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Case description
A 60-year-old woman, born in Sri Lanka and with long-standing diabetes, developed subacute onset pain. The pain had started in the left lower leg, but within a few weeks extended to all four limbs, thorax and abdomen, though sparing the head. She described the pain as ‘like pin and needles’ with burning sensations. It was constant, with fluctuating intensity over day and night, up to 10 out of 10. There were no associated neurological or systemic symptoms, and no autonomic symptoms. Two months after symptom onset, she was admitted under rheumatology. An exhaustive rheumatological workup was normal, including immunological blood workup, MR scans of all skeletal muscles and sacroiliac joints, and X-rays of hands, knees and feet.
We met her for the first time at our neuromuscular clinic 3 months after symptom onset.
Vital observations and general examination were normal, and cranial nerves were intact. There was no limb nor axial weakness. Deep tendon reflexes were normal. There were no cerebellar signs and gait was normal. Sensory testing (discriminative touch, vibration, temperature, pain and proprioception) was preserved, apart from a diffuse hyperalgesia and allodynia.
Question 1: what is the differential diagnosis?
A subacute diffuse pain syndrome has a broad differential diagnosis, including rheumatological pathology, fibromyalgia, toxic-induced myopathies and various other conditions. The associated allodynia/hyperalgesia suggests a neurological origin. At this stage, the main hypothesis is a small fibre neuropathy, which would explain the normal epicritic sensibility (discriminative touch, vibration and proprioception). Patients with small fibre neuropathy usually report reduced or absent sensitivity to cold, heat and noxious stimuli, which was not the case here. However, sensory loss can occasionally be masked by simultaneous hyperalgesia and allodynia. Moreover, the patient had no obvious symptoms of dysautonomia though this can be compatible with small fibre neuropathy, when C fibres are preserved. A central nervous system lesion, particularly in the …
Footnotes
Contributors TB and VL drafted and revised the manuscript. MT revised the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Provenance and peer review. Not commissioned. Externally peer reviewed by David Bennett, Oxford, UK.
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