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Chapter 8 CFIN4

Chapter 8 Solutions

8-1 a. r̂ = (0.2)(19%) + (0.7)(9%) + (0.1)(4%) = 10.5%

b.  = (0.2)(19 - 10.5)2 + (0.7)(9 - 10.5)2 + (0.1)(4 - 10.5)2 = 20.25 = 4.5%

4.5%
c. CV = = 0.429
10.5%

8-2 a. r̂ = (0.45)(32%) + (0.35)(-4%) + (0.2)(-20%) = 9.0%

b.  = (0.45)(32 - 9)2 + (0.35)( −4 − 9)2 + (0.2)( −20 − 9)2 = 465.4 = 21.573%

21.573%
c. CV = = 2.397
9%

8-3 a. r̂A = (0.3)(30%) + (0.2)(10%) + (0.5)(-2%) = 10%

r̂B = (0.3)(5%) + (0.2)(15%) + (0.5)(25%) = 17%

b.  A = (0.3)(30 - 10)2 + (0.2)(10 − 10)2 + (0.5)( −2 − 10)2 = 192 = 13.856%

B = (0.3)(5 - 17)2 + (0.2)(15 − 17)2 + (0.5)(25 − 17 )2 = 76 = 8.718%

13.865%
c. CV A = = 1.387
10%

8.718%
CV B = = 0.513
17%

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Chapter 8 CFIN4

8-4 To answer the question, the coefficient of variation for each investment must be computed.

Investment r̂  CV
Stock M 6.0% 4.0% 0.667 = 4%/6%
Stock N 18.0 12.0 0.667 = 12%/18%
Stock O 12.0 7.0 0.583 = 7%/12%

According to the CV measure, Stock O has the best risk/return relationship; its risk per unit of return is
the lowest at 0.583.

8-5 To answer the question, the coefficient of variation for each investment must be computed.

Investment r̂  CV
F 16.0% 7.0% 0.438 = 7%/16%
G 27.0 13.0 0.481 = 13%/27%

According to the CV measure, Investment F has the better risk/return relationship; its risk per unit of
return is the lower at 0.438.

8-6 $9,000 invested in one stock with an 18 percent expected return

$21,000 invested in a second stock with an 8 percent expected return

 $9,000   $21,000 
r̂P =   18% +  $9,000 + $21,000  8%
 $9,000 + $21,000   

= 0.3(18%) + 0.7(8%) = 11.0%

8-7 Portfolio return:

Amount Weight Return Portfolio Return

Investment (1) (2) (3) (4) = (2) x (3)

DEF $ 30,000 0.30 = $30,000/$100,000 4.0% 1.2%

KJL 25,000 0.25 = $25,000/$100,000 24.0 6.0
TUV 45,000 0.45 = $45,000/$100,000 14.0 6.3
$100,000 1.00 13.5%

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Chapter 8 CFIN4

8-8 Portfolio beta:

Investment Weight Beta Portfolio beta

(1) (2) (3) (4) = (2) x (3)

$ 350,000 0.35 = $350,000/$1,000,000 1.0 0.35

250,000 0.25 = $250,000/$1,000,000 0.2 0.05
400,000 0.40 = $400,000/$1,000,000 2.5 1.00
$1,000,000 1.00 1.40

rp = rRF + (rM – rRF)(βp) = 3% + (9% – 3%)1.4 = 11.4%

Alternative solution: First compute the return for each stock using the CAPM equation
[rRF + (rM – rRF)βj], and then compute the weighted average of these returns.

rRF = 3% and rM – rRF = 9%.

rj = rRF + (rM – rRF)βj

Investment Beta = 3% + (9% – 3%)βj Weight rP
(1) (2) (3) (4) (5) = (3) x (4)

$ 350,000 1.0 9.0% 0.35 3.15%

250,000 0.2 4.2 0.25 1.05
400,000 2.5 18.0 0.40 7.20
Total $1,000,000 1.00 11.40%

rp = 9.0%(0.35) + 4.2%(0.25) + 18.0%(0.40) = 11.4%.

8-9 a. r̂ABC = (0.1)(22%) + (0.6)(12%) + (0.3)(2%) = 10.0%

r̂RST = (0.1)(-2%) + (0.6)(12%) + (0.3)(30%) = 16.0%

b.  ABC = (0.1)(22 - 10)2 + (0.6)(12 − 10)2 + (0.3)(2 − 10)2 = 36 = 6.000%

RST = (0.1)( −2 − 16)2 + (0.6)(12 − 16)2 + (0.3)(30 − 16)2 = 100.8 = 10.040%

c. Compute the expected return of the portfolio

Probability rABC rRST Portfolio Return: 60% ABC; 40% RST

0.1 22.0% -2.0% 12.4% = 0.6(22%) + 0.4(–2%)
0.6 12.0 12.0 12.0 = 0.6(12%) + 0.4(12%)
0.3 2.0 30.0 13.2 = 0.6( 2%) + 0.4(30%)
Expected return 10.0% 16.0% 12.4% = 0.6(10%) + 0.4(16%)

rP = 0.1(12.4%) + 0.6(12.0%) + 0.3(13.2%) = 12.4%

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accessible website, in whole or in part.
Chapter 8 CFIN4

P = (0.1)(12.4 - 12.4)2 + (0.6)(12 − 12.4)2 + (0.3)(13.2 − 12.4)2 = 0.288 = 0.537%

d. The portfolio standard deviation is much lower than the standard deviation for either of the
investments, because the investments’ returns are negatively correlated. Notice that when
Investment ABC’s return is highest, Investment RST’s return is lowest, and vice versa. In fact, the
two investments’ returns are strongly negatively correlated, which resulted in a substantial
reduction is risk when the two investments were combined to form a portfolio.

8-10 Total investment = $60,000

ws = 0.40
wX = 0.60
βs = 1.5
βP = 2.1

βP = 2.1 = 0.4(1.5) + 0.6(βX)

0.6(βX) = 2.1 – 0.6 = 1.5

βX = 1.5/0.6 = 2.5

Check: If βX = 2.5 and βs = 1.5, the portfolio’s beta coefficient is:

βP = 0.4(1.5) + 0.6(2.5) = 2.1

 $40,000   $10,000 
8-11 new = 1.2   + 2.2  $40,000 + $10,000  = 1.2(0.8) + 2.2(0.2) = 1.4
 $40,000 + $10,000   

8-12 Information that is given:

Total current value $120,000

Number of stocks (current portfolio) 4
Beta coefficient, βCurrent 0.8

Because the beta coefficient for the portfolio will be 1.0 after the stock is sold for $48,000, we know that
the remaining stocks, which are worth $72,000 = $120,000 – $48,000, must have a weighted average
beta equal to 1.0. And, in combination, the weighted average beta for the stocks that make up the
current (pre-sale) portfolio must be 0.8, which means that the following situation must exist:

0.8 = ($48,000/$120,000)(Beta of stock being sold) + ($72,000/$120,000)(1.0)

0.8 = 0.40(βStock) + 0.60(1.0)

βStock = (0.8 – 0.6)/0.4 = 0.5

Check: βCurrent = ($48,000/$120,000)(0.5) + ($72,000/$120,000)(1.0) = 0.2 + 0.6 = 0.8

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accessible website, in whole or in part.
Chapter 8 CFIN4

8-13 Information that is given:

Total current value $200,000

Number of stocks (current portfolio) 6
Beta coefficient, βCurrent 1.5

Because the beta coefficient for the portfolio will be 1.3 after the stock is sold for $40,000, we know that
the remaining stocks, which are worth $160,000 = $200,000 – $40,000, must have a weighted average
beta equal to 1.3. And, in combination, the weighted average beta for the stocks that make up the
current (pre-sale) portfolio must be 1.5, which means that the following situation must exist:

1.5 = ($40,000/$200,000)(Beta of stock being sold) + ($160,000/$200,000)(1.3)

1.5 = 0.20(βStock) + 0.80(1.3)

βStock = (1.5 – 1.04)/0.2 = 2.3

Check: βCurrent = ($40,000/$200,000)(2.3) + ($160,,000/$200,000)(1.3) = 0.46 + 1.04 = 1.5

8-14 rRF = 3%
RRM = 6%
β = 1.5

r = 3% + (6%)1.5 = 12%

8-15 rRF = 4%
rM = 12%
β = 2.5

r = 4% + (12% - 4%)2.5 = 24%

8-16 rRF = ?
rM = 12.5%
β = 0.8
rZR = 11%

11% = rRF + (12.5% - rRF)0.8

11% = rRF +12.5%(0.8) – 0.8rRF

rRF = (11% - 10.0%)/0.2 = 5%

Check: If rRF = 5%, rZR = 5% + (12.5% - 5%)0.8 = 11%

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accessible website, in whole or in part.
Chapter 8 CFIN4

8-17 rRF = 5%
rM = 11%
βV = 2.0
βW = 0.5

rV = 5% + (11% - 5%)2.0 = 17%

rW = 5% + (11% - 5%)0.5 = 8%

The required return for Stock V is 9% = 17% - 8% higher than the required return for Stock W.

8-18 Original information:

rQ = 11%
rRF = 4%
rM = 9%

Based on this information, we can compute the stock’s beta coefficient:

rQ = 11% = 4% + (9% - 4%)βQ

βQ = (11% - 4%)/5% = 1.4

Original RPM = 9% - 4% = 5%

Correct RPM = 5% + 1% = 6%

Correct rQ = 4% + (6%)1.4 = 12.4%

8-19 Given information:

rRF = 3.5%
RPM = 7%
βU = 0.9
P0 = $28
D0 = $1.75
g = 4%

Stock U’s required rate of return is rU = 3.5% + 7%(0.9) = 9.8%

Stock U’s expected rate of return is:

$1.75(1.04)
r̂U = + 0.04 = 0.105 = 10.5%
$28

In this case, the expected rate of return, r̂U , is greater than the required rate of return, rU, which means
the $28 selling price is too low. Investors should want to buy the stock, which will increase the price of
the stock to its equilibrium value of $31.38:

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accessible website, in whole or in part.
Chapter 8 CFIN4

$1.75(1.04) $1.82
P̂0 = = = $31.38
0.098 − 0.04 0.058

8-20 Given information:

P0 = $37.50
D0 = $2
rRF = 4%
rM = 10%
βStock = 1.1

rStock = 4% + (10%- 4%)1.1 = 10.6%

Based on the dividend discount model, we know the following relationship exists:

$2(1 + g)
$37.50 =
0.106 − g

Solving for g, gives the following result:

$2(1 + g)
$37.50 =
0.106 − g

$37.50(0.106 − g) = $2 + $2g

$3.975 − $37.50g = $2 + $2g

$39.50g = $1.975

$1.975
g= = 0.05 = 5.0%
$39.50

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but not always connected with, right motor paralysis we have the
inability to use words in speaking, known as aphasia, aphemia,
alalia, and others. The first of these names is the one most
frequently used. Agraphia is the inability to use words in writing.

On the receptive side we have the inability to understand language

as presented to the eye (word- or psychic blindness) or to the ear
(word- or psychic deafness). A case of the former condition has
already been spoken of. One still more singular was reported by
Mdlle. Skwortzoff,37 where the patient, not being blind, could not
understand letters presented to the eye, but could read with the
fingers and understand raised letters like those used by the blind. In
a case of the latter kind a man whose ears were normal, and who
could distinguish different sounds, answered questions, but entirely
at random, though he could read and understand what was written.
All these defects are manifestly connected with a peculiar loss of
memory, and hence the word amnesia is used sometimes to cover
part of the group, and amnesic as an adjective to qualify aphasia.
37 Comptes Rendus de la Société de Biologie, 1883, p. 319.

It should, of course, be understood that the muscles are not

paralyzed, so that glottis, lips, tongue, and fingers are capable of
making the necessary movements to produce words, and, on the
other hand, that the senses of sight and hearing are intact. Aphasia
was confounded by some of the older writers with paralysis of these
organs, and the whole grouped together under the name of alalia.
Even now the distinction is not always clearly observed.

The act of speaking, according to Kussmaul,38 consists in three

stages or processes: the preparation in the intelligence and feelings
of the matter to be uttered; the diction, or the formation of the words
internally, together with their syntax; the articulation, or formation of
words outwardly, irrespective of their connection with one another in
the matter spoken. Defects in the first condition have already been
spoken of. In the entire absence of mind, as in the deepest apoplexy,
aphasia can hardly be said to exist, and it is only later that it
becomes manifest. If the second stage is defective, amnesic aphasia
exists, and if the third, ataxic. In the great majority of cases of
aphasia the loss of memory is the most important factor; and as this
exists whatever be the mode in which it is desired to express the
idea, amnesic aphasia is accompanied by agraphia. In those cases,
however, in which the patient retains a few words, they are not
always the same for speech and writing. Occasionally an instance is
found where a person can write perfectly well and possesses
complete intelligence, but is unable to speak a word. This is pure
ataxic aphasia, and is certainly rare. An ataxic agraphia is less easy
to detect, since the aphasic patient is likely to be paralyzed upon the
right side, and thus unable to write, even if he remembers the words,
until educated upon the left side.
38 Ziemssen's Cyclopædia.

There are many degrees and kinds of amnesic aphasia, and, in fact,
every case is a study by itself. The slightest might be called
physiological; at any rate, it is sufficiently common among people
supposed to be well, and consists in the failure to recollect in time for
use the name, most frequently of a person, but sometimes of a thing,
which is really well known, is recognized at once if suggested, and
perhaps returns spontaneously at a later period. Another person may
forget only some words which are not recalled at any time, or parts
of words. A man appeared among the out-patients at St.
Bartholomew's Hospital who had his name written on a piece of
paper, because he could not say it, but could carry on a long
conversation. There were a few other words he could not say. The
more complete cases have no vocabulary at all, or only a few words
or syllables applied to all purposes, and perhaps an exclamation or
two. In these cases the patient may know perfectly well that he is not
expressing his ideas, and he may recognize perfectly well the word
when it is told to him or reject a wrong one. If he be, as happens in
nearly all cases, unable to pronounce the word after he has
recognized it as the one he wished for, there is a combination of
ataxic and amnesic aphasia. Incorrect or deficient words may be
corrected or supplemented by gestures or intonation. “Yes” may do
duty without confusion for “yes” or “no,” according to the tone.
Oaths may be retained, and sometimes an exclamation may be
uttered with perfect propriety of application which cannot be
repeated deliberately a moment afterward. This emotional use of
words may be considered akin to the movement executed by
paralyzed limbs under the stimulus of a movement taking place
elsewhere, and may lead to an erroneous prognosis of recovery.
This curious fact, that more or less automatic expressions are
possible when deliberately-willed pronunciation is not, is a probable
explanation for the observation which has occasionally been made
that an aphasic patient is able to sing words which he cannot speak.

Paraphasia is the use of the wrong words, or of phrases which carry

an entirely different meaning from that intended, as when
Trousseau's patient receives a guest with politeness and invites her
to be seated with the words “cochon, animal, fichue bête,” or an old
paralytic, when a lady declines to drive with him, answers with great
suavity, “It don't make any damnation to me whether you go or not.”

Word-blindness is more common than word-deafness, and is a

frequent accompaniment of aphasia. Rostan, the well-known author
of the work on softening of the brain, experienced an attack of
aphasia lasting a few hours. The symptom which first attracted his
attention was the inability to understand the book, by no means
abstruse, which he was reading. He was, however, able carefully to
observe his own symptoms, and made signs to be bled, which
operation was followed by relief.

Gouty aphasia has been described in a man aged thirty-seven who

on several occasions became aphasic, with recovery in a short time.
This condition was connected with localized paralysis, and once with
entire right hemiplegia. Afterward it was accompanied by
convulsions. In the intervals the patient was in fair health.39 It is
difficult to imagine the lesion in this case. The reporter speaks of
“sudden blocking by a gouty thrombus,” but nothing is known of any
thrombus which can disappear so rapidly. Ball40 describes twelve
attacks of aphasia occurring within nine months, and accompanied
by slight paresis and convulsive movements in the right hand. The
patient suffered habitually from migraine. He supposes the cause to
have been a temporary anæmia.
39 Brit. Med. Journ., Aug. 28, 1880.

40 L'Encephale, 1883, 2.

Aphasia may be entirely unconnected with motor paralysis, and is

then likely to be of shorter duration, though just as complete. Most of
these cases probably do not depend upon a lesion of the same kind
as when aphasia is only one of several severe symptoms. It shows
how delicate a function of the brain memory for words may be, and is
possibly the result of a temporary malnutrition or a change in the
vascular supply. It has been observed in various conditions of
debility and after acute disease. Rostan was diabetic. It has been
seen after chloroform narcosis, after santonin (5 cgr.), after fright,
and is said to be one of the ordinary symptoms after the bite of
venomous serpents. Aphasia and paraphasia may be met with in
thorough bromization, and, naturally enough, may be part of the
symptomatology of general paralysis. In other cases, even when it is
the principal symptom, it depends upon an organic lesion, and is not
infrequently the precursor of a more fully-developed attack. The
diagnosis is of great importance, and other traces of paralysis should
be carefully sought for. This symptom is far more common with
occlusion of the vessels than with hemorrhage, though not unknown
with the latter.41
41 Lancet, Oct. 11, 1884, p. 655.

By far the most common situation of the softening or hemorrhage

which gives rise to aphasia is in the third left frontal convolution
(convolution of Broca) or the white substance immediately underlying
it. The island of Reil may be involved in some cases where but little
damage is done to the third frontal.

In a respectable minority of cases aphasia may be associated with

left hemiplegia. A case where a tumor in the third right frontal
convolution was found in a case of aphasia is reported by
Habershon.42 It is not stated whether the patient was left-handed.
Some of these cases constitute those exceptions which prove the
rule, inasmuch as the patient is left-handed, and Hughlings-Jackson
has shown that the relationship of aphasia to the side which is
congenitally pre-eminent, and which is in the vast majority of human
beings the right side, is not destroyed by a partial education of the
other side to such acts as writing or using a knife.
42 Med. Times and Gaz., 1881, i.

A lesion in the pons may give rise to aphasia or something closely

resembling it, but it is probable that a careful distinction of true
aphasia, both amnesic and aphasic, from paralysis or inco-ordination
of the muscles of speech, would reduce the number of these cases,
and bring the symptom into closer relations with the usual cortical
lesions.

A case of congenital aphasia with right hemiplegia has been

described.43 When six years old the boy was well developed, though
less so on the paralyzed side; intelligent; heard well, but could say
only a few words, and those badly. Whatever the lesion, which is
thought by the author to have been in the speech-centre, but which
may not improbably have been in the pons, it is interesting, as
showing that the development of the speech-centre is certainly not
accomplished by education.
43 Centralblatt f. d. Med. Wiss., 1873, p. 299.

Post-paralytic chorea is an affection the nature of which is indicated

by its name. As the hemiplegia disappears, irregular movements are
developed in the paralyzed limbs, sometimes closely resembling
ordinary chorea, and at others consisting of irregular movements, as
closing and spreading of the fingers, with curious and bizarre
stiffenings, extensions, and contractions, sometimes known as
athetosis, or in others still a tremor resembling paralysis agitans.
These usually cease during sleep. It is very apt to be associated with
hemianæsthesia more or less complete, though this may be
represented by only a certain amount of numbness. A hemiathetosis
has been observed to be gradually developed from a post-
hemiplegic hemichorea of the more ordinary form.44
44 Archiv für Psychiatrie, xii. 516.

This affection is not a common one, and Weir Mitchell states that it is
common in inverse proportion to the age. He thinks it possible that
some of the congenital choreas may be the result of, or at least
closely connected with, intra-uterine cerebral paralysis. It remains for
years or for life. In the absence of history such a case might present
difficulties of diagnosis from the more usual hemichorea, which is not
infrequently accompanied by considerable weakness of the affected
side.

The temperature in the early days of both hemorrhage and embolism

has been described. At a later period of the hemiplegia it remains in
the neighborhood of normal. The temperature of the affected side is
often higher than that of the sound one for an indefinite period, but in
many cases sinks below if atrophy takes place. The time at which
the change occurs is extremely variable. Out of ten cases reported
by Folet,45 in two of them for three years and one year after the
attack the paralyzed side was eight-tenths and six-tenths of a degree
respectively the warmer. In three others, of twenty months, four and
six years, it was the same on both sides, and in the remaining five
the paralyzed limb was a little the cooler. In the last eight there was
more or less atrophy.
45 Gaz. hébd., 1867.

The coincidence of rise of temperature with vascular relaxation has

already been noted under the head of Cerebral Hemorrhage. It is not
difficult to explain why a vascular paralysis in a comparatively well-
nourished limb, especially when the heart is vigorous, may, by
allowing a larger amount of warm blood to circulate, raise the
temperature, when the same paralysis with atrophied muscles, weak
heart, and impaired general health, merely furnishes a larger
reservoir in which the slowly-moving blood may be cooled. The
accompanying charts represent the difference of temperature
between the two sides in two cases of hemiplegia, the first, O. G. T.
(Fig. 41), from embolism, and the second, J. B. (Fig. 42), from
hemorrhage, the observation being made within two or three weeks
of the attack. The dotted line is from the paralyzed side. A subjective
feeling of coldness is not uncommon in paralyzed limbs.

FIG. 41.

FIG. 42.
The modifications undergone by the urine in a case of cerebral
hemorrhage are increase of quantity amounting to polyuria, the urine
becoming limpid and afterward returning to the usual color; a
diminution in the quantity of urea coinciding with the fall of
temperature, and afterward a return to the normal or even above it.
When this augmentation is considerable, it constitutes at the same
time with a marked elevation of temperature an unfavorable
prognostic sign.46 In a case under the observation of the writer,
probably of thrombosis, the acid urine has been remarkable for the
amount of mucus contained in it, so that it pours from one vessel to
another like white of egg. There is a small amount of pus, but no
vesical irritation whatever.
46 Ollivier, Archives de Physiol., 1876.
Since the trophic centres for the muscles are situated in the spinal
cord, cerebral hemiplegia, which does not cut off their connection,
does not produce the rapid wasting seen in some cases of spinal
paralysis, unless descending degeneration involves the anterior gray
columns. The limbs preserve their fulness for a time, although the
muscular masses become flabby and slowly atrophy for want of use.
This atrophy, however, seldom becomes extreme. The skin of the
hands becomes dry, the folds at the knuckles disappear, and the
hand loses its expression, looking more like a stuffed glove. The
change, however, is not much greater than may be seen in a hand
kept for a long time in a bandage. The growth of the nails is retarded,
as may be seen by staining them with nitric acid.

If there is any tendency to œdema, as when nephritis is complicated

with hemiplegia, the swelling is likely to be much greater upon the
paralyzed side. In the adult, of course, there can be no question of
the growth of limbs, but when a child becomes hemiplegic from
cerebral disease, the limbs grow more slowly and remain smaller, as
in a case of ordinary infantile palsy or anterior poliomyelitis.

Much importance has been attached to the fact that large sloughs
form with great rapidity upon the nates of the paralyzed side, and
Charcot says that this tendency is greater than can be accounted for
in any mechanical way. He therefore thinks that a direct trophic
influence of the brain upon nutrition is shown. At the very most,
however, that can only be a contributory cause, and the freedom of
other portions from a similar condition—and that, too, in regions
farther removed from the centres of circulation—makes it highly
improbable that anything more is necessary to account for it than the
less sensitiveness of that side to irritation from urine, roughnesses in
the bed, or pressure, and hence neglect. The writer, among a very
considerable number of hemiplegias, fatal and otherwise, does not
remember to have seen a well-marked case of the kind. Scrupulous
cleanliness and changing the position sufficiently often make the
preference for the paralyzed side a very slight one.
Arthropathies, consisting in a vegetating, and sometimes an
exudative, synovitis, and accompanied by swelling, redness, and
pain, are sometimes observed, especially in the upper extremity.
They do not appear until fifteen days or a month after the attack.

The most significant change which occurs in the course of a

hemiplegia is the development of increased reflexes and rigidity and
contracture. After some weeks or months, during which the aspect of
the case has not essentially changed, the limbs remaining in the
same condition, it will be found on examination that the patellar
reflex has become quite energetic, and ankle clonus developed upon
the paralyzed side; the arm reflexes from the triceps, biceps, and
supinator longus are much exaggerated. This has the same meaning
as when similar phenomena are found with spinal disease, and
signifies descending degeneration of the postero-lateral columns of
the spinal cord, the crossed peduncular tracts. This degeneration
may sometimes be traced completely down from the situation of the
lesion in the cortical motor centres through the basal ganglia, crura,
decussation, and cord. The fuller development of this condition is the
contracture or rigidity, which was at one time referred to secondary
changes taking place in the neighborhood of the original lesion, as
well as to a purely reflex action having no relation to the
degeneration of the cord.

The arms are usually flexed at the elbow, the wrists on the arm, and
the fingers in the hand. Sometimes, however, the arm is straight. The
leg, which is not always affected to the same extent, is generally in
extension, though the toes are likely to be flexed. Attempts to move
the limbs are resisted strongly, and in such a way as to show the
reflex nature of the phenomenon. If an attempt be made to open the
fingers of a contractured hand slowly and carefully, it can be often
accomplished and the hand held open with but little pressure, but if it
is twitched the fingers resist like a spring. The violent attempt to
overcome rigidity is often painful.

In some rare cases rapid atrophy of the muscles of one limb may
take place. This has been found to coincide with extension of
degenerative changes in the cord to the anterior gray columns.

Late rigidity is an unfortunately clear symptom. There is little if any

hope of complete recovery of the use of the limb after it has made its
appearance, though it does not prevent walking. After long-continued
contracture the activity of the muscles diminishes, but the increase of
connective tissue and changes in the joints hold the limb in its fixed
position, and the contracture is a more passive one. The electrical
reactions of the muscles and their nerves in cerebral hemiplegia are
not materially altered, but the neuro-muscular irritability may be
somewhat increased for a time by the irritating influence of the
cerebral lesion.

In most cases of flaccid cerebral hemiplegia the electrical irritability is

somewhat decreased, though retaining the normal character with
both currents. Since the muscles and their nerves retain their
connection with the spinal nuclei which are their trophic centres, and
these nuclei are uninjured, their nutrition does not undergo the
changes which affect electric excitability.

When descending degeneration takes place there may be found,

coinciding with increased reflex activity and contracture, increased
sensitiveness to the electric currents. If the degeneration extend to
the anterior columns, as happens in rare cases, the muscles waste
rapidly and exhibit the reactions of anterior poliomyelitis—i.e.
degenerative.

What has just been said applies to the muscles paralyzed by a

central lesion. If, however, with or without a complete hemiplegia, a
limited lesion, as in the pons, affects the nucleus of a nerve, the
peripheral distribution of that nerve is cut off from its nutritive centre,
and it undergoes the usual changes which lead to the reaction of
degeneration, so that, in some unusual forms of paralysis, the two
kinds of reaction, normal and degenerative, may be present in
different sets of muscles.

DIAGNOSIS.—The apoplectiform attack due to hemorrhage or

occlusion of the cerebral arteries is to be distinguished from narcotic
poisoning, specially by opium or alcohol, or by coal gas; epilepsy
with its succeeding coma; uræmia (so called) or cerebral symptoms
connected with renal disease; comatose form of pernicious
intermittent; diabetic coma; sunstroke; hysteria, and various other
forms of intracranial disease, especially meningitis; concussion and
compression of the brain, which often involve hemorrhage; the
apoplectiform attacks of intracranial syphilis and of general paralysis,
as well as the congestive attacks (coup de sang, rush of blood to the
head).

The first of these distinctions is, in a practical point of view, among

the most important and often the most difficult, so that distinguished
authorities insist not only on the difficulty, but impossibility, of making
a positive diagnosis in every case. The physician who is most
familiar with all the different conditions which may cause coma is
least likely to jump at a conclusion.

Persons are constantly being picked up in the street partially or

wholly unconscious, or found alone in a room without history and
away from friends. The physician must then form his opinion from
the present condition, which without a history may be very obscure,
though with one it might present no difficulty. An empty laudanum- or
whiskey-bottle may be of assistance, the former of much, but the
latter of less. The smell of the breath may give a hint, but even if the
smell of alcohol be detected, considering the widespread belief in its
virtues as a panacea, it may be as well the result of amateur
therapeutic attempts as an indication of the cause of the attack.
Neither does it follow that because a man has been or is drunk he
has no organic disease in his brain. Alcohol should simply make us
more careful to examine for possible injuries. In regard to both these
poisons—and in fact in the diagnosis of these conditions generally—
the first thing to be sought for, after assuring one's self that the
patient can breathe and is likely to do so for a few minutes, is some
evidence of hemiplegia. This is not so easy as it might appear at first
sight, since the general muscular relaxation may be so complete as
to cover up local manifestations. The face, however, may show
inequality in its lines or one cheek flap more loosely than the other.
The patient is not likely to undertake voluntary movements at the
request of the physician, but he may make semi-voluntary ones if
annoyed by the examination. The flaccidity of the arms may vary.
Irregularity of the pupils is a piece of evidence to be received with
some caution, as it may be habitual or the result of disease in the
eye. Conjugate deviation of the eyes and head is a form of paralysis,
or sometimes of unilateral spasm, which when present is of great
significance. In opium-poisoning—and to a less extent in alcoholic
coma—the pupils are much contracted, while they are not always so
in apoplexy. Respiration is usually much more rapid in apoplexy than
in opium-poisoning, and this, in the absence of distinct signs of
hemiplegia, would be one of the most important means of distinction.
The pulse is more nearly normal in frequency, while that of opium is
either slow and hard or more often frequent and feeble.

After the time for the initial depression has passed, rapidly-rising
temperature is very strong evidence in favor of apoplexy. If the
patient be only partially unconscious and able to protest against
being handled, to make some short answers, or even be inclined to
be combative, this is not to be taken as evidence of alcohol.
Hemiplegia may then be noticed. This condition of excitement may
be observed in the early stage of an apoplectic attack before it
deepens into coma. Unfortunately, when the lesion is situated in
certain portions of the brain, as in the extremities of either the frontal
or occipital lobes, there may be no paralysis, but then also there is
less likelihood of the extreme symptoms we are supposing to be
present. In the cerebellum, however, the symptoms may be very
severe without hemiplegia, and the diagnosis correspondingly
difficult. Vomiting, not caused by the presence of large quantities of
food or liquor, and persisting after the stomach is once emptied,
would be of some value in this case, but it would often be necessary
to wait for a diagnosis. Cerebellar hemorrhage is, however, a very
rare accident, and cerebellar embolism sufficiently large to cause
apoplectiform symptoms still more so. A limited lesion in the pons
may cause gradually-increasing stupor without distinct paralysis.
Chloroform, especially if swallowed, and chloral might possibly give
rise to difficulties in the way of diagnosis, and would have to be
distinguished on the same general principles as alcohol and opium.

The poisonous gases arising from burning coal, consisting chiefly of

carbonic oxide and dioxide, or illuminating gas, consisting of
carburetted hydrogen with a little carbonic oxide, cause
unconsciousness, coma, and sometimes convulsions and vomiting.
In case of a person found unconscious in bed the possibility of
poisoning by one of these should not be lost sight of, nor, on the
contrary, assumed to be a cause without investigation. A case has
been reported where, after acute poisoning by coal gas, there
occurred, presumably as the result of local anæmia, alternate
paralysis, convulsions, and aphasia.47 The new water-gas process is
said to furnish a product considerably richer in the poisonous
carbonic oxide than that now most in use.
47 Boston Med. and Surg. Journal, Nov. 26, 1885.

The stupor succeeding an epileptic convulsion resembles apoplexy,

and the fact that cerebral hemorrhage may be accompanied by
some convulsions increases the possible similarity, but it requires
only a short time for epilepsy to make itself manifest, either by a
renewal of the convulsions or a rapid recovery without paralysis.
According to Trousseau, however, many attacks of so-called
congestion of the brain are really epilepsy. Puerperal eclampsia
comes under the same head, but when convulsions are violent they
may give rise to actual hemorrhage. Unilateral epileptiform
convulsions are likely to be dependent on organic disease of the
brain, usually not of the kind at present under consideration, but
more frequently of a tumor.

Among the cerebral symptoms connected with renal disease, and

not involving organic change in the brain, may be found
unconsciousness, deep coma, and convulsions. It is obvious that the
presence of a few hyaline casts and a little albumen will not decide
the matter, since these may be present from many causes, and
especially the changes in the circulation accompanying apoplexy.
Neither will the most indubitable evidence of Bright's disease, such
as dropsy, hypertrophy of the heart, rigid arteries, with fatty and waxy
casts in the urine, do so, for, as we have already seen, not only is
there nothing in the presence of nephritis to exclude apoplexy, but
the very form, the interstitial, which, from the supervention of coma
not preceded by other very severe symptoms, most nearly
counterfeits apoplexy, is also the most likely to give rise to actual
cerebral hemorrhage. The extreme and frequent cephalalgia which is
so distressing a symptom in cases where there is no cerebral lesion
may also be the precursors of hemorrhage.

If we have a history, the gradual onset of the symptoms, deepening

unconsciousness without any paralytic or unilateral symptoms,
especially if accompanied by a diminution in the amount of urine or
contained urea or a marked change in the character of the casts,
renders it probable that we are dealing with so-called uræmia alone.
In the absence of history hemiplegia must be the chief dependence,
but it would not be difficult to imagine a case of embolism of the
basilar artery with softening of the pons which would defy a positive
diagnosis.

Pernicious intermittent fever appears in a so-called comatose form,

which, if it were to be accompanied, as in a case related by Bemiss
in the second volume of this work, by paralysis of one arm, might
present difficulties of diagnosis. If it were known that the attack had
been only of short duration, the elevation of temperature would, as in
the case of sunstroke, decide in favor of the fever, but if it had lasted
some hours, this symptom would be of no value, as the temperature
may rise to an equal height in apoplexy.

Diabetic coma is a much less common affection than apoplexy. The

peculiar odor (aceton) of the breath, if present—which is not always
the case—might be diagnostic. The peculiar long and deep
respirations would awaken suspicion which would be confirmed by
an examination of the urine.

Sunstroke, with its sudden onset, complete unconsciousness, and

rapidly rising temperature, may present a very close resemblance for
a while to apoplexy, and in fact has been known as heat apoplexy.
Age, temperature, and surroundings would give strong probabilities
one way or the other, and if the temperature of the patient were at
first below the normal and did not rise for an hour or two, it would
certainly not be sunstroke and would be apoplexy, while if the
temperature were very high a few minutes after the patient had been
observed to cease work or become unconscious, the evidence in
favor of sunstroke would be equally strong.

It might appear that hysteria need hardly enter into our

consideration, and could hardly be mistaken for apoplexy, but most
experienced physicians could relate instances where serious organic
disease has been made light of under the name of hysteria, and
many inexperienced ones could tell of the opposite and safer
mistake. An occasional case of deep coma presents itself where,
although the age and sex of the patient awaken strong suspicion, we
cannot at once be sure that no organic lesion is present; and if, in
addition, the patient should be affected with hemiplegia—a
combination which, although rare, is by no means beyond the limits
attainable by this perplexing disease—an immediate positive
diagnosis would be difficult. Absence of facial paralysis, which might
be made manifest by some irritation like pinching or an attempt to
raise the eyelids, would be of much value under these
circumstances. The hysterical physiognomy might be well enough
marked to be almost conclusive by itself. The urine and feces are not
likely to be passed involuntarily in hysteria, as they are in apoplexy.

Injuries to the head should be carefully looked for in any case with
unknown history. Actual fracture, which perhaps leads to no
depression of bone, may give rise to hemorrhage, probably
meningeal, which will cause the usual symptoms, and a shock which
is not accompanied by fracture may cause considerable laceration of
the brain with consequent hemorrhage. In the latter case, however,
unless the brain be already predisposed by arterial disease, the
laceration and hemorrhage will not be extreme and the symptoms
will be those of concussion. The diagnosis can hardly be said to be
between hemorrhage and concussion, but whether the hemorrhage
be the result of concussion—a question which can hardly be
answered without the history and observation of the further progress.
Cuts and bruises may result from a fall caused by the shock, and
pericranial ecchymoses may result from cerebral hemorrhage
through the vaso-motor system without the intervention of accident.

Rapid meningitis of the vertex, with predominance of the effusion

upon one side, may closely simulate compression from hemorrhage.
At the base, by the time it has become severe enough to cause
unconsciousness, it is likely to have affected the ocular muscles, and
perhaps given rise to other paralyses less regular in their distribution
than the ordinary hemiplegia. Ophthalmoscopic examination would
be of value in these cases if—which is not very likely to happen—
there is no history. The temperature in meningitis is more likely to be
irregular and less rapidly and uniformly rising than in a severe
hemorrhage or occlusion. In many cases emaciation, dry tongue,
and constipation with sunken abdomen will testify to a previous
illness, while after a few hours' observation the progress of the case
will make the diagnosis more clear.

In differentiating cerebral hemorrhage or ordinary embolism from the

apoplectiform attacks met with in syphilitic intracranial disease, it is
rather a question of etiology than of diagnosis in the narrower sense,
since unconsciousness and hemiplegia coming on with syphilis are
often dependent upon a condition of the vessels closely resembling
that which gives rise to the ordinary forms; that is, we are dealing in
either case with an endarteritis which has furnished the basis for the
deposit of a thrombus, and the question is, Of what nature is the
endarteritis? It is obvious that this is only to be answered by a
knowledge of the history, not necessarily of a primary or secondary
lesion, but of previous disease. The syphilitic taint may often be
suspected from the irregularity of the paralysis, the cranial nerves,
for instance—especially the ocular—being much more frequently
affected in syphilitic than in ordinary hemiplegia. After partial
recovery or amendment the characteristics of irregularity and
changeableness will be more strongly marked.
The pathology of hemiplegia and apoplectiform attacks, often
transitory, in the course of general paralysis is not certain, but it is
probable that they are due to sudden congestions of regions of some
extent already in a condition of chronic periencephalitis or to cerebral
œdema. The question of the existence of the previous disease can
only be settled after the return of the patient to consciousness.
Usually, these attacks are not of the severest kind, and are not
necessarily attended with loss of consciousness, which, when it
occurs, is usually not of long duration. An apoplectiform attack
occurring in a young or middle-aged person who has neither cardiac
nor renal disease, rapidly recovered from or changing its character,
should awaken strong suspicions of either general paralysis or
syphilis, or both.

The characteristic of the so-called congestion of the brain, or coup

de sang, is a close resemblance to ordinary apoplexy, but without
hemiplegia and usually with a rapid and complete recovery. A
diagnosis from apoplexy cannot be made at once, except so far as
hemiplegia can be shown to be either distinctly present or absent.

As has already been stated, the doctrine of the dependence of real

apoplectiform attacks upon cerebral congestion alone has been
vigorously combated by distinguished clinicians; and certainly the
diagnosis of congestive (and the same may be stated even more
strongly of so-called serous) apoplexy should never be made until
after the rigorous exclusion of every other possibility.

After the severer apoplectic symptoms have passed off, and in cases
where they have never been present, the diagnosis, so far as most
of the conditions mentioned above is concerned, is divested of many
of its difficulties when we are dealing with cases of well-marked
hemiplegia. The chief points left are the distinctions from the
apoplectiform attacks of general paralysis, cerebral syphilis, and
cerebral tumor, which are to be made as already pointed out.

Slighter and more localized paralyses, such as may occur with

limited lesion of the pons or where a hemorrhage having a large
focus in the substance has escaped under the membranes and
presses on some cranial nerve, would present more difficulties.
Paralyses which are very limited, and at the same time complete, are
not likely to arise from hemorrhage or embolism, though it is possible
that they may do so, but the diagnosis is to be considered rather
under the head of local palsies than of cerebral disease. General
rules cannot be laid down for slighter cases, and each case must be
diagnosticated for itself. In many of them the electrical diagnosis
would be of great value and often decisive.

Hysteria remains, as always, ready to counterfeit anything, but the

following case shows that the error is not always on that side: F. S
——, a young woman, was brought to the hospital, apparently
conscious and understanding what was going on, but unable or
unwilling to speak or to protrude her tongue. There was no history
except that she had probably been in the same condition for thirty-six
hours. There was paralysis of the right side, including the face, and
marked anæsthesia of the same side, quite distinctly limited at the
median line; temperature 97.8°, pulse 60, respiration 20. The next
day she seemed perfectly conscious, but did not speak. The faradic
brush to her face caused loud outcries, and the facial paralysis was
diminished. This condition remained nearly the same, the patient
appearing half conscious, but passing urine in bed. Four days later
there was marked diminution of sensation and motion on the left
(previously sound) side, as well as the right. The note two days later
was, “Shuts and opens her eyes when told, and moves eyeballs in
every direction, but there is apparently no voluntary motion except
slight of the head. Incontinence of urine and feces.” A week later the
temperature rose to 100.4°, pulse 140, and she died. The autopsy
showed red adherent thrombus in the left carotid, extending into the
cerebrals, with extensive anæmic necrosis of the cortex and a part of
the corpus striatum. On the right there was a grayish thrombus and
softening of the cortex, while the great ganglia were not affected.

A woman of thirty-two had repeated attacks of loss of consciousness

and somnolence lasting several hours, but leaving her apparently
well. The case was considered hysteria, but the patient died in a
similar attack. Degeneration of the cerebral arteries and hemorrhage
were found.48
48 Christian, Centralblatt f. d. Med. Wiss., 1873, 864.

Post-paralytic chorea might present difficulties of diagnosis from

hysteria or malingering, though the difficulty is quite as likely to be on
the other side.

The diagnosis, however, is not complete until the lesion is located

with some precision and its nature determined, although it must be
confessed that when we have got as far as this the diagnosis in most
cases is of more interest to the physician than to anybody else,
except to a slight extent for prognosis, so that the event may be
anticipated by a few hours. As to the localization of the lesion, recent
experiments and observations, involving not only lesions of the kind
we are here discussing, but tumors and injuries as well, permit this to
be done with a reasonable degree of certainty. The general article on
Cerebral Localization may be referred to by the reader for the
minuter points, but certain groups of symptoms may be indicated
here which are available to some extent before the complete return
of the patient to consciousness.

In the vast majority of cases the lesion is situated upon the side of
the brain opposite to the paralysis, except in some instances of
cerebellar lesion, while in the peculiar form known as alternate
paralysis due to lesion of the pons it is on the opposite side to the
paralysis of the limbs and on the same side with the facial. It should
be distinctly stated, however, that there are exceptions which are
inexplicable on the present basis of cerebral anatomy. It is well
known that only a part of the motor tracts cross to the other side of
the cord at the decussation, and also that the proportion between the
fibres which do and those which do not cross is a variable one. It has
been suggested, in some cases of the kind mentioned, that all the
motor fibres, instead of only a minority, as is usual, pass down on the
same side of the cord as their origin. This has not been
demonstrated. The number of such cases are so small that it need
not be taken into account in diagnosis, and if the practitioner should