Walking means the act of walking. It is a harmonious and complex movement of
the body that is produced following a simultaneous and coordinated action
between trunk, pelvis and limbs (lower, but also higher due to the presence of
the oscillatory movement of the arms). Following many studies it has been
established a methodological criterion for the quantitative evaluation of both
movement and posture, ie the analysis of the path that regards numerous areas,
from the medical-rehabilitative to the sport. The reduction or loss of walking
ability is also one of the most considered parameters in the assessment of the
degree of disability in an individual. For this reason, we will now consider, in
relation to the alteration of the path they produce, the various gaits that
express neurodisability.
The gait anomalies will be considered here:
Ankle gait
Mowing gait
Propulsive gait
Spastic gait
Stepping gait
The gait gait is a characteristic gait gait, an important sign of muscular
dystrophy, atrophy of spinal muscles or, rarely, of congenital hip dislocation.
The gait is the result of the progressive dysfunction of the pelvic girdle
muscles mainly the gluteus medius, the hip flexors and the hip extensors. The
weakness of these muscles hinders the stabilization of weight distribution on
the hip during walking. inducing the opposite hip to lower and the trunk to lean
towards that side in order to maintain balance. Generally, the legs take a wider
support base and the trunk is moved backwards to improve stability, accentuating
lordosis and abdominal protrusion.In severe cases, muscle contractions of the
leg and foot can cause equine-varus foot combined with circling or buckling of
the legs.
Ask the patient (or a family member if the patient is a child) when the gait
disturbance first appeared and has recently worsened. To assess the extent of
pelvic girdle hyposthenia and leg muscles, ask if the patient falls frequently
or has difficulty climbing stairs, getting up from a chair or walking. Also,
find out if you started walking late or keeping your head upright. To obtain a
family history, focusing on problems of muscle weakness and gait and congenital
motor disorders. Inspect and palpate the muscles of the leg, especially the
calves, to evaluate their size and tone. Evaluate the positivity of the sign of
Gower, or of climbing, which indicates muscle hyposthenia. Next, evaluate the
muscle strength and function of the shoulders, limbs and hands, looking for any
hyposthenia or asymmetric movements.
In Duchenne muscular dystrophy, anserine gait becomes clinically evident around
3-5 years of age. Walking worsens as the disease progresses, until the child
loses the ability to walk and becomes wheelchair dependent, usually between 10
and 12 years. The early signs are often mild: delay in learning to walk,
frequent falls, walking or abnormal posture and intermittent pain in the calf.
Frequent late findings include lordosis with protrusion of the abdomen, a
positivity of the sign of Gower and equine-varus foot. As the disease progresses,
its effects become more prominent, typically include rapid muscular hypotrophy,
which begins in the legs and spreads to the arms (although the muscles of the
calf and upper limb can become hypertrophic, hard, and elastic in consistency ),
muscle contractures, limitation of dorsiflexion of the feet and extension of the
knees and elbows, obesity and sometimes mild mental retardation. Serious
complications appear when kyphoscoliosis develops, leading to respiratory
failure and ultimately to death due to heart or respiratory failure. In Becker's
muscular dystrophy, the anserine gait generally becomes evident in late
adolescence, worsens slowly during the third decade and culminates in a total
inability to ambulate. Hypostenia hyposthenia first appears in the pelvic and
upper limb muscles. Progressive atrophy with hypertrophy of the selected muscles
produces lordosis with abdominal protrusion, poor balance, positive Gower sign
and sometimes mental retardation. In facetoscapolomeral muscular dystrophy that
usually occurs late in children and during adolescence, anserine gait appears
after muscle atrophy has spread downward, from the muscles of the face and
shoulder girdle to the pelvic girdle and legs. . Early signs include the
progressive weakness and atrophy of facial muscles, shoulders and arms, light
lordosis and pelvic instability.
In Kugelberg-Welander disease, anserine gait appears precociously (usually after
two years of age) and generally progresses slowly, culminating in total
inability to ambulate up to 20 years later. Related findings may include muscle
atrophy of the legs and pelvis, which progresses to the shoulders, or a
positivity of the sign of Gower, ophthalmoplegia, fasciculations of the tongue.
In Werdnig-Hoffmann's disease, anserine gait generally begins when the child
learns to walk. 1 reflections may be absent. Walking worsens progressively,
culminating in complete inability to ambulate in adolescence. Associated
findings include lordosis with abdominal protrusion and hyposthenia of the hips
and thighs.
It receives the name of "mowing" in relation to the old neurological definition
based on the displacement of the paretic lower limb that during the walk seems
to mimic the image of the sickle that cuts the grain. This gait is typical of
subjects with hemiparesis due to ischemic stroke. Resulting from bilateral
spastic paresis (diplegia), the mowing gait affects both legs and is of little
or no effect on the arms. The patient's legs are slightly bent at the level of
the hips and knees, so it seems as if he is running around. At each step, her
thighs come forward and her knees touch or cross each other in a scissors-like
movement. His steps are short, regular and laborious, as if he were wading
through deep water. His feet can be plantar flexed and rotated inside, with a
shortened Achilles tendon; as a result, he walks on the fingers or on the pad of
the foot and can drag his fingers on the ground.
Ask the patient (or a family member, if the patient can not answer) about the
onset and duration of the gait. Has it progressively deteriorated or remained
constant? Ask for previous trauma, including birth trauma
In the spastic form of this pathology, patients walk on their toes with a mowing
gait. Other aspects include tendon hyperreflexia, increased reflex reflexes,
rapid alternation of contraction and muscle relaxation, hyposthenia, hypotrophy
de (the affected limb and a tendency to contractures.
Exceptionally, the mowing gait arises during the late phase of recovery of
bilateral occlusion of the anterior cerebral artery. The patient can also show a
paraparesis of the leg muscles and atrophy, incoordination, paresthesias,
urinary incontinence, confusion and personality changes.
A mowing gait develops in the later stages of this degenerative disease and
worsens constantly. The associated findings resemble those of a herniated disc:
severe back pain, which can radiate to the jute, legs and feet, muscle spasms,
sensory and motor disorders, asthenia and muscular atrophy.
The mowing gait may appear several months before the onset of hepatic failure (see
hepatic profile). Other findings may include asterixis, generalized convulsions,
jaundice, purpura, dementia and fetor hepaticus.
A progressive mowing gait generally develops gradually, with rare remissions.
The characteristic hyposthenia, usually in the legs, varies from a minimum
fatigue to the paraparesis with urinary urgency and constipation. Related
findings include facial pain, visual disturbances, paresthesia, incoordination
and a loss of proprioceptive and vibratory sensitivity to the ankle and toes.
The gait. mowing is sometimes found to be a late sign in untreated anemia. In
addition to the classic triad of symptoms related to this disorder, such as
weakness, sore tongue, numbness and tingling limbs, the patient may have pale
lip, gums and tongue, a slightly jaundiced selera and pale or pale yellow skin ,
proprioceptive disorders, incoordination, visual disturbances (diplopia,
obnubilation).
The mowing gait may develop during the recovery phase at partial compression of
the spinal cord, especially with a lesion below C6. Associated findings may
include loss of sensation or paresthesia, hyposthenia or paresthesia, paralysis
distal to the lesion, and bladder and intestinal dysfunction.
The mowing gait may develop gradually as a result of thoracic or lumbar tumors. Other findings reflect the location of the tumor and may include root pain, subscapularis, shoulder, inguinal, leg or hips, muscle spasms or fasciculations, muscle atrophy, sensory disturbances, such as paraesthesia and a feeling of tightness in the abdomen and chest. , increase of tendon reflexes, bilateral Babinski reflex, spastic neurogenic bladder, sexual dysfunction.
A progressive mowing gait generally develops gradually, with rare remissions.
The characteristic hyposthenia, usually in the legs, varies from a minimum
fatigue to the paraparesis with urinary urgency and constipation. Related
findings include facial pain, visual disturbances, paresthesia, incoordination
and a loss of proprioceptive and vibratory sensitivity to the ankle and toes.
The gait. mowing is sometimes found to be a late sign in untreated anemia. In
addition to the classic triad of symptoms related to this disorder, such as
weakness, sore tongue, numbness and tingling limbs, the patient may have pale
lip, gums and tongue, a slightly jaundiced selera and pale or pale yellow skin ,
proprioceptive disorders, incoordination, visual disturbances (diplopia,
obnubilation).
The mowing gait may develop during the recovery phase at partial compression of
the spinal cord, especially with a lesion below C6. Associated findings may
include loss of sensation or paresthesia, hyposthenia or paresthesia, paralysis
distal to the lesion, and bladder and intestinal dysfunction.
The mowing gait may develop gradually as a result of thoracic or lumbar tumors. Other findings reflect the location of the tumor and may include root pain, subscapularis, shoulder, inguinal, leg or hips, muscle spasms or fasciculations, muscle atrophy, sensory disturbances, such as paraesthesia and a feeling of tightness in the abdomen and chest. , increase of tendon reflexes, bilateral Babinski reflex, spastic neurogenic bladder, sexual dysfunction.