The propulsive gait is characterized by a rigid and curved posture, in which the
head and neck of the patient are inclined forward, the arms flexed, rigid are
held away from the body, the fingers are extended, the knees and hips are
rigidly He flexed. During walking, this posture manifests itself with a forward
displacement of the center of gravity of the body and consequent alteration of
the balance, causing the appearance of increasingly rapid, short and dragged
steps with involuntary accelerations (festination) and loss of control over
movement forward (Propulsion) or backwards (retropulsion). The propulsive gait
is a cardinal sign of advanced Parkinson's disease and is caused by the
progressive degeneration of the ganglia, which are mainly responsible for the
movement of smooth muscles. As this sign develops gradually and the effects that
accompany it are often erroneously attributed to aging, the propulsive gait
often remains unnoticed or unrelated to stages of severe disability.
Ask the patient when he presented the first changes in gait and if he has recently worsened. Since you may have difficulty remembering, having attributed the gait to "old age", you must be able to obtain information from family members or friends, especially from those who see the patient only sporadically. Furthermore, an accurate pharmacological history should be obtained, which includes both the type of drug and the dosage. Ask the patient if he has taken sedatives, especially phenothiazines. If you know you have Parkinson's and take levodopa, pay special attention to the dosage, as an overdose can cause an acute exacerbation of the signs and symptoms. If Parkinson's disease is not known or suspected, ask the patient if he has been exposed to acute or chronic carbon monoxide or manganese. Begin the objective examination by testing the reflexes and the sensory and motor function of the patient, paying attention to any abnormal reaction
The propulsive gait often appears several weeks after the acute carbon monoxide
poisoning. Early effects include muscle stiffness, coreoatetotic movements,
generalized myoclonus convulsions, mask facies and dementia.
Manganese intoxication
Chronic overexposure to manganese can cause an insidious, often permanent
propulsive gait. Characteristic initial signs include fatigue, hyposthenia and
muscle stiffness, dystonia, rest tremor, coreoatetosic movements, mask facies
and personality change.
The characteristic and permanent propulsive gait soon presents itself as a drag.
As the disease progresses, walking becomes slower. Cardinal signs of the disease
are the progressive muscular rigidity, which can be uniform (lead tube rigidity)
or jerks (toothed wheel rigidity), akinesia, an insidious tremor that begins in
the fingers, increases with stress or during d anxiety and decreases choruses
intentional movements and sleep. In addition to gait, akinesia generally also
produces a monotone voice, sialorrhea, facial amimia, bent posture, dysarthria,
dysphagia or both. Sometimes, it is also due to oculogyric crises or
blepharospasm.
Other causes
Drugs.
A propulsive gait and other extrapyramidal effects may result from the use of phenothiazines, other antipsychotics (especially haloperidol, tiotixene and loxapine) and, exceptionally, metoclopramide and methirosin. These effects are usually temporary and disappear within a few weeks of discontinuation of therapy. Because of the gait and associated motor impairment, the patient may have problems performing daily life activities. We must help it in an appropriate manner, while at the same time encouraging its independence and autonomy. Recommend to the patient and his / her family members to spend a lot of time on these activities, especially walking, since he is particularly susceptible to falls due to fable and poor balance. Encourage the patient to continue walking; for security reasons, remember to stay with him while walking, especially if you are in unfamiliar or steep places. The need to entrust it to a physiotherapist for therapeutic activities and to slow down the pace may occur.
A spastic gait sometimes described as a paretic or hyposthenic gait is a rigid
gait, with dragging of the foot caused by the unilateral hypertreat of the leg
muscles. This gait indicates focal damage of the corticospinal tract. The
affected leg becomes stiff, with a noticeable decrease in flexion of the hip and
knee, and sometimes with plantar flexion and equino-varus foot. Since the
patient's leg does not move normally to the hip or knee, the foot tends to crawl
or crawl, scratching the fingers on the ground. For compensation, the pelvis of
the affected side tilts upward in an attempt to lift the fingers, causing the
patient to abduct and circumduce the leg. Furthermore, the swing of the arm is
obstructed by the same side of the affected leg. Spastic gait usually develops
after a period of flaccidity (hypotonia) of the affected leg. Whatever the
cause, the gait is usually permanent once developed.
It is necessary to find out when the patient has accused the disorder for the
first time and whether the disorder has developed suddenly or gradually. Ask him
if he increases and decreases or if he has progressively escalated. Does fatigue,
heat, baths or hot showers make walking worsens? This exacerbation typically
occurs in multiple sclerosis. Focus the history of neurological disorders,
recent head trauma and degenerative diseases. During the physical exam, test and
compare strength, mobility and sensory functions in all the arts. Also, observe
and palpate to evaluate muscle weakness or atrophy.
In this pathology, spastic gait generally develops slowly after a period of
muscle weakness and fever. The first signs and symptoms of abscess reflect
endocrine hypertension (IEC), headache, nausea, vomiting and local or
generalized crises. Late, seat-specific symptoms may include hemiparesis,
tremors, visual disturbances, nystagmus and pupillary anisocoria. The patient's
level of consciousness can range from drowsiness to stupor.
Depending on the location and the type of tumor, the spastic gait usually
develops gradually and worsens over time. Associated symptoms may include signs
of IEC (headache, nausea, vomiting and local or generalized crises), papilledema,
loss of sensation on the affected side, dysarthria, ocular paralysis, aphasia
and personality change.
Spastic gait generally appears after a period of muscle weakness and hypotonia
on the affected side. Associated symptoms may include unilateral muscle atrophy,
loss of feeling and falling foot, aphasia, dysarthria, dysphagia, visual field
deficits, diplopia, ocular paralysis.
Spastic gait generally follows the acute phase of a head injury. The patient may
also have local or generalized crises, personality changes, headache and local
neurological signs, such as aphasia and decreased visual field.
A spastic gait begins insidiously and follows the typical sky of this pathology
with remissions and exacerbations. The gait, as well as other signs and symptoms,
often gets worse in hot weather or after a hot bath or shower. A characteristic
weakness, which usually affects the legs, varies from a minimum fatigue, to the
paraparesis with urinary urgency and constipation. Other signs include facial
pain, paraesthesia, incoordination, alterations in proprioception and
vibrational sensitivity to the ankles and toes and visual changes.
Special considerations
Since leg muscle contractures are commonly associated with spastic gait, it is
necessary to promote both active and passive physical activity. The patient may
have poor balance and a tendency to fall towards the paretic side, so we must
stay with him while he is walking. Provide a cane or a cane, as shown. If
necessary, entrust the patient to a physiotherapist to re-educate the gait and
in case he should wear orthotics or braces to maintain proper alignment of the
foot to stand up and walk.
The stepping gait generally comes from the falling foot caused by hyposthenia or
paralysis of the pretibial and peronial muscles, usually due to lower motor
neuron injury. The falling foot induces weakness of the foot with the fingers
resting on the ground and crawling on the ground during walking. For
compensation, the hip rotates outward and the hip and knee flex exaggeratedly to
lift the leg advancing from the ground. The foot is thrown forward and the
fingers strike the ground first, producing a sound. The pace of the gait is
usually regular, with a uniform pitch and posture of the upper body and normal
arm swing. The stepping gait may be unilateral or bilateral and permanent or
transient, depending on the location and the type of neurological damage.
Begin by asking the patient about the onset of gait disturbance and any recent
variation in its characteristics. Does any member of the family have a similar
gait? Check to see if the patient has had a traumatic injury to the buttocks,
hip, legs or knees. Ask about the history of chronic diseases that may be
associated with polyneuropathy, such as diabetes mellitus, polyarteritis nodosa
and alcoholism. While collecting the medical history, observe if the patient
crosses the legs while sitting because this may result in compression of the
peroneal nerve.
Inspect and palpate the calves and feet of the patient to assess muscle atrophy
and hypotrophy. Using a pin, test any sensory deficits along the entire length
of both legs.
Emerging generally after healing from the acute phase of this pathology, the
stepping gait may be mild or severe and unilateral or bilateral; it is always
permanent. Hypostenia usually begins in the legs, extends to the arms and face
within 72 hours and may progress to total motor paralysis and respiratory
failure. Other signs include the falling foot, transient paresthesia, nasal
voice, dysphagia, sweating, tachycardia, orthostatic hypotension and
incontinence.
The unilateral stepping gait and the falling foot generally appear with delayed
hyposthenia and atrophy of the leg muscles. However, the most obvious symptom is
severe back pain, which can radiate to the buttocks, games and feet, often
unilaterally. Subsequently, a sciatica appears, often associated with muscle
cramps and sensory and motor deficits. Paraesthesia and fasciculations may
appear.
Stepping gait and falling foot generally show obvious fluctuations with the
cycle of periodic remissions and flare-ups typical of this disease. Hypostenia,
which usually affects the legs, can vary from a minimum of fatigue to the
paraparesis with urinary urgency and constipation. Related findings include pain
in facades, visual disturbances, paresthesia, incoordination and loss of
sensitivity to
ankle and toes.
The bilateral stepping gait and the sagging foot develop insidiously in this
disease. 1 foot muscles, peroneal and ankle dorsiflexor are affected first.
Other early signs and symptoms include paresthesia, pain and cramps in the feet
and legs along with a feeling of cold, edema and cyanosis. As the disease
progresses, all leg muscles become weak and atrophic, with hypoactivity or
absence of deep tendon reflexes (RTP). Belatedly, atrophy and sensitivity
deficits extend to the hands and arms.
The unilateral transient stepping gait appears suddenly but resolves with the
decompression of the peroneal nerve. The gait is associated with the falling
foot, hypostenia and reduced sensitivity on the lateral surface of the calf and
the foot.
The stepping gait, usually permanent and unilateral, often develops after the
acute phase, generally preceded by fever, asymmetric muscle hyposthenia, coarse
fasciculations, paresthesia, RTI 'hypoactive or absent and paralysis and
permanent muscle atrophy. Dysphagia, urinary retention and difficulty in
breathing may occur.
Diabetic polyneuropathy is a rare cause of bilateral stepping gait, which
appears as a late but permanent effect. This sign is preceded by burning pain in
the foot and is accompanied by leg hyposthenia, anesthesia and skin ulcers.
In polyarteritis nodosa with polyneuropathy, the unilateral or bilateral
stepping gait is a late finding. Related findings include mild sciatica,
abdominal pain, haematuria, fever and increased blood pressure.
In alcoholic polyneuropathy, the stepping gait appears 2 to 3 months after the
onset of vitamin B deficiency. Uandatura can be bilateral and resolves by
treating vitamin deficiency. The initial signs include paresthesia in the feet,
muscular hyposthenia of the leg and sometimes sensory ataxia.
Trauma of the spinal cord.
In an outpatient patient, a spinal cord injury can cause stepping. The effects
vary with the severity of the lesions and may include unilateral or bilateral
drop foot, neck and back pain, tenderness and vertebral deformities.
Paraesthesia, sensitivity deficit, asymmetric or absent RTP, hyposthenia or
muscular paralysis can develop distally to the lesion. The patient can also
develop faecal and urinary incontinence.
Special considerations
The patient with a stepping gait can quickly get tired when he walks because
of the extra effort he does to lift his foot off the ground. When he gets tired,
he can trip over his toes, falling. To avoid this, we must help the patient
recognize his limitations and encourage him to rest properly. Entrust it to a
physiotherapist, if necessary, to re-educate the gait and for the possibility
that it should wear orthotics or braces to maintain correct alignment of the
foot-
neurology index