As adults, our normal walking gait sees us bend one knee and lift our foot, then swing our lower leg forward, with the foot flexed and raised upwards, so it clears the ground. Then, we use the other leg to propel us forward, by raising our heel off the ground and pushing using the ball of our foot, as our toes flex.
As we walk, we unconsciously swing our arms to balance us and, unless we’re injured in some way, can usually walk at a speed that feels natural, without worrying unduly about falling.
What is Parkinsonian Gait?
In contrast to normal adult gait, Parkinsonian Gait – also called Parkinson’s Walk – is characterized by very short, shuffling steps, in which the feet do not lift far from the floor. There is little to no flexion in the knee, ankle or foot, so the foot is placed flat on the ground, resulting in extremely short stride length.
The ability to bend the knee, flex the foot and roll onto the ball of the foot is critical to the ability to begin moving. Because Parkinsonian Gait lacks the knee and foot flexion of our normal movement, it’s often difficult for those who experience it to start walking. Uneven surfaces, slopes and steps can prove almost impossible to navigate and the inability to swing or turn the leg can make turning slow and awkward.
Instead of the body being upright, those with Parkinsonian Gait often lean slightly forward, with a hunched posture. To avoid overbalancing, it’s common to see rapid, short steps that seem to propel the individual forward, and reduced arm movement is often noticeable.
What Causes Parkinsonian Gait?
While the cause of Parkinson’s Disease itself is unknown, it is characterized by damage to the basal ganglia – a group of structures that sit in the base of the forebrain and top of the midbrain.
The basal ganglia is one of many stations in the communication circuit translating and moving neural impulses back and forth between the brain and the rest of the body.
The communication begins in the motor cortex – the part of the brain controlling voluntary movement – that creates a command, such as “move your legs.” This command moves to the basal ganglia, which produces dopamine, the brain chemical that facilitates the movement of messages between the brain and the body. The dopamine opens up the pathways for the signal to travel down to the rest of your body.
As Parkinson’s progresses, the disease kills nerve cells in a subsection of the basal ganglia, the “substantia nigra”, which produces dopamine. As the supply of dopamine drops, the pathways between the brain and the body have trouble opening up. Without those pathways, the brain has greater difficulty sending impulses to the legs, arms, and other parts of the body involved with walking.
The body begins exhibiting symptoms such as inability to control the length and speed of steps, as well as decreased range of motion and sudden increases in pace (known as “festination”). These are the typical symptoms of the small, shuffling steps that exemplify Parkinsonian gait.
Why Does Parkinson’s Cause This Specific Gait Disorder?
As with all things related to Parkinson’s Disease, precise causes of the walking pattern known as Parkinsonian Gait aren’t known, but researchers have found abnormalities in muscle function that may provide some answers.
Normal movement process sees muscles work in pairs to enable us to flex our joints. Agonist muscles contract, while antagonist muscles relax or extend. For example, our quadriceps – the muscles at the front of our thigh – contract to bend our knee, while the hamstrings lengthen to allow it to bend. The reverse then occurs to straighten the knee again.
However, it’s normal to have some degree of muscular co-activation, where the muscle pairs both contract at the same time, to support movement and provide stability for a joint. This is particularly obvious when we are deliberately controlling movement.
Abnormal co-activation sees both the agonist and antagonist muscles contract at the same time, to a degree that does not allow the joint to flex much, if at all. In particular, researchers have found a greater degree of antagonistic muscle activity in people with Parkinson’s Disease. While the agonist muscles are contracting to try to create movement, the antagonist muscles should be extending. Instead, they are contracting, holding the knee or elbow rigid and inflexible.
Many researchers believe that this overactive and involuntary contraction of antagonist muscles is responsible for this peculiar walking pattern in individuals with Parkinson’s. Given the significant evidence that the basal ganglia and cerebellum also play a vital role in muscle co-activation, it seems likely that it is damage to the basal ganglia that is also in play here.
Abnormal muscle co-activation may also be responsible for the poor balance that people in the later stages of Parkinson’s often experience, where it’s difficult to maintain a steady and upright posture.
In particular, it may explain why these problems with balance tend to result in leaning or falling backwards. The antagonist muscles lie at the back of the legs. When they contract – without the opposing contraction from the front of the legs – the center of balance is shifted backwards, making it difficult to stay upright.
How Does Parkinson’s Walk Interact with Other Parkinson’s Symptoms?
Two other symptoms associated with Parkinson’s Disease can make walking, and moving, even more difficult, especially as the disease progresses.
Slow movement – referred to using the Greek term Bradykinesia – is another of the symptoms used to diagnose Parkinson’s. In addition to generally sluggish movement, a decreased blink rate, and reduced facial expression, those with Bradykinesia find the fine motor control required for writing, or doing up buttons, challenging.
Additionally, those with Parkinsonian Gait often experience freezing episodes – known as Freezing of Gait – during which they feel “stuck in cement,” and unable to lift their feet from the ground.
Parkinson’s freezing in particular can make walking risky, as it significantly increases the likelihood of falling. As a result, many with Parkinsonian Gait simply limit their movement as much as possible to avoid injury.
Rewiring the Basal Ganglia to Support Movement
Movement supports and assists our most basic bodily functions, from our circulation to our digestive system. It also allows us independence and quality of life, so retaining the ability to move to the greatest extent possible is vital.
The brain is a remarkable organ, and as anyone who has ever worked to regulate or control their emotions will know, it can be tricked, distracted, or simply taught to think in a different way.
Research dating back to the 1980s showed that audio or visual cues can be successfully used to improve movement for people with Parkinson’s. These cues allow the brain to find alternative ways to transmit instructions to the body, bypassing damaged neural pathways and creating new ones.
Research has shown that people using these cues can extend their length of stride, increase their pace, avoid freezing episodes and overcome freezes when they do occur. They’re also far less prone to falls, and subsequent injury.
The increased confidence and sense of wellbeing that comes with improving Parkinsonian Gait is matched with the physical benefits of improving muscle tone, flexibility and bone density, which allows the body to stay healthier, for longer.
The Parkinson’s Foundation offers information on therapies and approaches to managing Parkinson’s and is an excellent resource for tips and medical-based options.