Acute sensory inflammatory demyelinating polyneuropathy and central diabetes insipidus

Abstract

Guillain-Barre syndrome (GBS) is characterized by acute, progressive monophasic course with a predominance of motor disorders in typical cases; it develops due to an aberrant immune response in some viral and bacterial infections. As ganglioside complexes are the direct cause of acute dysimmune neuropathy, it is assumed that the combined damage of peripheral nerves structure, and neurohypophysis and hypothalamus, may be based on similar immunopathogenetic mechanisms. Here we present the first case of a patient with diabetes insipidus and acute inflammatory dysimmune damage to sensory and autonomic peripheral nerve fibers due to secondary hypothalamic-pituitary system lesion. Due to the long-term persistence of arthralgias, accompanied by a low-grade fever and a single positive denatured DNA IgG antibodies test, atypical variant of GBS, hypophysitis, we differentiated the patient's condition with systemic rheumatic diseases, primary and secondary vasculitis. Those nosologies were not confirmed during the examination and observation; porphyrias and thyroid gland damage as etiological factors of nervous system damage were also excluded.This case report demonstrates the need for a prompt determination of the nature of the pathological process that causes damage to peripheral nerves' fibers and the neuroendocrine system to select an adequate treatment strategy.

Keywords

• guillain-barre syndrome
• diabetes insipidus
• neuropathic pain