This document provides information about radial nerve palsy and peripheral nerve injury classification. It discusses:
- The anatomy of peripheral nerves and how they can be injured through ischemia, compression, traction, laceration or burning.
- A classification system for nerve injuries from neuropraxia (reversible conduction block) to axonotmesis (axon interruption but nerve continuity) to neuronotmesis (nerve trunk division).
- Clinical signs of nerve injury like numbness, muscle weakness, and abnormal posture. Electrodiagnostic studies and tests like the Tinel's sign that can help assess nerve recovery are also outlined.
anatomy of median nerve,course in arm and struthers ligament, branches in the forearm, carpal tunnel and course in hand, high and low median nerve injuries, principles of surgical management, pronator teres syndrome, anterior interosseous nerve syndrome, open and endoscopic carpal tunnel release
PNI with Relevant Anatomy, Etiology, Mechanism of Degenration and Regenration, Saddon's and Sunderland Classifications, Clinical symptoms and Examination (Tests) of Brachial Plexus, Radial & Median Nerve.
anatomy of median nerve,course in arm and struthers ligament, branches in the forearm, carpal tunnel and course in hand, high and low median nerve injuries, principles of surgical management, pronator teres syndrome, anterior interosseous nerve syndrome, open and endoscopic carpal tunnel release
PNI with Relevant Anatomy, Etiology, Mechanism of Degenration and Regenration, Saddon's and Sunderland Classifications, Clinical symptoms and Examination (Tests) of Brachial Plexus, Radial & Median Nerve.
Peripheral nerve injuries-ASSESSMENT AND TENDON TRANSFERS IN RADIAL NERVE PALSYsuchitra_gmc
A presentation to understand peripheral nerve injuries assessment, evaluation and management. Includes principles of tendon transfer and techniques of tendon transfer for radial nerve palsy. Also, post operative rehabilitation is included.
Nerve injury is an injury to nervous tissue. There is no single classification system that can describe all the many variations of nerve injuries. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve.
Seddon2 classified nerve injuries into three broad categories; neurapraxia, axonotmesis, and neurotmesis.
Degeneration & regeneration of nerve fiber.ppt by Dr. PANDIAN M.Pandian M
INTRODUCTION
CLASSIFICATION OF NERVE INJURIES
INJURY OF THE NERVE CELL BODY
INJURY OF THE NERVE CELL PROCESS
CHANGES IN THE DISTAL SEGMENT OF THE AXON
CHANGES IN THE PROXIMAL SEGMENT OF THE AXON
CHANGES IN THE NERVE CELL BODY
RECOVERY OF THE NEURONS FOLLOWING INJURY
REGENERATION OF AXONS IN THE PERIPHERAL NERVES
REGENERATION OF AXONS IN THE CNS
Similar to Peripheral Nerve Injury: Radial Nerve Palsy (20)
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. Anatomy
• Peripheral nerves are bundles of axons conducting
efferent impulses from cells in the anterior horn of spinal
cord to muscles and afferent impulses from peripheral
receptors via cells in posterior root ganglia to the cord.
• In peripheral nerves, all motor axons and the large
sensory axons are coated with myelin, a multilayered
lipoprotein membrane derived from the accompanying
schwann cells
• Every few mm the myelin sheath is interrupted, leaving
short segments of bare axon called the nodes of ranvier.
3. • Outside the schwann cell
membrane, the axon is covered
by a connective tissue stocking,
the endoneurium
• The axons that make up a nerve
are separated into bundles
(fascicles) by a fairly dense
membranous tissue, the
perineurium.
• The group of fascicles that make
up a nerve trunk are enclosed in
an even thicker connective tissue
coat, the epineurium.
4.
5. • The nerve is supplied by blood vessels that run
longitudinally in the epineurium before penetrating
the various layers to become the endoneurial
capillaries
• The tiny blood vessels have their own sympathetic
nerve supply coming from the parent nerve and
stimulation of these fibres (intraneural
vasoconstriction) may be important in conditions
such as reflex sympathetic dystrophy and other
unusual pain syndromes
6. Pathology
• Nerves can be injured by ischaemia, compression,
traction, laceration or burning.
• Damage varies in severity from transient and
quickly recoverable loss of function to complete
interruption and degeneration
7. Transient ischaemia
• Acute nerve compression causes numbness and
tingling within 15 minutes, loss of pain sensibility after
30 minutes and muscle weakness after 45 minutes.
• Relief of compression is followed by intense
paresthesia lasting unto 5 minutes , feeling is restored
within 30 seconds and full muscle power after about
10 minutes.
• These changes are due to transient endoneurial
anoxia and leave no trace of nerve damage.
8. Neuropraxia
• Reversible physiological nerve conduction block in
which there is loss of some types of sensation and
muscle power followed by spontaneous recovery
after a few days or weeks
• D/t mechanical pressure causing segmental
demyelination and is seen typically in crutch palsy,
pressure paralysis in the states of drunkenness
(saturday night palsy) and the milder types of
tourniquet palsy.
9. Axonotmesis
• More severe, seen typically after closed fractures and
dislocations.
• axonal interruption, with loss of conduction but the nerve is in
continuity and neural tubes are intact.
• Distal to lesion and for a few mm retrograde, axons disintegrate
and are resorbed by phagocytes; Wallerian degeneration;
Accompanied by marked proliferation of schwann cells and
fibroblasts lining the endoneurial tubes.
• Numerous fine unmyelinated tendrils grow from proximal stumps,
many of which find their way into the cell clogged endoneurial
tubes at the speed of 1-2 mm per day
10. Neuronotmesis
• Division of nerve trunk, as may occur in an open
wound.
• Regenerating fibres mingle with proliferating
schwann cells and fibroblasts in a jumbled knot, or
neuroma at the site of injury.
11. Double crush phenomenon
• Proximal compression of a peripheral nerve renders
it more susceptible to the effects of a second, more
peripheral injury.
• Peripheral entrapment syndromes are often
associated with cervical or lumbar spondylosis.
13. Sunderland,1978
• 1st degree injury;
-Transient ischaemia and neurapraxia; reversible
-Motor function is more profoundly affected than sensory function. Sensory
modalities affected in order of decreasing frequency as ; proprioception, touch,
temperature and pain. Sympathetic fibers are most resistant to this type of injury.
-Sympathetic function return promptly and motor function is last to return
-Simulataneous return of motor function in proximal and distal musculature; i.e.
no motor march.
-No advancing tinel sign
14.
15. • 2nd degree injury;
-Axonal degeneration but because endoneurium is preserved, regeneration can lead to complete or near
complete recovery without need for intervention.
-Motor reinnervation is accomplished in a progressive manner from proximal to distal in the order in
which nerve branches leave the parent trunk
-Commonly an advancing tinel sign can be followed along the course of nerve usually at the rate of 1
inch per month, tracing the progression of regeneration.
• 3rd degree injury;
-Endoneurium is disrupted but perineurial sheaths are intact
-Chances of axons reaching their targets are good but fibrosis and crossed connections limit recovery.
-Advancing tinel sign is usually present
-Complete return of neural function does not occur, distinguishing this from a second degree injury.
16. • 4th degree injury
-Only epineurium is intact but the internal damage is severe.
-Retrograde degeneration is more severe and the mortality among the neuronal
soma is higher, resulting in a significant reduction in the number of surviving
axons.
-Essentially nerve continuity is maintained only be scar tissue, preventing proximal
axons from entering distal endoneurial tubes.
-No advancing tinel sign
-Recovery is unlikely; injured segment should be excised and the nerve repaired
or grafted
17. • 5th degree injury
-Nerve is completely transected, resulting in a variable distance between neural
stumps.
-Occur only in open wounds and usually identified at the time of surgical
exploration.
-No chance of recovery without repair.
• 6th degree (Mackinnon) or mixed injuries occur in which a nerve trunk is
partially severed and the remaining part of the trunk sustains fourth degree,
third degree, second degree or rarely even first degree injury.
18. Etiology
• Peripheral nerves may be injured by metabolic or
collagen diseases; malignancies; endogenous or
exogenous toxins; or thermal, chemical or
mechanical trauma
19.
20. Clinical features
• Numbness, paresthesia or muscle weakness in the
related area
• Signs of abnormal posture (eg. wrist drop in radial nerve
palsy)
• Areas of altered sensation should be accurately tapped
• Sudomotor changes may be found in the same
topographic area; skin feels dry due to lack of sweating
• Neurological examination must be repeated at intervals
21. • In chronic nerve injuries, anaesthetic skin may be
smooth and shiny, with evidence of diminished
sensibility.
• Wasting of muscle groups
• Fixed postural deformities
22. Assessment of nerve
recovery
• Motor recovery is slower than sensory recovery
• Degree of injury/History
-Low energy injury;neurapraxia
-High energy injury; Sunderland 3rd and 4th injury
-Open injury; 5th degree
23. Tinels sign
• Peripheral tingling or dysaesthesia provoked by percussing the nerve along its
course.
• It should be tested in distal to proximal direction
• A positive tinel sign is presumptive evidence that regenerating axonal sprouts
that have not obtained complete myelinization are progressing along the
endoneurial tube.
• Negative in neurapraxia
• In axonotmesis, positive at the site of injury due to sensitivity of regenerating
axon sprouts. After a delay of few days or weeks, the tinel sign advance at rate
of 1 mm per day
• Failure of tinels sign to progress suggests 4th or 5th degree injury and need for
early exploration
24. • Sweat test
-Sympathetic fibres within peripheral nerve are
resistant to mechanical trauma
-Presence of sweating within the autonomous zone of
an injured peripheral nerve reassures the examiner to
a degree, suggesting that complete interruption of
nerve has not occurred.
-Iodine starch test, Ninhydrin print test.
25.
26. Electrodiagnostic studies
• Most common electrodiagnostic methods used to study
peripheral nerve injuries are nerve conduction studies and
EMG.
• Provide the most objective and quantitative means of
evaluating and following patients with peripheral nerve injury
• Allow localization of disorders of roots or peripheral nerves,
measure type and severity of injury and provide prognostic
information.
• Full neuropathic changes are not observed in these studies
for 2 or 3 weeks after injury
27. Nerve conduction study
• Stimulation of peripheral nerve by an electrode placed
on the skin overlying the nerve readily evokes a
response from the muscle innervated by that nerve
• This response can be seen, palpated and measured;
• Immediately after injury, conduction proximal and distal
to the insult usually elicits a normal response.
• As wallerian degeneration ensues(within 5-10 days),
there is a progressive reduction in the amplitude and
alteration in the configuration of the evoked potentials.
28. • After 10-12 days, in case of axonal injury, wallerian
degeneration will have occurred with resultant
failure to obtain sensory and motor responses with
distal stimulation.
• In contrast , distal responses are preserved in
neuropraxia because underlying axons are intact.
• Therefore, if an acute injury is suspected and
nerve continuity is in question, it is best to
perform NCS 10-14 days after injury.
29.
30. EMG
• If a muscle loses its nerve supply, the EMG will show denervation potentials by
the third weeks which excludes neurapraxia.
• EMG changes evolve over weeks and months, rather than days as seen with
NCS.
• Without normal trophic influences from nerve, muscle displays abnormal electric
irritability in the form of spontaneous fibrillation potentials, postive sharp waves
or fasciculations.
• Spontaneous electrical activity in muscle fibers develops 2-6 weeks after
denervation and continues until muscle fiber degenerates completely or is
reinnervated by nerve
• During voluntary contraction, the amplitude, duration, rate of firing and
recruitment pattern of MUPs provide information about the progress of nerve
regeneration and chronicity of injury.
31.
32. Intraoperative peripheral nerve studies
• Invaluable in identifying the appropriate circumstance for nerve grafting..
• In case of nerves that are severely injured but still in continuity, some fail to
regenerate adequately.It is in these circumstances that intraoperative studies are
well suited
• For patients who have evidence of early reinnervation on conventional EMG (6-9
months), no need of nerve grafting.
• When a greater distance needs to be traversed by nerve regeneration, EMG
evidence of axons reaching their target muscle may be delayed fo 12-24 months.
By waiting that long to decide that there was no spontaneous regeneration, it would
be too late to use nerve grafting.
• Intraop studies allow surgeon to get information earlier about the presence or
absence of axonal regeneration through the site of injury
33.
34.
35. Principles of treatment
Nerve exploration;
-Indications
• If the nerve was seen to be divided and needs to be
repaired
• If the type of injury suggest that the nerve has been
divided or severely damaged
• If recovery is inappropriately delayed and the diagnosis
is in doubt
36. • Vascular injuries, unstable fractures, contaminated soft tissues
and tendon division should be dealt with before the nerve lesion
• Nerve must be handled with suitable instruments
• Bipolar diathermy and magnification are essential
• Nerve stimulator is essential if scarring makes recognition
uncertain
• If microsurgical equipment and expertise are not available, then
the nerve lesion should be identified and wound closed pending
transferal to an appropriate facility
37. Primary repair
• Divided nerve is best repaired as soon as this can be done safely
• Stumps are anatomically orientated and fine (10/0) sutures are inserted in
the epineurium.
• No tension on the suture line
• Sufficient relaxation of tissues to permit tension free repair can usually be
obtained by positioning nearby joints or by mobilising and re routing the
nerve.
• If this doesn't solve the problem, then primary nerve graft must be
considered
• Limb is splinted in a position to ensure minimal tension on the nerve;
Splintage for 3 weeks and then physiotherapy started
38.
39. Delayed repair
Late repair i.e weeks or months after the injury, may
be indicated because
• closed injury was left alone and shows no signs of
recovery at the expected time
• diagnosis was missed and the patient presents late
• primary repair has failed
40. • When the nerve is in continuity, it is difficult to know
whether resection is necessary or not
• If the nerve is only slightly thickened and feels soft,
or if there is conduction across the lesion, resection
is not advised
• If neuroma is hard and no conduction on nerve
stimulation, it should be resected, paring back the
stumps until healthy fascicles are exposed
41. Dealing with gap
• Methods of closing troublesome gaps include
-Nerve mobilization
-Nerve transposition
-Joint flexion
-Nerve grafts
-Bone shortening
• Gaps of 2 cm in median nerve, 4-5 cm in ulnar nerve and 6-8 cm in sciatic
nerve can usually be closed
• Elsewhere gaps of more than 1-2 cm usually require grafting
42.
43. Transposition
• Ulnar nerve at the elbow- anterior transposition
• Median nerve can be transposed anterior to the
pronator teres if the lesion is distal to its branches to
the long flexor muscles of the forearm
• Tibial nerve can be placed superficial to the soles or
gastrocnemius
44. Position of extremity
• Flexion knee and elbow no more than 90 degree
• Flexion of wrist no more than 40 degrees
• External rotation and abduction helpful when repairing
radial and axillary nerves
• Elevation of shoulder girdle in brachial plexus injury.
• Extension of hip in sciatic injury.
45. Nerve guides
• Nerve gaps can regenerate through a tube which
excludes surrounding tissue from each end
• Tubes can be autogenous vein, freeze dried
muscle, silicone or metal; soluble guides which
dissolve over weeks or months are also used
• Offers a simple way of avoiding a nerve graft yet
achieving results which are at least as good in both
digital nerves and probably in main trunks
46. Nerve grafting
• Free autogenous nerve grafts can be used to bridge
gaps too large for direct suture (Sural nerve is most
commonly used)
• Vascularized grafts
47. Nerve transfer
• In root avulsions of upper brachial plexus, too
proximal for direct repair, nerve transfer can be
used
• Spinal accessory nerve can be transferred to the
supra scapular nerve
48. Techniques of nerve repair
Endoneurolysis (Internal neurolysis)
• Epineurium is incised longitudinally proximal to lesion, beginning not
more than 0.5 cm from the level of gross changes in the nerve as
determined by palpation.
• Flaps of epineurium on each side may be retracted laterally by nylon
sutures and are undermined widely. The funiculi are separated.
• If most of fascicle are intact and can be separated and traced
through neuroma, nothing further should be done.
• If stimulation fails to elicit a response and few if any intact fascicle
can be found, resection of neuroma and neurorrhaphy are probably
indicated.
49. Partial neurorrhaphy
• Indicated in Partial
severance of larger
nerves, such as the
sciatic nerve and the
cords and trunks of
brachial plexus.
54. Tendon transfer
• Motor recovery may not occur if the axons,
regenerating at about 1 mm per day, do not reach
the muscle within 18-24 months of injury.
• It is most likely when there is a proximal injury in a
nerve supplying distal muscles
55.
56. Prognosis
• Type of lesion
• Level of lesion
• Type of nerve
• Size of gap
• Age
• Delay in suture
• Associated lesions
• Surgical techniques
57. Brachial plexus injury
• Brachial plexus injuries can involve any degree of injury
at any level of the plexus.
• More severe injury such as rupture of plexal segments
or root avulsions are associated with higher energy
trauma
• Brachial plexus injuries include
-traumatic injury
-obstetric brachial plexus injury (Erb’s /Klumpke’s palsy)
58. Epidemiology
• Complete involvement of all roots is most common
(75-80% of traumatic BPIs)
• C5-C6 upper trunk (Erb’s palsy); 20-25%
• C8-T1 or lower trunk (Klumpke’s palsy); 0.6-3%
59.
60. • High speed vehicular accidents
• On Caudally forced shoulder predominantly affect
upper brachial plexus
• Forced arm abduction predominantly affect lower
roots
61. Prognosis
• Recovery of reconstructed plexus can take unto 3
years
• Infraclavicular plexus injuries have better prognosis
• Upper plexus injuries have improved prognosis
• Root avulsion (preganglionic injuries) have worst
prognosis
62. Preganglionic Vs Postganglionic
• Histamine test /Triple response (redness, wheal,
flare)
• Horner’s syndrome, winging of scapula associated
with preganglionic lesion
• Post ganglionic has better prognosis
63.
64.
65. • Xray
• CT myelograpy
-Gold standard for defining level of nerve root injury
• MRI
-Indicated if suspect injury is distal to nerve roots
• NCT/EMG
66. • Non Operative
-Observation alone waiting for recovery
-Most managed with closed observation
-Advancing Tinel sign is best clinical sign of effective
nerve regeneration
• Operative
67. Surgical techniques
• Direct nerve repair; Rarely possible due to traction and
usually only possible for acute and sharp penetration injuries
• Nerve graft ; Preferable to graft lesions of upper and middle
trunk
• Nerve transfer (Neurotization); Involves transfer of working
but less important motor nerve to a nonfunctioning more
important denervated muscle
• Muscle /Tendon transfer
68. Radial Nerve Palsy
• Radial nerve is most commonly injured peripheral
nerve accounting for 70% of all the peripheral nerve
injuries of upper extremity
74. Aetiology & Clinical features
Very high radial nerve palsy; Total palsy
• Crutch palsy
• Aneurysm of axillary vessels
High radial nerve palsy; Loss of wrist,thumb and finger extension, elbow extension
spared
• SOH fracture
• Tourniquet palsy
• Saturday night palsy
• Injections
75. Low radial nerve palsy; Loss of thumb and finger
extension; Elbow extension spared with weak wrist
extension and radial deviation.
• Dislocation of elbow, Fracture neck of radius
• Enlarged bursa
• Rheumatoid synovitis of elbow
76. History
• Mechanism of injury
• Timing of injury
• Loss of motor sensory function
• Interval recovery of function in patient presenting late
O/E
• Assessment of motor function (Individual muscles)
• Assessment of sensory function
• Assessment of involved joints
80. Non operative
• Splints
• wrist drop can be successfully
treated by splints
• Burkhalter has observed that grip
strength may be increased by 3-5
times by simply stabilising the wrist
with splints
81. Internal splint
• Burkhalter proposed early transfer of PT-ECRB to restore wrist
extension as an adjunct to nerve repair.
• It restores power grip quickly and effectively since wrist extension is
restored
• Advantages;
-It works as a substitute during nerve regrowth and largely eliminates
an external splint.
-Subsequently transfer aids the newly innervated and weak wrist
extensor.
-It continues to act as a substitute in case nerve regeneration is poor or
absent
82. Indications for surgery
• In sharp injury, exploration is indicated for
diagnostic, therapeutic and prognostic purposes.
• When nerve deficit follows blunt or closed trauma
and no clinical or electrical evidence of regeneration
has occurred after an approriate time, exploration of
nerve is indicated.
83. Timing of surgery
• Primary repair gives the best result with respect to
motor, sensory recovery. Indicated in clean sharp
nerve injuries and carried out in first 6-8 hours.
• Secondary repair preferrable only in crush injuries
where patient life is seriously endangered. Done at
delay of 3-6 weeks
84. • Nerve exploration to be done if no
return after a longer waiting period
• Seddon has suggested the maximum
length of time that may be required
for motor recovery to first manifest
itself can easily be calculated by
measuring the distance on the xray
from the fracture site to the point of
innervation of brachioradialis
muscle(approx 2 cm above lateral
epicondyle)
90. References
• Apley’s system of orthopaedics and fractures, 9th
edition.
• Campbell operative orthopaedics,12th edition.
• Greens operative hand surgery
• orthobullets.com
• Internet sources