Gait Training in Stroke

Original Editor - Sheik Abdul Khadir

Top Contributors - Sheik Abdul Khadir, Stacy Schiurring, Kim Jackson, Garima Gedamkar, Lucinda hampton, Vanessa Rhule, Naomi O'Reilly, Evan Thomas, Simisola Ajeyalemi, Admin, WikiSysop, Adam Vallely Farrell, Vidya Acharya, Rucha Gadgil, Wanda van Niekerk, Lauren Lopez, 127.0.0.1 and Aminat Abolade  

Introduction to Gait 

The ability to walk independently is a prerequisite for most daily activities. The capacity to walk in a community setting requires the ability to walk at speeds that enable an individual to cross the street in the time allotted by pedestrian lights, to step on and off a moving walkway, in and out of automatic doors, walk around furniture, under and over objects and negotiate kerbs.A walking velocity of 1.1-1.5 m/s is considered to be fast enough to function as a pedestrian in different environmental and social contexts. It has been reported that only 7% of patients discharged from rehabilitation met the criteria for community walking which included the ability to walk 500 m continuously at a speed that would enable them to cross a road safely (Hill et al. 1997). 

The major requirements for successful walking (Forssberg 1982) are:

• support of body mass by lower limbs
• propulsion of the body in the intended direction
• the production of a basic locomotor rhythm
• dynamic balance control of the moving body
• flexibility, i.e. the ability to adapt the movement to changing
  environmental demands and goals.
  

Gait in Stroke 

Poststroke hemiplegic gait is a mixture of deviations and compensatory motion dictated by residual functions, and thus each patient must be examined and his/her unique gait pattern identified and documented. Walking dysfunction is common in neurologically impaired individuals, arising not only from the impairments associated with the lesion but also from secondary cardiovascular and musculoskeletal consequences of disuse and physical inactivity. Muscle weakness and paralysis, poor motor control and soft tissue contracture are major contributors to walking dysfunction after stroke.

Typical kinematic deviations and adaptations 

Initial stance (heel/foot contact and loading)

• Limited ankle dorsiflexion - decreased activation of anterior tibial muscles ; contracture and/or stiffness of calf muscles with premature activation.
  
•  Lack of knee flexion (knee hyperextension) - contracture of soleus ; limited control of quadriceps 0-15°

Mid-stance

• Lack of knee extension (knee remains flexed 10-150 with excessive ankle dorsiflexion) - decreased activation of calf muscles to control movement of shank forward at ankle (ankle dorsiflexion) ; limited synergic activation of lower limb extensor muscles.
• Stiffening of knee (hyperextension). This interferes with preparation for push-off -  contracture of soleus ; an adaptation to fear of limb collapse due to weakness of muscles controlling the knee.
• Limited hip extension and ankle dorsiflexion with failure to progress body mass forward over the foot - contracture of soleus.
• Excessive lateral pelvic shift </u

Late stance (pre-swing)

• Lack of knee flexion and ankle plantarflexion, prerequisites for push-off and preparation for swing - weakness of calf muscles.

Early and mid-swing

• Limited knee flexion normally 35-40° increasing to 60° for swing  and toe clearance - increased stiffness in or unopposed activity of two-joint rectus femoris ; decreased activation of hamstrings.

Late swing (preparation for heel contact an'''d loading)

• Limited knee extension and ankle dorsiflexion jeopardizing heel contact and weight-acceptance - contracted or stiff calf muscles ; decreased dorsiflexor activity.

Spatiotemporal adaptations

These include: 

• decreased walking speed
• short and/or uneven step and stride lengths
• increased stride width
• increased double support phase
• dependence on support through the hands.