<unk>  (or polyradiculoneuropathy) is considered an autoimmune disorder destroying myelin, the protective covering of the nerves. Typical early symptoms are "tingling" (sort of electrified vibration or paresthesia) or numbness in the extremities, frequent (night) leg cramps, loss of reflexes (in knees), muscle fasciculations, "vibration" feelings, loss of balance, general muscle cramping and nerve pain.<unk>  is extremely rare but under-recognized and under-treated due to its heterogeneous presentation (both clinical and electrophysiological) and the limitations of clinical, serologic, and electrophysiologic diagnostic criteria. Despite these limitations, early diagnosis and treatment is favoured in preventing irreversible axonal loss and improving functional recovery. There is a lack of awareness and treatment of<unk> . Although there are stringent research criteria for selecting patients for clinical trials, there are no generally agreed-upon clinical diagnostic criteria for<unk>  due to its different presentations in symptoms and objective data. Application of the present research criteria to routine clinical practice often misses the diagnosis in a majority of patients, and patients are often left untreated despite progression of their disease.<unk>  has been associated with diabetes mellitus, HIV infection, and paraproteinemias. Variants with paranodal autoantibodies Some variants of<unk>  present autoimmunity against proteins of the node of Ranvier. These variants comprise a subgroup of<unk>  neuropathies with IgG4 autoantibodies against the paranodal proteins neurofascin-155, contactin-1 and caspr-1. These cases are special not only because of their pathology, but also because they are non-responsive to the standard treatment. They are responsive to Rituximab instead. Also some cases of combined central and peripheral demyelination (CCPD) could be produced by neurofascins. Autoantibodies of the IgG3 Subclass in<unk>  Autoantibodies to components of the Ranvier nodes, specially autoantibodies the Contactin-associated protein 1 (CASPR), cause a form of<unk>  with an acute "Guillain-Barre-like" phase, followed by a<unk>  phase with progressive symptoms. Different IgG subclasses are associated with the different phases of the disease. IgG3 Caspr autoantibodies were found during the acute GBS-like phase, while IgG4 Caspr autoantibodies were present during the<unk>  phase of disease.
Chronic inflammatory demyelinating polyneuropathy
Tropical neuropathy
Critical illness polyneuropathy
Paraneoplastic cerebellar degeneration
Hereditary motor and sensory neuropathy
Alcoholic polyneuropathy
CMV polyradiculomyelopathy
Peripheral mononeuropathy