A 36-year-old woman, with no previous history, who started with paraesthesia in the thumb of the right hand followed, 2 days later, by weakness in pincer movement. Two days later, she developed dorsiflexion paresis of the left foot and painful paresthesia on the dorsum of the left foot. She was admitted one week after the start of the week of evolution, with grade 3 paresis on the Medical Research Council (MRC) scale of the right opponens and abductor pollicis brevis (ACP) and grade 4 MRC of the muscles dependent on the left external popliteal sciatic muscle (CPE) together with tactile and painful hypoaesthesia in the first and second fingers of the right hand and on the dorsum of the left foot. He was in good general condition with no fever, skin lesions or adenopathies. Five days after admission, new neurological alterations appeared, consisting of grade 3 MRC paresis of the deltoid and left triceps brachii and paraesthesia in the external face of the left arm and both calves.
Complementary studies performed included erythrocyte sedimentation rate (ESR), haemogram, elemental biochemistry of blood and urine, cerebrospinal fluid (CSF) study, coagulation study including platelets, mean platelet volume, prothrombin time, International Normalised Ratio (INR) and fibrinogen, proteinogram, immunoglobulins, complement C3 and C4 fractions, cryoglobulins, antibody antibody antibody, antibody antibody antibody, immunoglobulin antibody, antibody antibody antibody antibody, antibody antibody antibody antibody, antibody antibody antibody antibody, cryoglobulins, antinuclear antibodies (ANA), anti-neutrophil cytoplasm antibodies (ANCA), anti-cardiolipin antibodies IgG and IgM and anti-ganglioside GM1 and GD1b, rheumatoid factor, serology for lues (RPR), Borrelia burgdorferi and hepatitis B and C, Mantoux, electrocardiogram (ECG), chest X-ray, brain, thoracic and abdominal magnetic resonance imaging (MRI). The findings of these examinations were within the normal range.
During admission, two neurophysiological studies were performed, as detailed in table 1. The first, performed 9 days after the onset of symptoms, highlighted the absence of motor potential (MP) of the left SPC and a reduction in the amplitude of the right median MP with wrist, elbow and axillary stimuli compared to that obtained with palmar stimulation. The electromyogram (EMG) of the right PCA showed a simple maximal effort pattern with few motor unit potentials (MUPs) of normal characteristics and no spontaneous activity. No spontaneous or voluntary activity was recorded in the left tibialis anterior (TA). In the second study performed at 15 days of evolution, changes in the sensory conduction of several nerves, which had previously shown no alterations, were observed. These included a reduction in the amplitude of the sensory potential of the left superficial peroneal nerve, absence of sensory responses in the sural nerves and in the right median nerve on stimulation of the third finger, and a decrease in the amplitude of those obtained from the first and second fingers. As in the first study, no PMs were obtained from the left SPC. The amplitude of the PMs of the right median was reduced, including that corresponding to stimulation on the palm, which had decreased with respect to that of the previous study. EMG showed spontaneous activity in the form of fibrillations and positive waves, abundant in the right PCA and scarce in the left TA and pedio. As in the previous study, the H-reflex and F waves of ulnar, posterior tibial, left medial and right CPE were normal and no proximal motor conduction blocks were observed in the left medial and both ulnar nerves, with normal values up to Erb's point.

A biopsy of the left sural nerve showed axonal degeneration and perivascular inflammatory infiltrate compatible with vasculitis infarction.

Treatment with 60 mg/day of prednisone was started, with subjective improvement of muscle weakness and painful paraesthesias. Subsequently, the prednisone dose was gradually reduced. At 9 months, 45 mg every other day, improvement of paresthesias in the lower extremities and proximal strength in the left upper extremity. Sensory-motor deficit persisted in the right hand and marked paresis in the left EPC territory. A third neurophysiological study performed at 9 months showed no significant changes with respect to the previous one, except for the reappearance of the low-amplitude sensory potential in the right sural nerve. In the EMG, moderate spontaneous activity persisted in the right PCA and left AT, with markedly deficient maximal effort patterns and PUMs with signs of active, irregular (polyphasic and polyturns) and unstable reinnervation.