In multiple sclerosis, myelin loss produces a failure in the conduction of the axonal action potential that is associated with clinical exacerbations, but axonal conduction can recover as a result of the expression of new sodium channels along demyelinated axons, providing a substrate for the remission of clinical deficits (. Several factors help determine how fast an action potential travels down an axon (called conduction velocity). The biophysical characteristics of a neuron, including the size of its axonal diameter and the permeability of the membrane, help scientists determine what is known as the length or space constant (lambda or α) of each neuron. Why is this value l important? That is directly proportional to the conduction velocity, so the factors that determine okr also determine the conduction velocity of a neuron.
Let's not forget that speed excites the CNS and the brain, and the faster a signal arrives, the more the brain likes it. In multiple sclerosis, an unknown trigger causes immune cells to start attacking and breaking down the myelin sheath. Over time, repeated damage causes hard scar tissue, known as plaques, to form in the nerve. Nerve cells are surrounded by an insulating layer called myelin.
In multiple sclerosis, the myelin sheath becomes inflamed or damaged. This interrupts or slows down nerve impulses and leaves areas of scarring along the nerves. Multiple sclerosis can also damage the nerve cells themselves, not just their myelin lining. Therefore, a patient with optic tract demyelination, for example, may suffer from temporary conduction blockage and blindness when the head is heated as a result of using a hair dryer.
Murine model of demyelination in multiple sclerosis that highlights the activation of the inflammatory process. Multiple sclerosis (MS) is caused by progressive damage to myelin, which covers and protects extensions of nerve cells called axons. Multiple sclerosis is an immune-mediated disease in which the body's immune system attacks nerves in the brain and spinal cord. A series of compound action potentials showing conduction through an ethidium bromide demyelinating lesion induced in rat dorsal columns 23 days earlier.
The consequence is that the duration of action potentials fractionally shortens with heating and this reduces the current available to depolarize the demyelinated membrane to its activation threshold. During development, before coating with glial cells, axons have a diffuse distribution of Nav1.2 along the axolemma (20, 7) and it is presumably these that support impulse conduction before myelination (150). In this way, many sodium channels can be opened almost simultaneously and, in excitable cells, such as neurons, this can create the “explosion” of internal current that characterizes an action potential. Sometimes, it's important for you and your doctor to see how your symptoms or test results change over time before making a diagnosis of multiple sclerosis.
Although successful conduction is theoretically favored by a small axon diameter, it was observed in demyelinated axons up to 5.5 μm in diameter (5), suggesting that most demyelinated central axons will be physically capable of driving under ideal conditions (although many do not in practice). These deficits are mainly attributed to the blockage of axonal conduction, and demyelination is probably the most important cause of this. As the old symptoms revived instead of new ones, it is presumed that the deficits were due to the blockage of conduction in axons that had been previously damaged by the disease process, but the mechanism remained unclear. Therefore, at low nitric oxide concentrations, demyelinated axons would be preferentially affected, providing a plausible explanation for the transient exacerbation caused by the administration of Campath-1H.
Based on observations in experimental lesions, there is little doubt that remyelinated axons will conduct impulses, although this has not yet been demonstrated in MS. Sensory axons are once again more susceptible than motor axons, and the demyelination affecting the sensory axons of the cervical spine can cause the perception of an electrical shock or a tingling sensation when stretching the cervical cord when bending the neck forward (Lhermitte symptom) (73, 8). The pathology of MS alters myelin structures, impairs conduction and leads to neurodegeneration). .
