CHEM2 Instructor’s Manual

Solutions Manual for CHEM 2 Chemistry in Your World

2nd Edition by Hogg ISBN 113396298X 9781133962984
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1. Definitions
a. A cation is an ion with a positive charge.
b. An anion is an ion with a negative charge.
c. Atoms react to acquire an electron configuration with 8 electrons in the outermost shell to
match the configuration of the nearest noble gas.
d. The formula unit is the simplest element ratio for an ionic compound like NaCl instead of
Na2Cl2.
2. Definitions
a. Nonmetals are elements that form negative ions and acidic oxides, are nonconductors of
heat and electricity. They are found in the upper right corner of the Periodic Table.
b. A compound consisting of two different elements like carbon monoxide, CO
3. Definitions
a. a pair of electrons shared between two atoms
b. four electrons (2 pairs) shared by two atoms
c. six electrons (3 pairs) shared between two atoms
d. pair of valence electrons on an atom that are not shared with another atom
e. a pair of electrons shared between two atoms
f. either a double or a triple bond
4. Definitions
a. A covalent bond exists between two atoms that share two or more electrons
b. An ion consisting of two or more different elements, like PO43−
c. The type of bond that exists between two oppositely charged ions like Na+ and Cl−.
d. a compound formed between two elements
5. Definitions
a. bond between two atoms that share electrons equally
b. bond between two atoms that do not attract shared electrons equally

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Chapter 5 CHEM2

6. The octet rule says that atoms lose and gain electrons to reach the nearest noble gas electron
configuration. Sodium, 2-8-1, would lose one electron to achieve the 10 electron neon noble
gas electron configuration, 2-8. A nonmetal like oxygen, 2-6, would gain two electrons to
achieve the 2-8 electron configuration of neon.
7. Definition/description
a. A hydrocarbon is a compound consisting only of carbon and hydrogen.
b. a compound consisting only of carbon and hydrogen with only single bonds
c. a compound consisting only of carbon and hydrogen with one or more multiple bonds
between carbon atoms
d. Alkenes are hydrocarbons with one or more carbon-carbon double bonds.
8. A Ca3+ ion is not possible because the energy required to remove a third electron is much
greater than the energy available in chemical reactions. This third electron would need to
come from the set of electrons in the noble gas 2-8-8 electron configuration for argon.
9. Predict the ions
a. Br1−
b. Al3+
c. Nal+
d. Ba2+
e. Ca2+
f. Ga3+
g. I1−
h. S2-
i. Group 1A atoms lose one valence electron to form a +1 ion, see 9c above.
j. Group 7A atoms have seven valence electrons and gain one to form a 1- ion, see 9g.
10. An ion with 12 protons and 10 electrons will have a +2 charge; magnesium has 12 protons,
Mg2+. The number of protons stays the same. The number of protons exceeds the number of
electrons by 2.
11. Formulas and names
a. AlI3 aluminum iodide
b. SrCl2 strontium chloride
c. Ca3N2 calcium nitride
d. K2S potassium sulfide
e. Al2S3 aluminum sulfide
f. Li3N lithium nitride
12. Electrostatic attractions between positive and negative ions in an ionic lattice hold the solid

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 CHEM2 Instructor’s Manual

together. These attractions are not limited to the nearest ions. The example is a NaCl lattice.
Each ion is attracted to all the oppositely charged ions in the lattice. The attraction decreases
as the distance between oppositely charged ions increases.
13. Nomenclature
a. calcium sulfate
b. sodium phosphate
c. sodium bicarbonate
d. potassium hydrogen phosphate
e. sodium nitrite
f. copper(II) nitrate
14. Variants
a. water or dihydrogen monoxide
b. molecular oxygen or dioxide
c. hydrogen peroxide or dihydrogen dioxide
15. Formulas
a. Lithium is in Group 1A so it forms the Li1+ ion. Tellurium is in Group 6A and forms the
Te2− ion. The formula for the neutral ionic combination is Li2Te.

b. MgBr2
c. Ga2S3
16. a. CaCl2
b. SrCO3
c. Mg(OH)2
d. Fe2O3
e. K2PO4
17. a. With a ratio of three telluride anions for every two bismuth cations, the most likely
formula is Bi2Te3.
b. Bismuth cations have a +3 charge, so for bismuth telluride to be electrically neutral, the
telluride anion must have a charge of –2.
18. Because the ammonium cation has a charge of +1, the charge of the perchlorate anion must
be –1 for the compound to be electrically neutral.
19. a. (NH4)3PO4
b. Na2SO4
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Chapter 5 CHEM2

c. CuCl2
d. Cr(NO3)3
e. KBr
f. CaCO3
g. NaClO
20. Ionic bonds differ from covalent because of the differences in the kinds of atoms that are
bonded. Ionic bonds are formed between atoms of widely different electron attracting power;
the more electron attracting atom gains one or more electrons to become a negative ion and
the less electron attracting atom loses one or more electrons to become a positive ion.
Covalent bonds are formed between atoms of similar electron attracting power; the two
atoms share one or more pairs of electrons to give complete octets; neither atom gains or
loses a whole electron. Metals typically combine with nonmetals to form ionic bonds while
nonmetals and nonmetals combine to form covalent bonds.
21. Types of bonding
a. ionic
b. covalent
c. ionic
d. covalent
e. covalent
22. Inorganic compounds
F O Cl S Br Se
Na NaF Na2O NaCl Na2S NaBr Na2Se
K KF K2O KCl K2S KBr K2Se
B BF3 B2O3 BCl3 B2S3 BBr3 B2Se3
Al AlF3 Al2O3 AlCl3 Al2S3 AlBr3 Al2Se3
Ga GaF3 Ga2O3 GaCl3 Ga2S3 GaBr3 Ga2Se3
C CF4 CO2 CCl4 CS2 CBr4 CSe2
Si SiF4 SiO2 SiCl4 SiS2 SiBr4 SiSe2
23. Formulas and names
a. NO, nitrogen monoxide
b. SO3, sulfur trioxide
c. N2O, dinitrogen oxide
d. NO2, nitrogen dioxide
24. a. Covalent, nitrogen tribromide
b. Ionic, zinc iodide
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 CHEM2 Instructor’s Manual

c. Covalent, carbon tetrachloride

d. Covalent, hydrogen bromide
e. Ionic, chromium(III) oxide

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Chapter 5 CHEM2

25. Lewis structures

a. b. c. d.

e. f. g. h.
26. Ionic bonding exists between oppositely-charged ions. The polar covalent bond exists
between atoms that share electrons unequally. The nonpolar bonding exists between atoms
that share electrons equally (atoms with similar attractions for electrons).
27. Shapes

a. Tetrahedral b. Trigonal-pyamidal c. Bent

28. Polarity
a. The electron attracting power differences determine the polarity of the bonds. The farther
apart two elements are in the periodic table the more polar the bond. The C—Cl bond is
more polar because they are farther apart in the periodic table.
b. The C—F bond is more polar than the C—Cl bond.
29. The octet rule states that in order for an atom to be stable it must have a total of 8 electrons or
4 pairs (either lone or bonding pairs) around it. A molecule with an odd number of electrons
will have one electron that is not paired and not satisfy the octet rule. For example, NO has
11 valence electrons with only oxygen satisfying the octet rule with 8 valence electrons while
nitrogen only has 7 electrons and will never satisfy the octet rule unless nitrogen gains an
electron.
30. eleven valence electrons
31. H—F because the difference in electronegativity is the greatest. Fluorine draws electrons
away from hydrogen more than chlorine and bromine because it has the highest
electronegativity.

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 CHEM2 Instructor’s Manual

32. Polarity of molecules

a. Polar; O is the negative end and C is the positive end. The arrow indicates the direction
electrons shift in the molecule.
b. Nonpolar; the bonds are nonpolar. The molecule is tetrahedral and symmetric.
c. Nonpolar; the bonds are polar but the planar triangular shape puts the center of positive
charge and the center of negative charge in the middle of the boron atom.
d. Polar; F is the negative end and H is the positive end.
33. Polarity of molecules
a. Polar; oxygen draws electrons and makes that end of the molecule negative.
b. Nonpolar; there are no polar bonds in the butane molecule.
c. Polar; nitrogen draws electrons so the nitrogen end of the molecule is negative; the
molecule is a trigonal pyramid.
34. States of Matter
a. The gaseous state has no definite shape or volume; a gas takes the shape and volume of
its container. Gases are compressible.
b. A liquid has definite volume and assumes the shape of the container. The liquid
molecules are free to move past each other, allowing the liquid to flow and assume the
shape of its container. Liquids are relatively incompressible.
c. The solid state has definite shape and definite volume. The molecules or ions making up
the solid are in direct contact and located at fixed positions. The solid is incompressible
due to direct contact between the particles.
35. Pairs in ethanol
a. The total valence electron count is done by adding all contributions from each atom.
Valence electrons Valence electrons Valence electrons Total valence
from hydrogen from oxygen from carbon electrons
6×1 1×6 2×4 20
b. 8 single bonds
c. 8 bonding pairs
There are 2 nonbonding pairs of electrons on the oxygen (see figure below).

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Chapter 5 CHEM2

36. a electron geometry = tetrahedral; molecular geometry = tetrahedral

b. electron geometry = tetrahedral; molecular geometry = trigonal pyramidal
37. (b) solid
38. A gas has the greatest average distance between particles. Gas compressibility is evidence for
this.
39. The number of gas molecules in a given volume of gas decreases as you move away from the
earth's surface. The fewer number of molecules collide with any object less often and exert
less push or pressure. Additionally, the force of Earth's gravity decreases with altitude. This
results in less weight or force per unit area at greater altitudes.
40. Particles in a liquid are in constant motion; this is shown when one liquid diffuses in another
(a drop of ink or food coloring will slowly spread throughout a glass of water even though
you do not stir the mixture). Particles in a liquid are close together. This makes liquids nearly
incompressible.
41. Gas molecules are constantly moving. The gas molecules of the perfume vapor diffuse away
from the person wearing the perfume.
42. Pressure in an automobile tire decreases in cold weather because average kinetic energy goes
down and molecules collide less often with the tire walls. The tire volume remains the same
at all temperatures.
43. Water has an unusually high normal boiling point and surface tension. Additionally it
expands on freezing.
44. H bonding
The hydrogen bond (shown as a faint line) in
Hydrogen bonds H water exists between a hydrogen atom in one
O O
H
water molecule and an oxygen atom in a
O H
H H
H H
different water molecule. One oxygen atom is
O typically hydrogen bonded to two different water
H molecules.
45. Evaporation of water from one's skin draws energy from the skin. This produces a resulting
"chilling" sensation. We are cooled when the energy flows into the evaporating liquid.
46. Structure and Hydrogen bonding
a. Yes. Hydrogen is covalently bonded to a very electron attracting oxygen atom. The
hydrogen in the O-H group can hydrogen bond to an oxygen in another molecule.
b. Yes. In ammonia, hydrogen is covalently bonded to a very attracting nitrogen atom. The
N-H bond is very polar and hydrogens in one
NH3 can hydrogen bond to a nitrogen in a
different NH3 molecule.
c. No. Sulfur dioxide, SO2, has no hydrogens so
no hydrogen bonding is possible even though it is a bent polar
molecule.

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 CHEM2 Instructor’s Manual

d. No. Carbon dioxide, CO2, has no hydrogens so it cannot show

hydrogen bonding. It is a linear nonpolar molecule.
e. No. Methane does not show hydrogen bonding even though it has
four hydrogens. The electron attracting power of hydrogen and carbon are similar. The C-
H bond is not polar enough to produce hydrogen bonding between methane molecules.
f. Yes. Hydrogen is covalently bonded to fluorine in HF.
The electron attracting powers are very different. This is
the most polar bond formed by a hydrogen atom. The
hydrogen in one HF molecule can hydrogen bond to fluorines in neighboring HF
molecules.
g. No. The hydrogens are bonded to the carbon atoms not the oxygen.
The electron attracting power of carbon and hydrogen are similar so
the bonds are not polar enough to produce hydrogen bonding.
47. The solubility of an ionic substance is dependent on the strength of the attraction between the
ions and the strength with which the solvent (water, here) can hold on to dissolved ions. The
insolubility must be a result of an attraction between barium and sulfate ions that is stronger
than the attraction between water and barium or sulfate ions.
48. Without hydrogen bonding the boiling point for ammonia would be −100°C. See Figure 5.9.
49. There are great distances between particles in the gas state while particles in the liquid and
solid states are in direct contact. The gas molecules are separated by distances equal to about
1000 molecular diameters. This is empty space, a vacuum.
50. Because heat is being released, the process is exothermic.
51. The increased pressure creates more collisions of gas molecules with the solvent surface.
These more frequent collisions create more opportunities for the gas to dissolve in the
solvent. Champagne, sparkling waters, Coca-Cola, and Pepsi are examples.
52. Attractive forces between particles in the surface layer are unbalanced because the particles
are attracted by the bulk of the liquid below the surface. Water has a high surface tension
because of the strong intermolecular forces between molecules.
53. The concentration of dissolved oxygen is controlled by the relation C = kP. The
concentration of dissolved oxygen is 0.0109 g O2/L when the pressure is 1 atm. This means
that when the O2 pressure decreases from 1 atm to 0.5 atm the concentration of oxygen will
decrease by ½ to 0.00545 g/L. Rounded to 1 sf this becomes 0.005 g/L.
54. three times as much
55. solid because temperature is lower than mp .
56. When acetone is at −50°C and 1 atm, this is warmer than the melting point of −95°C and
colder than the normal boiling point of boils at 56.5°C. Acetone will be a liquid.
57. below 646°C, at approximately 500°C.

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Chapter 5 CHEM2

58. Octane, C8H18, should have a boiling point between the boiling points for heptane, C7H16;
98.4°C and nonane, C9H20; 150°C. The boiling points can be assumed to increase by a
regular amount with every additional CH2 unit. The boiling point increased by 29.7°C when
the molecule size increased from hexane to heptane. From heptane to nonane the boiling
point change is 52.4°C. The boiling point for octane should be about halfway between the
heptane and nonane boiling points. This would make it about 26-30°C more than 98.4°C. A
boiling point in the range of 124-128°C for octane is a reasonable answer.

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whether their seat is central or peripheral. We will notice here some
of the prominent symptoms resulting from nerve injuries which may
be useful in distinguishing peripheral from central lesions, although
in many cases it is only by the careful consideration of all symptoms
and the impartial weighing of all attending circumstances that a
probable conclusion can be arrived at.

The rapid loss of muscular tone and the early atrophy of the muscles
is a mark of paralysis from nerve-injury which distinguishes it from
cerebral paralysis, even when the latter occupies circumscribed
areas, as is sometimes the case in cortical brain lesion. In spinal
paralysis also the muscles retain their tone and volume (the latter
being slightly diminished by disuse), except in extensive destruction
of gray matter, when all tonicity is lost, and in lesions of the anterior
horns of gray matter (poliomyelitis), when there is loss of muscular
tone and marked atrophy. The first of these spinal affections may be
distinguished by the profound anæsthesia and by the paralysis being
bilateral—by the implication of bladder and rectum and the tendency
to the formation of bed-sores; such symptoms being only possible
from nerve-injury when the cauda equina is involved. In poliomyelitis
the complete integrity of sensation—which is almost always
interfered with at some period after nerve-injury—and the history of
previous constitutional disturbance will aid us in recognizing the
diseased condition. While the reflexes are wanting in peripheral, they
are, as a rule, retained, and often exaggerated, in cerebral and
spinal paralysis; the exceptions being in the two lesions of the cord
above mentioned, in which the reflex arc is of course destroyed by
the implication of the gray matter. Loss or alteration of sensation,
where it occurs from nerve-injury, generally shows itself in the
distribution of the nerve, while the sensitive disturbances from
disease or injury of the brain or spinal cord are less strictly confined
to special nerve territories. The trophic disturbances arising from
nerve-irritation are distinctively characteristic of nerve-injury.

But it is in the behavior of the nerves and muscles to electricity that

we find some of the strongest points on which to base a diagnosis of
nerve-injury, and, although not always conclusive as to the seat of
lesion, it enables us to reduce within very narrow limits the field for
discrimination. The degenerative reaction which we have seen takes
place in muscles the continuity of whose nerves have been
destroyed, or in which degenerative changes have taken place in
consequence of injury to their nerves, is never found in muscles
paralyzed from the brain. In spinal paralysis resulting from
transverse myelitis the electrical excitability of the nerves and
muscles may be increased or diminished, but there is no
degenerative reaction. In progressive muscular atrophy a careful
electrical examination may discover the degenerative reaction in the
affected muscles; but it is too obscure, and there are besides too
many characteristic symptoms in that disease, to allow of a practical
difficulty in diagnosis from its presence. In poliomyelitis anterior
(infantile paralysis and the kindred affection in the adult) we have, it
is true, the quantitative, qualitative changes of degenerative reaction,
such as are seen after nerve-injury, and in such cases its presence
is not conclusive of peripheral lesion. Here we may be assisted by
remembering that while in poliomyelitis sensation is intact, in nerve-
injury it is almost always affected in a greater or less degree,
although it may have been recognizable but for a short time. In lead
paralysis we also have the degenerative reaction, but whether the
seat of lesion in that affection is central or peripheral is an undecided
question.

TREATMENT OF NERVE-INJURIES.—The therapeutics of nerve-injuries

belong largely to surgery. When there is complete division of a nerve
the ends should be united by suture at the time of injury. When this
has not been done, and after the lapse of time no return of function
is observed, the ends of the nerve should be sought for, refreshed
with the knife, and brought together by suture. There is the more
hope that such a procedure will be successful as we know that after
a time the fibres of the peripheral portion of the nerve may be
regenerated, even when there has been no reunion, and thus be in a
condition to render the operation successful. It is a matter for
consideration whether in injuries in which a certain portion of the
nerve, not too great in extent, has been crushed or otherwise
obviously destroyed, it would not be best to excise the destroyed
portion and bring the ends together. Whether the use of electricity,
the galvanic current, hastens the regeneration and restitution of the
injured nerves cannot be affirmed with certainty, although in practice
this has seemed to us to be the case, and the known catalytic action
of the current gives us a possible explanation of such beneficial
effects. But, however this may be, it is certain that with the first
symptoms of returning function in the nerves and muscles the use of
electricity obviously accelerates the improvement. And, again, in the
treatment of the results of nerve-injury, such as paralysis,
anæsthesia, pain, it is in the careful and very patient use of the
electric currents, both faradic and galvanic, that most confidence is
to be placed; the galvanic being generally most applicable and giving
the better results. The symptoms of nerve-irritation are amongst
those most difficult to treat successfully. Counter-irritation, heat, cold,
electricity, may all be tried in vain, and as a last resource against
pain, ulceration, and perverted nutrition we may be obliged to resort
to nerve-stretching, or neurotomy. Under the head of Neuritis much
must be said of treatment applicable to the inflammation, acute and
chronic, resulting from nerve-injuries.

INFLAMMATION OF NERVES.

Neuritis.

Although inflammation of the nerves has been for a long time a

recognized disease, its frequency and the extent and importance of
its results have been appreciated only within a comparatively short
time. The observations upon neuritis were formerly almost
exclusively confined to acute cases, the results of traumatic lesions
or the invasion of neighboring disease, while the more obscure forms
occurring from cold, toxic substances in the circulation, constitutional
disease, etc., or those apparently of spontaneous origin, escaped
attention, or were classed according to their symptoms simply as
neurosis, functional disease of the nerves, or affections of the spinal
cord. Hence the classic picture of neuritis is made to resemble
exclusively the acute inflammation of other tissues, and tends to
blind as to the subtler but not less important morbid processes in the
nerves which at present we must classify as inflammation, though
wanting, it may be, in some of the striking features seen in
connection with inflammatory processes elsewhere. In short, we
must not look for heat, redness, pain, and swelling as absolutely
necessary to a neuritis.

Entering into the structure of the peripheral nerves we have the true
nervous constituent, the fibres, and the non-nervous constituent, the
peri- and endoneurium, in which are found the blood-vessels and
lymph-channels. Though intimately combined, these tissues,
absolutely distinct structurally and functionally, may be separately
invaded by disease; and although it may not be practicable nor
essential in every case to decide if we have to do with a
parenchymatous or interstitial (peri-) neuritis, it is necessary to keep
in mind how much the picture of disease may be modified according
as one or the other of the constituents of the nerve are separately or
predominantly involved. Thus, a different group of symptoms will be
seen when the vascular peri- and endoneurium is the seat of
inflammation from that which appears when the non-vascular nerve-
fibres are themselves primarily attacked and succumb to the
inflammatory process with simple degeneration of their tissue.
Furthermore, it is not too speculative to consider that the different
kinds of nerve-fibres may be liable separately or in different degrees
to morbid conditions, so that when mixed nerves are the seat of
neuritis, motor, sensitive, or trophic symptoms may have a different
prominence in different cases in proportion as one or other kind of
fibres is most affected.

ETIOLOGY.—Traumatic and mechanical injuries of nerves are the

most common and best understood causes of neuritis. Not only may
it be occasioned by wounds, blows, compression, and other insults
to the nerves themselves, but jolting and concussion of the body,
and even sudden and severe muscular exertion, have been recorded
as giving rise to it. We readily understand how neuritis is caused by
the nerves becoming involved in an inflammation extending to them
from adjacent parts, although the nerves in many instances show a
remarkable resistance to surrounding disease. Less easily
understood but undoubted causes of neuritis are to be found in the
influence of cold, especially when the body is subjected to it after
violent exertion. Although the causal connection is unexplained, we
find neuritis a frequent sequel of acute diseases, as typhoid fever,
diphtheria, smallpox, etc. In the course of many chronic
constitutional affections, as syphilis, gout, elephantiasis græcorum,
we encounter neuritis so frequently as to make us look for its cause
in these diseases. Finally, neuritis may develop apparently
spontaneously in one or many nerves.

MORBID ANATOMY.—The macroscopic appearance of nerves affected

by neuritis is very varied, according as the disease is more interstitial
or parenchymatous, acute or chronic. Sometimes the nerve is
swollen, red, or livid, the blood-vessels distended, with here and
there points of hemorrhage, the glistening white of the fibres being
changed to a dull gray. Sometimes the nerves are reduced to gray
shrunken cords. When the perineurium has been the principal seat
of the inflammation we may have swellings at intervals along the
course of the nerve (neuritis nodosa, perineuritis nodosa acuta) or,
as in chronic neuritis, the trunk of the nerve may be hard and
thickened from proliferation of the connective tissue, sclerosis of the
nerve. The nerve does not always present the appearance of
continuous inflammation, but the evidence of neuritis may be seen at
points along its course which are separated by sound tissue. These
points of predilection are usually exposed positions of the nerve or
near joints. Often the nerve appears to the naked eye normal, and
the characteristic changes of neuritis are only revealed by the
microscope. The microscopical changes in neuritis may extend to all
of the constituents of the nerve, and present the ordinary picture of
acute inflammation, hyperæmia, exudation, accumulation of white
corpuscles in the tissues, and even the formation of pus, the nerve-
fibres exhibiting in various degrees the destruction of the white
substance of Schwann and the axis-cylinder. Or, as in chronic
neuritis, the alterations may consist in the more gradual proliferation
of the peri- and endoneurium, which, contracting, renders the nerve
dense and hard and destroys the nerve-fibres by compression. In
acute as well as in chronic neuritis the perineurium may be
exclusively affected, the fibres remaining normal (Curschman and
Eisenlohr). The nerve-fibres themselves may be the primary and
almost exclusive seat of the neuritis, exhibiting more or less
complete destruction of all their constituent parts, except the sheath
of Schwann, without hyperæmia and with little or no alteration of the
interstitial tissue. Sometimes the fibres are affected at intervals, the
degeneration occupying a segment between two of Ranvier's nodes,
leaving the fibre above and below normal (nèvrite segmentaire peri-
axile, Gombault). All of these lesions of the nerve-fibres may be
recovered from by a process of regeneration, the fibres showing a
remarkable tendency to recover their normal structure and function.

SYMPTOMS OF NEURITIS.—When a mixed nerve is the seat of an acute

neuritis, with hyperæmia of its blood-vessels, it becomes swollen by
inflammatory exudation, and can be felt as a hard cord amongst the
surrounding tissues. It is not only highly sensitive to direct pressure,
but muscular exertion, or even passive movement of the part, excites
pain. Spontaneous pain is one of the most prominent symptoms, and
is sometimes so severe and continuous as to destroy the self-control
of the patient, and demand the employment of every agent we
possess for benumbing sensibility and quieting the excited system.
At first there may be hyperæsthesia of the skin in the region of the
distribution of the nerve, but a much more constant and significant
symptom is cutaneous anæsthesia, which generally makes its
appearance early in the course of the disease. The degree and
extent of the anæsthesia varies very much in different cases, but is
seldom total, except over small areas, even when the inflammation
has seriously damaged the nerve-fibres. This is explained by the
sensibility supplied to the part by neighboring nerves, as already
described in treating of traumatic nerve-injuries. Very characteristic
of acute neuritis are various abnormal sensations (paræsthesiæ)
which are developed in a greater or less degree during the progress
of the disease, and are described by the patients as numbness,
tingling, pins and needles, burning, etc. In a case of acute neuritis of
the ulnar nerve seen by the writer the patient was much annoyed by
a persistent sensation of coldness in the little and ring fingers, which
caused him to keep them heavily wrapped up even in the warm
weather of summer. When motor symptoms make their appearance
they begin with paresis of the muscles, which may increase rapidly
to paralysis. As this is the result of destructive changes, more or less
complete, in the motor nerve-fibres, we will have, as would be
expected, accompanying the paralysis the symptoms already
detailed in the consideration of nerve-injuries with destruction of
continuity—namely, absence of muscular tone, loss of skin and
tendon reflexes, increased mechanical excitability, atrophy of
muscles, and the different forms of degenerative reaction, with loss
of faradic contractility. When spasm or tremor has been observed in
acute neuritis of mixed nerves, it is a matter of doubt whether it is not
to be explained by reflex action of the cord excited by irritated
centripetal fibres. Various trophic symptoms may show themselves,
as herpes zoster or acute œdema. Erythematous streaks and
patches are sometimes observed upon the skin along the course of
the inflamed nerve-trunks. In chronic neuritis, into which acute
neuritis generally subsides or which arises spontaneously, the
symptoms above described are very much modified; indeed, cases
occur which exist for a long time almost without symptoms. While the
affected nerve may be hard and thickened by proliferation of its
connective tissue, pain, spontaneous or elicited by pressure, is not of
the aggravated character present in acute neuritis, and may be quite
a subordinate symptom. It has more of a rheumatic character, is less
distinctly localized, more paroxysmal, and has a greater tendency to
radiate to other nerves. It is probable that many ill-defined, so-called
rheumatic pains which are so frequently complained of are the result
of obscure chronic neuritis. Anæsthesia and various paræsthesiæ
are often more prominent symptoms than pain. Sometimes there is a
hyperæsthesic condition of the skin, in which touching or stroking the
affected part causes a peculiarly disagreeable nervous thrill, from
which the patient shrinks, but which, however, is not described as
pain.
The motor symptoms in chronic neuritis of mixed nerves often
remain for a remarkably long time in abeyance or may be altogether
wanting. They may appear as tremor, spasm, or contraction, these,
however, being probably reflex phenomena. Most commonly there is
paresis, which may deepen into paralysis with atrophy of muscles
and degenerative reaction. The trophic changes dependent on
chronic neuritis are frequently very prominent and important. The
skin sometimes becomes rough and scaly, sometimes atrophied,
smooth, and shining (glossy skin). Œdema of the subcutaneous
cellular tissue is often seen, for example, on the dorsum of the hand,
where it may be very marked. The hair of the affected part shows
sometimes increased growth, sometimes it falls off. The nails may
become thickened, ridged, and distorted. Deformity of joints with
enlargement of the ends of the bones is not infrequently met with as
the result of chronic neuritis. In short, we may meet with all of those
trophic changes which have been described as arising from nerve-
irritation, and which occur in chronic neuritis as the result of
compression of nerve-fibres by the contraction of the proliferated
connective tissue in the nerve-trunk.

The symptom-complex varies greatly in neuritis, so that there is

hardly a symptom which may not be greatly modified or even
wanting in some cases—a fact, which, as we have already said, may
be explained by the morbid process fixing itself exclusively or in
different degrees upon one or other of the component parts of the
nerve-trunk, or, it may be, upon fibres of different functional
endowment. Thus pain, usually one of the most prominent symptoms
of neuritis, may be quite subordinate, or even absent, in cases of
neuritis acute in invasion and progress. In a case of neuritis of the
ulnar nerve seen by the writer, beginning suddenly with numbness
and paresis, and rapidly developing paralysis, atrophy of muscles,
loss of faradic contractility, with degenerative reaction, there was no
pain during the disease, which ended in recovery.7 On the other
hand, in mixed nerves the sensitive fibres may be long affected,
giving rise to pain and various paræsthesiæ before the motor fibres
are implicated, or these last may escape altogether.
 7 “Two Cases of Neuritis of the Ulnar Nerve,” Maryland Medical Journal, Sept., 1881.

The swollen condition of the nerve, so characteristic in many cases

of neuritis where the perineurium is the seat of a hyperæmia, is
wanting in cases where the stress of the attack is upon the nerve-
fibres themselves. Again, the trophic changes induced in the tissues
by a neuritis may predominate greatly over the sensitive or motor
alterations. Thus, in the majority of cases in which herpes zoster
occurs it is without pain or paræsthesia. Indeed, in chronic neuritis
the symptoms show such variations in different cases that it is
difficult to give a general picture of the disease sufficiently
comprehensive and at the same time distinctive. The prognosis in
acute neuritis is generally favorable, although it must depend in a
great measure upon the persistence of the cause producing it. Thus,
if it has been excited by the inflammation of neighboring organs it
cannot be expected to disappear while these continue in their
diseased condition. In other cases the symptoms may subside with
comparative rapidity; and so great is the capacity of the nerve-fibres
for regeneration that recovery may be complete and nothing remain
to indicate the previous inflammation. The nerve, however, that has
once suffered from neuritis shows for a long time a tendency to take
on an inflammatory action from slight exciting causes. If there has
resulted an atrophy of muscles, we must expect some time to elapse
before they recover their functional activity and normal electric
reaction.

Acute neuritis most frequently passes into the chronic form, and it
may then drag on indefinitely, stubbornly resisting treatment and
giving rise to permanent derangement of sensibility, loss of muscular
power, or perverted nutrition. Neuritis shows a tendency to spread
along the affected nerve centripetally, sometimes reaching the spinal
cord, and, as it has appeared in some cases, even the brain, causing
tetanus or epilepsy.

Reflex paralyses, which at one time were believed to be the not

infrequent result of nerve-irritation and inflammation, affecting from a
distance the functions of the spinal cord, have been shown to be the
effect of an extension of the lesion of the inflamed nerve to the cord,
causing organic disease. Instances of the extension of a neuritis to
distant nerves, as those of an opposite extremity, without the
implication of the spinal cord (neuritis sympathica), are most
probably cases of multiple neuritis, to be considered farther on.

The DIAGNOSIS of cases of traumatic neuritis can scarcely present a

difficulty. Acute neuritis with spontaneous pain, swelling, and
tenderness of the nerve, presents distinctive features hardly to be
confounded with any other affection, although thrombosis of certain
veins, as the saphenous, may present some of its symptoms. To
distinguish chronic neuritis or the cases wanting those obvious
symptoms just indicated (many cases of sciatica) from neuralgia is a
more difficult task. The following distinctive points may be noted: In
neuritis the persistent and continuous character of the pain helps us
to distinguish it from the more paroxysmal exacerbations of
neuralgia, and its tendency, often seen, to spread centripetally
spontaneously or when pressure is made on the nerve, may be also
considered as characteristic of neuritis. Cutaneous anæsthesia,
paresis, and atrophy of muscles are distinctive in any case of a
neuritis rather than a neuralgia. Herpes zoster and other trophic
changes speak strongly for a neuritis.

In the TREATMENT of neuritis the first indication is to get rid, as far as

possible, of such conditions as may cause or keep up the
inflammation, as, for instance, the proper treatment of wounds, the
removal of foreign bodies, the adjustment of fractures, the reduction
of dislocations, the extirpation of tumors, etc. Absolute repose of the
affected part in the position of greatest relaxation and rest is to be
scrupulously enforced. In acute neuritis local abstraction of blood by
leeches and cups in the beginning of the affection is of the greatest
advantage and should be freely employed. The application of heat
along the course of the inflamed nerve has appeared to us
preferable to the use of ice, although this also may be employed with
excellent effect. The agonizing pain must be relieved by narcotics,
and the hypodermic injection of morphia is the most efficient mode of
exhibition. Salicylic acid or salicylate of sodium in large doses
contributes to control the pain. Iodide of potassium in large doses
appears to act beneficially, even in cases with no syphilitic
complications. In subacute or chronic neuritis local bloodletting is not
as imperatively demanded as in the acute form, although it is
sometimes useful. Here counter-irritation in its various forms and
degrees, even to the actual cautery, is to be recommended. An
excellent counter-irritation is produced by the application of the
faradic current with the metallic brush. It appears from general
experience that the counter-irritation has the best effect when
applied at a little distance from the inflamed nerve, and not directly
over its course. In the galvanic current we possess one of the very
best means not only for relieving the symptoms of chronic neuritis,
but for modifying the morbid processes in the nerve and bringing
about a restoration to the healthy condition. Its application is best
made by placing the anode or positive pole as near as possible to
the seat of the disease, while the cathode or negative pole is fixed
upon an indifferent spot at a convenient distance. The positive pole
may be held stationary or slowly stroked along the nerve. Finally, in
protracted cases nerve-stretching may be resorted to with great
benefit. It probably owes its good effects to the breaking up of minute
adhesions which have formed between the sheath of the nerve and
the surrounding tissues, and which act as sources of irritation.

Multiple Neuritis, Multiple Degenerative Neuritis, Polyneuritis.

Cases of this important form of neuritis have been observed and

recorded since 1864, but the resemblance of its symptoms to those
of certain diseases of the central nervous system (poliomyelitis,
Landry's paralysis, etc.) has prevented its general recognition, and it
is only within the last few years that its distinctive pathological
lesions have been demonstrated and its diagnosis made with
considerable certainty. We can hardly overrate the importance of this
in view of the great difference in gravity of prognosis between it and
other diseases with which it may be confounded.
Multiple neuritis consists in a simultaneous or more or less rapidly
succeeding inflammation of several or many usually bilaterally
situated nerves, with a greatly preponderating, almost exclusive,
lesion of the motor fibres. Commonly the disease attacks the lower
extremities and progresses upward, although occasionally it has
been seen to begin in the arms. It does not confine itself to the
nerves of the extremities and trunk, but often involves the phrenics,
causing paralysis of the diaphragm, and frequently invades one or
more of the cranial nerves, notably the vagus, thus giving rise to the
rapid heart-beat so often seen in the disease. In the cases of
multiple neuritis observed the muscles of deglutition have never
been paralyzed. The sphincter ani and bladder have likewise
escaped. All degrees of acuteness are observed in the course it
runs, from the cases terminating rapidly in death to those in which
the disease extends over months, slowly involving nerve after nerve,
until nearly all of the muscles of the body are paralyzed, when death
may result or a more or less complete recovery take place. The
invasion of the disease is in most cases sudden, even when its
subsequent course is chronic, and is often marked by decided
constitutional disturbance, as rigors, fever, delirium, albuminuria, etc.
Disturbances of sensation are prominent among the initial
symptoms, and are of great importance for the diagnosis of the
disease. Severe, spontaneous, paroxysmal pain of a shooting,
tearing character has ushered in most of the cases on record,
remitting, however, during their progress. Pain is not always present,
nevertheless, and cases not infrequently occur which run a painless
course. In some cases which have come under the writer's notice
spontaneous pain did not occur until some days after the disease
was fully declared by other symptoms. More constantly present, and
more characteristic of multiple neuritis, are the disturbances of
sensation which show themselves in subjective feelings of
numbness, tingling, pins and needles, coldness, burning, and other
paræsthesiæ, which appear at its outset and continue to be present
more or less during its course. Anæsthesia, not of a high degree nor
at all coextensive with the paralysis of the muscles—sometimes,
indeed, confined to very circumscribed areas—may be said to exist
always in multiple neuritis—a fact of great diagnostic value.
Hyperæsthesia of the skin is frequently seen. Hyperalgesia and
analgesia are sometimes observed. Hyperæsthesia of the muscles is
a very marked symptom in almost every case, and shows itself not
only upon direct pressure being made, but also in the pain elicited by
passive movements of the parts affected. Pressure upon nerve-
trunks does not cause pain as invariably as might have been
expected from the location of the disease. Delayed sensation has
been frequently observed.

Paresis of muscles, often commencing suddenly, is early seen in

multiple neuritis, and increases until there is more or less complete
paralysis, the most important feature of the disease. The paralyzed
muscles present the flabby condition characteristic of muscles
deprived of the tonic influence of the spinal cord. Atrophy, which is
not commensurate, however, with the paralysis, soon begins, and
may go on to an extreme degree. As the paralysis develops the
tendon reflexes are lost, and there may be diminution or loss of the
skin reflexes also. The paralyzed muscles lose their faradic
contractility, and exhibit diminution of electric excitability to the
galvanic current, and, finally, the various forms of degenerative
reaction. It is remarkable that neither the impairment of sensation nor
the paralysis is, as a rule, strictly confined to the areas of distribution
of particular nerves, but is diffused over regions of the body. Thus in
the limbs the motor and sensory symptoms are most marked at their
extremities, gradually diminishing toward the trunk. In some cases
multiple neuritis appears to have occasioned the inco-ordinate
movements of locomotor ataxy. In the progress of the disease a
rigidity and contracted condition of muscles may be developed,
occasioning a fixed flexion of some of the joints. Profuse sweating,
œdema of the hands and feet, trophic changes in the skin, mark at
times the implication of trophic and vaso-motor nerves. Bed-sores do
not occur.

The pathological changes in pure cases of multiple neuritis are found

in the nerve-trunks, mainly toward their peripheral terminations, and
in their muscular branches, the evidences of disease diminishing
toward the larger trunks, the nerve-roots being unaffected and the
spinal cord showing no lesions. Sometimes the affected nerves
present, even to the naked eye, unmistakable proof of acute
inflammation. They are reddened by hyperæmia, swollen by
exudation, and small extravasations of blood may be seen among
their fibres. The microscope shows congestion of the blood-vessels,
exudation of the white corpuscles, even to the formation of pus,
alteration of the endo- and perineurium; in short, all the evidence of
an interstitial inflammation, the nerve-fibres being comparatively little
altered, and suffering, as it were, at second hand. In most of the
cases, however, the nerves macroscopically present little or nothing
giving indication of disease. The microscopic changes, however, are
extensive, and pertain almost exclusively to the nerve-fibres
themselves. These are altered and degenerated, giving an
appearance almost precisely the same as already described in
treating of the changes occurring in nerves separated by injury from
the centres—Wallerian degeneration.8 There is no hyperæmia,
thickening, or change in the endoneurium. So great are these
differences in the microscopic appearance of the nerves in different
cases of multiple neuritis that objection has been raised to classing
the two varieties together, and it has been argued that we cannot
with right designate the cases in which hyperæmia and other
evidence of a general inflammation are absent as neuritis. It has
been, however, argued—apparently, to the writer, with better reason
—that the same morbid influence which at one time affects the
blood-vessels, causing their congestion and the passage through
their walls of the white corpuscles and the exudation of inflammation,
may at another time, by a direct and isolated influence upon the
nerve-fibres, cause their degeneration; in other words, that there
may be a parenchymatous neuritis, which shall affect only the nerve-
fibres. The vastly disproportionate implication of the motor fibres
would point to the fact of a selective infection in multiple neuritis of
certain fibres, as there is a selective infection in poliomyelitis of the
motor cells of the anterior horns of the spinal gray matter.
8 Gombault's observations (Arch. de Névrologie, 1880) would seem to show that
there is a difference in the lesion of the fibres in neuritis from that in simple Wallerian
degeneration, inasmuch as that in the former the first alteration is seen about the
 nodes of Ranvier, and occurs at points separated from each other by healthy fibre,
and also in the more tardy destruction of the axis-cylinder.

ETIOLOGY.—Much in the symptomatology of multiple neuritis,

especially of its invasion, strongly urges us to the conclusion that it is
a constitutional disease caused by an unknown morbid influence, the
stress of which falls upon the nervous system. This view receives
strong support from the history of the Japanese kak-ke or Indian
beriberi, a disease at times epidemic in those countries, and which
has the undoubted symptoms and the characteristic pathological
alterations of multiple neuritis. After many acute infectious diseases
neuritis of individual nerves is not uncommon, but the distinctive
characteristics of multiple neuritis have, so far, been observed
almost exclusively after diphtheria, to which it is not infrequently a
sequel. It has been observed as the result at least occurring in
intimate connection with polyarthritis, and the frequency with which it
has occurred in the phthisical is remarkable. There have been not a
few cases of multiple neuritis recorded as having been produced by
chronic alcohol-poisoning. A well-marked case has come under the
writer's observation in which the immediate cause was acute
poisoning by arsenious acid, a very large amount having been taken
at one dose by mistake. The poison of syphilis has been regarded as
standing in a causal relation to multiple neuritis. For the rest, the
exciting causes (probably acting in connection with a peculiar
condition of the system) have appeared to be exposure to cold, great
muscular exertion, direct mechanical injury to the nerves, as the
rough jolting of a wagon, or the inflammation of a nerve which has in
some unknown way extended to others.

The DIAGNOSIS of multiple neuritis in certain cases presents great

difficulty, from the close resemblance of its symptoms to those of
poliomyelitis. The prominent symptoms in the muscular system—viz.
paralysis, atrophy, the degenerative reaction—are the same in both.
It may be remarked, however, that in multiple neuritis the paralysis is
more generally diffused over the muscles of the affected limbs, while
in poliomyelitis it is more confined to the areas of distribution of
particular nerve-branches. Pain is common to the beginning of both
diseases, but it generally passes off more quickly and completely in
poliomyelitis. The persistent hyperæsthesia of the muscles is
wanting in poliomyelitis. But it is in the diminution and alteration of
sensation that we have the surest means of distinguishing between
the two affections. This symptom seldom or never fails to show itself
in multiple neuritis, although its area may be circumscribed and it
may be slight in degree, while it certainly makes no part of the
symptomatology of poliomyelitis. It has been asserted that the
implication of the cranial nerves so often seen in multiple neuritis
never occurs in poliomyelitis. When we consider the intimate
connection of the anterior horns of the spinal gray matter with the
motor nerve-fibres, it appears highly probable that the same morbid
influence may invade both simultaneously or in quick succession,
thus producing a complex of symptoms rendering a diagnosis very
difficult, and probably giving rise to some confusion in the recorded
symptoms of multiple neuritis. From Landry's paralysis multiple
neuritis is to be distinguished by the impairment of sensibility, the
loss of faradic contractility, and absence of the tendon reflex; from
progressive muscular atrophy, by the loss of sensibility and the much
more obvious degenerative reaction.

The PROGNOSIS of multiple neuritis is in the great majority of cases

not grave, so far as life is concerned, even when there is extensive
paralysis. Death may occur early in the acute form of the disease or
it may take place at the end of chronic cases. When the disease
proves fatal, it is from paralysis of the diaphragm and the other
muscles of respiration. Where the paralysis and atrophy have been
great, showing profound alteration of the nerves, a long time is
required for recovery, and more or less paralysis, contracture, or
defective sensibility may permanently remain.

The TREATMENT consists, at the outset, in rest and position, the local
abstraction of blood (in cases where the nerve-trunk is swollen and
tender), and the administration of such drugs as we suppose act
favorably upon the inflammation of the nerves. Salicylic acid or
salicylate of sodium seem to act beneficially in relieving the severe
pains in the outset of the disease. Iodide of potassium, gradually
increased until large doses are taken, has, in the experience of the
writer, seemed to beneficially modify the course of multiple neuritis.
The necessary relief of pain is best obtained by hypodermic
injections of morphia, supplemented by heat applied to the affected
nerves. To these means may be added rubbing with chloroform and
applying to the painful parts cloths dipped in a 5 per cent. solution of
carbolic acid. After the acute stage has been passed and in chronic
cases, just as soon as we have reason to suppose that the
degenerative process in the nerves has come to a standstill, we
possess in the use of electricity the means of hastening the
regeneration of the nerve-fibres, strengthening the paralyzed
muscles, and restoring the sensation. The galvanic current is to be
preferred, and it is to be applied to the crippled nerves and muscles
—sometimes stable for its electrolytic action, sometimes interrupted
to obtain its exciting and stimulating effect. The excitement to nerves
and muscles by the use of the faradic current has also its uses in
hastening recovery. Protracted treatment and much patience are
required to overcome contractions and restore the nerves and
muscles, and the effects of the disease may be seen for a long time
in the weakness and diminished electric reaction of the muscles.

Anæsthesia of Peripheral Origin.

A prominent and important symptom of the lesion of peripheral

nerves is the diminution and loss of cutaneous sensibility. Besides
the anæsthesia caused by the affections of the fibres themselves,
which has been touched upon in the preceding pages, it may be
produced by morbid states of the peripheral end-organs or
cutaneous terminations of the nerves. Cold applied to a nerve-trunk
may produce alterations which for days after cause numbness and
paræsthesia in the surface to which it is distributed, and the
application of cold to the surface of the body, as we know from
common observation, causes blunting of the cutaneous sensations,
especially that of touch. In this way, from exposure to the
atmosphere at low temperatures, to cold winds, or by the immersion
of the body in cold water, the end-organs of the nerves in the skin
are morbidly affected, and anæsthesia results, the so-called
rheumatic anæsthesia. Many substances, as acids, notably carbolic
acid, alkalies, narcotics, etc., act upon the cutaneous end-organs in
a way to destroy their capacity for receiving or transmitting
impressions and produce a more or less persistent anæsthesia of
the skin. In the anæsthesia so often observed in the hands and
forearms of washerwomen we have an example of the action
probably of several of these causes, as the frequent plunging of the
hands into cold water and the action upon the skin of alkalies and
alkaline soaps. The diminution or interruption of the circulation
through the skin, as in ischæmia from spasm of the minute arteries
due to an affection of the vaso-motor nerves, is also a cause of
cutaneous anæsthesia. In lepra anæsthetica (Spedalskhed) the
cutaneous anæsthesia is dependent upon a neuritis of the minute
branches in the skin. The local anæsthesia met with so often in
syphilis, though its pathology is doubtful, is not improbably
sometimes caused by an affection of the peripheral nerves
(neuritis?) and their end-organs. After many acute diseases,
diphtheria, typhoid fever, etc., we have cutaneous anæsthesia in
connection with muscular paralysis, the cause of both being a
neuritis. The patient is made aware of the loss of sensation by some
interference with his usual sensations and movements. If he puts a
glass to his lips, the sensation is as if a bit were broken out of the
rim; his accustomed manipulations are awkward, because of the
want of distinct appreciation of the objects he holds; he fumbles in
buttoning his clothes or he stumbles unless looking to his steps. An
examination, nevertheless, almost always reveals that the
anæsthesia is greater than would have been supposed from the
subjective feelings of the patient; indeed, cases occur in which he is
not aware of an existing defect of sensation. But a careful
examination is not only required to determine the extent, but by it
alone can we arrive at a knowledge of the quality of the anæsthesia
—viz. whether there is a loss of all of the different kinds of sensation,
whether they are affected in an unequal degree, or whether some
have entirely escaped. Thus we must test for the acuteness of the
simple sense of touch by comparing the sensations elicited by the
contact of small surfaces of unequal size, as the point and head of a
pin or pencil, observing the appreciation by touch of the patient for
different substances, as woollen, silk, linen, cloth, or comparing the
sensation of the anæsthesic part with the same part on the opposite
healthy side of the body. The sense of locality and space may be
examined by placing at the same instant upon the skin of the patient,
his eyes being closed, two points (the anæsthesiometer or the points
of a compass), and observing his capacity for appreciating the
impression as double. As there is an enormous difference of
acuteness of the space-sense in the skin of different parts of the
body (see textbooks of physiology)—ranging from the tip of the
tongue, where the touch of two points separated 1.2 mm. gives a
double sensation, to the thigh, where the points must be separated
77 mm. to be felt as two—we must be careful to consider in making
the examination the normal space-perception of the region. Care
must be taken not to repeat the test too often, as a rapid education
of the surface to a more delicate appreciation of the impressions is
the result. In certain abnormal conditions from spinal disease we
have a condition of polyæsthesia in which the impression of one
point is felt as two or more. The sense by which we appreciate the
pressure of objects must be tested by placing upon the surface to be
examined, in succession, objects of different weight, care being
taken to have the area which touches the skin and the temperature
the same in each. The parts to be tested must be firmly supported,
and all muscular contraction on the part of the patient prevented.
The temperature sense is examined by the application of hot and
cold water or bodies of different temperature. We sometimes meet
with a perversion of this sense in which the application of a cold
surface to the skin gives the sensation of warmth, and the contrary.
In testing the sense of temperature and the sense of pressure it is
not the absolute capacity of appreciating on the part of the patient
that we investigate, but the power of discriminating between different
degrees of temperature or pressure. The sense of pain must likewise
be tested, since morbid conditions occur in which it may be caused
more readily than is normal by exciting the cutaneous nerves, and
that, too, in parts which have in a great measure or quite lost the
sense of touch; or, on the other hand, touch may be retained, while
irritation of the skin can excite no feeling of pain (analgesia). We
have in the faradic current an excellent means of testing the
cutaneous sensibility, inasmuch as it excites the skin over the
various parts of the body about equally, and it can be employed in
very gradually increasing or decreasing strength. Its effects on the
affected part must be compared with those produced on the healthy
surface of other parts of the patient's body or on healthy individuals.

Frequently accompanying cutaneous anæsthesia, but constituting no

part of it, are various paræsthesiæ, as formication, pins and needles,
burning, etc. Pain, sometimes of great intensity, is not infrequently
connected with it (anæsthesia dolorosa). The paræsthesiæ and pain
are the result of irritation in some portion of the conducting tracts,
and, together with the trophic changes so often seen in connection
with nerve-injuries, they have been already considered under that
head.

It is a very important point to make the diagnosis between central

and peripheral anæsthesia, but it is often a matter of great difficulty,
and sometimes not to be made at all. The history of the case must
be carefully considered, and an examination made for symptoms of
brain or spinal disease, the existence of nerve lesions, or if there is a
history of toxic influences, etc. In peripheral anæsthesia the reflexes
which may be normally excited from the affected surface are
wanting, in contradistinction to anæsthesia of central origin, in which
they are most generally retained or even increased. Concomitant
trophic changes speak strongly for a peripheral origin, as do also
paralysis and atrophy of muscles. Loss of some of the forms of
sensation, with retention of others—i.e. partial paralysis of sensation
—indicate a central origin.

The TREATMENT of peripheral anæsthesia must look, in the first place,

to removal, if possible, of its cause, and the treatment of diseased
conditions, if any exist, of the nerve-trunks, as neuritis, mechanical
injuries, etc. Local applications of a stimulating character may be
advantageously used upon the anæsthesic parts. By far the most
effective stimulant to the diseased nerves is the faradic or galvanic