An Inconvenient Duke Anna Harrington

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Books. Change. Lives.

Copyright © 2020 by Anna Harrington
Cover and internal design © 2020 by Sourcebooks
Cover design by Katie Anderson
Cover image by Shirley Green
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 Contents

Front Cover

Title Page

Copyright

Prologue

One

Two

Three

Four

Five

Six

Seven

Eight

Nine

Ten
Eleven

Twelve

Thirteen

Fourteen

Fifteen

Sixteen

Seventeen

Eighteen

Nineteen

Twenty

Twenty-One

Twenty-Two

Twenty-Three

Twenty-Four

Twenty-Five

Twenty-Six

Twenty-Seven

Epilogue

Excerpt of A Duke Too Far

One
About the Author

Back Cover
 Dedicated to Bruiser
for keeping me company during the long hours on the porch writing
this.
And a very special thank you to
Sarah Younger, Sarah Otterness, and Cat Clyne.
 Prologue

April 1814
To General Marcus Braddock
Coldstream Guards, 2nd Battalion,
Household Division
Bayonne, France

Dear General Braddock,

It is with a grieving heart that I write to you to tell you of the

passing of your sister Elise.
There was a terrible accident. She was on her morning ride in
the park and was thrown from her horse. The horse guards who
found her assured me that she did not suffer. While there is
nothing I can write that will lessen your pain, I pray you might
find some comfort in that.
I know that your attention must now be fixed on your men and
on the fight you are waging against Napoleon, but please be
assured that I will do everything I can to support your sister
Claudia and Elise’s daughter, Penelope, while you are away.

Yours in shared grief—

Danielle Williams

June 1814
 To the Honorable Danielle Williams
No. 2 Bedford Square, Mayfair
London, England

Dear Miss Williams,

Although the news was bitter, I thank you for your kind letter. It
brings me solace to know that Elise was so dearly loved by you. I
am more grateful than I can express to know that you are
looking after Claudia and Pippa during this time of mourning.

With gratitude—
Marcus Braddock

January 1816
To the Honorable Danielle Williams
No. 2 Bedford Square, Mayfair
London, England

Dear Miss Williams,

My regiment’s work in Paris will be ending soon, and I will be

returning to London. I would very much appreciate the
opportunity to call on you. I wish to thank you in person for the
kindnesses that you and your aunt have shown to my family
during my absence.

Yours sincerely,
Marcus Braddock

February 1816
To General Marcus Braddock
British Embassy
Hôtel de Charost, rue du Faubourg Saint-Honoré
 Paris, France

Dear General,

Your appreciation is more than enough. Please do not feel

obligated to call on us, as I know how busy your homecoming
will surely be. I wish you the best with your new endeavors.
Please give my love to Claudia and Penelope.

Yours in friendship—
Danielle Williams

April 1816
To the Honorable Danielle Williams
No. 2 Bedford Square, Mayfair
London

Dear Miss Williams,

I have returned home but discovered unsettling information

regarding my sister Elise. I must insist on meeting with you.
Please reply with the best day and time for me to call upon you.

Marcus Braddock

April 1816
To the General His Grace the Duke of Hampton
Charlton Place, Park Lane
London

Dear Duke,

While I wish to congratulate you on your new title, I must decline

your offer to receive you. Elise was my dearest friend—in truth,
more like a sister. To speak of her death will only refresh our
 shared grief and remind us of all that we have lost when your
return should be met with joy. I could not bear it and wish to
grieve for her in peace. Please understand.

Sincerely,
Danielle Williams

May 1816
To the Right Honorable the Viscountess Bromley
& the Honorable Danielle Williams
No. 2 Bedford Square
Mayfair, London

You are cordially invited to attend a birthday celebration in honor

of the General His Grace the Duke of Hampton, on Saturday, May
5, at 8 p.m. Please send your acceptance to Miss Braddock,
Charlton Place, Park Lane, London.

And the handwritten note tucked inside with the invitation…

Danielle, please attend. The party will not be the same without
you. And to be honest, I will need your support to survive the
evening. You know how Marcus can be at events like this. That it
is for his own birthday will most likely make him all the worse.
And Pippa misses you as much as I do.

~Claudia

Danielle Williams bit her bottom lip as she read the note, dread and
guilt pouring through her in equal measure.
God help me.
There was no refusing this invitation.
 One

May 1816
Charlton Place, London

Marcus Braddock stepped out onto the upper terrace of his town
house and scanned the party spreading through the torch-lit gardens
below.
He grimaced. His home had been invaded.
All of London seemed to be crowded into Charlton Place tonight,
with the reception rooms filled to overflowing. The crush of bodies in
the ballroom had forced several couples outside to dance on the
lawn, and the terraces below were filled with well-dressed dandies
flirting with ladies adorned in silks and jewels. Card games played
out in the library, men smoked in the music room, the ladies retired
to the morning room—the entire house had been turned upside
down, the gardens trampled, the horses made uneasy in the mews…
And it wasn’t yet midnight.
His sister Claudia had insisted on throwing this party for him,
apparently whether he wanted one or not. Not only to mark his
birthday tomorrow but also to celebrate his new position as Duke of
Hampton, the title given to him for helping Wellington defeat
Napoleon. The party would help ease his way back into society, she’d
asserted, and give him an opportunity to meet the men he would
now be working with in the Lords.
But Marcus hadn’t given a damn about society before he’d gone off
to war, and he cared even less now.
No. The reason he’d agreed to throw open wide the doors of
Charlton Place was a woman.
The Honorable Danielle Williams, daughter of Baron Mondale and
his late sister Elise’s dearest friend. The woman who had written to
inform him that Elise was dead.
The same woman he now knew had lied to him.
His eyes narrowed as they moved deliberately across the crowd.
Miss Williams had been avoiding him since his return, refusing to let
him call on her and begging off from any social event that might
bring them into contact. But she hadn’t been able to refuse the
invitation for tonight’s party, not when he’d also invited her great-
aunt, who certainly wouldn’t have missed what the society gossips
were predicting would be the biggest social event of the season. She
couldn’t accept and then simply beg off either. To not attend this
party would have been a snub to both him and his sister Claudia, as
well as to Elise’s memory. While Danielle might happily continue to
avoid him, she would never intentionally wound Claudia.
She was here somewhere, he knew it. Now he simply had to find
her.
He frowned. Easier said than done, because Claudia had
apparently invited all of society, most of whom he’d never met and
had no idea who they even were. Yet they’d eagerly attended, if only
for a glimpse of the newly minted duke’s town house. And a glimpse
of him. Strangers greeted him as if they were old friends, when his
true friends—the men he’d served with in the fight against Napoleon
—were nowhere to be seen. Those men he trusted with his life.
 These people made him feel surrounded by the enemy.
The party decorations certainly didn’t help put him at ease. Claudia
had insisted that the theme be ancient Roman and then set about
turning the whole house into Pompeii. Wooden torches lit the
garden, lighting the way for the army of toga-clad footmen carrying
trays of wine from a replica of a Roman temple in the center of the
garden. The whole thing gave him the unsettling feeling that he’d
been transported to Italy, unsure of his surroundings and his place in
them.
Being unsure was never an option for a general in the heat of
battle, and Marcus refused to let it control him now that he was on
home soil. Yet he couldn’t stop it from haunting him, ever since he’d
discovered the letter among Elise’s belongings that made him doubt
everything he knew about his sister and how she’d died.
He planned to put an end to that doubt tonight, just as soon as he
talked to Danielle.
“There he is—the birthday boy!”
Marcus bit back a curse as his two best friends, Brandon Pearce
and Merritt Rivers, approached him through the shadows. He’d
thought the terrace would be the best place to search for Danielle
without being seen.
Apparently not.
“You mean the duke of honor,” corrected Merritt, a lawyer turned
army captain who had served with him in the Guards.
Marcus frowned. While he was always glad to see them, right then
he didn’t need their distractions. Nor was he in the mood for their
joking.
A former brigadier who now held the title of Earl of Sandhurst,
Pearce looped his arm over Merritt’s shoulder as both men studied
him. “I don’t think he’s happy to see us.”
 “Impossible.” Merritt gave a sweep of his arm to indicate the
festivities around them. The glass of cognac in his hand had most
likely been liberated from Marcus’s private liquor cabinet in his study.
“Surely he wants his two brothers-in-arms nearby to witness every
single moment of his big night.”
Marcus grumbled, “Every single moment of my humiliation, you
mean.”
“Details, details,” Merritt dismissed, deadpan. But he couldn’t hide
the gleam of amusement in his eyes.
“What we really want to know about your birthday party is this.”
Pearce touched his glass to Marcus’s chest and leaned toward him,
his face deadly serious. “When do the pony rides begin?”
Marcus’s gaze narrowed as he glanced between the two men.
“Remind me again why I saved your miserable arses at Toulouse.”
Pearce placed his hand on Marcus’s shoulder in a show of genuine
affection. “Because you’re a good man and a brilliant general,” he
said sincerely. “And one of the finest men we could ever call a
friend.”
Merritt lifted his glass in a heartfelt toast. “Happy birthday,
General.”
Thirty-five. Bloody hell.
“Hear, hear.” Pearce seconded the toast. “To the Coldstream
Guards!”
A knot tightened in Marcus’s gut at the mention of his former
regiment that had been so critical to the victory at Waterloo yet also
nearly destroyed in the brutal hand-to-hand combat that day. But he
managed to echo, “To the Guards.”
Not wanting them to see any stray emotion on his face, he turned
away. Leaning across the stone balustrade on his forearms, he
muttered, “I wish I could still be with them.”
 While he would never wish to return to the wars, he missed being
with his men, especially their friendship and dependability. He
missed the respect given to him and the respect he gave each of
them in return, no matter if they were an officer or a private. Most
of all, he longed for the sense of purpose that the fight against
Napoleon had given him. He’d known every morning when he woke
up what he was meant to do that day, what higher ideals he served.
He hadn’t had that since he returned to London, and its absence ate
at him.
It bothered him so badly, in fact, that he’d taken to spending time
alone at an abandoned armory just north of the City. He’d purchased
the old building with the intention of turning it into a warehouse,
only to discover that he needed a place to himself more than he
needed the additional income. More and more lately, he’d found
himself going there at all hours to escape from society and the
ghosts that haunted him. Even in his own home.
That was the punishment for surviving when others he’d loved
hadn’t. The curse of remembrance.
“No, General.” Pearce matched his melancholy tone as his friends
stepped up to the balustrade, flanking him on each side. “You’ve left
the wars behind and moved on to better things.” He frowned as he
stared across the crowded garden. “This party notwithstanding.”
Merritt pulled a cigar from his breast pocket and lit it on a nearby
lamp. “You’re exactly where you belong. With your family.” He puffed
at the cheroot, then watched the smoke curl from its tip into the
darkness overhead. “They need you now more than the Guards do.”
In his heart, Marcus knew that, too. Which was why he’d taken it
upon himself to go through Elise’s belongings when Claudia couldn’t
bring herself to do it, to pack up what he thought her daughter,
Penelope, might want when she was older and to distribute the rest
to the poor. That was how he’d discovered a letter among Elise’s
things from someone named John Porter, arranging a midnight
meeting for which she’d left the house and never returned.
He’d not had a moment of peace since.
He rubbed at the knot of tension in his nape. His friends didn’t
need to know any of that. They were already burdened enough as it
was by settling into their own new lives now that they’d left the
army.
“Besides, you’re a duke now.” Merritt flicked the ash from his cigar.
“There must be some good way to put the title to use.” He looked
down at the party and clarified, “One that doesn’t involve society
balls.”
“Or togas,” Pearce muttered.
Marcus blew out a patient breath at their good-natured teasing.
“The Roman theme was Claudia’s idea.”
“Liar,” both men said at once. Then they looked at each other and
grinned.
Merritt slapped him on the back. “Next thing you know, you’ll be
trying to convince us that the pink ribbons in you horse’s tail were
put there by Penelope.”
Marcus kept his silence. There was no good reply to that.
He turned his attention back to the party below, his gaze passing
over the crowded garden. He spied the delicate turn of a head in the
crowd—
Danielle. There she was, standing by the fountain in the glow of
one of the torches.
For a moment, he thought he was mistaken, that the woman
who’d caught his attention couldn’t possibly be her. Not with her
auburn hair swept up high on her head in a pile of feathery curls,
shimmering with copper highlights in the lamplight and revealing a
long and graceful neck. Not in that dress of emerald satin with its
capped sleeves of ivory lace over creamy shoulders.
Impossible. This woman, with her full curves and mature grace,
simply couldn’t be the same excitable girl he remembered, who’d
seemed always to move through the world with a bouncing skip.
Who had bothered him to distraction with all her questions about the
military and soldiers.
She laughed at something her aunt said, and her face brightened
into a familiar smile. Only then did he let himself believe that she
wasn’t merely an apparition.
Sweet Lucifer. Apparently, nothing in England was as he
remembered.
He put his hands on both men’s shoulders. “If you’ll excuse me,
there’s someone in the garden I need to speak with. Enjoy
yourselves tonight.” Then, knowing both men nearly as well as he
knew himself, he warned, “But not too much.”
As he moved away, Merritt called out with a knowing grin. “What’s
her name?”
“Trouble,” he muttered and strode down into the garden before she
could slip back into the crowd and disappear.
 Two

Danielle Williams smiled distractedly at the story her great-aunt

Harriett was telling the group of friends gathered around them in the
garden. The one about how she’d accidentally pinched the bottom of
—
“King George!” The crux of the story elicited a gasp of surprise,
followed by laughter. Just as it always did. “I had no idea that the
bottom I saw poking out from behind that tree was a royal one.
Truly, doesn’t one bottom look like all the rest?”
“I’ve never thought so,” Dani mumbled against the rim of her
champagne flute as she raised it to her lips.
Harriett slid her a chastising glance, although knowing Auntie,
likely more for interrupting her story than for any kind of hint of
impropriety.
“But oh, how high His Majesty jumped!” her aunt continued,
undaunted. As always. “I was terrified—simply terrified, I tell you! I
was only fourteen and convinced that I had just committed high
treason.”
Although Dani had heard this same story dozens of times, the way
Harriett told it always amused her. Thank goodness. After all, she
needed something to distract her, because this evening was the first
time she’d been to Charlton Place since Marcus Braddock had
returned from the continent. The irony wasn’t lost on her. She was
on edge with nervousness tonight when she’d once spent so much
time here that she’d considered this place a second home.
“A pinch to a king’s bottom!” Harriett exclaimed. “Wars have been
declared over less offending actions, I assure you.”
Dani had been prepared for the unease that fluttered in her belly
tonight, yet the guilt that gnawed at her chest was as strong as
ever…for not coming to see Claudia or spending time with Pippa, for
not being able to tell Marcus what kindnesses Elise had done for
others in the months before her death. But how could she face him
without stirring up fresh grief for both of them?
No. Best to simply avoid him.
“Had it been a different kind of royal bottom—say, one of the royal
dukes—I might not have panicked so. But it was a king’s bottom!”
She had a plan. Once Harriett finished her story, Dani would
suddenly develop a headache and need to leave. She would give her
best wishes to Claudia before slipping discreetly out the door and in
the morning pen a note of apology to the duke for not wishing him
happy birthday in person. She’d assure him that she’d looked for him
at the party but had been unable to find him. A perfectly believable
excuse given how many people were crammed into Charlton Place
tonight. A complete crush! So many other people wanted their
chance to speak to him that she most likely couldn’t get close to him
even if she tried. Not that she’d try exactly, but—
“Good evening, Miss Williams.”
The deep voice behind her twined down her spine. Marcus
Braddock. Drat it all.
So much for hiding. Her trembling fingers tightened around the
champagne flute as she inhaled deeply and slowly faced him. She
held out her gloved hand and lowered into a curtsy. “Your Grace.”
Another random document with
no related content on Scribd:
cerebellar tract—or, rather, a large part of the periphery of the lateral
column—may be sclerosed in this disease. In this way, since the
direct pyramid tract in the anterior, the greater part of the border of
the lateral, and the entire posterior column are degenerated, the
sclerosis resembles a marginal ring113 in shape.
113 Archiv für Psychiatrie, xiv. p. 384.

Anatomically, the sclerosis of the family form of tabes resembles that

form of combined sclerosis in which the lateral and posterior
columns are together affected. It is probably due to a defective
development of these tracts, rendering them liable to premature
decrepitude or increasing their vulnerability. The latter alternative is
exemplified in those cases where some acute disease of childhood,
such as scarlatina or measles, acted as an exciting cause.

DIAGNOSIS.—There are two affections some of whose leading

symptoms are so closely imitated by those of this disease that they
may be confounded with it on first sight. These are tabes dorsalis—
of which the family form is still regarded a variety, as the name
indicates—and disseminated sclerosis. In the gait the former, in the
nystagmus and scanning speech the latter, disorder is approximated.
The distinction from true tabes has already been dilated on. (See
Tabes.) The fact that relatives—usually the sisters and brothers—of
the patient are affected in the same way in their youth speaks in
favor of the family form. The deep reflexes are not abolished early,
as in tabes, nor are anæsthesias or paræsthesias early symptoms,
as in the latter. The speech-disturbance and nystagmus, which in
most cases develop later in the family form, serve to distinguish it
from true tabes in the advanced stage. It is at this period that the
disease may resemble a disseminated sclerosis. The hereditary or
family character does not aid us in making a discrimination here, as
there is also a family form of the latter disease. But the absence of
intention tremor, which we would assume to be present in a case of
disseminated sclerosis of the cerebral type, and of optic-nerve
atrophy serves to distinguish the two. Musso claims that the speech-
disturbance is also different in character. There certainly is more
lingual ataxia in the family form of tabes, and less of typical
scanning, but I am doubtful about our ability to differentiate these
characters in all cases. The following table includes the main points
of difference, clinically considered, between the acquired and the
family form of tabes:

Tabes Dorsalis. The Family Form.

Prodromata. Marked and constant. Absent or slight.
Static ataxia (Romberg Early and constant. Absent.
symptom).
Involvement of upper extremities. Usually late. Early.
Ataxia of tongue, eyes, and Absent or unnoticeable. Always developed.
trunk-muscles.
Paresis. Rare. Characteristic.
Anæsthesia. Present in some form. Absent or slight.
Paræsthesia. Constant. Rare.
Sexual desire. Becomes extinguished. Remains unaffected.
Deep reflexes. Abolition usually initial. Abolition in course of
disease.114
Sphincters. Involvement is characteristic Involvement late, if at all.
and early.

114 There are conflicting observations on this point.

Disseminated Sclerosis.

SYNONYMS.—Multiple cerebro-spinal sclerosis (also spinal and

cerebral form), Insular cerebro-spinal sclerosis, Focal sclerosis,
Multilocular sclerosis; Herd-sklerose (Ger.); Sclerose en plaques
disseminées, Sclerose en plaques generalisées (French).

The occurrence of disseminated patches of gray degeneration in the

nervous axis was observed by Cruveilhier and Türck, but they
regarded the affection rather from the anatomical than the clinical
standpoint, and it was left for Frerichs to recognize its important
position among the chronic affections of the brain and spinal cord.
The earlier German investigators who followed him were cautious in
generalization, and it was not until Vulpian, Charcot, and their
followers announced the discovery of infallible diagnostic criteria that
disseminated sclerosis received that attention at the hands of the
profession which it merits. But the more thorough researches made
during the last two decades have shown that this announcement was
premature. The best authorities recognize the existence of a large
number of cases in which the supposed pathognomonic signs of
disseminated sclerosis are absent, notwithstanding the existence of
characteristic lesions, and thus the more cautious earlier
investigators are justified in the reserve they had maintained.

It is in perfect harmony with the irregular location of the disease and

the lack of any constant rule governing the distribution of the
sclerotic foci that there is no constant clinical picture by which its
existence can be accurately determined in all cases. The diagnosis
of tabes dorsalis, of spastic paralysis, of amyotrophic lateral
sclerosis, and of transverse myelitis rests on exact and constant
signs, but that of disseminated sclerosis does not. The dictum of
Charcot, that there is always intention tremor and nystagmus in
disseminated sclerosis, has long been overthrown. Well-determined
cases are on record by De Fleury and Westphal, and a number have
been observed by myself, where there was no tremor or no
increased tremor with intended movement, and no nystagmus, nor
any other of the pathognomonic symptoms so considered by Charcot
and his followers.

The morbid process of disseminated sclerosis consists in the

development of patches of sclerosed tissue, scattered apparently
without any regularity or rule through the brain and spinal cord. They
are the results of insidious inflammatory changes. The symptoms
marking their presence may include nearly every known focal and
general symptom studied by neurologists, varying with the number,
size, and distribution of the foci. Usually there is some disturbance of
motility, both ataxic and paretic; in the majority there is tremor, which
in a large proportion of cases is of a distinctive character, and
disturbance of the functions of the cranial nerves, amblyopia, color-
blindness, mental enfeeblement; and, above all, apoplectiform
seizures are frequent.

Some writers discriminate between cases in which the lesions are

limited to, or most intense in, the spinal cord, and those in which the
brain is chiefly or exclusively involved, and hence they speak of a
spinal, a cerebral, and a cerebro-spinal form. This discrimination is
not sufficiently supported by clinical evidence to be of any practical
value. Each case is to be studied by itself during life and after death,
and to be regarded as one of a series in which the lesion may be
concentrated in any one segment of the cerebro-spinal axis. It
seems that when the sclerotic foci are limited to or chiefly located in
the spinal cord, the clinical signs are less pronounced than where
the brain is seriously involved; those cases in which the symptoms
are latent, or so vague that they cannot be distinguished from spinal
irritation or spinal exhaustion, have been found to be of the spinal
type. The cases of this character thus far observed are not
sufficiently numerous to justify the creation of special subdivisions.115
115 According as the formation of the sclerotic foci preponderates in a given segment
of the nervous axis, the early signs of the disease may consist in disturbances of the
cerebral or the spinal functions, and we may speak accordingly of a cerebral or spinal
invasion type. But the principle of classification adopted by several recent writers,
which would rank the spinal type among the spinal diseases, the cerebral type among
the cerebral diseases, and which is compelled to erect a third category for the
reception of the cerebro-spinal type under the name of cerebro-spinal diseases, is a
bad one. Modern pathology recognizes the existence of affections which involve
whole fibre-systems, which are intracerebral in one and intraspinal in other parts of
their course, such as tabes and amyotrophic sclerosis, which would therefore have to
rank among the cerebro-spinal, and not among the spinal affections, with which the
authors referred to classify them.

CLINICAL HISTORY.—Prodromal.—Disseminated sclerosis is usually

inaugurated by a long initial period in which the symptoms are not
characteristic, and in which, unless there be decisive pupillary or
optic-nerve symptoms present, the nature of the disease is not
recognized. The patients feel weak and tired; walking is difficult, and
an element of unsteadiness suggests the development of a tabic
disorder. In other cases ankle-clonus is found and tremor of the foot
on extension (dorsiflexion); it is discovered that the unsteadiness is
due to weakness or to rigidity of the muscles, and thus the
impression of a developing spastic paralysis may be created. But
symptoms on the part of the cranial nerves soon show that the case
is one of disseminated sclerosis. Sometimes a marked belt
sensation is developed, and other forms of paræsthesia are not
uncommon; nay, the symptoms of spastic paralysis and tabes
dorsalis may be mingled. Diplopia of the same transitory character
as in tabes usually accompanies the gradually-developing speech
trouble. The reflex and mechanical excitability of the muscles is
increased in all cases where the lateral column is extensively
involved and the gray substance of the cord is—as it usually is in the
main—intact. In some cases a slight tap on the knee when held in
the position required to demonstrate the knee-jerk produces
oscillatory movements of the limb; as the patient endeavors to
suppress these they become more violent, extend to the trunk and
head, and may eventually involve the opposite side. In those cases
which show the cerebral-invasion type headache, vertigo, and
speech disturbance, temporary darkening of the visual field, and loss
of memory are the earliest symptoms directing attention to the
existence of serious disease.

Whether the spinal or the cerebral symptoms preponderate, they

continue increasing slowly and with temporary variations, which are
particularly marked in the cerebral-invasion type. As a rule, the
sensory disturbances are not pronounced at this time, but later, after
the initial symptoms have existed for a few years, they become
intense, and often extremely distressing. Those most complained of
by the patient are neuralgic, lancinating, and other pains. The
lancinating pains are, as a rule, not as severe as those of tabes
dorsalis, but they are apt to be associated with a dull heavy pain
which is located in a whole extremity, referred to the deep structures,
and very persistent. This diffuse pain sometimes occupies all of the
lower half of the body. As in tabes, the pain may be regarded the
forerunner of anæsthesia, which rarely, however, reaches a high
degree or an extensive distribution. Its distribution, like that of the
other peripheral symptoms of disseminated sclerosis, is commonly
irregular. Like the motor disturbance, which at this period consists in
a combination of paretic and spastic—occasionally of ataxic—
symptoms, it is most marked in the lower extremities.

In the majority of cases there is a peculiar tremor, which usually

presents the character to which Charcot directed attention—namely,
that it increases when the patient attempts to carry out a voluntary
movement, and disappears, or at least diminishes, when the
muscles of the part in question are at rest. This is the important
symptom known as the tremor on intended movement or intention
tremor. One of the time-honored means of testing it is to order the
patient to take a glass of water and pass it to his mouth. While he
reaches out for it some oscillatory unsteadiness is observed, but on
grasping, this is increased, and on raising the glass the oscillations
increase till he spills the water; if he succeeds in carrying it to his
mouth, there is a clattering against the teeth, and but for the
steadying aid of his mouth he would throw it aside by the violence of
the disturbing movements. In incipient cases this intention tremor is
best shown with delicate movements, and the more distinctly the
more slowly they are performed. It has been suggested that the
peculiar character of the lesion of disseminated sclerosis has some
relation to the intention tremor. It is a remarkable feature of the
morbid process that it leaves the axis-cylinder comparatively intact,
beyond any other form of myelitis or encephalitis. The myelin,
however, is destroyed, and the consequence is that the naked axis-
cylinders lie in a newly-formed connective tissue, which has not the
same faculty the myelin has of isolating the nervous impulses
conducted through the axis-cylinders. The result is, that when a
nervous impulse, such as a voluntary movement, travels through a
sclerotic focus, it may become deflected to neighboring fibres going
to another muscle or muscular bundle than the one intended to be
innervated. An unintended motion results; the patient makes a
stronger effort, intended for the right channel, but again it slips off, to
use a coarse simile, and thus a number of erroneous messages are
transmitted, and an equal number of disturbing motions respond to
these messages.

Whether this histological explanation be correct or not, the tremor is

probably due to the lesion of the peduncular tracts of the brain. At
least, this is rendered plausible for the tremor on intended
movement, which indicates an interference with the transmission of
voluntary impulses. Whether, as Pasternatzky116 claims, the extreme
muscular oscillation seen in advanced cases is due to irritation of the
cortical motor fields, it is impossible to decide. No strong evidence
can be adduced in favor of his view. A few cases have been
described (Schüle, Jolly, and Greiff); and, in my opinion, such are far
more numerous than is usually supposed, where the tremor did not
have the so-called characteristic feature of ceasing in conditions of
rest, claimed by Charcot, but continued as in paralysis agitans.117 A
collection of cases by Erb, Ordenstein, and Greiff shows clearly that
with a typical dissemination of sclerotic foci in the cord the tremor on
intended movement may be entirely absent, while no case is known
where the crus and pons were involved to a similar extent in which it
was absent. So it seems that a cerebral lesion is necessary to
produce this symptom in its characteristic form.
116 Jahrbücher für Psychiatrie, iii. 3, 1882.

117 For several years I had been puzzled by the fact that Charcot's formula failed to
correspond to the clinical picture in the majority of cases, and I registered such cases
as incipient multiple sclerosis or as a connecting group between paralysis agitans and
that disease.

In advanced cases of disseminated sclerosis the intention tremor

becomes generalized; previously noticed, perhaps, only in one arm,
it now affects all the limbs and the muscles which maintain the trunk
and head in static equilibrium. The result is, that even when the
patient is at rest sitting in a chair, his body, and particularly his head,
are agitated by a violent and coarse tremor, which is increased on
rising and walking, as well as on attempting to use the hands.
Delicate mechanical occupations become impossible, and the
handwriting shows a characteristic change, the forward strokes of
the letters and the curvilinear back strokes, as well as the dots and
crosses, registering the tremor of the hand in their peculiar
irregularity.

The speech is usually rough and broken, and sometimes enunciation

is impeded in a peculiar way, the patient appearing to scan his
words. Krause118 has found relaxation of the vocal cords in a
remarkable degree to underlie the change in phonation. The
scanning of speech appears to be due to impeded innervation of the
lips and tongue. When the patient is told to protrude his tongue, he
does so either in spasmodic instalments of movement or with a
sudden jerk after delay. The same delay and apparent halting are
noticed in the mimic expressions that are observed in speech. The
features sometimes express an emotion opposite to the one
experienced by the patient.119
118 Neurologisches Centralblatt, 1885.

119 This symptom is found where there are other reasons for suspecting the existence
of large foci in the pons. I have observed it in one case of tumor of this region, and
one of a focal disease of undetermined anatomical nature in the same location, in a
remarkable form. In the former case the patient not only exhibited the facial
contortions of hearty laughter when she felt as if about to break out in tears, and
broke out in tears when she felt amused, with perverse regularity, but both emotional
manifestations occurred simultaneously. The other case is still under observation.
There was complete anarthria in the first, and nearly complete anarthria in the second
case—a fact not unrelated to the inferred site of the lesion, and which may be
associated with the fact that where the perverse mimic expression occurs in
disseminated sclerosis the speech-disturbance often has an anarthric character.

Whether diplopia occur as an early symptom or not, nystagmic

oscillation of the eyeballs is commonly found in the developed
affection. This nystagmus is usually universal, noted in associated
movements in every direction, and aggravated by excitement, by
constrained positions, and by any act of innervation of the eye-
muscles. It may be looked upon as an intention tremor of the latter,
and attributed to sclerotic foci in the cerebral axis, particularly in the
tegmental part of the pons varolii.

The deep reflexes are in some cases but slightly affected. Where
spastic phenomena preponderate, they are exaggerated, and where
the posterior root-zones are involved in the lesion, they may be, as in
tabes dorsalis, diminished or absent. The nutrition of the muscles is
not impaired in the early stages, and indeed most functions which
depend for their proper performance on the intact condition of the
gray substance, such as the power of retaining the urine, micturition,
and the functions of the rectum, are properly performed at this
period. The cutaneous reflexes are not markedly abnormal in the
majority of cases. They sometimes become diminished in the last
stages.

In cases regarded as disseminated scleroses and similar disorders

approximating the combined form of sclerosis, Westphal120 noticed a
paradoxical muscular phenomenon which is the reverse in action of
the tendon reflexes. It is best observed in the tibialis anticus: if the
foot be extended (dorsiflected)—in other words, if the origin and
insertion of this muscle be approximated—the muscle contracts
firmly, keeping the foot in the enforced position, as if frozen into that
attitude. The same occasionally occurs if the patient voluntarily
extends his foot. Westphal observed the same phenomenon in the
disease described by him in which the symptoms of disseminated
sclerosis are present, but the corresponding lesion is not visible.121
120 Archiv für Psychiatrie, x. p. 243.

121 Ibid., xiv. p. 132. It is a noteworthy fact that this sign has been observed by its
discoverer also in paralysis agitans.

In a number of cases the mind becomes involved. Simple dementia

is the commoner condition, and some indication of passive mental
enfeeblement is found sooner or later in the history of the disease in
the majority of cases. In addition, there may be a morbid emotional
condition, usually in the direction of depression. I have been struck
by the frequent association of a melancholic state with large foci in
the oblongata. When it is borne in mind that the patient exhibits
tremor and speech-disturbance in addition to his mental trouble, it
will be understood that with some modifications of the typical signs
the case may simulate one of paretic dementia; and there are cases
in which it is exceedingly difficult to decide whether they belong to an
aberrant type of disseminated sclerosis or to the sclerotic type of
paretic dementia. There are some which constitute veritable
connecting-links between the two affections.122
122 Zacher, Archiv für Psychiatrie, xiii. p. 168; the writer, Journal of Nervous and
Mental Diseases, April, 1877, and Insanity, its Classification, Diagnosis, and
Treatment, p. 240.

Like tabes dorsalis, the progress of disseminated sclerosis is often

marked by episodes. Some of these differ in no way from the
visceral crises of posterior-column sclerosis; every form of these
symptoms found with that affection may occur in the present one,
while episodes involving the cerebral functions are much more
common. The latter manifest themselves as apoplectiform or
epileptiform seizures. They are preceded by headache and vertigo,
or, if these be continuously present, by an aggravation of them; then
unconsciousness develops, either accompanied by convulsions or
not, and the face is flushed, the pulse full and frequent, and the
temperature raised. Consciousness returns in a few hours or a day,
the attack rarely lasting more than two days, and it is found that the
patient is hemiplegic. But, unlike the hemiplegia found after vascular
rupture, embolism, or structural cortical disease, it is rapidly
recovered from.

In a case of Gnauck's an attack of scotoma scintillans, associated

with a noise of thunder in the right ear and pricking pains on the right
side of the face, preceded anæsthesia and the formation of a small
defect of the visual field.

There is a close resemblance between these apoplectiform and

epileptiform seizures and those of paretic dementia, not alone in
clinical character, but also in the surprisingly complete and rapid
recovery from the more serious symptoms. But just as in paretic
dementia, especially in its advanced stage, each seizure leaves the
patient somewhat more impaired in mind and body than he was
before, so it is in disseminated sclerosis; each attack marks a step
forward in the invasion of the morbid state.

Eye-trouble is much less frequently a premonitory sign of

disseminated sclerosis than of tabes. A few such cases are on
record. Magnan observed the development of the characteristic
symptoms of disseminated sclerosis fourteen years after an
amaurosis which followed typhoid; and Gnauck reports another in
which first a right ptosis, and then a right amblyopia, preceded the
ordinary symptoms. In exceptional cases this premonitory eye-
trouble may, like that of tabes, rapidly lead to extreme amblyopia or
even amaurosis. The visual disturbances are remarkable for their
rapid changes. They appear within a short period, attain their
maximum rapidly, and may occasionally retrograde as quickly. They
develop under two forms—the central and the peripheral scotoma,
or, rather, limitation of the visual or color field. The former, like the
amblyopia of alcoholic and nicotine intoxication, consists in an
inability to differentiate between red and green in the centre of the
visual field. It never, in my experience, proceeds as far as the toxic
amblyopias; that is, to the complete extinction of vision.123 The
peripheral limitation of vision may be for both quantitative and
qualitative light-perception, but it is not, as a rule,124 concentric as in
tabes, but sector-like.
123 Gnauck says that the central color-blindness may become total, and the red-green
blindness extend to the periphery.

124 Concentric limitation of ten to thirty degrees has been noted for color-perception.

The atrophy of the optic nerve in disseminated sclerosis is typically

partial, in the majority of cases manifesting itself as a sharply-
marked discoloration of the temporal half of the papilla. In others the
nasal half of the papilla also becomes discolored, but so much less
intensely that the difference between the earlier involved and later
involved portions is quite easy. It is doubtful whether the subjective
visual disturbance is always an indication of the extent to which the
optic nerve is involved. There are good reasons for believing those
amblyopias and limitations of the field of vision which show marked
remissions and exacerbations to be due to some dynamic central
condition involving the visual centres and tracts. Thus it has been
observed that almost total amaurosis occurred after an apoplectiform
attack, to disappear later on. Occasionally the amblyopia is bilateral
and the optic-nerve lesion unilateral. The frequency of this affection
is stated by Gnauck125 as follows: In one half the cases there is
diminished vision, and in half this half optic-nerve atrophy with
limitation of the visual field. It is only in exceptional cases that an
optic neuritis can be determined to have preceded the atrophy.
125 Of 50 cases, 22 had no visual trouble, 8 showed simple diminution of perception,
5 added limitation, and 15 changes of the optic disc, a case of total atrophy and
amaurosis being included in the latter.

The pupils are perfectly normal in some cases; in others myosis of

the spinal type is observed; and this I found to be nearly constant in
all advanced cases. Irregularity in outline and inequality exist in a
small proportion, and reflex iridoplegia is found in about 10 per cent.
of the cases.

Thus far, the symptoms which occur either in a majority or in a large

percentage of cases have been enumerated. The typical course of
disseminated sclerosis may be stated as consisting in their gradual
development and intensification, covering a period of from four to
twenty or more years. There are a number of cases in which so
many of the symptoms regarded as typical are either absent or
where some given symptom-group preponderates over the others to
such an extent that they require special mention.

It is not difficult to understand that disseminated sclerosis may ape

other forms of spinal disease. Its symptoms depend on the location
of the sclerotic foci. If these are situated chiefly in the crossed-
pyramid tract, spastic phenomena will predominate, and the case
may resemble a spastic paralysis.126 If they be distributed in both the
posterior and lateral columns, the symptoms will resemble those of a
combined form of sclerosis in which the tabic and spastic signs are
associated, as far as they do not, in the nature of the case,
neutralize each other. This was well shown in a case of De Fleury's.
Not infrequently an unusually large focus involves the entire
transverse section of the cord, and the case becomes complicated
by the symptoms of a transverse myelitis. In such a case, described
by Rovigli,127 a large transverse focus in the cord had led to
ascending secondary degeneration in the column of Goll and
descending degeneration of the crossed pyramid tract. In a large
series, instances of which are related by Kilian,128 Siemens,129
Schultze,130 Zacher,131 and Greiff,132 the disseminated foci were
complicated by a diffuse lesion distributed like that of a diffuse or
fascicular myelitis; and there seems to exist every connecting-link
between ordinary chronic myelitis, strictly so called, and
disseminated sclerosis.
126 Gnauck, Neurologisches Centralblatt, 1884, p. 315.

127 Rivista sperimentale di Freniatria e di Medicina leqale, x. p. 227.

128 Archiv für Psychiatrie, vii. p. 28. He designates this form sclerosis continua
multiplex.

129 Ibid., x. p. 135.

130 Ibid., xi. p. 216.

131 Ibid., xiii. p. 168.

132 Ibid., xiv. p. 287.

Not only does disseminated sclerosis occasionally imitate or

approximate the regular (fascicular) affections of the cord, as well as
diffuse cerebro-spinal affections, but it may appear under the mask
of a nuclear oblongata paralysis.133 And cases are on record where,
in addition to the disseminated sclerosis, there occurred sclerotic
atrophy of an entire hemisphere or of its capsular tracts, thus leading
to a hemiplegic resemblance of the motor paralysis. In my
experience the cases presenting the type of a nuclear oblongata
paralysis run a more rapidly fatal course than others. The shortest
history in my series, one of four years, was of such a case. A
number of instances are on record by careful observers—and are
probably much more numerous than is commonly suspected—where
no decisive evidence of spinal or cerebral disease could be detected
during life, and yet disseminated foci of sclerosis existed in the
nerve-centres. In such cases the symptoms may be in the direction
of simple nervous prostration, more commonly of spinal irritation. I
have now under observation a case which for years had been
regarded as one of spinal irritation, and which made that impression
on me until I discovered the existence of optic-nerve atrophy, which
was the only indication that the symptoms depended on gross
structural disease.134
133 It is customary to speak of symptoms referable to the oblongata as bulbar. The
designation bulbus rachidicus is now obsolete, and just as we speak of a capsular
hemiplegia, a pons paralysis, or a spinal hemiplegia, so we should say an oblongata
paralysis, discriminating between the nuclear, the neural, and the tract affections by
means of a prefix.

134 At present the symptoms of disseminated sclerosis are unmistakable. Cases are
mentioned by Strümpell and others in which they remained indecisive throughout.

Among the anomalous forms of disseminated sclerosis there is one

which is characterized by the preponderance of paraplegia and
contractures in a combination which is usually found in spinal
diseases of a different type. The coexistence of dementia, however,
usually enables the observer to determine that the lesion is both
cerebral and spinal, although those signs which might enable him to
decide the disseminated focal character may be absent.

MORBID ANATOMY.—In advanced cases of disseminated sclerosis the

lesion is visible to the naked eye on the surface of the brain and
spinal cord. Grayish maculas, sometimes elevated, more rarely a
little sunken, and occasionally showing a buff or reddish tinge, are
seen on the surface of the spinal cord, the oblongata, pons, and
crura. On making sections across the region of the spots, it is found
that the color-change is not superficial, but extends inward, involving
large parts of the transverse area of the cord or the cerebral axis;
and patches lying more deeply in their substance are revealed
whose existence could not have been suspected from a mere
surface inspection. Exceptionally, patches are found involving the
entire transverse section of the spinal cord in a length of a half to two
inches. And, similarly, in the brain nearly the entire area of the pons
or one of the crura or an entire division of the internal capsule may
be occupied by a sclerotic focus. Otherwise, they may vary from
almost microscopic dimensions to the size of a chestnut or even
larger. Bourneville135 has described cases in which the nerve-centres
appeared normal to the naked eye, while the microscope revealed
the existence of sclerotic foci. It is, however, unlikely that the fresh
brain- and cord-tissue, when the site of disseminated sclerosis, will
appear perfectly healthy to the naked eye under fairly good
illumination. Much less intense lesions than those of disseminated
sclerosis reveal their presence by changes in color and consistency.
135 Mouvement medicale, 1869, No. 27.

On examining the diseased spots more narrowly, they are found to

be slightly diaphanous. Usually, they are rounded or elliptical, but
they are often drawn out, as it were, in the most irregular shapes,
and not infrequently appear to be the result of a confluence of
originally remote and separate foci. In the cord they are sometimes
wedge-shaped, extending inward from the periphery. To the touch
they appear firm—sometimes not much more so than the normal
tissue, contrasting with it as hard-boiled white of egg would contrast
with soft-boiled; in advanced cases they become of almost leathery
consistency, and there are instances recorded where they actually
creaked under the knife. A clear fluid usually runs from their cut
surface, and the latter does not jut up on section like normal nerve-
tissue.

The distribution of the diseased areas follows no known law. They

may be numerous and of large size in one segment of the nervous
axis, and small, few in numbers, or even absent, in others. In some
altitudes of the cord the lateral, in others the posterior, in still others
the anterior, columns are chiefly involved. The cerebrum usually
contains a larger number of foci irregularly scattered in the centrum
ovale of Vieussens, the internal capsule and its surrounding ganglia,
as well as in the corpus callosum. Throughout the nervous axis it
seems that the lesion chiefly affects the white substances, and even
the roots of the peripheral nerves, both cranial and spinal, are
occasionally found to contain small foci, gray, firm in consistency,
and as distinctly outlined as those of the central organs.

The morbid process consists in an atrophy and gradual

disappearance of the myelin, which is preceded, if not caused, by an
increase of the enveloping interstitial substance. This change is of
the same character as that found in chronic myelitis. The septa and
trabeculæ of connective tissue become thicker, formless connective
substance and fibrillar tissue, which seems to arise in, if not in part
from, it, constituting the new formation. The neuroglia-nuclei are
increased, enlarged, and develop into spider-shaped cells, whose
long processes contribute (according to some authors exclusively) to
the newly-formed fibrillar network.

While the myelin undergoes wasting, the axis-cylinders remain intact

for a long period, and even in intensely sclerosed regions they may
be found in nearly their normal number, but naked and in direct
contact with the pathological fibrillæ. Some of them become
hypertrophied, increasing to twice, thrice, and, according to Leyden,
even more, of their normal diameter. This change seems to
inaugurate the last phase of the process: the axis-cylinders,
becoming sclerosed and brittle, ultimately disappear, and no trace, or
at best but doubtful traces, of the normal nerve-tissue are left behind.
The blood-vessels, following the rule of the sclerotic process, take
part in it. Their walls become thickened, richly nucleated, and the
lumen becomes narrowed in consequence. In the smaller vessels
complete obliteration of the lumen is sometimes observed.

The gray substance is not involved as frequently as the white, but it

opposes no barrier to the extension of the morbid process when
once established in its neighborhood. The nerve-cells show the
same resistance which the axis-cylinder does; that is, they retain
their outline and fibre-connections a long time in the midst of the
diseased area. But eventually they become discolored, undergo
hyaline or granular disintegration, their processes shrink, and finally
they disappear.

Ribbert and Zacher consider the sclerosis of tabes and the

disseminated affection to be much more similar than Leyden and
Charcot supposed. They locate the starting-point of the morbid
process in the vascular and connective tissues; and Greiff, in
harmony with this view, finds that the foci occur most frequently in
those parts of the cord where the connective-tissue trabeculæ are
most numerous, as in the posterior columns and at the junction of
the anterior and lateral columns.

Although the morbid foci appear to the naked eye to be uniform, and
to be sharply demarcated in the normal tissue, closer examination
shows that the areas of maximum lesion are surrounded by a narrow
transition zone by which the lesion seems to mark its eccentric
progress, and occasionally a focus of intense disease lies in a
diffused area of slight changes, resembling those of diffuse myelitis.
Sometimes the cord appears to be almost continuously involved by a
lesion of moderate intensity, and a few disseminated foci in the brain
alone prove that the case belongs to this form of sclerosis.

A few years ago Greiff described what he considered a new lesion in

multiple sclerosis, under the name of disseminated vitreous
degeneration of the cerebral cortex.136 I have been familiar with this
lesion since 1876: it can be produced at will in perfectly healthy
brains, and consists in a precipitation of leucine crystals extracted
from the brain-substance by the action of alcohol. His accompanying
figure137 represents this artificial lesion very accurately; and Greiff, if
he fails to recognize that his vitreous degeneration is a spurious
lesion, at least identifies it with the miliary sclerosis of Bucknill and
Tuke and the spheres of Schüle, which are now generally
recognized to be the results of post-mortem manipulations and not
actual lesions.138
 136 Archiv für Psychiatrie, xiv. p. 286.

137 Ibid., xiv., Plate ii. Fig. 5.

138 Attention was first called to the artificial nature of these bodies by the writer in the
Journal of Nervous and Mental Diseases, October, 1877, and a more accurate
description was given in the Chicago Medical Review of 1880, and in a demonstration
before the New York Neurological Society in 1883. In commenting on the latter a
German critic stated that the facts related had been long known in Germany
(Neurologisches Centralblatt, 1883, p. 283). On inquiring of the critic what publication
contained any reference to this discovery, he frankly stated that he knew of none, but
had had in mind what he considered a tradition of the laboratory. It was in the same
year that Greiff worked at the Heidelberg laboratory under the eminent supervision of
Fürstner, and it was a few years previous that Schüle, one of the collaborators of
Ziemssen's Cyclopædia, had made the same mistake. So it seems that the tradition is
in some danger of expiring, and that it would do no harm to accept the caution, even
though it travel across the Atlantic in the reverse of the usual direction. It has been
amply confirmed by Savage and Plaxton (Journal of Mental Science, October, 1882,
and April, 1883).

In judging as to the nature and intensity of the inflammatory process

which leads to the development of the sclerotic foci, it must be
remembered that we are acquainted thus far only with the terminal
period of the disease, when, as is to be presumed, the active
inflammatory changes have gone by or are in the background. It is
very probable that the newly-formed tissue is more nucleated in early
periods than is found in the cases which constitute the material of
pathological laboratories. In a case of protracted nervous exhaustion
accompanied by spinal irritation in an alcoholic subject who was
murdered, and whose brain and cord I had an opportunity of
examining, I found, both in the cord and brain, districts in which the
white substance showed a slight grayish discoloration and increased
consistency. Minute examination failed to show any qualitative
change in the conducting elements, but the interstitial tissue was
hypertrophied, richly nucleated, and showed Frommann's cells in
abundance.
ETIOLOGY.—Heredity has been observed in a number of cases by
Duchenne, Erb, and Frerichs. The latter two had each an opportunity
of recording this inheritance in several members—sisters or brothers
—of the same family. In these cases the transmitted affection
developed in adult life. Dreschfeld, however, cites a case where two
brothers developed its symptoms in a marked degree in infancy. As
an associated feature it is found with some cases of congenital
defect. Thus Pollak139 discovered disseminated sclerosis in an infant
which had a defective corpus callosum and exhibited the
characteristic signs of the focal affection side by side with the
imbecility due to imperfect cerebral development. As a rule, the
disease is developed after the twentieth year. But cases have been
related (De Fleury) where the patient developed the disease and
died with an apoplectiform onset in earlier life. One of the youngest
on record is described by Hödemacker.140 The subject developed the
disease at the seventh year, and died with it at the fourteenth, having
shown the characteristic symptoms, besides more muscular atrophy
than is common. The sclerosis in this case belonged to the type
which has been referred to as a connecting-link between diffuse and
disseminated sclerosis. Pelizæus141 reports five cases developing in
the same family in early life, corresponding somewhat in their
relation to multiple sclerosis of advanced life, as the family forms of
tabes and spastic paralysis correspond to the typical adult forms of
those diseases. All the cases were of males, and the ancestral taint
had been present in male members of the family, passing through
the females to their progeny without breaking out in the mothers.
Each branch of this family appeared to develop its own peculiar type
of the disorder.
139 Deutsches Archiv für klinische Medizin, Bd. xxiv. p. 404.

140 Ibid., vol. xxiii. p. 442.

141 Archiv für Psychiatrie, xvi. p. 698.

CAUSES.—Disseminated sclerosis may develop as a sequel of an

acute myelitis. An excellent observation of Singer,142 in which a
unilateral optic-nerve atrophy of central origin occurred after
recovery from an acute inflammation of the cord, proves that
sclerotic foci may develop secondarily to an acute process. Westphal
believes that obstruction to the circulation, both of blood and lymph,
in the cord may act as a predisposing factor in the production of
multiple sclerosis. He rests this opinion on a case where the cord
had been compressed by a tumor, and sclerotic foci of probably later
date were found in the neighboring segments of the cord.
142 Prager medizinisch Wochenschrift, 1885, No. 8.

The myelitic affection discovered by the same observer143 to be an

occasional sequel of typhus, smallpox, diphtheria, measles, and
erysipelas is a true disseminated sclerosis. The foci are usually very
small and very numerous. A focal sclerosis of the posterior columns
of the disseminated type has been found by Brigidi-Bandi in a case
of pellagra which presented ataxic symptoms.144
143 Archiv für Psychiatrie, iii. p. 376, iv.; Oertel, Deutsches Archiv für klinische
Medizin, viii.; Damaschino, Gazette médicale de Paris, 1871, p. 505. In one case now
under observation a typical disseminated sclerosis developed in a robust young man
of thirty after typhoid fever.

144 Lo sperimentale, December, 1879.

Among the exciting causes, prolonged exposure to wet and cold are
acknowledged to occupy an important position. The frequent
combination of these factors with over-exertion and depressing
emotions among the poorer classes probably account for its great
frequency among them. In some cases excessive grief has been the
only discoverable etiological factor: in three of my own cases this
was so prominent and connected a feature that I could not doubt its
influence, if not as a primary at least as an exciting cause.145 Fright
has been distinctly connected with the outbreak of the disease in a
number of cases.146 There is considerable unanimity among
observers regarding the effects of shock and injury in producing
disseminated sclerosis, usually of that anomalous type which
approximates the diffuse or fascicular form. Railway spine is
undoubtedly the mask of a disseminated inflammatory trouble in a