes in fast axonal transport during experimental nerve compression at low pressures. Experimental Neurology 1984; 84; 29-36. Dahiin L B, McLean WG. Effects of graded experimental compression on slow and fast axonal transport in rabbit vagus nerve. Joumal of the Neurological Sciences. 1986; 72: 19-30. Dahiin L B, Sjostrand J, McLean WG. Graded inhibition of retrograde axonal transport by compression of rabbit vagus nerve. Joumal of the Neurological Sciences 1986; 76: 221-230. Upton A R M, McComas A J. The double crush in nerve entrapment syndromes. Lancet 1973; 2: 359-362. Cherington M. Proximal pain in carpal tunnel syndrome. Archives of Surgery 1974; 108: 69. Hurst L C, Weissberg D, Carroll R E. The relationship of double crush to carpal tunnel syndrome. Joumal of Hand Surgery 1985; 202-204. Dyro F M. Peripheral entrapments following brachial plexus lesions. Electromyography and Clinical Neurophysiology 1983; 23: 251-256. Principles of neuromobilization for treating musculoskeletal disease, Micha³ Dwornik, Dariusz Bia³oszewski,Izabela Korabiewska, Zbigniew Wroñski,Orr ttopediia Traumatologia Rehabilitacja © MEDSPORTPRESS, 2007; 2(6); Vol. 9, 111-121
THANK YOU!
Dr. LAKSHMI PAVANI P. (PT)
SPINE
Mechanical interface
Neural
Innervated tissue
FLEXION AND EXTENSION
Mechanical interface- spinal canal
Flexion of the whole spine causes elongation of the spinal neural structures because they, and their canal are located behind the axis of rotation of the spinal segments.
Neural tissues-
Tension and strain are the two responses for flexion. The amount of tension is not clearly known but strain from lumbar extension to flexion in lumbar dura can reach 30%, scaral nerve roots 16% (Adams & Logue; Yuan et al 1988)
Sliding and convergence:
Sliding of the neural structures is complex in spine and specific sequences of movements their own sliding. Eg: Neck flexion produces cephalad sliding of neural structures in lumbar region (Breig 1978). However SLR produces caudad sliding of the nerve roots in the lumbosacral foraminae ( Goddard & Reid; Breig 1978).
LATERAL FLEXION AND LATERAL GLIDE
Mechanical interface
The key event with lateral flexion in relation to mechanical interface is that the intervertebral foraminae close down ipsilateral side and open on the contralateral side (Fujiwara et al 2001).
Neural effects:
Lateral flexion produces increased tension in the neural structures on the convex side of the spine and reduce tension on the concave side (selvaratnam et al 1988).
Increase in tension occurs in two ways:
The first is that lateral flexion itself produces elongation of the interface and neural tissues on the convex side.
The second is by causing an increase in distance between the spine and the periphery by sideway translation of the vertebrae (Louis 1981)
Uses: 1.
Structural differentiation
2.
Sensitization
Others: 1.
Contralateral neurodynamics
2.
Bilateral neurodynamic techniques
GENERAL NEUROPATHODYNAMICS
Mechanical interface dysfunctions
Neural dysfunctions
Innervated tissue
dysfunctions
MECHANICAL INTERFACE DYSFUNCTIONS Closing dysfunctions
• Reduced closing
Opening dysfunctions
• Reduced opening
Patho-anatomical dysfunctions Pathophysiological dysfunctions
• Excessive closing
• Excessive opening
• Eg: spondylolisthesis • malignancy • inflammation
CLOSING DYSFUNCTIONS
Reduced closing
Symptoms: Key behavioral aspect is symptoms increase with closing movements. Physical findings: 1.
Posture:
In acute and severe dysfunctions a protective deformity is frequently apparent. This deformity is always in the opening direction so as to reduce the pressure in the adjacent neural structure.
Excessive closing
Symptoms:
Provoked by closing mechanism
Hypermobility, instability or habitual closing exist.
Eg: Hyper-lordotic lumbar spine. History:
Habitual posture or posture imperfection is common.
Sometimes a history of trauma and features of instability also
Opening dysfunctions
Reduced opening
Symptoms:
Usually aches and pains in the localized area with or without referred pain.
Opening movements provoke pain and are usually restricted.
History:
Usually H/O trauma exists in which patient has been forced into opening positions.
The body then compensates during healing process by causing inflammation and muscular spasm such that opening movements are reduced to avoid further provocation.
Eg: spine
Physical findings:
The reduced opening dysfunction produces a protective spasm on the ipsilateral side unlike closing type has on contralateral side. This deformity is specially designed to reduce tension in the interfacing and neural tissues.
Palpation:
tenderness, muscle spasm Eg: L4-S1 segments may be accompanied by tenderness and spasm of the ipsilateral erector spinae as they limit contralateral flexion.
Excessive opening
Symptoms:
Aches and pains and can produce referred pain
Pins and needles, numbness can occur in this dysfunction.
Symptoms are intermittent and they are produced when provoking movements occur.
Physical findings:
No deformity is seen
Opening movements are increased and that is eventually leading to this disorder.
Eg: cervical contralateral flexion and rotation.
Palpation:
Tenderness over specific areas is often present. Hypermobility produces mechanical irritation of the relevant structures.
NEURAL DYSFUNCTIONS
Neural sliding dysfunction Neural tension dysfunction
Hypermobility
AIMS AND OBJECTIVES OF NEUROMOBILIZATION
Neuromobilization is aimed at reconstructing normal neuromechanical condition, i.e. adapting the nervous system to constantly changing loads and mechanical tension.
It involves stretching and pulling nerve trunks, spinal roots, spinal nerves, spinal cord and spinal meninges by effecting movement of joints in precisely isolated positions.
Physiotherapeutic treatment, including neuromobilization, ought to be performed in the earliest possible stage of disease, before the occurrence of irreversible morphological changes and should include all affected tissues.
Neuromobilization should involve the entire length of the nerve trunk.
The primary objective in neuromobilization is to improve neuromechanical function through mobilization of peripheral nerves, spinal roots, spinal meninges and the perineural connective tissue.
Neuromobilization techniques restore normal neuromechanical function of both peripheral nerves and the central nervous system.
CLINICAL TESTS Clinical tests performed in connection with neuromobilization consist of:
Testing of exteroceptive sensation (superficial sensation, two-point discrimination) and proprioceptive sensation ,vibrations.
Examination of indicator muscle function (innervated mostly by one segment)
Testing muscle reflexes
Examination of nerve trunk tension (nerve trunk tension tests)
Examination of nerve trunk mobility (nerve trunk mobility tests)
The essential examination conducted before performing neuromobilization involves nerve trunk tension and mobility tests. Positive results of these tests include:
Elicitation of a symptomatic pain reaction characteristic of a particular condition,
Differential symptoms in symmetry tests (performed on the opposite upper limb)
Confirmation of the symptoms by discriminatory testing of other tissues
Confirmation of the symptoms by palpation of the nerve trunk through irritation.
Tension tests consist in stretching a given nerve, spinal cord or meninges by moving joints in areas where these structures are found in such a way as to enable the maximum possible adjustment of the nervous system.
The stretching effect is increased by angular placement of the joint and also by joint traction.
A positive test result reflects a lack of elasticity in the conducting structures.
Eg: Hematoma located in the perineurium.
Mobility tests induce a shift of the nervous system by placing the examined fragment of neural tissue in a rest (relaxed) position, while a shift in relation to perineural tissues occurs as a consequence of stretching the nerve proximally or distally to the injury site.
A positive test result reveals a limitation in the supportive connective tissue in the nerve or the presence of external compression factors.
Positive results enable the tests to be used as mobilization techniques.
The initial position for a mobilization procedure is determined by a positive tension test or a positive mobility test.
Impulsation (stretching and pulling) is conducted through the joint situated proximally or distally to the treated segment of the nervous system.
Impulses stretching the trunks of peripheral nerves should not stretch the neural tissue more than
up to 8% of the entire nerve length, since that might produce early symptoms of nerve ischemia. (Lundborg et al,1970)
Blood supply is completely blocked when neural tissue is stretched by 15% (Lundborg et al 1970)
Thus, a procedure must correspond to the patient's condition and may never cause pain. The number, duration and frequency of impulses is determined on the basis of patient response.
Initially, two series of impulsation procedures of a few seconds' duration are performed at a frequency of 2-4 impulsations per second.
As the patient's condition improves, the duration of the procedure is extended to 20-30 seconds, with increasing amplitude of movement in the joint through which the impulsation, longer duration of a single impulse and more series of impulsations.
In chronic conditions, between 10 and 60 stretches are performed lasting up to 20 seconds.
However, it must be emphasized that this method is based on the principle of painlessness corresponding with concept of “painlessness and opposite motion”- ( Maigne R et al,1996 ), which holds that the patient should not feel any pain either during or after the procedure.
While producing tension of a nerve trunk, the therapist does not know which structure has caused
the dysfunction. In the course of the procedure the stretching force is received by the tissue which has lost elasticity. The remaining structures gradually adapt to the progressing tension and rearrangement ( Maigne R et al,1996 ).
CONTRAINDICATIONS
Acute injuries to the central and peripheral nervous system,
Tumors of the nervous system and spinal cord,
Infection and acute inflammation,
Fever,
Unstable neurological symptoms,
Pain at rest,
CONTRAINDICATIONS
Cauda equina injury symptoms (disturbed bladder or bowel function, disturbed function of the rectal sphincters, major neurological defects of upper and lower limbs),
Spinal instability (osseous or ligamentous),
Congenital anomaly of the spinal column and peripheral nerves (dysplasia, aplasia, hyperplasia, neoplasia etc.)
Lack of patient compliance.
The above contraindications apply to all neuromobilization techniques.
Following a neuromobilization procedure (which must not cause any pain to the patient), pain is reduced while the scope of painless movement and muscle relaxation improve
A painless procedure will normally not give rise to any undesirable effects.
Properly performed neuromobilization procedures contribute to:
Pain reduction
Improved perfusion of the neural tissue
Reduced edema of the neural tissue
Improved axonal transport (orthodrome and antidrome)
Reduced sympathetic tone
Restoration of normal neuromechanical function
Restoration of normal physiological function of the nerve cells.
NEURODYNAMIC TESTS
Observation
Planning the examination (Levels of examination)
LEVELS OF NEURODYNAMIC TESTING Level 0 (zero): Testing is contraindicated. Any contraindication for manual therapy generally exists for neurodynamic testing Level 1: Limited examination
Indications:
When symptoms are easily provoked and takes long time to settle after movement.
In cases of severe pain.
Presence of any neurological deficit.
When symptoms show a progressive worsening after physical examination.
Level 2: Standard examination Indications:
Problem is not easily provoked and symptoms are not severe.
Neurological impairment is absent.
When pain is not severe during examination.
Contraindications:
When there is bony instability, hypersensitivity, irritability/ co-existing pathology
Level 3 examination:
Indications:
When level 2 testing is normal and didn’t reveal sufficient information
Symptoms are stable and not easily provoked
When there is no co-existing pathology that might adversely affect the nervous system
Contraindications:
Same as level 2
Summary Level 0
• contraindicated
Level 1
• limited
Level 2
• standard • Neurodynamically sensitized
Level 3
• Neurodynamic sequencing • Multi-structural
• Symptomatic position/ movement
GENERAL POINTS TO BE NOTED
Explanation to the patient
Bilateral comparison
Test the unaffected side first
Maintain each movement precisely
Be gentle and do not hurry
Evoke VS provoke
Short duration of testing
The application of neuromobilization in musculoskeletal conditions is effective provided that the patient is properly diagnosed and the pathology is functional.
Neuromobilization procedures should be performed in musculoskeletal system diseases on condition that the results of tension and mobility tests are positive.
Different musculoskeletal conditions require conditionspecific neuromobilization techniques. It must be borne in mind that neuromobilization is a component of conservative treatment and should not be used in monotherapy but included in a therapeutic regimen together with other physiotherapeutic procedures and pharmacotherapy.
REFERENCES
Butler D, Mobilisation of the nervous system. New York: Churchill Livingstone; 1991
Haftek J. Stretch injury of peripheral nerve: acute effects of stretching on rabbit nerve. Joumal of Bone and Joint Surgery 1970; 52B; 354-365.
Lundborg G. Ischemic nerve injury: experimental studies on intraneural microvascular pathophysiology and nerve function in a limb subjected to temporary circulatory arrest. Scandinayian Joumal of Plastic and Reconstructive Surgery 1970; 6: 1-113.
Selander D, Mansson L G, Karlsson L, i wsp. Adrenergetic [RACZEJ adrenergic] vasoconstriction in peripheral nerves in the rabbit. Anesthesiology 1985; 62; 6-10.
Gilliatt R W. Physical injury to peripheral nerves: physiologic and electrodiagnostic aspects. Mayo Clinic Proceedings 1981; 56; 361-370.
Triano J J, Luttges MW. Nerve irritation: a possible model of sciatic neuritis. Spine 1982; 7; 129-136.
Rydevik B, Brown M D, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9: 7-15.
Dahiin L B, Rydeyik B, McLean W G, i wsp. Changes in fast axonal transport during experimental nerve compression at low pressures. Experimental Neurology 1984; 84; 29-36. Dahiin L B, McLean WG. Effects of graded experimental compression on slow and fast axonal transport in rabbit vagus nerve. Joumal of the Neurological Sciences. 1986; 72: 19-30. Dahiin L B, Sjostrand J, McLean WG. Graded inhibition of retrograde axonal transport by compression of rabbit vagus nerve. Joumal of the Neurological Sciences 1986; 76: 221-230. Upton A R M, McComas A J. The double crush in nerve entrapment syndromes. Lancet 1973; 2: 359-362. Cherington M. Proximal pain in carpal tunnel syndrome. Archives of Surgery 1974; 108: 69. Hurst L C, Weissberg D, Carroll R E. The relationship of double crush to carpal tunnel syndrome. Joumal of Hand Surgery 1985; 202-204. Dyro F M. Peripheral entrapments following brachial plexus lesions. Electromyography and Clinical Neurophysiology 1983; 23: 251-256. Principles of neuromobilization for treating musculoskeletal disease, Micha³ Dwornik, Dariusz Bia³oszewski,Izabela Korabiewska, Zbigniew Wroñski,Orr ttopediia Traumatologia Rehabilitacja © MEDSPORTPRESS, 2007; 2(6); Vol. 9, 111-121
THANK YOU!
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