Cerebral Congestion

A Vanished Disease
Gustavo C. Rom\l=a'\n,MD, FACP

concept of "cerebral conges-

\s=b\ The
tion" as a cause of apoplexy was first
proposed by Morgagni in 1761, and had a
profound influence in the treatment of
stroke during the next 150 years. It
accounted not only for cerebral hemor-
rhage, but also for lacunes (Dechambre,
1838), \l=e'\tatcribl\l=e'\(Durand-Fardel, 1842),
depression, maniac outbursts, head-
aches, coma, and seizures. According to
tion based on the sounds heard over
the brachial artery with the compres¬ TRACTATUS
sion cuff. Therefore, prior to the 20th
century, the concept of "cerebral
hyperemia" prevailed. Hammond5 be¬
lieved that cerebral congestion was
"more common, according to my expe¬
APOPLEXIA:
rience, than any other affection of the
the result of men¬
1N J^ O HVJVS
nervous system ...

tal strain or emotional distur¬ afftfttonts caufa penitiùs

Hammond (1871, 1878), cerebral conges-
tion was "more common ... than any oth-
er affection of the nervous system." This
notion fell into oblivion when an accurate
method for bedside determination of
blood pressure became available (Riva\x=req-\
Rocci, 1896; Korotkov, 1905) allowing for
better understanding of the neurologic
complications of arterial hypertension.
(Arch Neurol 1987;44:444-448)
Apoplexy due to cerebral hemor¬
rhage has been known for over
300 years. However, the fact that arte¬
rial hypertension constitutes its main
cause only became established with
the use of the sphygmomanometer for
bedside determination of the blood
pressure. Devised in 1896 by Riva-
Rocci1 and modified in 1901 by von
Recklinghausen,2·3 it became widely
used after Nikolai S. Korotkov4
bance ... an outgrowth of our civiliza¬ inquintur & curattv
tion, and of the restless spirit of
enterprise and struggle for wealth so exponiíHf
characteristic of the American peo¬ Ex Docìrina Hippocratìs.
ple." As late as 1888, the role of arte¬
rial hypertension in neurologic dys¬ ¿iulhrc Francisco Bayis
function could only be assumed.
Gowers6 expressed this notion as fol¬ Dottore Medico.
lows: "Putting aside traumatic influ¬
ences, the force that ruptures an
artery is the pressure of the blood
within it. But as long as the walls of
an artery are in a healthy state, they TOLOSA,
very rarely give way, however great Ixcudcbat B. GUILLEMETTE,
may be the pressure to which they are Typographus , Tub Signo Divi
exposed." Bernardi, ante Collegium
EARLY CONCEPTS PP. Socia. JESU.
'» -—4
In 1677, Francisco Bayle7 reviewed M. DC. LXXVJI.
the opinions prevailing in his time
regarding the cause of apoplexy in his
Cum Ptrmijju Suftncrum*
Tractatus de Apoplexia (Fig 1). Galen Fig 1. Tractatus de Apoplexia by Francisco
thought that obstruction of the cere¬ Bayle, 1677.
—

described, in 1905, the auscultatory bral ventricles by thick pituitary

method of blood pressure determina-
Accepted for publication Jan 9, 1987.
From the Department of Neurology, Texas
Tech University Health Sciences Center School
of Medicine, Lubbock.
Presented in part at the 38th Annual Meeting
of the American Academy of Neurology, New
Orleans, April 1986.
Reprint requests to Department of Neurology,
Room 4A124, Texas Tech University Health Sci-
ences Center School of Medicine, Lubbock, TX
79430 (Dr Rom\l=a'\n).
phlegm blocked the action of the ani¬
mal spirit. Vesalius invoked compres¬
sion of the nerves at the base of the
brain as a cause. Apoplexy was also
known to be caused by a failure of the
influx of blood to the brain, either due
to obstruction of the arteries, or
"from an arterial tear with effusion of
blood in such amount as to prevent
the action of the vital spirit." Bayle7
also quoted Lachambre's original the-
ory of "cerebral atonia." Lachambre
believed that a sudden loss of the
coherence of the brain could produce
compression of the blood vessels and
interruption of the circulation, proba¬
bly basing his hypothesis on the
observation of edema and cerebral
softening (ramollissement cerebral) in
patients with ischemie strokes. Bayle7
stated that cerebral inflammation

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 could also cause apoplexy by ruptur¬
ing the blood vessels, thus explaining
the presence of blood in the interstice
of the brain tissue. Following Hippo¬
crates, he concluded that "the true
cause" of apoplexy was melancholia or
black bile:
Nothing is more obvious than the fact that
a sudden detention and accretion of circu¬
lating bile is a cause of interruption of the
function of the vital spirit. The acidity of
the bile not only interrupts the flow of
blood, but also causes erosion of the blood
vessels. The dominant melancholia of
patients with apoplexy indicates that black
bile is the most logical and rational expla¬
nation for the cause of apoplexy.7
Bayle's contribution was the report
of calcified atheromatous lesions of
the carotids in a patient with apo¬
plexy. However, he failed to refer to
the work of Johann Jacob Wepfer,8
Historiae Apoplecticorum, published
a few years earlier in 1658, in which
the presence of "polypous concre¬
tions" in the internal carotid arteries
was also mentioned as a cause of
stroke. Wepfer8 also gave one of the
earliest descriptions of intracranial
hemorrhage. "The year 1655, the sev¬
enth day of November, the fifth day
after the full moon," he was sum¬
moned by the Most Reverend Lord
Abbot to assist one of his monks who
had collapsed from apoplexy, proba¬
bly a subarachnoid hemorrhage. "The
first hour after midday of the same
day he ceased to live I opened the
...
head: The whole brain, ventricles &
surface were contaminated by blood
in large amount & crumbly This
however is certain, no external violent
...
cause, be it a blow, be it a fall, was the
cause of such ruptures of the blood¬
vessels."
According to Berhman,9 the first
description of congestion of the brain
is found almost a century later, in
1761. In his De sedibus et causis mor-
borum, Giovanni Morgagni10 described
a case of a 62-year-old man who was
found dead in his bed two hours after
eating. Blood distended the cerebral
blood vessels enlarging even the capil¬
laries. Morgagni concluded that death
was produced by cerebral congestion.
THE 19TH CENTURY
In a review of classic works on
apoplexy published in 1820, John
Cooke" correctly pointed out to the
frequent inclusion of brain tumors,
accesses, cysts, and other alien con¬
ditions in patients thought to have
suffered from apoplexy. He concluded
that all forms of apoplexy were essen¬
tially "sanguineous," and
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produced by a too great fullness of blood in
the head, and with a view to lessen this
fullness, blood-letting, purging, and revel-
lents have been recommended. Under these
circumstances, the greatest reliance has
been placed on bleeding In some cases
of this kind, the opening of the temporal
...
arteries or jugular veins has been thought
advisable."
In 1827, Abercrombie12 described a
patient who died of "simple apoplexy"
and whose brain showed an increased
degree of vascularity. Sir George Bur¬
rows' Disorders of Cerebral Circula¬
tion," published in 1846, favored the
idea of cerebral hyperemia and dis¬
posed of Monro and Kellie's theory1416
which stated that the absolute quanti¬
ty of blood within the cranium
remained nearly unchanged in all cir¬
cumstances. Therefore, in addition to
venesection, Burrows13 also recom¬
mended ligature of the common carot¬
id artery for the treatment of stroke,
and a rotatory machine devised to
"drive the blood from the head toward
the lower extremities. The centrifugal
force thus suddenly created powerful¬
ly diminishes the momentum of the
blood moving into the cranium. The
diminished arterial pressure in the
cerebral substance soon produces a
sense of exhaustion or complete syn¬
cope."
William Alexander Hammond17
wrote the first American textbook on
neurology, entitled A Treatise on Dis¬
eases of the Nervous System.'6 A Sur¬
geon-General, he was dismissed from
the army after a questionable verdict
at court-martial, but was later
restored to his full rank of Brigadier-
General. Hammond was one of the
founding fathers of both the New
York Neurological Society (1872) and
the American Neurological Associa¬
tion (1875).19 The first chapter of
Hammond's Treatise'* is devoted to
"cerebral congestion." He classified it
in an active form, resulting from
increase in arterial cerebral blood
flow, and in a passive form, due to
venous congestion. The clinical mani¬
festations of active cerebral conges¬
tion included a premonitory stage,
characterized by difficulty sleeping,
restlessness, intellectual confusion,
memory problems, emotional upset
and occasional illusions, hallucina¬
tions, or delusions. Headache, heat,
and a sensation of fullness or disten-
tion of the head were believed to be
common, along with vertigo, roaring
or rumbling noises in the ears, flashes
of light, or scotomata:
Ophthalmoscopic examination, which
should never be omitted, shows the vessels
of the retina to be increased in number,
diameter, and tortuosity, and occasionally
the optic disk is found more or less con¬
gested The face is flushed, the carotids
and temporals throb with more than ordi¬
...
nary force Bleeding from the nose is not
infrequent... The articulation is thick,
...
and sometimes whole syllables are slurred
over in a slovenly way.18
Following these prodromata, the
patient could develop a form of apo¬
plexy with hemiplegia, as was seen in
16 of Hammond's 29 cases; an epilep¬
tic form, observed in nine cases, or a
maniacal form characterized by a par¬
oxysm of psychomotor agitation,
which was present in four of his cases.
He remarked that "what is called
temporary insanity, mania ephemera,
or impulsive insanity, generally
depends upon cerebral congestion.
The subject, therefore, is of vast
importance in its medico-legal rela¬
tions."
The signs and symptoms of the pas¬
sive form of cerebral congestion were
essentially identical to those men¬
tioned above. In his practice, Ham¬
mond5 had seen 507 cases of active
congestion and 115 of the passive
form. With regard to the postmortem
changes of cerebral congestion, he
wrote: "There are certain appearances
seen in the brain of those who died of
cerebral congestion which are charac¬
teristic, although it must be confessed
that some or all of them are occasion¬
ally absent."
In 1878, Hammond published his
book, Cerebral Hyperaemia: The
Result of Mental Strain or Emotional
Disturbance1 (Fig 2), which expanded
the ideas presented the first chapter
of his Treatise'*. In the preface he
wrote, "The last few years have wit¬
nessed the death of many distin¬
guished persons from the direct
results of excessive brainwork or the
passional excitement so commonly
produced in men and women by the
multitude of causes in operation upon
them." He enumerated a myriad of
symptoms that most likely repre¬
sented chronic depression or situa-
tional stress, although it is conceiv¬
able that he also included cases of
hypertensive encephalopathy, tran¬
sient ischemie attacks, cerebral hem¬
orrhage, ischemie stroke, chronic sub-
dural hematoma, and other condi¬
tions.
By the end of the 19th century,
important works on cerebral conges¬
tion had been published. In Paris, a
clinicopathologic correlation by La-
borde20 appeared in 1866. A review
article written by Russell Reynolds
and Charlton Bastian21 of the Nation¬
al Hospital for the Paralysed and

Fig 2. Cerebral Hyperaemia by William A. Hammond, 1878.
—
Epileptics was published in London in
1868. From the same institution came
the authoritative work of William R.
Gowers, A Manual of Diseases of the
Nervous System,5 whose American
edition was published in Philadelphia
in 1888. Gowers5 judiciously re¬
marked:
Of all regions of cerebral pathology, that of
congestion of the brain is perhaps the most
obscure. We have very little precise knowl¬
edge regarding it, and, as is often the case,
theory has flourished in proportion to the
deficiency of fact... Hence, an extensive
symptomatology was elaborated and built
upon an erroneous foundation.
With regard to the clinical symp¬
toms of cerebral congestion, Gowers5
limited the diagnosis of this entity to
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those cases, "occurring in the second
half of life, characterized by sudden
loss of consciousness (the so-called
'congestive apoplexy') and some¬
times by transient hemiplegia, pass¬
ing away in a few days." However, he
noted that many of those cases could
have resulted from a small hemor¬
rhage or infarction of the brain with
brief symptoms, and he also ad¬
dressed the possibility of transient
cerebral ischemia, indicating that
"vascular obstruction may occur and
cause no lasting symptoms." He indi¬
cated that the diagnosis of congestion
of the brain should be reserved for
those instances "when the attack is
brief, passes away completely, is
attended with the signs of what is
termed "plethora," and especially
when it recurs more than once, still
without enduring symptoms." In con¬
trast to Hammond,6 Gowers5 empha¬
sized that the presence of focal symp¬
toms, such as minimal hemiparesis,
excluded the diagnosis, and that
cephalic sensations of vague or definite
character are alone of no diagnostic value.
Such sensations are specially common in
hypochondrial patients are intensified
by annoyance and by brain work, and are
...
vastly increased by attention. They are
purely nervous sensations, pseudoneural-
gic in nature, and there is not the slightest
justification for attributing them to con¬
gestion of the brain.
NEUROPATHOLOGIC STUDIES
In 1838, Amedée Dechambre22 pub¬
lished a "Memoir on the Curability of
Cerebral Softening" in the Gazette
Medicale de Paris, which constitutes
the first description of lacunes.23
These small cavitary lesions of the
brain are strongly linked to hyperten¬
sion.24 In 1843, Maxime Durand-Far-
del25 in his Treatise on Cerebral Soft¬
ening referred to these lacunar lesions
in the chapter "On the curability and
forms of healing of cerebral soften¬
ing." He concluded that these cavities
could result from distension of cere¬
bral blood vessels during life, from
recurrent bouts of brain congestion,
or could be "nothing more than the
trace of (cerebral) softenings that
healed." In 1842, Durand-Fardel26
described état criblé in the brain of
elderly patients. This "peculiar alter¬
ation of the white matter" (Fig 3) was
depicted in his book Clinical and
Practical Treatise on Diseases of the
Elderly,21 published in 1854 in Paris—
probably one of the earliest works in
the neurology of aging:
What I will describe below has not been
described before Here is the aspect of
the condition I have named cribriform
...
state of the brain When one sections
transversally a cerebral hemisphere, the
...
white matter appears cribbled by a great
number of small, round holes, with well-
drawn edges. Around these cavities the
cerebral tissue is generally healthy, with¬
out changes in color or consistency. The
majority of these holes could have the size
of the cavity produced by a fine needle
inserted in the white matter until the trace
remains in the cerebral pulp; still others
could contain the head of a small
pin When one places the section under a
...
continuous current of water, it is possible
to observe that from each one of these
holes, a small, ruptured blood vessel es¬
capes and floats These holes or cri-
...
blures, are openings created artificially of
channels normally present in the bulk of
the nerve substance to contain a blood
vessel. It is permissible to consider this
 Fig 3.—Original description of état criblé
alteration as being the result of repeated
episodes of cerebral congestion.27
Durand-Fardel considered état cri¬
blé to be abnormal, and correlated its
presence in the brain with clinical
manifestations such as dementia and
chronic delirium. He also noted that it
could occur in normal elderly brains,
but remarked that in these instances
"these criblures are rare, very narrow
and frequently can only be observed
with great difficulty."
By the end of the 19th century,
opinions were divided with regard to
the cause of lacunes. Bourneville
(1873)28 and Brissaud (1899),29 believed
that they resulted from small soften¬
ings, while Landouzy (1877)30 and
Laborde (1866)20 concluded that
lacunes resulted from "small foci of
capillary hemorrhage." Proust
(1866)31 and Raymond (1835)32 af¬
firmed that either cause was possible.
Despite the lucidity of the initial
descriptions, the difference between
lacunes and état criblé, remained
blurred in the literature until very
recently.33·34
The major contribution to the study
of lacunes was undoubtedly made by
Pierre Marie35 and his students Fer-
rand36 and Católa,37 while they were
working at Bicêtre Hospice for the
Elderly. First presented at the 13th
International Congress of Medicine
held in Paris, August 2-9,1900,36 their
hospice work was the subject of a
now-classic article by Pierre Marie35
(Fig 4). That article, clearly defined
and differentiated lacunes from other
cavitary lesions of the brain, such as
état vermoulu (motheaten state). The
latter was characterized by cortical
destruction of vascular origin, produc¬
ing the so-called granular atrophy of
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by Durand-Fardel. Fig 4.—Pierre Marie's original article
tion," 1901.
the cerebral cortex, with punched-out
foci of cavitated cicatricial softenings,
situated entirely in the cortex. He also
noted the postmortem nature of cere¬
bral porosis (état de fromage de Gru¬
yère) (a condition described by Mor¬
gagni10) produced by gas-forming bac¬
teria. Poirier and Derousné33 have
reviewed the evolution of the concept
of lacuna cerebri from 1838 to the
present time, and recommended that
lacunes be classified into three types:
sequelae from small infarctions (type
I), sequelae from reabsorption of
small hemorrhages (type II), and
lacunes due to dilatation of the peri-
vascular space (type III).34
That cerebral congestion was inti¬
mately linked to cerebral hemorrhage
was mentioned for the first time in
Laborde's Cerebral Congestion and
Softening (1866). Laborde correctly
stated that "the links which bind cere¬
bral congestion and cerebral hemor¬
rhage together are frequently the
minute aneurysms described by Bou¬
chard. Congestion may have some¬
thing to do with their formation as it
certainly has with the final rupture
leading to effusion of blood." In fact,
Charcot and Bouchard38·39 had demon¬
strated the presence of microaneu-
rysms in the penetrating lenticulo-
striate and pontine arterioles of
patients with cerebral hypertensive
hemorrhages, and postulated that
rupture of these miliary aneurysms
was the cause of the hemorrhage. This
concept was confirmed almost 100
years later by Ross Russell.40
The anatomists of the Middle Ages,
in particular Valsalva and Morgagni,
already knew the relationship be¬
tween brain hemorrhage and organic
heart disease, especially hypertrophy
on "Lacunar foci of disintegra¬
of the left ventricle. Such a link was
mentioned in the case of the anato¬
mist Marcello Malpighi, physician to
the Pope, who died of apoplexy on
November 29, 1694, after many years
of suffering from palpitations and
hematuria. The autopsy was per¬
formed by George Baglivi41:
The Heart was larger than ordinary, espe¬
cially the Walls of the left Ventricle; the
right Kidney was half as big as the left and
the Stones that were bred in the Kidneys,
presently slipt into the Bladder. The cavity
of the right Ventricle of the Brain con¬
tained an Extravasation of about 2 Pints of
black clotted Blood, which was the Cause of
his Apoplexy and his Death. The Blood
Vessels of the Brain were dilated and broke
on all Hands.
Further confirmation of these rela¬
tionships was provided by Richard
Bright4244 in the 19th century. As pre¬
viously mentioned, the development of
modern concepts of arterial hyperten¬
sion and its effects on the brain was
the direct result of the availability of
a simple indirect method for measur¬
ing arterial blood pressure at the bed¬
side. Hypertension explained the cere¬
bral pathologies briefly reviewed
here, and the concept of "cerebral
hyperemia" slowly fell into oblivion.
The author is indebted to Pr. J.-C.
Gautier,
MD, Hôpital de la Salpêtrière, Paris, who encour¬
aged this research, and to C. M. Poser, MD, and
J. T. Hutton, MD, for review of the text and
helpful criticism. Rev. Father H. Bedoya, CM,
MA, JCD, PhD, provided invaluable help with
translation of the Latin texts.
References
1. Riva-Rocci S: Un nuovo sfigmomanometro.
Gazz Med Torino 1896;47:981-1001.
2. Von Recklinghausen H: Ueber Blutdruck-
messung beim Menschen. Arch Exp Pathol Phar-
makol 1901;46:78-87.
 3. Von Recklinghausen H: Unblutige Blutruck-
messung. Arch Exp Pathol Pharmakol 1906;
55:375, 412, 463.
4. Korotkov NS: A contribution to the problem
of methods for the determination of the blood
pressure. Izvestiya Imperatorskoi Voenno-Medi-$
tsinskoy Akademii 1905;11:365-367. (Translated
in Ruskin A: Classics in Arterial Hypertension.
Springfield, Ill, Charles C Thomas Publishers,
1956, pp 127-133.)
5. Hammond WA: Cerebral Hyperaemia: The
Result of Mental Strain or Emotional Distur-
bance. New York, GP Putnam's Sons, 1878.
6. Gowers WR: A Manual of Diseases of the
Nervous System. Philadelphia, P Blakiston Son &
Co, 1888.
7. Bayle F: Tractatus de Apoplexia: In quo
hujus affectionis causa peniti\l=u'\sinquiritur &
curatio exponitur: Ex doctrina Hippocratis. Tolo-
sae, B Guillemette, 1677.
8. Wepfer JJ: Observationes anatomicae, ex
cadaveribus eorum, quos sustulit apoplexia, cum
exercitatione de ejus loco affecto. Schaffhausen,
Caspari Suteri, 1658. (In Major RH: Classic
Descriptions of Disease With Biographical
Sketches of the Authors. Springfield, Ill, Charles
C Thomas Publishers, 1945, pp 474-477.)
9. Berhman S: Congestion of the brain, in Rose
FC, Bynum WF (eds): Historical Aspects of the
Neurosciences. New York, Raven Press, 1982, pp
179-184.
10. Morgagni GB: De sedibus, et causis morbo-
rum per anatomen indagatis libri quinque. Vien-
na, Ex Typographica Remondiana, 1761.
11. Cooke J: A Treatise on Nervous Diseases.
London, Longman, Hurst, Rees, Orme, and
Brown, 1820.
12. Abercrombie J: Pathological and Practical
Researches on Diseases of the Brain and Spinal
Cord. Edinburgh, Waugh and Innes, 1828.
13. Burrows G: On Disorders of the Cerebral
Circulation and on the Connection Between
Affections of the Brain and Disease of the Heart.
London, Longman, Brown, Green, and Long-
mans, 1846.
14. Monro A (Secundus): Observations on the
Structure and Functions of the Nervous System.
Edinburgh, W Creech, 1783.
15. Kellie G: Reflections on the pathology of
Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 06/19/2015
the brain. Trans Med Chir Soc Edinburgh 1824;
1:123-169.
16. Gawel M: The development of concepts
concerning cerebral circulation, in Rose FC,
Bynum WF (eds): Historical Aspects of the Neu-
rosciences. New York, Raven Press, 1982, pp
171-178.
17. McHenry LC Jr: Surgeon-General William
Alexander Hammond. Milit Med 1963;128:1199.
18. Hammond WA: A Treatise on Diseases of
the Nervous System. New York, D Appleton & Co,
1871.
19. McHenry LC Jr: The founding of the Amer-
ican Neurological Association and the origin of
American neurology. Ann Neurol 1983;14:153\x=req-\
154.
20. Laborde JV: Le Ramollissement et la Con-
gestion du Cerveau Principalement Consid\l=e'\r\l=e'\s
chez le Vieillard: \l=E'\tudeClinique et Pathog\l=e'\ni-
que. Paris, A Delahaye, 1866.
21. Reynolds JR, Bastian HC: System of Medi-
cine. New York, Macmillan Publishing Co Inc,
1868, vol 2, p 413.
22. Dechambre A: M\l=e'\moiresur la curabilit\l=e'\du
ramollissement c\l=e'\r\l=e'\bral.Gaz M\l=e'\d1838;6:305\x=req-\
314.
23. Rom\l=a'\nGC: The original description of
lacunes. Neurology 1986;36:85.
24. Rom\l=a'\nGC: Lacunar dementia, in Hutton
JT, Kenny AD (eds): Senile Dementia of the
Alzheimer's Type. New York, Alan R Liss Inc,
1985, pp 131-151.
25. Durand-Fardel M: Trait\l=e'\du Ramollisse-
ment du Cerveau, Paris, JB Bailli\l=e'\re,1843.
26. Durand-Fardel M: M\l=e'\moiresur une alt\l=e'\r-
ation particuli\l=e'\rede la substance c\l=e'\r\l=e'\brale.Gaz
M\l=e'\d1842;10:23-26, 33-38.
27. Durand-Fardel M: Trait\l=e'\Clinique et Pra-
tique des Maladies des Vieillards. Paris, JB Bail-
li\l=e'\re,1854.
28. Bourneville M: De l'h\l=e'\mianesth\l=e'\sieli\l=e'\ea
une l\l=e'\siond'un h\l=e'\mispheredu cerveau. Prog M\l=e'\d
1873;1:244-246.
29. Brissaud E: Lecons sur les Maladies Ner-
veuses, Deuxi\l=e'\meS\l=e'\rie(H\l=o^\pitalSaint-Antoine).
Paris, Masson, 1899.
30. Landouzy L: H\l=e'\mipl\l=e'\giedroite, contrac-
ture tardive et atrophie musculaire des membres
droits. Prog M\l=e'\d1877;5:992-994.
31. Proust A: Des Diff\l=e'\rentesFormes de
Ramollissement du Cerveau. Paris, Th\l=e'\se
d'Agr\l=e'\gationde M\l=e'\decine,1866.
32. Raymond J: Sur la pathog\l=e'\niede certains
accidents observ\l=e'\schez les vieillards: Leurs rap-
ports probables avec l'ur\l=e'\mie. Rev M\l=e'\d
1885;5:705-738.
33. Poirier J, Derouesn\l=e'\C: Le concept de
lacune c\l=e'\r\l=e'\bralede 1838 \l=a`\nos jours. Rev Neurol
1985;141:3-17.
34. Poirier J, Derouesn\l=e'\C: Cerebral lacunae: A
proposed new classification. Clin Neuropathol
1984;3:266.
35. Marie P: Des foyers lacunaires de d\l=e'\sint\l=e'\-
gration et de diff\l=e'\rentsautres \l=e'\tatscavitaries du
cerveau. Rev M\l=e'\d1901;21:281-298.
36. Ferrand J: Essai sur l'H\l=e'\mipl\l=e'\giedes Vieil-
lards: Les Lacunes de D\l=e'\sint\l=e'\grationC\l=e'\r\l=e'\brale.
Paris, Jules Rousset, 1902.
37. Catola G: \l=E'\tudeclinique et anatomo-
pathologique sur les lacunes de d\l=e'\sint\l=e'\gration
c\l=e'\r\l=e'\brale.Rev M\l=e'\d1904;24:778-809.
38. Charcot JM, Bouchard C: Nouvelles recher-
ches sur la pathog\l=e'\niede l'h\l=e'\morrhagiec\l=e'\r\l=e'\-
brale. Arch Physiol Norm Pathol 1868;1:110-27,
643-665.
39. Bouchard C: A Study of Some Points in the
Pathology of Cerebral Haemorrhage. London,
Simpkin, Marshall, and Co, 1872.
40. Russell RWR: Observations on intracere-
bral aneurysms. Brain 1963;86:425-442.
41. Baglivi G: The history of the sickness of
Marcellus Malpighi, the Pope's physician: With
an account of the dissection of his corps. The
Practice of Physick. London, Bell, 1704, p 461. (In
Major RH: Classic Descriptions of Disease With
Biographical Sketches of the Authors. Spring-
field, Ill, Charles C Thomas Publishers 1945, pp
476-477.)
42. Bright R: Reports of Medical Cases Selected
With a View of Illustrating the Symptoms and
Cure of Diseases by a Reference to Morbid Anat-
omy. London, Longman, 1827.
43. Bright R: Reports of Medical Cases: Dis-
eases of the Brain and Nervous System. London,
Longmans, vol 2, 1831.
44. Bright R: Cases illustrative of the effects
produced when the arteries and brain are dis-
eased. Guy's Hosp Rep 1836;1:9-12.