the local œdema may appear together or in succession. The patient
notices a thickening of the skin, which becomes dry, rough, and scaly.
The thickening is uniform and involves the entire body. It is most
marked where the subdermal connective tissue is loose, as in the
cheeks, lips, eyelids, and in all parts where the skin is thrown into
folds. The hands and feet do not escape. The thickened skin is hard,
and does not pit on pressure, thus differing from ordinary œdematous
swelling. It appears of a waxy color, and is free from perspiration,
the sweat-glands becoming atrophied from pressure. The hair may fall
out or become woolly and brittle, and may change its color. In a few
cases spots of pigment have appeared on various regions.[87] The nails
are brittle. The teeth are carious. The mucous membranes show similar
changes, and the mouth and tongue, rectum and vagina, may be so
swollen as to impair their respective functions. Digestive
disturbances, constipation alternating with diarrhœa, and uterine
hemorrhages, which occur, are ascribed to this cause. Albumen is
occasionally found in the urine, but is not a constant symptom. The
nervous symptoms are constant. The patients complain of paræsthesiæ
and anæsthesia of the extremities or over the entire body, and the
special senses may be impaired, as well as the tactile sense. They are
very liable to severe attacks of neuralgia. They suffer from
subjective sensations of cold, and are easily affected by changes of
temperature. Motion is interfered with; tremors occur early; movements
become slow and awkward; the gait is unsteady; the voice is rough and
nasal; but no true paralysis or muscular atrophy has been observed.
The patella-tendon reflex is occasionally lost, but not in all cases.
[Footnote 87: Allan McLane Hamilton, _Journ. Nerv. and Ment. Dis._,
1885, April, p. 180.]
These symptoms have been ascribed to the pressure of the mucin upon
the terminal filaments of the nerves, and also to changes in the
central nervous system. That the latter theory is probably correct is
shown by the occurrence of mental symptoms in the majority of cases.
The patients become apathetic and all mental action is slowly
performed. Indifference to surroundings, loss of memory, and inability
to concentrate the attention may be succeeded by transient delirium,
hallucinations, and occasionally by delusions of persecution, and the
patient finally lapses into a state of imbecility. If the disease
develops in early life, education is impossible, and the patient
remains in an infantile condition.
Whether the changes in the nervous system are due to pressure by
deposit of mucin (Hadden), or are due to an altered nutrition of the
most delicate tissues of the body consequent upon the general
metabolic derangement (Horseley), is undetermined. In experimental
myxœdema the degenerative processes have been found in the
nerve-cells.
There are no symptoms referable to the heart or lungs, and if
cirrhosis of the kidney and liver develop, their symptoms supervene
upon and are secondary to those of myxœdema. High arterial tension has
been noticed in the majority of the cases.
The COURSE of the disease is a chronic one, and is progressive. There
are, however, intermissions in the severity of the symptoms in some
cases. Recovery does not occur.
{1273} DIAGNOSIS.—The diagnosis from the accumulation of fat is made
by observing the thickening of the nose, lips, fingers, and tongue,
and the changes in the skin and its appendages. Scleroderma is not
universal like myxœdema. In scleroderma the skin is harder and more
adherent to subjacent parts, is not transparent and waxy, and the
nervous symptoms are wanting. Cretinism seems to be closely allied to
myxœdema, but is only observed before the age of seven and is
accompanied by hypertrophy of the thyroid gland.
TREATMENT.—The treatment is only palliative. Simple nutritious diet,
especially milk diet, with the use of such tonics as iron and quinine,
has been found useful. The progress of the disease is hastened by
exposure to cold, and in a very warm climate the symptoms may remain
stationary for several years. Jaborandi or pilocarpine has been used
in some cases with a moderate degree of success. Nitro-glycerin, gr.
1/100, has also been of benefit. For the paræsthesiæ and anæsthesia of
the early stage the faradic brush has been applied, and for the motor
weakness the faradic current, with the effect of relieving but not
curing these symptoms. During the attacks of neuralgia morphine may be
employed.
Inflammation.—The most important trophic disturbances are those which
consist of an actual disintegration of tissue. These are very
numerous. Herpes zoster, certain forms of eczema and pemphigus, lepra
anæsthetica, scleroderma, acute ulceration of the fingers, perforating
ulcer of the foot, acute bed-sores, keratitis with anæsthesia of the
cornea, sympathetic ophthalmia, and various forms of joint disease,
are examples of such trophic diseases.[88] For the discussion of the
skin and eye diseases mentioned the reader is referred to special
articles on those subjects. In regard to lepra anæsthetica, it may be
mentioned that in this disease lesions have been found both in the
sensory nerves and in the posterior cornua of the spinal cord.[89]
[Footnote 88: Leloir, “Tropho-neuroses,” _Nouveau Dictionnaire de
Médecine et Chirurgie practiques_, 1885.]
[Footnote 89: Virchow, “Nerven Lepra,” _Geschwülste_, ii. 521;
Tschirijew, _Travaux du Laboratoire de Vulpian_, 1879.]
I have reported[90] a case of acute ulceration of the ends of the
fingers and toes occurring in an anæmic girl aged twelve, and
persisting for more than a year, associated with cyanosis of the hands
and feet, and with a tendency to rapid ulceration of any part of the
body which happened to be exposed to pressure. The hair of the
eyebrows, eyelids, and to a less extent that of the scalp, fell out
during the disease. There was no local asphyxia and no appearance of
gangrene; hence the case was not one of Raynaud's disease. Its
symmetrical distribution, the lack of any constitutional organic
disease or of any local cause for the production of the ulceration,
and the anæmic and nervous condition present, all pointed to a
disturbance of the central nervous system. It did not yield to
treatment, either local or general or electrical. Mills has seen a
similar case.[91]
[Footnote 90: _Journal Nerv. and Ment. Disease_, Feb., 1886, clinical
cases.]
[Footnote 91: Mills, _Amer. Journ. Med. Sci._, Oct., 1878.]
Perforating ulcer of the foot begins on the sole, beneath any of the
metatarso-phalangeal articulations, preferably the first or the fifth,
or under the heel, as a small pustule under the epidermis. This
ruptures, and the ulcer which results begins to extend in a direction
vertical to the surface, involving the deeper tissues or even opening
into the joint and destroying the bone. It appears rather like a sinus
than an ulcer, and is {1274} remarkable from the fact that it is not
painful and is insensitive to touch, although it may prevent the
patient from walking on account of extreme tenderness. The epidermis
around the sinus is thickened and insensitive, and there may be
anæsthesia of the entire sole of the foot, and even of the leg,
although this is due to the neuritis present, which is also the cause
of the ulcer, rather than to the ulceration. The circulation is
sluggish in the affected extremity; it becomes cyanotic on exposure to
cold, and seems peculiarly liable to become œdematous. The œdema may
go on to suppuration, and involve the articulations, and ankylosis of
the smaller joints may follow. This, too, is to be traced to the
neuritis. The skin of the foot becomes pigmented, and may be dry or
covered with offensive sweat. As the patient cannot walk while the
ulcer remains, the condition demands treatment. Rest, moist warm
applications, antiseptic lotions, scraping out the sinus, and other
surgical means appropriate to the treatment of ulcers and sinuses do
not often prove of benefit, and in obstinate cases recourse has been
had to amputation of the foot. Electrical treatment has been tried in
vain.
Such perforating ulcers may occur symmetrically on both feet, and may
be numerous. They also occur rarely on the hands. They have been
observed not infrequently in locomotor ataxia, occurring either early
or late in the disease,[92] and have appeared in patients suffering
from dementia paralytica. The only constant lesion found is a
degeneration of the peripheral nerve supplying the affected part.
[Footnote 92: For bibliography see Ross, _Diseases of Nervous System_,
2d ed., i. p. 256, and Blum, _Berliner klin. Wochen._, 1875, Nos.
13-15.]
Acute bed-sores (decubitus) develop in many cases of spinal and
cerebral disease, but not in all. It is argued that anæsthesia of a
part or simple pressure upon a part or irritation of an anæsthetic
part will not explain their occurrence, and that they must be traced
to a destruction of trophic centres in the cord or brain. No amount of
attention to the position and cleanliness of the patient is thought to
be sufficient to prevent them in some cases, and their progress is
often so rapid as to remove them from the category of simple
ulceration. Their most frequent seat is upon the buttocks, over the
sacrum, on the heels, and over the scapulæ; but it is believed that in
the conditions in which they appear in these places pressure on any
part may cause one. They begin within a few hours after the occurrence
of the lesion as irregular mottled patches of redness, in which there
soon appear small or large vesicles filled with dark serum. These
rupture, leaving little areas of ulcerated surface, which soon unite
to form a large ulcer with softened, infiltrated, and bloody base and
ragged edges. The tissues around and within the ulcer have a tendency
to slough and to become gangrenous, and the process goes on rapidly
until a considerable area of the surface is completely destroyed,
together with the deeper structures, fat, muscles, and fasciæ, down to
the bone, which may become necrosed. Acute cystitis is so frequently
associated with acute bed-sore that it is traced to the same nervous
cause, though here, again, another explanation is possible. The
constitutional disturbance produced by these two affections may be
increased by a true septicæmia, to which the patient succumbs; or
metastatic abscesses may be formed, and pyæmia cause death; or,
lastly, the ulcer on the back may lay bare the vertebræ and erode
their ligaments, thus opening a way for the extension of suppuration
to {1275} the meninges of the spinal cord. The duration may be from a
few days to two weeks, and the prognosis is very grave.
Chronic bed-sores develop in a similar manner, although all the
processes described occur more slowly and are much less severe. They
do not show the tendency to extend so widely or so deeply, nor to
become gangrenous. They remain stationary after attaining a certain
size, and the tissues seem to lack all tendency to reproduction and
repair. When the central lesion which they follow begins to pass away
they heal; sometimes local treatment is successful; but in many cases
they persist for years, always threatening the life of the patient
from the possibility of their sudden aggravation or from the
occurrence of the complications already mentioned in connection with
the acute process.
Since neither form of decubitus occurs after lesion of the anterior
cornua of the spinal cord, nor in sclerosis of the posterior or
lateral columns, nor in those cases of locomotor ataxia in which
extensive invasion of the posterior cornua is present, while they are
particularly frequent as a complication of general myelitis,
hemorrhage in the cord, and syringo-myelitis, it is argued that the
trophic centres whose destruction is the cause of these bed-sores lie
in the central gray matter of the cord, near to the central canal. In
unilateral lesion of the cord the bed-sore occurs on the anæsthetic
side of the body—_i.e._ on the side opposite to the seat of the
lesion—a fact which may indicate a decussation of the trophic
nerve-fibres in the cord,[93] but which has also been urged in proof
of the theory that the sore is always due to irritation of an
insensitive surface.
[Footnote 93: Recklinghausen believes that these cases of disturbance
of nutrition can be explained by injury of anæsthetic parts in which
vaso-motor disturbances of central origin exist (_Handbuch d. Path. d.
Ernahrung_, pp. 236, 237).]
The treatment of bed-sores belongs to the domain of surgery, the same
methods being pursued as in the case of any large ulcer. The
application of electricity to the sore has been tried, but the results
are not sufficiently encouraging to warrant its recommendation.
Joint affections of neurotic origin are discussed in the articles upon
Locomotor Ataxia, Hemiplegia, and Hysteria.
It is evident from this review that the nervous centres have some
influence upon the activity of the cells of which the body is made up,
and that they control the processes of growth, function, repair, and
reproduction. The facts are too numerous, too varied, and too positive
to admit of any other explanation. Trophic disturbances must therefore
be considered as a set of symptoms referable to various lesions of the
nervous system. It is evident from the preceding discussion that they
may be produced by disease of the peripheral nerves; by disease of the
ganglionic cells, which nourish those nerves; by disease of the spinal
cord, especially in the region of the central gray matter; and,
finally, by disease of the brain. Whether in the last condition the
effect is a direct one, or is produced secondarily by an irritation of
the spinal centres, cannot yet be determined. There are no trophic
centres as yet localized in the cerebrum, but the pathological facts
already mentioned warrant the conclusion that such centres will not
long elude search. Certain facts observed in cases of infantile
hemiplegia point to the motor area of the cortex as the seat of
trophic centres for the motor mechanisms; since it is found that when
the motor cortex is destroyed in early life the bones and muscles
{1276} which it controls fail to develop properly. Trophic centres for
sensory mechanisms are not yet discovered. Certain investigations of
Luciani recently published[94] point to the cerebellum as the part of
the brain which governs the general nutrition of the body, but these
need confirmation.
[Footnote 94: _Alienist and Neurologist_, July, 1885.]
* * * * *
CONCLUSION.—While an attempt has been made here to consider vaso-motor
and trophic neuroses separately, it must be admitted that in very many
conditions the two are coincident. This follows inevitably from what
has been stated regarding the localization of the vaso-motor and
trophic centres in the spinal cord, and regarding the course of the
vaso-motor and trophic nerves from the spinal centres to the
periphery. These two classes of centres and nerves lie side by side in
the central and peripheral organs, and it is less surprising that they
should be jointly affected than that one should ever be involved
alone. In any case of lesion of the peripheral nerves or of the
central nervous system they may be expected. In all cases they are to
be regarded as symptoms of such lesions rather than as distinct
diseases.
{1277}
INDEX TO VOLUME V.
A.
Abdomen, state of, in lead colic, 684
in tubercular meningitis, 726, 727
Abscess of the brain, 791, 792
of the spinal cord, 808
Achromatopsia, hysterical, 247
Aconite and aconitia, use of, in neuralgia, 1224, 1227
hypodermically in exacerbations of cerebral syphilis, 1015
Acoustic sensory disturbances in nervous diseases, 40, 41
Acrodynia, 1254
Acute affections produced by heat, 387
alcoholism, 586
cerebral anæmia, 776
encephalitis, 791
myelitis, spinal, 810
poisoning by alcohol in lethal doses, 596
simple meningitis, 716
spinal meningitis, 749
pachymeningitis, 747
Æsthesodic system of encephalon, localization of lesions in, 81
of spinal cord, localization of lesions in, 69
Affective mental disease, 153
Age, influence on causation of acute spinal meningitis, 750
of catalepsy, 315
of cerebral anæmia, 777
of chorea, 441
of chronic lead-poisoning, 680, 686, 688
of disseminated sclerosis, 883
of embolism and thrombosis of cerebral veins, 951
of epilepsy, 470
of family form of tabes dorsalis, 871
of general paralysis of the insane, 77
of hæmatoma of the dura mater, 707
of hysteria, 216
of hystero-epilepsy, 293
of insanity, 116, 117
of intracranial hemorrhage and apoplexy, 927
of labio-glosso-laryngeal paralysis, 1173
of migraine, 406, 1230
of myxœdema, 1271
of neuralgia, 1217
of paralysis agitans, 433
of progressive unilateral facial atrophy, 694
of syphilitic affections of nerve-centres, 1000
of tabes dorsalis, 856
of the opium habit, 650
of thrombosis of cerebral veins and sinuses, 983
of tubercular meningitis, 725
of tumors of the brain, 1029
spinal cord, 1090
of writers' cramp, 512
relation of, to limitation of the myelitis in infantile paralysis,
1147
Agraphia in hemiplegia, 957
Akinesis in nervous diseases, definition of, 42-44
Alalia (see _Speech, Disorders of_).
Alexia in nervous diseases, 31
Albuminuria in chronic lead-poisoning, 682, 689
Alcohol, influence on causation of acute meningitis, 716
of cerebral hyperæmia, 765
of intracranial hemorrhage and apoplexy, 929, 933
of tabes dorsalis, 854
of writers' cramp, 512
use of, in alcoholism, 642, 644
in cerebral anæmia, 789
in heat-exhaustion, 388
in insomnia, 380, 381
in the chloral habit, 677
in the opium habit, 673, 675
in thermic fever, 397
Alcoholic abuse as a cause of epilepsy, 472
insanity, 175, 202, 630-633
ALCOHOLISM, 573
Classification, 573
Definition, 573
Diagnosis, 637
of acute alcoholism, 637
of chronic alcoholism, 638
of dipsomania, 639
of hereditary alcoholism, 639
Etiology, 575
Alcohol, physiological action of, 580, 586
Alcoholic beverages, varieties and characters of, 578-580
Exciting causes, 578
Heredity, influence on causation, 576
Moral, social, and personal condition, influence on causation,
575, 578
Predisposing causes, 575
History, 574
_Pathological Action of Alcohol_, 586
_Acute Alcoholism_, 586-598
Symptoms, 587
Effects in persons of unsound mind, 594
Effects of different alcohols, 589-591
of acute narcotic poisoning, 597
of acute poisoning in lethal doses, 596
of convulsive form, 593
of corrosive poisoning, 596
of irregular form, 592
of maniacal form, 592
of ordinary form, 587
Pathological anatomy, 595
Varieties, 588
_Chronic Alcoholism_, 598-633
Symptoms, anatomical changes, etc., 599
Alcoholic cachexia in, 616
Atheroma in, 612
Biliary catarrh in, 607
Blood, disorders of, 615
Blood-vessels, disorders of, 612
Cerebral, 616
Delirium, alcoholic, and delirium tremens, 626, 630
Dyspeptic, 601, 602
Genito-urinary disorders, 612-614
Glands, disorders of, 602
Heart, disorders of, 610-612
Insanity, alcoholic, 630-633
Intestinal disorders, 601
Kidneys, disorders of, 613
Larynx, disorders of, 607
Liver, disorders of, 603-607
Locomotive apparatus, disorders of, 614
Lungs, disorders of, 608
Moral sense, perversion of, 624
Motion, disorders of, 620
Mouth and throat, disorders of, 599
Muscles, disorders of, 614
Nervous system, disorders of, 616
Obesity in, 615
Paralysis, alcoholic, 621
Pleuræ, disorders of, 610
Psychical disorders, 624
Respiratory system, disorders of, 607
Sensibility, general, disorders of, 619
Skin, disorders of, 615
Special sense, disorders of, 622
Spinal disorders, 619
Stomach, disorders of, 600
Tremor in, 620
Visceral derangements, 599
Will and intellect in, 625
_Dipsomania_, 635
Symptoms and nature, 636, 637
_Hereditary Alcoholism_, _symptoms and forms_, 634
Prognosis, 639
Synonyms, 573
Treatment, 640
Alcohol, withdrawal of, 642, 644
Ammonia, use of, 641, 642, 645
Baths and douches, use of, 641, 642, 643
Bromides, use of, 642, 645, 646
Cannabis indica, piscidia, and hyoscyamus, use of, 645
Chloral, use of, 641, 645, 646
Coca and cocaine, use of, 643, 646
Diet in, 643, 644
Emetics in, 642
Iron, use of, 643
Hypophosphites and cod-liver oil, use of, 644, 646
of acute form, 641
of chronic form, 642
of delirium tremens, 644
of dipsomania and hereditary forms, 645
Paraldehyde, use of, 641, 642, 645, 646
Prophylaxis, 640, 642
Quinia and opium, use of, 642, 643, 645, 646
Strychnia, use of, 641, 643, 646
Alcoholism, influence on causation of insanity, 119
Allochiria in tabes dorsalis, 832
Alum, use of, in lead colic, 691
Amaurosis in chronic lead-poisoning, 689
Amenorrhœa in the insane, treatment, 136
Ammonia, use of, in acute alcoholism, 641, 642, 643
in thrombosis of cerebral veins and sinuses, 989
Ammonio-sulphate of copper, use, in neuralgia, 1229
Ammonium chloride, use, in neuralgia, 1229
Amnesia in nervous diseases, 28
Amputation, question of, in tetanus, 559
Amyl nitrite, use of, in angina pectoris, 1238
in catalepsy, 338
in cerebral anæmia, 788
in chorea, 456
in epilepsy, 502
in hysteria, 286
in hystero-epilepsy, 311
in migraine, 414, 1232
in vaso-motor neuroses, 1256
Amyotrophic lateral sclerosis, 867
Anæmia as a cause of neuralgia, 1218
of thrombosis of cerebral veins and sinuses, 984
of vertigo, 425
and chlorosis, influence on causation of hysteria, 220
general, as a cause of spinal anæmia, 806
of the brain, 774, 777
of the spine, 805
Anæmic headache, 402
Anæsthesia, hysterical, 246
in acute myelitis, 819
in chronic alcoholism, 620
spinal meningitis, 753
in hemiplegia, 955
in hystero-epilepsy, 298
in injuries of nerves, 1182, 1185, 1186
in neuritis, 1191, 1192
in spinal meningeal hemorrhage, 752
meningitis, 750
syphilis, 1025
in symmetrical gangrene, 1259
in tumors of the brain, 1042
of the spinal cord, 1092
in unilateral spinal paralysis, 1166
of peripheral origin, 1198
Causes, 1199
Diagnosis, 1200
Symptoms, 1199-1201
Treatment, 1201
Varieties of, in nervous diseases, 35, 37
Analgesia, definition of, 35
hysterical, 246
Angina pectoris (see _Neuralgia_).
Angiomata in brain tumors, 1049
Angio-paralysis in vaso-motor neuroses, 1252
Angio-spasm in vaso-motor neuroses, 1262
Anidrosis in progressive unilateral facial atrophy, 696
Ankle-clonus in amyotrophic lateral sclerosis, 868
in diffuse spinal sclerosis, 888
in nervous diseases, 54
in spastic spinal paralysis, 862, 864
Anterior cornua, changes in, in amyotrophic lateral sclerosis, 867
in infantile spinal paralysis, 1133-1144
Antipyrine, use, in thermic fever, 397, 398
Antispasmodics, use, in hysteria, 278
Anus and rectum, neuralgia of, 1240
Aphasia in nervous diseases, 31
in cerebral anæmia, 776
hemorrhage, 941
syphilis, 1008
hemiplegia, characters and varieties of, 956, 960
post-epileptic, 481
Aphonia, hysterical, 239
Apoplexy, 917
of the brain, meningeal, 710
Apoplectic attack, symptoms of, 933-952
constitution, peculiarities of, 930
Apoplectiform attacks in tumors of the brain, 1040
type of acute myelitis, 817
Argyll-Robertson pupil in nervous diseases, 40, 51
in tabes dorsalis, 830
Arsenic, use of, in chorea, 454
in malarial form of cerebral anæmia, 790
in neuralgia, 1224
in paralysis agitans, 438
in tetanus, 559
in tremor, 432
in writers' cramp, 538
Arteries, cerebral, atheroma of, 991
in cerebral meningeal hemorrhage, 711
diseases of, in intracranial hemorrhage and apoplexy, 922
Arterial spasm in spinal anæmia, 806
Arthralgia, the, of chronic lead-poisoning, 684
Arthropathies in hemiplegia of apoplexy and intracranial hemorrhage,
962
in tabes dorsalis, 837
Asafœtida, use, in hysteria, 278, 285
Assimilation, alterations of, in nervous diseases, 59
Asthma, hysterical, 245
Asylums in the treatment of opium and alcohol habit, question of, 671
treatment of insane by removal to, 128, 130-135
Ataxia in tabes dorsalis, 831, 833, 848
in tumors of the brain, 1041
in tumors of the spinal cord, 1094
muscular, in general paralysis of the insane, 189, 193
Ataxic tremor, in nervous diseases, 47
Atheroma, in chronic alcoholism, 612
of the cerebral arteries, 991
Athetosis, definition and symptoms, 457
pathology, prognosis, and treatment, 46