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Physical Properties of
Diamond and Sapphire
Physical Properties of
Diamond and Sapphire

Roshan L. Aggarwal
Anant K. Ramdas
CRC Press
Taylor & Francis Group
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Boca Raton, FL 33487-2742

© 2019 by Taylor & Francis Group, LLC

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International Standard Book Number-13: 978-0-367-23508-6 (Hardback)

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Library of Congress Cataloging-in-Publication Data

Names: Aggarwal, R. L. (Roshan Lal), 1937- author. | Ramdas, Anant K., author.
Title: Physical properties of diamond and sapphire / Roshan L. Aggarwal and
Anant K. Ramdas.
Description: First edition. | Boca Raton, FL : CRC Press/Taylor & Francis
Group, 2019. | Includes bibliographical references and index.
Identifiers: LCCN 2019006297| ISBN 9780367235086 (hardback : acid-free
paper) | ISBN 9780429283260 (ebook)
Subjects: LCSH: Diamonds. | Sapphires.
Classification: LCC QE393 .A384 2019 | DDC 549/.27--dc23
LC record available at https://lccn.loc.gov/2019006297

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 This monograph is dedicated to our parents
(Chet Ram Aggarwal and Lila Vati Aggarwal and
Lakshminarayanapuram AnanthakrishnaIyer Ramdas
and Kalyani Ramdas), our spouses (Pushap Lata
Aggarwal and Vasanthalakshmi Ramdas), our
children (Rajesh Aggarwal and Achal Aggarwal),
and our grandchildren (Isha Aggarwal, Neena
Aggarwal, Akash Aggarwal, and Ashok Aggarwal).
Contents

Preface, xi
Acknowledgments, xiii
Authors, xv

Chapter 1   ◾    Introduction 1

1.1 DIAMOND 3
1.1.1 Color of Natural Diamonds 3
1.1.2 Physical Properties of Diamond 3
1.2 SAPPHIRE 6
1.2.1 Colors of Sapphire 6
1.2.2 Physical Properties of Sapphire 8

Chapter 2   ◾    Crystal Structure and Growth 9

2.1 DIAMOND 9
2.2 SAPPHIRE 12

Chapter 3   ◾    Mechanical Properties of Diamond 17

3.1 HARDNESS 17
3.2 TENSILE STRENGTH 17
3.3 COMPRESSIVE STRENGTH 18
3.4 YOUNG’S MODULUS 18
3.5 ELASTIC CONSTANTS 20

vii
viii   ◾    Contents

Chapter 4   ◾    Mechanical Properties of Sapphire 21

4.1 HARDNESS 21
4.2 TENSILE STRENGTH 21
4.3 YOUNG’S MODULUS 23
4.4 ELASTIC CONSTANTS 24

Chapter 5   ◾    Thermal Properties of Diamond 25

5.1 THERMAL EXPANSION 25
5.2 SPECIFIC HEAT 27
5.3 THERMAL CONDUCTIVITY 30

Chapter 6   ◾    Thermal Properties of Sapphire 33

6.1 THERMAL EXPANSION 33
6.2 SPECIFIC HEAT 34
6.3 THERMAL CONDUCTIVITY 35

Chapter 7   ◾    Optical Properties of Diamond 37

7.1 TRANSMISSION RANGE 37
7.2 REFRACTIVE INDEX 38
7.3 ABSORPTION SPECTRUM 40

Chapter 8   ◾    Optical Properties of Sapphire 43

8.1 TRANSMISSION AND ABSORPTION 43
8.2 REFRACTIVE INDEX 44

Chapter 9   ◾    Light Scattering of Diamond 47

9.1 RAMAN SCATTERING 47
9.2 BRILLOUIN SCATTERING 52
 Contents   ◾   ix

Chapter 10   ◾    Light Scattering of Sapphire 55

10.1 RAMAN SCATTERING 55
10.2 BRILLOUIN SCATTERING 59

Chapter 11   ◾    Sapphire Lasers 63

11.1 CHROMIUM-DOPED SAPPHIRE LASER 63
11.2 TITANIUM-DOPED SAPPHIRE LASER 63

REFERENCES, 67

INDEX, 73
Preface

T his monograph is intended to provide readers with

the physical properties of diamond and sapphire, which
are both gemstones and have similar properties. Diamond is
an optically isotropic crystal. Sapphire is a uniaxial crystal
with refractive indices nE and nO for polarization parallel and
perpendicular to the optic axis, respectively. This monograph
includes crystal structure and growth, mechanical properties,
thermal properties, optical properties, light scattering, and
sapphire lasers. Mechanical properties include hardness, tensile
strength, compressive strength, and Young’s modulus. Thermal
properties include thermal expansion, specific heat, and thermal
conductivity. Optical properties include transmission, refractive
index, and absorption. Light scattering includes Raman scattering
and Brillouin scattering. Sapphire lasers include chromium-doped
and titanium-doped lasers. The sources for the material in this
monograph are journal articles and others as acknowledged in the
references.

xi
Acknowledgments

W e thank Dr. Marc Bernstein for his approval to write

this monograph. We thank Dr. William Herzog and
Dr. Mordechai Rothschild for discussions regarding this work. We
thank Casey Reed for drafting some of the figures.

xiii
Authors

Roshan L. Aggarwal retired from Massachusetts Institute of

Technology (MIT) effective April 1, 2016, after 51 years of service.
He is currently working as part-time flexible technical staff in
Group 81 “Chemical, Microsystem, and Nanoscale Technologies”
at MIT Lincoln Laboratory. Previously, he was technical staff at
MIT Lincoln Laboratory for 30 years (1986–2016), senior research
scientist in the MIT Physics Department for 12 years (1975–1987),
associate director at the MIT Francis Bitter National Magnet
Laboratory for 7 years (1977–1984), and technical staff at the MIT
Francis Bitter National Magnet Laboratory for 12 years (1965–
1977). Dr. Aggarwal is a fellow of the American Physical Society,
a senior member of the Optical Society of America, a fellow of the
Punjab Academy of Sciences, and a recipient of the Albert Nelson
Marquis Lifetime Achievement Award.

Anant K. Ramdas retired as the Lark-Horovitz Distinguished

Professor Emeritus of Physics in 2016 after 60 years of service at
Purdue University. He received his PhD in Physics from Poona
University, India, in 1956; his thesis advisor was Prof. C. V. Raman.
Professor Ramdas is a recipient of the Alexander von Humboldt
Foundation Senior U. S. Scientist Award, recipient of the Raman
Centenary Medal of the Indian Academy of Sciences, Frank Isakson
Prize of the American Physical Society, Sigma Xi Faculty Research
Award, Ruth and Joel Spira Award for excellence in undergraduate

xv
xvi   ◾    Authors

teaching, and Herbert Newby McCoy Award of Purdue University.

Prof. Ramdas is a fellow of the American Physical Society, fellow
of the Optical Society of America, fellow of the American Vacuum
Society, fellow of the American Association for the Advancement
of Science, and fellow of the Indian Academy of Sciences.
 Chapter 1

Introduction

D iamond has fascinated mankind since the early ages for

its aesthetic beauty. Diamond is a girl’s best friend because it
is both expensive and associated with romantic love. Diamond is
the birthstone for April.
Diamonds are gemstones, which are crystals of carbon.
Diamond crystals are also grown in the laboratory. Natural
diamonds come in a variety of colors, including white, yellow
(Sobolev and Lavrent’Ev 1971), pink (King et al. 2002), and blue
(King et al. 1998). Most diamonds are white. Yellow, pink, purple,
and blue diamonds are rare and hence expensive.
Figure 1.1 shows the purplish-red, red, and orangy-red colors
of diamonds produced by Lucent Diamonds using a multistep
process that involves high pressure–high temperature (HPHT)
annealing, irradiation, and low-pressure annealing at relatively
low temperatures (Wang et al. 2005).
The wavelength ranges for the red, orange, yellow, green, blue,
and violet colors are approximately 675–741, 600–675, 538–600,
482–538, 450–482, and 379–422 nm, respectively (Loeffler and
Burns 1976).
Both ruby and sapphire are corundum (α-aluminum oxide)
crystals. The birthstone months for ruby and sapphire are July

1
2   ◾    Physical Properties of Diamond and Sapphire

FIGURE 1.1 Colors of diamonds (shown on the color wheel) produced

by Lucent Diamonds using a multistep process for natural type Ia
diamonds. (After Wang, W. et al., Gems Gemol. 41, 6, 2005.)

and September, respectively. Ruby is red (∼675–741 nm), whereas

sapphire is typically blue (∼450–482 nm) but also occurs in
yellow (∼538–600 nm) and green (∼482–538 nm) colors. The
red (∼675–741 nm) color of ruby is due to chromium. Yellow
sapphires are due to iron. Blue and green sapphires are due to iron
and titanium pairs. The physical properties of ruby and sapphire
are the same.
 Introduction   ◾   3

1.1 DIAMOND
1.1.1 Color of Natural Diamonds
Colors of diamonds are caused by optical absorptions due to
impurities (nitrogen, hydrogen, boron) and defects (Fritsch 1998).
Nitrogen is responsible for the yellow (∼538–600 nm) color of
diamonds as shown in Figure 1.2 (Chrenko et al. 1971).

FIGURE 1.2 Absorption spectrum of yellow diamond. (After Chrenko,

R. M. et al., Philos. Mag. 23, 313, 1971.)

Boron, which shows absorption starting at 3.35 µm and

continuing with decreasing intensity into the visible range, is
responsible for the blue (∼450–482 nm) color of diamonds, as
shown in Figure 1.3 (King et al. 1998).
Figure 1.4 shows the ultraviolet-visible-near infrared (UV-V-NIR)
absorption spectrum of purple diamonds (Titkov et al. 2008). The
absorption spectrum in Figure 1.4 exhibits increasing absorption
below 450 nm and a broad absorption band centered at about 550 nm.
The N3-related zero phonon line (ZPL) is observed at 415 nm.

1.1.2 Physical Properties of Diamond

Diamond is a large-gap semiconductor with an indirect gap of
5.48 eV (226 nm) and direct gap of 7.12 eV (174 nm) (Logothetidis
et al. 1992). Diamond is optically transparent in the ultraviolet,
visible, infrared, and far infrared. Diamond has a high refractive
4   ◾    Physical Properties of Diamond and Sapphire

FIGURE 1.3 Absorption spectrum of boron-containing natural type IIb

diamond compared with that of natural type IIa diamond. (After King,
J. M. et al., Gems Gemol. 246, 1998.)

FIGURE 1.4 UV-VIS-NIR absorption spectrum of purple diamonds.

(After Titkov, S. V. et al., Gems Gemol. 44, 56, 2008.)
 Introduction   ◾   5

index of 2.46–2.41 for visible light (0.40–0.65 µm), which gives cut
diamonds their brilliance (Palik 1985).
Natural diamonds, which are formed deep within the earth
under extreme heat and pressure, contain unique birthmarks that
are either internal (inclusions) or external (blemishes). Diamonds
without these birthmarks are rare and very expensive. Diamonds
are assigned a clarity grade using the GIA International Grading
System under 10× magnification. The GIA covers 12 clarity grades:
flawless (FL), internally flawless (IFL), very very slightly included
(VVS1 and VVS2), very slightly included (VS1 and VS2), slightly
included (SI1 and SI2), and included (I1, I2, and I3).
The density of diamond is 3.515 g/cm3; that is, it has a C12 concen-
tration of 1.762 × 1023 cm−3. The weight of diamonds is expressed in
carats. One carat is equal to 200 mg and has a volume of 56.9 mm3.
Diamond is harder and conducts heat better than any other
known material. The relative hardness of diamond is 10 Mohs;
Mohs chose 10 well-known minerals and arranged them in order
of their scratch hardness in descending order in 1822. The thermal
conductivity of diamond at 300 K is 900 W/m · K compared to that
of 386 W/m · K for copper (Touloukian et al. 1971). The physical
properties of hardness and thermal conductivity make diamond
an excellent choice for many technological applications, such
as cutting, polishing, protective coatings, and heat conduction.
Diamonds used for technological applications are produced using
the chemical vapor deposition (CVD) method.
There are four types of natural diamonds: (1) type Ia, which contains
pairs and other aggregates of substitutional nitrogen atoms; (2) type
Ib, which contains single/isolated substitutional nitrogen atoms; (3)
type IIa, which is relatively free of nitrogen and other impurities; and
(4) type IIb, which contains substitutional boron atoms.
Most diamonds are excellent insulators. The electrical resistivity
is on the order of 1011–1018 Ωm. Boron-doped natural blue diamonds
are p-type semiconductors. However, certain blue-gray diamonds
that contain hydrogen are not semiconductors. Phosphorus-doped
diamond films, produced by CVD, are n-type semiconductors.
6   ◾    Physical Properties of Diamond and Sapphire

1.2 SAPPHIRE
1.2.1 Colors of Sapphire
Ruby is red sapphire due to Cr3+ ions. Figure 1.5 shows the optical
absorption of ruby in the visible range. There are two absorption
bands in the violet, and green and yellow regions. There is negligible
absorption in the red, which is responsible for the red color of ruby.

FIGURE 1.5 Absorption spectrum of ruby. (After Loeffler, B. M., and

R. G. Burns, Am. Sci. 64, 636, 1976.)

Blue sapphires are due to the absorption of Ti4+-O2–-Fe2+

at 18,000 cm−1 (556 nm) for perpendicular-to-c polarization
and 14,200 cm−1 (704 nm) for parallel-to-c polarization. Green
sapphires are due to the absorption of Fe2+-O2–-Fe3+ at 11,500 cm−1
(870 nm) for perpendicular-to-c polarization and 10,000 cm−1
(1000 nm) for parallel-to-c polarization. Figure 1.6 shows the
room-temperature absorption spectrum of blue-green sapphire
for perpendicular-to-c polarization (Ferguson and Fielding 1971).
 Introduction   ◾   7

FIGURE 1.6 Room-temperature absorption spectrum of a natural blue-

green sapphire for the perpendicular-to-c polarization. (After Ferguson,
J., and P. E. Fielding, Australian J. Chem. 25, 1371, 1972.)

Yellow sapphires are due to the absorption of single Fe3+ ions

and pairs of Fe3+ ions (Ferguson and Fielding 1972). Figure 1.7
shows the room-temperature spectra of yellow sapphire containing
0.99% Fe for (a) parallel-to-c polarization and (b) perpendicular-
to-c polarization.

FIGURE 1.7 Absorption spectra of a natural yellow sapphire containing

0.99% Fe by weight. (a) Parallel-to-c polarization, and (b) perpendicular-
to-c polarization. (After Ferguson, J., and P. E. Fielding, Australian J.
Chem. 25, 1371, 1972.)
8   ◾    Physical Properties of Diamond and Sapphire

1.2.2 Physical Properties of Sapphire

Sapphire is corundum, which is aluminum oxide (α-Al2O3). Sapphire
is typically blue but also occurs in red (ruby), yellow, and green colors.
Natural ruby and sapphire are often found in the same geological
setting (Wenk and Bulakh 2004). Significant sapphire deposits are
found in Australia, Thailand, Sri Lanka, China, Madagascar, East
Africa, and North America (Wise 2004). Except for the difference
in color, the physical properties of ruby and sapphire are the same,
described under physical properties of sapphire in this monograph.
Sapphire belongs to the trigonal crystal system; the crystal
class is hexagonal scalenohedral (3 m). The lattice constants are
a = 4.785 and c = 12.991 A.
The density of sapphire is 3.98 g/cm3, resulting in an Al2O3
concentration of 1.762 × 1023 cm−3. The melting point of sapphire
is 2303 K. The relative hardness of sapphire is 9 Mohs, which is the
second-hardest material; diamond is the hardest known material,
with a hardness of 10 Mohs. The bulk modulus of sapphire is
240 GPa (2.40 × 1012 dyn/cm2). Its shear modulus is 145 GPa
(1.45 × 1012 dyn/cm 2), and its Young’s modulus is 345 GPa
(3.45 × 1012 dyn/cm2).
The optical transmission range of synthetic color-free sapphire
is 0.17–5.5 µm. The refractive index of sapphire at 532 nm is
nO = 1.7717 and nE = 1.76355.
The specific heat of sapphire is 761 J/kgK at 291 K. The thermal
coefficients of linear expansion at 323 K are 6.66 × 10−6/K and
5 × 10–6/K parallel and perpendicular to the c-axis, respectively.
The values of thermal conductivity at 300 K are 23.1 W/mK and
25.2 W/mK parallel and perpendicular to the c-axis.
Sapphire is an excellent insulator. The electrical resistivity is on
the order of 1018 Ωm at 298 K, 1013 Ωm at 773 K, and 108 Ωm at
1273 K. Values of the dielectric constant of sapphire at 298 K for
the frequency range 103–109 Hz are 11.5 and 9.3 for parallel and
perpendicular to the c-axis.
 Chapter 2

Crystal Structure
and Growth

2.1 DIAMOND
Diamond consists of carbon atoms. Each carbon atom is surrounded
by four nearest atoms, which form a regular tetrahedron whose
center is the atom in question. The unit cell for the diamond crystal
structure is face-centered cubic (fcc) with a basis that consists of
two carbon atoms associated with each lattice site. The length a
of the diamond unit cell is equal to 3.56683 Å. The positions of
the two basis atoms are 000 and (1/4)(1/4)(1/4). Figure 2.1 shows
the crystal structure of a diamond with the tetrahedral bond
arrangement of carbon atoms. There are eight atoms in a unit cell.
Artificial diamonds are produced using a high-pressure
(1 × 105 kg/cm 2) and high-temperature (>2300 K) process
developed by Bundy et al. at Research Laboratory, General Electric
Company, Schenectady, New York (Bundy et al. 1955). The size
of the diamonds thus produced ranges from less than 100 µm to
more than 1 mm along an edge. Artificial (synthetic) diamonds
are now a commonplace item of commerce. Figure 2.2 shows
artificial diamonds.

9
10   ◾    Physical Properties of Diamond and Sapphire

FIGURE 2.1 Crystal structure of diamond showing the tetrahedral

arrangement of carbon atoms.

FIGURE 2.2 Artificial diamonds: (a) 1-mm diamond shown with

phonograph needle, and (b) 0.2–0.5 mm octahedra. (After Bundy, F. P.
et al., Nature 176, 51, 1955.)
 Crystal Structure and Growth   ◾   11

Figure 2.3 shows the x-ray diffraction pattern of artificial and

natural diamonds.

FIGURE 2.3 X-ray diffraction pattern of laboratory-made (artificial)

diamond and natural diamond. (After Bundy, F. P. et al., Nature 176,
51, 1955.)

Chang et al. reported diamond crystal growth by plasma

chemical vapor deposition in 1988 (Chang et al. 1988). Figure 2.4
shows a schematic of the 2450-MHz discharge tube reactor used
by Chang et al.

FIGURE 2.4 Schematic of the 2450-MHz discharge tube reactor. (After

Chang, C.-P. et al., J. Appl. Phys. 63, 1744, 1988.)
12   ◾    Physical Properties of Diamond and Sapphire

A single-crystal diamond growth rate >20 mm/hr was achieved

using this reactor. Figure 2.5 shows a high-quality single-crystal
diamond grown using 100 H2/4 CH4/0.5 O2 sccm at 30 Torr with
a 100-W discharge.

FIGURE 2.5 High-quality single-crystal diamond formed in the 2450-

MHz discharge tube reactor. (After Chang, C.-P. et al., J. Appl. Phys. 63,
1744, 1988.)

2.2 SAPPHIRE
The crystal structure of sapphire (corundum) was first determined
by Pauling and Hendricks (1925). The chemical formula is Al2O3.
The crystal class is hexagonal system with rhombohedral class 3 m.
The lattice constants are a = 4.785 Å and c = 12.991 Å. Figure 2.6
shows a schematic of the packing of O2– ions (light circles) and Al3+
ions (black circles). The lattice constant a is equal to the distance of
the O2– ion from the c-axis passing through the Al3+ ions.
A vertical-pulling technique is used for the growth of highly
perfect sapphire single crystals (Cockayne et al. 1967). Figure 2.7
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current, and it should be used in the way that will produce the
greatest amount of excitation in the cutaneous end-organs. This is
best done by applying the faradic current to the dry skin with the
metallic brush, or by allowing the cathode of the galvanic current to
rest upon it for some time.

The PROGNOSIS in peripheral anæsthesia is in the main favorable, but

it must, of course, depend much on the gravity of the lesion causing
it, as mechanical injury, pressure, neuritis, cold, etc. Rheumatic
anæsthesia, the result of exposure to cold, is in general readily
recovered from. Vaso-motor anæsthesia yields in most cases without
difficulty to treatment. Washerwoman's anæsthesia and allied cases
are intractable, and often resist the patient and well-conducted
application of remedies.

As a concrete picture of peripheral anæsthesia we will give a

description of anæsthesia of the fifth nerve—the rather that in its
consideration we meet with some of the most interesting and
important complications occurring in connection with paralysis of
sensitive nerves. The fifth nerve may have either of its three
branches separately affected, giving rise to anæsthesia limited to the
distribution of that branch, or all of its fibres may be simultaneously
involved, giving rise to complete anæsthesia of the nerve. In the
latter case the lesion of the nerve in all likelihood exists at some
point of its course between the apparent origin from the pons and the
ganglion of Gasser, which rests upon the apex of the petrous portion
of the temporal bone. Beyond this point the nerve divides into its
three branches. Amongst the causes of trigeminal anæsthesia are
injuries, tumors, syphilitic thickening of the dura mater, neuritis, etc.,
affecting the nerve within the cranial cavity. In complete anæsthesia
of the fifth nerve the parts implicated are the skin of the forehead to
the vertex, the nose, the lips, and chin up to the median line, the
cheek and temporal region, including the anterior portion of the ear,
the conjunctiva, the mucous membrane of the nose, the mucous
membrane of the mouth, and partly of the fauces of the same side.
The tongue is deprived not only of common sensation on the
affected side in its anterior two-thirds, but the sense of taste is also
lost over the same region, by reason that the fibres of the chorda
tympani, the nerve of taste for this region of the tongue, are derived
from the fifth nerve. If the whole thickness of the nerve-trunk is
involved, including the small motor root, there is, in connection with
the anæsthesia, paralysis of the muscles of mastication on the side
affected, which may be distinguished by the want of hardening of the
masseter when the jaws are forcibly brought together, and by the
thrusting of the chin over to the paralyzed side when the mouth is
widely opened, caused by the want of action of the external
pterygoid muscle, which allows the condyle on the paralyzed side to
remain in the glenoid fossa, while the condyle of the opposite side is
pulled forward upon the articular eminence by the sound pterygoid.
The face is of a dusky or livid color, and cooler than natural. Ulcers
of a stubborn character in the mucous membrane of the cheek may
be caused by the patient unconsciously biting the insensitive parts.
An inflammation of the conjunctiva is frequently set up, which may
extend to the cornea, causing ulceration, perforation,
panophthalmitis, and destruction of the eye (ophthalmia neuro-
paralytica). This has been regarded by some as caused by trophic
changes in the tissues, the direct result of irritation or destruction of
trophic fibres connected with the ganglion of Gasser. Experiments
made upon animals, however, seem to show that the inflammation of
the eye depends upon the irritation caused by the intrusion of foreign
bodies, which, owing to the loss of sensation, are not appreciated,
and which from loss of reflex action are not removed by winking nor
washed away by an increased lachrymal secretion, as in the healthy
eye. It may be that although the latter is the true explanation of the
origin of the inflammation, nevertheless the tissues may have lost
their normal power of resistance to its invasion by reason of nutritive
changes consequent upon the lesion of trophic fibres running in the
trunk of the nerve. The reflexes ordinarily induced by irritation of the
parts in their normal state are lost. Irritation of the conjunctiva causes
no winking of the lids nor secretion of tears, and titillation of the
nostrils no movements of the muscles of the face nor mucous or
lachrymal secretion. The movements of the face are less lively on
the affected side, not on account of paralysis of the muscles, but
from the loss of that constant play of reflex activity in them which
takes place in the normal condition. The loss of the reflexes
distinguishes peripheral trigeminal anæsthesia from that of cerebral
origin, in which they may still be excited by irritating the anæsthesic
surfaces. In trigeminal anæsthesia, which sometimes occurs from
the effect of cold upon the surface of the face, the mucous surfaces
are not affected.

The SYMPTOMS and DIAGNOSIS of peripheral paralysis having been

already given under the heads of Injuries of Nerves and Neuritis, a
consideration of the distribution of any motor nerve will enable us to
anticipate the distinguishing features of the paralysis dependent
upon it. With each the picture will be modified according to the
position of the muscles paralyzed and the motor functions destroyed.
It now remains to give the symptoms, diagnosis, and treatment of the
paralysis of an individual motor nerve, which may serve as an
example and paradigm, in the consideration of which points of
interest and instruction may be touched upon applicable to all other
cases.

Peripheral Paralysis of the Facial Nerve (Bell's Paralysis).

Of all the peripheral paralyses, probably that of the seventh is the

one we are most frequently called upon to treat and the symptoms of
which are the most complex and interesting. The frequency of its
paralysis is due to the length and peculiarity of its course, enclosed
as it is in a bony canal which permits no increase of its volume
without compression, the run of its terminal branches through parts
liable to inflammation and disease (parotid gland), and their final
distribution to parts exposed to all vicissitudes of heat and cold and
in constant danger of mechanical injury. The complexity and interest
of the symptoms of its paralysis depend in a great measure upon the
intimate connections it forms at different points of its course with the
fibres of other nerves of entirely different functions (acoustic and
fifth).
The seventh nerve is liable not only to intercranial compression from
tumors, inflammation of the meninges, syphilitic processes, etc., but
its long course through the petrous portion of the temporal bone
renders it liable to injury from fracture or caries, and its close
proximity to the middle ear causes it often to suffer from the
diseased conditions of the bony walls or mucous lining membrane of
that chamber, its paralysis being not infrequently the result of simple
aural catarrh. After the exit of the nerve from the stylo-mastoid
foramen it is imbedded in the parotid gland, and sometimes suffers
from compression produced by an inflammation or abscess in that
organ or by enlarged lymphatic glands in the neighborhood. Surgical
operations, so often demanded for disease of the bones or soft parts
of the face, may necessitate the lesion of its trunk or branches. The
exposed position of this nerve is sometimes the occasion of its injury
at the very outset of the life of the individual, when the application of
the forceps to the head has been resorted to in delivery. But the
most frequent cause of facial paralysis appears to be the exposure
of one side of the face directly to cold—as sleeping in a draught of
air, sitting at the open window of a railroad coach, etc. Here the
causal connection appears evident from the rapidity with which the
paralysis usually follows, although cases occur in which an interval
of hours or days elapses after the exposure before the paralysis
declares itself. Although this is usually designated rheumatic
paralysis, there is nothing to connect it with that disease, nor are
rheumatics more liable to it than others. Under such circumstances
the paralysis is probably brought about by the occurrence of a
neuritis of the nerve-trunk, which is compressed by the hyperæmia,
and it may be by an inflammatory exudation against the bony walls
surrounding it, until not only does it lose the power of conduction, but
its fibres undergo the degenerative process. In some cases the
neuritis thus excited by exposure to cold attacks the nerve after it
has issued from the bony canal, and then the resulting injury to the
fibres is much less grave. Although in some cases there are
prodromal symptoms, as stiffness or pain in the face, generally the
paralysis occurs suddenly, very often being first observed upon
awaking. The patient may be first made aware of the paralysis by an
inability to drink without the fluid dribbling from the affected side of
the mouth or by the overflow of tears from the eye of the same side.
When the paralysis is recent and the face in complete repose, there
may be little or no deformity to mark the condition of the muscles.
When, however, the patient speaks or the slightest emotional or
reflex movements of the face are excited, as laughing, frowning, etc.,
it becomes obvious from the bizarre grimace caused by a one-sided
contraction. After the paralysis has existed for some time the
contrast of the two sides of the face is marked. The paralyzed side is
characterized by a vacancy of expression to which the staring,
unwinking eye contributes. From loss of the tonicity of the muscles
the angle of the mouth droops, and the expressive furrows and lines
about the brow, below the eye, and beside the nose are smoothed
out and obliterated. Speech is affected, inasmuch as the paralysis of
the lip interferes with the pronunciation of the labials, and all
attempts to purse up the mouth, as in whistling, is abortive. The eye
not only remains open, the lids motionless, but there is partial
eversion of the lower lid (lagophthalmos), and the tears, no longer
directed to the punctum (paralysis of Horner's muscle), flow over the
cheek. The natural impulse to reflex winking caused by evaporation
from the conjunctiva or by the contact of particles of dust is
answered by a rolling of the eyeball upward to wipe the cornea
beneath the momentarily relaxed and drooping upper lid. Excited
respiration causes no movement of the ala of the nose on the
affected side, but in deep inspiration, in contrast to the normal
elevation of the ala, it is flattened down by the suction of the
inrushing current of air. In masticating, the cheek bulges out from
want of power in the paralyzed buccinator to press the food inward
against the opposing movements of the tongue. In persons who
have the rather unusual power of voluntarily moving the ear we may
detect the paralysis of the muscles concerned in those movements—
a useful point in diagnosis. Moreover, on the sound side of the face
the features have not entirely the natural appearance. The angle of
the mouth is drawn upward and the naso-labial line more deeply
impressed than natural. This results not from excessive contraction,
but from the muscles remaining in the position they have taken
during contraction, the antagonistic tonic traction from the opposite
side, which would have restored them to their normal position, being
wanting. This may be in a measure remedied by mechanical
appliances which will keep up an elastic pull from the paralyzed side,
or by restoring the muscles after contraction to position with the
hand. The tongue rests symmetrically in the floor of the mouth, and
is thrust out straight, although in appearance it is pushed toward the
side paralyzed—a deceptive appearance produced by the
asymmetrical position of the mouth. In some cases there is partial
paralysis of the velum palati, the half arch on the affected side
hanging lowest, and if we cause the patient to make the sound of ah
the opposite side of the palate is alone drawn upward. The uvula
may also participate in the paralysis, but the explanation of its
position, sometimes directed away from, sometimes toward, the side
of the paralysis, cannot be given. In proportion to the amount of the
paralysis of the soft palate will be the prominence of the symptoms
caused by it, such as difficulty in deglutition, a nasal tone in
speaking, and the escape of fluids through the nostril in swallowing.
The sense of hearing is often affected coincidently with facial
paralysis. Thus by reason of their close juxtaposition the same cause
may in common affect the acoustic and the facial, causing imperfect
hearing, subjective noises, etc. The hearing is frequently affected by
diseased conditions of the middle ear, which also cause a facial
paralysis. Still another defect of hearing, however, is caused by the
paralysis of the facial nerve itself. The stapedius muscle, supplied by
a branch of the facial, is the antagonist of the tensor tympani, and
when it is paralyzed the over-tense tympanic membrane vibrates
more readily to sound-waves, and a condition of uncomfortably
exaggerated sensitiveness to sounds is the result (hyperacuisis).
The rarely-occurring symptom of dryness of the mouth on the side of
the paralysis receives its explanation in the well-known fact of the
presence of secretory fibres for the salivary gland in the chorda
tympani, which are derived from the facial. We observe sometimes,
in connection with facial paralysis, that the patient complains of
certain subjective sensations of taste, as sour or metallic, and an
examination will in some cases reveal that the sense of taste is lost
on the anterior two-thirds of the tongue on the side of the paralysis.
The fibres which convey the sense of taste pass centripetally from
the tongue in the chorda tympani nerve, join the facial just within the
stylo-mastoid foramen, and continue united with it to the geniculate
ganglion of the facial, at which point they leave it to pass in the great
superficial petrosal to the spheno-palatine ganglion, and thence to
the trunk of the fifth nerve. Loss of sensation over the face only
occurs in cases where the fifth nerve has been simultaneously
affected with the facial, which may occur from exposure to cold.

It is obviously of importance in cases of facial paralysis to determine

if they are of central or peripheral origin. The most prominent
symptoms which mark a peripheral paralysis are the implication of all
the branches of the nerve, the loss of the reflexes, the development
of the degenerative reaction, and atrophy of the muscles. In facial
paralysis of cerebral origin the frontal and orbital branches are not at
all or but slightly affected, leaving the eye with its natural
appearance, in contrast to the lagophthalmos, and the open eye
which does not close even in sleep. In cerebral paralysis the reflexes
are normal and the muscles retain their natural electric reaction.
Accompanying brain symptoms assure the diagnosis. In facial
paralysis of bulbar origin the electric reactions are diminished, and
we have a complex of symptoms made up in a great measure by the
implication of neighboring nerves. After the diagnosis of a peripheral
facial paralysis has been made, by a careful consideration of the
symptoms we may with more or less accuracy determine at which
point of the nerve the lesion is situated. If there is paralysis of all the
muscles of the face, without alteration of taste or hearing, the electric
reaction of nerve and muscles normal, the nerve is affected outside
of the stylo-mastoid foramen. This is usually the form of slight
rheumatic paralysis. If we discover that the muscles of the external
ear are paralyzed, it shows that the point of lesion is just within the
stylo-mastoid foramen, where the posterior auricular branch is given
off from the facial. If with paralysis of the face there is alteration of
the sense of taste, with dryness of the mouth, without interference
with hearing, the trunk of the nerve is affected within the Fallopian
canal, involving the chorda tympani fibres below the point where the
stapedius nerve is given off. If to the above symptoms there is added
over-sensitiveness to sounds, hyperacuisis, and there is no paralysis
of the palate, we have the nerve affected still higher up, but below
the geniculate ganglion. If the geniculate ganglion is involved, there
is, in addition to the foregoing, symptoms of paralysis of the palate.
If, now, the lesion is above the geniculate ganglion, we will have
eliminated the symptom due to implication of the chorda tympani,
which leaves the trunk of the facial at the geniculate ganglion, and
the sense of taste is unaffected, while there remains paralysis of the
face, dryness of the mouth (the secretory fibres run in the trunk of
the seventh), hyperacuisis, and paralysis of the palate.

It was in facial paralysis that the first observations upon the

degenerative reaction in muscles were made, and it is in that
affection that these electric phenomena have been best studied, and
give us the clearest indications for prognosis and treatment in
peripheral paralysis generally. In rheumatic facial paralysis, the most
common form of peripheral facial paralysis, the electric reactions of
the paralyzed muscles enable us to classify the cases into three
groups, the prognosis and duration of which vary very much. In the
first group are the slight forms of facial paralysis. Here the faradic or
galvanic current, applied to nerve or muscles, causes an ordinary
contraction; the electric reactions are normal. These cases scarcely
require treatment, and recover in two or three weeks. In a second
group are those cases in which within a short time after the invasion
of the paralysis (two weeks) complete degenerative reaction is
observed. This degenerative reaction, with the accompanying
anatomical changes in nerve and muscle, has already been treated
of in this article, and it is sufficient here to say that it is marked by
total loss of electric excitability, both faradic and galvanic, in the
nerve, loss of faradic and increased galvanic excitability in the
paralyzed muscles, with a reversal of the normal reply of the
muscles to the different poles of the galvanic battery. These cases
constitute the severe form of rheumatic facial paralysis, and the
prognosis is grave, recovery takes place only after months, and even
after the lapse of years traces of the disease remain in the imperfect
action of the muscles. A third group of cases are of a gravity
intermediate between these two. In them is present the milder form
of degenerative reaction; that is, there is a diminution, but not a total
loss, of electric excitability in the nerve for both the galvanic and
faradic currents; but in the muscles there is a marked increase of
galvanic excitability, with qualitative change—i.e. greater contraction
upon application to them of the positive than of the negative pole.
These cases may be expected to recover in from four to eight
weeks, the muscles still exhibiting the degenerative reaction after
voluntary motion has returned. Among the symptoms to be
particularly noticed in the progress of the severe forms of facial
paralysis are spasmodic twitchings or spasms of the muscles on the
affected side of the face, about the angle of the mouth, and around
the eye, occurring spontaneously or when voluntary movements are
made. Also a state of tonic contraction and rigidity may develop in
some of the muscles, causing a permanent elevation of the angle of
the mouth, a narrowing of the opening of the eye, or a rigidity of the
cheek. These symptoms have been erroneously attributed to the use
of electricity in the treatment, but they occur as frequently in cases in
which it has not been employed. Traumatic facial paralysis, as from
wounds, surgical operations, use of the forceps in delivery, or
paralysis from compression of the nerve, as from tumors, syphilitic
thickening of the dura mater, etc., do not require a detailed mention
here, as such cases come under the head of nerve-injuries, already
discussed. Paralysis of both facials (diplegia facialis), in so far as it is
caused by peripheral nerve lesion, is an accidental occurrence, and
need not be considered as a separate form of facial paralysis. It is
often the result of central disease.

The TREATMENT of peripheral facial paralysis must begin with the

effort to remove its cause. If syphilis is suspected, mercury and
iodide of potassium must be freely used. If the cause is an affection
of the middle ear, this must be treated. Wounds or traumatic injuries
must receive the necessary surgical attention. In addition, in such
cases electricity must be employed in the manner presently to be
described. In cases of rheumatic facial paralysis the treatment will
vary with their gravity. In the lighter form in which the nerve is
affected outside of the Fallopian canal, recovery takes place in a
comparatively short time, even without treatment, but is hastened by
the use of the faradic or galvanic current daily along the branches of
the nerve. In the severe form we must open the treatment by an
attempt to combat the condition of inflammation—of inflammatory
exudation—which we suppose exists within the Fallopian canal.
Local blood-letting by leeching upon the mastoid process may be
appropriately used in the very first outset of the paralysis. Iodide of
potassium, given persistently in large doses during the earlier period
of the disease, appears to act beneficially independently of any
syphilitic taint. Electricity is the remedy, however, on which most
reliance is to be placed in the treatment of rheumatic facial paralysis,
and the manner of its application may be taken as a model of how it
should be employed in all cases of peripheral paralysis. The galvanic
current, on account of its power of penetrating to the deeper parts
and its catalytic action, is to be preferred for the direct electrical
treatment of the nerve which should be instituted in recent cases. Its
action is best obtained by placing the positive pole behind the ear on
the affected side, the cathode behind the opposite ear, and passing
a moderate current across the base of the skull (the affected nerve
being thus in the course of the current) for one or two minutes.
Occasionally the position of the poles may be reversed. Besides this
direct application of galvanism to the point of lesion, it is necessary
to make a peripheral application of electricity to the branches of the
nerve and to the paralyzed muscles. For this we use both the faradic
and galvanic currents. The galvanic current is used by applying the
positive pole stationary behind the ear, while the negative pole, with
an electrode of suitable size, is stroked over each branch of the
nerve and applied to each muscle, a current being used sufficiently
strong to produce decided contractions. This peripheral application
should be made once daily, the time of application being from two to
five minutes. The application of the faradic current is made by simply
placing one electrode upon an indifferent spot, and moving the other
over the face, with a current strong enough to cause contractions if
the muscles still respond to it, or if they do not of such strength as
the patient can bear without discomfort. Without doubt, one of the
beneficial effects of peripheral electrization is the reflex excitement of
the facial above the point of lesion through the irritation of the
terminations of the fifth nerve in the skin. A certain advantage
derived from it is that it maintains the tone of the paralyzed muscles,
which in the case of the orbicularis palpebrarum is of great
importance in preventing the eversion of the lower lid and the
overflow of the tears. As it is impossible during the first days
succeeding the paralysis to distinguish severe cases from those of
the middle form, it is best to begin the treatment of all cases in the
manner above described. The use of strychnia in rheumatic facial
paralysis, both internally and by hypodermic injection, may be
mentioned on account of the widespread preposession in its favor,
and to point out distinctly its utter futility.

Mechanical appliances and manipulation are used with advantage in

the treatment of facial paralysis to prevent the paralyzed muscles
about the mouth and cheek from being drawn out of place and over-
stretched by the action of the sound ones of the opposite side, thus
having their tonicity and nutrition impaired.

Contractions and rigidity of muscles receive little benefit from the use
of electricity, and must be treated by mechanical procedures, such
as stretching, massage, etc.

Neuromata.

The term neuromata was applied to all tumors involving the nerve-
trunks at a time when their histological differences had not been
studied and they were all supposed to be composed of nerve-tissue;
and even yet the name is conveniently retained, because, although
differing widely histologically, tumors situated upon the nerves have
a very similar clinical history.

Neuromas must be divided into true and false, the true consisting of
nerve-tissue, the false, or pseudo-neuromas, being composed of
many varieties, having this only in common, that they are seated
upon the nerves.

The true neuromas are again subdivided into those in which the
nerve-tissue composing them resembles exactly the fibres of the
peripheral nerves, showing with the microscope the double-
contoured white substance of Schwann surrounding an axis-cylinder,
and those in which the tumor is made up of fibres which Virchow has
shown to be non-medullated nerve-fibres—i.e. the axis-cylinder
without the white substance of Schwann. These two forms have
been distinguished by the names myelinic and non-myelinic. The
true neuromas are non-malignant, although showing the tendency to
recur after extirpation, are of slow growth, and as a rule do not
increase to a very great size. The best type of the myelinic neuromas
is found in the spherical or spindle-shaped enlargements at the cut
ends of nerves, particularly in the stumps of amputated limbs, where
they are found oftenest intimately connected with the cicatricial
tissue, though sometimes lying free. They consist of true medullated
fibres mixed with some fibrous tissue. The fibres composing them
are derived partly from splitting up and proliferation of the fibres of
the nerve itself, partly are of new formation, the appearances
strongly recalling the process of regeneration in nerves. Myelinic
neuromas consist of fibres and nuclei so closely resembling in
microscopic appearance the fibromas that they have hitherto been
confounded with them; and there is a difference among the highest
authorities as to the certainty of their diagnosis, and, in
consequence, of the frequency of their occurrence. The true
neuromas may include in their structure all of the fibres of the nerve-
trunk or only a portion of them (partial neuroma)—a fact of
importance in their symptomatology. Of the false neuromas, the
fibromas are by far the most frequently met with. They appear as
knots, more or less hard, upon the course of the nerve-trunk, which
they may involve completely or partially. They are often excessively
painful to the touch or spontaneously, most of the so-called tubercula
dolorosa belonging to the fibro-neuromas. Fibromas sometimes
occur along the trunk and branches of a nerve, forming a plexus of
knotted cords (plexiform neuroma). Fibro-sarcomas are not an
infrequent form of neuroma.

Myxomas often occur upon the peripheral nerves, and are frequently
multiple, their points of predilection being the larger trunks, as the
sciatic, ulnar, etc. They show their characteristic soft structure, and
are usually spindle-shape, assuming a rounder form as they attain a
large size. The various forms of sarcoma occasionally form tumors
upon the nerves, attacking generally the large trunks. Carcinomatous
tumors beginning upon the nerves sometimes occur, but as a rule
these growths involve the nerve by extension to it from adjacent
parts.

Syphilitic gummata have been found almost exclusively upon the

intracranial portion of the cranial nerves.

Gliomas appear to affect only the optic and acoustic nerves. Lepra
nervorum (lepra anæsthetica) produces usually a spindle-form
thickening upon the nerve-trunks, but sometimes there are more
distinct knots, which may be felt beneath the skin, bead-like, along
the course of the nerves of the extremities.

Like the true neuromas, the false neuromas, developing from the
neurilemma and perineurium, may involve the whole or only a part of
the fibres of a nerve, or the nerve-fibres may run at the side of the
tumor—different conditions, which may alter materially the effects
produced upon the nerve.

Neuromas, both false and true, may occur not only singly, but often
in large numbers, many hundreds having been counted upon an
individual. Sometimes they are numerous upon a single nerve-trunk
and its branches, and again they may appear scattered over nearly
all of the nerves of the body, even to the cauda equina and roots of
the nerves. According to Erb,9 isolated neuromas are more frequent
in females, while multiple neuromas are found almost exclusively in
men. Neuromas vary greatly in size, as we might expect from the
very great difference of their nature and structure; sometimes no
larger than a pea, they may attain the size of a child's head.
9 Ziemssen's Handbuch.

ETIOLOGY.—In cases of multiple neuromata it would seem as if there

was a constitutional condition or diathesis as the foundation of the
affection. This we may the more readily believe as there appears
good evidence to show that the tendency to the formation of these
nerve-tumors is sometimes hereditary, and some of them are
congenital.

Idiots and cretins have been observed to suffer in undue proportion

with multiple neuromas. We find a direct exciting cause of neuromas
in mechanical injuries of nerves, wounds, blows, pressure, etc. Thus,
as has been already seen, true neuromas occur in the divided ends
of the nerves after amputations or otherwise where a nerve-trunk
has been divided (cicatricial neuroma). As such neuromas are in
some degree the result of inflammation, it is probable that they may
sometimes be caused by chronic neuritis.

For a large number of neuromas no cause can be assigned, and we

must at present consider them as originating spontaneously.

SYMPTOMS.—The position and connections of neuromas being so

different, sometimes simply in contact with the nerve; sometimes
situated in the thickness of the nerve-trunk, the fibres being pressed
aside and spread out upon the surface of the tumor; sometimes
involving in their tissue a part or the whole of the nerve-fibres,—we
cannot but expect a very marked difference in their clinical history.
Not a few cases occur in which the presence of neuromas, even in
large numbers, gives rise to no symptoms during life, and their
existence has been revealed only upon a post-mortem examination.

The symptom most common to neuromas, and one to be expected

from their mechanical interference with the nerves, is neuralgic pain
—sometimes extreme, local or shooting along the course of the
nerves, stubborn, and hardly to be alleviated by remedies. It is
paroxysmal, notwithstanding the unvarying character of its cause, in
consonance with the tendency to periodical activity which prevails in
the nervous system. Sometimes the pain is increased notably by
atmospheric changes. The pain may sometimes be arrested by firm
pressure upon the nerve above the seat of the tumor. In some cases
pressure upon the neuroma, or even handling it, causes great pain.
The intensity of the pain does not depend upon the size of the tumor,
some of the smallest having earned the appropriate name of
tubercula dolorosa. The continued irritation of a neuroma sometimes
produces a condition of general nervous excitability, which shows
itself in hysterical and even in true epileptic convulsions.
Occasionally there are abnormal sensations (paræsthesiæ),
formication, numbness, etc., in the distribution of the nerve affected,
and when from pressure or histological changes the fibres are
destroyed anæsthesia results.

The interference with the conductivity of the motor fibres, which

occurs less frequently than alterations of sensation, shows itself in
cramps, tumors, paresis, and paralysis, according to its degree.

Neuromas may destroy life by the continued excessive pain, which

wears down the strength and depresses the vitality. Death may be
caused by their peculiar situation; as, for instance, upon the cauda
equina, where they produce paraplegia, paralysis of the sphincter
and bladder, and trophic changes.

The DIAGNOSIS of neuromas can only be made when they are

sufficiently superficial to be recognized by the touch, and along with
the symptoms above detailed the tumor is situated upon the known
course of a nerve, to which, moreover, its attachment allows a lateral
movement.

The only TREATMENT available for neuromas is extirpation, which must

be conducted with a view to sparing any fibres of the nerve not
involved in the tumor. Where it is necessary to divide the nerve in the
removal of the tumor, as small a portion as possible must be
excised, with the hope of a regeneration and reuniting of the cut
ends. The success of extirpation depends largely upon the nature of
the neuroma. The true neuromas, while they often show a strong
tendency to recur after removal, are benign and show no metastasis.
For the false neuromas the prognosis will be in accordance with their
benign or malignant character.
NEURALGIA.
 BY J. J. PUTNAM, M.D.

DEFINITION.—It is customary to describe as neuralgic those pains for

which no adequate cause can be assigned in any irritation of the
sensory nerves from outside, which recur paroxysmally, are
unattended by fever, and are distributed along the course of one or
more nerves or nerve-branches.

The general use of the term neuralgia further implies the common
belief that there is a disease or neurosis, not covered by any other
designation, of which these pains are the characteristic symptom. Of
the pathological anatomy of such a disease, however, nothing is
known; and if it could be shown for any given group of cases that the
symptoms which they present could be explained by referring them
to pathological conditions with which we are already familiar, these
cases would no longer properly be classified under the head of
neuralgia.

The attempt has frequently been made, and on good grounds, in

obedience to this reasoning, to cut down the list of the neuralgias,
strictly so called, and to account for many of the groups of symptoms
usually classified under that head by referring them to anæmia or
congestion of the sensory nerves, to neuritis, etc.

One of the best and most recent statements of this view is that of
Hallopeau,1 who, although he does not wholly deny the existence of
a neurosis which may manifest itself as neuralgia, goes so far as to
maintain that the gradual onset and decline and more or less
protracted course so common in the superficial neuralgias, such as
sciatica, suggest rather the phases of an inflammatory process than
the transitions of a functional neurotic outbreak, and that, in general
terms, a number of distinct affections are often included under the
name of neuralgia which are really of different origin, one from the
other, and resemble each other only superficially. This subject will be
discussed in the section on Pathology, and until then we shall, for
convenience' sake, treat of the various neuralgic attacks as if they
were modifications of one and the same disease.
1 Nouveau Dict. de Méd. et de Chir. pratiques, art. “Névalgies.”

GENERAL SYMPTOMATOLOGY.—The neuralgias may be conveniently

divided into—1, external or superficial; 2, visceral; 3, migraine and
the migrainoid headaches.

Superficial Neuralgia.

The most prominent symptom of a neuralgic attack of the superficial

nerves is of course the pain, and sometimes, from first to last, no
other sign of disease is present. In an acute attack the pain is usually
ushered in by a sense of discomfort, which the patient vainly tries to
shake off, or by a feeling of weight and pressure or of numbness and
prickling, or of itching. Sometimes, though far less often than in the
case of migraine, there are prodromal signs of a more general
character, such as a feeling of thirst2 or of mental depression or
drowsiness.
2 Spoken of by Mitchell's patient with neuralgia of the stump (see below).

A dart of pain may then be felt, which soon disappears, but again
returns, covering this time a wider area or occupying a new spot as
well as the old. The intensity, extension, and frequency of the
paroxysms then increase with greater or less rapidity, but, as a rule,
certain spots remain as foci of pain, which radiates from them in
various directions, principally up or down in the track of the nerve-
trunk mainly implicated. The pain rarely or never occupies the whole
course and region of distribution of a large nerve or plexus, but only
certain portions, which may be nearly isolated from one another.
In an acute attack the affected parts may at first look pale and feel
chilly, and later they frequently become congested and throb.
Mucous surfaces or glandular organs in the neighborhood often
secrete profusely, sometimes after passing through a preliminary
stage of dryness.

The skin often becomes acutely sensitive to the touch, even though
firm, deep pressure may relieve the suffering. Movement of the
painful parts, whether active or passive, is apt to increase the pain.
When the attack is at its height, the pain is apt to be felt over a larger
area than at an earlier or a later period, and may involve other
nerves than those first attacked. Thus, a brachial becomes a cervico-
brachial neuralgia or involves also the mammary or intercostal
nerves. A peculiarly close relationship exists between the neuralgias
of the trigeminal and of the occipital nerves. It is said that when the
attack is severe the corresponding nerves of the opposite side may
become the seat of pain. This is perhaps remotely analogous to the
complete transference of the pain from one side to the other which is
so characteristic of periodical neuralgic headaches, especially if they
last more than one day.

Some cutaneous neuralgias pass away after a few hours' or a night's

rest, after the manner of a migraine or a headache, and patients in
whom this takes place are, as a rule, constitutionally subject to
neuralgia or other neuroses. Toward the end of such an attack there
is often a copious secretion of pale, limpid urine. In a large class of
cases, on the other hand, the attack is of several days' or weeks', or
even months' or years', duration, with remissions or intermissions
and exacerbations, which may be either periodical or irregular.

The most marked periodicity of recurrence is seen with the

neuralgias of malarial origin, which may take on any one of the
typical forms of that disease.

These malarial neuralgias affect pre-eminently, though not

exclusively, the supraorbital branch of the fifth nerve; but it should
not be forgotten that there is also a typically periodical supraorbital
neuralgia of non-malarial origin, of which the writer has seen several
pronounced examples, the pain usually recurring regularly every
morning at eight or nine o'clock and passing away early in the
afternoon. The same periodicity is seen, though less often, in other
neuralgias. Thus, Trousseau3 speaks of neuralgic attacks from
cancer of the uterus in a young woman, which recurred daily at
exactly the same hour. Some of the traumatic neuralgias show the
same peculiarity to a marked degree.
3 Clin. Méd.

In many neuralgias, on the other hand, the exacerbations are worse

at night, like the pains of neuritis. In the intervals between the attacks
the pain may be wholly absent, or may persist, usually as a dull
aching.

After a neuralgia has lasted a few days—sometimes, indeed, from

the outset if the attack is severe—it is usually found that definite
spots of tenderness have made their appearance at certain limited
points on the course of the nerve. These are the famous points
douloureux which Valleix described with such minute accuracy,
believing them to be invariably present in true neuralgias. This is
certainly not strictly the case, though they are very common. They
are not necessarily coincident with the foci of spontaneous pain, as
Valleix supposed, but do correspond in general to the points at which
the affected nerve emerges from its bony canal or from deep
muscles and fascia, and to portions of its area of distribution in the
skin. The spinous process corresponding to an affected spinal nerve
may also become tender, but this is probably to be looked on, like
the same symptom in so-called spinal irritation, not as a sign of local
disease, but as due to a general reaction on the part of the nervous
system, and as a fact of a different order from the tenderness along
the nerve.

The termination of an acute neuralgic attack is usually gradual, like

its onset, although in some cases of headache, and in other
neuralgias to a less degree, there comes a moment when the patient
suddenly declares that he is free from pain.