Spinal Cord Disease Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Patel is a 66-year-old man who presents with a three-week history of progressive mid-thoracic back pain, worse at night, and three days of progressive leg weakness with numbness ascending to his waist. He has a history of metastatic prostate cancer, Gleason grade 8, diagnosed two years ago, on androgen deprivation therapy with enzalutamide and known sclerotic bone metastases. [1]

On examination he is alert, afebrile and haemodynamically stable. He has a spastic paraparesis — power 3 out of 5 in the hip flexors and 2 out of 5 at the ankles — with increased tone, brisk reflexes, ankle clonus, and extensor plantar responses. There is a sharp sensory level to pinprick at T10 bilaterally, with reduced vibration below the knees and impaired joint position sense at the toes. He has a distended bladder, a post-void residual of 450 mL, reduced perianal sensation and lax anal tone. [1]

His main problems are:

1. Acute malignant spinal cord compression from prostate cancer at the T10 level — emergency dexamethasone and MRI required
2. Urinary retention — catheterisation required
3. Severe back pain — opioid analgesia required
4. VTE risk from cancer and immobility — prophylaxis required
5. Metastatic prostate cancer — ongoing oncology management
6. Psychological and functional impact — multidisciplinary support required." [1]

Examiner probing questions and model answers

Q1: "You have given dexamethasone 16 mg. Why that dose and not a higher loading dose?" [1]

"The standard dose for malignant spinal cord compression is 16 mg loading followed by 8 mg twice daily, tapered after definitive treatment. The Vecht 1989 randomised trial compared a conventional regimen — 10 mg loading then 16 mg per day — against a high-dose regimen — 100 mg loading then 96 mg per day — and found no difference in pain relief, ambulation, or bladder function, but significantly more toxicity in the high-dose group, including psychosis, gastric perforation, and serious infection. This established the conventional dose as the standard of care and high-dose regimens are no longer recommended. I would give 16 mg immediately because the clinical diagnosis of cord compression is secure, and the steroid buys time by reducing cord oedema while I arrange the definitive MRI and treatment." [1]

Q2: "The MRI shows a single compressive mass at T10. Do you operate or give radiotherapy?" [1]

"I would apply the Patchell criteria. The Patchell 2005 randomised trial, published in the Lancet, compared direct decompressive surgery plus radiotherapy against radiotherapy alone in patients with a single area of malignant spinal cord compression. The trial was stopped early because surgery was clearly superior — 84 percent of the surgery group were ambulatory at the end of treatment versus 57 percent with radiotherapy alone, the median duration of ambulation was 122 days versus 13 days, and among non-ambulatory presenters, 62 percent with surgery versus 19 percent with radiotherapy regained walking. Survival was also significantly longer in the surgery group. [1]

This patient meets all the Patchell criteria: a single compressive site at T10, an expected survival well over 3 months given the trajectory of metastatic prostate cancer on enzalutamide, paraplegia for less than 48 hours, and he appears fit for surgery. I would therefore recommend direct decompressive surgical resection followed by radiotherapy. The one consideration is that prostate cancer is moderately radiosensitive, so if he were not a surgical candidate — for example, if he had multiple compressive sites, a poor prognosis, or was medically unfit — radiotherapy alone, typically 8 Gy in a single fraction or 20 Gy in 5 fractions, would be the appropriate alternative." [1]

Q3: "He has already lost the ability to walk. What is his chance of regaining ambulation?" [1]

"The single most important predictor of ambulation after treatment is the neurological status at presentation. For patients who are ambulatory at presentation, over 80 percent remain ambulatory with treatment. For those who are non-ambulatory but not paraplegic — as this patient is — approximately 30 to 60 percent regain walking with surgery. For those who are completely paraplegic for more than 48 hours, the chance of regaining ambulation is under 10 percent. This patient has been non-ambulatory for approximately 18 hours, so he is still within the window where surgery offers the best chance of recovery. I would be honest with him and his family that recovery is possible but not guaranteed, and that intensive rehabilitation will be essential regardless of the outcome." [1]

Q4: "He has been paraplegic for three days by the time surgery is arranged. Does surgery still help?" [1]

"The Patchell criteria exclude patients with paraplegia for more than 48 hours because the cord has typically undergone irreversible infarction by that point, and the trial did not show benefit in that group. At three days of paraplegia, I would discuss with the neurosurgical team whether surgery is still indicated — it may be offered for pain control or to prevent further neurological deterioration, but the primary goal of restoring ambulation is much less likely. I would lean toward radiotherapy and continued dexamethasone for palliation, with a focus on pain control, bladder and bowel management, pressure-area care, and rehabilitation to optimise wheelchair independence. I would involve the palliative care team and have an honest conversation with the patient and family about the changed prognosis." [1]

Q5: "How would you manage his urinary retention in the longer term?" [1]

"Immediately, I would insert an indwelling urinary catheter to relieve the 450 mL retention and prevent bladder overdistension injury. In the longer term, the management depends on his neurological recovery. If his cord compression is relieved and sphincter function returns, I would trial without a catheter once his power improves. If he has a persistent neurogenic bladder — either a spastic (UMN) bladder with small involuntary contractions and urgency, or a flaccid bladder with overflow incontinence — I would involve the urology and continence teams for bladder training, anticholinergics or intermittent self-catheterisation, and regular monitoring for urinary tract infection and renal function. Long-term catheterisation increases the risk of infection, stones, and urethral injury, so I would aim for the least invasive continence strategy that works for him." [1]

Q6: "What is your communication plan with the patient and family?" [1]

"I would speak to him and his family in plain language, away from the busy emergency department. I would explain that his prostate cancer has spread to a bone in his spine and is pressing on his spinal cord, which is why his legs have become weak and he has lost bladder control. I would explain that this is a serious but treatable complication — I have given him a steroid to reduce the swelling, and we are arranging an urgent scan and a surgical and radiation oncology opinion. I would set realistic expectations: the goal is to preserve or restore his ability to walk and to control his pain, but I cannot guarantee full recovery. I would involve the oncology team to discuss his systemic cancer treatment, the palliative care team for symptom management, and the social work and psychology teams for emotional and practical support. I would arrange regular family meetings and document all discussions." [1]

Short Case Discussion

Scenario: "Examine this patient's neurological system. They were admitted two days ago with progressive leg weakness."

Candidate presentation (model): [1]

"I examined Mr Patel's neurological system. He is alert and cooperative, seated in a wheelchair with an indwelling urinary catheter. [1]

Cranial nerves are intact. In the upper limbs, tone, power, reflexes and coordination are normal, with downgoing plantar responses. [1]

In the lower limbs, tone is increased bilaterally. Power is 3 out of 5 in the hip flexors, 4 out of 5 in the knee extensors, and 2 out of 5 at the ankles and feet, symmetric. Reflexes are pathologically brisk at the knees and ankles, with sustained clonus at both ankles. Both plantar responses are extensor. [1]

Sensation is reduced to pinprick below the T10 dermatome bilaterally — a clear sensory level. Vibration sense is absent at the ankles and reduced at the knees. Joint position sense is impaired at the toes. Light touch is relatively preserved. [1]

Coordination cannot be fully assessed in the legs due to weakness. [1]

In summary, these findings — a spastic paraparesis with a T10 sensory level, hyperreflexia, ankle clonus, extensor plantar responses, and urinary retention — localise to a thoracic spinal cord lesion at or above the T10 cord segment. The pattern is most consistent with malignant spinal cord compression." [1]

Examiner: "Localise the lesion." [1]

"The lesion is in the thoracic spinal cord at or above the T10 segment. The evidence is: the UMN pattern of weakness (spastic, hyperreflexic, extensor plantar) places the lesion in the corticospinal tract — above the anterior horn cell. The sharp T10 sensory level to pinprick places the lesion at or above the T10 cord segment (the spinothalamic fibres enter and cross at the level of entry, so the sensory level corresponds to the cord level, with a one-to-two-segment offset from the vertebral body level). The bilateral nature of the deficits and the preserved cranial nerves exclude a cerebral or brainstem lesion. The sphincter involvement (urinary retention, reduced perianal sensation) is consistent with a cord lesion above the sacral segments." [1]

Examiner: "How would you distinguish this from a cauda equina lesion?" [1]

"The key distinction is upper motor neuron versus lower motor neuron signs. This patient has UMN signs — increased tone, hyperreflexia, clonus, and extensor plantar responses — which localise to the cord (above the conus medullaris, which ends at L1 to L2). A cauda equina lesion, which compresses the lumbosacral nerve roots below the conus, produces LMN signs — flaccid weakness, absent reflexes, downgoing plantar responses — with saddle anaesthesia and urinary retention. The clinical pictures can overlap in terms of sphincter dysfunction, but the reflex pattern is the discriminator: this patient's brisk reflexes and extensor plantars confirm a cord (UMN) lesion, not a cauda equina (LMN) lesion." [1]

Examiner: "What is the significance of the preserved light touch but loss of pinprick below the level?" [1]

"This pattern — preserved light touch with loss of pain and temperature — reflects the different pathways for these modalities. Pain and temperature travel in the spinothalamic tract (anterolateral column), which is damaged in a compressive cord lesion. Light touch travels in both the spinothalamic tract and the dorsal columns, so partial preservation of light touch can occur even when the spinothalamic tract is disrupted, because the dorsal column component of light touch is intact. This 'dissociation' between pinprick and light touch is not as marked as in a central cord lesion (syringomyelia, where the dissociation is the hallmark), but it reflects the fact that light touch has a dual pathway." [1]

Examiner: "What is the first investigation you would arrange?" [1]

"Emergency MRI of the whole spine with gadolinium, within 24 hours. This is the single most important investigation because it confirms the compressive lesion, defines its level and extent, identifies any other compressive sites (which would change the surgical decision), and guides the surgical or radiotherapy planning. I would not arrange a CT of the spine as the first investigation because it shows bone but not the cord or the epidural tumour — a normal CT does not exclude cord compression. The MRI must be whole spine because the clinical sensory level may not correspond exactly to the compressive level, and there may be multiple sites of disease." [1]