Parkinsonian gait (or festinating gait, from Latin festinare [to hurry]) is the type of gait exhibited by patients with Parkinson's disease (PD). It is often described by people with Parkinson's as feeling like being stuck in place, when initiating a step or turning, and can increase the risk of falling. This disorder is caused by a deficiency of dopamine in the basal ganglia circuit leading to motor deficits. Gait is one of the most affected motor characteristics of this disorder although symptoms of Parkinson's disease are varied.

Parkinsonian gait is characterized by small shuffling steps and a general slowness of movement (hypokinesia), or even the total loss of movement (akinesia) in the extreme cases. Patients with PD demonstrate reduced stride length, walking speed during free ambulation and cadence rate, while double support duration is increased. The patient has difficulty starting, but also has difficulty stopping after starting. This is due to muscle hypertonicity.

Parkinsonian gait

Abnormal gait characteristics

Patients with Parkinson's disease exhibit gait characteristics that are markedly different from normal gait. While the list of abnormal gait characteristics given below is the most discussed, it is certainly not exhaustive.

Parkinsonian gait

Heel to toe characteristics

Whereas in normal gait, the heel strikes the ground before the toes (also called heel-to-toe walking), in Parkinsonian gait, motion is characterised by flat foot strike (where the entire foot is placed on the ground at the same time) or less often and in the more advanced stages of the disease by toe-to-heel walking (where the toes touch the ground before the heel). In addition, PD patients have reduced foot lifting during the swing phase of gait, which produces smaller clearance between the toes and the ground.

Parkinsonian gait

Patients with Parkinson's disease have reduced impact at heel strike and this mechanism has been found to be related to the disease severity with impact decreasing as the disease progresses. Also, Parkinson patients show a trend towards higher relative loads in the forefoot regions combined with a load shift towards medial foot areas. This load shift is believed to help in compensating for postural imbalance. The intra-individual variability in foot strike pattern is found to be surprisingly lower in PD patients compared with normal people.

Vertical ground reaction force

In normal gait, the vertical ground reaction force (GRF) plot has two peaks – one when the foot strikes the ground and the second peak is caused by push-off force from the ground. The shape of the vertical GRF signal is abnormal in PD. In the earlier stages of the disease, reduced forces (or peak heights) are found for heel contact and the push-off phase resembling that of elderly subjects. In the more advanced stages of the disorder where gait is characterized by small shuffling steps, PD patients show only one narrow peak in the vertical GRF signal.

Falls and freezing of gait

Falls and freezing of gait are two episodic phenomena that are common in Parkinsonian gait. Falls and freezing of gait in PD are generally thought to be closely intertwined for several reasons, most importantly: both symptoms are common in the advanced stages of the disease and are less common in the earlier stages, with freezing of gait leading to falls in many instances. Both symptoms often respond poorly and sometimes paradoxically to treatment with dopaminergic medication, perhaps pointing to a common underlying pathophysiology. It is possible to demonstrate poor and paradoxical dopaminergic medication response through a challenge paradigm in which gait is assessed after withdrawal from medication and in the full ON medication state.

Freezing of Gait: Freezing of Gait (FOG) is typically a transient episode – lasting less than a minute, in which gait is halted and the patient complains that his/her feet are glued to the ground. When the patient overcomes the block, walking can be performed relatively smoothly. The pathophysiology of the phenomenon is poorly understood but likely extends across a disseminated functional-anatomic network. Sadly, current treatments for FOG offer only limited benefits but a range of novel approaches are being actively explored, and thought is being given to how future research strategies are best coordinated.