Impact of cervical lymph node dissection on accessory spinal nerve XI function: Case series and literature review
Saout Arrih Badr1, Bijou Walid1, Oukessou Youssef1
1Department of Otolaryngology, Head and Neck surgery, Ibn Rochd University Hospital, Faculty of Medicine and Pharmacy, Hassan II University, Casablanca, Morocco.
Introduction:
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.
Methods:
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).
Results:
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).
Conclusion:
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.
