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Gait – Anatomy

Introduction

All levels of the neuroaxis contribute to gait although most gait abnormalities are motor in nature. In assessing gait it is important to not only watch the lower extremities but also the upper extremities for normal associated movements.


Localizing Value

There are 7 basic pathological gaits that should be recognized by their characteristic pattern. These pathological gaits are:

  • Hemiplegic
  • Spastic diplegic
  • Neuropathic
  • Myopathic
  • Parkinsonian
  • Chorea
  • Ataxic

These gaits have localizing value because they can indicate levels (an “y” axis as well as an “x” axis) of neurological disease or systems abnormalities (such as cerebellar or basal ganglia). Normal gait is demonstrated in the normal neuro exam section of this tutorial. The pathological gaits are demonstrated in the abnormal neurological exam section. An antalgic gait is usually secondary to a musculoskeletal injury of the lower limb (hip, knee, ankle) resulting in a softer foot strike and characteristic limp; the cause of pathology in these cases is usually easily confirmed by basic history, inspection and palpation findings.


Adapted, with permission from the University of Nebraska School of Medicine By Paul D. Larsen, M.D. and Suzanne S. Stensaas, Ph.D.

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Gait – Normal Exam

Station

The patient should be able to stand still with her feet less then shoulder width apart.


Natural Gait

The patient should be able to walk with a smooth, coordinated gait. There should be normal associated movement of the upper extremities.


Heel and Toe Walking

A good way to test balance as well as strength of the distal lower extremities is to have the patient heel and toe walk.


Tandem Gait

Have the patient walk heel-to-toe. The patient should be able to balance without falling or stepping to the side.


Adapted, with permission from the University of Nebraska School of Medicine By Paul D. Larsen, M.D. and Suzanne S. Stensaas, Ph.D.

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Gait – Abnormal

Hemiplegic Gait Demonstration

The patient has unilateral weakness and spasticity with the upper extremity held in flexion and the lower extremity in extension. The foot is in extension so the leg is “too long” therefore, the patient will have to circumduct or swing the leg around to step forward. This type of gait is seen with a UMN lesion.


Diplegic Gait Demonstration

The patient has spasticity in the lower extremities greater than the upper extremities. The hips and knees are flexed and adducted with the ankles extended and internally rotated. When the patient walks both lower extremities are circumducted and the upper extremities are held in a mid or low guard position. This type of gait is usually seen with bilateral periventricular lesions. The legs are more affected than the arms because the corticospinal tract axons that are going to the legs are closest to the ventricles.


Neuropathic Gait Demonstration

This type of gait is most often seen in peripheral nerve disease where the distal lower extremity is most affected. Because the foot dorsiflexors are weak, the patient has a high stepping gait in an attempt to avoid dragging the toe on the ground.


Myopathic Gait Demonstration

With muscular diseases, the proximal pelvic girdle muscles are usually the most weak. Because of this the patient will not be able to stabilize the pelvis as they lift their leg to step forward, so the pelvis will tilt toward the non-weight bearing leg which results in a waddle type of gait.


Parkinsonian Gait Demonstration

This type of gait is seen with rigidity and hypokinesia from basal ganglia disease. The patient’s posture is stooped forward. Gait initiation is slow and steps are small and shuffling; turning is en bloc like a statue.


Choreiform Gait Demonstration

This is a hyperkinetic gait seen with certain types of basal ganglia disorders. There is intrusion of irregular, jerky, involuntary movements in both the upper and lower extremities.


Ataxic Gait Demonstration

The patient’s gait is wide-based with truncal instability and irregular lurching steps which results in lateral veering and if severe, falling. This type of gait is seen in midline cerebellar disease. It can also be seen with severe lose of proprioception (sensory ataxia)


Hemiplegic Gait

This girl has a right hemiparesis. Note how she holds her right upper extremity flexed at the elbow and the hand with the thumb tucked under the closed fingers (this is “cortical fisting”). There is circumduction of the right lower extremity.


Diplegic Gait

This man has an UMN lesion affecting both lower extremities. He has spasticity and weakness of the legs and uses a walker to steady himself. There is bilateral circumduction of the lower extremities.


Neuropathic Gait

This girl has weakness of the distal right lower extremity so she can’t dorsiflex her foot. In order to walk she has to lift her right leg higher then the left to clear the foot and avoid dragging her toes on the ground.


Myopathic Gait

This young boy has pelvic girdle weakness, which produces a waddling type of gait. Note the lumbar hyperlordosis with the shoulders thrust backwards and the abdomen being protuberant. This posture places the center of gravity behind the hips so the patient doesn’t fall forward because of weak back and hip extensors.


Parkinsonian Gait

This man’s gait is bradykinetic and his steps are smaller then usual. There is also the pill-rolling tremor in his hands. He turns en bloc and there is decreased facial expression.


Choreiform Gait

Note the involuntary, irregular, jerky movements of this woman’s body and extremities, especially on the right side. There are also choreiform movements of the face. A lot of her movements have a writhing, snake-like quality to them, which could be called choreoathetoisis.


Ataxic Gait

This woman’s gait is wide-based and unsteady. She has to use a walker or hold on to someone in order to maintain her balance (note how hard she has to work with the hand that she’s holding on with in order to maintain her balance). Her ataxia is even more apparent when she tries to turn.


Adapted, with permission from the University of Nebraska School of Medicine By Paul D. Larsen, M.D. and Suzanne S. Stensaas, Ph.D.

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