Cord through the Lumbar Enlargement: The æsthesodic system is shaded;
the kinesodic system unshaded. Parts of the æsthesodic system: (1)
Posterior nerve-roots; (2) posterior gray horns; (3) fasciculi cuneati
(columns of Burdach, inclusive of posterior root-zones); (4) fasciculi
graciles (columns of Goll, or posterior median columns); (5) ascending
cerebellar fasciculi; (6) columns of Clarke. Parts of the kinesodic
system: (7) Anterior roots; (8) anterior columns (inclusive of
anterior root-zones); (9) anterior gray horns; (10) crossed pyramidal
fasciculi; (11) direct pyramidal fasciculi (columns of Türck) [10 and
11 are the intraspinal prolongation of the cerebral motor tract]; (12)
lateral columns of ill-defined limits and unknown functions; P. R.,
posterior roots; P. S., posterior septum; A. R., anterior roots;
A. F., anterior fissure.]
In a general way it may be stated that lesions of the kinesodic system
are characterized positively by the isolated existence or predominance
of {72} motor symptoms, by impairment of muscular nutrition, and by
De R.; also by contractures. The reflexes are almost never normal,
being either exaggerated or lost. Negative symptoms are—absence of
sensory symptoms, of ataxia, and of vesical or rectal symptoms.
(_a_) Lesions of the anterior gray horns (9) are revealed by most
definite and characteristic symptoms. There occurs a flaccid paralysis
involving more or less extensive groups of muscles in the extremities,
rarely truncal muscles, and never those of organic life. In a few
weeks the paralyzed muscles undergo atrophy, sometimes to an extreme
degree, and various degrees of De R. are present. Cutaneous and
tendinous reflexes are abolished. The bladder and rectum are normal.
Sensory symptoms absent, and if present consist only of mild
paræsthesiæ, which are probably due to postural pressure upon
nerve-trunks or to disturbance of the peripheral circulation. There is
no tendency to the formation of bed-sores, but circulation and
calorification are reduced in the paralyzed members. It should be
remembered that paralysis due to systematic lesion of the anterior
gray horns is never typically paraplegic, with horizontal limit-line
of sensory symptoms, a cincture feeling, and vesical paralysis.
{73} The above symptom-grouping is characteristic of lesion of the
anterior horns en masse; in other words, of poliomyelitis. In that
form of systematic disease of the anterior horns which consists
primarily and chiefly of a degeneration or molecular death of the
ganglion cells there is no true paralysis; the atrophy of muscles is
infinitely slower, and it proceeds in various muscles fasciculus by
fasciculus, the wasting being usually preceded by fibrillary
contractions, and being almost always symmetrically located on the two
sides of the body (affecting analogous or homologous parts). The
electrical reactions are abnormal, in that musculo-faradic reaction is
lost in exact proportion to the wasting; so that in a large muscle one
part may contract normally, while the adjacent fasciculi do not. It is
as yet uncertain whether De R. occur in this disease (progressive
muscular atrophy). Calorification and circulation are much less
impaired than in poliomyelitis; the negative symptoms are much the
same.
It is sometimes difficult to distinguish poliomyelitis from
generalized neuritis. The diagnosis is to be made by the presence in
the latter disease of marked sensory symptoms—neuro-muscular pains,
numbness, slight anæsthesia—and by a grouping of symptoms coinciding
with the distribution of nerve-trunks and branches. No assistance can
be derived from electrical tests, as both diseases yield more or less
typical De R.
(_b_) Lesions of the spinal pyramidal tract (of fasciculi 10 and 11)
are followed by motor symptoms only—viz. paralysis and contracture—or,
in other words, by a spastic paralysis. Sensibility is unaffected; the
bladder, rectum, and truncal muscles are not distinctly paralyzed; the
reflexes are much increased, and ankle-clonus is often present. The
electrical reactions of the paralyzed muscles are normal,
qualitatively at least. The diagnosis of localization may be pushed
still farther by the following considerations:
(1) When the condition of spastic paralysis is unilateral, of
hemiplegic distribution, and follows an attack of cerebral disease of
some sort, we may feel sure that both the crossed and the direct
fasciculi of the pyramidal (10 and 11) belonging to one cerebral motor
tract are degenerated throughout the length of the spinal cord, the
crossed fasciculus on the paralyzed side and the direct on the healthy
side (same side as injured hemisphere). It would thus appear that
lesion of the direct pyramidal fasciculus (11) produces no
symptoms,[4] except, of course, in those rare cases in which it is
larger than its associated crossed fasciculus.
[Footnote 4: Unless it be the increase of reflexes which is so often
observed on the non-paralyzed side in hemiplegics.]
(2) The above symptoms may be bilateral, as observed in children as a
congenital or early-acquired condition. In such cases the four
fasciculi of the motor tract are degenerated or undeveloped, in
correspondence with a symmetrical bilateral lesion of the motor area
of the cerebrum—imperfect development or early destruction.
(3) When the legs alone are the seat of spastic paralysis, with
increased reflexes, spastic or tetanoid gait, without sensory
symptoms, the diagnosis of a primary sclerosis of both lateral columns
(inclusive of 10) of the spinal cord is justified.
(_c_) Lesions of antero-lateral columns of the cord (8 and 12),
primary and independent of lesions of the anterior horns or of the
crossed {74} pyramidal fasciculus, cannot now be diagnosticated during
life. These large masses of fibres include fasciculi whose functions
are probably motor; others (especially in 12) whose functions,
according to recent experiments, may be sensory; and still others
which are associating or commissural.
(_d_) Various combinations of the above lesions occur, and may be
recognized positively during life: (1) Combined sclerosis of the
posterior columns and of the crossed pyramidal fasciculi (3 and 10),
indicated by ataxia with paralysis, absence of patellar reflex,
tendency to contracture, pains, and anæsthesia less marked than in
typical posterior spinal sclerosis. This symptom-group is usually
found in children; it is pre-eminently a family disease, and is known
as Friedreich's disease. Similar cases also occur in adults as a
strictly personal disease. (2) Secondary degeneration of the pyramidal
tract (10 and 11), with more or less localized atrophy of cells in the
anterior horns (9) coexists in two forms: First, in a few cases of
cerebral hemiplegia with contracture, and pathological atrophy of
various muscles on the paralyzed side; second, as a distinctly spinal
bilateral affection, characterized by a spastic or tetanoid state of
the lower extremities, and a mixture of atrophic paralysis (vide
(_a_)), with contracture in the arms and hands. This latter form is
the amyotrophic lateral sclerosis of Charcot.
SECOND QUESTION.—BEING GIVEN SYMPTOMS INDICATING A TOTAL TRANSVERSE
LESION OF THE SPINAL CORD, ONE INVOLVING ITS VARIOUS SYSTEMS AT A
CERTAIN LEVEL, TO DETERMINE THE ELEVATION OR FRONTO-CAUDAL SITUATION
OF THE LESION.
This question is usually easy of solution by the following method:
Since a transverse lesion of the spinal cord gives rise to both motor
and sensory symptoms of horizontal, paraplegic distribution caudad of
the lesion, the first thing to do is to determine accurately the upper
level of the symptom, either the line of anæsthesia or the limit of
paralysis. The former is always much more definite than the latter,
and usually serves as the guide to diagnosis, indicating accurately
the uppermost part of the lesion. In the thorax the levels of sensory
and motor symptoms nearly coincide, but in the extremities the
operation of Van der Kolk's law of distribution of motor and sensory
fibres of nerve-trunks must be borne in mind, although it does not
apply as strictly in this case as in nerve lesions strictly speaking.
Gowers's diagram will prove very serviceable in making a diagnosis of
transverse lesions, and will also prove of use in the study of
vertebral injury and disease, as it indicates with sufficient accuracy
the relation between vertebræ (spinous processes) and segments of the
spinal cord. (Vide Fig. 2.)
The following are the principal transverse localizations of disease
which are usually recognized during life by the above procedure:
(_a_) Lesions of the cauda equina (by tumors, caries, or fracture of
the bones, etc.) produce paralysis, anæsthesia, atrophy of muscles,
with De R., in the range of distribution of the sciatic nerves mainly.
The sphincter ani is paralyzed and relaxed, while the bladder remains
normal as a rule. In all essential respects this paraplegiform, but
not paraplegic, affection resembles that following injury to mixed
nerve-trunks. It is in reality an intra-spinal peripheral paralysis.
The more exact location of the lesion, in the absence of external
physical signs (fracture, etc.), may be {75} approximately determined
by a study of the distribution of the symptoms and their relation to
nerve-supply.
(_b_) Lesions of the lower end of the lumbar enlargement, or conus
medullaris, behind the first lumbar vertebra, will give rise to the
same symptoms as (_a_). The expression, lumbar part of the spinal
cord, should be more carefully used than it is at present in the
discussion of spinal injuries and spinal-cord diseases, disease of the
lumbar enlargement being common enough, but disease of the lumbar part
of the cord very rare. In the discussion of railway cases, more
especially, it is often forgotten that the spinal cord practically
ends behind the first lumbar vertebra.
(_c_) Lesions of the middle and upper parts (segments) of the lumbar
enlargement are evidenced by true paraplegia, without paralysis of the
abdominal muscles. In some cases the quadriceps group, supplied by the
crural nerve, is not paralyzed. The constriction and the limit of
anæsthesia are about the knees, at mid-thigh, or near the groin in
different cases. The paralyzed muscles, as a rule, retain their
irritability and show normal electrical reactions; the cutaneous and
tendinous reflexes are preserved or increased. The sphincter is
usually paralyzed, while the bladder is relatively unaffected.
(_d_) Transverse lesion of the dorsal spinal cord produces the
classical type of paraplegia—_i.e._ paralysis and anæsthesia of all
parts caudad of the lesion. The limit of anæsthesia and the
constriction band are nearly horizontal, and their exact level varies
with the height of the lesion, from the hypogastric region to above
the nipples. Below the level of anæsthesia, which indicates by the
number of the dorsal nerve the upper limit of the cord lesion, there
are complete paralysis, retention of urine, constipation with relaxed
sphincter ani, greatly exaggerated reflexes in the lower extremities,
even to spinal epilepsy; the muscles preserve their volume fairly
well, and their electrical reactions are normal—sensibility in all its
modes is abolished; bed-sores are easily provoked. Retention of urine
is an early symptom in lesion of the middle dorsal region of the
cord—sometimes, in our experience, preceding symptoms in the legs.
(_e_) A transverse lesion of the cord at the level of the last
cervical and first dorsal nerves—_i.e._ in the lower part of the
cervical enlargement—gives rise to typical paraplegia with a sensory
limit-line at or just below the clavicle, but also with some very
peculiar symptoms superadded. These characteristic symptoms are in the
upper extremities, and consist of paralysis and anæsthesia in the
range of distribution of the ulnar nerves. In the arms the anæsthesia
will be found along the lower ulnar aspect of the forearm, the ulnar
part of the hands, the whole of the little fingers, and one half of
the annuli. There will be paralysis (and in some cases atrophy with
De R.) affecting the flexor carpi ulnaris, the hypothenar eminence,
the interossei, and the ulnar half of the thenar group of muscles,
producing in most cases a special deformity of the hand known as
claw-hand or main-en-griffe. Another important symptom of a transverse
lesion in this location is complete paralysis of all the intercostal
and abdominal muscles, rendering respiration diaphragmatic and making
coughing and expectoration impossible. The breathing is abdominal in
type, and asphyxia is constantly impending.
(_f_) A transverse lesion of the upper part of the cervical
enlargement, below the origin of the fourth cervical nerve, gives rise
to symptoms {76} designated as cervical or total paraplegia. The lower
extremities and trunk are as in (_d_) and (_e_), but besides both arms
are completely paralyzed and anæsthetic. The limit of anæsthesia
usually extends along the clavicles to the acromion processes, or a
little below, near the deltoid insertions. All reflexes caudad of this
line are vastly increased, either with tonic or clonic contractions.
In some cases of pressure upon the cervical cord by tumors, caries of
vertebræ, etc. the tetanoid or spastic state of the extremities (the
lower more especially) may precede paralysis for a long time; as the
compression increases paralysis becomes more and more marked, while
the reflexes remain high. This constitutes the clinical group we
described in 1873 as tetanoid pseudo-paraplegia.
(_g_) Transverse lesions of the spinal cord from the decussation of
the pyramids to the fourth cervical nerve are very rare, and usually
of traumatic origin. They produce complete paralysis of the entire
body, and also of the diaphragm (third and fourth cervical nerves),
thus causing death by apnœa in a very short time.
(_h_) In ascending paralysis (Landry) the above symptom-groups,
excepting (_a_), (_b_), are met with at successive stages of the
disease, often by almost daily accession, until finally respiration
ceases.
(_i_) The height of a transverse localized lesion (_e.g._ a
stab-wound) of one lateral half of the spinal cord is to be determined
by the various groupings of symptoms stated in the preceding
paragraphs, the chief guide being the limit-line between the sensitive
and anæsthetic portions of the body, measured vertically. The symptoms
are, however, distributed in a very remarkable manner on either side
of the median line. The paralysis will be found on the same side as
the lesion, often accompanied by hyperæsthesia, vaso-motor paralysis,
and loss of muscular sense, while the anæsthesia is on the other side
of the body. When such a lesion occurs below the first dorsal nerve,
the symptom-group is designated as hemiparaplegia; when the lesion is
higher up, so as to paralyze the arms, the affection is termed spinal
hemiplegia (Brown-Séquard).
Above the decussation of the pyramids total transverse lesions are
practically unknown, so that the second question need not be followed
farther.
By means of the data above given we are also enabled to determine the
length—_i.e._ fronto-caudal extension—of the systematic lesions of the
cord.
The symptoms of transverse lesions of the spinal cord are not
exclusively caudad of the lesion, and some very striking ones are
observable in the head. In lesions of the upper part of the dorsal
cord and of the cervical enlargement (_e_, _f_, _g_) we observe
vaso-motor and pupillary symptoms, due to injury of the spinal origin
of the cervical sympathetic nerve; the pupils are contracted; the
cheeks and ears congested and unnaturally warm; the cutaneous
secretions are increased. In other words, the symptoms about the head,
frontad of the lesion, are the same as those we produce experimentally
in animals by section of the cervical sympathetic or of the lower
cervical cord. In hemi-lesion of the cord, in man as in animals, these
symptoms are unilateral, on the same side as the injury.
Another point to be remembered in the study of transverse lesions of
the spinal cord is that the lesion may involve enough of the anterior
{77} gray horns to give rise to atrophic paralysis with De R. in some
few muscles deriving their motor innervation from the focus of
disease. This is not rarely seen in cervical paraplegia.
THIRD QUESTION.—BEING GIVEN VERY LIMITED MOTOR OR SENSORY SYMPTOMS OF
SPINAL ORIGIN, TO DETERMINE THE EXACT LOCATION OF THE FOCAL LESIONS
CAUSING THEM.
(_a_) In the range of sensory disturbances this question rarely
presents itself for solution. Localized anæsthesia and pain of spinal
origin (except the fulgurating pains of tabes) are rare, and we do not
know the relation of cutaneous areas with the spinal segments as well
as we know the motor innervations. It should be stated here, however,
that the location of a fixed pain and of a zone of anæsthesia is often
of great value in determining what spinal nerve is affected, just
outside of the cord itself, by such directly-acting lesions as
vertebral caries, spinal pachymeningitis, tumors upon the spinal cord,
etc. Among the various symptoms of Pott's disease of the spine, fixed
pains in one side of the trunk, in one thigh, or in the upper
occipital region, etc. is a sign against which the physician should
always be on his guard, as it is a very early and valuable indication
of the existence of an affection which requires special treatment as
soon as a diagnosis can be made.
(_b_) Localized motor symptoms of spinal origin calling for a
diagnosis of the focal lesions causing them are frequent, and are
mostly met with in two affections—viz. progressive muscular atrophy
and poliomyelitis. The problem is now capable in many cases of an
approximately exact solution by the deductive application of our
knowledge of the intimate connection between certain muscles and
muscular groups and limited portions or segments of the spinal cord
(anterior gray horns more especially). This knowledge has been
accumulated and organized from ordinary anatomy, physiological
experiments, and more especially from carefully-made autopsies with
microscopic examination of the cord. We cannot present this subject
better than by reproducing a tabular statement of these results
prepared by M. Allen Starr.[5] Future autopsies may correct this
table, and in making use of it the occurrence of anomalous
nerve-distribution should be remembered:
LOCALIZATION OF FUNCTIONS IN THE VARIOUS SEGMENTS OF THE SPINAL CORD.
-----------+------------------------+--------------+---------------
Segment. | Muscles. | Reflexes. | Sensation.
-----------+------------------------+--------------+---------------
2d-3d C. | Sterno-mast. trapezius.| . . . . . . | Neck and back
| Scaleni and musc. of | | of head.
| neck. | |
| Diaphragm. . . . . . . | Hypochon- |
| | drium (?). |
| | |
4th C. | Diaphragm. . . . . . . | Dilatation | Neck.
| | of pupil. |
| Supra- and | On irritation| Upper shoulder.
| infra-spinatus. | of neck. |
| Deltoid. . . . . . . . | 4th-7th C. | Outer arm.
| Biceps and | |
| coraco-brach. | |
| Supinator longus. | |
| Rhomboid. | |
| | |
5th C. | Deep muscles of | Scapular. | Back of should-
| shoulder-blade. . . | 5th C.-1st D.| er and arm.
{78} | Deltoid. . . . . . . | . . . . . . | Outer side of
| | | arm and
| | | forearm.
| Biceps and | | Ant. upper
| coraco-brach. . . . | . . . . . . | two-thirds of
| | | arm.
| Supinator longus. | |
| Pectorales. | |
| Serratus magnus. | |
| Triceps. | Elbow tendon.|
| Rhomboid, teres minor. | 5th-6th C. |
| | |
6th C. | Biceps, brach. antic. | . . . . . . | Outer side of
| | | arm and
| | | forearm.
| Pectorales. . . . . . | . . . . . . | Inner and front
| | | of forearm.
| Serratus magnus. | |
| Triceps. | |
| Extensors of wrist and | Wrist |
| fingers. . . . . . | tendons. |
| Flexors of wrist. . . | Wrist |
| | tendons. |
| Pronators, supinator | 6th-8th C. |
| brevis. . . . . . . | |
| | |
7th C. | Triceps, long head. . | . . . . . . | Inner and back
| | | of arm and
| | | forearm.
| Extensors of wrist and | |
| fingers. | |
| Flexors of wrist and | Palmar. . . | Radial
| fingers. . . . . . | | distribution
| | | in the hand.
| Pronators of wrist. . | 7th-8th C. |
| Subscapular. | |
| Latissimus dorsi. | |
| Teres major. | |
| | |
8th C. | Extensors of thumb. . | . . . . . . | Forearm and
| Flexors of wrist and | | hand, median
| fingers. | | and ulnar
| Intrinsic muscles of | | distribution.
| hand. | |
| | |
1st D. | Extensors of thumb. . | . . . . . . | Ulnar
| Intrinsic muscles of | | distribution
| hand. | | to hand,
| Thenar and hypothenar | | little
| eminences. | | finger.
| | |
2d-12th D. | Muscles of back and | Epigastric | Skin of back
| abdomen. . . . . . | skin. | and abdomen,
| | 4-7 D. | and over
| | Abdominal | upper gluteal
| | skin. | region.
| | 7-11 D. |
| Erector spinæ muscles. | Hypochon- |
| | drium (?). |
| | |
1st L. | Ilio-psoas. . . . . . | Cremasteric. | Skin over groin
| Sartorius. . . . . . | 1st-3d L. | and front of
| | | scrotum.
| | |
2d L. | Ilio-psoas. . . . . . | Patellar | Outer side of
| | tendon. | thigh.
| Sartorius. . . . . . | 2d-4th L. |
| Flexors of knee, | Bladder and |
| Remak (?) . . . . . | sexual |
| | centres. |
| | 2d-4th L. |
| | |
3d L. | Quadriceps femoris. . | . . . . . . | Front of thigh.
| Adductores femoris. | |
| | |
4th L. | Adductores femoris. . | Rectal | Inner side of
| | centre. | thigh and leg
| Extensores femoris. . | 4th L.-2d S. | to ankle.
| Tibialis anticus. . . | Gluteal. |
| Peroneus longus. . . | 4th-5th L. |
| Flexors of knee | |
| (Ferrier (?)). | |
{79} | | |
5th L. | Outward rotators of | . . . . . . | Lower part of
| thigh. . . . . . . | | gluteal
| | | region.
| Flexors of knee | . . . . . . | Back of thigh.
| (Ferrier). | |
| Flexors and extensors | . . . . . . | Leg and foot,
| of toes. | | outer part.
| Peronei. | |
| Muscles of calf of leg.| |
| | |
1st S. | Muscles of calf of leg.| Foot clonus. | Leg and foot,
| Long flexor of great | Achillis | except inner
| toe. . . . . . . . | tendon. | part.
| Intrinsic muscles of | Plantar. |
| foot. . . . . . . . | |
| | |
2d S. | Intrinsic muscles of | Plantar. | Perineum, anus.
| foot. . . . . . . . | |
-----------+------------------------+--------------+---------------
[Footnote 5: “The Localization of Functions of the Spinal Cord,”
_American Journal Neurology and Psychiatry_, iii., 1884.]
The above table should be studied in connection with Gowers's diagram
of the vertebral column and spinal cord (Fig. 2, p. 53), for the
thorough study of cases of neural and spinal localization. Additional
details of much value with respect to the peripheral nerve
distribution are accessible in the works of Ranney[6] and Ross[7].
[Footnote 6: _The Applied Anatomy of the Nervous System_, N. Y., 1881,
p. 355 _et seq._]
[Footnote 7: _Handbook of Diseases of the Nervous System_, Am. ed.,
Philada., 1885, p. 356 _et seq._]
III. The Localization of Lesions in the Medulla Oblongata.
In general terms, lesions of the oblongata are characterized by the
early appearance and prominence of motor symptoms in the mouth,
throat, and larynx, and by bilaterality of the symptoms. Remote
symptoms consist of disturbances in the cardiac action and in the
functions of some intra-abdominal organs. There may also be more or
less paralysis of all the extremities. These lesions may conveniently
be classified, like those of the cord, into systematic and focal.
A. SYSTEMATIC LESIONS OF THE OBLONGATA.—1. Systematic lesions of the
æsthesodic system of the oblongata are, for purposes of practical
diagnosis, unknown at the present time.
2. Systematic lesions of the kinesodic system of the oblongata, on the
other hand, are often positively recognizable during the patient's
life.
(_a_) The most strictly systematic and most frequent of these lesions
is that of secondary (Wallerian) degeneration of the pyramids, the
prolongation of the cerebral motor tract. This morbid change gives
rise to no distinct bulbar symptoms, and it can only be diagnosticated
inferentially or inclusively by determining the existence of secondary
degeneration of the entire pyramidal tract, from the occurrence of
hemiplegia followed by contracture and increased reflexes. If the
phenomena present be those of double spastic hemiplegia, there is
surely degeneration of both pyramids.