Purpose: Claudication is a common complaint of elderly patients. Lumbar spinal stenosis (LSS) and peripheral arterial disease (PAD) are the two main etiologies, producing neurogenic and vascular claudication respectively. Physicians initially diagnose claudication based on a “typical” symptom profile. The reliability of this symptom profile to accurately diagnose LSS or PAD as a cause of claudication is unknown, leading to the potentially unnecessary utilization of expensive and overly sensitive imaging modalities. Furthermore, clinicians rely on this symptom profile when directing treatment for patients with concurrent imaging positive for LSS and PAD. This study evaluates the reliability of various symptom attributes, which classically have characterized and differentiated the two.

Method: Patients presenting at a tertiary care center’s vascular or spine clinics with a primary complaint of claudication were enrolled in the study. Diagnosis of either LSS or PAD was confirmed with imaging for each patient. They answered 14 questions characterizing their symptoms. Sensitivity, specificity, positive and negative likelihood ratio (PLR and NLR) was determined for each symptom attribute.

Results: The most sensitive symptom attribute to rule out LSS is “triggering of pain with standing alone” (0.96). Four symptom attributes demonstrated a high PLR and three had low NLR for diagnosing neurogenic claudication (PLR= 3.08, 2.51, 2.14, 2.9; NLR=0.06, 0.29, 0.15). In vascular patients, calf symptoms and alleviation of pain with simply standing had a high PLR and NLR (PLR= 3.08 and 4.85; NLR= 0.31 and 0.36).

Conclusion: Only four of 14 “classic” symptom attributes are highly sensitive for ruling out LSS, and should be considered by primary care physicians before pursing expensive diagnostic imaging. Six symptom attributes should be relied upon to differentiate LSS and NLR. Numbness, pain triggered with standing alone, located in the buttock and thigh, and relieved following sitting, are symptom attributes which reliably characterize neurogenic claudication.

Purpose: Magnetic resonance imaging (MRI) and Computerized tomography (CT) are commonly used for the diagnosis and assessment of lumbar spinal stenosis. The available literature has not identified which modality is superior. We compared the reliability and accuracy of CT and MRI in the assessment of lumbar spinal stenosis.

Method: We performed a prospective review of CT and MRI scans of 54 patients referred for surgical consultation. One orthopaedic spine fellow and one neuro-radiologist reviewed the CTs and MRIs. A qualitative and quantitative analysis was performed. Intra-observer and inter-observer reliability was determined using Kappa coefficient. The patient’s official reports were correlated with analysis performed by the two reviewers. Owsestry and SF-36 data was correlated with the qualitative and qualitative assessment of stenosis on CT, MRI using the Pearson’s R coefficient.

Results: MRI – substantial inter-observer agreement was achieved between surgeon and neuro-radiologist as well as between surgeon and reporting radiologist (κ= 0.74 and κ=0.64 respectively). Moderate agreement was found between neuro-radiologist and reporting radiologist (κ=0.57). Almost perfect intra-observer reliability for MRI was achieved by the two expert reviewers (κ=0.91 for surgeon and κ=0.92 for neuro-radiologist). CT – moderate inter-observer agreement (κ=0.58) was found between surgeon and neuro-radiologist. Fair agreement was found between neuro-radiologist and reporting radiologist and between surgeon and reporting radiologist (κ=0.30 and 0.32 respectively). Substantial intra-observer agreement was found for the surgeon (κ=0.77) while the neuro-radiologist achieved almost perfect agreement (κ=0.96).

Conclusion: This study directly demonstrates that MRI is likely a more reliable tool than CT, but neither correlates with functional status.

Purpose: Recent studies have examined the systemic inflammation that occurs following spinal cord injury (SCI) (Gris et al. 2008). It is believed that this systemic inflammation plays a role in the respiratory, renal and hepatic morbidity of SCI patients, ultimately contributing to mortality post-injury. Evidence of this inflammatory response has been shown as early as two hours post SCI (Gris et al. 2008) Intravital microscopy is a powerful tool for assessing inflammation acutely and in ‘real-time’ (Brock et al. 1999). This tool would be useful for demonstrating the acuteness of a systemic inflammatory response post-SCI, and for assessing the degree of inflammation to different severities of SCI. The liver has been shown to play a particularly important role in the initiation and progression of the early systemic inflammatory response to spinal cord injury (SCI), therefore the purpose was to evaluate hepatic inflammation immediately after SCI. We hypothesized that SCI would cause immediate leukocyte recruitment and that the magnitude of inflammation would increase with increasing severity of cord injury.

Method: Male Wistar rats (200–225g) were randomly assigned to one of the following groups: uninjured, trauma-injured (laminectomy and no cord injury), cord compressed or cord transected. Spinal cord-injured rats were anesthetized by isoflurane, a dorsal laminectomy was performed, and the 4th thoracic spinal segment was injured by a moderately severe clip-compression injury or by a severe complete cord transection injury. Uninjured rats and trauma-injured rats served as controls. At 0.5 and 1.5 h after SCI rats had the left lobe of their livers externalized and visualized using intravital video microscopy.

Results: At 0.5 hours the total number of leukocytes per post-sinusoidal venule was significantly increased after cord compression and cord transection compared to that in uninjured and trauma-injured rats (P< 0.05). Of these leukocytes significantly more were either adherent or rolling along venule walls compared to uninjured and trauma-injured rats (P< 0.05). Of the rolling leukocytes 2–fold more were observed after cord transection compared to cord compression. At 1.5 h the total number of leukocytes per post-sinusoidal venule and the number of adherent leukocytes was significantly increased only after cord transection.

Conclusion: Injury to the spinal cord but not trauma alone causes immediate leukocyte recruitment to the liver within 0.5 h after injury. Also, leukocyte recruitment increases with increasing severity of injury. This is the first study to use intravital microscopy to visualize systemic inflammation in the liver following SCI.