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BMJ Case Rep. 2010; 2010: bcr1220092529.
Published online 2010 October 11. doi:  10.1136/bcr.12.2009.2529
PMCID: PMC3028046
Unusual presentation of more common disease/injury

Sciatic neuropathy as first sign of metastasising prostate cancer


Peripheral neuropathies are among the most common neurological diseases and have numerous causes, including diabetes, alcohol, hereditary, toxic, metabolic, infectious, inflammatory, ischaemic and paraneoplastic. Often, however, no definitive cause is identified and the condition is termed idiopathic neuropathy. Here we describe a patient who was initially diagnosed with idiopathic sciatic neuropathy but who was eventually diagnosed with prostate cancer. This is an uncommon manifestation of prostate cancer, and the diagnostic was difficult because prostate-specific antigen (PSA) was normal and the positron emission tomography scan negative. Changes in PSA should always raise the suspicion of prostate cancer, just as idiopathic progressive neuropathy should always raise the suspicion of an underlying malignancy, even when standard diagnostics fail to explain the patient's symptoms.


We found the patient hard to diagnose. Despite MRI-verified pathology, normal prostate-specific antigen (PSA) and negative positron emission tomography (PET) made clinical picture less than clear. We hope that others can learn from our experience, that idiopathic neuropathy may indeed be an unusual first-manifestation of prostate cancer.

Case presentation

A 71-year-old man, former smoker, referred to the department of neurology from the department of vascular surgery with progressive pain in the right thigh. At time of referral, the pain has been present for at least 2 years, but the patient reports aggravation through the last 6 months, with pain (murmurs) in the thigh aggravated after 200–300 m walk, difficulty in maintaining balance and increased fatigue. The department of vascular surgery found an ankle blood pressure of 80/85 mm Hg (L/R) and an ankle-brachial index of 48/52% and intermittent claudication on the right leg that could, only partly, be related to arterial insufficiency. The patient had experienced problems passing urine for 2 years, and had been examined at the department of urology, where a rectal examination showed a prostate of normal size and texture. Sonography of the prostate was normal, with a slight hypertrophy (32 ml). PSA was 1.7. The patient had been examined urodynamically, including cystometry and because the pressure/flow examination showed no obstruction the patient was diagnosed with detrusor insufficiency (bladder atony). For this the patient performed intermittent self-catheterisation.

Physical examination upon admission at the department of neurology was unremarkable apart from difficulty in walking the line and decreased right-sided muscle strength for knee flexion (strength 4) and extension (5-) and foot plantar flexion (3) and extension (5-) in contrast to normal responses on the left. In the right leg, the proprioception and the sense of vibration were decreased from the ankle level, and the plantar response could not be elicited. Spinal stenosis was suspected, and CT showed slight spinal stenosis at L3–L4 without spinal root affection. Blood work, including haematological, biochemical and immunological tests were all normal, apart from a slightly elevated sedimentation rate (18 AU). Nerve conduction velocity test of the right tibial nerve showed no motor response and no sensory response from the right sural nerve. Electromyography (EMG) showed neurogenic changes with denervation in the right anterior muscle and mild neurogenic changes in the right medial vastus muscle. The neurophysiological examination pointed towards a right-sided sciatic neuropathy with possible involvement of the lumbosacral plexus. There were normal findings on the left side.

Within weeks, the patient reported intensifying of the pain which impaired walking. MRI of the lumbar-sacral plexus did not show relevant pathology. The patient strength had faded; knee flexion (strength 3) and extension (4) and foot plantar flexion (2) and extension (3), and hallucis extension (2). The patients most pronounced deficits were distally, in the innervations area of the sciatic nerve; a new MRI showed thickening of the nerve from the sacral bone and through obturator foramen with oedema in the area (figures 1 and and2).2). The department of neurosurgery was contacted and advised against nerve biopsy due to the risk of nerve lesion, but recommended a PET scan. 18-Fluorodeoxyglucose-PET (FDG-PET) showed slightly increased activity in the prostate but it was assumed that this was due to hypertrophy, no malignancy was suspected. Four months later the patient reported a 5 kg weight loss and oedema of the right leg. The motor responses were unchanged but the patient was now troubled by faecal incontinence. A medullary compression syndrome was suspected and MRI showed a possible S3-affection by a process as well as thickening of the sciatic nerve and pathological signals from the right pubic bone. CT showed osteolytic/sclerosing changes in the right pubic bone and the inferior ramus of the ischium. PSA was now 7.1 but it was assumed that this was due to the intermittent self-catheterisation. 99-mTc-MDP bone scintigraphy showed intense signals from the right inferior ramus. A biopsy from the bone showed adenocarcinoma staining positive for KL-1, CK18, epithelial membrane antigen and PSA, but negative for other markers, thus diagnosing the tissue as a metastasis from a carcinoma of the prostate, Gleason 4 + 4. Trans-rectal sonography showed malignant transformation of the prostate, and it was deemed superfluous with prostate biopsies. The patient was again referred to the department of urology and treated conservatively with Zoladex (goserelin) and palliative radiotherapy. PSA before start of treatment was >11, and <0.1 after start of treatment.

Figure 1
MRI-picture. Arrow shows thickened sciatic nerve on right side.
Figure 2
MRI-picture. White arrow shows thickened sciatic nerve on right side. Dotted arrows show oedema in gluteus medius and piriformis muscles.

Outcome and follow-up

This treatment has improved the pain and the function of the right ankle but the patient still needs help to get around. The patient is still followed in the out-patient clinic at the department of urology and neurology.


These findings emphasise the importance of considering idiopathic neuropathy a preliminary diagnosis as long as a manifest cause can not be excluded.

In some cases peripheral neuropathy is the first symptom of an underlying malignancy.1 In a prospective study in patients with peripheral sensory neuropathy of unexplained cause, more than one third developed cancer, and prostate cancer in approximately 10%,2 whereas a retrospective study found lower incidence (7.5%) of cancer-related neuropathy in patients originally diagnosed with idiopathic peripheral neuropathy.3 Our patient, however, presented with motor symptoms. Neurological complications may be observed in 20% of patients with prostate cancer and are more common with advanced disease.4 Typically, the neurological complications result from metastasis to the spine with resulting paraplegia or radiculopathy. In one large series, 19% of cases of spinal cord and cauda equina compression were the consequence of spinal metastasis from prostate cancer.5 Neoplastic lumbosacral plexopathy occurs with some abdominal and pelvic malignancies. The tumour might spread along prostatic nerves into the lumbosacral plexus via perineural spread.6 In our patient, EMG helped locate the lesion to the plexus or the sciatic nerve. In a case series, four out of five patients presented with osteosclerotic metastases of prostate cancer and gait difficulties were diagnosed with motor neuropathy, whose predilection region was one of two distal motor trunks sciatic nerve.7

How may diagnostics be improved?

PSA levels are used to monitor possible prostate cancer.8 In our patient, PSA was normal throughout and only marginally raised at the time of diagnosis. Upon first visit to the department of urology, the PSA was 1.68. Eighteen months later, PSA was 4.09 and 1 year later, just before start of treatment, 9.06. Many patients with localised prostate cancer might however, have normal PSA levels,9 but changes in PSA should always raise the suspicion of prostate cancer.

Magnetic resonance neurography often identifies an abnormal increased signal in the proximal sciatic nerve in patients with extraspinal sciatica and allows more accurate diagnosis of sciatic nerve entrapment in suspected cases.10

In our case, 18-FDG-PET exam was negative. FDG-PET has limited use in diagnosis and staging of clinically organ-confined disease,11 apart from case reports.12 13 FDG-PET might be useful for detecting locally recurrent and/or metastatic disease.14 FDG-PET thus appears to have the most prognostic value for patients with prostate cancer, particularly those undergoing radical prostatectomy.15 In a retrospective study, 18-FDG-PET detected local or systemic disease in 31% of patients with PSA relapse.16 Other tracers might be more favourable, as reported for 11-C-choline compared to 18-FDG-PET,17 and 11-C-choline PET/CT have been shown to provide an added value for skeletal manifestations.18

Learning points

  • [triangle] Unusual first-manifestation of prostate cancer.
  • [triangle] Diagnostic difficult – MR-verified pathology, normal PSA and PET-negative tumour.
  • [triangle] Changes in PSA should always raise the suspicion of prostate cancer.
  • [triangle] Idiopathic progressive neuropathy should always raise the suspicion of an underlying malignancy, even when standard diagnostics fail to explain the patient's symptoms.


Competing interests None.

Patient consent Obtained.


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