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An unusual cause of paraplegia
  1. S A M Saeeda,
  2. D Francisb,
  3. R Brooksb
  1. aUniversity Department of Geriatric Medicine, North Staffs Combined Health Care NHS Trust, City General Hospital, Stoke-on-Trent, UK, bQueen Elizabeth Medical Centre and Walsall Manor Hospital, Walsall, West Midlands, UK
  1. Dr Saad A M Saeed, Springfield Unit, City General Hospital, Stoke-on-Trent, Staffs ST4 6QG, UKsaad_saeed{at}

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A 56 year old machine operator presented with mild weakness and sensory disturbance in his lower limbs after he woke up from an arthroscopy operation. At the time he did not seek medical attention. His symptoms progressed over the next four months to the degree that he was unable to stand and he developed back pain radiating to the legs, urinary frequency, hesitancy, and incontinence of urine. There was no history of claudication in the legs. He was a heavy smoker and suffered from ischaemic heart disease and type 2 diabetes mellitus.

On examination he was overweight. Straight leg raising test was within normal limits. Neurological examination showed normal cranial nerves and normal upper limbs. Lower limb examination revealed grade 3/4 proximal limb weakness with absent ankle jerks and equivocal plantar responses. Light touch and pinprick sensation was impaired in L1–S3 distribution bilaterally with impaired vibration. Coordination was normal. The remaining physical examination was otherwise unremarkable.

Laboratory examination showed high inflammatory parameters with an erythrocyte sedimentation rate of 33 mm in the first hour and a C reactive protein of 68 mg/l. The following tests were either normal or negative: full blood count, biochemistry profile, immunoglobulins, serum vitamin B12, serum and red blood cell folate, vasculitis, thrombophelia, and paraneoplastic screens, angiotensin converting enzyme level, and Treponema pallidumhaemagglutination test.

Lumbar puncture showed a cerebrospinal fluid (CSF) opening pressure of 260 mm with high CSF protein at 1.9 g/l (normal 0.1–0.4) with no evidence of oligoclonal band. CSF glucose 5.7 mmol/l (blood glucose 10.4 mmol/l), 73 red cells/high power field and no leucocytes or abnormal cells on cytospin. There was no evidence of xanthochromia.

Computed tomography and magnetic resonance imaging (MRI) scans of the brain were normal; however, an MRI scan of the spinal cord was abnormal (fig 1).

Figure 1

(A) Axial and (B) sagittal MRI. T2 weighted scan of the spinal cord.

After he was given specific medical treatment he became paraplegic (leg power 0/4) and lost bladder sensation. An urgent spinal angiogram confirmed the diagnosis (fig 2).

Figure 2

Spinal angiogram. Two pictures of the anterioposterior view.

He had specific interventional treatment after which he had some improvement in sensation in the lower limbs, only to be replaced by unpleasant dysthesia, but he started passing urine normally. Lower limb strength improved to grade 2–3/4, although he was not weight bearing.

Eight months after the initial presentation he continued to improve, although he required a wheelchair for mobility.


What differential clinical diagnoses would you consider?
What do the spinal MRI scans show?
What was the first treatment given which was followed by paraplegia?
What is the pathological abnormality suggested by the spinal angiogram?
What specific treatment did the patient receive?

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