Management of cervical spinal cord injury in ankylosing spondylitis: the intervertebral disc as a cause of cord compression

1992 ◽  
Vol 77 (2) ◽  
pp. 241-276 ◽  
Author(s):  
David W. Rowed
Keyword(s):  
Spinal Cord ◽  
Ankylosing Spondylitis ◽  
Intervertebral Disc ◽  
Spinal Cord Compression ◽  
Recurrent Dislocation ◽  
Cord Compression ◽  
Flexion Deformity ◽  
Extradural Hematoma ◽  
Halo Vest ◽  
Content Type

✓ Twenty-one patients with universal syndesmophytosis due to ankylosing spondylitis were identified in a consecutive series of 1578 patients with acute spine and spinal cord injuries. They were predominantly male, older than spinal cord-injured patients in general, and most were injured by falls. Approximately one-half were managed by halo-vest immobilization alone with good clinical and radiological outcomes. The remainder required surgery either for recurrent dislocation or for spinal cord compression associated with neurological deterioration. Extradural hematoma, a recognized cause of spinal cord compression in ankylosing spondylitis patients with spinal fractures, was encountered in two patients. Herniated intervertebral disc as a cause of spinal cord compression in ankylosing spondylitis does not appear to have been previously reported and was recognized three times in the present series, once in association with extradural hematoma. The pathology of ankylosing spondylitis is such that the nucleus pulposus tends to be spared, allowing disc herniation to occur in the heavily ossified spine. In virtually all patients, satisfactory correction of the flexion deformity could be safely accomplished following spinal fracture. It is concluded that fracture/dislocations of the cervical spine should be managed initially by halo-vest immobilization, without prior traction and with careful incremental correction of flexion deformity. Decompression is performed as required for extradural hematoma or intervertebral disc herniation, and internal fixation is carried out for recurrent dislocation.

Spinal cord compression by extramedullary hemopoietic tissue in sickle cell anemia

1975 ◽  
Vol 43 (4) ◽  
pp. 483-485 ◽  
Author(s):  
Abdel A. Ammoumi ◽  
Joanna H. Sher ◽  
Daniel Schmelka
Keyword(s):  
Spinal Cord ◽  
Sickle Cell ◽  
Spinal Cord Compression ◽  
Sickle Cell Anemia ◽  
Cord Compression ◽  
Content Type ◽  
Hemopoietic Tissue ◽  
Fine Print ◽  
Mass Recovery

✓ The authors report a patient with sickle cell anemia who suffered from paraplegia of 18 months duration due to spinal cord compression by a hemopoietic mass. Recovery following removal of the mass was complete.

scholarly journals Symptomatic thoracic ossification of the ligamentum flavum in a patient with ankylosing spondylitis: Report of a case and review

2021 ◽  
Vol 12 ◽  
pp. 596
Author(s):  
Abolfazl Rahimizadeh ◽  
Parviz Habibollahzadeh ◽  
Walter L. Williamson ◽  
Housain Soufiani ◽  
Mahan Amirzadeh ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ankylosing Spondylitis ◽  
Spinal Cord Compression ◽  
Marked Improvement ◽  
Ligamentum Flavum ◽  
Cord Compression ◽  
Case Description ◽  
Thoracic Spinal Cord ◽  
Decompressive Laminectomy ◽  
Thoracic Spinal

Background: Thoracic spinal cord compression due to both ankylosing spondylitis (AS) and ossification of the ligamentum flavum (OLF) is rare. Case Description: A 33-year-old male with AS presented with a paraparesis attributed to MR documented T9-T10 OLF/stenosis. He was successfully managed with a decompressive laminectomy; this resulted in marked improvement of his deficit. Conclusion: Thoracic OLF and AS rarely contribute T9-T10 spinal cord compression that may be readily relieved with a decompressive laminectomy.

Spinal cord compression due to Masson's vegetant intravascular hemangioendothelioma

1995 ◽  
Vol 82 (1) ◽  
pp. 125-127 ◽  
Author(s):  
David G. Porter ◽  
Andrew J. Martin ◽  
Conor L. Mallucci ◽  
Catherine N. Makunura ◽  
H. Ian Sabin
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Vascular Lesion ◽  
Content Type ◽  
Fine Print

✓ The authors present the case of spinal cord compression in a 16-year-old boy due to the rare vascular lesion, Masson's vegetant hemangioendothelioma.

The therapeutic window for spinal cord decompression in a rat spinal cord injury model

2005 ◽  
Vol 3 (4) ◽  
pp. 302-307 ◽  
Author(s):  
Christopher B. Shields ◽  
Y. Ping Zhang ◽  
Lisa B. E. Shields ◽  
Yingchun Han ◽  
Darlene A. Burke ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Stenosis ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Therapeutic Window ◽  
Content Type ◽  
Significant Difference ◽  
Cord Injury ◽  
Fine Print

Object. There are no clinically based guidelines to direct the spine surgeon as to the proper timing to undertake decompression after spinal cord injury (SCI) in patients with concomitant stenosis-induced cord compression. The following three factors affect the prognosis: 1) severity of SCI; 2) degree of extrinsic spinal cord compression; and 3) duration of spinal cord compression. Methods. To elucidate further the relationship between varying degrees of spinal stenosis and a mild contusion-induced SCI (6.25 g-cm), a rat SCI/stenosis model was developed in which 1.13- and 1.24-mm-thick spacers were placed at T-10 to create 38 and 43% spinal stenosis, respectively. Spinal cord damage was observed after the stenosis—SCI that was directly proportional to the duration of spinal cord compression. The therapeutic window prior to decompression was 6 and 12 hours in the 43 and 38% stenosis—SCI lesions, respectively, to maintain locomotor activity. A significant difference in total lesion volume was observed between the 2-hour and the delayed time(s) to decompression (38% stenosis—SCI, 12 and 24 hours, p < 0.05; 43% stenosis—SCI, 24 hours, p < 0.05) indicating a more favorable neurological outcome when earlier decompression is undertaken. This finding was further supported by the animal's ability to support weight when decompression was performed by 6 or 12 hours compared with 24 hours after SCI. Conclusions. Analysis of the findings in this study suggests that early decompression in the rat improves locomotor function. Prolongation of the time to decompression may result in irreversible damage that prevents locomotor recovery.

Cerebrospinal fluid lactate and electrolyte levels following experimental spinal cord injury

1976 ◽  
Vol 44 (6) ◽  
pp. 715-722 ◽  
Author(s):  
Douglas K. Anderson ◽  
Leon D. Prockop ◽  
Eugene D. Means ◽  
Lawrence E. Hartley
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Spinal Cord Tissue ◽  
Post Injury ◽  
Content Type ◽  
Protein Levels ◽  
Cord Injury ◽  
Csf Lactate

✓ Cerebrospinal fluid (CSF) lactate, sodium (Na+), potassium (K+), calcium (Ca++), magnesium (Mg++), and chloride (Cl−) levels were determined for 17 to 21 days following experimental spinal cord compression in cats. Laminectomies were performed at L-2 under general anesthesia with aseptic techniques. Paraplegia was produced by applying a 170-gm weight transdurally for 5 minutes. Significant increases in CSF lactate levels were observed on the first through ninth days post injury with peak levels (50% above normal) occurring at Day 5. The only significant postinjury CSF electrolyte changes were elevation in Ca++ concentration on Days 3, 9, 11, 13, and 15, elevation in K+ concentration on Days 9 and 11 and decline in Cl− levels on the first day. The CSF K+ increase probably reflected cellular loss of K+ from damaged tissue whereas the Ca++ rise may have resulted from increased CSF protein levels. The prolonged elevation of CSF lactate indicates that tissue hypoxia plays a role in spinal cord compression paralysis, and that there is a continuing hypoxia of metabolically active spinal cord tissue for several days post injury.

Atlantoaxial stabilization in rheumatoid arthritis

1991 ◽  
Vol 74 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Stephen M. Papadopoulos ◽  
Curtis A. Dickman ◽  
Volker K. H. Sonntag
Keyword(s):  
Rheumatoid Arthritis ◽  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cord Compression ◽  
Atlantoaxial Subluxation ◽  
High Rate ◽  
Content Type ◽  
Operative Stabilization ◽  
Asymptomatic Patients ◽  
Fine Print

✓ Atlantoaxial subluxation in patients with rheumatoid arthritis is common. Operative stabilization is clearly indicated when signs and symptoms of spinal cord compression occur. However, many recommend early operative fusion before evidence of appreciable neural compression occurs because 1) the myelopathy in these patients may be irreversible; 2) the overall prognosis is poor once symptoms of cord compression are present; and 3) the risk of sudden death associated with atlantoaxial subluxation is increased even in asymptomatic patients. The authors believe that rheumatoid arthritis patients in relatively good health without advanced multisystem disease and less than 65 years of age should be considered for operative stabilization if mobile atlantoaxial subluxation is greater than 6 mm. Seventeen patients with severe rheumatoid arthritis and atlantoaxial subluxation treated with a posterior arthrodesis are presented. A new method of fusion, devised by the senior author (V.K.H.S.), was utilized in all cases. Indications for operative therapy in these patients included evidence of spinal cord compression in 11 patients (65%) and mobile atlantoaxial subluxation greater than 6 mm but no signs or symptoms of cord compression in six patients (35%). Thirteen patients developed a stable osseous fusion, two patients a well-aligned fibrous union, one patient a malaligned fibrous union, and one patient died prior to evaluation of fusion stability. The details of the operative technique and management strategies are presented. Several technical advantages of this method of fusion make this approach particularly useful in patients with rheumatoid arthritis. Because of multisystem involvement of this disease, a high rate of osseous fusion is often difficult to achieve.

Spinal echinococcal cyst: treatment using computerized tomography—guided needle aspiration and hypertonic saline irrigation

1997 ◽  
Vol 87 (3) ◽  
pp. 464-467 ◽  
Author(s):  
Sergey Spektor ◽  
John M. Gomori ◽  
Liana Beni-Adani ◽  
Shlomo Constantini
Keyword(s):  
Spinal Cord ◽  
Hypertonic Saline ◽  
Computerized Tomography ◽  
Spinal Cord Compression ◽  
Complete Resolution ◽  
Needle Aspiration ◽  
Cord Compression ◽  
Resonance Imaging ◽  
Saline Irrigation ◽  
Content Type

✓ A multilocular extradural cervical spinal hydatid cyst that causes severe spinal cord compression and quadriplegia is relatively rare and difficult to treat. In a patient with this disorder, computerized tomography—guided needle aspiration of the cyst loculations and irrigation using hypertonic saline eliminated the need for emergency surgery and provided complete resolution of the patient's quadriplegia. The subsequent course of the disease was controlled by treatment with albendazole. Magnetic resonance imaging performed 4 months after the procedure demonstrated collapsed cysts and absence of spinal cord compression.

Cardiovascular response to experimental spinal cord compression

1973 ◽  
Vol 38 (3) ◽  
pp. 326-331 ◽  
Author(s):  
Eduardo E. Eidelberg
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Blocking Agent ◽  
Cord Compression ◽  
Left Ventricular ◽  
Cervical Cord ◽  
Content Type ◽  
Ectopic Beats

✓ Anesthetized, and unanesthetized decerebrate, cats were used to study the arterial pressor response to spinal cord compression. To produce a cervical compression it was necessary that the cervical cord be functionally connected to the thoracic cord, pressor response by the reverse was not true. A pressor response above 200 mm Hg systolic was associated with electrocardiographic (EKG) signs of left ventricular overload and ventricular ectopic beats. These changes were not prevented by atropine, hexamethonium, or propanolol. Both the pressor response and the EKG abnormalities were prevented by an alpha-adrenergic blocking agent. The authors conclude that alpha-adrenergically mediated arterial vasoconstriction is the effector mechanism in the pressor response to increased intracranial pressure or cord compression.

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