Spinal cord compression
Malignant spinal cord (and cauda equina) compression is a complication seen relatively frequently in palliative care. Without rapid diagnosis and management it cause significant morbidity due to weakness in the legs +/- arms. When suspected, it should generally be investigated with an urgent (same-day) MRI and where treated with high-dose steroids and urgent neurosurgical and radiation oncology consultation. If treatment is instituted promptly there is a greater chance of recovery or maintaining reasonable neurological function. Without treatment spinal cord rapidly progresses with paralysis but even with prompt treatment, the development of spinal cord compression often heralds a relatively poor prognosis because it indicates the presence of progressive cancer.
The spinal canal is surrounded by the vertebral body, lamina, pedicles and spinous processes. Deep to this lies the epidural space which contains fat and vessels. Deep to this lies the dura and CSF (thecal sac) and deep to this lies the spinal cord (L1 and above) or the cauda equina (L2 and below). Nerve roots exit bilaterally at each level of the vertebra.
In the spinal cord itself, upper motor neurons ipsilaterally descend the spinal cord and at the level of nerve root exit they connect to lower motor neurons in the anterior horn.
Aetiology and Epidemiology
Around 5% of patients with advanced cancer develop spinal cord compression, although the risk varies depending on cancer type.
The most common causes of spinal cord compression are:
- Multiple myeloma
- Non-Hodgkin's lymphoma
- Prostate cancer
- Breast cancer
- Lung cancer
Spinal cord compressions are most common in thoracic spine (60% of cases) and least common in the cervical spine (10% of cases) with the remainder occur in the lumbar spine (30% of cases).
The usual mechanism of malignant spinal cord compression is metastatic spread to a vertebra followed by malignant invasion of the epidural space with compression of the the thecal sac. Oedema associated with obstruction of the epidural venous plexus occurs with eventual development of spinal cord infarction.
Spinal cord compression typically develops relatively rapidly over hours and days. Symptoms and signs vary based on the level of spinal cord involvement, although pain is almost always present.
Pain is often the initial feature of spinal cord compression and occurs in 9 out of 10 patients. Pain often develops a number of weeks prior to the development of other neurological features. The pain is well localized pain and gradually progresses. It is often worse lying down and at night. If the pain is significantly worse on movement then this can suggest spinal instability; and if it acutely worsens, this might suggest pathological fracture.
The pain may radiate along the distribution of a nerve root.
Bilateral weakness is present in the majority of patients at diagnosis. Motor signs will be consistent with the level of the spinal cord lesion. For example, spinal cord compression at the L3 vertebra will be associated with lower motor neuron signs in the legs (e.g. reduced tone, reduced power, absent reflexes, downgoing plantar response) whereas compression at a thoracic vertebra will result in upper motor neuron signs (e.g. increased tone, reduced power, increased reflexes, upgoing plantar response). If there is compression at the cervical spine there will also be some arm weakness, with lower motor neuron signs at the level of the compression and upper motor neuron signs below it.
Occasionally the compression is very lateral only and this results in weakness at the nerve root distribution of that level.
The majority of patients have reduced sensation or numbness below the level of the lesion. In a cauda equina lesion, there is sensory loss around the anus.
Bladder and bowel dysfunction
Bladder or bowel dysfunction (especially urinary retention) is relatively common, occurring in about 50% of patients with malignant spinal cord compression. It is unusual for this to occur without any motor or sensory loss, however compression at the level of the conus medullaris may be associated with pain and urinary symptoms but normal motor and sensory exam.
The mechanism of bowel and bladder dysfunction relates primarily to the disruption of the normal neural pathways. The intrinsic nerve supply (myenteric plexus) of the intestine normally maintains peristalsis in the intenstines however the intestine also receives extrinsic innervation via the vagus nerve and via the smpathetic nervous system from T10 to L3 and the parasympathetic nervous system from S2-S4 (remembering that the conus medullaris is at T12/L1). In spinal cord injuries above the conus medullaris increased pelvis muscle tone develops with the problem of an inability to relax the external anal sphincter leading to constipation with faecal impaction. In lesions above at the conus medullaris or below, a lower motor neuron patter develops with reduced muscle and sphincter tone and incontinence mixed with constipation.
Generalized weakness with troiuble mobilizing is common in progressive advanced cancer. In cases where there is known advanced progressive cancer and there is gradual weakness and immobility associated with fatigue and cachexia and there are no other specific neurological signs or back pain, then spinal cord compression should not be high on the list of differentials. In cases where there is an acute and rapid change in power then spinal cord compression should be considered as a possibility with other differentials determined based on the neurological features, including:
- Vertebral metastases - cause severe pain, localized pain but any weakness will occur due to pain
- Cerebral metastases - weakness is much more likely to be unilateral with upper motor neuron signs and back pain is not a usual feature
- Spinal cord metastses (i.e. intramedullary metastases) - more likely to see a Brown-Sequard Syndrome type picture.
- Leptomengingeal metastases (e.g. in the cauda equina) - back pain is often absent although there may e radicular pain; confusion is often present
- Malignant invasion of a nerve plexus - back pain is usually absent but there is typically severe local (lateral to the midline) and radicular pain with unusual unilateral sensory loss and focal weakness
The definitive diagnosis of spinal cord compression required MR imaging. Frequently there is a delay in diagnosis for a number of reasons, including patients not seeking medical help sooner and GPs and hospital doctors taking a number of days to recognize the condition.
Magnetic resonance imaging is the gold standard test to investigate suspected spinal cord compression and will show tumour encroaching on the thecal sac. In addition to showing the cord and thecal sac well, MR also gives good images of the bone and surrounding soft tissue.
In cases where MRI is contraindicated (e.g. medchanical valves or pacemakers), the best alternative imaging modality is a CT myelogram. With this procedure, contrast is injected into the CSF prior to imaging. Additionally CSF can be sent to the lab to look for evidence of leptomeningeal disease if this is being considered as a differential.
If neither an MRI nor CT myelogram is possible, then a CT scan alone can be performed although this does not show clear detail of the spinal cord or thecal sac. It does however show bone well and if there is significant metastatic damage of the cortex near the spinal canal then this suggests the possibility of spinal cord compression at this level.
A whole body bone scan will show bony metastases and if one is occurring at a level consistent with a patient's signs then this could be considered evidence of spinal cord compression at this level. Bone scans do not show detail of the thecal sac or spinal cord.
The most important predictors of post-treatment mobility are:
- Pre-treatment mobility
- Rapidity of treatment
It is important to warn patients who are thought to be at higher risk of spinal cord compression of the possibility so that they seek urgent treatment for back pain associated with weakness (as often patients wait many days to seek a medical opinion).
Administration of high dose steroids on suspiscion of spinal cord compression is key. Studies shown that urgent steroids improve mobility with one study (where 96mg of dexamethasone was given daily) showing that following definitive therapy (radiotherapy) 81% of patients who received steroids were ambulating versus 63% in the non-steroid group of patients. The appropriate dose is unclear and although some studies have given very high doses (e.g. 96mg IV daily), others have shown no difference in efficacy between 96mg daily and 16mg daily. Higher doses of steroids are associated with a heightened risk of adverse effects. Thus a reasonable approach is:
Dexamethasone 16 SC daily (or oral)
This should be followed by urgent definitive therapy (e.g. surgery and/or radiotherapy) and the dose of steroid then tapered over a number of weeks (e.g. 2-4 weeks).
Neurosurgery and/or Radiotherapy
Urgent neurosurgery and/or urgent radiotherapy are the treatments of choice for spinal cord compression. The decision of whether or not pursue these of course depends on many factors such as the patient's pre-spinal cord compression performance score and expected prognosis, but as a general rule, unless the patient is thought to be in the last few weeks of life, it is usually appropriate to seek definitive therapy as this greatly increases the chance of the patient maintaining mobility.
Neurosurgery should be considered as the first line therapy prior to radiotherapy particularly if:
- There is spinal instability
- The tumour is likely to be relatively radioresistant
In cases where there is spinal instability the best option is surgical decompression (especially when there is obvious epidural disease or a bone fragment clearly compressing the spinal cord) because this reduces pain (and radiotherapy will not) as well as improves chances of maintaining mobility. In cases of instability without bone fragments or epidural disease pressing on the spinal cord, a vertebroplasty may be a reasonable alternative as it can be helpful in reducing pain.
There is no universal agreed understanding of an unstable spine. A scoring system known as the Spine Instability Neoplastic Score (or SINS) is often employed, although this has not formally been validated in any studies. Where the score is greater than 6, it is appropriate to consider a surgical opinion.
|Spinal Instability in Neoplasia Score|
|Pain on standing or moving|
|No (pain may be present but not worswe on standing or moving)||1|
|Completely pain free||0|
|Location of lesion|
|At a junction (C1-2, C7-T2, T11-L1, L5-S1)||3|
|At a mobile area (C3-C6, L2-L4)||2|
|At a semi-rigid area (T3-T10)||1|
|At a rigid area (S2-S5)||0|
|Type of lesion|
|> 50% collapse||3|
|< 50% collapse||2|
|No collapse with > 50% of vertebral body involved||1|
|None of the above||0|
|Tumour involvement of facet, pedicle, costovertebral joint|
|Determine Score by Adding Together All Figures|
Current techniques for surgery include resection of any tumour in the epidural space with reconstruction with methylmethacrylate and spinal stabilization with screw an rod fixation. Radiotherapy is delayed after surgery (for 1-2 weeks if reconstruction is done with methylmethacrylate or for 6 weeks of bone grafting is used). Evidence for tumour decompressive surgery and spinal stabilization prior to radiotherapy is good. In a large study, patients with metastatic spinal cord compression and a single site of disease who had been paraplegic for less than 48 hours were randomized to urgent surgery + radiotherapy or urgent radiotherapy alone. High doses of steroids were used (96mg daily). There was a significantly higher mobility rate in patients treated with surgery, with 84% able to walk if surgery was undertaken versus 57% post-radiotherapy alone. Furthermore, median ambulatory duration was 122 days versus 13 days between the two groups. A large proportion of patients who underwent surgery (10 of 16) regained the ability to walk whereas this was not the case in those who underwent radiotherapy alone. The positive benefits of surgery were only in younger patients however, under the age of 65. Surgery does however have significant and serious complications.
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The best analgesia is urgent treatment but whilst commencing treatment and post-treatment use of opioids + neuropathic agents such as gabapentin are the mainstay of analgesia.
The immobility caused by spinal cord compression results in a high risk of development of DVT and routine prophylaxis is usually appropriate at least in the initia stage. In patients who do not regain mobility and who are deteriorating then the value of DVT prophylaxis can be questioned.
Consiptation is commonly an issue due to a combination of poor mobility, opioids and dysregulation of the autonomic nervous system. A combination of oral softeners and and stimulants are generally appropriate and may help establish a regular bowel habit and minimize constipation. However, patients may require regular stimulant enemas (e.g. daily after breakfast) followed by various manouvres to help the evacuation of all stool (e.g. deep breathing, abdominal pressure, the Valsalva manouvre and insertion of a finger into the anus with slow rotation over 30 seconds repeated every 5 minutes).
- Sorensen S et al. Effect of high-dose dexamethasone in carcinomatous metastatic spinal cord compression treated with radiotherapy: a randomised trial. Eur J Cancer. 1994; 30A(1):22.
- Vecht CJ et al. Initial bolus of conventional versus high-dose dexamethasone in metastatic spinal cord compression. Neurology. 1989;39(9):1255.
- Patchell RA et al. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomised trial. Lancet. 2005.