Guillain Barre Syndrome

Guillain Barre syndrome is an inflammatory disorder that damages the body's immune system. The condition results in weakness and numbness in extremities and finally, paralysis. Though the exact cause of Guillain-Barre syndrome is highly debated, the condition could be brought on by something as common as a stomach flu...
Guillain-Barré syndrome is a health condition that is the result of an immune response to foreign antigens. The response to infectious agents damage host nerve tissues in a sort of antigenic mimicry and the targeted gangliosides are in fact complex glycosphingolipids. Trigger factors like Campylobacter jejuni are the primary antecedent infections that spark the onslaught of Guillain-Barré syndrome. The result is a ruthless attack / inflammation of myelin that brings on muscle paralysis. The condition is commonly accompanied by distinct autonomic disturbances.

Guillain Barre Disease

Guillain-Barré syndrome is a condition that refers to acute inflammatory demyelinating polyneuropathy or AIDP. It is an autoimmune disorder that affects the peripheral nervous system. The condition is triggered by an infectious process and is clinically included within peripheral neuropathies. The condition manifests in the form of ascending paralysis and a weakness in the legs. The pain and numbness spreads to the upper limbs and reaches as far as the face. The total collapse of the deep tendon reflexes can only be addressed via prompt treatment. There have been instances of the condition culminating in death, in the case of severe pulmonary complications and/or dysautonomia setting in.

Causes of Guillain Barre Syndrome

Guillain-Barré syndrome is primarily the result of immuno-pathological reaction and rarely, serum sickness. This autoimmune disorder has six subtypes which include acute inflammatory demyelinating polyneuropathy or AIDP, Miller-Fisher syndrome or MFS, acute motor axonal neuropathy or AMAN, acute motor sensory axonal neuropathy or AMSAN, acute panautonomic neuropathy and Bickerstaff’s brainstem encephalitis or BBE.

The primary causes or triggers include:
  • Autoimmune response against Schwann cell membranes.
  • Attack on the motor nodes of Ranvier, the axoplasm of peripheral nerves.
  • Attack on sensory nerves, leading to severe axonal damage.
  • Accompanying cardiovascular involvement and dysrhythmias.
  • Irregular hyperintense lesions in the brainstem - pons, midbrain and medulla.
The patients and doctors bank heavily on physiotherapy. The treatment plan, at all times, involves a detailed and dedicated progressive training program and guidance to improve functional movement. The role of the Speech and Language Therapist is very important for the patient to regain communication ability, after a tracheostomy. Although on record is the fact that with the help of timely action recovery ideally begins from the 4th week onwards, the phase could well stretch beyond a year.

Guillain Barre Syndrome Treatment

The disorder is characterized by:
  • Lower limb weakness.
  • Dysesthesias in the arms and facial muscles.
  • Bulbar weakness in the lower cranial nerves.
  • Oropharyngeal dysphagia.
  • Respiratory difficulties.
  • Sensory loss, loss of proprioception and areflexia.
  • Loss of sensation, with regards to pain and temperature.
  • Bladder dysfunction.
  • Spinal cord disorder.
  • Fever and fluctuations in blood pressure.
  • Paralysis and central pontine demyelination.
Recovery, in the case of Guillain-Barré syndrome, is possible only if remyelination occurs. However, on the contrary, axonal degeneration occurs, which is again a condition that can be corrected only when an opposite 'regeneration' is triggered. Recovery is not only slow, but also only after a major residual damage. Myelin and axon loss are the typical features of the condition. The condition is addressed after a thorough clinical analysis with the help of plasmapheresis and/or intravenous immunoglobulins. Supportive care plays a key role in recovery and in strengthening the patient's resolve and immunity to regain previous functional capacity. Supportive care demands monitoring of vital functions. The treatment options include:
  • High-dose intravenous immunoglobulins.
  • Plasmapheresis.
  • Physical Therapy, directed towards ADL independence.
  • Glucocorticoids, in some cases.

By Gaynor Borade
Published: 5/8/2009
 
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