Spinal Cord Disease — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Ramesh Patel, 66 years old, retired schoolteacher. [1]

Presenting illness (3 months ago): Three weeks of progressive thoracic back pain and three days of leg weakness with ascending numbness to his waist. He was diagnosed with acute malignant spinal cord compression at T10 from a prostate cancer metastasis. He received dexamethasone 16 mg immediately, emergency MRI confirmed a single compressive epidural mass at T10 with cord signal change, and he met the Patchell criteria for surgery. He underwent T9 to T11 posterior decompression and stabilisation with instrumented fusion, followed by radiotherapy (20 Gy in 5 fractions). He regained some motor function but remains partially dependent. [1]

Past history: Metastatic prostate cancer (Gleason 8, T4N1M1), diagnosed 2 years ago. Androgen deprivation therapy (enzalutamide). Hypertension. Ex-smoker (40 pack-years). No prior neurological disease. [1]

Current medications: Enzalutamide 160 mg daily, tamsulosin 400 micrograms daily, gabapentin 600 mg three times daily (for neuropathic pain), oxycodone modified-release 10 mg twice daily, paracetamol 1 g four times daily, senna two tablets at night, enoxaparin 40 mg subcutaneously daily, omeprazole 20 mg daily, a multivitamin. [1]

Current functional status: Mobilises with a frame for short distances (10 to 20 metres); uses a wheelchair for longer distances. Can stand and transfer with assistance of one person. Needs help with dressing (lower half) and bathing. Has a suprapubic catheter for persistent neurogenic bladder. Reports ongoing neuropathic burning pain in both legs below the knees, worse at night. [1]

Examination findings (trainee elicits):

• Alert, oriented, cooperative. Speech fluent.
• Cranial nerves intact.
• Upper limbs: normal tone, power 5 out of 5 throughout, reflexes 1+, downgoing plantars, normal coordination.
• Lower limbs: increased tone (modified Ashworth 2), power 4 out of 5 in the hip flexors and knee extensors, 3 out of 5 at the ankles and feet (dorsiflexion and plantarflexion), symmetric. Reflexes 3+ at the knees and ankles, with 3 to 4 beats of clonus at both ankles. Both plantars are extensor.
• Sensory: a sensory level to pinprick at T10 bilaterally. Vibration absent at the ankles, reduced at the knees. Joint position sense impaired at the toes.
• Gait: spastic, uses a frame, short steps, circumduction.
• Suprapubic catheter in situ, urostomy bag draining clear urine.
• No pressure injuries. Surgical scar well healed. [1]

Investigations (current):

• MRI whole spine (1 month ago): post-operative changes at T9 to T11 with no residual cord compression; no new compressive sites; stable sclerotic bone metastases elsewhere.
• PSA (2 weeks ago): 45 (down from 340 at presentation, reflecting response to enzalutamide and radiotherapy).
• Renal function and FBC: normal.
• Bone scan: stable sclerotic metastases, no new lesions. [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Patel is a 66-year-old retired schoolteacher who, three months ago, presented with acute malignant spinal cord compression at the T10 level from a prostate cancer metastasis. He was managed with immediate dexamethasone, emergency MRI, and surgical decompression with instrumented fusion at T9 to T11, followed by radiotherapy (20 Gy in 5 fractions). He now has a residual partial paraparesis and is reviewed in the rehabilitation clinic for ongoing management. [1]

His main problems are:

1. Residual partial paraparesis (power 4 out of 5 proximally, 3 out of 5 distally in the legs) with a T10 sensory level — intensive neurological rehabilitation required
2. Neuropathic pain in both legs below the knees — optimise pharmacological and non-pharmacological management
3. Neurogenic bladder managed with a suprapubic catheter — urology review for long-term strategy
4. Metastatic prostate cancer responding to enzalutamide (PSA down from 340 to 45) — ongoing oncology surveillance
5. VTE prophylaxis — current enoxaparin; review the ongoing indication
6. Opioid dependence risk — review the pain regimen and consider opioid weaning
7. Functional and psychological impact — social work, psychology, and community support." [1]

Management plan: [1]

1. Neurological rehabilitation: Intensive multidisciplinary inpatient or outpatient rehabilitation — physiotherapy for strength, transfers, gait re-education, balance and fall prevention; occupational therapy for activities of daily living, home modification (rails, shower chair, ramp access), and equipment prescription (wheelchair, frame). Serial motor assessment (MRC sum score) to track recovery. The surgical decompression was within the Patchell window, so continued improvement is possible over 6 to 12 months. [1]

2. Neuropathic pain management: The burning leg pain is neuropathic (cord injury). His current gabapentin 600 mg three times daily (1800 mg total) is suboptimal — I would titrate upward to a target of 1800 to 3600 mg per day in divided doses, adding a second-line agent (pregabalin or duloxetine) if monotherapy is insufficient. I would review the oxycodone requirement — the goal is to minimise opioid exposure (constipation, dependence, falls) while maintaining function. A pain specialist referral would help with the opioid taper and consideration of non-pharmacological strategies (transcutaneous electrical nerve stimulation, desensitisation). [1]

3. Bladder management: The suprapubic catheter is appropriate for his current level of function and continence. I would involve the urology and continence teams to assess for a trial of intermittent self-catheterisation or bladder training as his function improves; perform regular urine cultures and renal function monitoring (annual ultrasound); and prescribe an anticholinergic if he develops detrusor overactivity. [1]

4. Oncology management: His PSA response to enzalutamide (340 to 45) is encouraging. I would continue the enzalutamide, arrange serial PSA monitoring every 3 months, and maintain the bone scan surveillance for new metastatic sites. I would liaise with his oncologist about the role of additional bone-targeted therapy (denosumab or zoledronic acid) for skeletal-related events. [1]

5. VTE prophylaxis: The risk of venous thromboembolism is high (cancer and residual immobility) and persists while he is significantly immobile. I would continue enoxaparin 40 mg subcutaneously daily while he is unable to mobilise independently, and transition off once his mobility improves and his risk falls. I would monitor for bleeding and adjust the dose if renal function changes. [1]

6. General medical management: Continue omeprazole for gastric protection (now off dexamethasone, so review the ongoing indication), optimise blood pressure control, encourage bone health (calcium, vitamin D, weight-bearing where possible), and screen for depression (a common and under-recognised complication of spinal cord injury). [1]

7. Psychological and social support: The diagnosis of MSCC and the residual disability carry a high risk of depression, anxiety, and loss of identity (he was an active schoolteacher). I would screen with the PHQ-9, involve the clinical psychology team, and arrange social work input for home modifications, community supports, and financial planning. A peer support group for spinal cord-injured patients can be valuable. [1]

Examiner discussion questions

Q: "He is still on enoxaparin at 3 months. When do you stop it?" [1]

"The risk of VTE in cancer patients with significant immobility is high — approximately 15 to 30 percent without prophylaxis. The risk persists while the patient is unable to mobilise independently. I would continue enoxaparin while Mr Patel is wheelchair-dependent and has limited independent ambulation, and transition off it once his mobility improves to the point where his VTE risk approaches that of an ambulatory patient. I would not transition to long-term oral anticoagulation unless he develops a separate indication, such as atrial fibrillation or a confirmed thromboembolic event. I would monitor his renal function and platelet count and adjust the dose if needed." [1]

Q: "How would you distinguish residual cord dysfunction from a new compressive lesion if he deteriorated?" [1]

"Any new or worsening neurological deficit in a patient with a history of MSCC requires urgent re-imaging to exclude a new compressive site or local recurrence. I would arrange an emergency MRI whole spine with gadolinium. A new compressive lesion would show as an epidural mass with cord compression at a new level or at the surgical site. If the MRI is clear, I would consider alternative explanations — radiation myelopathy (typically occurs 6 to 24 months after radiotherapy, within the radiation field), a paraneoplastic process, or a metabolic or vascular cause. The clinical pattern and the MRI are the key discriminators. Serial neurological examinations are essential to detect subtle deterioration early." [1]

Q: "What is his long-term prognosis?" [1]

"His neurological prognosis depends on the degree of recovery over the next 6 to 12 months. He was non-ambulatory but paraparetic (not paraplegic) at presentation and was decompressed within the Patchell window, which offers the best chance of recovery. At 3 months he has partial paraparesis (4 out of 5 proximally, 3 out of 5 distally) and can ambulate with a frame — this is a meaningful recovery. Further improvement is likely over the next 6 to 9 months, though he may be left with residual distal weakness and sensory loss. His oncological prognosis depends on the response to enzalutamide — his PSA has fallen from 340 to 45, which is encouraging, and patients with hormone-responsive prostate cancer can survive for years with good quality of life. The main threats to his quality of life are further skeletal-related events (new cord compression or pathological fractures), neuropathic pain, and the complications of immobility (pressure injuries, UTIs, VTE, depression). Close multidisciplinary follow-up is essential." [1]

DCE Short Case — Neurological Examination of a Cord Lesion

Instruction

"Examine this patient's neurological system. He was admitted two weeks ago with progressive leg weakness from spinal cord compression. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Spastic paraparesis — increased tone, weakness worse distally, hyperreflexia, extensor plantar responses.
• A clear sensory level — to pinprick at T10, marking the upper border of the cord lesion.
• Dorsal column loss below the level — impaired vibration and proprioception.
• Sphincter involvement — indwelling catheter for neurogenic bladder.
• Preserved upper limbs and cranial nerves — localising the lesion below the cervical cord. [1]

Systematic examination routine

1. Observe from the end of the bed: posture in the wheelchair, catheter bag, any surgical scar, wasting or fasciculations.
2. Cranial nerves: usually normal in a thoracic cord lesion — perform a quick screen to exclude a higher lesion.
3. Upper limbs: full motor, reflex, sensory and coordination examination — normal in a thoracic lesion, confirming localisation below the cervical cord.
4. Lower limbs motor: assess tone (increased), power (reduced, worse distally), reflexes (pathologically brisk with clonus), plantar responses (extensor).
5. Lower limbs sensory: test pinprick dermatomally from the feet upward to find the sensory level; test vibration at the ankles, knees and hips; test joint position sense at the toes; compare light touch with pinprick to identify any dissociation.
6. Sphincter examination: check perianal sensation and anal tone (if appropriate and consented).
7. Gait: if ambulatory, observe for spastic gait (stiff, circumducting, short steps). [1]

Presentation template

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

Cranial nerves are intact. The upper limbs are normal — tone, power 5 out of 5, reflexes 1+, downgoing plantars, coordination intact. [1]

In the lower limbs, tone is increased bilaterally. Power is 4 out of 5 in the hip flexors and knee extensors, and 3 out of 5 at the ankles and feet, symmetric. Reflexes are pathologically brisk at 3+ in the knees and ankles, with 3 to 4 beats of 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]

In summary, these findings — a spastic paraparesis with a T10 sensory level, hyperreflexia with clonus, extensor plantar responses, impaired dorsal column modalities below the level, and a neurogenic bladder — localise to a thoracic spinal cord lesion at or above the T10 cord segment, consistent with his history of malignant spinal cord compression managed surgically." [1]

Discussion questions

Q: "Localise the lesion." [1]

"The lesion is in the thoracic spinal cord at or above the T10 segment. The UMN pattern — spastic weakness, hyperreflexia, clonus, extensor plantar — places the lesion in the corticospinal tract, above the anterior horn cell. The sharp T10 sensory level places the lesion at or above the T10 cord segment. The preserved upper limbs and cranial nerves exclude a cervical or cerebral lesion. The neurogenic bladder is consistent with a cord lesion above the sacral segments. The combination of a motor level and a sensory level at the same dermatome is the hallmark of a complete or near-complete cord lesion." [1]

Q: "What is the significance of the dorsal column loss?" [1]

"The impaired vibration and proprioception below the level reflect dorsal column involvement. The dorsal columns carry ipsilateral vibration, proprioception and fine touch, and they cross only in the medulla, so a cord lesion produces ipsilateral dorsal column loss below the level. In this patient the dorsal column loss is bilateral and below T10, consistent with a bilateral cord lesion at that level. The dorsal column loss contributes to his unsteadiness and fall risk — he cannot feel where his feet are, which is why a positive Romberg (worse balance with eyes closed) is a feature of dorsal column disease." [1]

Q: "How does the sensory level help you determine which vertebral body is compressed?" [1]

"There is a one-to-two-segment offset between the clinical sensory level and the vertebral body level, because the dorsal roots enter the cord at a point that is typically one to two segments above the overlying vertebral body in the thoracic spine. A T10 sensory level therefore corresponds to a cord lesion around T10, but the compressive mass is often found at the T11 or T12 vertebral body. This is why I always image the whole spine rather than just the clinical level — to avoid missing the lesion due to the anatomical offset." [1]

Q: "What is the role of rehabilitation in his ongoing management?" [1]

"Intensive multidisciplinary rehabilitation is the cornerstone of his long-term management. The goals are to maximise functional independence (mobility, transfers, activities of daily living), prevent complications (pressure injuries, contractures, UTIs, DVT, depression), and optimise quality of life. Physiotherapy focuses on strength, gait re-education, balance and fall prevention, and spasticity management (stretching, standing frame, baclofen or botulinum toxin for focal spasticity). Occupational therapy addresses activities of daily living, home modification, and equipment prescription. The continence and urology teams manage the neurogenic bladder. The psychology team addresses the emotional impact. Rehabilitation should continue for 6 to 12 months as recovery from cord compression is prolonged, and serial motor assessments (MRC sum score) track progress. The surgical decompression was within the Patchell window, so continued improvement is anticipated." [1]