| 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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