Ieva Navickaitė¹

¹ Lithuanian University of Health Sciences, Academy of Medicine, Faculty of Medicine, Kaunas, Lietuva

Abstract

Guillain–Barré syndrome (GBS) is a postinfectious neurological disorder characterized by rapidly progressive, symmetrical weakness of the extremities and areflexia or hyporeflexia. GBS is a rare disease with an annual global incidence of approximately 1–2 per 100,000 person-years. Two-thirds of GBS cases are preceded by infection of either respiratory or gastrointestinal tract. Molecular mimicry between microbial and nerve antigens is thought to be the main cause of this disorder. Specific antibodies bind to their targets in the nervous tissue and induce its lesion. GBS usually starts with weakness and sensory signs in the legs that progress to the arms and cranial muscles. However, GBS can also present in an atypical manner. Miller Fisher syndrome is characterized by ophthalmoplegia, areflexia and ataxia. In some cases, weakness can be localized to specific regions of the body such as the face (bilateral facial palsy with paraesthesias), upper limbs (pharyngeal–cervical–brachial weakness) or lower limbs (paraparetic variant). The diagnosis of GBS is based on clinical history, neurological examination, CSF examination and electrodiagnostic studies. Both intravenous immunoglobulin and plasma exchange are equally effective treatments for GBS. An important part of GBS treatment is early detection and management of various complications including respiratory failure, wide range fluctuations of the arterial blood pressure and pulse as well as other autonomic disturbances. Approximately 80% of patients with GBS are able to walk independently 6 months after disease onset. The most common long-term residual complications include neuropathic pain, weakness, fatigue and depression. Death occurs in 3–7% of cases, most commonly due to cardiovascular and respiratory complications.

Keywords: Guillain–Barré syndrome; pathogenesis; diagnostic criteria; treatment; complications.