MadSci Network: Neuroscience |
Before I attempt to answer this question, let me back up and give some introductory information regarding the myelin sheath and cardiac arrhythmia so that other interested people can follow. The nervous system is made up of cells called neurons that communicate with each other (and other cells like muscle cells) by sending electrical impulses (called action potentials) down long cellular extensions called axons. Now, as it turns out (I won't go into the theory here), the rate at which an action potential can travel down an axon is inversely proportional to the resistance of the cytoplasm within the axon (usually referred to as the axoplasm) and also inversely proportional to the capacitance of the axonal membrane. Since having high speed signaling is very important for survival, evolution has come up with two solutions to this problem. In invertebrates, the solution has been to either become very small (so axons are very short and therefore the speed of the action potential is not so critical) or to have very large diameter axons (which reduces the resistance of the axoplasm). In vertebrates, a very elegant solution was found. Basically, a membrane gets wrapped around the axon many times to form an insolating covering called a myelin sheath. The idea is that this covering greatly decreases the capacitance of the axonal membrane and thus speeds up action potentials without needing to increase the diameter of the axon. This is very lucky for us because without myelin, it would be impossible to have a highly complex nervous system because there would be no room to fit all the large-diameter axons. Myelin itself is actually not part of the neuron, but is in fact the result of an associated cell wrapping itself around the axon many many times to form the sheath. These associated cells are called oligodendrocytes (if they are in the central nervous system - CNS) or Schwann cells (if they are in the peripheral nervous system - PNS). Thus, as it turns out, there are two types of myelin diseases - those that affect the CNS myelin and those that affect the PNS myelin. The most well-recognized of these diseases is multiple sclerosis (MS), which causes (for unknown reasons) a loss of parts of the CNS myelin and results in all kinds of problems due to slow (or sometimes absent) action potentials. Also, over the life span of an individual, there is a very slow progressive loss of myelin - but this loss (when compared to MS for example) is still very small and therefore it is normally unnoticeable. There is also a similar slow loss of the neurons themselves with age. However, in the heart there is no myelin. The heart is made of muscle cells called cardiac myocytes which are definitely NOT neurons. The cardiac pacemaker is also made of modified cardiac myoctyes and is directly attached to the heart (the SA node). This makes the heart a self-contained beating machine and can actually be removed from the body (don't try this at home) and still continue beating! So there is nothing that a demyelination disease can do to affect this system. Now an arrhythmia is caused when the timing of the heartbeat is not normal. There are actually many types of arrhythmias, many of which are very common and not even dangerous. The four most common causes of this condition are as follows: 1. underlying heart disease (such as coronary artery disease or valve problems, etc.) 2. abnormal electrolyte levels (such as potassium for example) that effect the electrophysiology of the heart. 3. congenital problems (very unusual) 4. alcohol, tobacco, or stimulants (like caffeine) For an older patient, causes #1 and #4 are BY FAR the most common. All of these causes affect the heart directly (as would be expected since the heart is self-contained). However, this heart is actually not completely self-contained. The heart rate is controlled by two different sets of neurons originating from the brain stem. The vagus nerve causes the heart to slow down, while the sympathetic fiber causes it to speed up. Thus, there is a push-pull system that allows the brain stem to control the heart rate. Since these neurons (as well as the circuitry in the brain stem itself) are myelinated, they could in principle be affected by demyelination. So, if this control system went haywire could it cause cardiac arrhythmia? The only indication I could find in the medical literature that this could happen are a few reports of MS patients that also have certain forms of cardiac arrhythmia. I have included the references below. But it must be stressed that you can find a few reports of practically anything in the medical literature and certainly most MS patients have no associated heart problems at all. To show any real association between MS and arrhythmia would require a very expensive large scale statistical study that no one is likely to fund anytime soon. Then, of course, if you DO happen to prove that an association exists, it still might have nothing to do with demyelination because certainly MS is a much more complex disease than just simply a selective demyelinator. So it is possible that an older patient with normal low-levels of age-induced demyelination could have cardiac arrhythmias as a result of this? Yes - but it would be the first recognized case! And of course it would be very difficult to establish that demyelination was in fact the cause. If I were examining a patient, I would more easily believe that perhaps I missed some subtle form of heart disease, or that the patient has been exposed to some form of toxin or is using too much alcohol, drugs, or caffeine. I hope I've answered most of your questions! Take care, Dave REFERENCES: Drouin E, et al. Abnormalities of cardiac repolarization in multiple sclerosis: relationship with a model of allergic encephalomyelitis in rat. Muscle Nerve. 1998 Jul;21(7):940-2. Schroth WS, et al. Multiple sclerosis as a cause of atrial fibrillation and electrocardiographic changes. Arch Neurol. 1992 Apr;49(4):422-4. Chagnac Y, et al. Paroxysmal atrial fibrillation associated with an attack of multiple sclerosis. Postgrad Med J. 1986 May;62(727):385-7.
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