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Poststreptococcal neuropathy
  1. SIMON J HICKMAN,
  2. RICHARD B GODWIN-AUSTEN
  1. Department of Neurology
  2. Department of Neurophysiology, University Hospital, Queen’s Medical Centre, Derby Road. Nottingham NG7 2UH, UK
  1. Dr Richard B Godwin-Austen (emeritus consultant), Department of Neurology, University Hospital, Queen’s Medical Centre, Derby Road, Nottingham NG7 2UH, UK.
  1. LESLEY M HENDERSON
  1. Department of Neurology
  2. Department of Neurophysiology, University Hospital, Queen’s Medical Centre, Derby Road. Nottingham NG7 2UH, UK
  1. Dr Richard B Godwin-Austen (emeritus consultant), Department of Neurology, University Hospital, Queen’s Medical Centre, Derby Road, Nottingham NG7 2UH, UK.

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Streptococcal infection can lead to a wide range of sequelae. Peripheral nervous system injury is not well known as one of its possible complications. We report a case with a typical history for a poststreptococcal vasculitis causing an axonal neuropathy of the right common peroneal nerve.

A 17 year old girl was referred by her general practitioner due to the sudden onset of numbness on the dorsum of her right foot associated with stamping her foot on walking. She had been well until 6 weeks previously when she developed tonsillitis for which she received a 1 week course of oral penicillin V. She was also taking minocycline for mild acne. As her throat recovered she developed symmetric distal polyarthralgias and night sweats which persisted as the numbness developed. There was no history of trauma or compression of the common peroneal nerve at the neck of the fibula.

On examination she had a right foot drop with weakness of ankle dorsiflexion (Medical Research Council grade 3/5). There was sensory loss in the distribution of the common peroneal nerve. She was otherwise neurologically intact with normal reflexes. There were no skin lesions and her joints were quiescent.

She had an erythrocyte sedimentation rate of 87mm/h, a C reactive protein concentration of 112 mg/l and an antistreptolysin-O titre (ASOT) of 1600 units/ml. Autoimmune screen, antineuronal antibodies, and cryoglobulins were all negative apart from an atypical perinuclear antineutrophil cytoplasmic autoantibody (p-ANCA) IgG titre of 160. Renal function was normal and there were no casts on urine microscopy.

Nerve conduction studies showed uniform reduction of compound motor action potential amplitude from all sites of stimulation of the right peroneal nerve with mild slowing of conduction velocity. Sensory studies disclosed an absent response from the right superficial peroneal nerve (table). F Wave late responses were normal in the right tibial (with true H response) and left peroneal nerves, but delayed and inconstant in the right peroneal nerve. Needle EMG was normal in the right tibialis posterior muscle providing evidence against the lesion being at the L5 root level. There were, however, only two units recruited from the right tibialis anterior with small responses of long duration and no spontaneous activity. The tests confirmed a mainly axonal neuropathy of the right common peroneal nerve with no evidence of entrapment.

Table Nerve conduction study results confirming a mainly axonal neuropathy of the right common peroneal nerve

Because of its link with autoimmune disease the minocycline was stopped although it was not thought to have precipitated her condition.1 She was treated initially with oral prednisolone but developed a vasculitic skin rash over the dorsum of both feet. A biopsy showed deposits of C3 and fibrin in the walls of some superficial dermal vessels consistent with a vasculitis. A 3 day course of intravenous methylprednisolone was followed by azathioprine and prednisolone. The decline in her ASOT and inflammatory markers mirrored the improvement in her systemic symptoms although on stopping immunosuppression after a 2 month course she developed erythema nodosum necessitating further steroid therapy. Her foot drop has improved although she has persistent sensory loss.

In conclusion this is a 17 year old girl with a typical poststreptococcal syndrome associated with constitutional symptoms, arthralgias, microscopic polyangiitis, and later erythema nodosum. As part of her illness she developed a mononeuropathy with no evidence to suggest a specific antineuronal process and likely to be due to a necrotising vasculitis. It is unlikely that the streptococcal infection has unmasked a connective tissue disorder due to the negative autoimmune screen apart from the atypical p-ANCA and her improvement as the ASOT fell. Vasculitis after streptococcal infection has been well described.2 There are also reports of vasculitis causing neuropathies often as part of a connective tissue disorder.3 Surprisingly, streptococcal infection is not a well known antecedent of peripheral nervous system disease, even Guillain-Barré syndrome. There is a report of a 22 year old man who developed a flaccid tetraparesis, raised creatine kinase, and immune complex-mediated rapid progressive glomerulonephritis after a group A streptococcal infection. A sural nerve biopsy showed an inflammatory axonal neuropathy.4 There are also two cases of mononeuritis multiplex reported after β-haemolytic streptococcal infections.2 5 Biopsy of the sural nerve from one of these patients revealed a necrotising vasculitis. Poststreptococcal immune-mediated vasculitis should therefore be more widely recognised as one of the causes of a vasculitic neuropathy.

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