Guillain-Barré Syndrome
Guillain-Barré Syndrome (GBS) is a rapidly progressive polyradiculoneuropathy that can lead to acute or subacute paralysis. This disorder is marked by a raise in the level of cerebrospinal fluid (CSF) protein in the absence of CSF pleocytosis.
With many distinct variants, GBS is commonly seen in much of the Western world in the form of Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) characterised by varying degrees of secondary axonal damage.
John B. Winer, from Queen Elizabeth Hospital in Birmingham, describes the clinical features of the disorder as pyramidal in distribution with ankle dorsiflexion and knee and hip flexion often severely affected.
Aberrant macrophage activity has been suggested by various pathological studies to be the main instrument of causing damage to the nerves but various antibodies may also target myelin or axon tissues.
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Neurologic symptoms need to be given primary consideration in the diagnosis and treatment of the condition with early assessments revealing prolonged distal motor latency, delayed F-waves and transient conduction blocks.
As mentioned by Willison et al., nerve conduction studies can help to support diagnosis by discriminating between axonal and demyelinating subtypes; nerve conduction abnormalities are most prominent two weeks after the onset of weakness.
The authors recommend the following measures of supportive care to prevent and manage complications associated with GBS – cardiac and haemodynamic monitoring, prophylaxis for deep vein thrombosis, management of possible bladder and bowel dysfunction, early initiation of physiotherapy and rehabilitation, and psychosocial support.
A comprehensive rehabilitative programme should be implemented for providing stability and support to the feet in a corrected posture.
Stretching exercises in conjunction with foot supportive devices can also help treat some of the secondary biomechanical effects of GBS; this is achieved by stabilising the medial longitudinal arch and improving ankle range of motion to reduce load on the soft tissue supportive structures around the ankle.
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References:
- Willison, H. J., Jacobs, B. C., van Doorn, P. A. (2016) Guillain-Barré syndrome. The Lancet 388: March 2016. DOI: 10.1016/S0140-6736(16)00339-1
- Winer, J. B. (2014) An Update in Guillain-Barré Syndrome. Autoimmune Diseases: January 2014, Vol. 2014. DOI: 10.1155/2014/793024
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