Dorsal spinal cord herniation at the thoracolumbar junction presenting with scalloping of ossification of the ligamentum flavum: case report

2020 ◽  
Vol 32 (1) ◽  
pp. 56-60
Author(s):  
Takahiro Makino ◽  
Shota Takenaka ◽  
Gensuke Okamura ◽  
Yusuke Sakai ◽  
Hideki Yoshikawa ◽  
...  

Dorsal spinal cord herniation is reportedly a rare condition. Here, the authors report an unusual case of dorsal spinal cord herniation at the thoracolumbar junction presenting with scalloping of ossification of the ligamentum flavum (OLF). A 75-year-old woman with a 2-year history of bilateral leg dysesthesia presented with progressive gait ataxia. Neurological examination showed bilateral patellar tendon hyperreflexia with loss of vibratory sensation and proprioception in her bilateral lower extremities. CT myelography revealed a posterior kink and dorsal herniation of the spinal cord at T11–12, with OLF between T10–11 and T12–L1. In addition, scalloping of the OLF was observed at T11–12 at the site of the herniated spinal cord. This scalloping was first noted 9 years previously and had been gradually progressing. The patient underwent surgical repair of the spinal cord herniation. Subsequently, her spinal cord herniation and vibratory sensation and proprioception in both legs partly improved, but gait ataxia remained unchanged. Dorsal spinal cord herniation reportedly occurs under conditions of vulnerability of the dorsal dura mater. In this case, acquired vulnerability of the dorsal dura mater owing to previous epidural catheter placement into the thoracolumbar space may have resulted in dorsal spinal cord herniation.

Author(s):  
Haruki Funao ◽  
Satoshi Nakamura ◽  
Kenshi Daimon ◽  
Norihiro Isogai ◽  
Yutaka Sasao ◽  
...  

2019 ◽  
Author(s):  
Jessie Atterholt ◽  
Mathew J Wedel

Bony ridges occur on the walls of the neural canal in caudal vertebrae of numerous sauropod dinosaurs. These neural canal ridges (NCRs) are anteroposteriorly elongated but do not extend to the ends of the canal. To date, we have observed NCRs in caudal vertebrae of Alamosaurus, Apatosaurus, Astrophocaudia,Brontomerus, Camarasaurus, and Diplodocus. Numerous similar structures occur in extant vertebrates: (1) Neurocentral joints are ventral to NCRs in sauropod caudal vertebrae, and NCRs occur in unfused juvenile arches. Hypothesis rejected. (2) Attachment scars from ligamentum flavum occur at the ends of the dorsal roof of the canal, not the midpoint of the lateral edges, and this mammalian ligament was probably absent in dinosaurs. Hypothesis rejected. (3) Smooth ridges separate the spinal cord from the dorsal spinal vein and paramedullary airways in some crocodilians and birds, respectively. However, these septa persist to the ends of the canal, giving it an 8-shape, unlike the discrete NCRs of dinosaurs. Hypothesis rejected. (4) Bony attachments for denticulate ligaments occur in some non-mammalian vertebrates. The dura mater around the spinal cord fuses to the periosteum of the neural canal in non-mammals, so the denticulate ligaments that support the spinal cord can leave ossified attachment scars. These spinal cord supports have been identified in teleosts, salamanders, and a juvenile lizard, and they are the best match for the morphology of the NCRs in sauropod vertebrae. Functions of NCRs remain obscure. Denticulate ligaments are largest in regions of the vertebral column that experience strong lateral flexion. The hypothesis that NCRs supported the spinal cord of sauropods during lateral tail-whipping is attractive, but inconsistent with our recent discovery of NCRs in a hadrosaur caudal. NCRs are a new osteological correlate of the peripheral nervous system in dinosaurs, and highlight the need for more study in this area.


2019 ◽  
Author(s):  
Jessie Atterholt ◽  
Mathew J Wedel

Bony ridges occur on the walls of the neural canal in caudal vertebrae of numerous sauropod dinosaurs. These neural canal ridges (NCRs) are anteroposteriorly elongated but do not extend to the ends of the canal. To date, we have observed NCRs in caudal vertebrae of Alamosaurus, Apatosaurus, Astrophocaudia,Brontomerus, Camarasaurus, and Diplodocus. Numerous similar structures occur in extant vertebrates: (1) Neurocentral joints are ventral to NCRs in sauropod caudal vertebrae, and NCRs occur in unfused juvenile arches. Hypothesis rejected. (2) Attachment scars from ligamentum flavum occur at the ends of the dorsal roof of the canal, not the midpoint of the lateral edges, and this mammalian ligament was probably absent in dinosaurs. Hypothesis rejected. (3) Smooth ridges separate the spinal cord from the dorsal spinal vein and paramedullary airways in some crocodilians and birds, respectively. However, these septa persist to the ends of the canal, giving it an 8-shape, unlike the discrete NCRs of dinosaurs. Hypothesis rejected. (4) Bony attachments for denticulate ligaments occur in some non-mammalian vertebrates. The dura mater around the spinal cord fuses to the periosteum of the neural canal in non-mammals, so the denticulate ligaments that support the spinal cord can leave ossified attachment scars. These spinal cord supports have been identified in teleosts, salamanders, and a juvenile lizard, and they are the best match for the morphology of the NCRs in sauropod vertebrae. Functions of NCRs remain obscure. Denticulate ligaments are largest in regions of the vertebral column that experience strong lateral flexion. The hypothesis that NCRs supported the spinal cord of sauropods during lateral tail-whipping is attractive, but inconsistent with our recent discovery of NCRs in a hadrosaur caudal. NCRs are a new osteological correlate of the peripheral nervous system in dinosaurs, and highlight the need for more study in this area.


1999 ◽  
Vol 260 (3) ◽  
pp. 173-176 ◽  
Author(s):  
Kirk W. Barron ◽  
John E. Croom ◽  
Crystal A. Ray ◽  
Margaret J. Chandler ◽  
Robert D. Foreman

1991 ◽  
Vol 69 (6) ◽  
pp. 877-885 ◽  
Author(s):  
D. Nicholson ◽  
T. D. White ◽  
J. Sawynok

The effects of forskolin, Ro 20-1724, rolipram, and 3-isobutyl-1-methylxanthine (IBMX) on morphine-evoked release of adenosine from dorsal spinal cord synaptosomes were evaluated to examine the potential involvement of cyclic AMP in this action of morphine. Ro 20-1724 (1–100 μM), rolipram (1–100 μM), and forskolin (1–10 μM) increased basal release of adenosine, and at 1 μM inhibited morphine-evoked release of adenosine. Release of adenosine by Ro 20-1724, rolipram, and forskolin was reduced 42–77% in the presence of α, β-methylene ADP and GMP, which inhibits ecto-5′-nucleotidase activity by 81%, indicating that this adenosine originated predominantly as nucleotide(s). Significant amounts of adenosine also were released from the ventral spinal cord by these agents. Ro 20-1724 and rolipram did not significantly alter the uptake of adenosine into synaptosomes. Although Ro 20-1724 and rolipram had only limited effects on the extrasynaptosomal conversion of added cyclic AMP to adenosine, IBMX, a phosphodiesterase inhibitor with a broader spectrum of inhibitory activity for phosphodiesterase isoenzymes, significantly inhibited the conversion of cyclic AMP to adenosine and resulted in recovery of a substantial amount of cyclic AMP. As with the non-xanthine phosphodiesterase inhibitors, IBMX increased basal release of adenosine and reduced morphine-evoked release of adenosine. Adenosine released by IBMX was reduced 70% in the presence of α, β-methylene ADP and GMP, and release from the ventral spinal cord was 61% of that from the dorsal spinal cord. Collectively, these results indicate that forskolin and phosphodiesterase inhibitors release nucleotide(s) which is (are) converted extrasynaptosomally to adenosine. For forskolin, Ro 20-1724, and rolipram, the nucleotide released could be cyclic AMP. Morphine releases adenosine per se, and forskolin and phosphodiesterase inhibitors reduce this release. The lack of increase in the action of morphine with phosphodiesterase inhibitors in particular does not support a role for stimulation of cyclic AMP production by morphine in the release of adenosine. The reduction in morphine-evoked release of adenosine by forskolin and phosphodiesterase inhibitors suggests either (a) that a reduction in cyclic levels by morphine promotes adenosine release, or (b) that cyclic AMP interferes with the release process.Key words: forskolin, Ro 20-1724, 3-isobutyl-1-methylxanthine, cyclic AMP, morphine, adenosine release, spinal cord.


2016 ◽  
Vol 617 ◽  
pp. 6-13 ◽  
Author(s):  
Fangting Xu ◽  
Juan Huang ◽  
Zhenghua He ◽  
Jia Chen ◽  
Xiaoting Tang ◽  
...  

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