31th October, 2020

MODULE EXAMINATION NEUROMUSKULER DIVISION II

Brachial Plexus Injury

Presented By:
Aulia Angraini, MD

Supervised By:
Dr. Vitriana, MD, Physiatrist Consultant

Novitri, MD, Physiatrist Consultant

Farida Arisanti, MD, Physiatrist Consultant

Physical Medicine and Rehabilitation

Department Faculty of Medicine of Padjadjaran
University Dr. Hasan Sadikin Hospital
Bandung 2020
1. Why does the neuropraxia type brachial plexus injury recovery faster than the
axonotmesis type?
The peripheral nerve injuries can be caused by a variety of mechanisms, broadly
classified as systemic conditions or local pathologies. Nerve injury may involve axonal
loss, myelin loss, or commonly a combination of both. In 1943, Sir Herbert Seddon
described the three basic types of nerve injuries, and referred to them as neurapraxia,
axonotmesis, and neurotmesis, using a mild/moderate/severe surgical model. Sir Sydney
Sunderland described five degrees of peripheral nerve injury [Table 1]. The first degree
corresponds to neurapraxia and the second degree to axonotmesis as described above.
The third, fourth, and fifth degrees involve injury to endoneurial tubes, perineurium, and
epineurium, respectively.
Neurapraxia, the first-degree injury, is the most common response to blunt trauma
causing a temporary conduction block with demyelination at the site of injury. Clinically,
it results in sensory dysfunction. The Tinel sign is absent and electrophysiologic studies
are negative. The recovery may take a few days up to 12 weeks.
Axonotmesis is the second-degree injury leading to axonal loss while the
connective tissue layers are preserved. The distal targets of peripheral nerves release
trophic factors for growth and survival of axons and neuronal cell bodies that enhance
formation of proximal axonal sprouts. Chemotactic factors released from distal targets
also help guide sprouting axons to the appropriate destination. Clinically, motor and/or
sensory dysfunction is present and Tinel sign is positive at the site of injury.
Electrophysiologic study reveals decreased nerve conduction velocity and regional
muscle denervation changes with fibrillations.
Neurotmesis is the third-degree and the most severe nerve injury, where the nerve
is physically divided. No conduction on electrophysiology and no recovery are expected
unless surgery is performed.
Therefore, neuropraxia will recovery faster than the axonotmesis because
neuropraxia is the mildest where the nerve and the axonal continuity are maintained, and
there is only nerve demyelination. In axonotmesis, the continuity of the nerve sheath is
maintained while there is a breakdown of the axonal continuity by Wallerian
degeneration.
2. What happens to the wallerian degeneration process?
Traumatic injury to peripheral nerves results in the loss of neural functions. Recovery by
regeneration depends on the cellular and molecular events of Wallerian degeneration that
injury induces distal to the lesion site, the domain through which severed axons
regenerate back to their target tissues. Innate-immunity is central to Wallerian
degeneration since innate-immune cells, functions and molecules that are produced by
immune and non-immune cells are involved. The innate-immune response helps to turn
the peripheral nerve tissue into an environment that supports regeneration by removing
inhibitory myelin and by upregulating neurotrophic properties. The characteristics of an
efficient innate-immune response are rapid onset and conclusion, and the orchestrated
interplay between Schwann cells, fibroblasts, macrophages, endothelial cells, and
molecules they produce. Wallerian degeneration serves as a prelude for successful repair
when these requirements are met. In contrast, functional recovery is poor when injury
fails to produce the efficient innate-immune response of Wallerian degeneration.
3. What are the causes of shoulder subluxation?
Shoulder subluxation is defined as partial or incomplete dislocation of the glenohumeral
joint or translation between the humeral head and glenoid fossa while the humeral head is
in contact with the glenoid fossa. The weakness of rotator cuff muscles or laxity of the
glenohumeral ligaments causes the humeral head to easily slip out of the glenoid fossa
and results in glenohumeral subluxation.

The etiology can be classified as traumatic, non-traumatic and neuromuscular

causes. For the traumatic cause, it is more frequent in active young individuals. Shoulder
subluxation is prevalent in boxers. However, a non-contact sport with repetitive shoulder
movements and a hand in the outstretched position can also cause subluxation. For the
non-traumatic cause, the etiology could be multifactorial. The patients may have
suboptimal shoulder muscle control or tendon/ligament injury in the rotator cuff interval.
These 2 patterns of shoulder instability can be defined as TUBS syndrome (traumatic,
unilateral dislocations with a Bankart lesion, often requiring surgery) and AMBRI
syndrome (atraumatic, multidirectional, bilateral shoulder subluxation/dislocations, often
treated with rehabilitation, and sometimes requiring inferior capsular shift), respectively.
The neuromuscular causes, such as stroke, cerebral palsy, and brachial plexus injury can
also lead to shoulder subluxation.
There are two factors that keep the stability of shoulder:
1. Static Factors
 Articular congruence
 Articular version
 Glenoid labrum
 Capsule and ligament
2. Dynamic Factors
 Rotator cuff
  Biceps tendon
 Scapulothoracic motion
 Negative pressure
 Proprioception

Subluxation mechanism at stroke people:

4. What causes joint stiffness in a patient with a brachial plexus injury?

Pain is one of the most negatively affecting factors on the quality of life patients with BPI
(brachial plexus injury), is a common symptom after BPI, accounting for 67% to 71%.
Pain after BPI is usually neuropathic, with rates of neuropathic pain reported as high as
95%. It is usually caused by trauma or traumatic neuropathy to the musculoskeletal
system, but other kinds of pain associated with nociceptive pain and complex reginal pain
syndrome can also occur. Nociceptive pain results from tissue injury that activates the
pain receptor, and also associated with inflammation, which often leads to peripheral
hyperexcitability of the nociceptive system. Causes of nociceptive pain associated with
BPI include myofascial pain, tendinitis, postoperative lesion, and muscle overload due to
unbalanced movement and joint pain. A wide continuum of injuries, from contusions to
ruptures, produce weakness, initially from the injury itself, and secondarily from
inactivity and disuse following the injury during the recovery phase. Pain, whether in an
injured muscle or in a joint on which the muscle acts, reduces the individual’s willingness
to move the muscle. When a muscle is not used at its normal functional level, weakness
ensues. When paralysis happens, the joints can stiffen and make movement more
difficult.
5. What we should do after tendon transfer?
4-6 weeks after surgery patient were given time not to move his hand. After that the main
thing to do is to do the stretching to prevent joint stiffness and prepare the muscle for the
next step which is strengthening. After that is patient have to do the strengthening
program.
In steindler postoperative rehabilitation, the patient is maintained with the elbow in a
long-arm splint or cast holding the elbow in 110 degrees of flexion along with forearm
pronation. Starting 4 weeks after surgery the patient is extended 10 degrees each week in
a brace that can control the maximum amount of elbow extension. The patient is allowed
to begin passive and active flexion exercises 6 weeks after surgery. A flexion contracture
of 30 degrees is desirable because this will provide an improved mechanical advantage
for elbow flexion. Strengthening exercises are delayed until 12 weeks after surgery.
 REFERENCE

1. Braddom RL, Chan L, Harrast MA, eds. Physical Medicine and Rehabilitation. 4th ed.
Philadelphia, PA: Saunders/Elsevier; 2011.
2. Chhabra A, Ahlawat S, Belzberg A, Andreseik G. Peripheral nerve injury grading simplified on MR
neurography: as referenced to Seddon and Sunderland classifications. Indian J Radiol Imaging.
2014 Jul;24(3):217.
3. Rotshenker S. Wallerian degeneration: the innate-immune response to traumatic nerve injury. J
Neuroinflammation. 2011 Dec 1;8(1):109.
4. Vitoonpong T, Chang KV. Shoulder Subluxation. [Updated 2020 Aug 29]. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK507847/
5. Park HR, Lee GS, Kim IS, Chang JC. Brachial plexus injury in adults. The Nerve. 2017 Apr
30;3(1):1-1.
6. Andrea S, Morehouse, Susan, et all. Review Article : Brachial Plexus Injury. Elsevier.
7. Sakellariou VL, Badilas NK, et all. Review Article : Treatment Options for Brachial
Plexus Injury. ISRN Orthopedics. Doi :10.1155/2014/314137
8. Peggy AH, Dolores BB. Brunsstorm’s Clinical Kinesiology. 6th ed. Philadelphia, PA:
Davis company; 2012.