Chapter 3: Movement, Falls, and Parkinson’s disease

What is the number one concern for the person with Parkinson’s? Falling! People with PD are at a much higher fall risk than their peers. Complications from falls are one of the leading causes of death in the PD population.

In this chapter, we will take an even more in depth look at several symptoms of PD and learn how they may correlate to a higher risk of falling.

Looking at this study; 100 patients with Parkinson’s disease and 5 patients with progressive supranuclear palsy were questioned about the frequency, circumstances, and consequences of falling. Parkinsonian symptoms were scored using the unified rating scale. Thirty-eight percent of parkinsonian patients fell, and 13% fell more than once a week. 13% experienced broken bones, 18% received hospitalization, 3% ended up confined to a wheelchair, and fear of walking occurred. Postural hypotension was uncommon and did not correlate to falling. Sensory loss, dementia, heart disease, and the use of antihypertensive medications were not related to falling. Falling did correlate with postural instability, bradykinesia, and rigidity but not with tremor. (Koller WC1, 1989)

In the following text, we hear from my friend, Dr. Massimo Marano, a Rome, Italy based neurologist who’s on the cutting edge in his field. Dr. Marano gives us in depth input regarding movement and falls in relation to Parkinson’s disease.

By Dr. Massimo Marano

Impaired movements in Parkinson’s disease

Human voluntary and automated movement are regulated by a complex neuronal network, constituted by neuronal elements which are greatly impaired in Parkinson’s disease (PD).

The integrated activity of the “basal ganglia” (a group of neuronal elements sited in the deep part of the encephalon) with cerebellar and cortical structure provides the real time control of motor performances. The clinical motor picture of a patient affected by PD is broad. Various elements are melted together with different combinations as the disease progresses.

There are some main features that characterize this disease and differentiate PD from other similar conditions such as atypical parkinsonisms. The so called “cardinal” motor features are tremor, muscular rigidity and bradykinesia that present with typical pattern and drug responsiveness. Gait and postural impairment are also included in this topic, being highly descriptive of the PD clinical picture. The motor onset is asymmetrical (e.g. unilateral limb presentation with loss of dexterity and/or tremor). As the disease spreads, it is then bilateral involving limbs and the trunk and leads to postural deformities in the end stage. A certain quote of asymmetry is maintained throughout the disease course. This is due to the asymmetric degeneration of the nigrostriatal system, which is a dialogue network between the basal ganglia, spreading to the cortex, and supported by the activity of dopamine producing neurons. Pharmacological interventions are efficacious, especially in the early stage of the disease. Therapies aim at restoring the dopaminergic neurotransmission with synthetic L-DOPA (L-hydroxyl-o-phenylalanine, the main precursor of the brain neurotransmitter dopamine) and other products that indirectly stimulate the dopamine dependent pathway or maintain the dopamine efficacy. This implies that the PD disease course would be strongly influenced by drug efficacy and side effects. Long term anti-PD drug intake together with the neuronal degeneration build up the background for motor complications, namely fluctuations. These side effects are caused by dopamine receptor sensitivity, which increases with drug exposure, and are essentially characterized by the waxing and waning of PD symptoms during the day. Patients who present with alternating motor deterioration (drug “wearing off”) and drug related recovery (“On drug”) may realize complications by the onset of involuntary movements (dyskinesias).

The most famous and pictorial PD sign is the tremor. The tremor is an involuntary rhythmical movement due to the alternating contraction of an agonist muscle (or group of muscles) with the respective antagonist. Tremor has various faces and could affect a specific region (e.g. the hand, the foot or the mouth), a segment (e.g. a limb or the head) or the whole body. In general, tremor onset could raise while the patient is holding a position or maintaining a posture (e.g. maintaining the cup of coffee; “postural” tremor), or while a limb is reaching a position or a particular point in space (e.g. put a key in the door lock; “kinetic” tremor), or while the affected part of the body is at rest (e.g. sitting relaxed on a sofa or just walking without holding anything in the hand; “resting” tremor). A specific kind of tremor is caused by a specific dysfunction in one or more node of the motor circuit. A PD patient could be affected by various kinds of tremors. However, the tremor at rest is the hallmark of this disease. The resting tremor has been called several pictorial names (due to its presentation) such as a “pill rolling” or “counting coins” tremor. It has a low frequency (3 to 5 Hertz) compared to other tremors and breaks out or tends to get worse with stressful situations, low temperatures, and mental processes such as calculations. Of note, 30-40% of PD patients do not experience resting tremor, so being unaffected by tremor does not mean they have a different disease than PD. Anti-PD medications that globally relieve all cardinal symptoms are not always effective on tremor and physicians could adopt other drugs (e.g. benzodiazepine, beta blockers) or surgery to treat tremor.

Bradykinesia has a Greek etymology and literally means slowness of movement. Parkinson’s disease patients have difficulties in starting, maintaining and stopping an automated movement such as alternating arm swings while walking. Fine voluntary movements are coarse and executed slowly; repeated alternating movements, such as finger tapping progressively lose amplitude as the motor task is performed.

A patient could complain of hypokinesia (reduced) or akinesia (absence of movement) in several aspects of their life. A good example of akinesia is the difficulty in rotating into the bed during the nighttime (i.e. when anti-PD drugs level in blood is generally lower). Nowadays it is rarely seen, but patients could also voluntarily reach a specific position and acquire that fixed posture being unable to automatically get back to the previous one.

Parkinsonian face is hypokinetic. Consequently, the facial mimic is poor, and the face exhibits various grades of hypomimia. This begins as reduced blink rate and worsens with the presence of fixed postures of the lower face. 

Micrographia is a typical result of PD symptoms on an acquired semi-automated fine skill movement such as the handwriting. Micrographia is also one of the first PD complaints: writing becomes smaller or even unreadable.

The quality of global movements gets worse in time in terms of pace and rhythm, but also in coordination (adiadochokinesia, inhability of performing rapid alternating movement). The voice could become soft and the reduction in swallowing frequency leads to hypersalivation.

Parkinson’s disease patients often suffer from muscle stiffness. Rigidity involves flexor muscles, in particular. In idiopathic PD, this kind of stiffness follows a specific pattern due to the degeneration of mesencephalic neurons. The trunk and limbs are flexed, and the latter are adducted, resulting in typical PD postures. Limb and neck rigidity are measured by the neurologist as the resistance that muscles provide against a passive movement of two limb segments (or the neck) around the shared joint. Such resistance presents in a “plastic” way. The examiner sensation may feel “as if he is trying to bend lead pipe”. In their routine life, patients manifest their stiffness with the acquisition of preferential involuntary rigid postures, deformities and pain.

Parkinson’s disease could frequently present other motor features that are not specific for the disease. These frequently include dystonia and myoclonus. Apraxia could also be part of the motor disorder however it is not properly a motor phenomenon, but a cognitive symptom. Dystonia is determined as a sustained involuntary co-contraction of agonist and antagonist muscles that could induce a twisting posture to a part, or a segment or multiple parts of the body. Various postural PD features are caused by dystonia, such as anterocollis or trunk bending, but L-DOPA could also lead to sustained altered muscle contraction. Foot dystonia with foot inversion is typical of the wearing off period or in the early morning. This is generally unilateral, featuring the side of onset of the disease. Blepharospasm (paroxysmal involuntary sustained bilateral contraction of the orbicularis oculi) could present, less frequently, and during the wearing off time. Myoclonus is a very brief jerky involuntary movement. It frequently characterizes atypical parkinsonisms (e.g. multiple system atrophy, cortico-basal syndrome) but could be evoked by L-DOPA. It is common that a patient starting L-DOPA therapy realizes the appearance of sporadic, brisk “whole body” jerks. In this case, it is of benign origin and not leading to any kind of disability.

Camptocormia and reduced stride length are the hallmark of parkinsonian posture and gait respectively. The camptocormia consists in the forward trunk bending. This is frequently associated with the lateral bending that is generally directed to the opposite side respective to the most involved one. The lateral flexion assumes a particularly severe entity in the so called “Pisa” syndrome: a postural deformity caused by a dystonic contraction with a side bending and a mild rotation of the trunk on the sagittal plain. This could cause severe disability and significantly impair patient gait scheme. In general, parkinsonian patients present an increased basal tone of flexor muscles leading to neck in addition to trunk flexion, limb flexion, and adduction. The parkinsonian gait reflects the posture and is characterized by reduced stride length and “festination” (typical parkinsonian gait characterized by fast repeated short strides).

The other unique parkinsonian gait feature is “freezing”. It is not specific for PD, since it could present also in atypical parkinsonism (e.g. a progressive supranuclear palsy subtype). Freezing is a sudden gait akinesia and manifests with the patient’s feet suddenly “freezing” on the floor. Freezing pathogenesis involves both motor and cognitive neuronal networks and it is not a simple hypodopaminergic phenomenon. Freezing could affect all movements, even speech (resembling stuttering). Freezing of gait, however, specifically occurs while walking and is related to the gait motor program. Sensory cues (visual or auditory) could help the patient in relieving freezing episodes since they help the patient in activating other compensatory neuronal pathways (e.g. stepping or…dancing!). Cognitive processes, especially executive functions can affect gait, and cognitive tasks such as dual task can precipitate gait troubles. Leg movements and posture are highly integrated in generating a protective postural reflex. The human body reacts to a dangerous perturbation status with a reflex and eventually with a voluntary act. Reflexes are quick and aim to protect the body from potential damages. Balance perturbations triggering a postural reflex can be tested by the neurologist with the “pull test.” This consists of pulling the patient backward and evaluating the postural response in maintaining the correct balance. This is demonstrated by the patient eventually taking a step backwards to break a fall. Postural reflex and balance are also necessary to perform tasks such as standing from a chair. This is one of the main complaints of PD patients. Many tend to fall backward on the chair and need help to gain the standing position.

Voice, face expressions, repeated alternating movements of the four limbs, passive movements around joints, rest position or forced posture maintenance, raising from a chair, walking, and pull test are examined in the Unified Parkinson’s Disease Rating Scale (UPDRS) to test PD bradykinesia, rigidity, tremor, posture and gait. Also, turning while walking or passing through doors or narrow spaces should be examined to test freezing and which side is more affected by the freezing phenomenon. The unilateral, bilateral, and axial involvement with or without gait/standing abilities are reassumed in the Hoehn and Yahr (and modified Hoehn and Yahr) score, the most reliable validated disease progression scale.

Take home messages:

From impaired movement to falls – motor and non-motor contributors.

Parkinson’s disease is a complex condition which directly involves multiple neurological functions (e.g. movement, senses and cognition) and indirectly affects the locomotor system. The autonomic nervous system is greatly impaired by the disease, and a large part of the PD “non-motor” symptoms are derived by an autonomic dysfunction. Among non-motor PD features, it is worthy to acknowledge orthostatic hypotension. This is caused by the autonomic failure in regulating arterial blood pressure and cardiac frequency in response to postural changes. Another frequent change is the urinary incontinence and nocturia, which greatly impairs patient quality of living.

Motor and non-motor PD features determine a risk of falling (PD-related risk factors). Up to 90% of PD patients fall at least once in their life, with up to 65% experiencing recurrences. Gait and balance issues are the main determinants of falls while non-motor complaints could significantly contribute to generate a fall or a contingent situation with a high falling risk. Aging itself may expose patients to fall risk due to other comorbidities (mainly cardiovascular, locomotor, drug related) (PD-unrelated risk factors). Moreover, it is also worthy to understand that the PD population is exposed to multidrug therapy and such drugs are generally highly active on the cardiovascular and neurological systems. For instance, L-DOPA (the gold standard in PD pharmacotherapy) could worsen orthostatic hypotension such as alpha-blockers (substances that are commonly adopted for the treatment of prostate hypertrophy).

Falls are dramatic events that can profoundly mark patient life as they can lead to severe injuries (e.g. fractures, bleedings) and hospitalization. The effect of a single fall on quality of life and survival can be very significant and we know that PD patients are exposed to high fall and fall recurrences risk.

Preventing falls is a multidisciplinary intervention that must be tailored to patient needs.

A main target is to identify fallers and estimate fall risk. Various questionnaires are available to investigate previous falls and fall risk. Clinical scales can be adopted to quantify and monitor patient gait and balance. Patients should always be tested for cognitive function by an experienced examiner since mild executive dysfunction could have a significant impact on outcomes. The intervention should be implemented based on individual patient medical factors and disease features to ameliorate patient lifestyle and implement physical activity and rehabilitation.

Physical therapy and rehabilitation should be focused on PD features that integrate posture, gait, and balance exercises along with cognitive reinforcements. If possible, the caregiver should be involved in training in order to implement patient compliance and patient education.

Other than anti-PD therapy, no pharmacological agents have been produced to act specifically against falls. Some pharmacological trials have been conducted and benefits have been realized in targeting cognitive function and the autonomic contribution on falls. However, the best available intervention implements physical therapy, occupational therapy, and other entertaining activities (dances, martial arts or sports) that primarily train balance and limb mobility in a non-traumatic way. Finally, once a faller is identified and the best preventive strategy is predisposed, the health care provider should act on the patient perceived risk of falling and the consequent “fear of falling” which could greatly impair patient autonomy and lead to immobility and its consequences (i.e. reduced muscle weakness and gait skills).

Take home messages:

More fall facts

We certainly learned a lot from Dr. Marano about movement and falls in relation to Parkinson’s. Now, let’s look at additional information.

Fallers are people who fall:

Once a person falls, they enter the “faller” category and are considered a faller.

Idiopathic fallers:

These are people who fall for no apparent reason.

Depression and falls / Falls and depression:

In a January 2017 interview with neurologist, Dr. Alfonso Fasano, we discuss depression and falling in the Parkinson’s population. Here’s a question to ponder; do falls cause depression or does depression cause falls? As Dr. Fasano states in our interview, it’s much like the chicken and the egg. Which came first? It is reasonable to surmise that they exacerbate each other. Watch the full interview at the book support website:

Falls and awareness or recognition of fall risk:

Figure 2.1 represents a “Fall Awareness Spectrum.” This is a modified version of a similar chart you’ll see in the interview (listed above) with Dr. Alfonso Fasano.

NOTE: The Activities-specific Balance Confidence (ABC) Scale is a 16 item, self-administered-assessment. Participants rate their confidence in balance in activities of daily living. A score of 0 equals no confidence. A score of 100% equals total confidence.

** See Assessments chapter for and example and download instructions.

Figure 2.1

Cognitive decline often accompanies Parkinson’s and can increase the risk of falling. (Josefa M. Domingos, 2015)

Once a person falls and enters the faller category, their likelihood of falling increases greatly.

We want to avoid the first fall. Intervention strategies described later in this book can help to put off that first fall further into the future, or hopefully to avoid falling altogether.

It’s true. A single fall CAN be deadly. Imagine falling backwards and hitting your head on a sharp or blunt object. This can lead to an instant death.

If the fall doesn’t kill the person, complications from a fall may lead to death. All to often, you’ll hear about a person with PD who falls and ends up in the hospital (much like the study cited in the beginning of this chapter). With breathing issues being a major concern and cause of death for people with PD, pneumonia may enter the picture and lead to death.

Multitasking or dual tasking may become a challenge for the person with PD. With cognitive decline often entering the picture, the focus on movement may be compromised when performing another task simultaneously. This increases fall risk. (Linlin Gao, 2017)

The fear of falling increases fall risk and can lead to more falls. (Allan L. Adkin PhD James S. Frank PhD Mandar S. Jog MD, 2003)

Diminished dopamine production along with cognitive decline will often lead to delayed reaction time. Additionally, delayed reaction time is often related to age and increases risk of falling.

Lack of dopamine in the retina can cause a multitude of visual disturbances and increase risk of falling. (Carlijn D.J.M. Borm, 2019)

Delusions and hallucinations can be debilitating for anyone. Complications from Parkinson’s disease pathology can increase likelihood of experiencing these. For example, a person with PD is walking and sees something or someone that isn’t there. Depending upon what is happening in the hallucination, fall risk may increase. In my travels, I have met many people who experience delusions and as a result, have experienced a fall. Factors have included; trying to move out of the way of the object or person who isn’t there, stepping and tripping over an object that isn’t there, etc.


Falls are the number one concern for the person with Parkinson’s. In later chapters, we will discuss strategies and training concepts to help improve mobility, balance, stability, and to reduce fall risk and falls.

This is a summary list of a few factors that often trigger falls:

  • (Huh YE1, 2016)

Summary sources

(Huh YE1, 2016)

(Gray & Hildebrand, 2000)

(Aaron Kucinskia, 2015)

(Rudzińska M, 2013)