Acute sensorimotor polyneuropathy as an early sign of polyarteritis nodosa. A case report.

We examined a patient aged 31 who had a sudden burning paraesthesia, pain and numbness in the lower legs together with an increased temperature of 39°C. Clinical examination showed asymmetrical sensory polyneuropathy more clearly seen in the lower legs and the left wrist, with high ESR (up to 44 mm/h), leukocytosis, slight anemia and proteinuria. CSF was normal. After three weeks the temperature suddenly increased again up to 39°C and severe flaccid distal tetraparesis was seen more clearly with foot drop in the left lower leg and dense oedema in the left wrist, purple cyanosis and haemorrhagic foci appeared on the skin of the toes, feet, lower legs and left wrist. ESP increased up to 65 mm/h, CK was 200 IU (normal ≤ 190 IU) and hypergammaglobulinaemia developed. An EMG study showed sensorimotor, mainly axonal, polyneuropathy with different degrees of involvement of some nerves and with conduction block in the left ulnar nerve. Muscle biopsy revealed findings of inflammatory vasculitis that resembled polyartheritis nodosa with secondary denervation atrophy and non-specific myositis. The patient was treated with high doses of prednisolone, dexamethasone and cyclophosphamide with plasmapheresis. Motor disturbances and pain decreased and the patient began walking with a stick. However, the necrosis of the toes gradually progressed to dry gangrene and amputations of the toes were carried out three months after the disease began. At that time the patient had the clinical features of multisystem disease with progressive heart, lung, liver and kidney failure. The patient died suddenly of pulmonary artery thrombo-embolism a year after the onset of the disease. An autopsy confirmed the diagnosis of polyarteritis nodosa (PN). Thus, in this patient the asymmetrical sensory polyneuropathy progressed rapidly in symmetrical sensorimotor peripheral polyneuropathy which preceded the clinical multisystem involvement in polyarteritis nodosa.

Blood test detecting autoantibodies to N-methyl-D-aspartate neuroreceptors for evaluation of patients with transient ischemic attack and stroke.

BACKGROUND: Stroke is a multisystemic disorder that includes mechanisms of thrombosis and neurotoxic coupling. Key metabolites of the molecular cascade following biochemical events appear simultaneously in brain tissue, the blood-brain barrier, and brain vessels, activating the immune system and generating autoantibodies (aAbs) to brain-specific antigens. We developed an ELISA blood test to measure aAbs to a subtype of N-methyl-D-aspartate (NMDA) receptors, which are the key markers of neurotoxicity underlying cerebral ischemia. We investigated the diagnostic accuracy of serum aAbs to NR2A/2B, a subtype of NMDA receptors, in assessing transient ischemic attack (TIA) and ischemic stroke (IS) and its ability to distinguish cerebral ischemia from intracerebral hemorrhage (ICH). METHODS: Autoantibodies to NR2A/2B were measured in 360 serum samples: 105 from TIA/stroke patients and 255 from controls, including patients with controlled hypertension/atherosclerosis and gender- and age-matched healthy individuals. RESULTS: Patients with TIA (n = 56) and acute IS (n = 31) had significantly higher NR2A/2B aAb concentrations than controls (P <0.0001). The test sensitivities for TIA and IS were 95% and 97%, respectively, and predictive values were 86% and 91% at a cutoff point of 2.0 micro g/L. The area under the ROC curve was 0.99. Monitoring NR2A/2B aAbs within 72 h differentiated IS and ICH (P <0.001) and was confirmed by magnetic resonance imaging and computed tomography. CONCLUSIONS: NR2A/2B aAbs are independent and sensitive serologic markers capable of detecting TIA with a high posttest probability and, in conjunction with neurologic observation and neuroimaging, ruling out ICH. The test may help assess risk of TIA in routine general practice and may potentially be useful in assisting diagnosis of acute IS in the emergency setting.