Neurophysiology

Myelin acts as an electrical insulator in the brain and spinal cord. This lipid sheath is produced by oligoden-drocytes in the brain and spinal cord. One oligodendrocyte insulates 1-100 axons. The myelin, produced in layers or lamellae, is interrupted by nodes of Ranvier. At the node of Ranvier there is a high density of sodium channels, which are responsible for sodium ion shifts for depolarization. These areas allow for production and propagation of action potentials. Conduction is a saltatory (not a continuous) process. The internodal areas (areas between the nodes of Ranvier under the myelin sheath) have a low proportion of sodium channels and a high proportion of potassium channels, especially in the perinodal region. These potassium channels oppose depolarization. Depolarization produces an electrical charge, which is conducted through the myelinated segment to the next node for depolarization. Myelin increases the speed of conduction and efficiency. With demyelina-tion, slowing of action potentials and conduction block occur. Conduction block prevents propagation of any axon action potential. Sodium channels develop along the demyelinated internodal area as a way to allow for propagation of an action potential, although this is slower. This reorganization of the demyelinated axon results in a higher than normal density of sodium in demyelinated regions. Other factors may interfere with conduction, such as circulating immune factors or edema. In addition to reorganization of sodium channels, resolution of edema or clearance of these factors may restore conduction. Synaptic changes and conduction through normal unmyelinated axons may also restore function.

It is known that small changes in temperature and electrolytes can produce conduction block in demye-linated axons. Patients' symptoms may recur when they have an elevated body temperature as a result of illness or increased environmental temperature. Uth-offs phenomenon is one of the best known of these phenomena. With elevation of body temperature, such as during exercise, individuals develop decreased visual acuity in an eye previously affected by optic neuritis. Symptoms resolve when body temperature returns to normal. Trains of impulses can also block propagation of action potentials by prolongation of the refractory period—the time during which a neuron cannot depolarize. Clinically, this occurs as patients complain of fatigability of muscle strength with repetitive use of any extremity, such as occurs during walking. It is possible that modification of the sodium and potassium channels in demyelinated neurons may result in improvement in clinical symp-toms.4-Aminopyridine, a potassium channel blocker, is a drug that improves symptoms for patients with MS, especially those who are heat sensitive. Currently, it is not a Federal Drug Administration (FDA)-approved drug, but further research into modification of sodium and potassium channels may lead to therapies, that provide improved conduction in de-myelinated axons.

Paroxysmal symptoms of MS are a unique feature of the disease that have their basis in the physiology of demyelinated axons. These symptoms include episodes ofrecurrent hemibody sensory symptoms, paroxysmal dysarthria, and paroxysmal pain such as trigeminal neuralgia. These phenomena may be a result of ephaptic transmission, which occurs when adjacent demyelinated axons communicate in a lateral fashion and result in recurrent abnormal stimuli. Lhermitte's phenomena is a transient electric shock-like sensation in the spine and/or extremities believed to be due to increased mechanosensitivity of demyelinated axons in the spinal cord and it results when neck flexion causes mechanical changes in the spinal cord.

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