Spinal Cord Disease — Written Clinical Reasoning

SAQ 1 — Metastatic Spinal Cord Compression: Emergency Management (20 marks, 30 minutes)

Prompt: Outline your integrated assessment and management plan for this patient, covering the immediate recognition and stabilisation, the diagnostic pathway, the definitive treatment decision (surgery versus radiotherapy) with the evidence supporting it, the dose and rationale for corticosteroids, the supportive care bundle, and the prognostic communication with the patient and family. Justify each decision with reference to evidence and guideline recommendations. [1]

Model Answer

Diagnosis and problem list (3 marks): [1]

This is acute malignant spinal cord compression (MSCC) from prostate cancer metastasis at the thoracic level. The diagnosis is clinical: a known cancer patient with progressive nocturnal back pain (the earliest and most common symptom, present in over 95 percent of MSCC cases), a clear T10 sensory level, UMN weakness below the lesion (spastic paraparesis with hyperreflexia, clonus, and extensor plantars), and sphincter disturbance (urinary retention, reduced perianal sensation, lax anal tone). The sphincter involvement indicates advanced compression and a worse prognosis. The problems are: [1]

1. Acute thoracic MSCC from prostate cancer — emergency dexamethasone and MRI required.
2. Metastatic prostate cancer on androgen deprivation — oncology input for systemic disease control.
3. Urinary retention — catheterisation required to prevent bladder injury.
4. Severe nociceptive back pain and likely neuropathic pain — opioid-based analgesia required.
5. VTE risk from immobility and cancer — pharmacological prophylaxis.
6. Functional and psychological impact of a potentially life-changing diagnosis. [1]

Immediate stabilisation (4 marks): [1]

I would recognise this as a neurological emergency immediately. The single best predictor of ambulation after treatment is ambulation at presentation — and this patient has already lost ambulation — so every hour matters. My immediate actions: [1]

• Dexamethasone 16 mg IV immediately. This reduces cord oedema by suppressing the inflammatory response to compression, buying time for definitive imaging and treatment. The conventional regimen is 16 mg loading then 8 mg twice daily, tapered after definitive treatment. I would give it before the MRI because the clinical diagnosis is secure.
• Catheterisation for the 450 mL retention to prevent bladder overdistension and injury.
• Notify the spinal surgery, radiation oncology and oncology teams in parallel — the decision between surgery and radiotherapy is made once the MRI defines the compressive site(s).
• Analgesia — opioid-based (regular paracetamol plus an opioid such as oxycodone or morphine) for the nociceptive bone pain, and consider a gabapentinoid for the neuropathic component.
• DVT prophylaxis with low-molecular-weight heparin (enoxaparin 40 mg subcutaneously daily) plus intermittent pneumatic compression, as cancer and immobility confer a high VTE risk.
• Gastric protection with a PPI alongside the dexamethasone, and glucose monitoring for steroid-induced hyperglycaemia. [1]

Diagnostic pathway (3 marks): [1]

• Emergency MRI whole spine with gadolinium within 24 hours. This is the gold standard — it shows the cord, the compressive mass, the epidural space, and any other sites of compression or spinal metastasis. A plain CT or X-ray does NOT show the cord and cannot exclude compression.
• If MRI is contraindicated (pacemaker), CT myelography is the alternative.
• I would not perform a lumbar puncture — there is no indication for CSF analysis in MSCC, and an LP below a compressive lesion risks neurological deterioration.
• Bloods: FBC, coagulation, U&E, LFTs, bone profile, PSA, and group-and-save in case of surgery. [1]

Surgery versus radiotherapy — the Patchell decision (5 marks): [1]

The definitive treatment decision depends on the Patchell 2005 randomised trial criteria. The Patchell trial (PMID 16112300, published in the Lancet) compared direct decompressive surgery plus radiotherapy against radiotherapy alone in patients with a single area of MSCC. The trial was stopped early at interim analysis because surgery was clearly superior: 84 percent of the surgery group remained or became ambulatory versus 57 percent with radiotherapy alone; the median duration of ambulation was 122 days versus 13 days; among non-ambulatory at presentation, 62 percent with surgery versus 19 percent with radiotherapy regained walking; and survival was significantly longer with surgery (median 126 versus 100 days). [1]

The Patchell criteria for surgical candidacy are: (1) a single compressive site, (2) predicted survival greater than 3 months, (3) paraplegia for less than 48 hours, (4) a fit surgical candidate, and (5) consideration of tumour radiosensitivity (surgery preferred for radioresistant tumours like renal cell, melanoma, sarcoma). [1]

For this patient with prostate cancer: prostate cancer is moderately radiosensitive, and the decision depends on the MRI findings. If there is a single compressive site at the T10 level and he is fit for surgery with a predicted survival of more than 3 months (reasonable given the prognosis of metastatic prostate cancer), I would recommend direct decompressive surgery followed by radiotherapy — especially because he has already lost ambulation, and the Patchell data show surgery doubles the chance of regaining walking in non-ambulatory presenters. If the MRI shows multiple compressive sites, or if he is not a surgical candidate, I would give palliative radiotherapy (typically 8 Gy single fraction or 20 Gy in 5 fractions) plus continued dexamethasone, tapering after treatment. [1]

Dexamethasone dose and rationale (2 marks): [1]

The standard dose is 16 mg loading then 8 mg twice daily, tapered over 2 to 3 weeks after definitive treatment. I would NOT use high-dose regimens (96 to 100 mg per day) because the Vecht 1989 trial (PMID 2771077) showed no additional benefit over the conventional dose, with significantly more toxicity (psychosis, gastric perforation, perforation, infection). This is the most commonly tested pharmacology fact in MSCC. I would prescribe a PPI for gastric protection and monitor blood glucose. [1]

Supportive care and complications (2 marks): [1]

• Bladder management: indwelling catheter initially, then trial of void once the neurological status improves.
• Bowel management: regular aperients to prevent constipation (compounded by opioids and immobility).
• Pressure area care: regular turning, pressure-relieving mattress — the patient has reduced sensation and cannot feel pressure damage.
• Rehabilitation: early physiotherapy and occupational therapy input for mobility, transfers, and activities of daily living.
• Psychological support: the diagnosis of MSCC and the threat of permanent paraplegia are devastating — I would involve the social work and psychology teams and ensure the family is supported. [1]

Prognostic communication (1 mark): [1]

I would speak to him and his family in plain language: "You have a condition where the cancer has spread to a bone in your spine and is pressing on your spinal cord — this is why your legs have become weak and you have lost the feeling of needing to pass urine. This is a serious complication, but we can treat it. I have given you a steroid medicine to reduce the swelling, and we are arranging an urgent scan to see exactly where the pressure is. Depending on the scan, you may need an operation to relieve the pressure, followed by radiotherapy. The aim is to keep you walking and to control your pain. The sooner we act, the better the chance of preserving your leg function. I cannot promise full recovery, but we will do everything we can to maximise your independence." I would set realistic expectations, involve the oncology and palliative care teams for systemic disease management, and arrange regular family updates. [1]

SAQ 2 — Subacute Combined Degeneration from Nitrous Oxide Abuse (10 marks, 15 minutes)

Prompt: A 26-year-old electrician presents with a two-week history of progressive tingling in his hands and feet, unsteadiness when walking (worse in the dark), and a sensation of electric shocks down his spine when he flexes his neck. He has been inhaling nitrous oxide canisters ("whippets") recreationally, up to 150 per day, for the past eight months. On examination he has a spastic paraparesis (power 4 out of 5 in both legs), brisk knee jerks with absent ankle jerks, extensor plantar responses, a strongly positive Romberg sign, impaired vibration sense at the ankles and knees, and impaired joint position sense at the toes. Pinprick and temperature are reduced in a glove-and-stocking distribution. His full blood count shows a haemoglobin of 135 g/L with a mean corpuscular volume of 102 fL. His serum B12 is 165 pmol/L (reference range 150 to 700). Outline your diagnostic reasoning, the investigations you would arrange, your management plan, and your communication with the patient. [1]

Model Answer

Diagnostic reasoning — subacute combined degeneration from nitrous oxide (3 marks): [1]

This is subacute combined degeneration (SCD) of the spinal cord from recreational nitrous oxide abuse, with a superimposed peripheral neuropathy. The clinical picture is the classic mixed UMN and LMN pattern: posterior column signs (impaired vibration and proprioception, positive Romberg, Lhermitte phenomenon — the electric shock sensation on neck flexion indicates dorsal column irritation in the cervical cord), corticospinal tract signs (spastic paraparesis, extensor plantars), and a coexisting peripheral neuropathy (absent ankle jerks despite brisk knee jerks, glove-and-stocking sensory loss). The macrocytosis (MCV 102 fL) supports a B12-related process. [1]

The key teaching point is that nitrous oxide irreversibly oxidises the cobalt ion in vitamin B12 from its active Co(1+) state to an inactive form, producing a functional B12 deficiency even when the serum B12 level is normal or low-normal (as in this case at 165 pmol/L). The serum B12 can be misleading in nitrous oxide-related myelopathy — the diagnostic markers are methylmalonic acid (MMA) and homocysteine, which are elevated because both B12-dependent enzymes (methionine synthase and methylmalonyl-CoA mutase) are functionally impaired. The Garakani 2016 systematic review (PMID 27523455) documented SCD and myeloneuropathy as the most common neurological consequences of nitrous oxide abuse, and this is now one of the most common causes of subacute combined degeneration in young adults. [1]

Investigations (3 marks): [1]

• Serum methylmalonic acid and homocysteine — elevated, confirming functional B12 deficiency. These are the most sensitive markers, especially when the serum B12 is borderline.
• FBC and blood film — macrocytosis with hypersegmented neutrophils (over 5 lobes).
• Folate — check concurrently; combined deficiency is common.
• Intrinsic factor antibodies and parietal cell antibodies — to screen for coexisting pernicious anaemia.
• MRI cervical and thoracic spine — T2 hyperintensity in the dorsal columns, classically an "inverted V" sign in nitrous oxide myelopathy, confirms the structural cord involvement and excludes a compressive lesion.
• Nerve conduction studies — may show an accompanying axonal peripheral neuropathy.
• Copper and caeruloplasmin — copper deficiency causes an identical syndrome and should be excluded.
• Comprehensive metabolic panel — to assess for other complications of substance use. [1]

Management plan (3 marks): [1]

• Immediate cessation of nitrous oxide — this is the root cause and must stop.
• High-dose intramuscular hydroxocobalamin (vitamin B12) 1000 micrograms on alternate days for 2 weeks (or until no further neurological improvement), then 1000 micrograms every 2 to 3 months for maintenance until the nitrous oxide use has definitively ceased and the B12 status is normalised. I would use IM rather than oral because the neurological involvement is established and IM ensures reliable replacement.
• Never give folate alone — if folate is also low, give it with or after B12, never before. Folate alone can correct the anaemia while allowing the subacute combined degeneration to progress irreversibly.
• Rehabilitation — physiotherapy for gait re-education, fall prevention, and proprioceptive training.
• Psychology and addiction support — address the recreational substance use with counselling and harm-reduction strategies.
• Serial monitoring — repeat neurological examination and consider repeat MRI to document resolution. [1]

Communication (1 mark): [1]

I would explain in plain language: "The gas you have been inhaling — nitrous oxide, or whippets — has inactivated the vitamin B12 in your body, which your nerves need to make their protective coating. This has caused inflammation in your spinal cord, which is why you feel tingling and can't walk steadily. The good news is that if you stop using the gas and we replace your B12 with injections, you have a good chance of recovery, though it may take months and you may be left with some residual symptoms. I strongly advise you to stop using nitrous oxide completely, because continuing could cause permanent damage. I'll also arrange counselling and support to help you with this." I would be honest about the uncertainty of the recovery trajectory, document the advice, and arrange close follow-up. [1]