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Intraoperative measurements of nerve root blood flow during discectomy for lumbar disc herniation
Shinichi Hida1, Masatoshi Naito, Masahiro Kubo
1Department of Orthopaedic Surgery, Fukuoka University, School of Medicine, Fukuoka, Japan. hidas@cis.fukuoka-u.ac.jp
Study Design:
Nerve root blood flow was intraoperatively measured before and after discectomy for lumbar disc herniation and compared with clinical features.
Objective:
To investigate the relation between nerve root blood flow changes and symptoms associated with lumbar disc herniation.
Summary Of Background Data:
Several authors have reported that recovery of intraneural blood flow, which restores the supply of oxygen and other nutrients to the nerve tissue, is strongly related to the rapid improvement of nerve function after discectomy for lumbar disc herniation. However, no previous study has quantitatively assessed blood flow in the human nerve root.
Methods:
Nerve root blood flow was monitored in 21 patients with lumbar disc herniation using laser Doppler flowmetry (ALF 21 N; ADVANCE, Tokyo, Japan) during discectomy. Possible correlations were investigated between the blood flow rates and the following clinical features: age, duration of sciatica, presence or absence of neurologic deficits, latency to pain relief, and morphology of herniated discs.
Results:
The blood flow rate in 16 patients who reported immediate relief after discectomy was much greater than in 5 patients whose pain was not relieved immediately after surgery (141% 8%, = 0.0364). The increase in the blood flow rate after discectomy was five times greater in patients with neurologic deficits than in patients without neurologic deficits (158% 36%, = 0.0638).
Conclusions:
The results of the current study suggest that immediate relief from pain and resolution of neurologic deficits soon after surgery are the result of early recovery from nerve root ischemia after discectomy, and that ischemia caused by mechanical nerve root compression is mainly related to the mechanisms underlying sciatic pain production and neurologic deficits.
