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Guillain–Barré syndrome (also called "GBS") is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. [3] Typically, both sides of the body are involved, and the initial symptoms are changes in sensation or pain often in the back along with muscle weakness, beginning in the feet and hands, often spreading to the arms and upper body. [3]
The next morning he had generalised aches, the day after sharp abdominal pain and a fever increasingly raged. Bedridden in pain, he gradually lost the ability to move, to the point, 8 days later of just flickering his eyes or twitch his hands. His cognition was not affected. The symptoms all fit with Guillain–Barré syndrome. His minimal ...
His main symptoms were fevers; symmetric, ascending paralysis; facial paralysis; bowel and bladder dysfunction; numbness and hyperesthesia; and a descending pattern of recovery. He was diagnosed with poliomyelitis and underwent years of therapy, including hydrotherapy at Warm Springs, Georgia.
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Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically, there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier. [citation needed]
There is certainly overlap between Guillain–Barré syndrome, Miller Fisher syndrome and Bickerstaff brainstem encephalitis, as well as other conditions associated with anti-ganglioside antibodies such as chronic ophthalmoplegia with anti-GQ1b antibody and the pharyngo-cervico-brachial variant of GBS.
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Autoantibodies to components of the Ranvier nodes, specially autoantibodies the Contactin-associated protein 1 , cause a form of CIDP with an acute "Guillain-Barre-like" phase, followed by a chronic phase with progressive symptoms. Different IgG subclasses are associated with the different phases of the disease.