Gait

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A gait disturbance is a gait pattern that deviates from a "normal" gait. Synchrony, fluency, smoothness, and symmetry may be affected. A gait disturbance can be caused by problems at any level of the neuraxis, and they can be classified on an anatomical basis. This type of classification scheme categorises gait disturbances into low-level, middle-level, and high-level gait disorders. Particularly in the elderly, multiple factors may be in play causing a gait disturbance. [1]

Gait Cycle

Gait is a cyclic process take place between the time a foot touches the ground and when the same foot returns to the ground once again.

The stance phase of a limb is when some part of the foot is touching the ground. It makes up 60% of the gait cycle and incorporates heel strike, foot flat, mid-stance, and push-off (heels-off and toes-off). The swing phase is when it is off the ground. This phase has an acceleration, mid-swing, and deceleration components.

Gait Cycle Terminology; graphical representation of stride and step lengths

Gait Disorder Classifications

Higher, Middle, and Lower Level Gait Disorder Anatomical Correlations. [1]
Levels Anatomical Level Balance and Gait Pattern
Higher Psychological / psychiatric Variable: slow, buckling knees
Higher Cortical and subcortical Different patterns: cautious, parkinsonian, ataxic, spastic, magnetic, gait ignition failure, disequilibrium
Middle Basal ganglia Parkinsonian / dystonic / choreic
Middle Thalamus Astasia / ataxia
Middle Cerebellum Cerebellar ataxia
Middle Brain stem Ataxia / spasticity
Middle Spinal cord Spastic gait / tabetic gait
Lower Peripheral nerve
Proprioception, vestibular visual
Sensory ataxia / vestibular disequilibrium / visual disequilibrium
Lower Neuromuscular junction Waddling
Lower Muscle Waddling, steppage, Trendelenburg
Lower Skeleton Antalgic / compensatory for deformities

See below for a demonstration of neurological gait conditions (Hemiplegic, Parkinsonian, Cerebellar, Stomping, Scissoring, Trendelenburg, Foot-drop, Choreiform)

Lower Level Gait Disorders

Lower level gait disorders are caused by pathology of the muscles, skeleton, peripheral nerves, peripheral vestibular system, and anterior visual pathway.[1]

Antalgic Gait

The occurs when there is a protective adaptation to minimise pain during weightbearing. The patient removes weight from the painful side as quickly as possible. The stance phase of the affected side, and the swing phase of the unaffected side are lessened. Stride length and velocity are decreased.

Trendelenburg and Waddling Gaits

The distance from the midline to the femoral head is almost twice that between the abductors and femoral head. The abductors generate very large forces across the hip weight bearing area, about 3 times that of upper body weight.[2] Trendelenburg gait manifests as ipsilateral lurching of the torso with a contralateral hip drop during the stance phase of the affected side. It is caused by unilateral hip abductor weakness.[1] There is an exaggerated up and down motion of the pelvic.

A waddling gait pattern is seen with weakness of the bilateral hip abductors as well as in bilateral hip joint osteoarthritis or other bilateral hip joint diseases. The gait is wide based, and has short steps. There is increased alternating lateral body sway, and excessive drop of the hips. By swaying laterally the patient places their weight down the centre of gravity through each hip to reduce pain. There may be increased arm abduction and an exaggerated lumbar lordosis. [1]

The abductor lurch is seen with further abductor mechanism weakness, where the trunk muscles come into play. The entire body and shoulder tilts to the diseased side in the stance phase of the ipsilateral limb. The abductor lurch can also occur in the setting of a painful hip. By tilting the body to the affected side the centre of gravity is shifted towards the centre of the femoral head, thereby reducing the reaction force and resultant pain. In this situation there is no drop of the hemipelvis as seen with a Trendelenburg gait.

Short Limb Gait

To compensate for length, the pelvis on the affected short side tilts down (hip hiking). This allows the longer limb to more easily clear the ground. The foot may supinate or there may be toe walking. The longer limb may compensate by flexing at the hip or knee.[2]

Steppage Gait

This is seen with weakness of food dorsiflexion, which may be due to peroneal nerve injury, radiculopathy, and demyelinating neuropathy. It may be unilateral or bilateral. The patient exaggerates knee and hip flexion to avoid tripping. The step is high and short, and at the end of each swing phase the foot may slap the floor.[1]

Gluteus Maximus or Extensor Lurch

Normally the gluteus maximus prevents the torso toppling forward in the stance phase, because the centre of gravity is anterior to the hip. With gluteus maximus weakness, the torso lurches backwards at heel strike on the affected side. This is a compensatory mechanism to interrupt forward motion of the trunk due to a weakness of hip extension. The pelvis is thrusted forward, and the torso backwards, in order to shift the centre of gravity more posteriorly.[2]

Flexion Contracture of Hip or Knee

This results in increased lumbar lordosis, stopping, and a short stride length. Evaluate this laterally.[2]

Knee Considerations

Evaluate varus and valgus thrusting by squatting or sitting to inspect the patient from the level of their knees. Varus thrust is the most common. In the stance phase the knee collapses into varus with the lateral border laterally thrusting. This can be seen in advanced osteoarthritis, varus from malunited tibial plateau fracture, and tibia varum. A ligamentous laxity will usually add a recurvatum thrust visualised laterally. Valgus thrust is less common, and patients may circumduct their limb to avoid knocking their knees.[2]

A stiff knee gait with the knee extended may be seen with patients avoiding patellofemoral pain. This can also be seen when compensating for quadriceps weakness with locking in the stance phase. On the other hand, a stiff knee gait with the knee flexed - even 5 degrees can cause a gait disturbance - can result in a short stride, a heel strike replaced by an almost flat foot to start phase, and a jerky up-down motion from apparent shortening.[2]

Ankle and Foot Considerations

An equinus contracture can be seen as a high stepping gait during the swing phase of the affected side. There is an abnormally early heel raise, with hyperextension of the ipsilateral knee to compensate for the contracture.[2]

Patients with a stiff 1st MTP joint walk mainly on the lateral border of their foot. This may be more easily visualised by observing for lateral wear on their shoes. There is a hurried push-off, which occurs directly from the heel.[2]

In pes planus the heel raise is avoided, and so the heel and ball of the foot rise together. The toes are usually splayed outwards.[2]

Sensory Ataxia

The sensory ataxic gait is wide based with a variable step length and marked stride-to-stride variability. There is usually unsteadiness. Romberg sign is often positive. This gait pattern is not specific to any anatomical location, and may be seen in pathology of proprioception (sensory ataxia), cerebellum (cerebellar ataxia), pons, and thalamus.[1]

Visual Disequilibrium

Acute visual distortion such as using new prescription glasses may cause a sense of loss of balance. There may be cautiousness in gait, with tentative steps and an increased base of support.[1]

Vestibular Disequilibrium

Acutely there may be vertigo, nystagmus, and a tendency to fall onto the affected side. Chronically, the symptoms may be less marked, but the gait is often still wide based and cautious. There is difficulty with Romberg test and tandem walking, but assistance is not required to walk.[1]

Sensory Disequilibrium

There is conflict among inputs from the visual, proprioceptive, and vestibular pathways. Loss of two of these pathways, or loss of one without CNS adaptation, may lead to this becoming chronic. The gait is slow and cautious, and there is increased bipedal support.[1]

Middle Level Gait Disorders

In middle level gait disorders are caused by lesions in the ascending or descending sensorimotor tract, cerebellar dysfunction, bradykinesia, and hyperkinetic movement disorders.[1]

Spastic Gait and Scissoring

Corticospinal tract lesions cause spastic gaits that can be hemi or paraparetic depending on whether the lesion is unilateral or bialteral. There is often an associated weakness. [1]

Spastic hemiparetic gaits show lower limb hyperextension with difficulty in hip and knee flexion and excessive plantarflexion and inversion of the foot. The arm may have a flexor posture or may dangle. The support base is narrowed, and there is a semicircular movement at the hip during the swing phase which is needed to clear the ground due to the hyperextension of the leg. With more mild spasticity and good proximal muscle strength the patient may clear the floor during the swing phase with increased hip flexion.[1]

Spastic paraparetic gaits is more common in spinal cord injury and there is some shared features with hemiparetic gaits. Arm swing and the posture of the upper limb may be relatively normal depending on the lesion level.[1]

Spastic diplegic gait is a bilatearl hemiparetic gait with particular features. The knees and hips are significantly flexed. The hips are adducted during the gait cycle causing a scissoring pattern from leg crossing. Compared to bilateral hemiparesis, in spastic diplegia the upper limbs and bulbar muscles are much less affected than the lower limbs.[1]

Cerebellar Ataxia

Parkinsonian Gait

Choreic Gait

Dystonic Gait

Higher Level Gait Disorders

These gait disorders are caused by impairment of the cortico-basal ganglia-thalamocortical pathways. Gait disorders in this category include cautious gait, fear of falling, freezing of gait, and frontal and subcortial disequilibrium.

Psychiatric disorders may also affect the gait cycle.

Examination

There should be a general, neurological, and musculoskeletal examination in order to localise the lesion. The gait should be assessed by observing the gait parameters, posture, range of motion, and tandem walking. The Romberg test and a vestibular examination may be indicated. The neurological examination should focus on pyramidal signs, tremor, sensory changes, and dysmetria. The general examination may include a brief cardiorespiratory and ophthalmologic examination. A general screening and focused musculoskeletal examination should be performed.

Investigations

References

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Biller, José. Practical neurology. Philadelphia: Wolters Kluwer, 2017.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 https://www.slideshare.net/ggkar/gait-for-dnb.