CHAPTER 7
Nervous Tissue
123
CLINICAL CORRELATION
Figure 7-6C.
Multiple Sclerosis.
Luxol fast blue stain.
Multiple sclerosis (MS)
is an
autoimmune infl
ammatory
demyelinating disease
of the CNS, in which the body’s
immune system destroys the myelin sheath that cov-
ers and protects the nerves. It most often affects young
women between 20 and 40 years of age. Signs and symp-
toms depend on the location of affected nerves and sever-
ity of the damage and may include numbness or weakness
of limbs, visual impairments (double or blurring vision),
unusual sensations in certain body parts, tremor, and
fatigue. A typical case would have multiple episodes with
some resolution between episodes. Genetics and child-
hood infections may play a role in causing the disease.
Pathologically, MS produces
multiple plaques of demy-
elination
(illustrated) with the loss of oligodendrocytes
and astroglial scarring and possible axonal injury and
loss. Glucocorticoids and immunomodulatory agents are
treatments of F
rst choice.
Region of photomicrograph
Lateral
ventricle
C
Corpus callosum
Normal myelin
Plaques with
degenerated
myelin
Corpus
callosum
Figure 7-6A.
Myelinated and unmyelinated axons.
The
myelin sheath
consists of a tight spiral wrapping of the
lipid-rich cell membrane of a
Schwann cell
in the PNS or an
oligodendrocyte
in the CNS. As the Schwann cell envelops the
axon, the wrapping process proceeds from outside to inside
(
black arrow, 1
) and the cytoplasm is excluded, bringing the
inner surfaces of the cell membrane together (
red arrows, 1
).
The closely apposed inner surfaces of the membrane form
the
major dense line
in the spiraling myelin (±ig. 7-7B,
inset
).
When the myelination is complete, the axon is surrounded
by many layers of membrane, which function as “insula-
tion,” increasing the speed and efF
ciency of nerve conduction
(
2
). The smallest axons in the PNS and CNS lack the thick
coating of myelin that is present in medium and large axons.
These axons lie in grooves in the cell bodies of supporting
Schwann cells (
3
and ±ig. 7-7B) and have much slower con-
duction velocities than myelinated axons.
A
Myelinated axon
J. Lynch &T. Yang
1
3
2
Nuclei of
Schwann cells
Schwann cell
cytoplasm
Myelin
Axons
Unmyelinated axons
B
Node
of Ranvier
Schwann cell
Nucleus
Axon
Clefts of Schmidt-Lanterman
Clefts of Schmidt-Lanterman
Clefts of Schmidt-Lanterman
Figure 7-6B.
Myelinated peripheral nerve axons (nodes
of Ranvier).
Trichrome stain,
3
272
A preparation of teased
myelinated axons
is shown here. The
myelin coating is not continuous. Each axon is enveloped by
numerous Schwann cells, each covering a distance of between
a few millimeters and a few tens of millimeters. Between each
pair of Schwann cells is a gap, the
node of Ranvier
, where
the bare axon membrane is exposed to the extracellular envi-
ronment. It is at these nodes that voltage-gated channels are
concentrated and the membrane becomes active during nerve
conduction. Action potentials jump from one node to the next,
a process which increases both the speed and the metabolic
efF ciency
of nerve conduction in large myelinated nerves. The
clefts of Schmidt-Lanterman
contain cytoplasm that provides
metabolic support for the membrane of the myelin coating.
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