Disease relevance of Polyradiculoneuropathy

• We found markedly increased serum levels of IL-2 in patients with Guillain-Barré syndrome and to a much lesser extent, in patients with chronic idiopathic demyelinating polyradiculoneuropathy [1].
• Guillain-Barré syndrome (GBS), chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), and multiple sclerosis (MS) are disorders with presumed immunopathogenesis [2].
• Coexistence of CNS and PNS chronic demyelination has been rarely demonstrated in chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) and in MS, but the occurrence of acute polyradiculoneuropathy in a patient with MS is even more unusual [3].

High impact information on Polyradiculoneuropathy

• Factors involved in the development of an insidious polyradiculoneuropathy in association with a procainamide-induced, lupuslike syndrome were explored [4].
• Systemic lupus erythematosus with anti-Hu antibodies and polyradiculoneuropathy [5].
• In contrast to SP duration, which proved to be an independent variable giving supplementary information over the usual CMCT measurement, SP onset latency correlates well with CMCT and peripheral nerve conduction slowing, as in polyradiculoneuritis [6].
• The distribution of P2 in the human nervous system parallels the incidence and severity of lesions in acute polyradiculoneuritis [7].
• The increase in hydrophobic amino acids and lysine in CSF from patients with acute polyradiculoneuropathy is consistent with transudation over the blood-CSF barrier following an infection [8].

Chemical compound and disease context of Polyradiculoneuropathy

• Cyclosporin A in the treatment of chronic demyelinating polyradiculoneuropathy [9].
• Severe sensorimotor polyradiculoneuropathy after ingestion of ethylene glycol [10].
• Suramin is unique in causing subacute, demyelinating polyradiculoneuropathy [11].
• A significant increase in apoptosis was also induced by cerebrospinal fluid samples from patients with acute polyradiculoneuropathy, suggesting the presence of neurotoxic factor(s) here also [12].
• The close temporal correlation between clinical relapse and recurrence of the IgG paraprotein and its permanent absence in stable clinical remission after carmustine treatment suggest a causal relationship between the paraprotein and the polyradiculoneuropathy [13].

Biological context of Polyradiculoneuropathy

• Hereditary neuropathy with liability to pressure palsy (HNPP) is an inherited disease caused by a deletion or point mutation in the peripheral myelin protein 22 (PMP22) gene, which may manifest as a recurrent polyradiculoneuropathy [14].

Anatomical context of Polyradiculoneuropathy

• Class and IgG subclass distribution of antibodies against peripheral nerve myelin in sera from patients with inflammatory demyelinating polyradiculoneuropathy [15].
• We explored the expression of TACE (ADAM-17) in sciatic nerves from Lewis rats with experimental autoimmune neuritis (EAN), an animal model of the Guillain-Barré syndrome (GBS), an immune-mediated polyradiculoneuropathy [16].

Gene context of Polyradiculoneuropathy

• Recurrent polyradiculoneuropathy and PMP22 defects [14].
• Antibodies in sera from patients with inflammatory demyelinating polyradiculoneuropathy react with ganglioside LM1 and sulphatide of peripheral nerve myelin [17].
• This case suggests that acute polyradiculoneuropathy may represent a rare but serious side-effect of statin treatment [18].
• A 40-year-old man with cervical dystonia developed an acute inflammatory demyelinating polyradiculoneuritis after botulinum toxin type A treatment [19].
• This chimpanzee's ascending, symmetrical, monophasic, flaccid paralytic illness, with albuminocytologic dissociation in CSF, and recovery following supportive treatment, was characteristic of inflammatory polyradiculoneuropathy, known as Guillain-Barré syndrome in human beings [20].

References