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Neuropathodynamics: Dr. Lakshmi Pavani P. (PT)
Neuropathodynamics: Dr. Lakshmi Pavani P. (PT)
Mechanical interface
Neural
Innervated tissue
FLEXION AND EXTENSION
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
• Reduced closing
Closing dysfunctions • Excessive closing
• Reduced opening
Opening dysfunctions • Excessive opening
• Eg: spondylolisthesis
Patho-anatomical dysfunctions
• malignancy
Pathophysiological • inflammation
dysfunctions
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
Hypermobility
AIMS AND OBJECTIVES OF
NEUROMOBILIZATION
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.
The stretching effect is increased by angular placement of the joint and also by joint traction.
A positive test result reveals a limitation in the supportive connective tissue in the nerve or the
presence of external compression factors.
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.
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
Fever,
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),
Congenital anomaly of the spinal column and peripheral nerves (dysplasia, aplasia,
Observation
Planning the examination (Levels of examination)
LEVELS OF NEURODYNAMIC TESTING
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
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.
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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
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