Parkinsonian gait

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Parkinsonian gait indoor 01.jpg
Parkinsonian gait (indoor)
Parkinsonian gait outdoor.jpg
Parkinsonian gait (outdoor)
Features of PD gait are more obvious in the side view. [1]

Parkinsonian gait (or festinating gait, from Latin festinare [to hurry]) is the type of gait exhibited by patients with Parkinson's disease (PD). [2] 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. [3] 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.

Contents

Parkinsonian gait is characterized by small shuffling steps and a general slowness of movement (hypokinesia), or even the total loss of movement (akinesia) in extreme cases. [4] [5] [6] Patients with PD demonstrate reduced stride length, walking speed during free ambulation and cadence rate, while double support duration is increased. [7] [8] [9] [10] The patient has difficulty starting, but also has difficulty stopping after starting. This is due to muscle hypertonicity. [11]

Abnormal gait characteristics

Parkinson's disease patient showing a flexed walking posture pictured in 1892, from Nouvelle Iconographie de la Salpetriere, vol. 5. Paralysis agitans-Male Parkinson's victim-1892.jpg
Parkinson's disease patient showing a flexed walking posture pictured in 1892, from Nouvelle Iconographie de la Salpètrière, vol. 5.

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.

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) [12] 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. [13]

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. [14]

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. [15] [16] 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.[ citation needed ]

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. [17] 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. [18]

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. [19] Sadly, current treatments for FOG offer only limited benefits but a range of novel approaches are being actively explored, [20] and thought is being given to how future research strategies are best coordinated. [21]

The most common form of FOG is 'start hesitation' (which happens when the patient wants to start walking) followed in frequency by 'turning hesitation' [22] [23] FOG can also be experienced in narrow or tight quarters such as a doorway, whilst adjusting one's steps when reaching a destination, and in stressful situations such as when the telephone or the doorbell rings or when the elevator door opens. As the disease progresses, FOG can appear spontaneously even in an open runway space. [17] It is proven that psychological interventions can help reduce negative effect of psychosocial factors, like anxiety or depression, that can worsen freezing of gait or tremor in Parkinson's patients. [24] Based on that, every patient could benefit from psychological intervention, not only to reduce anxiety, depression, pain, and insomnia, but also to reduce effect of psychosocial factors in worsening of motor symptoms.

Falls: Falls, like FOG are rare in the earlier stages of the disorder and becomes more frequent as the disease progresses. Falls result mainly due to sudden changes in posture, in particular turning movements of the trunk, or attempts to perform more than one activity simultaneously with walking or balancing. Falls are also common during transfers, such as rising from a chair or bed. PD patients fall mostly forward (45% of all falls) and about 20% fall laterally. [17] Falls that occur frequently very early in the disease course may signify that another diagnosis (such as progressive supranuclear palsy) should be considered. [25]

Postural sway

Postural instability in upright stance is common in end-stage PD and compromises the ability to maintain balance during everyday tasks such as walking, turning and standing up from sitting. An inability to adequately balance the body's center of mass over the base of support combined with inflexibility in body movements (due to increased rigidity) causes patients with advanced PD to fall. Whereas postural sway in normal stance usually increases in patients with balance disorders arising from stroke, head injury and cerebellar ataxia it is often reduced in patients with PD. The reason for this because in PD the problem appears to be a lack of flexibility in shifting postural responses. This inflexibility increases the tendency to fall in these patients. [26] [27]

Electromyographic studies

Electromyographic (EMG) studies of the leg muscles in PD patients have shown an extreme reduction in the activation of the tibialis anterior muscle in the early stance and in the early and late swing phases, and a reduction in triceps surae muscle bursting at push-off. The quadriceps and hamstring muscles on the other hand, show prolonged activation in the stance phase of gait. [28] This implies that PD patients have higher passive stiffness of ankle joints, show larger background EMG activity and more co-contraction of leg muscles in stance. Stiffer joints lead to abnormal postural sway in the PD patients. [29] [30]

Gait improvement strategies

Drugs

L-dopa (activates D1 receptor) most widely used drug for Parkinson's treatment Levodopa.png
L-dopa (activates D1 receptor) most widely used drug for Parkinson's treatment

The most widely used form of treatment is L-dopa in various forms. L-dopa is able to pass the blood–brain barrier as a prodrug and is decarboxylated in the brain to the neurotransmitter dopamine by the enzyme aromatic-L-amino-acid decarboxylase. In this way, L-DOPA can replace some of the deficit in dopamine seen in Parkinsonism. Due to feedback inhibition, L-dopa results in a reduction in the endogenous formation of L-dopa, and so eventually becomes counterproductive.

Effect on gait parameters: The stride length and the kinematic parameters (swing velocity, peak velocity) related to the energy are Dopa-sensitive. Temporal parameters (stride and swing duration, stride duration variability), related to rhythm, are Dopa-resistant. [31]

Effect on falls and freezing of gait: Levodopa treatment decreases the frequency and the akinetic type of FOG, with a tendency for shorter FOG episodes. Results indicate that this is primarily because L-dopa increases the threshold for FOG to occur but the fundamental pathophysiology for FOG did not change. [32] It has also been shown that other dopamine agonists like ropinirole, pramipexole and pergolide that have a strong affinity to D2 receptors (as opposed to L-dopa which has a strong D1 receptor affinity) increase the frequency of FOGs. [33]

Effects on postural sway: Parkinson's disease have abnormal postural sway in stance and treatment with levodopa increases postural sway abnormalities. [34] During movement, it has been shown that early autonomic postural disturbances are only partially corrected while the later occurring postural corrections are not affected by dopamine. These results indicate that non-dopaminergic lesions play a role in postural imbalance in PD patients. [35]

Metronome used to deliver rhythmic auditory cues for Parkinsons disease patients Digital metronome 2.jpg
Metronome used to deliver rhythmic auditory cues for Parkinsons disease patients
Metronome sound used as auditory cues

Auditory and visual cues

Basal ganglia dysfunction in PD causes it to stop acting as an internal cue for gait in Parkinson's patients. Hence various external sensory cues like auditory and visual cues have been developed to bypass the basal ganglia's cueing functions.

Visual cues: The visual cues are commonly transverse lines or rods on the floor (floor markers). Such cues have been shown to improve stride length and velocity in Parkinsonian gait by substituting kinaesthetic feedback with visual feedback for regulating movement amplitude. [36] In addition gait initiation has been shown to be significantly improved in PD patients compared with auditory cues. [37] Visual cues administered by "laser canes" have been reported to improve gait initiation. [38] Virtual reality glasses have also been developed recently to aid walking in PD patients. [39]

Auditory cues: The auditory cues are commonly rhythmic cues generated by a metronome or equivalent, sometimes embedded in music, set at or slightly above the subject's usual cadence. Rhythmic auditory cues have been associated with increases in velocity and cadence and sometimes stride after gait has been initiated. Auditory cues have been shown to have little or no effect in gait initiation. [37] Moreover, there are prediction algorithms to support more efficient auditory cueing. [40] These algorithms predict freezing episodes so that a cueing can be initiated.

Deep brain stimulation

Deep Brain Stimulation on a Parkinson's patient. The picture shows the process of implantation of a DBS electrode into a patient's brain. Parkinson surgery.jpg
Deep Brain Stimulation on a Parkinson's patient. The picture shows the process of implantation of a DBS electrode into a patient's brain.

Deep brain stimulation (DBS) in the pedunculopontine nucleus, a part of the brainstem involved in motor planning, [41] has been shown to improve gait function in patients with Parkinson's disease. [42]

DBS in the subthalamic nucleus (STN) and the globus pallidus have also been shown to have positive effects on gait abnormalities presented by Parkinson's Disease patients. DBS in the STN has been reported to reduce freezing of gait significantly at 1 and 2 year follow up. [43] Contradictory results have been reported on the effects on DBS on postural stability [34] [44] The results seem to be highly location specific. The studies which do report positive effects suggest that the effectiveness of DBS in improving postural stability is due to its ability to affect non-dopaminergic pathways (in addition to dopaminergic pathways) which are believed to cause postural sway in PD patients. [34] Several studies suggest that STN stimulation with low frequencies (60–80 Hz) better alleviates gait deficits than with the commonly used high frequencies (>130 Hz). [45]

Other treatments strategies

Attention strategies: By consciously paying more attention to walking and rehearsing each step before actually making it, PD patients have shown to improve their gait. Sometimes, a companion walking alongside reminds the patient to concentrate on gait or they create a visual cue to step over by putting a foot in front of the person with PD over which the person must step. This causes the patient to focus their attention on the stepping action, thus making this a voluntary action and hence bypassing the faulty basal ganglia pathway (which is responsible for involuntary actions like walking). Avoidance of dual tasks that require motor attention or cognitive attention has also been shown to normalize gait in the PD patients. [46] [47]

Exercise: Physical therapy and exercise have been shown to have positive effects on gait parameters in PD patients. [48]

Physiotherapists may help improve gait by creating training programs to lengthen a patient's stride length, broaden the base of support, improve the heel-toe gait pattern, straighten out a patient's posture, and increase arm swing patterns. [49]

Research has shown gait training combining an overhead harness with walking on a treadmill has shown to improve both walking speed and stride length. [50] The harness assists the patient in maintaining an upright posture by eliminating the need to use a mobility aid, a practice which normally promotes a forward flexed posture. [49] It is believed the activation of the central pattern generator leads to the improvement in gait pattern. [49]

Improving trunk flexibility, along with strengthening of the core muscles and lower extremities has been associated with increased balance and an improvement in gait pattern. [51] Aerobic exercises such as tandem bicycling and water aerobics are also crucial in improving strength and overall balance. [51] Due to PD's progressive nature it is important to sustain an exercise routine to maintain its benefits. [51]

Strategies such as using a vertical walking pole can also help to improve upright postural alignment. The therapist may also use tiles or footprints on the ground to improve foot placement and widen the patient's base of support. [49] Creative visualization of walking with a more normalized gait pattern, and mentally rehearsing the desired movement has also shown to be effective. [51]

The patient should also be challenged by walking on a variety of surfaces such as tile, carpet, grass, or foamed surfaces will also benefit the individual's progress towards normalizing their gait pattern. [49]

Comparison with other gait disorders

Subcortical arteriosclerotic encephalopathy (SAE), also called lower-body parkinsonism, and cerebellar ataxia are two other gait disorders whose symptoms seem to closely resemble that of Parkinson's. However, through regression analysis studies have revealed that in Parkinson's, increasing the velocity of walking changes the stride length linearly (which resembles that of controls). However, in SAE and cerebellar ataxia stride length had a disproportionate contribution to increasing velocity, indicating that SAE and cerebellar ataxia have common underlying mechanisms different from those of Parkinson's. [43]

Socio-economic impact

Mobility issues associated with falls and freezing of gait have a devastating impact in the lives of PD patients. Fear of falling in itself can have an incapacitating effect in PD patients and can result in social seclusion leaving patients largely isolated leading to depression. Immobility can also lead to osteoporosis which in-turn facilitates future fracture development. This then becomes a vicious circle with falls leading to immobility and immobility facilitating future falls. Hip fractures from falls are the most common form of fracture among PD patients. Fractures increase treatment costs associated with health care expenditures in PD. [17] Also, when gait is affected it often heralds the onset of Lewy body dementia. [52] [53] [54]

Related Research Articles

<span class="mw-page-title-main">Parkinsonism</span> Medical condition

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. These are the four motor symptoms found in Parkinson's disease (PD) – after which it is named – dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and many other conditions. This set of symptoms occurs in a wide range of conditions and may have many causes, including neurodegenerative conditions, drugs, toxins, metabolic diseases, and neurological conditions other than PD.

<span class="mw-page-title-main">Multiple system atrophy</span> Neurodegenerative disorder

Multiple system atrophy (MSA) is a rare neurodegenerative disorder characterized by autonomic dysfunction, tremors, slow movement, muscle rigidity, and postural instability and ataxia. This is caused by progressive degeneration of neurons in several parts of the brain including the basal ganglia, inferior olivary nucleus, and cerebellum.

<small>L</small>-DOPA Chemical compound

l-DOPA, also known as levodopa and l-3,4-dihydroxyphenylalanine, is made and used as part of the normal biology of some plants and animals, including humans. Humans, as well as a portion of the other animals that utilize l-DOPA, make it via biosynthesis from the amino acid l-tyrosine. l-DOPA is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), which are collectively known as catecholamines. Furthermore, l-DOPA itself mediates neurotrophic factor release by the brain and CNS. In some plant families, l-DOPA is the central precursor of a biosynthetic pathway that produces a class of pigments called betalains. l-DOPA can be manufactured and in its pure form is sold as a psychoactive drug with the INN levodopa; trade names include Sinemet, Pharmacopa, Atamet, and Stalevo. As a drug, it is used in the clinical treatment of Parkinson's disease and dopamine-responsive dystonia.

Dyskinesia refers to a category of movement disorders that are characterized by involuntary muscle movements, including movements similar to tics or chorea and diminished voluntary movements. Dyskinesia can be anything from a slight tremor of the hands to an uncontrollable movement of the upper body or lower extremities. Discoordination can also occur internally especially with the respiratory muscles and it often goes unrecognized. Dyskinesia is a symptom of several medical disorders that are distinguished by their underlying cause.

<span class="mw-page-title-main">Progressive supranuclear palsy</span> Medical condition

Progressive supranuclear palsy (PSP) is a late-onset neurodegenerative disease involving the gradual deterioration and death of specific volumes of the brain. The condition leads to symptoms including loss of balance, slowing of movement, difficulty moving the eyes, and cognitive impairment. PSP may be mistaken for other types of neurodegeneration such as Parkinson's disease, frontotemporal dementia and Alzheimer's disease. The cause of the condition is uncertain, but involves the accumulation of tau protein within the brain. Medications such as levodopa and amantadine may be useful in some cases.

Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinson's disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.

Parkinson-plus syndromes (PPS) are a group of neurodegenerative diseases featuring the classical features of Parkinson's disease with additional features that distinguish them from simple idiopathic Parkinson's disease (PD). Parkinson-plus syndromes are either inherited genetically or occur sporadically.

<span class="mw-page-title-main">Fall prevention</span> Interventions to prevent injury in domestic settings

Fall prevention includes any action taken to help reduce the number of accidental falls suffered by susceptible individuals, such as the elderly (idiopathic) and people with neurological or orthopedic indications.

In the management of Parkinson's disease, due to the chronic nature of Parkinson's disease (PD), a broad-based program is needed that includes patient and family education, support-group services, general wellness maintenance, exercise, and nutrition. At present, no cure for the disease is known, but medications or surgery can provide relief from the symptoms.

<span class="mw-page-title-main">Droxidopa</span> Synthetic amino acid/norepinephrine prodrug

Droxidopa is a synthetic amino acid precursor which acts as a prodrug to the neurotransmitter norepinephrine (noradrenaline). Unlike norepinephrine, droxidopa is capable of crossing the protective blood–brain barrier (BBB).

Dopamine-responsive dystonia (DRD) also known as Segawa syndrome (SS), is a genetic movement disorder which usually manifests itself during early childhood at around ages 5–8 years.

<span class="mw-page-title-main">Dopamine dysregulation syndrome</span> Medical condition

Dopamine dysregulation syndrome (DDS) is a dysfunction of the reward system observed in some individuals taking dopaminergic medications for an extended length of time. It typically occurs in people with Parkinson's disease (PD) who have taken dopamine agonist medications for an extended period of time. It is characterized by problems such as addiction to medication, gambling, or sexual behavior.

<span class="mw-page-title-main">Parkinson's disease</span> Long-term degenerative neurological disorder

Parkinson's disease (PD), or simply Parkinson's, is a chronic degenerative disorder of the central nervous system that affects both the motor system and non-motor systems. The symptoms usually emerge slowly, and as the disease progresses, non-motor symptoms become more common. Early symptoms are tremor, rigidity, slowness of movement, and difficulty with walking. Problems may also arise with cognition, behaviour, sleep, and sensory systems. Parkinson's disease dementia is common in advanced stages.

Signs and symptoms of Parkinson's disease are varied. Parkinson's disease affects movement, producing motor symptoms. Non-motor symptoms, which include dysautonomia, cognitive and neurobehavioral problems, and sensory and sleep difficulties, are also common. When other diseases mimic Parkinson's disease, they are categorized as parkinsonism.

Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and athetosis.

<span class="mw-page-title-main">History of Parkinson's disease</span> History of Parkinsons disease

The history of Parkinson's disease expands from 1817, when British apothecary James Parkinson published An Essay on the Shaking Palsy, to modern times. Before Parkinson's descriptions, others had already described features of the disease that would bear his name, while the 20th century greatly improved knowledge of the disease and its treatments. PD was then known as paralysis agitans. The term "Parkinson's disease" was coined in 1865 by William Sanders and later popularized by French neurologist Jean-Martin Charcot.

Kinesia paradoxa is a phenomenon most often seen in people with Parkinson's disease where individuals who typically experience severe difficulties with the simple movements may perform complex movements easily. Specifically, kinesia paradoxa focuses on walking, referring to the sudden ability to demonstrate smooth, fluid movements in people that previously had problems with walking easily. This new discovery does not just happen to an individual randomly, but must be stimulated using various types of visual or auditory cues.

The temporal dynamics of music and language describes how the brain coordinates its different regions to process musical and vocal sounds. Both music and language feature rhythmic and melodic structure. Both employ a finite set of basic elements that are combined in ordered ways to create complete musical or lingual ideas.

<span class="mw-page-title-main">Mesencephalic locomotor region</span>

The mesencephalic locomotor region (MLR) is a functionally defined area of the midbrain that is associated with the initiation and control of locomotor movements in vertebrate species.

Gait variability seen in Parkinson's Disorders arise due to cortical changes induced by pathophysiology of the disease process. Gait rehabilitation is focused to harness the adapted connections involved actively to control these variations during the disease progression. Gait variabilities seen are attributed to the defective inputs from the Basal Ganglia. However, there is altered activation of other cortical areas that support the deficient control to bring about a movement and maintain some functional mobility.

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