Cervical Spinal Cord Compression Attributable to a Calcified Intervertebral Disc in a Patient with X-linked Hypophosphatemic Rickets: Case Report and Review of the Literature

Neurosurgery ◽  
2002 ◽  
Vol 51 (1) ◽  
pp. 239-243 ◽  
Author(s):  
Martin Soehle ◽  
Adrian T.H. Casey
Keyword(s):  
Spinal Cord ◽  
Intervertebral Disc ◽  
Spinal Cord Compression ◽  
Spinal Canal ◽  
Facet Joint ◽  
Cord Compression ◽  
Spinal Canal Stenosis ◽  
Hypophosphatemic Rickets ◽  
Cervical Cord ◽  
Canal Stenosis

Abstract OBJECTIVE AND IMPORTANCE X-linked hypophosphatemic rickets is a common inherited phosphate-wasting disorder, but it is a rare cause of spinal cord compression. We present the first reported case of a calcified intervertebral disc causing spinal canal stenosis in X-linked hypophosphatemic rickets. CLINICAL PRESENTATION A 44-year-old woman presented with paresthesia of her left arm and a loss of grip in both hands. Magnetic resonance imaging revealed a calcified intervertebral disc, as well as a posterior osteophytic bar causing marked cervical cord compression at C6/C7. INTERVENTION An anterior cervical discectomy at C6/C7 and fusion with autologous bone graft were performed. The patient then exhibited significant improvement. CONCLUSION A review of the 16 published cases demonstrates that thickening of the vertebral laminae, facet joint hypertrophy, and ossification of the intervertebral discs, posterior longitudinal ligament, and/or ligamentum flavum contribute to spinal canal stenosis in X-linked hypophosphatemic rickets. Those changes are caused by the disease itself and are unlikely to be related to long-term vitamin D treatment. Eleven of 16 patients were reported to have experienced favorable outcomes after surgery.

scholarly journals T1 Mapping Quantifies Spinal Cord Compression in Patients With Various Degrees of Cervical Spinal Canal Stenosis

2020 ◽  
Vol 11 ◽  
Author(s):  
Ilko L. Maier ◽  
Sabine Hofer ◽  
Eva Eggert ◽  
Katharina Schregel ◽  
Marios-Nikos Psychogios ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Spinal Canal ◽  
T1 Mapping ◽  
Cord Compression ◽  
Spinal Canal Stenosis ◽  
Canal Stenosis ◽  
Cervical Spinal Canal

scholarly journals Quantification of spinal cord compression using T1 mapping in patients with cervical spinal canal stenosis – Preliminary experience

2019 ◽  
Vol 21 ◽  
pp. 101639 ◽  
Author(s):  
Ilko L. Maier ◽  
Sabine Hofer ◽  
Arun A. Joseph ◽  
K. Dietmar Merboldt ◽  
Eva Eggert ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Spinal Canal ◽  
T1 Mapping ◽  
Cord Compression ◽  
Spinal Canal Stenosis ◽  
Canal Stenosis ◽  
Cervical Spinal Canal

scholarly journals Could spinal canal compression be a cause of polyneuropathy?

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Richard Bostelmann ◽  
Samis Zella ◽  
Hans Jakob Steiger ◽  
Athanasios K. Petridis
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Spinal Canal ◽  
Unknown Origin ◽  
Diabetic Polyneuropathy ◽  
Cord Compression ◽  
Spinal Canal Stenosis ◽  
Short Report ◽  
Canal Stenosis

Causality between spinal cord compression and polyneuropathy is difficult to define, especially under the circumstances that polyneuropathy can have many causes. Seven patients with spinal cord compression and electrophysiological signs of polyneuropathy were treated surgically on decompression of their spinal canal stenosis in the time from April 2010 to January 2013. Median follow up time was 9 months (2-23 months). Causes of polyneuropathy were: 1 patient with methotrexate-induced polyneuropathy, 1 endocrine-dysfunction-induced, 2 with diabetic- polyneuropathy, and 3 patients had unknown reasons. The localization of the spinal canal stenosis was also varying: 2 patients suffered of cervical spinal canal stenosis and 5 of lumbar. Decompressive surgery led to pain relieve in all patients initially. Surprisingly, also symptoms of polyneuropathy seemed to regress in all 7 patients for the first 5 months after surgery, and in 5 patients for the time of 9 months after surgery. There are two points we would like to emphasize in this short report. Since 5/7 patients with polyneuropathy and spinal canal stenosis improved clinically after surgery, surgery has a place in the treatment of such a combined pathology. Since it seems to be a possible causality between polyneuropathy of unknown origin and spinal cord stenosis, decompression of the spinal canal could also be a therapeutic step in a specific kind of polyneuropathy. Which patients could possibly have a spinal canal stenosis induced polyneuropathy remains a subject of further studies.

scholarly journals Clinical implications morphometric study of the cervical spine on MRI

2019 ◽  
Vol 10 (2) ◽  
Author(s):  
Swati S.More ◽  
Anita R. Gune ◽  
Jeetendra K. Patil
Keyword(s):  
Spinal Cord ◽  
Vertebral Body ◽  
Spinal Cord Compression ◽  
Spinal Canal ◽  
Cord Compression ◽  
Cervical Region ◽  
Canal Stenosis ◽  
Cervical Spinal Canal ◽  
Canal Diameter ◽  
Increased Risk

Degenerative changes, history of trauma or inflammation usually progressed to cervical spinal canal stenosis.  This condition leads to cervical spondylosis neuropraxia and cervical spondylotic myelopathy (CSM). SAC (space available for the cord) value is important to understand the symptoms of spinal cord compression in cervical canal stenosis. The aim of our study is to establish cervical spinal canal morphometry in Western Maharashtra population observed by MRI of cervical region.70 subjects aged between 18-70 years. The sagittal vertebral body diameter, the sagittal spinal canal diameter and the sagittal spinal-cord diameter were measured at the C3 - C7 level. The SAC was determined. For each variable a two-way ANOVA was performed, sagittal canal diameter, sagittal spinal cord diameter and SAC were significant with p-value P< 0.0001**. Mean vertebral body diameters observed were 1.49-1.51. Values of SAC observed were C3-1.5 cm, C4- 1.51cm, C5- 1.49cm, C6- 1.5cm, C7- 1.49cm. Average sagittal spinal canal diameter from C3-C7 was 14.1± 1.3 mm. The range of SAC was between 6.4-9.5mm, least at the C5 level. We conclude that subjects in our study do not have an increased risk of spinal cord compression.

Cervical myelopathy in patients with ossification of the posterior longitudinal ligament

2009 ◽  
Vol 10 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Macondo Mochizuki ◽  
Atsuomi Aiba ◽  
Mitsuhiro Hashimoto ◽  
Takayuki Fujiyoshi ◽  
Masashi Yamazaki
Keyword(s):  
Spinal Cord ◽  
Conservative Treatment ◽  
Spinal Canal ◽  
Clinical Course ◽  
Posterior Longitudinal Ligament ◽  
Treated Group ◽  
Spinal Canal Stenosis ◽  
Canal Stenosis ◽  
Residual Space ◽  
Surgical Group

Object The authors assessed the clinical course in patients with a narrowed cervical spinal canal caused by ossification of the posterior longitudinal ligament (OPLL), but who have no or only mild myelopathy. Additionally, the authors analyzed the factors contributing to the development and aggravation of myelopathy in patients with OPLLinduced spinal canal stenosis. Methods Between 1997 and 2004, the authors selected treatments for patients with cervical OPLL in whom the residual space available for the spinal cord was ≤ 12 mm. Treatment decisions were based on the severity of myelopathy at presentation. Twenty-one patients with no or mild myelopathy (defined as a Japanese Orthopaedic Association [JOA] scale score ≥ 14 points) received conservative treatment, with a mean follow-up period of 4.5 years. In 20 patients with moderate or severe myelopathy (JOA scale score < 14 points), the authors performed surgery via an anterior approach. The clinical course in these patients was assessed with the JOA scale and the OPLL types were classified. The authors evaluated the range of motion between C-1 and C-7, the developmental segmental sagittal diameter, the percentage of spinal canal diameter occupied by the OPLL (% ratio), and the residual space available for the spinal cord on cervical radiographs; T2-weighted MR images were examined for high signal changes (HSCs). Results In the conservative treatment group, 8 patients showed improvement, 12 remained unchanged, and 1 patient's condition became slightly worse during the observation period. Fifteen patients in this group had mixedtype, 3 had continuous-type, 2 had localized-type, and 1 had a segmental-type OPLL. In the surgically treated group, there were 12 patients with segmental-type, 10 patients with mixed-type, and 1 with localized-type OPLL. The mean range of motion at C1–7 was 36.4° in the conservatively treated group and 46.5° in the surgical group (p < 0.05). No significant difference was seen between the groups in terms of developmental segmental sagittal diameter, % ratio, or residual space available for the cord. No HSCs were noted in the conservative group, while 17 patients in the surgical group had HSCs (p < 0.05). Conclusions In the present study, the authors demonstrate that the mobility of the cervical spine and the type of OPLL are important factors contributing to the development and aggravation of myelopathy in patients with OPLLinduced spinal canal stenosis. The authors advocate conservative treatment in most patients with OPLLs who have no or only mild myelopathy, even in the presence of spinal canal narrowing.

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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