The initial symptoms of GBS are often sensory. Pain in the leg or legs may occur, and is often accompanied by a tingling sensation in the feet. In most affected individuals weakness becomes noticeable within 1 to a few days and may progress rapidly. The weakness usually involves the feet and legs first, but can be more severe in the arms, the breathing muscles, or the muscles involved in swallowing and chewing. The weakness progresses to paralysis sufficient to require ventilator support for breathing in perhaps 20% of affected individuals. Improvement usually begins within 2-4 weeks and can be rapid. However, at least 15% of affected individuals have long term symptoms after recovery, such as weakness in the ankles, and a small group has very poor recovery, usually reflecting axonal loss. The peripheral nerve fibers relevant to the Guillain Barre syndrome run from the spine (or the lower part of the skull) out to the muscles, the skin, and the internal organs. They are necessary to carry the message for movement, feeling, and to produce the reflexes that doctors test with reflex hammers (such as the reflex at the knee). Each nerve fiber is very small in diameter but very long. The fibers running to the foot in a 6-footer begin within the lower part of the spine, and thus may be 31/2 feet long. Yet even the largest are only about 1/3000 of an inch in diameter. They are made up of a single long continuous cell process, called the axon, that arises from and is part of a nerve cell or neuron. Spaced every 1/100- 1/25 mm along the axon are Schwann cells. Each Schwann cell makes special wrap of membrane the surrounds the axon and is called myelin [Figurs 1].Myelin acts as an insulator that has the effect of speeding the rate of electrical impulse conduction down the fiber. Each nerve has thousands of these individual nerve fibers, in the same way that a telephone switchboard requires large numbers of wires. Normal function of each nerve fiber depends on a normal axon and normal Schwann cells and myelin, and normal function of the whole nerve in turn requires that most of the individual nevre fibers be normal. In the Guillain Barre syndrome the immune system damages individual nerve fibers. In most instances the brunt of the immune attack is borne by the mylein, so that myelin is damaged and destroyed in some Schwann cells [Figure 2]. Removal of even a single myelin sheath can prevent passage of electrical signals along the nerve, and thus render it functionless. This process is called demyelination. Recovery of function by remyelination can occur surprisingly quickly - within days - once the immune attack stops, usually within 1 month in GBS. New myelin can be laid down within days, yet not every affected individual recovers rapidly or completely. The reason is that some demyelinated axons don't survive, but instead break down from the site of the immune attack all the way to their end. This breakdown of the axon all the way to its target happens whenever an axon is cut, a process named afer its first describer in the 1850's, Augustus Waller, and is thus termed Wallerian degeneration. After Wallerian degeneration, recovery requires not just remyelination, but regeneration of the axon, a notoriously slow process that at best advances about an inch/month. In addition, in a form of the Guillain Barre syndrome that is less frequent in North America, the axon may be the primary target of the immune attack (axonal GBS). In this instance the axon is cut by the immune attack, and the region distal to the site of attack breaks down.