Ephaptic and ectopic transmissions are abnormal signals from the central nervous system. As MS patients experience disease progression, they accrue damage to their central nervous system. Axons break and lesions form. Research shows that axon breakage occurs before myelin loss and lesion formation. As nerves lose their myelin coating, they start shorting out and the transmissions don't get to their destination.
Aside from the MS exacerbation or flare, there are other types of situations that cause temporary symptoms.
Uhthoff's Phenomenon is the worsening of symptoms when the body is overheated. It seems to cause problems with nerve conduction, adding 'static' to the signal.
Paroxysmal symptoms of MS are temporary neurological disturbances. They're like MS attacks, but they're short lived - anywhere from a few seconds to a few minutes. However, they can occur several times a day. They're caused either by ectopic or ephaptic transmission. As the nerves lose their myelin coating, they transmit poorly or 'short out,' meaning that the axons are no longer able to carry the electrical impulse. Researchers call this condition 'conduction blocking.'
Demyelinated axons can become overexcitable at the MS lesion. They start sending out signals that originate at the site of the lesion, rather than from the brain or sensory neurons. That nerve impulse goes out in both directions to the neuron. A neuron transmits electricity through the flow of ions like potassium and sodium from the outside of the neuron to the long, branching part of the neuron, known as the axon. These ions carry positive charges, which triggers the axon to fire at the site of demyelination. So a lesion in the spine can suddenly decide to fire, all by itself, and cause symptoms around the area, because the surrounding nerves are getting stray signals from the demyelinated area. It's similar to what happens when somebody uses their garage door opener and your television shuts off.
Apparently just a little change in charge can be enough to cause the axon to fire. Researchers believe that active axons that are near the demyelinated region are enough to trigger the nerve to fire - like the electricity from one nerve is jumping and going to the other. Ephaptic transmission can result in the simultaneous firing of a number of axons together. This is why a simple touch can result in pain - the touch sensation is passing through an area of demyelination, causing demyelinated pain axons to fire as well.
If these paroxysmal symptoms interfere with your life, it's time for medication. Anti-epilepsy drugs are currently used to reduce symptoms, but there is research to find better solutions. Carbamazepine is believed to block sodium channels and the flow of charged sodium ions, causing a reduction in the random firing of axons. Unfortunately it also causes a worsening of neurological function. Oxcarbazepine also blocks sodium channels, and is effective in treatment of paroxysmal pain, but also causes a worsening of MS symptoms. Gabapentin is another anti-epileptic drug found to be effective in preventing paroxysmal symptoms. It seems to increase gamma aminobutyric acid (GABA) levels in the brain, which helps decrease electrical activity. My neurologist has prescribed Keppra for me, which has similar effects. The drug binds to a synaptic vesicle protein, SV2A, which is believed to impede nerve conduction across synapses.
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