Impact of cervical lymph node dissection on accessory spinal nerve XI function: Case series and literature review

TL;DR

Cervical lymph node surgery often harms the accessory spinal nerve, causing muscle atrophy and sensory issues, with recovery taking up to 18 months.

Contribution

This study provides new electrophysiological criteria to distinguish nerve injury types and identifies risk factors for post-surgery complications.

Findings

Cervical lymph node dissection frequently causes axonotmesis in the accessory spinal nerve, confirmed by EMG.

Malignant pathology significantly worsens functional outcomes, and anatomical variations increase complication risks.

Clinical improvement is observed at 6 months, but electrophysiological abnormalities persist, indicating prolonged recovery.

Abstract

Cervical lymph node dissection can damage the accessory spinal nerve, causing motor and pain disorders. This study evaluates the impact of these lesions and investigates the associated risk factors.

Prospective study of 29 patients who underwent cervical lymph node dissection. Assessment of accessory spinal nerve function was performed by clinical examination and electromyogram on day 28 and 6 months post-operatively. The EMG parameters analyzed were onset latency and motor amplitude. Electrophysiological and clinical criteria were established to distinguish neurapraxia from axonotmesis: neurapraxia was defined by conduction block with normal distal latencies (<3 ms) and preserved amplitudes (>5 mV), while axonotmesis was characterized by prolonged latencies (≥3 ms) and reduced amplitudes (≤5 mV) with signs of axonal degeneration. Statistical analysis was performed using Mann-Whitney, Wilcoxon, and McNemar tests and linear regression (p < 0.05).

Damage to the accessory spinal nerve was common after cervical lymph node dissection: trapezius atrophy (72 %), scapular detachment (32 %), C2 hypoesthesia (34 %). EMG revealed a mean latency of 2.78 ms (34 % pathological) and a mean amplitude of 3.04 mV (84 % less than 5 mV). Malignant pathology significantly influenced EMG amplitude (p = 0.026). At 6 months, significant improvement was observed: recovery of joint amplitudes, reduction in muscle atrophy (p < 0.05), reduction in hypoesthesia to 5.1 %, and improvement in EMG latencies (2.6 % pathological vs. 30.8 % initially).

Cervical lymph node dissection frequently causes damage to the accessory spinal nerve in the form of axonotmesis. Despite gradual clinical improvement (recovery of joint range of motion, reduction in muscle atrophy), electrophysiological abnormalities persist at 6 months, reflecting a prolonged recovery process requiring 12 to 18 months. Individual anatomical variations justify personalized management. This study highlights the importance of prolonged follow-up and appropriate preventive strategies to optimize functional recovery after dissection.

•Cervical lymph node dissection causes functional alterations of the accessory spinal nerve XI even when it is not severed, with axonotmesis-type lesions confirmed by electromyography.•The study reveals high rates of complications: atrophy of the trapezius and sternocleidomastoid muscles, scapular detachment, and sensory disturbances.•Malignant pathology significantly worsens functional impact, advanced age is correlated with sensory disorders, and certain anatomical variations (non-bifurcated nerve) predispose to complications.•A statistically significant clinical improvement is observed at 6 months for strength, trophicity, and mobility, but recovery is not complete, highlighting the importance of specialized follow-up and surgical prevention.

Cervical lymph node dissection causes functional alterations of the accessory spinal nerve XI even when it is not severed, with axonotmesis-type lesions confirmed by electromyography.

The study reveals high rates of complications: atrophy of the trapezius and sternocleidomastoid muscles, scapular detachment, and sensory disturbances.

Malignant pathology significantly worsens functional impact, advanced age is correlated with sensory disorders, and certain anatomical variations (non-bifurcated nerve) predispose to complications.

A statistically significant clinical improvement is observed at 6 months for strength, trophicity, and mobility, but recovery is not complete, highlighting the importance of specialized follow-up and surgical prevention.

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