CHAPTER XXIII

LOCOMOTION AS AN AID IN DIAGNOSIS

One need not be a very experienced physician to know that there is a

group of diseases, mostly of the nervous system, which at a certain

point of their evolution, stamp the sufferer with a characteristic mode

of locomotion. To observe such a modification of the normal walk is

often sufficient to make a correct diagnosis.

It is strange, however, how little attention this important subject

has received from the medical profession. In fact, other than the work

of the brothers Weber, who established the physiology and mechanism

of human locomotion, of Neugebauer and of Gilles de la Tourette, who

developed the ichnogram method of gait study, scarcely anything of

importance has been done along these lines for the last quarter of

a century. The study of the mode of locomotion in various diseases

and ailments remains, therefore, a fertile field of research for the

podiatrist.

=Elements of Locomotion.= The act of locomotion or the _power_ of

progression is not a simple one. Various co-related movements combine

to form what we ordinarily term the _walk_. The three chief elements

are: (1) _Posture_, (2) _Station_, and (3) _Gait_. These three factors

may be influenced by local or general diseases, either separately or

together.

=Posture.= Posture is the term applied to the position of the body

in space and is not of much interest to the podiatrist except as

corroborative of the two other elements of locomotion. It has, however,

its value in diagnosis and the new practitioner of podiatry will do

well to learn to observe the position of the body at various angles

and in various diseases. One should learn early, for instance, that

_immobility_ is not always due to paralysis. It may be due to _pain_,

as in rheumatism or to a disinclination to move as in scurvy, rickets

or any condition causing dyspnea. The _restlessness_ in fevers and in

large hemorrhages, as well as the _throwing about_ in renal, gallstone

or intestinal colics, is known to all. Equally characteristic are

the _agitation_ and irregular movements in chorea and hysteria;

the _gun-hammer posture_ in cerebrospinal meningitis, and the

_opisthotonos_ in tetanus and strychnine poisoning.

=Station.= Station is the _power_ of standing more or less firmly

on one’s feet. It includes _attitude_ which is the _manner_ of

standing, i.e., the relation of the rest of the body to the erect

position. The carriage of the head and shoulders should be noted; the

shape of the entire body whether bending _forward_, as in “stooped

shoulders” (faulty attitude habit) and in paralysis agitans, or bending

_backward_, as in ascites and abdominal tumors, should be closely

studied and differentiated from the actual lordosis which is seen

in spinal diseases, in advanced pregnancy, in pseudo-hypertrophic

paralysis and in cretinism. The strictest attention should be paid to

the attitude of the lower limbs, their individual shapes and their

relation to each other when the erect position is assumed. The degree

of firmness with which the individual stands should always be taken

into consideration before a final diagnosis is made. _Swaying_ is the

term applied to any departure from the ideally rigid erect attitude and

perpendicular station. The normal individual, with eyes open and heels

close together, sways about one inch forward and three-quarters of an

inch from side to side. In functional and static ataxias, the swaying

may become so extreme as to produce absolute incapacity to stand.

=Gait.= This term means the specific _manner_ of walking. It is a

narrower term than locomotion which is the _power_ of walking. It

is, however, the chief factor in the act of progression and in the

majority of cases it is characteristic enough to stamp itself indelibly

on the normal as well as on the diseased individual. While in character

reading, gait expression may not be as popular as face expression, it

is often more reliable and in certain diseases it is simply invaluable

as an aid in diagnosis.

METHODS OF DIAGNOSIS

=A.--The Observation Method.= This is the usual method of ascertaining

the gait of an individual. It is practised by the average physician and

podiatrist and consists in observing the patient while he or she walks

up and down the room, taking notice of the peculiarities of gait which

may develop. The patient may be allowed to roam freely about the room

or should be directed to follow a carpet seam or a crack in the floor

at right angles to a previous line of vision. This may be varied by

opening or closing the eyes, stretching out the arms, with legs wide

apart, or keeping them close together. Brisk walking should alternate

with a slower gait and the effect of stopping abruptly and turning

sharply at command should be closely observed.

It is best to have the patient uncovered from the hips down. In women,

the nightgown or chemise can be pulled tightly between the thighs and

fastened anteriorly with a safety pin.

=Caution.= Due allowance should be made for nervousness and a careful

watch must be maintained against a serious fall.

[Illustration: Fig. 1

ICHNOGRAM OF A NORMAL GAIT]

=B.--The Ichnogram Method= consists in studying the impressions left by

_both_ soles (previously colored) when walking on paper for a distance

of about twenty-five feet. Ichnograms (from the Greek--_ichnos_--trace,

and _gramma_--to write) as a method of gait diagnosis are more exact

than the method of observation and should supplement it. Besides, they

inform us, at the same time, of the state of the plantar arch as each

_pelmatogram_ (the impression of a single foot) shows more or less

clearly a posterior oval which changes but little, and an anterior oval

as well as toe marks which undergo characteristic contour changes,

depending on the state of the ligaments, of the tarsal and metatarsal

bones and phalanges, and the relation of these structures to the

musculature and innervation of the foot.

Comparatively little has been accomplished along this line of endeavor,

although it offers a vast and fruitful field for podiatric research.

In fact this branch of podiatry deserves a special treatise, and it

will be discussed in fuller detail in our forthcoming book on Podiatry

Orthopedics.

[Illustration: Fig. 2

A. PELMATOGRAM OF A NORMAL FEMALE FOOT

B. MODIFIED PELMATOGRAM SHOWING WEIGHT BEARING POINTS]

[Illustration: Fig. 3

PELMATOGRAM OF A MALE, SHOWING FLAT FOOT]

=Classification of Gaits.= Strictly speaking there are only three types

of gait: (1) the _paretic_, (2) the _ataxic_ and (3) the _choreic_.

In some diseases there may be a combination of the three, while in

others one type of gait predominates during the early stage and another

during the later developments. At times, one comes across a gait that

combines characteristics of the three types and hence is difficult of

classification.

=I.--Paretic Gait.= _Paresis_ means a lessening of the normal motility

of a muscle, while the term _paralysis_ denotes entire absence of motor

power. We may have, therefore, two or three distinct paretic gaits

according to whether the muscle is slightly or severely weakened or

entirely paralyzed:

A.--The mild paretic gait.

B.--The moderate or flaccid paretic gait.

C.--The severe or spastic paretic gait.

=A.--The Mild Paretic Gait= is caused by muscular weakness due to a

large number of etiologic factors. It results in slowing of locomotion,

the steps being shortened on account of an exaggerated flexion at the

knee joint. The following are examples of mild paretic gaits:

(1) _The Pompous Gait._ The upper part of the body leans backward,

the back is hollowed, the abdomen is protuberant, the feet are widely

separated and appear to move with deliberation and dignity, giving the

impression of conscious importance--hence the name. This gait may be

seen in obesity, pregnancy, ascites, large abdominal tumors, cretinism

and rickets.

(2) _The Hobbling Gait._ The pelvis tilts towards the sound side,

while the trunk leans over to the affected side, causing more or

less pronounced _limping_. This gait is seen in people afflicted

with corns, rheumatism, gout, sciatica, plantar neuralgia, Morton’s

neuralgia, metatarsalgia, hip or knee joint disease or injury (recent

or old), sacro-iliac disease, sprains, inflammatory diseases of the

lower extremity, chimatlon, short leg, paralysis of one leg, abdominal

aneurism, and subacute and chronic appendicitis.

(3) _Intermittent Limping_ (disbasia angiosclerotica or intermittent

claudication) may be classified here and is a curious limping gait

which develops in arteriosclerosis of the lower extremities. There

are pain and fatigue on walking, which disappear after a short rest,

to reappear again soon after walking is resumed. The pulse is weak or

absent below the knee.

(4) _The Waddling or Goose Gait._ The pelvis and head of femur are

jerked forward at each step, knee advanced and extended only after

foot is flat upon the ground. There is more lordosis and swinging

of the body from side to side at each step, than in the pompous

gait. It resembles the gait of a goose. The patient cannot stand on

tiptoe. It is seen in: congenital dislocation of both hip joints and

in pseudo-hypertrophic muscular paralysis, a hereditary disease seen

mostly in boys under ten years of age, and characterized by inability

to get up from the floor.

(5) _The Wobbly Gait._ Resembles the above and is due to atrophy or

paralysis of the three glutei muscles and prevents the patient from

climbing. This inability to climb is also seen in those exhibiting the

waddling gait.

(6) _The Tottering Gait._ Seen in those who have taken large doses

of bromides for long periods; also in hydrocephalus, in Korsakoff’s

disease (psychosis polyneuritica) and in idiopathic muscular atrophy.

(7) _The Shuffling Gait_ is the gait seen in normal old age or senility

and is associated with slowly progressive loss of strength and

mentality. It is also seen in general paresis and is the “normal” gait

of the long-term prison inmate. The patient gives the impression of

being too lazy to lift his feet and instead pushes them along with his

legs.

(8) _The “Charlie Chaplin” Gait_ has been erroneously described as

an ataxic gait. It is rather a combination of the “funny part” of

several gaits in which the waddling, shuffling, tottering paretic gaits

predominate and to which some elements of the spastic paretic, as well

as the ataxic gaits, have been added. The inspiration must have come

originally to the celebrated movie star from some waddling cripple whom

he proceeded to imitate and later burlesqued.

=B.--The Moderate or Flaccid Paretic Gait.= In this form of the paretic

gait there is commonly a paresis of a certain group of muscles, usually

the extensors of the foot or the peronei, causing “toe drop” and

apparent lengthening of the affected extremity. It corresponds to the

“wrist drop” of the upper extremity. To compensate for the lengthening

of the limb, overflexion at the hip or knee, or at both joints, takes

place. The limb is flaccid or flabby.

The foot is lifted high up with each step in order to raise it clear

off the ground and avoid tripping. As the foot is brought down, heel

first, this gait may sometimes be confused with tabes and is therefore

sometimes referred to as the pseudo-tabetic gait. It is, however,

easily differentiated from the true tabetic gait by its characteristic

“high action” or “high stepping” quality which made Charcot compare it

to the gait of a horse and hence called it:

(1) _The Steppage Gait_, mostly seen in the chronic intoxications

producing neuritis. It resembles the gait of a man walking through

thick grass or brushwood and stepping over constantly recurring but

non-existent obstacles. The typical steppage gait is seen in arsenical

neuritis with ankle drop, also in alcoholic neuritis, polyneuritis

potatorum (ataxia of drunkards) and in lead neuritis (lead palsy,

plumbism, saturnism), in which first the peroneal muscles are affected,

later the extensor communis digitorum and finally the extensor

proprius hallucis. Phosphorus, copper and grain (ergotism) poisoning

may give rise to a neuritis in the lower extremities and produce the

characteristic steppage gait. Tuberculosis, malaria, diabetes and

diphtheria (motor form) may sometimes produce this gait. It may also

develop as a sequel of sunstroke (thermic fever, insolation) and in

fact following any disease which will cause peripheral neuritis of the

anterior tibial nerve.

(2) _The Prancing Gait_ is an exaggeration of the preceding gait.

It is seen in epidemic anterior poliomyelitis (infantile paralysis)

when the disease affects the anterior horn cells of the lumbar cord,

causing atrophy of the extensor muscles of the foot, resulting in

“foot drop.” It is also seen in acute ascending paralysis (Landry’s

disease), which is probably a form of poliomyelitis, and in progressive

hereditary muscular atrophy of the leg (Charcot-Marie-Tooth type) where

the muscles of the leg, not the foot, are primarily affected, i.e.,

first the peronei become atrophied, later the extensors of the toes

and finally the calcaneal muscles. Finally the prancing may be seen in

connection with certain tumors of the cord, unilateral hip disease,

dislocation or injury and in multiple neuritis and beriberi (epidemic

multiple neuritis).

=C.--The Spastic or Severe Paretic Gait.= The spastic gait is due to

the hypertonicity of the weakened muscles, the resulting stiffness

causing a slowing of locomotion and diminished excursion of the

affected limb. The hypertonicity is produced either by direct

stimulation of the motor cells in the anterior horn of the spinal cord,

as in traumatic myelitis, or by impulses coming down from the cerebral

cortex. The limb is spastic or rigid, due to the tonic spasm. When the

tonic spasm is of long standing, it is termed a _contracture_. The

lower extremity moves as a whole, the toes clinging to the ground,

scraping it and very often “catching.” Contrary to the moderate paretic

gait, this group presents difficulty in flexion which is partly

overcome by the elevation of the pelvis on the side of the swinging leg.

(1) _The Mowing or Hemiplegic Gait._ This is the prototype of

all spastic gaits and is encountered in its simplest form in all

hemiplegias, i.e., in paralysis of one side of the body, which may

be caused by cerebral hemorrhage, embolism, thrombosis, syphilis,

brain tumor, multiple sclerosis of a cerebral hemisphere, meningeal

hemorrhage or suppuration, Raynaud’s disease, general paresis of the

insane; sometimes it may be due to hysteria (functional hemiplegia)

or to uremia (transient hemiplegia). No matter what the cause of the

hemiplegia, there is always the typical mowing gait. This mowing

movement is due to the fact that the spastic limb swings lateralward,

describing an arc of a circle (outward), and strikes the ground in a

flail-like manner. Technically speaking, circumduction takes place by

tilting of the pelvis and the swinging of the foot outward and around

to the front. The patient afflicted with hemiplegia makes the same

movement with his limb as does the reaper with the hand in which he

holds the scythe. _Exception_: the only paralytic gait in which there

is no mowing movement occurs in hysterical (functional) paraplegia,

which is very rare. In this condition the leg is dragged forward

instead of outward.

_Important shoe sign in paraplegia._ The sole of the shoe is worn down

on the inner side.

(2) _The Small-step Gait_ (la marche à petits pas). This gait is seen

in cerebral softening following an apoplectic stroke, especially in

pseudo-bulbar paralysis; the steps are very short and the feet are

lifted from the ground with difficulty, the patient seeming to count

his steps.

(3) _The Cross-legged Gait._ This gait is due to a spasm of the

adductors of the thigh causing the knees to rub against each other,

resulting in cross-legged progression, the lower limbs having a

tendency to cross during locomotion. It is seen in both Little’s

congenital and Erb’s syphilitic form of lateral spinal sclerosis. In

the syphilitic form, a dragging and shuffling gait is often associated

with the cross-legged type.

(4) _The Ill-defined Spastic Gaits._ Ill-defined spastic gaits are seen

in tetany (paroxysmal tonic spasm) from any cause, and in amyotrophic

lateral sclerosis, which is the spastic form of progressive muscular

atrophy (Charcot’s disease). This involution disease, due probably to

developmental defects of the lateral pyramidal tracts, has the combined

symptoms of spastic spinal paralysis, anterior poliomyelitis and bulbar

palsy, hence the difficulty in classifying it. Myelitis (inflammation

of the spinal cord) may be due to trauma, alcoholism, syphilis,

vertebral caries (compression myelitis), tumors, aneurism, hemorrhages

into the cord, etc., and will exhibit various gaits according to

the stage and severity of the disease. It may begin with a mild

paretic gait passing through several stages of the spastic gait or to

complete paraplegia (paralysis of both lower extremities). In complete

paraplegia there is of course no gait, as the patient cannot walk,

there being a loss of the power of locomotion but not of progression (a

patient so afflicted may still move from place to place on his hands).

(5) _The Dragging Gait._ In hemiplegia one foot only is dragged.

Dragging of both feet is seen in multiple neuritis, hereditary peroneal

atrophy, spasmodic spinal paralysis and spinal and syphilitic spinal

paralyses.

(6) _The Dromedary Gait_, so called on account of its resemblance to

the gait of a camel, is seen in children suffering with progressive

torsion spasm (Flatau-Sterling disease).

Finally, spastic paretic gaits are often observed in pellagra (maidism,

Italian leprosy, Alpine scurvy) and in lathyrism (lupinosis), where

the slow toxic spinal sclerosis finally leads to spastic paraplegia

and loss of the power of locomotion; also in caisson disease (divers’

paralysis).

=II.--The Ataxic Gait.= The ataxic gait may be either:

A--The Static ataxic gait, or

B--The Functional ataxic gait

and these are termed either (1) spinal or (2) cerebellar, according to

the location of the lesion.

=A.--The Static Spinal Ataxic Gait= is the most easily recognized gait,

and once seen, is never forgotten. There is an exaggeration of all the

movements of locomotion. The hips are overflexed and rotated laterally,

the foot is raised suddenly and too high, the toes are lifted and the

whole limb is thrown suddenly forward with unnecessary vehemence and is

then brought down heel first or flat-footed, with a stamping sound. The

feet are kept wide apart and while in the air they move in an undecided

manner, as if the patient was doubtful where to put them. The eyes of

the afflicted person are glued to the ground or fixed to the limbs so

as to supplement the lack of muscular and articular sensation by the

sense of sight.

In the cerebellar type of this gait the movement excursion is not as

extensive as in the spinal type. A sudden turning movement or an abrupt

sitting posture is difficult or impossible to assume in this type of

locomotion.

In order to test static ataxia, the patient is made to stand heels

and toes together, whereupon marked swaying takes place. The swaying

is increased when the eyes are closed and the patient looks like a

“chicken on a clothes line.” If there is more than one inch forward

swaying and more than three-quarters of an inch lateral swaying, the

patient is considered ataxic.

In the disease known as tabes dorsalis, or locomotor ataxia of

syphilis, the swaying may be so pronounced as to produce absolute

incapability to stand or to walk.

=B.--The Cerebellar (functional) Ataxic Gaits.= These gaits are

produced by a disturbance of the equilibrium accompanied by vertigo

resulting in a very irregular swaying from side to side, resembling the

gait of an intoxicated person.

The patient makes short steps, keeps his feet wide apart, staggers,

rolls, sways to and fro and reaches a set point by zigzagging toward

it. The swaying is relieved when support is given under the armpits.

(1) _The Titubating Gait_ is a form of functional cerebellar ataxic

gait seen in the following affections: Friedreich’s (disease) ataxia;

hereditary cerebellar ataxia; dementia paralytica; ataxic paraplegia;

labyrinthine disease and to some extent in vertigo; syringomyelia; and

in some cases of general paresis, and various chronic intoxications

like lead or arsenic or alcohol poisoning affecting the cerebrospinal

system.

(2) _The Reeling or Staggering Gait_ is seen in acute alcoholic

intoxication and Mésnière’s disease (disease of the middle cerebellar

lobe).

=III.--The Choreic Gait.= The choreic gait, sometimes called _tremor_

gait, spasmodic or hysterical gait, is very variable in quality

depending on the cause of the tremor. It consists of a series of

quivering or trembling movements of varying intensity, but nearly all

due to clonic spasm and disappearing during sleep or passive motion.

This distinguishes it from the spastic or paraplegic gait in which

the spasm is tonic in quality, lasting from one minute to one month.

The clonic spasm, on the other hand, consists in rapidly alternating

contractions and relaxations of the muscle.

(1) _The Stumbling Gait_ is seen in chorea (St. Vitus’ dance) and

Huntington’s (hereditary) chorea, in Friedreich’s paramyoclonus

multiplex (which is not to be confounded with Friedreich’s ataxia),

in Unverricht’s progressive myoclonus, and in multiple sclerosis

of the spinal cord. The gait resembles that of a schoolboy, who

clownishly stumbles or trips over his heel to attract attention.

Technically it consists of spasmodic adduction, extension and outward

rotation of the legs which soon renders locomotion impossible. When

these abrupt twitchings and jerking movements, which are involuntary

and purposeless, affect only one-half of the body, we speak of the

condition as hemichorea. The patient appears restless, unsettled and

fidgety.

(2) _The Festination Gait_ is typical of the disease known as

paralysis agitans (Parkinson’s disease, shaking palsy) and is an

advanced choreic gait in which there may be observed the curious

phenomena of propulsion and retropulsion, i.e., the impossibility of

stopping, once the patient is pushed either forward or backward. In

some instances, when pulled suddenly backward, the patient will take

a few backward steps with increasing rapidity, also the body remains

in the characteristic posture of paralysis agitans; namely, in the

forward-leaning attitude. In festination “the body tries to overtake

its centre of gravity” (Trousseau).

(3) _The Saltatory Gait_ (“The jumpers”), is a very rare condition

occurring the instant the weight of the body is put upon the feet. It

consists in strong and rapid contractions of the muscles of the thigh

and leg causing the patient to jump up violently. It is probably a

hysterical spasm.

(4) _The Myotonia Gait_ occurs in Thomsen’s disease and consists of

tonic, _painless_ spasms whenever a certain group of muscles begin

to functionate. The steps are first checked and delayed; but this

gradually wears off. This curious condition returns again when the same

group of muscles are called into action. Owing to the tonic spasms,

this gait might have been properly classified as a spastic paretic

gait, were it not for the fleeting and irregular character of the

spasticity.

(5) _The Hysteria Gait_, known also as astasia-abasia, is notable by

the ease with which it may simulate any and all of the gaits described

above, the spastic as well as the flaccid types of paralyses,--even

the cross-legged gait, ending in complete inability to stand or walk.

It differs from all of them, however, in the ability of the patient to

perform all the nervous functions of the limb when lying in bed. The

hysterical gait may also end in:

_Catalepsy_ which is a state of muscular rigidity enabling a limb to

maintain a posture in opposition to gravity for one hour or more (waxy

flexibility). This curious phenomenon of retaining the leg or any other

part of the body in a fixed attitude (given to it by the operator)

is sometimes seen in catatonia, general paresis, brain tumors and,

(rarely) in meningitis.

(The above chapter was especially prepared for “Practical

Podiatry” by Paul Luttinger, M.D., Professor of Bacteriology in

The First Institute of Podiatry. It is the first compilation of

its kind ever published and should prove a valuable aid to both

practitioners of medicine and of podiatry--_Editor_).

Practical podiatry · 第 23 / 27 章