The images above are cross sectional depictions of two neurons and their associated axon. Neurons, as you can see, are strange looking cells with tentacles (axons and dendrites) that reach out and connect with other neurons in defined circuits. The connections made by these neurons are the means by which your nervous system receives information, interprets and manipulates information and acts on information. This information may come in the form of sights, sounds, tastes, smells, sensations or language. The information flow can also start from spontaneously generated thought and contemplation.
The myelin that is damaged in MS is shown in blue (called the myelinated internode in the picture) wrapped around segments of the axon (shown in blue green) with gaps between the myelinated internode that are called the Nodes of Ranvier (labeled Node in the picture). As you may know it is common in medicine to name things after their founder and a French physician in the late 19th and early 20th century named Ranvier discovered this peculiar feature of our nervous systems. The top image is a normal neuron-axon unit and the lower image depicts a neuron-axon unit that has been stripped of myelin in an area but with no permanent damage to the axon. Now why is this a problem?
- In the normal circumstance (shown in the top picture), electrical impulses created initially by receptors located in your skin (those that detect pain, touch and other things) travel upwards to your brain through these axons. Now these electrical impulses are able to move quickly enough because they literally jump from one node to another through a process called saltatory conduction. Since this not an electric wire transmitting electrons but a biologic membrane, the passage of electrical current occurs through the opening of sodium channels in the axon at the nodes of Ranvier. These sodium channels are shown as yellow lines in the outer part of the axons in the pictures above. Notice that these sodium channels are only located at the nodes. When the sodium channel opens there is an influx of sodium into the axon from outside the cell. This creates a difference in the electrical potential between the inside and the outside of the axon much like the battery in your car. This can then pass down the axon quickly as an electrical current because it jumps quickly from one node to the next.
- When a relapse occurs and the myelin is damaged around your axons, the exposed areas of the axon shown in the lower picture do not have many sodium channels. Therefore, electrical impulses traveling through this area are blocked which result in a loss of function or, in this case, a loss of sensation.
- As you begin to recover from a relapse, new sodium channels are formed along the damaged axons; sometimes with partial restoration of the myelin around the axon. These new areas of the axon that sprout sodium channels are very excitable. This means that it is possible to generate a spontaneous electric impulse at the site of injury that travels up to your brain and is interpreted as unusual sensations such as pins and needles or jabbing sensations or electrical sensations or a tight band sensation. This can occur spontaneously or as a response to a mechanical stimulus such as bending your neck forward (called Lhermitte’s phenomenon). In other words these sensations are no longer generated by cutaneous sensory receptors in your skin and are quite confusing to your nervous system. Depending upon the type of injury and recovery, these abnormal sensations can occur intermittently or constantly. Interestingly, neurons that carry sensory information tend to exhibit greater persistent sodium currents after they lose myelin. This is one reason why it is more common to experience abnormal sensations in MS than abnormal spontaneous movements. These sensations are often painful. The development of chronic constant pain usually requires the interaction of the demyelinated area with other areas of your nervous system.
- This is why we often treat these abnormal sensations with drugs like phenytoin (dilantin), carbamezipine (tegretol), and oxcarbezipine (trileptal) and gabapentin (Neurontin); all of these drugs block the voltage gated sodium channels that sprout along the axon after myelin is damaged. Now, as a former radio personality used to say, you know the rest of the story.
The difficult question is whether these new sodium channels that sprout all axons are harmful. There is some research that indicates that the effects of these sodium channels may lead to permanent damage to the neuron, but attempts so far to prevent this from occurring by administering drugs that block sodium channels have not been successful.