Disease modifying treatment available:
Time critical diagnosis and management:
Lateralising:
Guillain-Barre syndrome (GBS) describes an acute, monophasic, immune-mediated polyradiculoneuropathy.
| Subclassifications | Epidemiology | Clinical features |
|---|---|---|
| Acute inflammatory demyelinating polyradiculopathy | None | |
| Miller-Fisher syndrome | None | |
| Bickerstaff brainstem encephalitis | None | |
| Acute motor axonal neuropathy | None |
In many cases, GBS follows an infection. The most common infections implicated are Campylobacter jejuni, hepatitis E, CMV, EBV and Mycoplasma pneumoniae. Zika virus infection (and possibly vaccination), dengue and chikungunya virus have also been implicated but are less common in the UK. The preceding infection may in part determine the severity of disease and there is evidence that GBS following Campylobacter jejuni infection follows a more severe course. In a significant proportion of patients without clinical features of an infection and immunological response to an infection can be demonstrated.
The electrophysiological signatures and clinical features of the disease vary between populations. A demyelinating pattern is most common but in Asia axonal forms and motor-only variants are relatively more common.
Symptoms typically develop days to weeks after an infection (median 10 days). Back pain and acroparaesthesia are typically the earliest symptoms reported.
The disorder is almost always associated with areflexia or hyporeflexia and while this may not be present initially it normally develops over the course of the illness. Reports of patients with preserved or exaggerated reflexes have been published. Presumably MRIs of the neuraxis in these patients were normal excluding co-existing parainfectious myelopathy or encephalopathy.
In patients with ascending sensorimotor features and preserved reflexes myelopathy should be considered.
Guillain-Barre syndrome may cause the following:
| Laboratory Investigation | Result |
|---|