Injuries to the spinal cord are rarely isolated problems. Multiple trauma patients with spinal injuries can face significant long-term disability. In this retrospective, descriptive study we investigated the relationship between the level of spinal trauma and the injuries associated with this. We aimed to define the populations at risk and highlight trends identified.

METHODS: Analysis of 1500 trauma patients admitted to the Royal London Hospital by the Helicopter Emergency Medical Service (HEMS) over 6 years was undertaken. 265 patients of these patients had spinal cord injuries (SCI). Data was obtained from the HEMS trauma registry, patient records and interviews with patients.

RESULTS: 265 patients sustained SCI (mean age: 38 25% female). The most common mechanisms of injury were motor vehicle accidents (46%) and falls (29%) Attempted suicide was a common cause of SCI in our study group (mean age 32. M:F ratio 2:1) The most common associated injuries were limb and head trauma. C-spine injuries were the most common spinal injury and were associated with the highest mortality rates (37%). C-injuries presented with a bimodal age distribution, 84% had head trauma and 30% had significant chest injuries. In patients who sustained thoracic spinal injuries 71% had severe chest injuries and 34% had head injuries. The most common associated injury in lumbar spine trauma was injuries to the limbs or pelvis (68%). Injuries to the lumbar spine occurred more frequently in the 20–40 year old age groups.

Discussion: Mortality rate in our study was 26%. Mortality rates were highest in patients with cervical spine injuries (37%). The causes of mortality were from suicide attempts, falls and RTA. The mortality rates in these groups were 20%, 22% and 32% respectfully. Our review highlights significantly higher mortality in the over 60-age group. Our population had high numbers of suicide attempts. We highlight suicide attempts as a significant aetiology for SCI. All the deaths in the suicide group were as a result of jumping from high buildings. In patients over 60, c-spine injuries are by far the common level of SCI. Subdural haematomas occurred in almost 10% of patients with c- spine injuries. Any injury to the cervical spine should therefore prompt investigation for intracranial trauma. The GCS should be closely monitored and a low threshold for performing a CT scan is advisable. Thoracic spine injuries are strongly associated with severe chest injuries. Lumbar spine and sacral injuries are strongly associated with severe pelvic and lower limb injuries. Understanding the demographics and etiology is essential to allow effective planning for spinal services. Appreciating the injuries associated with SCI should ensure better care for patients, by recognizing problems earlier and using a multidisciplinary approach to optimize treatment and reduce morbidity and mortality.

Objective: The purpose of this study was to assess whether the use of high dose methylprednisolone (MPS) given to trauma patients with acute spinal cord injury improves neurological and long term functional outcomes.

Summary of Background Data: The National Acute Spinal Cord Injury Studies (NASCIS II and III) recommend the early administration of high dose MPS in the context of acute spinal cord injury. However, controversy exists surrounding its long term benefits.

Methods: A retrospective data analysis was performed using the Helicopter Emergency Medical Service (HEMS) trauma registry, medical records, and rehabilitation notes of 263 trauma patients with acute spinal injury admitted over a 6-year period. All survivors over 16 years of age with documented spinal cord injuries were selected. Frankel grade, Injury Severity Score (ISS), and Functional Independence Measure (FIM) scores (minimum FIM of 18 implies total dependence, and a maximum of 126 implies no disability) as indicators of neurological and functional morbidity were recorded at initial presentation, hospital discharge, and intervals up to 12 months post injury. Details of the age, gender, mechanism of injury, nature of injury and associated injuries were also recorded.

Results: There were 139 patients (107 males and 32 women) with documented acute spinal cord injuries, of which 74 patients had neurological deficits (Frankel A–D) at presentation. 49 patients were given high dose MPS within 8 hours of injury according to a standard protocol. The remaining 25 patients with documented neurological injury did not meet criteria or failed to receive the agent within the recommended time. The mean ISS scores were shown to be comparable in both groups. 59% (29/49) of patients who were given MPS showed an improvement of one or greater Frankel grade at the time of discharge whereas 52% (13/25) of patients who did not receive MPS showed a similar improvement in Frankel grades. We had long term functional outcome data (FIM scores) on 48% (67/139) of the total number of patients. At the time of discharge, the mean FIM scores for the MPS treated group and non MPS treated group were 68 and 90, respectively. Whereas at 12 months, there was no significant difference in the mean FIM scores between the two groups (both of which were > 100).

Conclusions: The Frankel grade assesses the degree of neurological impairment while FIM scores are a basic measure of the severity of disability regardless of the underlying impairment. In our study, patients given high dose MPS in the context of acute spinal cord injury showed some early improvement in Frankel grades. However, we have shown, there is no short term or long term benefit in terms of functional outcome by using MPS in trauma patients with acute spinal cord injury.

Purpose and Background: We have previously reported our investigations of nerve ingrowth into intervertebral discs (IVD) from patients with mechanical low back pain. We have shown that in discs that are painful on discography (pain level discs) nerves actively grow into the deep annulus fibrosus and nucleus pulposus. Nerve ingrowth accompanies blood vessel ingrowth and advances into the nucleus pulposus from the end plate. The morphology and neurochemistry of these nerves indicate them to be nociceptive.

The growth of non-myelinated pain fibres in other settings is regulated by the cytokine Nerve Growth Factor (NGF). In this study, we have investigated the production and distribution of NGF, or more particularly its active isoform – NGF-β, and its receptors, in diseased intervertebral discs in order to establish whether this cytokine might be responsible for the observed nerve ingrowth in this situation.

Methods: Tissue sections of 21 pain level, 15 non-pain level diseased and 12 normal intervertebral discs, taken at the time of spinal surgery, and from cadavers, were probed by radioactive in situ hybridisation (ISH) for expression of NGF-β, and by immunohistochemistry (IHC) for its high and low affinity receptors (trk-A and p75 respectively). In addition, either serial sections were stained with cell specific markers (CD31 – endothelial cell, PGP9.5 – neurones, GAP43 – actively growing nerves) or sections were doubled stained (two antibodies or both ISH and IHC).

Results: We have demonstrated that NGF-β is synthesised by the endothelial cells of blood vessels growing into the IVD from the end plate. The high affinity receptor is expressed by those small nerve fibres that accompany the vessels and in their offshoots in pain level discs that are growing from perivascular nerves into the disc. In addition to their expressing the nerve specific molecule PGP9.5, the trk-A positive cells also express the nerve growth associated protein GAP43.

Conclusion: The data indicate that nerve ingrowth into IVD is regulated by NGF-β. We have localised this production to the endothelial cells of ingrowing blood vessels. NGF-β is a potential therapeutic target for the management of back pain.

Purpose and Background: There is increasing evidence that events within the diseased intervertebral disc (IVD) are mediated by locally synthesised cytokines. A prominent histological, imaging and surgical feature of IVD disease is degradation of the cartilaginous discal matrix. Whilst the mechanism by which this is mediated is unknown, in other situations where connective tissues are degraded degradation is the result of production of matrix-degrading enzymes by local connective tissue cells stimulated by cytokines, particularly the beta isoform of interleukin-1 (IL-1β). Included amongst these disorders is osteoarthritis (OA) of diarthrodial joints. OA has many similarities to the discal “degeneration” seen in mechanical back pain syndromes. In the current study, we have used a combination of in-situ techniques to establish if IL-1β is responsible for stimulating matrix degradation in the IVD.

Methods: Using a combination of radioactive in-situ hybridisation (ISH) and competitive in situ zymography (ISZ) we have studied expression of IL-1β and IL-1R – its type 1 receptor (ISH) and matrix degradation (ISZ) in five diseased lumbar IVD taken at spinal fusion surgery and 10 cadaveric IVD (five normal and five diseased). The nucleus pulposus (NP) was separated from the annulus fibrosus and diced into 0.5cm cubes. Half the cubes (typically three) were fixed in formalin and processed into paraffin wax for ISH, and half were used for ISZ. For ISH, 5 μm sections of paraffin-embedded tissue were reacted with cDNA probes radiolabelled with 35S to 580 and 530 base segments of the IL-1β and IL-1R molecules. Hybridisation was disclosed using autoradiography. For ISZ, 50 μm vibratome sections were placed into wells on microscope slides precoated with gelatin. Sections were incubated for 10 days, half in culture medium and half in medium supplemented with human recombinant IL-1 receptor antagonist (IL-1Ra – an inhibitor of IL-1). Sections were photographed at daily intervals to detect evidence of gel degradation.

Results: Chondrocytes within patient and cadaveric diseased but not normal discs expressed mRNA for both IL-1β and IL-1R. By ISZ, the same cells degraded gelatin. Degradation was inhibited by recombinant IL-1Ra.

Conclusion: This study shows that chondrocytes of diseased discs express IL-1 and its receptor. The same cells produced matrix-degrading enzymes by a mechanism that can be inhibited by the IL-1 inhibitor IL-1Ra. IL-1 is a potential therapeutic target for the management of IV disc disease.