3. It is a neuropathy due to a structural abnormality, such as
compression, displacement, or traction of the nerve, or by
an intrinsic abnormality of the nerve, such as nerve cell
tumor
With these lesions, stretching and angulation of
the nerve may be as important a source
of injury as compression
7. Trauma, direct pressure and space-occupying lesions
at any level in the upper extremity
There are other situations that are not a direct cause of
nerve compression, but may increase the risk and may
predispose the nerve to be compressed specially when
the soft tissues are swollen like synovitis, pregnancy,
hypothyroidism, diabetes or alcoholism
9. Acute nerve compression
Pressures exceeding 20 mm Hg Reduced
epineurial blood flow
Pressures exceeding 30 mm Hg Inhibits
anterior and retrograde axonal transport
Pressures exceeding 80 mm Hg Cessation of
intraneurial blood flow
These changes are transitory Reversible in
short term
Example is Tourniquet palsy
13. A proximal level of nerve compression could cause more distal sites
to be susceptible to compression
The summation of compression along the nerve would result in
alterations of axoplasmic flow and subsequent pathology and
symptomatology
The possibility of a distal site of compression making the more
proximal nerve susceptible to secondary compression: A reverse
double crush
Systemic diseases such as obesity, diabetes, thyroid disease,
alcoholism, rheumatoid arthritis and neuropatthies lower the
threshold for the occurrence of a nerve compression and alter
axoplasmic transport rendering that nerve more susceptible to
develop compression neuropathy and act as a ‘crush’
14. DM is a significant predisposing factor for entrapment
neuropathies
TN-C(Tenascin-C) expression in the
endoneurium is closely correlated with nerve function
Metabolic and phenotypic abnormalities of endoneurial and
perineurial fibroblasts lies behind the vulnerability of DM patients
to entrapment neuropathy
In contrast to angiopathies, retinopathy, and nephropathy, three
representative complications of DM, mast cells do not
play significant roles in the onset or progression of the
entrapment neuropathy associated with DM
Ref: Histol Histopathol (2008) 23: 157-166
http://www.hh.um.es
15. Temporal sequence
Irritative or
inflammatory pain
Paraesthesia
(Tingling , Burning)
Ablative Numbness
Weakness and
atrophy
Dry, thin, hairless skin
Ridged, thickened,
cracked nails
Recurrent skin ulcerations
16. Clinical evaluation
History
Electro diagnosis: mainstay
• Nerve Conduction studies(NCS)
• Electromyography(EMG)
Electromyography (EMG)
EMG tests detect abnormal electrical activity in motor
neuropathy and can help differentiate between muscle and
nerve disorders
17. Sensory nerve conduction
studies are the earliest to show
abnormality of slowing (focal
demyelination) in the nerve
across the site of the
entrapment
Slow transmission rates and
impulse blockage tend to indicate
damage to the myelin sheath,
while a reduction in the strength of
impulses at normal speeds is a sign
of axonal degeneration
Motor conduction abnormalities
generally present later with
slowing across the site followed
by loss of axons (both sensory
and motor) if the entrapment is
unrelieved
Needle electromyography is
used to detect axon loss
which is chronic unless there
is a super added acute
external pressure on an
existing entrapped nerve
18. Nerve biopsy Although this test can provide valuable
information about the degree of nerve damage, it is an
invasive procedure that is difficult to perform and
may itself cause neuropathic side effects
Skin biopsy (examine nerve fibre endings) This
test offers some unique advantages over NCV tests
and nerve biopsy. Unlike NCV, it can reveal damage
present in smaller fibres; in contrast to conventional
nerve biopsy, skin biopsy is less invasive, has fewer
side effects, and is easier to perform
19. Magnetic resonance imaging (MRI) can show
muscle quality and size, detect fatty replacement of
muscle tissue, and can help rule out tumors, herniated
discs, or other abnormalities that may be causing the
neuropathy
Ultrasound: The impact of sonography on clinical
management has yet to be determined, even though
upper extremity nerves are well-depicted
Sonographically
20. Myelopathy
Brachial plexopathy
Radiculopathy
Other central nervous system disorders, that can
mimic peripheral nerve entrapment
Painful rheumatologic and orthopaedic disorders;
and other psychological entities, such as
somatoform and factitious disorders
21. Treat the
underlying cause
Infection
Toxin exposure
Medication
related toxicity
Vitamin
deficiencies
Hormonal
deficiencies
Autoimmune
disease
Management of
systemic diseases
Early management
of injuries
TREATMENT
Healthy lifestyle
Optimal weight
Balanced diet
Exercising
Limiting alcohol
consumption
Correcting vitamin
deficiencies
22. Symptom Management
1. Nonsteroidal anti-inflammatory drugs (NSAIDs) for mild
pain
2. Antidepressants (tricyclic antidepressants such as
amitriptyline or newer serotonin-norepinephrine reuptake
inhibitors such as duloxetine hydrochloride or venlafaxine)
3. Anticonvulsants (tricyclic antidepressants such as
amitriptyline or newer serotonin-norepinephrine reuptake
inhibitors such as duloxetine hydrochloride or venlafaxine)
4. Antiarrythmics (Mexiletine)
5. Narcotic agents ( Tapentadol)
23. 6. Topically administered medications
• Lidocaine
• Capsaicin
• Topical agents are generally most appropriate for
localized chronic pain such as herpes zoster neuralgia
(shingles) pain
7. TENS
8. Allied medicine (Acupuncture, massage etc.)
9. Orthosis
10. Surgery
11. Trans cranial magnetic stimulation
24. Steroid injections (such as cortisone or prednisolone) shrink the
swollen tissues and relieve pressure on the nerve
Corticosteroid injections are helpful for pregnant patients, as their
symptoms often go away within 6 - 12 months after pregnancy
Most doctors limit steroid injections to about three per year, because
they can cause complications, such as weakened or ruptured tendons,
nerve irritation, or more widespread side effects
Low-Dose Oral Corticosteroids: A short course (1 - 2 weeks) of oral
corticosteroid medicines may provide relief for some people, but the
relief does not usually last.
25. USG guided percutaneous injection, hydrodissection,
and fenestration
• An extension of blind steroid injection with advantage
of safety, accuracy of medication placement,
effectiveness, non invasiveness, ease of performance
and lower cost than open surgical release
REF: Vol.10,No.3,2010,Journal of Applied
research
26. CLASS AGENT(S) ACTION
Neutrophic Factors and
Chemoattractants
Ciliary Neutrophic factor
(CNTF)
Nerve growth factor
(NGF)
Insulin-like growth factors
(IGFs)
Brain-derived Neutrophic
factor
(BDNF)
NT-3
NT-4
Promote neuronal survival
and
regrowth
Attract and guide axon
Chemorepellent Factors Semaphorins
Netrins
Others
Selectively repel some
types of
axons
Inhibitors of Connective
Tissue
Formation
Inhibitors of fibroblasts
Collagenases
Others
Decrease fibrosis at the
site of
nerve injury to promote
axonal
regeneration
27. Nerve involved Site of entrapment
Median N.(wrist)
(Elbow)
Ulnar N. (wrist)
(Elbow)
Lower trunk or medial cord of
branchial plexus
Suprascapular N
Radial Nerve
(Elbow)
Carpal tunnel
Between heads of Pronator teres
Anterior Interosseous Nerve syndrome
Guyon’s canal (Ulnar tunnel)
Bicipital groove, Cubital tunnel
Cervical rib or band at thoracic outlet
Spinoglenoid notch
Radial tunnel—at point of
entrance into supinator muscle (arcade
of Frohse)
Posterior Interosseous Nerve syndrome
28. Median nerve in anterior
elbow. Passing between two
heads of Pronator teres muscle
and into the forearm beneath
the edge of the fibrous arch of
flexor digitorum sublimis
29. Possible areas for median nerve compression proximal
to the carpal tunnel:
The ligament of Struthers
The bicipital bursa
Anomalous arteries, and anomalous muscles (such as
Gantzer's muscle, an accessory FPL muscle)
Pronator syndrome
Anterior interosseous nerve syndrome
The last two remain the two most frequently referenced
compression neuropathies of the median nerve in the
forearm
30. Compression of the median nerve as it passes between the
two heads of the pronator teres muscle, Bicipital
aponeurosis
Compression is due to hypertrophy and imbalance of
regional tissues
Development of fibrous tissue
due to inflammatory processes
from repetitive stress,
decreasing range of motion and
increasing stresses
31. Symptoms
Insidious onset
No history of trauma
Aching pain in the proximal, volar forearm
Paraesthesias radiating into the median innervated fingers
Worsened by repetitive pronosupination movements and
wrist flexion
Carpenters, frequent computer users
with a mouse, weight lifters,
athletes especially yoga, golf and
tennis
PRONATOR SYNDROME
32. Discriminating clinically between PS and CTS:
Loss of sensation over palmar cutaneous branch territory
No Tinel's on the wrist
No nocturnal disturbance
Pain on resisted pronation from a neutral position, especially as the
elbow is extended
If resisted contraction of the FDS to the middle finger reproduces
symptoms, median nerve compression at the level of the fibrous arch
between the heads of the FDS might be suspected
If symptoms are elicited by resisted flexion of the forearm in full
supination, compression at the more proximal level of the lacertus
fibrosus might be considered
33. Site of compression essentially same for both Pronator
syndrome(PS) and AIN
PS:Vague volar forearm pain,Median nerve
parasthesias,minimum motor findings
AIN:Pure motor palsy of any or all three 1.FPL,2.FDP
of index and middle fingers,3.PQ.
Surgical indications for nerve decompression include
persistent symptoms for >6 months in patients with PS
or for a minimum of 12 months with no signs of motor
improvement in those with AIN syndrome
34. Pain may be present in the forearm along the course of the
nerve
Inability to make an “OK” sign when asked by the
examiner to flex his thumb interphalangeal joint and index
finger distal interphalangeal joint
In patients with mild AIN compression, subtle weakness
of these muscles may be the only clinical finding
Such weakness of the FPL and index finger FDP may be
uncovered by asking the patient to pinch a sheet of paper
between his thumb and index finger using only the
fingertips and then trying to pull the paper away
35. A patient with AIN syndrome may be unable to hold
on to the sheet of paper with just his fingertips and
may compensate by using a more adaptive grip in
which the interphalangeal joint of the thumb and
distal interphalangeal joint of the index finger remain
extended
Differential diagnosis
Brachial neuritis
Viral neuritis (Parsonage–Turner syndrome)
Rupture of the FPL tendon
36. Anterior view of radial nerve course.
PIN entrapment occurs because of
prominent radial recurrent artery(RRA),
medial edge of ECRB, proximal edge of
S (Arcade of frohse, RN (Radial nerve),
SRN (Superficial Radial Nerve)
37. Anatomy- Formed from posterior cord to emerge
between long and lateral heads of triceps, spiral
groove of humerus proceeding medially to laterally to
emerge between brachialis and brachioradialis on
lateral elbow to enter the radial tunnel
On exit from radial tunnel, the deep branch pierces the
supinator and exits the posterior aspect to emerge as
Posterior interosseous nerve
39. Anatomically, there are five potential sites of compression
of the Radial nerve in the area of the radial tunnel
• Fibrous bands of tissue anterior to the radiocapitellar joint
between the brachialis and brachioradialis
• The recurrent radial vessels that fan out across the PIN at the
level of the radial neck as the so-called leash of Henry
• The leading (medial proximal) edge of the extensor carpi radialis
brevis (ECRB)
• The proximal edge of the superficial portion of the supinator,
commonly referred to as the arcade of Fröhse
• The distal edge of the supinator muscle
40. Radial nerve compression can lead to either radial
tunnel syndrome or posterior interosseous nerve
syndrome (also called Supinator syndrome)
41. PIN is a branch of the radial nerve, originating in the
lateral intermuscular septum
Purely motor function
Innervates the supinator, extensor carpi ulnaris, extensor
digitorum communis, extensor digiti minimi, abductor
pollicis longus, extensor pollicis longus and brevis, and
extensor indicis proprius muscles
Most common in racquet sports, bowlers, rowers, discus
throwers, golfers, swimmers
All involve repetitive supination and pronation
May occur in synovitis, neoplasm etc
42. Symptoms and signs:
Inability to extend fingers and thumb
ECRL function intact—the wrist extends and radially
deviates
Whereas patients with PIN syndrome have a loss of motor
function, patients with RTS typically, present with mobile
wad and lateral forearm pain without motor involvement
43. Symptoms and signs:
Pain distal to lateral epicondyle, tenderness over the radial tunnel
along the path of PIN
Pain worsened by extending the elbow, pronating the forearm and
flexing the wrist
Pain with resisted active supination or wrist extension
Pain with active supination against resistance
Pain with wrist extension against resistance
Pain with resisted middle finger extension at the
metacarpophalangeal joint
No neurological deficit
Pain disappears after instilling local anaesthetic at the site of entry of
PIN
45. There is no motor weakness
Unlike a case of lateral epicondylitis the pain is not on the
lateral epicondyle of the humerus but slightly distal to it
It is described as being in the area of the mobile wad and
radial tunnel
Differential diagnosis:
Lateral epiconylitis
Osteoarthritis of the radial capitellar joint
Impingement of the articular branch of the radial nerve
Synovitis of the radiocapitellar joint
Muscle tear of the extensor carpi radialis brevis
46. Course of ulnar nerve from posterior
view. It travels deep to the flexor
carpi ulnaris muscle beneath the
arcuate ligament
47. Entrapment of the ulnar nerve is the second most common
compression neuropathy in the upper extremity after CTS
The arcade of Struthers is a band of fascia that connects the
medial head of the triceps with the intermuscular septum of the
arm
The cubital tunnel is a fibroosseous channel formed by the
olecranon process laterally, the posterior cortex of the medial
epicondyle medially, the elbow joint capsule and posterior
bundle of the medial collateral ligament anteriorly, and the
ligament of Osborne (the cubital retinaculum) posteriorly
49. •Truck drivers who lean the flexed
elbow against the open window of
their truck
•Constant cell-telephone users
•Baseball pitchers are also at risk
because of the valgus stress that is
induced in the late cocking and
early acceleration phases of
throwing
•Recurrent anterior
dislocation of the ulnar nerve
•Risk factors for ulnar nerve
dislocation
include cubitus varus deformity,
an absent or lax ligament of
Osborne, a hypertrophic medial
head of the triceps, or an
accessory head of the triceps
and the dislocation may be
associated with activities that
involve resisted elbow
extension, such as the early
acceleration phase of throwing
and bench press
CUBITAL TUNNEL SYNDROME
50. Entrapment neuropathies are far
more common than thought
These syndromes are
underdiagnosed
Early diagnosis can lead to
faster and near complete
recovery
Conservative management
followed by surgery in non
responsive cases gives good
results
51. Theodore T. Miller, William R. Reinus. Nerve
Entrapment Syndromes of the Elbow,
Forearm, and Wrist
Adam’s and Victor’s Principles of neurology
Entrapment Neuropathies John D. England,
MD
Nerves have both axial (e.g. the median artery) and segmental vasculature (e.g. the Superior Ulnar colateral artery) all along its course
The histopathology of chronic nerve compression follows a continuum that parallels patient sensory complaints, which progress from intermittent paraesthesia to constant numbness. Motor complaints progress from aching to weakness to atrophy
HISTOLOGY: ‘neuromatous’ enlargement just above the retinaculum with an abrupt reduction in size in the tunnel, distal to which the nerve regained its normal dimensions. The nerve bundles beneath the retinaculum were thinned with an increase in the endoneurium which had destroyed the ‘myelin sheaths’
The swelling showed a considerable increase in both the epineurial and intrafunicular connective tissue though the great bulk of the swelling was due to the former
Complete recovery of function after surgical decompression reflects remyelination of the injured nerve
Incomplete recovery in more chronic and severe cases of entrapment is due to Wallerian degeneration of the axons and permanent fibrotic changes in the neuromuscular junction that may prevent full reinnervation and restoration of function
Blood–Nerve barrier
The inner layers of the perineurium and the endothelial cells of the endoneurial microvessels create the blood–nerve barrier
These cells have tight junctions that are impermeable to many substances
Thus, the blood–nerve barrier provides a privileged environment within the endoneurial space
There are no lymphatic vessels within the endoneurial or perineurial spaces
As the duration of compression increases beyond several hours, more diffuse demyelination will appear, being the last event in injury to the axons themselves
This process begins at the distal end of compression or injury, a process termed wallerian degeneration. These neural changes may not appear at a uniform fashion among the whole neural sheath depending on the distribution of the compressive forces, causing mixed demyelinating and axonal injury resulting from a combination of mechanical distortion of the nerve, ischemic injury, and impaired axonal flow
Multiple and double crush syndrome
They noted a high incidence of carpal and cubital tunnel syndrome with associated cervical root injuries
’
This concept of double or multiple crush is important clinically in patients who demonstrate multiple levels of nerve compression, as failure to diagnose and treat these multiple levels of injury will result in failure to relieve patients’ symptoms. Systemic conditions such as obesity, diabetes, thyroid disease, alcoholism, rheumatoid arthritis and other neuropathies will similarly render a given individual more susceptible to the development of CTS and other compressions.
In a major mixed nerve (both sensory and motor), such as the sciatic or median nerves, signs of sympathetically mediated features may be prominent in chronic cases These changes manifest as the following
Dry, thin, hairless skin
Ridged, thickened, cracked nails
Recurrent skin ulcerations
Exceptions:
Deep branch of the ulnar nerve at Guyon canal and PIN (both predominantly motor) and the lateral femoral cutaneous nerve (LFCN; pure sensory) near the anterior superior iliac spine (ASIS)
The electromyography detects the voluntary or spontaneous generated electrical activity. The registry of this activity is made through the needle insertion, at rest and during muscular activity to assess duration, amplitude, configuration and recruitment after injury. Recruitment will be affected if demyelination occurs, but will not result in abnormal spontaneous activity. Meanwhile, axonal injury will result in both recruitment and abnormal spontaneous activity, which will not be seen on needle electromyography until 2 weeks after the initial insult
Nerve conduction assesses for both sensory and motor nerves. This study consists in applying a voltage simulator to the skin over different points of the nerve in order to record the muscular action potential, analyzing the amplitude, duration, area, latency and conduction velocity. The amplitude indicates the number of available nerve fibers. Some authors consider diminished amplitude below 50% to be suggestive of compression. In such cases, we will find a normal response to distal stimulation but no response proximal to the site of entrapment. If the compression progresses, our results will be compatible with axonal degeneration with diminished amplitude of the response with relative preservation of the conduction velocity and distal latency until the remaining axons are completely damaged
Exercise can reduce cramps, improve muscle strength, and prevent muscle wasting
Inflammatory and autoimmune conditions leading to neuropathy can be controlled in several ways
Immunosuppressive drugs such as prednisone, cyclosporine, or azathioprine may be beneficial. Plasmapheresis — a procedure in which blood is removed, cleansed of immune system cells and antibodies, and then returned to the body — can help reduce inflammation or suppress immune system activity. Large intravenously administered doses of immunoglobulins (antibodies that alter the immune system, and agents such as rituximab that target specific inflammatory cells) also can suppress abnormal immune system activity.
Neuropathic pain, or pain caused by the injury to a nerve or nerves, is often difficult to control. . The antidepressant and anticonvulsant medications modulate pain through their mechanism of action on the peripheral nerves, spinal cord, or brain and tend to be the most effective types of medications to control neuropathic pain. Tapentadol, a drug with both opioid activity and norepinephrine-reuptake inhibition activity of an antidepressant.
Surgical intervention can be considered for some types of neuropathies. Injuries to a single nerve caused by focal compression such as at the carpal tunnel of the wrist, or other entrapment neuropathies, may respond well to surgery that releases the nerve from the tissues compressing it. Some surgical procedures reduce pain by destroying the nerve; this approach is appropriate only for pain caused by a single nerve and when other forms of treatment have failed to provide relief. Peripheral neuropathies that involve more diffuse nerve damage, such as diabetic neuropathy, are not amenable to surgical intervention. Neutrophic factors
The AIN innervates the deep muscles of the forearm (FPL, FDP to the index and middle fingers, and pronator quadratus), a patient with a complete AIN palsy would present with
Absent motor function to all three of these muscles.
AIN comes out radially from the median nerve while most other branches come out Ulnarward
Anatomy
The nerve begins posterior to the axillary artery and travels through the triangular space and then continues along the spiral groove of the humerus. The branches to the triceps are given off before this transition. All branches (sensory or motor) beyond the spiral groove pertain to the hand and forearm (Anconeus is the exception). The nerve travels from the posterior compartment of the arm into the anterior compartment as it penetrates the lateral intermuscular septum approximately 10–12 cm proximal to the elbow. The radial nerve continues to travel distally and ultimately bifurcates into deep (PIN) and superficial (SRN) branches approximately 6.0–10.5 cm distal to the lateral intermuscular septum and 3–4 cm proximal to the leading edge of the supinator.[35,36] The PIN is a motor nerve that courses deep beneath the supinator muscle; the SRN is a sensory nerve that travels anteriorly on the undersurface of the brachioradialis and, in the distal one-third of the forearm, travels subcutaneously to provide sensation to the dorsoradial hand
The PIN travels through the radial tunnel. Distally innervating the ECRB, supinator, ECU, EDC, EDM, APL, EPL, EPB, and EIP. It does not innervate the extensor carpi radialis longus (ECRL). The radial tunnel[34] is a potential space 3–4 finger breadths long, lying along the anterior aspect of the proximal radius through which the PIN travels. The floor of the radial tunnel is created by the capsule of the radiocapitellar joint, which continues as the deep head of the supinator muscle.