Traumatic Brachial Plexus Injuries

What are traumatic brachial plexus injuries ?

These are traumatic lesions of the nerves that transmit motor and sensory signals from the spinal cord to the upper limb.

Peripheral nerves consist of nerve fibers (axons) surrounded by myelin (an insulating layer) and protective connective tissue. The brachial plexus is the complex nerve network arising from the cervical roots that supplies the shoulder, arm, forearm, and hand.

Following trauma, nerves may sustain injuries ranging from a transient “conduction block” to severe structural damage requiring surgical reconstruction. Accurate diagnosis is critical, as it determines whether observation or operative intervention is indicated.

How do they occur and which injury types are most common?

In everyday clinical practice, most injuries are closed and result from stretch or compression mechanisms.

Common mechanisms:

• Closed injuries (stretch/compression): e.g., motor vehicle accidents, falls, sports injuries.
• Penetrating trauma/transection: e.g., knife, glass—less common, but more likely to require primary repair.
• Traction of the roots: in high-energy trauma, root avulsion from the spinal cord may occur.

The magnitude, duration, and distribution of force determine the type of injury. Thus, two seemingly similar injuries may carry entirely different prognoses.

What are the “grades of injury” in peripheral nerves (neurapraxia, axonotmesis, neurotmesis)?

This classification reflects the degree to which the functional “architecture” of the nerve is disrupted and is crucial for prognosis.

1) Neurapraxia

• Injury primarily to the myelin (the “insulation”), resulting in a conduction block at the injured segment.
• Axons remain intact → recovery is typically complete.
• EMG usually does not show marked denervation changes.
• Prognosis: excellent; improvement over weeks to a few months, without surgery.

2) Axonotmesis

• Damage to the axons with development of Wallerian degeneration distally.
• The connective “scaffold” (structures that guide regenerating axons) is largely preserved.
• There is potential for axonal regeneration and gradual reinnervation.
• Prognosis: variable—depends on the distance from lesion to target (muscles/skin) and on nerve complexity/type.

3) Neurotmesis

• The most severe form: complete disruption of neural pathways where regeneration cannot proceed effectively.
• The nerve may be transected (loss of continuity) or may appear in continuity but with extensive intrafascicular fibrosis and neuroma formation that blocks axonal conduction.
• Prognosis: typically requires surgical reconstruction (repair/grafting/nerve transfers).

In practice, distinguishing axonotmesis from neurotmesis is not always immediate. This is why regular clinical reassessment and, when indicated, electrophysiological testing and targeted imaging are essential.

What does “root avulsion” mean and how is it different?

This is a particularly severe injury in which the spinal root is torn away from the spinal cord, fundamentally altering the reconstructive strategy.

Root avulsion is a preganglionic lesion: the root is completely detached from the spinal cord. In this scenario, nerve fibers cannot be restored by simple axonal reconstruction. Nerve transfers (redirecting functional nerves/branches) are often required to reinnervate critical functions.

Specialized electrophysiological studies may demonstrate characteristic patterns aiding diagnosis, while imaging (MR neurography or CT myelography) may reveal indirect signs that increase clinical suspicion.

What symptoms do they cause?

Symptoms depend on which part of the plexus/nerve is affected and whether motor, sensory, or mixed fibers are involved.

Common manifestations:

• Weakness in specific movements (e.g., shoulder abduction, elbow flexion, wrist/finger extension).
• Numbness/paresthesias in defined skin territories (dermatomal or peripheral nerve distribution).
• Neuropathic pain (burning, electric-shock sensations), particularly in plexus lesions.
• Muscle atrophy over time when reinnervation does not occur.
• Shoulder dysfunction (instability/subluxation) when stabilizing muscles are impaired.

Simple “numbness” after injury may be transient. However, complete weakness or persistence of symptoms warrants targeted evaluation.

How is the clinical evaluation performed and why is re-examination so important?

The clinical examination is the most reliable indicator of recovery, and follow-up reveals whether partial nerve regeneration is occurring or whether surgery is required.

Assessment includes:

• Neurological examination with documentation of muscle strength by myotome.
• Sensory testing to localize the distribution of deficits.
• Reflexes and special signs (e.g., features suggesting root involvement).
• Joint evaluation (shoulder/elbow/wrist) to prevent stiffness and secondary injury.

Reassessment at defined intervals is critical, as even minimal clinical improvement may indicate successful regeneration, whereas lack of progress at specific time points may necessitate surgical exploration.

What is the role of electrophysiological studies and when are they useful?

Electrophysiological tests document conduction, denervation, and reinnervation, complementing the clinical picture.

They may demonstrate:

• Neurapraxia: conduction block without marked denervation on electromyography (EMG).
• Axonotmesis/Neurotmesis: denervation changes and absence of voluntary motor units in affected muscles (early phase).
• Reinnervation: emergence of new motor units over time.

Timing is crucial: in very early stages, denervation findings may not yet be fully evident. The combination of clinical examination + serial EMG/nerve conduction studies is often the most reliable basis for therapeutic decisions.

What is the role of imaging (MRI/MR Neurography, CT myelography)?

Imaging helps identify severe injuries (especially root avulsion) and enables accurate surgical planning.

• MRI / MR Neurography (MRN): visualizes nerves/plexus, edema, enlargement, and indirect signs of avulsion.
• CT myelography: an alternative/complementary study in selected cases to assess root integrity and possible pseudomeningocele (a sign of avulsion).

Imaging does not replace the clinical examination, but when combined with EMG it can substantially enhance diagnostic accuracy and guide the timing of surgical intervention.

When is conservative management and physiotherapy sufficient?

In neurapraxic and many axonotmetic injuries, structured rehabilitation and systematic follow-up constitute the primary treatment.

Typically includes:

• Analgesia and control of neuropathic pain as needed.
• Physiotherapy to maintain range of motion and prevent contractures.
• Occupational therapy and splinting for functional support.
• Regular neurological reassessment and EMG at selected time points.

Conservative care is not “passive waiting.” It consists of active surveillance aimed at achieving milestones and identifying the optimal surgical window if needed.

When is surgical exploration/reconstruction required and what are the goals?

When there is no documented recovery from the initial injury, or when there are signs of neurotmesis or root avulsion, surgical reconstruction may be the only means to meaningfully alter functional outcome.

Indications:

• Absence of clinical/electrophysiological improvement within a reasonable time after injury.
• Strong suspicion of neurotmesis.
• Suspected/confirmed root avulsion.
• Complete paralysis of critical upper-limb functions (e.g., elbow flexion/shoulder abduction) without progress.

Goals of surgery:

1. Define the lesion type via intraoperative anatomical and electrophysiological assessment.
2. Resect scar/fibrosis/neuroma that obstructs regeneration and conduction.
3. Restore continuity (neurorrhaphy or grafting) or redirect nerve fibers (nerve transfers) to reinnervate critical functions.

Which surgical techniques are available (neurolysis, repair, nerve grafts, nerve transfers)?

Technique selection is based on defect length, nerve quality, and the functional target (shoulder, elbow, hand).

• External neurolysis: freeing the nerve from scar tissue when continuity is preserved and regeneration is evident.
• Primary repair: when nerve ends can be approximated without tension.
• Nerve grafts (often sensory donor nerves, e.g., from the lower limb): bridge gaps when tension-free repair is not feasible.
• Bioresorbable conduits in selected small gaps, case by case.
• Nerve transfers: redirecting functioning nerves/branches to reinnervate critical muscles, especially in root avulsion.

Fundamental principle: reconstruction must never be performed under tension. Tension increases the risk of failure and scarring.