Intermittent cauda equina compression due to narrow spinal canal

1972 ◽  
Vol 37 (1) ◽  
pp. 83-88 ◽  
Author(s):  
Hiroshi Yamada ◽  
Masaki Ohya ◽  
Tsuguo Okada ◽  
Zenji Shiozawa

✓ Five patients with intermittent claudication due to compression of the cauda equina in the presence of lumbar spinal canal stenosis or midline intervertebral disc protrusion are described. The characteristic myelographic evidence was complete obstruction during extension of the spine and release of the block with flexion. The cause of this syndrome is considered to be intermittent bulging of the ligamentum flavum into a narrow spinal canal so as to compress the cauda equina during extension of the back.

Spine ◽  
2007 ◽  
Vol 32 (25) ◽  
pp. 2805-2811 ◽  
Author(s):  
Hirofumi Kosaka ◽  
Koichi Sairyo ◽  
Ashok Biyani ◽  
Douglas Leaman ◽  
Richard Yeasting ◽  
...  

2015 ◽  
Vol 34 (7) ◽  
pp. 1241-1247 ◽  
Author(s):  
Yutaka Yabe ◽  
Yoshihiro Hagiwara ◽  
Masahiro Tsuchiya ◽  
Masahito Honda ◽  
Kouki Hatori ◽  
...  

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Chao Sun ◽  
Zhen Wang ◽  
Ji-Wei Tian ◽  
Yun-Hao Wang

The ongoing chronic inflammation and subsequent fibrosis play an important role in ligamentum flavum (LF) fibrosis and hypertrophy in patients with lumbar spinal canal stenosis (LSCS). Leptin is a chronic inflammatory mediator and involved in the fibrotic process in multiple organ systems. The present study aimed to investigate the role of leptin in LF fibrosis and its related regulatory mechanisms. The LF specimens were obtained during the surgery from 12 patients with LSCS (LSCS group) and 12 control patients with lumbar disc herniation (LDH) group. The morphologic changes and fibrosis score of LF were assessed by Hematoxylin and eosin (H&E) and Masson’s trichrome staining respectively. The location and expression of leptin in LF tissues were determined. Then, the LF cells were cultured and exposed to recombinant human leptin (rhleptin). Collagen I and III were used as fibrosis markers and IL-6 was used as the inflammatory factor. As a result, the LF thickness and fibrosis score in the LSCS group were significantly higher than those in the LDH group (P<0.05). Leptin was detected in the hypertrophied LF and its expression was substantially increased in the LSCS group and positively correlated with LF thickness and fibrosis score (P<0.05). Moreover, our in vitro experiments revealed that rhleptin treated LF cells elevated the expression of collagen I and III. Finally, leptin administration induced IL-6 expression via nuclear factor-κB (NF-κB) pathway in LF cell (P<0.05). Our study demonstrated novel molecular events for leptin-induced inflammation in LF tissue by promoting IL-6 expression and thus might have potential implications for clarifying the mechanism underlying LF fibrosis and hypertrophy.


Amyloid ◽  
2020 ◽  
pp. 1-6
Author(s):  
Masayoshi Tasaki ◽  
Masamitsu Okada ◽  
Akihiro Yanagisawa ◽  
Toshiya Nomura ◽  
Hiroaki Matsushita ◽  
...  

2015 ◽  
Vol 24 (10) ◽  
pp. 2315-2320 ◽  
Author(s):  
Masoud Poureisa ◽  
Mohammad Hossein Daghighi ◽  
Payam Eftekhari ◽  
Kaveh Rezaei Bookani ◽  
Daniel Fadaei Fouladi

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