What causes increased cervical lordosis
Spinal cord infarction due to suspected fibrocartilaginous embolism
- Neurological manifestations
We report one case of spinal cord infarction as a result of suspected fibrocartilaginous embolism (FCE).
A 23-year-old man had sudden neck and back pain followed by progressive weakness in his extremities after throwing a baseball. The history, neurological examination, and presentation of the spinal cord were consistent with the infarct of the spinal cord. We believe the cause was FCE.
Although rare, clinicians should be familiar with this diagnosis and the proposed mechanisms. There is no specific treatment for FCE-related spinal cord infarction, and the long-term prognosis depends largely on the degree of spinal cord injury.
There are many known causes of acute spinal cord infarction, including prolonged hypotension, aortic dissection, spinal cord vascular malformation, cardiac embolism, and as a complication of surgery. Fibrocartilaginous Embolism (FCE) is a rare and unknown cause of spinal cord infarction, first identified in 1961 by Naiman et al. 1 We report on a 23-year-old man with suspected FCE-related spinal cord infarction. Consent to publish the case report was obtained from the patient.
A 23-year-old Amish man with a family history of the Factor V Leiden mutation was playing baseball that morning when he suddenly developed pain in his right shoulder and felt a "crack". He continued to play but stopped 2 hours later when he developed a sore throat and back that lasted for over 15 minutes. Then he got into his horse-drawn carriage for the 10-minute drive home. He got out of the buggy and felt weak and unsteady. Symptoms worsened over the next hour when he was at home with an ice pack on his back. He was seen by a chiropractor with no relief for spinal manipulation. In the afternoon he felt a tingling sensation in his hands and feet and was unable to urinate. A Foley catheter was placed at a local hospital for urinary retention, but he refused admission and left the hospital. The next morning his extremities were much weaker and he presented to our hospital.
At the presentation he was feverish and other vital signs were normal. The neurological examination revealed a slight distal weakness in both upper extremities (handle 4/5 bilateral on its muscle strength rating scale) and a slight proximal weakness in both lower extremities (hip flexion 4/5 bilateral). The sensory examination showed a decrease in the sensation of pain and temperature below the level of T2, but a retention of the sensation of vibration. Muscle stretch reflexes were normal. His walk was unsteady. American Spinal Injury Association / International Standards for the Neurological Classification of Spinal Cord Injuries (ASIA / ISCoS) The exam table was rated D (Motor Incomplete). Magnetic resonance imaging of the cervical spine (MRI) showed abnormally increased intramedullary signal in the anterior spinal cord on T2-weighted images and short tau inversion recovery sequences (STIR) extending from the C3 / 4 level caudally to the C7 / T1 level extend. There was no increase in contrast and no evidence of a vascular fistula or malformation (Figure 1). The brain MRI with and without contrast agent was normal. The analysis of lumbar puncture and cerebrospinal fluid (CSF) revealed 4 nucleated cells per μl, 1000 red blood cells per μl, total protein 43 mg dl −1 and glucose of 65 mg dl −1 . The myelin basic protein was at 7.8 μL –1 increased although no oligocolonal bands or aquaporin 4 antibodies were detected. The tests for varicella zoster virus, West Nile virus, herpes simplex virus, JC virus, and Lyme were negative.
( a ) Axial cervical T2 MRI image with increased signal at the C5 level, mainly in the anterior spinal cord. ( b ) Sagittal cervical T2 MRI image, extending from the C3 / 4 level caudally to the C7 / T1 level, mainly in the anterior spinal cord.
Full size image
The patient was initially treated with intravenous methylprednisolone for possible transverse myelitis, but when an anterior spinal cord infarction was suspected, methylprednisolone was stopped and low-dose aspirin was started. Cholesterol tests were normal. He was heterozygous for the Factor V Leiden mutation and homozygous for the MTHFR mutation, while the test for the prothrombin 20210 mutation was negative. Methylmalonic acid and homocysteine levels were normal. Further work-up included CRP, HgbA1c, B12, fibrinogen, syphilis IgG, anti-cardiolipin antibodies, ANA, anti-double-stranded DNA, anti-ribosomal P, anti-Jo, anti-chromatin, anti-scleroderma 70, anti-SSA , Anti-SSB and anti-Sm / RNP antibodies, protein C, protein S, anti-thrombin - all negative or within normal limits. The computed tomography chest angiogram showed no evidence of aortic dissection. The motor and sensory examination of the patient remained stable throughout the entire course of the hospital (4 days), but hyperreflexia with ankle clonus developed. At discharge he was dependent on the catheter. The ASIA / ISCoS exam overview remained grade D (incomplete engine). During a two-month follow-up as an outpatient, his strength continued to improve. His Foley catheter was removed. He returned to his job as a lumberjack. He still had a T2 sensory level to temperature. In the 5-month follow-up examination, his ASIA / ISCoS exam still consisted of a grade D with normal strength in the lower extremities and minimal weakness in the handle 4/5, without a sensory level and improved gait too normal.
FCE is a rare and unknown cause of spinal cord infarction. 2 Although well described in animals, especially dogs, 3 Only 67 cases of FCE-related spinal cord infarction were reported in humans (41 histopathologically confirmed and 26 clinically suspected). 4 In these cases, the patients between the ages of 14 and 78 were predominantly female. Most symptoms appear after a minor traumatic event, i.e. falling, playing tennis, dancing, basketball, etc. 4, 5 In 76% of the cases, sudden back pain was the first symptom, followed by weakness that stretched from minutes to hours to paralysis. 4 Our patient suffered sudden right shoulder pain and a popping sensation while playing baseball, followed by pain in the cervix and upper back for 15 minutes. Within an hour he felt weak. This progression over time is important to distinguish an FCE-related spinal cord infarction from other causes of weakness. For example, inflammatory disease weakness usually progresses over days rather than hours. And while patients with spinal cord infarction can be found to have an increased CSF protein content, they usually do not have pleocytosis or an increased IgG index, the presence of which is more likely to indicate an inflammatory process. The neurological exam is also critical to diagnosing a spinal cord infarction. Secondary posterior cord infarction has been reported after FCE6, but most patients like ours have anterior spinal cord syndrome with preserved posterior column function (proprioception and vibration). Differential diagnosis also includes traumatic contusion of the spinal cord, which can develop over minutes to an hour. However, our patient had no history of trauma. The clinical feeling of a "pop" with sudden back pain and progression to weakness over an hour is more consistent with an FCE-related spinal cord injury.
Typical MRI findings of spinal cord infarction include diffusion restrictions, spinal cord edema, increased T2 signal changes in a vascular distribution pattern, and the lack of contrast enhancement. Our patient's cervical spine MRI showed abnormally increased intramedullary signal on T2-weighted images and STIR sequences extending caudally from C3 / 4 level to C7 / T1 level mainly in the anterior spinal cord with no related improvement occurred with a spinal cord infarction. The cervical, thoracic and lumbar vertebrae are anatomically aligned. Small Schmorl lumps in the lower thoracic and lumbar vertebrae are noted along the end plates. No focal bone marrow signal abnormality or ligament injury is noted. There is a loss of the cervical lordosis. The sensory level in our patient was at T2 level, although the MRI changes were higher. This could be explained by testing the distribution of C4, which is in close dermatome proximity to T2, or by a more severe injury in the spinothalamic tracts at the T2 level. The patient had a T2 value on a 2-month outpatient follow-up, which improved on a 5-month follow-up.
Several mechanisms have been proposed to explain infarcts related to the FCE spinal cord. The most common is the migration of pulposus nucleus material into the vasculature, which leads to embolization in spinal cord vessels. The anterior vertebral body and spinal cord are supplied by a single anterior spinal artery. The posterior vertebral body is supplied by radicular arterial branches and the posterior spinal cord by pairs of posterior spinal arteries. The vasculature of the intervertebral disc is well developed in infancy, but regresses by around 2 months of age and usually disappears completely by 11 to 16 years of age (although it can rarely last into the early 20s). However, in patients with degenerative disease, neovascularization can occur from the age of 50. 8 In the case of degeneration, the nucleus pulposus can also extend into the vertebral body (Schmorl node).
Emboli can access any of these routes - stubborn disc vasculature, neovascularization, or Schmorl's lumps. 4 In particular, it is believed that minor trauma leads to increased intervertebral pressure, which then causes migration of fibrocartilaginous embolic material into this vasculature via the arterial or venous route. In the arterial route, the emboli migrate retrograde to the radicular artery and anterograde to the spinal cord, leading to infarction. In the venous route, emboli migrate through the caval system and then migrate backwards to the Batson plexus and then to the spinal cord. 9
AbdelRazek, et al. 4 Suggested diagnostic criteria for diagnosing FCE-related spinal cord infarction, including a medical history consistent with the diagnosis, examination, and imaging of the spinal cord infarction and the exclusion of other causes. Although our patient was heterozygous for the Factor V Leiden mutation and homozygous for the MTHFR mutation, his experience of playing baseball with subsequent pain and progressive weakness for hours is consistent with a diagnosis of FCE spinal cord infarction.
Unfortunately, there is no specific surgical or medical treatment for FCE-related spinal cord infarction. Generally, patients are treated according to guidelines for spinal cord injury, including maintaining mean arterial pressure between 85 and 90 mm Hg, preventing respiratory complications, and intensive physical therapy. 10 In the literature, FCE-related spinal cord infarction has been associated with a high mortality rate, with surviving cases not reported until after 1996. 5 Deaths from respiratory complications (pulmonary embolism, pneumonia, and aspiration) were reported in 40% of cases. 4 For survivors, the long-term prognosis depends largely on the degree of spinal cord injury.
We have described a case of a young man with suspected FCE-related spinal cord infarction. Our patients' presentation was typical of medical history, symptoms, physical examination, and imaging findings. Although rare, clinicians should be familiar with this diagnosis and the proposed mechanisms. There is no specific treatment for FCE-related spinal cord infarction, and the long-term prognosis depends largely on the degree of spinal cord injury.
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