LAUSR

SIR, Peripheral nerve involvement is frequent in systemic vasculitis, typically either mononeuritis multiplex or sensorimotor peripheral polyneuropathy. However, these are distinctly uncommon in GCA [1, 2] and should prompt consideration of alternative causes of neuropathy and reconsideration of the underlying diagnosis of GCA. We present three cases of peroneal neuropathy in patients with recently diagnosed GCA presenting to our institution over a 2 month period. Patient 1 was a 57-year-old male who presented initially with bitemporal headache, recurrent amaurosis fugax, bilateral shoulder girdle pain and weight loss of 12 kg. Both temporal arteries (TAs) were tender. ESR was 26 mm/h and CRP was 16 mg/l. TA US demonstrated a positive halo sign. TA biopsy showed adventitial and intimal inflammatory infiltrates with no giant cells. He was diagnosed with GCA and had a complete response to 60 mg prednisolone. He re-presented 3 months later on a tapering dose of 20 mg prednisolone with acute left foot drop. He reported paraesthesia and a cold sensation on the dorsum of the foot. On examination, ankle dorsiflexion and eversion demonstrated reduced power of Medical Research Council (MRC) grade 3/5. He had no other symptoms and the remainder of the neurologic exam was normal. ESR was 6 mm/h and CRP was 1 mg/l, the remainder of his laboratory workup, including haemoglobin A1c, serum protein electrophoresis, ANCAs, ANA and viral serology, was normal. A nerve conduction study (NCS) confirmed a compressive left common peroneal neuropathy at the knee. He was managed conservatively with improvement in power to MRC grade 4+/5. Patient 2 was a 64-year-old man who presented initially with right temporal headache, decreased right eye visual acuity, weight loss of 19 kg and night sweats. Both TAs were normal, fundoscopy revealed a pale swollen right optic disk consistent with anterior ischaemic optic neuropathy. ESR was 56 mm/h and CRP 156 was mg/l. TA US demonstrated bilateral halo sign, CT angiogram of the head, neck and thorax was normal and TA biopsy failed to sample the artery. He was diagnosed with GCA and had a complete response to i.v. methylprednisolone. One month later he re-presented on 60 mg prednisolone reporting a left foot drop and numbness on the dorsum of the foot, which he believed may have been present since disease onset. On examination, left ankle dorsiflexion and eversion demonstrated reduced power of MRC grade 3/5. He had no other symptoms. ESR at this stage was 7 mm/h and CRP was 2 mg/l. The remainder of his laboratory workup was normal, aside from an ANA of 1:400 with nucleolar pattern and a negative extractable nuclear antigen panel. MRI of the brain and lumbosacral spine was normal. An NCS confirmed a compressive common peroneal neuropathy at the knee. He was managed conservatively with improvement in power to MRC grade 4+/5. Patient 3 was a 55-year-old man. He initially presented with bitemporal headache, recurrent left amaurosis fugax and bilateral shoulder girdle pain. The left TA was tender. ESR was 70 mm/h and CRP was 48 mg/l. TA US was normal. TA biopsy demonstrated an adventitial inflammatory infiltrate with no giant cells. He was diagnosed with GCA and commenced on prednisolone 60 mg with good response. He re-presented 2 months later on 20 mg prednisolone with sudden right foot drop and numbness on the dorsum of the foot. He reported onset after a prolonged period of sitting with crossed legs. On examination, right ankle dorsiflexion and eversion had reduced power of MRC grade 4/5. He had no other symptoms. ESR was 4 mm/h and CRP was 1 mg/l; the remainder of his laboratory workup was normal. His symptoms resolved over 2 weeks and an NCS performed after resolution was normal. Our case series highlights the importance of the correct determination of the aetiology of any new symptoms in patients with pre-existing vasculitis. The three patients described here were ultimately diagnosed with compressive common peroneal neuropathies, two most likely due to rapid weight loss and the other due to prolonged leg crossing. A prior diagnosis of GCA does not preclude the development of non-vasculitic neuropathies, including compressive neuropathies. The occurrence of peripheral neuropathy due to direct vasculitic involvement from GCA is disputed, but if it exists, it is rare [1]. Mononeuritis multiplex, however, is a characteristic feature of other forms of systemic vasculitis, in particular polyarteritis nodosa and the ANCA-associated vasculitidies [2]. The new onset of a mononeuropathy in these patients raised the possibility of an alternative diagnosis to GCA. However, careful clinical and laboratory evaluation revealed no evidence of other forms of systemic vasculitis; these cases also highlight the utility of electrophysiologic studies in the assessment of such patients with suspected peripheral nerve involvement. This distinction is an important one, as the presence of active systemic vasculitis other than GCA would have warranted treatment escalation with cyclophosphamide or rituxumab, with the attendant potential for adverse events this might entail [3, 4].