Fibrocartilaginous embolism--an uncommon cause of spinal cord infarction: a case report and review of the literature

Fibrocartilaginous embolism is a rare cause of spinal cord infarction. It is postulated that an acute vertical disk herniation of the nucleus pulposus material can lead to spinal cord infarction by a retrograde embolization to the central artery. An increased intradiskal pressure resulting from axial loading of the vertebral column with a concomitant Valsalva maneuver is thought to be the initiating event for the embolus. We present a previously healthy 16-year-old boy with sudden onset of back pain and progressive paraparesis within 36 hours after lifting exercises in a squat position. His clinical presentation and neuroimaging studies were consistent with spinal cord infarction resulting from a central artery embolus at the T8 spinal cord level. Laboratory investigation showed no evidence of infectious, autoimmune, inflammatory, or neoplastic causes. Although no histologic confirmation was obtained, lack of evidence for other plausible diagnoses in the setting of his clinical presentation and in the magnetic resonance imaging findings made fibrocartilaginous embolism myelopathy the most likely diagnosis. We postulated that some cases of transverse myelitis might actually be fibrocartilaginous embolism, making it a more prevalent cause of an acute myelopathy than commonly recognized. Relevant literature and current theories regarding the pathogenesis of fibrocartilaginous embolism myelopathy are reviewed.     

Widespread active inflammatory lesions in a case of HTLV-I-associated myelopathy lasting 29 years

An autopsy case of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM) of 29 years duration is reported. The patient had no history of surgery or blood transfusion and likely contracted HTLV-I sexually while traveling in an endemic area. At age 45, the patient began to experience gait disturbance; he later developed spastic tetraparesis. Autopsy revealed marked gross spinal cord atrophy, particularly in the middle to lower thoracic levels. Myelin and axonal degeneration were identified predominantly in the middle to lower thoracic spinal cord, extending into the medulla oblongata and lumbar cord. Inflammatory infiltrates of mononuclear cells were diffuse in the white and gray matter of the spinal cord and medulla oblongata, particularly in perivascular areas. These infiltrates were also observed in perivascular areas of the pons, midbrain, cerebellum, and cerebrum. More than half of the infiltrating cells were positive for the pan-T cell marker UCHL-1, but some were positive for the B cell marker SL-26. There were far more CD8-positive cells than CD4-positive cells in the spinal parenchyma and perivascular areas. Neurons in the anterior horn, Clarkes column, and intermediolateral column were relatively well preserved. Active chronic inflammation was indicated. Despite the 29-year history of HAM, the presence of an active inflammatory reaction is surprising. We discuss possible modulation of the histopathological manifestations of HAM by corticosteroid therapy.     

Neurological complications of primary Sjögren's syndrome

Objective: To better delineate the spectrum of neurological complications of primary Sjögren's syndrome (PSS). Methods: A detailed neurological investigation was prospectively performed in a group of 25 consecutive patients with PSS followed in an internal medicine department between June 1996 and December 1997 (Internal Medicine group). In addition, eleven patients with neurological complications of PSS were identified in the Neurological Department of the same institution during the same period (Neurological group). Results: In the Internal Medicine group, neurological complications were discovered in 10/25 (40 %) patients. Peripheral nervous system involvement was present in 4/25 patients from the Internal Medicine group and in 10/11 patients from the Neurological group and consisted mainly of axonal sensorimotor/sensory polyneuropathy. A motor neuron syndrome was identified in two patients. CNS involvement occurred in 7/25 patients from the Internal Medicine group and in 4/11 patients from the Neurological group. Three patients had spinal cord involvement. Cognitive dysfunction was the most frequent finding (5/25 in the Internal Medicine group, 3/11 in the Neurological group) characterized either by subcortical or corticosubcortical dysfunction. Cognitive impairment was not attributed to mood disturbance and was not associated with specific laboratory or radiological abnormalities. Conclusion: Neurological complications of PSS are frequent since they were present in 40 % (10/25) of patients in a consecutive series of patients from a department of Internal Medicine. Although PNS involvement predominates, complications of PSS affecting the brain or spinal cord are not rare, with subcortical dysfunction as the main finding.     

Spinal Cord Infarction Following Vertebral Angiography: Clinical and Pathological Findings

Abstract

Spinal cord damage from radiographic contrast material has been known to occur in both spinal and nonspinal angiographic procedures. Reported here is cervical spinal cord injury (SCI) during vertebral angiography. During the procedure, the patient displayed signs of acute cervical spinal cord irritation that should have been taken as a warning of impending injury. Autopsy 9 years later showed evidence of central cervical spinal cord necrosis. The pathological findings are similar to those seen in animal models of contrast media-induced SCI; and the pathophysiological mechanisms of such injury are discussed.     

Identifying Myelopathy Caused by Thoracic Syringomyelia: A Case Report

Myelopathy is a form of neurological disease caused by compression of the spinal cord. Upper and lower quarter screens are commonly used in identifying myelopathy, although most of the screen components demonstrate poor or unstudied diagnostic value. The purpose of this case report is to describe the diagnostic process in detecting syringomyelia, an intramedullary lesion that may cause myelopathy. The patient was a 47-year-old female with a thoracic syrinx that was discovered by spinal magnetic resonance imaging (MRI) following a complicated and delayed clinical diagnostic course. Following surgical intervention and a two-week inpatient rehabilitation stay, the patient was discharged using a rolling walker for ambulation and was performing most transfers with modified independence. A complicating pattern of signs and symptoms combined with a diagnostic process guided by poorly studied screen components demonstrates the diagnostic dilemma associated with identifying the cause of myelopathy within the thoracic spine. This also indicates the need for further investigation of individual and clustered components of the neurological screen to improve the ability to identify patients in need of complete imaging studies in a more timely fashion.     

Syringomyelia after decompressive laminectomy for cervical spondylosis

We describe a case of cervical spondylotic myelopathy in which deterioration occurred a month after decompressive laminectomy. Syringomyelia was then in evidence as seen by myelography and delayed metrizamide computed tomography scanning. The etiology of this finding and its possible relation to the course and treatment of cervical spondylotic myelopathy are discussed.     

Geographic variations in clinical presentation and outcomes of decompressive surgery in patients with symptomatic degenerative cervical myelopathy: analysis of a prospective,international multicenter cohort study of 757 patients

Background Context

Degenerative cervical myelopathy (DCM) is a progressive degenerative spine disease and the most common cause of spinal cord impairment in adults worldwide. Few studies have reported on regional variations in demographics, clinical presentation, disease causation, and surgical effectiveness.

Surgical outcomes in patients with mild symptoms,but severely compressed spinal cord from cervical ossification of the posterior longitudinal ligament

Surgical treatment is indicated in patients with moderate to severe myelopathy from cervical ossification of the posterior longitudinal ligaments (OPLL), but undertaking prophylactic surgery for asymptomatic or mildly symptomatic patients with a severely compressed spinal cord is debatable.Patients with <8 mm space available in the spinal canal on CT scan, were divided into groups I (mild symptoms, Japanese Orthopedic Association (JOA) score range 15–16) and II (moderate to severe symptoms, JOA score <14). Medical charts including operative records were reviewed to obtain preoperative, perioperative, and final postoperative follow-up data.Group I included 24 patients (20 men, mean age 52.42 years), and Group II included 46 patients (33 men, mean age 54.67 years). Compared to Group II, Group I had a shorter preoperative symptom duration (19.21 vs. 38.23 months, p = 0.046) and a more favorable JOA score at final follow-up (p = 0.007). The mean numbers of OPLL-involved segments were similar (Group I 2.96, Group II 3.09; p = 0.773) as were the mean numbers of operated segments (Group I 2.71, Group II 3.35; p = 0.076). Perioperative blood loss, operation duration, and hospital stay duration were significantly more favorable in Group I than in Group II. The numbers of surgery-related complications in the two groups were similar.Early surgical treatment for a favorable neurologic recovery with a low perioperative risk can be recommended in patients with severely compressed spinal cord from cervical OPLL who present with mild arm numbness. Surgery-related complications, however, should be carefully monitored regardless of symptom severity.